I am a neuropsychiatrist, epileptologist and electroencephalographer.
My address is-

DR P K Gupta.
MBBS (Hons), MD (Psych. Med)
61/5 Gandhi Road, Dehradun, UK,
India-248001
Ph- 91 135 2621343
Mo 9837425545
e mail dr.pkgupta@yahoo.com, dr.pkgupta@gmail.com
dr.pkgupta@hotmail.com
web site
http://www.deemagclinic.com
EDUCATION:
MBBS from University of Agra, (September 1979 to 1985)
(MBBS with Honours in ENT)
MD from University of Agra, India (August 1987-Aug 1989)
(Doctor of medicine in Psychiatry Agra University, degree earned in Aug 1989)
EXPERIENCE:
Internship from S N Medical college, Agra; and Doon Hospital Dehradun, India.
House physician at Dept of Medicine, Medical college, Agra, from 1986-1987
Resident in psychiatry from 1987-1989
Senior resident in psychiatry at SGRR Medical College, Patel Nagar, Dehradun India
in charge of inpatient and outpatient care in the above hospitals
PROFESSIONAL EXPERIENCE
35 years of experience in neuropsychiatry, epileptology and electroencephalography.
PROFESSIONAL AFFILIATIONS
Life Fellow- Indian Psychiatric Society
Member for life- Association of Physicians of India
Member – Indian Medical Association
Positions Held-
Honorary General Secretary Association of Physicians of India and President Elect Association of Physicians of India, Dehradun Branch.
Participated in more than 20 international conferences including conference of world psychiatric Association, Egypt, World Conference on Biological Psychiatry, Prague, American Geriatric Society meet, Washington, USA, and Conference of Neuropsychopharmacology, Stockholm, and meets organized by Kuoni academy (American academy of continued medical education).
Awards/ Honours received
medallist for leprosy eradication with vaccine (1984)
Name on School honours board for topping ICSE.
Honours in ENT MBBS final year 1985.
Worked as Consultant/Advisor in clinical neuropsychopharmacology to Intas, Torrent, Abbot India etc at various times

“Macbeth: How does your patient, doctor?

Doctor: Not so sick, my lord, as she is troubled with thick-coming fancies that keep her from rest.

Macbeth: Cure her of that! Canst thou not minister to a mind diseased, pluck from the memory a rooted sorrow, raze out the written troubles of the brain, and with some sweet oblivious antidote cleanse the stuffed bosom of that perilous stuff which weighs upon her heart.

Doctor: Therein the patient must minister to himself.”

― William Shakespeare, Macbeth

Contents
What are the general issues concerning neuro-psychiatry? 5
What is psychiatry? 6
What is anti-psychiatry? 6
What is history of psychiatry? 7
What is psychoanalysis? 7
What is Freudian psychoanalysis? 7
What is history of psychoanalysis? 8
What is hypnotherapy, or hypnotism? 8
What is the difference between psychiatry and neuropsychiatry? 8
What is the difference between neuropsychiatry and neuropsychology? 8
What is the difference between a psychiatrist and a neurologist? 8
When should a person go to a psychiatrist or a neurologist? 8
What is the difference between psychology and psychiatry? 9
What is hysteria? 9
What is intelligence? 9
What is emotional intelligence? 9
How can you develop EQ? 10
What is normal behaviour? 10
What is abnormal behaviour? 10
What is brain? 10
How is brain structure organised? 10
What are the primary functions of the brain? 11
How does ‘brain released hormones’ cause psychiatric disorders? 11
What is the stress hormone called? 11
What makes up the limbic system? 11
What are parts of the limbic system? 11
What does the limbic system control? 12
What is the main function of the limbic system? 12
What is the limbic system of the brain responsible for? 12
How does the limbic system work? 12
What is thalamus? 12
Is the hypothalamus part of the limbic system? 12
Is the amygdala in the limbic system? 13
How to calm down the amygdala? 13
Where is the seat of origin of normal or abnormal behaviour in humans? 13
What is a receptor? 13
What do receptors do? 13
What are the two types of neuron receptors? 13
What are cellular receptors? 13
What are intracellular receptors? 13
What are the receptors on the cell membrane? 14
What are receptor proteins responsible for? 14
What are receptor molecules? 14
What are types of receptors in brief? 14
What are different types of opiate receptors? 15
What are the categories of neurotransmitter receptor? 16
What is anatomy of neurotransmitter receptors? 16
What are types of neurotransmitter receptors? 17
What is catecholamine? 17
What is an agonist? 18
What are examples of agonist and antagonist drugs? 19
What is receptor agonist? 19
Is amphetamine an agonist or antagonist? 19
What are the examples of serotonin antagonists? 19
What is an example of an inverse agonist? 19
What is the difference between alpha and beta receptors? 19
What is the biochemistry and pharmacology of receptors? 19
What is dopamine system? 20
What is the mesolimbic dopaminergic pathway? 20
What is the function of dopamine? 20
How does dopamine affect mood? 20
How does dopamine cause depression? 20
What happens when dopamine is low in the brain? 20
What happens when dopamine is high in the brain? 20
What are symptoms of low Serotonin Levels? 20
What are symptoms of high serotonin levels in brain? 20
What is prostaglandin system? 21
What do endocannabinoid receptors do? 21
Does the human body produce cannabinoids? 21
How do opioids activate receptors? 21
What is the function of serotonin hormone? 21
What is the difference between adrenaline and noradrenaline? 21
What is norepinephrine responsible for? 21
What is the difference between a Neurotransmitters and a hormone? 22
What is pathology of receptors in various diseases? 22
What Is A Neurotransmitter? 22
What are neuromodulators? 23
What is the difference between a neurotransmitter and a neuromodulator? 24
What are some examples of neuromodulators? 24
Why are receptors and neurotransmitters so important for psychiatry? 24
What are components of mental state examination of a patient? 24
What are disorders of behaviour? 24
What is disorder of thought? 24
Which disorder shows disorder of thought? 24
What is disorder of mood? 25
Which disorder shows disorder of mood? 25
Which disorder shows disorder of memory? 25
What disorders result in poor or total loss of insight? 25
What are disorders of judgement? 25
Are disorders of behaviour, thinking, mood, insight and judgment along with other symptoms exclusive to certain diseases? 25
What is abnormal behaviour? 25
What is the difference between a behavioural disorder and a mental disorder? 26
What are the most common disruptive behaviours? 26
What are most Common Mental Illnesses and Disorders? 26
What is Mental Retardation? 26
What are the levels of mental retardation? 26
What are the causes of mental retardation? 26
What are the different types of mental retardation? 26
What is the most common genetic cause of mental retardation? 26
What are Down syndrome symptoms? 27
Is mental retardation as illness is considered a disability? 27
What are the different types of behavioural problems in children? 27
What is oppositional defiant disorder (ODD)? 27
What are the symptoms of conduct disorder? 27
What is autism? 27
What is autism syndrome? 27
What is the highest level of autism? 27
What are some signs of ADHD? 27
What are signs of mild Aspergers syndrome? 28
Did Alan Turing have Asperger’s syndrome? 28
What is Antisocial Personality Disorder? 28
What is Borderline Personality Disorder? 28
What is the definition of perversion? 28
What can we do about perversions? 28
What is anxiety? 29
How did anxiety evolve over the millenniums? 29
What is Anxiety Disorder? (GAD). 29
What are Phobias? 29
What is Obsessive Compulsive Disorder? 29
What are Panic Attacks? 29
What is post-traumatic stress disorder? 30
What is Schizophrenia? 30
What is evolution of psychosis? 30
What is schizophreniform psychosis? 30
What is schizoaffective psychosis? 30
What is brief psychosis? 30
What is Bipolar Disorder? 30
What is Depression? 31
What is the evolution of depression? 31
What is mania? 31
What is evolution of mania? 31
What is Eating Disorders? 31
What does amnesia tell us about memory? 31
How do you get amnesia? 31
What to do for amnesia? 32
How is amnesia diagnosed? 32
What are signs of dissociative identity disorder? 32
What is delirium? 32
What is delirium tremens (DT)? 32
What causes DT’s in alcoholics? 32
What causes delirium after surgery? 32
What is dementia? 32
How is delirium different than dementia? 33
What is addiction? 33
What is the most common addiction? 33
What is the most addictive drug? 33
What is alcohol addiction? 33
What is the difference between dependence and alcohol abuse? 33
What is pain? 33
What is evolutionary aspect of pain? 33
What is chronic fatigue syndrome? 33
Is chronic fatigue and fibromyalgia the same thing? 34
What is chronic pain? 34
What is headache? 34
What is the most common type of headache? 34
What is the difference between migraine and tension headache? 34
What is epilepsy? 34
How would you know if you have epilepsy? 34
What are the main types of seizures? 35
What are tonic clonic seizures? 35
What is a tonic seizure? 35
How long does a tonic seizure last? 35
What are myoclonic seizures? 35
What causes juvenile myoclonic epilepsy? 35
WHAT IS benign childhood epilepsy? 35
What is absence seizure? 35
What is a simple partial seizure? 36
What is complex partial seizure? 36
What are the signs of a partial seizure? 36
What is frontal lobe related seizures? 36
What are subtypes of frontal lobe seizures? 36
What is temporal lobe related seizure? 37
What are subtypes of temporal lobe related seizures? 38
What is parietal lobe related seizures? 38
What are subtypes of parietal lobe related seizures? 39
What is occipital lobe related seizures? 39
What are subtypes of occipital lobe related seizure? 40
What are pre – seizure symptoms? 40
What are the most common symptoms of mild seizures? 40
What is pre – seizure behaviour? 40
What medicines cause seizures? 40
What is aging? 40
What is it like living with mental disorders for patients, relatives and caregivers? 41
What does it mean to live with anxiety and depression? 41
What it’s like living with depression? 41
How to live with obsessive compulsive neurotic patient? 41
How to live with bipolar disorder? 42
How to support a loved one with schizophrenia? 42
How to live with personality disorder? 42
How to live with an alcoholic? 43
When should a person be considered an alcoholic? 43
How must a relative trying to deal with an addict, act? 44
What treatment are available for an addict? 45
What is biofeedback? 45
What can be the aetiology of anxiety and its management? 45
What medical disorders can directly cause anxiety? 46
What can be the result of anxiety? 46
How is anxiety treated? 46
What is the management of OCD? 46
How is panic disorder treated? 47
What is the treatment of phobias? 47
What is the treatment for Social anxiety disorder (social phobia)? 47
What is the treatment for specific phobias? 47
What is the treatment for Agoraphobia? 48
What is the drug treatment of depression? 48
How to manage psychotic symptoms? 48
What are additional Therapies for Depression? 48
How is Treatment-Resistant Depression managed? 49
What is a medical ECT? 49
How effective is ECT? 50
How does electroconvulsive therapy (ECT) work? 50
What are indications for ECT? 50
What are the contraindications of ECT therapy? 50
What are the long-term effects of ECT? 50
What are the immediate negative side effects of ECT? 50
What is the success rate of ECT? 50
What is Paediatric Depression? 50
What are the dangers in treating paediatrics patients for depression? 51
How do you treat resistant depression in paediatric population? 51
Is there a relationship between antidepressants and suicidality in youths? 51
So, what are the recommendations when treating paediatric depression? 52
What tests must be done before treating paediatric depression with TCAs? 52
How should depression during Pregnancy be treated? 52
What are the risks to infants whose mothers were on antidepressants? 53
What is postpartum Depression? 53
How to go about antidepressants and Breast-feeding? 53
Are special precautions necessary while using antidepressants in the Elderly? 54
When to hospitalize in depression? 54
What is fatal insomnia, (FI)? 55
What Complications can arise during treatment for Depression with SSRIs? 55
What is mania? 56
What are the physical signs of mania? 57
What can cause mania? 57
What are signs of mixed mania in bipolar disorder? 57
What medications trigger mania? 57
How to treat bipolar disorder in pregnancy? 57
What are the symptoms of hypomania? 57
What is the difference between mania and hypomania? 57
What drugs are used for Mania? 57
After how many episodes of bipolar I can be diagnosed? 58
What is bipolar ll. 58
What is alcohol withdrawal? 58
What is the cause? 58
How is it diagnosed? 58
How is it treated? 58
How long will the effects last? 59
How can I take care of myself? 59
What is amnesia? 60
What happens in the brain in amnesia? 60
What are the causes of amnesia? 61
How do you diagnose amnesia? 61
How do you manage amnesia? 62
What is Transient Global Amnesia (TGA)? 62
What are the causes of TGA? 62
What are the Symptoms and Signs of TGA? 62
What is Asperger syndrome and its management? 63
What is the cause of Asperger syndrome? 63
What are the symptoms Asperger syndrome? 63
How is Asperger syndrome diagnosed? 64
How is Asperger syndrome treated? 64
How long will the effects of Asperger syndrome last? 65
What are behavioural emergencies (BE)? 65
What are the causes of behavioural emergencies? 65
How are behavioural emergencies evaluated? 65
How must BE patients be approached? 66
How must the patients of behavioural emergency be restrained? 67
What can be the complications of restraints? 67
What is the treatment of BE? 68
What are types of BHS? 68
What are brief psychotic disorders and how to manage them? 69
What is Catatonia And its management? 69
What is cognitive therapy? 69
What is the theory behind this therapy? 69
How do your beliefs affect your thoughts? 69
What are the steps in cognitive therapy? 70
What is psychotherapy and how does it work? 70
What is the difference between psychotherapy and therapy? 70
What are the types of psychology therapy? 70
What are the different types of mental therapy? 70
How is psychotherapy used to treat depression? 70
How effective is Gestalt therapy? 71
What are the different types of counselling approaches? 71
What are the personality traits of a physical therapist? 71
What is placebo? 71
Why do placebos work? 71
What are the advantages of placebos? 71
What is the purpose of a placebo? 71
How effective are placebos? 71
What is a Nocebo? 71
What is the difference between placebo and nocebo? 72
What is placebo surgery? 72
What is a placebo procedure? 72
What is a placebo investigation?? 72
What is the process of meditation? 72
What is mindfulness? 72
What is the difference between meditation and mindfulness? 72
Why is meditation beneficial? 72
What are the benefits of mindfulness? 73
What are the best meditation techniques? 73
What is neuroplasticity and how does it help? 73
What are tremors? 73
What are essential tremors? 74
What are Parkinson’s tremors? 75
What are enhanced physiological tremors? 75
What are drug and metabolite induced tremors? 75
What are cerebellar tremors? 75
What are psychogenic tremors? 75
What are tremors in children? 76
What is the treatment of tremors? 76
What is delirium? 76
What are other commonly associated features of delirium? 76
What are subtypes of delirium? 77
How must delirium be managed? 77
What is the prognosis of delirium? 77
What is dementia, and its types? 78
What are the types of dementia? 78
What are the symptoms of dementia? 78
What happens in early stage of dementia? 79
What happens in intermediate stage of dementia? 79
What happens in late stage of dementia? 79
What is the differential diagnosis of dementia? 80
What tests must be employed to screen dementia? 80
What measures must the caregivers take in cases of dementia? 81
What is the treatment of dementia? 82
How must be the caregivers in family be assisted in dementia? 82
What are the legal issues in dementia? 83
What is Alzheimer’s Disease? 83
What is the pathology of Alzheimer’s dementia? 83
What are the Symptoms and Signs of Alzheimer’s dementia? 83
What is the difference between Alzheimer’s Disease and Lewy Body Dementia? 84
What is Vascular Dementia? 87
What are the types of vascular dementia? 87
What are the Symptoms and Signs of vascular dementia? 88
How do you diagnose vascular dementia? 88
What is the prognosis of vascular dementia? 88
What is the treatment of vascular dementia? 88
What is Lewy Body (LB) Dementia? 89
What is pathology of LB dementia? 89
What are the clinical features of LB dementia? 89
How do you diagnose LB dementia? 90
What is the treatment of LB dementia? 90
What is the prognosis of LB dementia? 91
What is HIV-Associated Dementia? 91
What is pathology of HIV-Associated Dementia? 92
What are Symptoms and Signs of HIV-Associated Dementia? 92
How do you Diagnose HIV-Associated Dementia? 92
What is the prognosis of HIV-Associated Dementia? 92
What is the Treatment of HIV-Associated Dementia? 92
What is Frontotemporal (FTD)Dementia? 92
What is the pathology of FTD? 92
What are the clinical features of FTD? 93
How to Diagnose FTD? 94
What is the Prognosis of FTD? 94
What is the treatment of FTD? 94
What is Normal–Pressure Hydrocephalus (NPH)? 94
What are the Symptoms and Signs of NPH? 94
How to diagnose NPH? 94
What is the Treatment of NPH? 95
What is Behavioural variant Frontotemporal Dementia (bvFTD) and how to manage it? 95
What is Sundowning and how to manage it? 95
How about the problem of treatment of opioid addiction in Punjab with buprenorphine? 96
What about management of dystonia? 97
What are the causes of dystonia? 97
How to diagnose dystonia? 98
What is Erectile dysfunction (ED)? 99
What are types of ED? 99
What are causes of ED? 99
What are drugs causing ED? 100
How to do a Clinical evaluation of ED? 100
How is ED investigated? 100
What is the Treatment of ED? 100
What is drug dependence? 102
What is addiction? 102
What is drug abuse? 103
What is illicit drug use? 103
What is recreational drug use? 103
What are narcotics? 103
What is schedule of drugs? 103
What are the principals of treatments of Addiction in general? 104
What are usual symptoms of drug withdrawal? 105
How to treat cocaine addiction? 105
How to treat alcohol addiction? 105
How to treat nicotine addiction? 106
How to treat marijuana addiction? 107
How to treat opiate addiction? 107
How to treat heroin addiction? 107
What are the uses of naltrexone? 107
What is the genetic influence on addiction? 108
What is the prognosis of addictive disorders? 109
What are the causes of death in addiction? 109
What is hypoglycaemia? 109
What are the causes of hypoglycaemia? 109
What is the treatment of hypoglycaemia? 110
How to assess and treat hyponatremia? 110
What are the principal Causes of Hyponatremia? 110
What is Syndrome of Inappropriate ADH Secretion-a cause of hyponatremia? 112
What are the Symptoms and Signs of hyponatremia? 112
How to diagnose hyponatremia? 113
What is the Treatment of hyponatremia? 113
What is hypothyroidism? 114
What are types of hypothyroidism? 114
What are symptoms and signs of hypothyroidism? 114
How to Diagnose hypothyroidism? 115
What is the Treatment of hypothyroidism? 115
What is Subclinical Hypothyroidism? 116
How should subclinical hypothyroidism be treated? 116
What is Irritable bowel syndrome (IBS)? 116
What are Symptoms and Signs of IBS? 116
How Is IBS diagnosed? 117
What is the Treatment of IBS? 117
What is migraine in general? 118
What are Triggers of migraine? 119
What is Treatment of migraine? 119
What are the Types of migraine? 120
What is tension headache? 122
Who Gets tension headaches? 122
What Are the Symptoms? 122
What is the Treatment of chronic tension headache? 123
What are cluster headaches? 123
What is the treatment of chronic cluster headache? 123
What is the best treatment for acute cluster headaches? 123
Why Psychiatrists have a major role in headache treatment? 123
What are Physical disorders mimicking mental disorders? 124
What is faith healing? 125
What to do for tardive dyskinesia? 125
What to do for benzodiazepine addiction? 126
What is schizophrenia in general? 127
What is prevalence of schizophrenia? 127
What are the causes of schizophrenia? 128
What are the issues in treatment of schizophrenia? 128
What is rehabilitation in schizophrenia? 129
When to hospitalise in schizophrenia? 129
How to interpret violence among mentally ill patients? 129
What is substance-induced mood disorder (SIMD)? 129
What is the most common substance induced mood disorder? 130
What is the cause of substance induced mood disorder? 130
What are the symptoms of SIMD?? 130
How is SIMD diagnosed? 130
How is SIMD treated? 130
How long will the effects of SIMD last? 131
How can I take care of myself from SIMD? 131
What is chronic pain? 131
How to evaluate chronic pain? 131
How to treat chronic pain? 132
Are there some treatments for depression that are not antidepressants? 132
What is new about catatonia? 134
What is therapeutic recreation? 135
How to manage common sleep problems? 135
How to manage dystonia? 137
How to go about managing Somatoform Disorders? 138
What is cognitive therapy? 139
What is the theory behind cognitive therapy? 139
How do your beliefs affect your thoughts? 139
What are the steps in cognitive therapy? 139
What are types of suicidal behaviours? 139
What to do in case of suicidal patient? 140
What are self-Harming Behaviours? 141
Why do people self-harm? 142
How are self-harming behaviours (SHB)treated? 142
What is a psychological autopsy and how can it help? 142
What are the signs and symptoms of Parkinson’s disease? 142
What are the causes of Parkinson’s disease? 143
What is the difference between Parkinson’s dementia and Alzheimer’s dementia? 143
What are the end stages of Parkinson’s Disease? 143
What is the treatment of Parkinson’s disease? 143
What procedures can be used in treatment of Parkinson disease? 143
What are Indications for EEG in psychiatric practice? 144
What is alcohol withdrawal (AW)? 145
What is the cause of AW? 145
How is AW investigated? 145
How is AW treated? 145
How long will the effects of AW last? 146
What are psychoactive drugs? 146
What are psychobiotics? 148
What are the investigations in a case of seizures? 148
What is the Treatment is a case of seizure? 149
What is the status of Pregnancy and seizures? 150
What should be advise to the patients of epilepsy about Personal safety? 150
What is Seizure first aid? 150
Why seizures, epileptic or non-epileptic, are seen in psychiatry OPDs? 151
Are dying patients optimistic? 151
What is transcranial magnetic stimulation (TCMS)? 152
What is artificial intelligence (AI)? 152
How can AI be of use to the healthcare industry? 152
Do you believe AI can work with specialists to help them arrive at a diagnosis? 153
What was your research programme using machine to detect diabetic retinopathy? 153
Is there a scope for full-scale rollout of these models in the foreseeable future? 153
What is the future in psychiatry? 153

    वक्रतुण्ड महाकाय सूर्यकोटि समप्रभ ।
    निर्विघ्नं कुरु मे देव सर्वकार्येषु सर्वदा ॥



    Yaa Devi Sarva-Bhutessu Buddhi-Ruupenna Samsthitaa |
    Namas-Tasyai Namas-Tasyai Namas-Tasyai Namo Namah || 



        Q & A IN NEURO-PSYCHIATRY

What are the general issues concerning neuro-psychiatry?

None of the other medical speciality are as poorly understood and as stigmatized as the speciality of neuro-psychiatry (or psychiatry in short) is. Some people call it psychological medicine. Some think it is psychology. Others think that doctors of psychiatry do only counselling. Not only is it stigmatized but people’s movement like anti-psychiatry movement has tried to discredit whatever good will it has. Some people has gone to the extent of starting a movement called survivors of psychiatry movement to make it look like a practice of holocaust. Psychiatry has suffered silently from being a medical science to being regarded as non-medical science. Noteworthy it is, that till recently, many a psychiatric conference were held under the banner of scientific societies, even in the nineteenth century rather than under the proper place of medical science society. This happened largely due to the facts that initially little pharmacotherapy was known about psycho-pharmacotherapy. In their vain attempt to do some help elaborate theories were proposed, many of them as ill-conceived as Freudian sexuality-oriented to repressed desires ones or other more scientific ones, to make some meaning out of the psychiatric patient’s behaviour. They only added to the ridicule of psychiatry among conventional medical science and men.
Fortunately, the last century also saw some amazing discoveries like the discovery of molecules chlorpromazine and imipramine, which added just the right armamentarium in the arsenal of stigmatised psychiatrists to leave the embraces of pure science and go under the banner of medical sciences. Since then psychiatry has not looked back and has now reached to the point that it is considered a coveted speciality both among students and practitioners alike.
This book is not a text book, nor a review book but a random read for students preparing for their MD and MBBS exams in psychiatry and for busy psychiatry enthusiasts to freshen up some topics of interests.
Psychiatry is akin to behavioural sciences and therefore understanding and managing behaviour is the prime requisite of psychiatrists.
Psychiatry involves understanding and treating anxiety, from GAD to obsessive anxiety to phobias, depression, from endogenous to reactive; Schizophrenia, from schizophreniform disorder to catatonia; bipolar disorder; from dementia to amnesia, borderline personality disorder to passive aggressive personality disorder, from alcoholism to drug addiction and erectile dysfunction to perversions. Since most of the treatment and pharmacotherapy involves drugs which act through receptors in the human body, the receptors will be touched upon.
Hypothyroidism is very common, almost a daily occurrence in practice, hyponatremia is also common in patients of dementia and those taking certain drugs. Hypoglycaemia though rare is dramatic and medical emergency with psychiatric presentation. I was once called to the home of a pathologist whose father was going berserk. He was diabetic and responded to intravenous glucose. And Tremors! In psychiatry tremors are the most common findings.
Since psychiatry involves human behaviour, does it help to keep human behaviour into the confines of stereotypes, or does it impact history and culture to do so. Since many artists and great leaders have suffered or conversely gained from psychiatric illnesses, it seems that anti-psychiatry movement people may have a point. Or do they?
Not only pharmacotherapy but psychotherapy is said to bring about a potent change in our perceptions and needs mention. If psychotherapy can bring about some desired results, does placebo helps. Does nocebo matters. Can faith healing help. Can meditation or mindfulness help. Can prayers help. Let us see.

So, let us start from basics to diagnosis and management to what future may hold for psychiatry.
What is psychiatry?
Psychiatry is the medical specialty devoted to the diagnosis, prevention, and treatment of mental disorders. These include various maladaptation related to mood, behaviour, cognition, and perceptions.
Ancient Egyptians when mummifying their kings’ body, used to insert a spatula through the nostrils and breaking the cribriform plate, scoop out the brain and discard it, while preserving all the other organs. That goes to show how little importance was attributed to brain. Such attitudes persisted even till modern times when heart was considered the seat of human body.
Lately however things have changed a bit. Let’s see how?
What is anti-psychiatry?
Anti-psychiatry is the view that psychiatric treatments are often more damaging than helpful to patients, and a movement opposing such treatments for almost two centuries. It considers psychiatry a coercive instrument of oppression due to an unequal power relationship between doctor and patient, and a highly subjective diagnostic process.
Anti-psychiatry originates in an objection to what some view as dangerous treatments. Examples include electroconvulsive therapy, insulin shock therapy, and brain lobotomy. An immediate concern is the significant increase in prescribing psychiatric drugs for children. There were also concerns about mental health institutions. All modern societies permit involuntary treatment or involuntary commitment of mental patients.
Anti-psychiatry group is active and working. Such view is more common in America than elsewhere. Recently in an annual meet of American Psychiatric society, a huge demonstration of anti-psychiatry group took place opposite the venue of the meet.
Things have gone a bit too ludicrous with movements like survivors of psychiatry and mad in America.

What is history of psychiatry?
Specialty in psychiatry can be traced in Ancient India. The oldest texts on psychiatry include the ayurvedic text, Charaka Samhita. Some of the first hospitals for curing mental illness were established during the 3rd century BCE.
During the 5th century BCE, mental disorders, especially those with psychotic traits, were considered supernatural in origin, a view which existed throughout ancient Greece and Rome. The beginning of psychiatry as a medical specialty is dated to the middle of the nineteenth century, although one may trace its germination to the late eighteenth century.
Specialist hospitals were built in medieval Europe from the 13th century to treat mental disorders but were utilized only as custodial institutions and did not provide any type of treatment.
The modern era of providing care for the mentally ill began in the early 19th century with a large state-led effort. Public mental asylums were established in Britain after the passing of the 1808 County Asylums Act. This empowered magistrates to build rate-supported asylums in every county to house the many ‘pauper lunatics’. Nine counties first applied, and the first public asylum opened in 1812 in Nottinghamshire. Parliamentary Committees were established to investigate abuses at private madhouses like Bethlem Hospital – its officers were eventually dismissed and national attention was focused on the routine use of bars, chains and handcuffs and the filthy conditions the inmates lived in. However, it was not until 1828 that the newly appointed Commissioners in Lunacy were empowered to license and supervise private asylums.
Looks familiar situation to our ‘Erwadi’ incident and subsequent enforcement of mental health act in India. Here in Erwadi, in south India, a group of chained mental patients were burnt to death in an accidental fire. The Supreme court intervened, resulting in implementation of mental health act, though passed much earlier in 1987, to ensure the rights and privileges of mental patients and regulating the practice of mental health care in India.
What is psychoanalysis?
It is a system of psychological theory and therapy which aims to treat mental disorders by investigating the interaction of conscious and unconscious elements in the mind and bringing repressed fears and conflicts into the conscious mind by techniques such as dream interpretation and free association.
Of course, it dated to the period when no drug treatment was prevalent in psychiatry and therefore, understandable.
What is Freudian psychoanalysis?
Psychoanalytic theory was developed by Sigmund Freud (1856-1939). Psychoanalytic theory revolutionized the understanding of mental life and human behaviour. Freud’s theories helped in understanding early development of sexuality and mental functioning in the infant and adult psychological illnesses.
Most of the mental disorders were said to be the results of repressed sexual desire. The Neo-Freudian, developed it as a cult and took it to ludicrous levels.
What is history of psychoanalysis?
The basic postulate of psychoanalysis, the concept of a dynamic unconscious mind, grew out of Freud’s observation that the physical symptoms of hysterical patients tended to disappear after apparently forgotten material was made conscious (see hysteria). He saw the unconscious as an area of great psychic activity, which influenced personality and behaviour but operated with material not subject to recall through normal mental processes. Freud postulated that there were a number of defence mechanisms —including repression, reaction-formation, regression, displacement, and rationalization—that protect the conscious mind from those aspects of reality it may find difficult to accept. The major defence mechanism is repression, which induced a “forgetfulness” for harsh realities. Observing the relationship between psychoneurosis and repressed memories, Freud made conscious recognition of these forgotten experiences the foundation of psychoanalytic therapy. Hypnosis was the earliest method used to probe the unconscious, but due to its limited effectiveness, it was soon discarded in favour of free association, which Freud interpreted as symbolic wish fulfilments, were considered a primary key to the unconscious, and their analysis was an important part of Freudian therapy.
What is hypnotherapy, or hypnotism?
Hypnosis — or hypnotherapy — uses guided relaxation, intense concentration, and focused attention to achieve a heightened state of awareness that is sometimes called a trance. The person’s attention is so focused while in this state that anything going on around the person is temporarily blocked out or ignored.
It was attempted by focusing on a moving pendulum and was thought to give good results in hysterical conditions.
It stands mostly discarded now.
What is the difference between psychiatry and neuropsychiatry?
The differences between psychiatry and neuropsychiatry have continued to evolve over the years. The short answer is that while both psychiatrists and neuropsychiatrists are doctors trained to treat mental health issues, they both follow a different focus.
What is the difference between neuropsychiatry and neuropsychology?
As nouns the difference between neuropsychiatry and neuropsychology. is that neuropsychiatry is (medicine) the branch of medicine dealing with disorders that have both neurological and psychiatric features while neuropsychology is a branch of neurology and of clinical psychology that investigates the physiological basis of psychological processes.
What is the difference between a psychiatrist and a neurologist?
Neurologists have focused objectively on organic structural nervous system pathology, especially of the brain, whereas psychiatrists have laid claim to the functional illnesses of the brain.
When should a person go to a psychiatrist or a neurologist?
The brain is the most complicated, yet least understood organ in the body; and central, as it is ultimately in charge of our bodies, including both voluntary and involuntary functions. This analogy, although imperfect, may help in understanding the difference: Psychiatrists focus on and treat symptoms originating in the brain that lead to abnormal voluntary functions, i.e.; human behaviours, whereas neurologists focus on and treat symptoms originating in the brain that produce abnormal involuntary functions. In the case of depression, for example, the patient will present with voluntary (meaning that the patient technically has physical control, although they choose not to engage in these behaviours if healthy) symptoms, like social isolation, increased or decreased sleep or weight and stopping activities they once found enjoyable. By contrast, a stroke patient will present with involuntary (meaning the patient could not physically stop these behaviours, because the body is in an “automatic” mode) symptoms, such as blurred vision, paralysis, headache, inability to communicate verbally and involuntary movements. However, because both disciplines deal with the brain/mind, the reality is that there is a tremendous overlap between the fields of psychiatry and neurology, and knowledge of both is essential to ensuring that all factors are considered in a diagnosis.
So, go to the neurologist if the symptoms are structural in nature, like stroke, go to a psychiatrist if the symptoms are functional in nature like depression or dementia.
What is the difference between psychology and psychiatry?
Psychology is the study of the mental processes and Behavior whereas psychiatry refers to the study of mental disorders. The main difference between the two fields is that while psychology adopts a broader approach to studying human life, psychiatry takes special notice on mental disorders, their diagnosis and treatment.
What is hysteria?
Hysteria an old-fashioned term for a psychological disorder characterized by conversion of psychological stress into physical symptoms (somatization) or a change in self-awareness (such as a fugue state or selective amnesia). The term has been replaced by somatisation disorders or conversion reaction.
It was more common in females. With the advent of modern psychopharmacology, hysterical reactions are being seen in lesser frequency.
What is intelligence?
Intelligence has been defined in many ways: the capacity for logic, understanding, self-awareness, learning, emotional knowledge, reasoning, planning, creativity, critical thinking, and problem-solving. More generally, it can be described as the ability to perceive or infer information, and to retain it as knowledge to be applied towards adaptive behaviours within an environment or context.
What is emotional intelligence?
It is the capacity to be aware of, control, and express one’s emotions, and to handle interpersonal relationships judiciously and empathetically.
The major components of emotional intelligence are personal competence and social competence. Developing emotional intelligence involves developing both personal competence and the social competence
What are the main components of Emotional Intelligence?
Self-awareness.: Recognize and understand your own moods and motivations…
Self-Regulation…
Internal Motivation…
Empathy…
What is emotional quotient? (EQ).
It is the level of a person’s emotional intelligence, often as represented by a score in a standardized test.
How can you develop EQ?
Pay attention to your emotional reactions to situations.
Introspect on why you respond the way you do.
Try to think of different ways to interpret harmful situations.
Find productive ways to cope with emotional stress if it remains.
Guidelines to develop social competence:
Pay attention to the emotions and behaviours of others.
Try to understand the behaviour of others by discussing it with third parties.
Identify the various ways to deal with situations.
Examine the effects of your actions.
What is normal behaviour?
Normality is a behaviour that can be normal for an individual (intrapersonal normality) when it is consistent with the most common behaviour for that person. Normal is also used to describe individual behaviour that conforms to the most common behaviour in society. It is in conformity with social norms.
What is abnormal behaviour?
There are four criteria mental health professionals use to help in the diagnosis of abnormal behaviour: statistic infrequency (statistical definition), disability or dysfunction (inability to function normally), personal distress (subjective discomfort), and social norm deviance.
What is brain?
It is an organ of soft nervous tissue contained in the skull of vertebrates, functioning as the coordinating centre of sensation and intellectual and nervous activity.
How is brain structure organised?
Brain structure is said to be like a grid. Just like Manhattan streets. Any disturbance in any part of brain is reflected in the corresponding part of the body accurately. Likewise, being a perceptive organ, any disturbance in particular part of brain at receptor level caused distinct symptoms. Frontal lobe disturbances causing personality problems, hippocampal disturbances causing memory problems, amygdala disturbance casing anger outbursts.
What are the primary functions of the brain?
Some of its main functions include processing sensory information, regulating blood pressure and breathing and releasing hormones.
How does ‘brain released hormones’ cause psychiatric disorders?
Sensory information is the domain of neurologists. Blood pressure regulation is the domain of cardiologist. Brain secretes a plethora of hormones. Hypothalamic disease may cause insufficient or inhibited signalling to the pituitary leading to deficiencies of one or more of the following hormones: thyroid-stimulating hormone, adrenocorticotropic hormone, beta-endorphin, luteinizing hormone, follicle-stimulating hormone, and melanocyte–stimulating hormone. Beta endorphin and TSH are important. Through TSH brain can modify the behaviour. Hypocretin neurons help regulate your sleep-wake cycles. These chemicals in your brain are at their highest levels when you’re awake. They naturally decrease during your normal bedtime. But when you have narcolepsy, hypocretin releases are low. This causes disruptions during the daytime, such as excessive sleepiness and fatigue. You may also tend to take more naps during the day. Reduced hypocretins are strongly linked to narcolepsy type This type of narcolepsy includes: disrupted sleep cycles, daytime fatigue, cataplexy (sudden loss of muscle control). Hypocretin losses can also affect other brain hormones, such as serotonin. This can cause sleep paralysis and hallucinations when you wake up. If you have type 2 narcolepsy, you may experience issues with sleep cycle regulation but don’t have issues with cataplexy. Melatonin is a hormone made naturally by your body. It is produced by the pineal gland in the brain but also found in other areas, such as the eyes, bone marrow and gut. It is often called the “sleep hormone,” as high levels can help you fall asleep. Melatonin maintains circadian rhythm. Low testosterone can produce erectile dysfunction, low libido, depression and fatigue. Insomnia hormones include estrogenic and testosterone. Oestrogen is a sleep-maintaining hormone. It is common to have an estrogenic deficiency in perimenopause and menopause and when your body is not producing enough natural estrogenic, your ability to get a full night’s sleep suffers as a result.
What is the stress hormone called?
Cortisol is often called the “stress hormone” because of its connection to the stress response, however, cortisol is much more than just a hormone released during stress.

What makes up the limbic system?
The limbic system was originally defined by Paul D. MacLean as a series of cortical structures surrounding the limit between the cerebral hemispheres and the brainstem: the border, or limbus, of the brain. These structures were known together as the limbic lobe. … The structures of the limbic system are involved in motivation, emotion, learning, and memory. Limbic system is very important in psychiatry.
What are parts of the limbic system?
The limbic system is a set of structures in the brain that deal with emotions and memory. It regulates autonomic or endocrine function in response to emotional stimuli and also is involved in reinforcing behaviour. Limbic System Structures are Amygdala: the almond-shaped mass of nuclei involved in emotional responses, hormonal secretions, and memory. The amygdala is responsible for fear conditioning or the associative learning process by which we learn to fear something. Cingulate Gyrus: a fold in the brain involved with sensory input concerning emotions and the regulation of aggressive Behavior. Fornix: an arching, band of white matter axons (nerve fibres) that connect the hippocampus to the hypothalamus. Hippocampus: a tiny nub that acts as a memory indexer – sending memories out to the appropriate part of the cerebral hemisphere for long-term storage and retrieving them when necessary. Hypothalamus: about the size of a pearl, this structure directs a multitude of important functions. It wakes you up in the morning and gets the adrenaline flowing. The hypothalamus is also an important emotional center, controlling the molecules that make you feel exhilarated, angry, or unhappy. Olfactory Cortex: receives sensory information from the olfactory bulb and is involved in the identification of odours. Thalamus: a large, dual lobed mass of Gray matter cells that relay sensory signals to and from the spinal cord and the cerebrum.
What does the limbic system control?
Because of the hypothalamus’s functions, the limbic system is directly in control of your “stress response” like crude pain perception, fear and emotions, and these key functions like Heart rate. Blood pressure. Breathing. Memory. Stress levels. Hormone balance.
What is the main function of the limbic system?
The limbic system is a group of related structures that help regulate emotion, memory, and certain aspects of movement. One of these structures, the hippocampus, is vital to the storage of recently acquired information — one of the brain’s most important functions.
What is the limbic system of the brain responsible for?
The limbic system (emotional motor system) is responsible for the experience and expression of emotion. It is located in the core of the brain and includes the amygdala, hippocampus and hypothalamus.
How does the limbic system work?
The limbic system represents the part of your brain devoted to the most basic survival structures that protect and regulate emotions and reactive states. Interconnecting pathways link the limbic system, located deep within your brain, to the hypothalamus, which controls thinking, behaviour and hormonal functions. Thus, basic emotional states like fear are directly liked to hypothalamus which controls the stress hormone release.
To summarise, amygdala which controls fear and anger, thalamus which controls pain perception, cingulate gurus which controls the aggressive behaviour, hippocampus which controls memory are all interconnected to hypothalamus which secretes the stress hormones, through white matter of fornix. These structures are also connected to cortex for indexing and other functions.
What is thalamus?
Thalamus is two masses of grey matter lying between the cerebral hemispheres on either side of the third ventricle, relaying sensory information and acting as a centre for pain perception. Overactivity of thalamus can cause chronic pains. It is here that some drugs like amitriptyline are said to act to reduce chronic pain
Is the hypothalamus part of the limbic system?
One of the most important functions of the hypothalamus is to link the nervous system to the endocrine system via the pituitary gland. The hypothalamus is located below the thalamus and is part of the limbic system. In the terminology of neuroanatomy, it forms the ventral part of the diencephalon.
Is the amygdala in the limbic system?
The amygdala is the gateway to the limbic system and passes sensory input on to the hypothalamus. The hypothalamus is the control center of the limbic system and is connected to the pituitary gland and the autonomic nervous system.
How to calm down the amygdala?
Calming the amygdala and activating the more resourceful forebrain can be done via intention as well. Simply visualize sending calming energy to the part of your brain just above the roof of your mouth where the dual-amygdalae are located.
It is here that mindfulness or meditation acts.
Where is the seat of origin of normal or abnormal behaviour in humans?
The microscopic seat of origin of normal or abnormal behaviour in humans is the receptor on cell surface especially of a neuronal cell in human brain. It is this place where drugs act to control behaviour. All cells have receptors. It is their mode of communication.
What is a receptor?
It is a protein on a cell wall that binds with specific molecules so that they can be absorbed into the cell in order to control certain functions.
What do receptors do?
A receptor’s main function is to recognize and respond to a specific ligand, for example, a neurotransmitter or hormone. Some receptors respond to changes in ‘transmembrane potential’ (the difference in electric potential between the inside and the outside of a cell).
What are the two types of neuron receptors?
There are two major types of neurotransmitter receptors: ionotropic and metabotropic. Ionotropic means that ions can pass through the receptor, whereas metabotropic means that a second messenger inside the cell relays the message (i.e. metabotropic receptors do not have channels). Metabotropic receptors are in fact G protein-coupled receptors.
What are cellular receptors?
Cell receptors, including hormone receptors, are special proteins found within and on the surface of certain cells throughout the body, including breast cells. These receptor proteins are the “eyes” and “ears” of the cells, receiving messages from substances in the bloodstream and then telling the cells what to do.
What are intracellular receptors?
Intracellular receptors are receptors located inside the cell rather than on its cell membrane. Classic hormones that use intracellular receptors include thyroid and steroid hormones. Examples are the class of nuclear receptors located in the cell nucleus and cytoplasm and the IP3 receptor located on the endoplasmic reticulum.
What are the receptors on the cell membrane?
Membrane receptors are specialized protein molecules attached to or integrated into the cell membrane. Through interaction with specific ligands (e.g., hormones and neurotransmitters), the receptors facilitate communication between the cell and the extracellular environment.
What are receptor proteins responsible for?
Receptor proteins are used to pass messages between cells. they are both components of the cell membrane are a protein that binds to a specific signal molecule, enabling the cell to respond to the signal molecule. they are responsible for picking up signals. A receptor protein is shaped like a boulder.
What are receptor molecules?
Receptor molecules, also known as neurotransmitters, transmit chemical signals from the end of the axon of a neuron to the end of the dendron of another neuron. These molecules help direct commands of the brain from the brain to the muscles so that the desired work (say breathe out for the lungs which is an involuntary action).
Receptor is a molecule on the cell surface (cell-surface or membrane receptor) or within a cell, usually in its nucleus (nuclear receptor) that recognizes and binds with specific molecules, producing some effect in the cell; e.g., the cell-surface receptors of immunocompetent cells that recognize antigens, complement components, or lymphokines; or those of neurons and target organs that recognize neurotransmitters or hormones.
What are types of receptors in brief?
α-r’s (α-adrenergic r’s) alpha-adrenergic receptors.
adrenergic r’s receptors for epinephrine or norepinephrine, such as those on effector organs innervated by postganglionic adrenergic fibres of the sympathetic nervous system. There are two types, alpha-adrenergic receptors and beta-adrenergic receptors.
β-r’s (β-adrenergic r’s) beta-adrenergic receptors.
B cell antigen r’s monomeric IgM, IgD, and (on memory cells only) IgG that is attached to the cell membrane of B lymphocytes (B cells); in conjunction with helper T cells, it triggers B cell activation on contact with antigen.
beta r’s (beta-adrenergic r’s) adrenergic receptors that are stimulated by epinephrine and blocked by agents such as propranolol. They are subdivided into two basic types: β1-receptors are found in the myocardium and cause lipolysis and cardiac stimulation, and β2-receptors are found in smooth and skeletal muscle and liver and cause bronchodilation and vasodilation. A third type, β3, is atypical; it is more sensitive to norepinephrine than to epinephrine, relatively resistant to propranolol blockade, and may be involved in lipolysis regulation in adipose tissue. Called also β-receptors and β-adrenergic receptors.
cell-surface receptor membrane receptor.
cholinergic r’s are membrane receptors on cells of effector organs, innervated by cholinergic nerve fibres and responsive to the acetylcholine secreted by these fibres. There are two types, muscarinic receptors and nicotinic receptors.
IgE r’s membrane receptors for IgE, found on mast cells and basophils.
opiate r’s (opioid r’s) receptors that combine with particular opiates to create analgesia and certain other effects. Several different ones have been identified and assigned Greek letters; the μ receptor gives superior analgesia, and the κ receptor is associated with a low degree of physical dependency.

What are different types of opiate receptors?
The different types of opioid receptors bind to their respective agonist counterparts.

Mu1,2,3 receptors (MOR) bind to endogenous ligands – beta-endorphin, endomorphin 1 and 2 with proopiomelanocortin (POMC) being the precursor.
The mu-1 receptor is responsible for analgesia and dependence.

The mu-2 receptor is vital for euphoria, dependence, respiratory depression, miosis, decreased digestive tract motility/constipation

Mu-3 receptor causes vasodilation. Kappa receptors (KOR) bind to dynorphin A and B (Prodynorphin as the precursor). They provide analgesia, diuresis, and dysphoria.

Delta receptors (DOR) bind to enkephalins (precursor being Proenkephalin). They play a role in analgesia and reduction in gastric motility.

Nociceptin receptors (NOR) bind to nociceptin/orphanin FQ (Pre-pronociceptin is the precursor) causing analgesia and hyperalgesia (depending on the concentration).
What are neurotransmitter receptors?
Neurotransmitter (NT) receptors are located on the surface of neuronal and glial cells. At a synapse, one neuron sends messages to the other neuron via neurotransmitters. Receptors can be located in different parts of the body to act as either an inhibitor or an excitatory receptor for a specific Neurotransmitter. An example of this are the receptors for the neurotransmitter Acetylcholine (ACh), one receptor is located at the neuromuscular junction in skeletal muscle to facilitate muscle contraction (excitation), while the other receptor is located in the heart to slow down heart rate (inhibitory)
What are the categories of neurotransmitter receptor?
Ionotropic receptors: neurotransmitter-gated ion channels, Ionotropic means that ions can pass through the receptor.
Ligand-gated ion channels (LGICs) are one type of ionotropic receptor or channel-linked receptor. They are a group of transmembrane ion channels that are opened or closed in response to the binding of a chemical messenger (i.e., a ligand), such as a neurotransmitter
The binding site of endogenous ligands on LGICs protein complexes are normally located on a different portion of the protein (an allosteric binding site) compared to where the ion conduction pore is located.
The direct link between ligand binding and opening or closing of the ion channel, which is characteristic of ligand-gated ion channels, is contrasted with the indirect function of metabotropic receptors, which use second messengers.
LGICs are also different from voltage-gated ion channels (which open and close depending on membrane potential), and stretch-activated ion channels (which open and close depending on mechanical deformation of the cell membrane)
Metabotropic receptors: G-protein coupled receptors
A mu-opioid G-protein-coupled receptor with its agonist
G protein-coupled receptors are involved in many diseases, and are also the target of approximately 30% of all modern medicinal drugs.
There are two principal signal transduction pathways involving the G protein-coupled receptors: the cAMP signal pathway and the phosphatidylinositol signal pathway
Neurotransmitter receptors are subject to ligand-induced desensitization: That is, they can become unresponsive upon prolonged exposure to their neurotransmitter
What is anatomy of neurotransmitter receptors?
Neurotransmitter receptor. A neurotransmitter receptor (also known as a neuroreceptor) is a membrane receptor protein that is activated by a neurotransmitter.
Chemicals on the outside of the cell, such as a neurotransmitter, can bump into the cell’s membrane and along the membrane we can find receptors.

What are types of neurotransmitter receptors?
The following are some major classes of neurotransmitter receptors
Adrenergic: α1A, α1b, α1c, α1d, α2a, α2b, α2c, α2d, β1, β2, β3
Dopaminergic: D1, D2, D3, D4, D5
GABAergic: GABAA, GABAB1a, GABAB1δ, GABAB2, GABAC
Glutaminergic: NMDA, AMPA, kainate, mGluR1, mGluR2, mGluR3, mGluR4, mGluR5, mGluR6, mGluR7
Histaminergic: H1, H2, H3
Cholinergic: Muscarinic: M1, M2, M3, M4, M5; Nicotinic: muscle, neuronal (α-bungarotoxin-insensitive), neuronal (α-bungarotoxin-sensitive)
Opioid: μ, δ1, δ2, κ
Serotonergic: 5-HT1A, 5-HT1B, 5-HT1D, 5-HT1E, 5-HT1F, 5-HT2A, 5-HT2B, 5-HT2C, 5-HT3, 5-HT4, 5-HT5, 5-HT6, 5-HT7
Glycinergic: Glycine
What is catecholamine?
Catecholamine (CA) is a monoamine neurotransmitter, an organic compound that has a catechol (benzene with two hydroxyl side groups next to each other) and a side-chain amine.
Catechol can be either a free molecule or a substituent of a larger molecule, where it represents a 1,2-dihydroxybenzene group.
Catecholamines are derived from the amino acid tyrosine, which is derived from dietary sources as well as synthesis from phenylalanine. Catecholamines are water-soluble and are 50% bound to plasma proteins in circulation.
Included among catecholamines are epinephrine (adrenaline), norepinephrine (noradrenaline), and dopamine. Release of the hormone’s epinephrine and norepinephrine from the adrenal medulla of the adrenal glands is part of the fight-or-flight response.
What is an agonist?
An agonist is a chemical that binds to a receptor and activates the receptor to produce a biological response. Whereas an agonist causes an action, an antagonist blocks the action of the agonist, and an inverse agonist causes an action opposite to that of the agonist.
Receptors can be activated by either endogenous agonists (such as hormones and neurotransmitters) or exogenous agonists (such as drugs), resulting in a biological response. A physiological agonist is a substance that creates the same bodily responses but does not bind to the same receptor.
An endogenous agonist for a particular receptor is a compound naturally produced by the body that binds to and activates that receptor. For example, the endogenous agonist for serotonin receptors is serotonin, and the endogenous agonist for dopamine receptors is dopamine.
Full agonists bind to and activate a receptor with the maximum response that an agonist can elicit at the receptor. One example of a drug that can act as a full agonist is isoproterenol, which mimics the action of adrenaline at β adrenoreceptors. Another example is morphine, which mimics the actions of endorphins at μ-opioid receptors throughout the central nervous system
A co-agonist works with other co-agonists to produce the desired effect together. NMDA receptor activation requires the binding of both glutamate, glycine and D-serine co-agonists. Calcium can also act as a co-agonist at the IP3 receptor.
A selective agonist is selective for a specific type of receptor. E.g. buspirone is a selective agonist for serotonin 5-HT1A.
Partial agonists (such as buspirone, aripiprazole, buprenorphine, or nor-clozapine) also bind and activate a given receptor, but have only partial efficacy at the receptor relative to a full agonist, even at maximal receptor occupancy. Agents like buprenorphine are used to treat opiate dependence for this reason, as they produce milder effects on the opioid receptor with lower dependence and abuse potential.
An inverse agonist is an agent that binds to the same receptor binding-site as an agonist for that receptor and inhibits the constitutive activity of the receptor. Inverse agonists exert the opposite pharmacological effect of a receptor agonist, not merely an absence of the agonist effect as seen with an antagonist. An example is the cannabinoid inverse agonist rimonabant.
A super agonist is a term used by some to identify a compound that is capable of producing a greater response than the endogenous agonist for the target receptor. It might be argued that the endogenous agonist is simply a partial agonist in that tissue.
An irreversible agonist is a type of agonist that binds permanently to a receptor through the formation of covalent bonds.
What is an antagonist for a receptor?
A receptor antagonist is a type of receptor ligand or drug that does not provoke a biological response itself upon binding to a receptor, but blocks or dampens agonist-mediated responses.
What are examples of agonist and antagonist drugs?
Examples of full agonists are heroin, oxycodone, methadone, hydrocodone, morphine, opium and others.
An antagonist is a drug that blocks opioids by attaching to the opioid receptors without activating them. Antagonists cause no opioid effect and block full agonist opioids. Examples are naltrexone and naloxone.
What is receptor agonist?
An agonist is a drug that activates certain receptors in the brain. Full agonist opioids activate the opioid receptors in the brain fully resulting in the full opioid effect. Examples of full agonists are heroin, oxycodone, methadone, hydrocodone, morphine, opium and others.
Is amphetamine an agonist or antagonist?
Amphetamine and methylphenidate are not (direct) dopamine agonists. Dopamine agonists are the substances that would specifically bind to dopamine receptors and activate them, thereby mimicking the effects of dopamine release. Amphetamine/methylphenidate are so-called indirect sympathomimetics.
What are the examples of serotonin antagonists?
Serotonin Antagonists boost serotonin by blocking its reuptake at nerve synapses, much like the SSRIs. Examples of Serotonin Antagonists are: trazodone and nefazodone. They are useful in case of persons suffering from anxiety and depression.
What is an example of an inverse agonist?
An agonist increases a receptor activity above its baseline, while an inverse agonist decreases the receptor activity below its baseline. For example, naloxone is a partial inverse agonist to μ-opioid receptors.
What is the difference between alpha and beta receptors?
Both alpha and beta receptors occur postsynaptic ally at the sympathetic junctions of some organs such as the heart, blood vessels, lungs, uterus, and fatty tissues. The main difference between alpha and beta receptors is that alpha receptors stimulate the effector cells whereas beta receptors relax the effector cells.
What is the biochemistry and pharmacology of receptors?
In biochemistry and pharmacology, receptors are chemical structures, composed of protein, that receive and transduce signals that may be integrated into biological systems. These signals are typically chemical messengers which bind to a receptor and cause some form of cellular/tissue response, e.g. a change in the electrical activity of a cell. There are three main ways the action of the receptor can be classified: relay of signal, amplification, or integration. Relaying sends the signal onward, amplification increases the effect of a single ligand, and integration allows the signal to be incorporated into another biochemical pathway. In this sense, a receptor is a protein-molecule that recognizes and responds to endogenous chemical signals. For example, an acetylcholine receptor recognizes and responds to its endogenous ligand, acetylcholine
What is dopamine system?
The dopamine system is a pathway in the brain in which dopamine is carried from one area of the brain to another. Dopamine is responsible for controlling the brain’s pleasure and reward centres
What is the mesolimbic dopaminergic pathway?
Among the eight dopaminergic pathways is the mesolimbic pathway. From the midbrain’s ventral tegmental area (VTA), this pathway transmits dopamine to the limbic system’s nucleus accumbens, a collection of neurons in the brain’s striatum.
What is the function of dopamine?
Dopamine is a neurotransmitter released by the brain that plays a number of roles in humans and other animals. Some of its notable functions are in: movement, memory, pleasurable reward, behaviour and cognition, attention and inhibition of prolactin production.
How does dopamine affect mood?
High levels of dopamine may result in impulsivity, feeling suicidal, aggressive behaviour, etc. Lower levels of serotonin are linked to mood swings, sugar cravings, worrying, insomnia, and sadness. There is some overlap between serotonin and dopamine that cannot be ignored.
How does dopamine cause depression?
Dopamine plays a big role in motivation and reward. If you’ve ever worked hard to reach a goal, the satisfaction your feel when you achieve it is partly due to a rush of dopamine. Some of the main symptoms of depression include: low motivation. feeling helpless. a loss of interest in things that used to interest you.
What happens when dopamine is low in the brain?
Few people have abnormally low dopamine and as a result aren’t able to get motivated or stay productive. Low dopamine: Tends to result in symptoms similar to Parkinson’s disease. People with abnormally low levels of dopamine may have difficulties with thinking, memory, and have slow reaction times.
What happens when dopamine is high in the brain?
High dopamine levels are implicated in the ethology of schizophrenia by causing a short of short circuits in brain causing hallucinations and thought disorders. This is treated by anti-psychotics which block the dopamine receptors in the brain.
What are symptoms of low Serotonin Levels?
Symptoms of Low Serotonin Levels are emotional numbness and social withdrawal – sufferers lose interest in social engagements…Depression – this is the classic sign of low serotonin levels and the reason drugs such as SSRIs act. Increased emotional sensitivity – this can present as low self-confidence, low self-esteem, Loss of interest in sexual activities etc
What are symptoms of high serotonin levels in brain?
It is important that serotine stays in normal range inside the brain. Serotonin syndrome is the result of taking medications that cause serotonin to increase to dangerous levels in the body. For example, if you are being treated for a chemical imbalance, like depression or bi-polar disorder, your physician may change your medication or increase your dosage. However, augmenting your dosage and your treatment can be dangerous. Too much serotonin is just as harmful, if not more, than having too little serotonin. When you have a surplus of serotonin in the brain, it could be deadly if left untreated.
What is prostaglandin system?
It is a large family of fast-acting lipid mediators primarily responsible for initiating inflammation, fever, and pain during the immune process. The production of prostaglandin can be controlled with anti-inflammatory drugs like aspirin.
What do endocannabinoid receptors do?
Endocannabinoids are naturally produced in the body and cannabis consumption increases the number of endocannabinoids present in the body. The endocannabinoid system remains under preliminary research, but may be involved in regulating physiological and cognitive processes, including fertility, pregnancy, during pre- and postnatal development, various activity of immune system, appetite, pain-sensation, mood, and memory, and in mediating the pharmacological effects of cannabis. The function of endocannabinoids and their receptors is to maintain homeostasis from the organism to the cell level by reversing damage in whatever way possible.
Does the human body produce cannabinoids?
The human body does produce cannabinoids. Endogenous Cannabinoids are neurotransmitters produced within our bodies that bind to cannabinoid receptors in the brain, immune system, and elsewhere. Examples include anandamide, 2-arachidonoylglycerol (2-AG), n-arachidonoyl dopamine (NADA), and virodhamine (OAE).
How do opioids activate receptors?
Endogenous Opioids often called endorphins (endogenous morphine -like substances), endogenous opioids – endorphins, enkephalins, and dynorphins – are amino acid chains (polypeptides) synthesized in the CNS with powerful analgesic properties. Endogenous opioids activate opioid receptors on the surface of nerve cells and the insides of the cells. Opioid drugs, on the other hand, activate receptors in these locations and additional parts of the cell.
What is the function of serotonin hormone?
Serotonin acts as a neurotransmitter, a type of chemical that helps relay signals from one area of the brain to another.
What is the difference between adrenaline and noradrenaline?
The activated parts of the body are different for the two with more receptors for adrenaline than for noradrenaline. The alpha effect of adrenaline is a very strong but beta effect is weak, whereas noradrenaline has a weak alpha effect. Adrenaline is mainly a hormone while noradrenaline is mainly a neurotransmitter.
What is norepinephrine responsible for?
Norepinephrine, also called noradrenaline, substance that is released predominantly from the ends of sympathetic nerve fibres and that acts to increase the force of skeletal muscle contraction and the rate and force of contraction of the heart. The nervous system responds to short-term stress with norepinephrine and epinephrine (adrenaline) which increase the heart rate and blood pressure. They also cause other actions within the body that prepare a person for a stressful situation.
What is the difference between a Neurotransmitters and a hormone?
Neurotransmitter is (biochemistry neuroscience) any substance, such as acetylcholine or dopamine, responsible for sending nerve signals across a synapse between two neurons. Hormone is (physiology) any substance produced by one tissue and conveyed by the bloodstream to another to effect physiological activity.
What is pathology of receptors in various diseases?
Pathophysiology of epilepsy is typically viewed as the shift in the balance between the inhibitory (γ-aminobutyric acid (GABA)) and the excitatory (glutamate) neurotransmission, in favour of the latter. This shift occurs due to both selective loss of inhibitory GABA-ergic neurons after precipitating epileptogenic insults (e.g., status epilepticus, stroke, and traumatic brain injury) and the reorganization of neuronal circuits that favour hypersynchrony of neuronal populations (e.g., aberrant connections formed by the axons of dentate granule cells of the dentate gyrus, known as mossy fibre sprouting). Deficit in GABA-mediated signalling and augmentation of glutamatergic transmission that have been documented in many (although not all) types of epilepsy represent the basis for the pharmacotherapy of the disease.
Pathology of addiction works through activation of opioid receptors results in inhibition of synaptic neurotransmission in the central nervous system (CNS) and peripheral nervous system (PNS).
Pathology of Depression is seen as a serotonin imbalance, and the most common class of anti-depressants (SSRIs) target the serotonin network.
Pathology of psychosis works through dopamine excess and anti-psychotics work through reducing this excess.
Pathology of Parkinson’s disease works through depletion of dopamine and carbidopa is given to boost sagging dopamine level.
Pathology of dementia is viewed through depletion of acetylcholine and acetylcholine esterase inhibitors are given to augment sagging acetylcholine levels.
What Is A Neurotransmitter?
A neurotransmitter is a substance that carries a message between brain cells (neurons). Neurotransmitter molecules are secreted by one neuron and detected by receptors in adjacent neurons. Mostly this happens at junctions between cells called synapses. Neurotransmitters can be excitatory, meaning they stimulate greater activation of the receiving neurons, or inhibitory, meaning they dampen down activation. Imbalances in neurotransmitters manifest as symptoms. Imbalances can be created by there being literally too much or too little neurotransmitter, but also by a problem with the receptors, or a problem with the brain’s mechanisms for mopping up neurotransmitters after they’ve done their job.
The brain’s main excitatory neurotransmitter is glutamate. In some disorders it appears there is an excess of glutamate, and this causes problems. Examples are Parkinson’s and possibly bipolar disorder. In the extreme case glutamate becomes toxic and can kill neurons (a process called excitotoxicity). Symptoms associated with excess glutamate are explosive emotions such as anger, rage, aggression and panic, also hyperactivity, migraines, insomnia, irritability and poor concentration, and perhaps mania.
The brain’s main inhibitory neurotransmitter is GABA. A lack of GABA is associated with anxiety. Many drugs that counter anxiety (anxiolytics) do so by stimulating GABA release.
Because GABA has the opposite effect of glutamate, there’s a lot of overlap between glutamate excess and GABA deficit.
What are neuromodulators?
An important sub-class of neurotransmitters are the neuromodulators, the main ones being serotonin, dopamine, noradrenalin and acetylcholine. They differ in that rather than directly carrying information, they affect the way cells respond to information. If the song playing on your stereo is glutamate and GABA, then the neuromodulators are like the volume, bass and treble controls. On the whole they seem to induce greater activation in the brain.
Dopamine is associated with drive and motivation. The brain secretes dopamine as a kind of reward signal, meaning we tend to want more of what just happened. Many addictive drugs such as cocaine stimulate dopamine.
It’s thought that several disorders are associated with dopamine deficit – including ADHD, addiction, and a variety of depression typified by emotional flatness and lack of motivation.
Dopamine stimulates the frontal part of the brain, especially the prefrontal cortex, a critical brain region for executive function – concentration / focus, planning and decision making, holding things in mind (short term memory) and emotional regulation. So, it makes sense that the symptoms of dopamine deficit are distractibility, low drive and motivation, and emotional flatness.
Serotonin is associated with mood – in particular serotonin deficit is linked to depression. Drugs that block the action of serotonin induce low mood, as does removing from the diet the nutritional building blocks of serotonin. The serotonin-deficient variety of depression is characterised more by feelings of misery as opposed to flatness and lack of drive (the dopamine variety). Serotonin is also associated with wakefulness and its dysregulation with sleep disturbance. (Dopamine deficit can also affect sleep but in this case, sleep seems to be excessive and unrefreshing.) OCD and some eating disorders also seem to be related to serotonin. Serotonin releasing neurons stimulate much of the brain.
Noradrenalin (also known as norepinephrine) is associated with arousal and vigilance. Experiments suggest noradrenalin is released when something new happens, that alerts our interest. So, like dopamine, noradrenalin is also associated with attention, concentration, short term memory and other executive functions. So, as you might expect, the major symptom associated with noradrenalin deficit is poor concentration and poor cognitive functioning. Like serotonin, noradrenalin secreting neurons stimulate all parts of the brain, and are associated with wakefulness. Chemically, noradrenalin is derived from dopamine. Nutrients that support the dopamine pathway, also support noradrenalin production.
Less is known about acetylcholine’s function in the brain, which appears complex, but it is connected to memory. It’s particularly prevalent in the hippocampus, a brain structure critical to memory. Acetylcholine producing neurons are among the first to die in Alzheimer’s which of course affects memory.
What is the difference between a neurotransmitter and a neuromodulator?
The key difference between neurotransmitter and neuromodulator is that neurotransmitter is a chemical substance released by the neuron to send signals to the next neuron, while the neuromodulator is a chemical substance released by the neuron to alter the effectiveness of the signal transmission.
What are some examples of neuromodulators?
Examples of neuromodulators are opioid peptides such as enkephalins, endorphins, dynorphins. Some neurotransmitters also act as neuromodulators: substance P, octopamine, serotonin, an acetylcholine are such examples.
Why are receptors and neurotransmitters so important for psychiatry?
Put simply, neurotransmitters are chemical messengers in the brain. The nerve cells of the brain use neurotransmitters to communicate with each other. The messages they send are believed to play a role in thought communication, mood regulation and thereby behavioural modulation. Disorders of such modalities results in psychiatric disorders and correction thereof results in treatment of the same.
What are components of mental state examination of a patient?
Appearance, Attitude, Behavior, Mood and affect, Speech, thought process, Thought content, Delusions, Overvalued Ideas, Obsessions, Phobias, Preoccupations, Suicidal thoughts, Perceptions, Cognition, Insight, Judgment. These are the parameters that govern behaviour of a patient and can be modulated through neurotransmitters, receptors and other manoeuvres.
What are disorders of behaviour?
Behavioural disorders in children may involve Inattention, hyperactivity, impulsivity, defiant Behavior, drug use, criminal activity and may include Attention Deficit Hyperactivity Disorder (ADHD), Oppositional Defiant Disorder (ODD) and Conduct Disorder. In adults some of the most common behavioural addictions are: Compulsive Gambling Disorder–Gambling Addiction. Compulsive Sexual Behavior Disorder–Porn and Sex Addiction, compulsive Eating Disorder (or Binge Eating Disorder)–Food Addiction, or anorexia. Compulsive Spending Disorder–Buying Addiction. Substance Use Disorder–Drug Addiction.
What is disorder of thought?
Thought disorder is a disorder of cognitive organization, characteristic of psychotic mental illness, in which thoughts and conversation appear illogical and lacking in sequence and may be delusional or bizarre in content. Appears due to high dopamine in the brain receptors and can be corrected by giving dopamine blocking agents like chlorpromazine hydrochloride.
Which disorder shows disorder of thought?
Thought disorder refers to the disorganized thinking as evidence by disorganized speech. The cause of formal thought disorder is not established. Research has implicated abnormalities in the semantic system in patients with schizophrenia. However, formal thought disorder is not unique to schizophrenia or psychosis. It is often a symptom of mania, and less often it can be present in other mental disorders such as depression.
What is disorder of mood?
Mood disorder, also known as mood (affective) disorders, is a group of conditions where a disturbance in the person’s mood is the main underlying feature.
Which disorder shows disorder of mood?
Mood disorders, also called affective disorders, are a group of illnesses that have as their distinguishing characteristic an experience of mood that is unusual for the circumstances. Common mood disorders include bipolar disorder, depression, postpartum depression, cyclothymia, schizoaffective disorder, and seasonal affective disorder.
Which disorder shows disorder of memory?
Memory loss is the predominant feature of amnesia and dementia, and other less common What is poor insight in schizophrenia?
What disorders result in poor or total loss of insight?
Poor insight is a prevalent feature of schizophrenia, and lack of awareness of schizophrenic symptoms is correlated with poor medication adherence and higher rates of recidivism. Poor insight is also common in bipolar disorder, and although insight is more state-dependent in bipolar disorder than in Schizophrenic disorders.
What are disorders of judgement?
Like insight, poor judgement is seen in many mental disorders but poor social judgement is seen in borderline personality disorder?
Are disorders of behaviour, thinking, mood, insight and judgment along with other symptoms exclusive to certain diseases?
No, but together they create a gamut of psychiatric disorders. For example, behaviour, thought, mood, insight and judgement are all impaired in schizophrenia.
What is abnormal behaviour?
The unusual or maladapted behaviour of many persons which do not fit into our common forms of behaviour is known as abnormal behaviour. Abnormality refers to maladjustment to one’s society and culture which surrounds him. It is the deviation from the normal in an unfavourable and pathological way.
Abnormal behaviour may be defined as behaviour that is disturbing (socially unacceptable), distressing, maladaptive (or self‐defeating), and often the result of distorted thoughts (cognitions). Several perspectives (models, approaches derived from data) and theories attempt to explain the causes of abnormal behaviour.
What is the difference between a behavioural disorder and a mental disorder?
Disorders of the brain include both behaviour disorders and other psychiatric illnesses. The primary difference between a behaviour disorder and another type of psychiatric disorder is the presence of choice. Psychiatric disordered patients may not have a choice. So, it becomes an illness.
What are the most common disruptive behaviours?
However, some children have extremely difficult and challenging behaviours that are outside the norm for their age. The most common disruptive behaviour disorders include oppositional defiant disorder (ODD), conduct disorder (CD) and attention deficit hyperactivity disorder (ADHD) and explosive anger disorder.
What are most Common Mental Illnesses and Disorders?
This includes a general census regarding which are the most frequent: They include anxiety disorders (Generalised anxiety disorders (GAD), phobias, Obsessive compulsive disorder, Panic attacks, social anxiety disorders, post-traumatic stress syndrome, etc., schizophrenias, bipolar disorder, major depression, addiction, headaches and epilepsy.
What is Mental Retardation?
Mental retardation is a condition in which people have below average intelligence that limits their ability to function normally. The condition, which is present from birth or childhood, has many different causes.
What are the levels of mental retardation?
The four levels of intellectual disability, sometimes referred to as mental retardation, are mild, moderate, severe and profound. Persons suffering from any level of intellectual disability have an intelligence quotient below 70.
What are the causes of mental retardation?
The main causes of mental retardation are, Genetic factors. About 30% of cases of mental retardation is caused by hereditary factors., Prenatal illnesses and issues, Childhood illnesses and injuries., Environmental factors, etc.
What are the different types of mental retardation?
The types of mental retardation usually fall into five categories caused by genetic mutations or abnormalities that develop before birth. They include cranial abnormalities, cretinism, phenylketonuria (PKU), Down syndrome, and non-syndromic mental retardation.
What is the most common genetic cause of mental retardation?
Fragile X syndrome is the most common inherited form of mental retardation and, after Down syndrome, the most common genetic form. It is X linked, with dominant inheritance, and the penetrance is lower in females.
What are Down syndrome symptoms?
Common Down syndrome signs are , a small head and short neck; a flat face, and upward slanting eyes; ears are flat and positioned lower than “normal, “the tongue protrudes and seems to be too large for the mouth, hands tend to be wide, with short fingers and there is just a single flexion crease in the palm.
Is mental retardation as illness is considered a disability?
Intellectual disability (ID), once called mental retardation, is characterized by below-average intelligence or mental ability and a lack of skills necessary for day-to-day living. People with intellectual disabilities can and do learn new skills, but they learn them more slowly.
What are the different types of behavioural problems in children?
Behavioural problems in children are Attention deficit hyperactivity disorder (ADHD), Oppositional defiant disorder (ODD), conduct disorder, Autism spectrum disorder (ASD) Anxiety disorder, Eating disorder, Depression, Bipolar disorder.
What is oppositional defiant disorder (ODD)?
Even the best-behaved children can be difficult and challenging at times. But if your child or teenager has a frequent and persistent pattern of anger, irritability, arguing, defiance or vindictiveness toward you and other authority figures, he or she may have oppositional defiant disorder (ODD).
What are the symptoms of conduct disorder?
Emotional symptoms of conduct disorder include: Lack of remorse: This may appear as an inability to feel guilty about doing something wrong, a failure to feel bad about hurting someone, or indifference to punishment for breaking the rules.
What is autism?
Autism is a developmental disorder of variable severity that is characterized by difficulty in social interaction and communication and by restricted or repetitive patterns of thought and behaviour.
What is autism syndrome?
Autism spectrum disorder (ASD) is a condition related to brain development that impacts how a person perceives and socializes with others, causing problems in social interaction and communication.
What is the highest level of autism?
ASD is divided into three levels that reflect severity: Level 1. This is the mildest level of ASD. Level 2. People at this level require more support, such as speech therapy or social skills training. Level 3. This is the most severe level of ASD.
What are some signs of ADHD?
Signs of Attention Deficit Hyperactivity Disorder (ADHD) are hyperkinesia and attention deficit with self-focused behaviour. A common sign of ADHD is what looks like an inability to recognize other Interrupting. Self-focused behaviour may cause a child with ADHD to interrupt others. They have trouble waiting for their turn.
What are signs of mild Aspergers syndrome?
Signs or Symptoms of Asperger syndrome include clumsy and uncoordinated motor movements, social impairment with extreme obtuseness, limited interests and/or unusual preoccupations, repetitive routines or rituals, speech and language peculiarities, and non-verbal communication problems. An average or above-average IQ is necessary for a diagnosis of Asperger’s. The child should see a neurologist or developmental paediatrician (again, someone familiar with autistic spectrum disorders) for a thorough neurological exam to rule out other medical conditions and to assess the need for medication.
Did Alan Turing have Asperger’s syndrome?
Alan Turing’s tendency to be severely logical – beyond the point of social survival – may in the end be what killed him. This can appear as a symptom of Asperger’s Syndrome – a form of autism claimed to be associated with mathematicians and computer scientists. Turing is widely considered to be the father of theoretical computer science and artificial intelligence. Despite these accomplishments, he was never fully recognised in his home country during his lifetime due to his homosexuality and because much of his work was covered by the Official Secrets Act.
What is Antisocial Personality Disorder?
This disorder is characterized by problems relating to other people. People who suffer from this disorder avoid all types of interactions with others. It doesn’t matter whether they are family members, acquaintances or strangers. The symptoms that are linked with this disorder could be: shyness, depression, solitude, violence, aggressiveness, among others. Additionally, they experience a large fear of rejection.
What is Borderline Personality Disorder?
Those who suffer from this mental illness have an impulsive and weak personality. This causes them to always doubt everything. They can be calm and then, within a few minutes, feel anxious, hopeless, or angry. You could say that they live their lives to the fullest, and often have loving and intense relationships and idolize their partner.
What is the definition of perversion?
Although the term perversion can refer to a variety of forms of deviation, it is most often used to describe sexual behaviours that are considered particularly abnormal, repulsive or obsessive.
What can we do about perversions?
In recent years there have been a variety of approaches to the treatment of sexual perversions. Generally, these approaches can be divided into five main categories: psychodynamic, cognitive-behavioural, relapse prevention, organic, and family systems. The psychodynamic and cognitive-behavioural orientations have largely dominated treatment, inasmuch as both of these approaches purport to treat the full spectrum of paraphiliac disorders. Relapse prevention techniques, which are being used increasingly in specialized treatment programs for sex offenders, can be initiated at the very onset of the treatment encounter. The organic and family systems approaches are somewhat delimited in that each of these perspectives treats a narrower range of deviant sexual disorders. For example, the organic approach, which until recently was confined to the administration of medroxyprogesterone acetate (MPA, Depo-Provera), is used for the seriously acting out and potentially dangerous patient for whom immediate control measures are indicated. The family systems approach has been mostly limited to the advanced stages of the treatment of some incest cases.
What is anxiety?
Anxiety is a feeling of worry, nervousness, or unease about something with an uncertain outcome.
How did anxiety evolve over the millenniums?
Anxiety is an extended version of the fight–or-flight response which evolved to keep us alive, from those early prehistoric days when there was threat to lives everywhere. We evolved in water and therefore carry a little of saline sea water in all of us. The internal physical milieu of all of us is saline like sea water. Likewise, the internal psychological milieu in all of us is anxiety predominant. But drag the fight-or-flight response into every situation and holding onto it until we are sick of anxiety, without a cause.
What is Anxiety Disorder? (GAD).
Anxiety disorders are one of the most common mental illnesses in the 21st century. They can appear in various stressful or distressing situations. This disorder can happen when there are changes in the life of an individual. It may appear difficult for the person to carry out their job, talk with family, meet strangers, etc. On the other hand, the general imbalance interferes in the person’s everyday life due to the fact that they are always worried about something: leaving the door open, someone robbing the car while it’s parked, something bad happening to a loved one, having a car accident, etc.
What are Phobias?
This is another one of the most common mental illnesses. Phobias go beyond a fear or dislike for a situation, object, or animal. It’s more than just not liking spiders or clowns. A phobia is an irrational disorder that doesn’t allow the person to enjoy life out of the fear that the cause of the phobia will appear.
What is Obsessive Compulsive Disorder?
When someone suffers from this anxiety-related disorder, they experience obsessive feelings, images, and ideas that aren’t real. They associate fear, stress, and continual distress and imagine daily problems. It goes beyond far organizing coat hangers or books because they don’t look properly in order. A person suffering from Obsessive Compulsive Disorder OCD may resort to extreme behaviours, like not stepping on lines on the floor, wanting to adjust everything they walk past, not being able to sleep if the closet door is open, organizing things multiple times, etc.
What are Panic Attacks?
This problem is appearing more and more frequently. In a panic attack, the person experiences difficulty breathing, feeling dizzy and nauseous, weakness, and a racing heart. It can also appear with other symptoms such as tingling in their hands, excessive sweating, feeling weak, and chest pains. It’s as if they are drowning and can’t control the situation. Panic attacks can happen at any moment, in any place, because of an irrational fear. They are incapacitating and can be hereditary. Without professional help, they can cause agoraphobia or fear of open spaces. They are afraid that they could have a panic attack at any given moment.
What is post-traumatic stress disorder?
Post-traumatic stress disorder (PTSD), also called post-traumatic stress syndrome, emotional condition that sometimes follows a traumatic event, particularly an event that involves actual or threatened death or serious bodily injury to oneself or others and that creates intense feelings of fear, helplessness, or horror.
What is Schizophrenia?
Schizophrenic people may hear voices or have delusions, which invade their thoughts and causes them to change how they act. For example, they tell the person to harm someone else or themselves. Someone who suffers from this disorder can noticeably change from day to day. They feel unable to control internal monologues of the characters.
Schizophrenia affects as many men as women, and usually appears between the ages of 16 and 30. The cause is still unknown. As for treatment, doctors generally opt for psychosocial therapy and antipsychotic drugs.
What is evolution of psychosis?
The link between creativity and psychosis has derived more support from a recent demonstration of a biologically relevant polymorphism of the promoter region of the neuregulin 1 gene, which is linked with schizophrenia,
What is schizophreniform psychosis?
Schizophreniform disorder is a type of psychotic illness with symptoms similar to those of schizophrenia, but lasting for less than 6 months. Like schizophrenia, schizophreniform disorder is a type of “psychosis” in which a person cannot tell what is real from what is imagined.
What is schizoaffective psychosis?
Schizoaffective disorder is a mental disorder in which a person experiences a combination of schizophrenia symptoms, such as hallucinations or delusions, and mood disorder symptoms, such as depression or mania.
What is brief psychosis?
Brief psychotic disorder. Brief psychotic disorder is a sudden, short-term display of psychotic behaviour, such as hallucinations or delusions, which occurs with a stressful event. Brief psychotic disorder is triggered by extreme stress, such as a traumatic accident or loss of a loved one.
What is Bipolar Disorder?
This falls under the term “mood disorders” and causes very exaggerated changes in emotions or manic episodes.
For example, this may include volubility, increased psychomotor activity, pressure of speech, flight of ideas, decreased sleep, roaring with laughter one minute, called manic phase and depressed mood, decreased sleep, decreased psychomotor activity, crying uncontrollably, called depressed phase, the next. The extreme behaviour can cause problems with social relations. This is based on the fact that the people close to them don’t know how to react to these drastic changes.
What is Depression?
This is one of the most common mental illnesses and in many cases goes beyond distress or passing sadness. Depressive disorder includes hopelessness, depression, agitation, decreased sleep, difficulty getting out of bed, feelings of inferiority and even suicidal thoughts. When these symptoms remain for weeks or months, they can change the person’s life. This causes serious problems in their interpersonal relationships.
What is the evolution of depression?
If depression was a disorder, then evolution had made a tragic mistake, allowing an illness that impedes reproduction — it leads people to stop having sex and consider suicide — to spread throughout the population. The alternative, of course, is that depression has a secret purpose. Depression allows people to ruminate and focus. The physical symptoms of depression might, in fact, protect you from a superior adversary. That way it is an evolution.
What is mania?
It is mental illness marked by periods of great excitement or euphoria, delusions, and overactivity.
What is evolution of mania?
The benefits of mania are pretty obvious. You can get more done than your fellow homo sapiens. You’re braver; you’re bolder. You’re willing to take greater risks and earn bigger rewards. You can talk yourself and all those around you to go into battle and conquer the neighbouring tribe. You might also be able to find more creative solutions to the problems facing humans at the time.
What is Eating Disorders?
In this group, you will find anorexia nervosa, which is characterized by the obsession to control the food they consume and distorted body image (although they may be very thin, the person thinks they’re fat when they look in the mirror). It also includes bulimia nervosa, consisting of unusual dietary patterns. This may include binging and then purging to eliminate what was eaten (through laxatives or vomiting). This can stem from depression and low self-esteem. Not so common.
What does amnesia tell us about memory?
Amnesia is “a disturbance in the memory of information stored in long-term memory, in contrast to short-term memory, manifested by total or partial inability to recall past experiences.”. Amnesia is a condition in which someone can’t recall stored memories.
How do you get amnesia?
Amnesia is a condition that can happen to a person that had severe trauma to the head like in a car accident or so. It could also be because of external pressure or stress, or… it could also be a problem of the brain and memory functions.
What to do for amnesia?
Amnesia from dementia is often incurable. However, your doctor may prescribe medications to support learning and memory. If you have persistent memory loss, your doctor may recommend occupational therapy. This type of therapy can help you learn new information and memory skills for daily living.
How is amnesia diagnosed?
To diagnose amnesia, your first rule out other causes of memory loss like Alzheimer’s disease or a brain tumour. Blood tests will test for malnutrition and infection that might influence memory, as in Wernicke-Korsakoff Syndrome.
What are signs of dissociative identity disorder?
Signs and symptoms depend on the type of dissociative disorders you have, but may include: Memory loss (amnesia) of certain time periods, events, people and personal information. A sense of being detached from yourself and your emotions. A perception of the people and things around you as distorted and unreal. A blurred sense of identity.
What is delirium?
Delirium is an acutely disturbed state of mind characterized by restlessness, illusions, and incoherence, occurring in intoxication, fever, and other disorders. Also called “acute confusional state,” delirium usually starts suddenly and can be frightening for the person experiencing it, as well as for those around them.
What is delirium tremens (DT)?
Delirium tremens (DTs) is the most severe form of alcohol withdrawal. It’s a psychotic condition characterized by confusion, illusions, hallucinations, tremors, anxiety, perspiration, rapid pulse and disorientation.
What causes DT’s in alcoholics?
Delirium tremens (DTs) is a rapid onset of confusion usually caused by withdrawal from alcohol. When it occurs, it is often three days into the withdrawal symptoms and lasts for two to three days. Physical effects may include shaking, shivering, irregular heart rate, and sweating.
What causes delirium after surgery?
A urinary tract infection or dehydration can cause delirium in certain people. The time after surgery (called the postoperative period) is a common time for delirium to develop, especially in older people. This may be related to pain or the use of anaesthesia or pain medications.
What is dementia?
Dementia is an overall term for diseases and conditions characterized by a decline in memory, language, problem-solving and other thinking skills that affect a person’s ability to perform everyday activities. Memory loss is an example. Alzheimer’s is the most common cause of dementia.
How is delirium different than dementia?
While dementia is a disturbance of memory, it also features a poor level of focus and concentration, the difference is that delirium’s is a sort of confusion where lack of focus stems from rapidly processed thoughts, rather than the stifled ability to conduct thought.
What is addiction?
Addiction is the fact or condition of being addicted to a particular substance or activity.
What is the most common addiction?
Among them, gambling, eating and internet use are problematic for many. The 10 most common addictions are alcohol, tobacco, drugs, gambling, shopping, sex, food, video games, the internet and the addiction to work.
What is the most addictive drug?
Heroin is generally considered the most addictive drug in the world. Studies have shown that just one dose of heroin can put a person on the fast track to addiction.
What is alcohol addiction?
Alcohol is a drug, and alcoholism is every bit as damaging as drug addiction. Alcohol addiction causes changes in the body and brain, and long-term alcohol abuse can have devastating effects on your health, your career, and your relationships.
What is the difference between dependence and alcohol abuse?
A simplified difference between alcohol abuse and alcohol dependence is that abuse describes the early stages of alcohol dependence. Dependence is a more complex and chronic condition. Therefore, while both indicate the consequences of problematic drinking, abuse has fewer symptoms.
What is pain?
Pain is an unpleasant sensation that can range from mild, localized discomfort to agony. Pain has both physical and emotional components. The physical part of pain results from nerve stimulation. Pain may be contained to a discrete area, as in an injury, or it can be more diffuse, as in disorders like fibromyalgia or chronic pain.
What is evolutionary aspect of pain?
The fact that pain states are associated with damaging experiences is the result of natural selection. Pain can be an adaptive trait and improve the survival value. In other cases, pain is only a by-product of natural selection.
What is chronic fatigue syndrome?
Chronic fatigue syndrome (CFS), also referred to as myalgia encephalomyelitis (ME), is a complex, fatiguing medical condition that causes worsening symptoms after physical or mental activity, a greatly lowered ability to do pre-illness activities and unrefreshing sleep.
Is chronic fatigue and fibromyalgia the same thing?
Chronic pain and fatigue are common symptoms of both fibromyalgia and chronic fatigue syndrome. The difference is that, in fibromyalgia, fatigue often takes a backseat to debilitating muscle pain. In chronic fatigue syndrome, people have an overwhelming lack of energy, but also can experience some pain.
What is chronic pain?
Chronic pain last for more than 3 months. It is very common (More than 1 crore cases per year in India). It is more common in females. Perhaps overactive thalamus causes chronic pain syndrome. Thalamolytic drugs like amitriptyline are so called because of their ability of block thalamus to produce unexplained chronic pains in the body.
What is headache?
Headache is the symptom of pain in the face, head, or neck. It can occur as a migraine, tension-type headache, or cluster headache. Frequent headaches can affect relationships and employment. There is also an increased risk of depression in those with severe headaches.
What is the most common type of headache?
90% of all headaches are primary headaches. Primary headaches usually first start when people are between 20 and 40 years old. The most common types of primary headaches are migraines and tension-type headaches. They have different characteristics.
Tension headache, also known as stress headache, or tension-type headache (TTH), is the most common type of primary headache. The pain can radiate from the lower back of the head, the neck, eyes or other muscle groups in the body typically affecting both sides of the head. Tension-type headaches account for nearly 70% of all headaches.
Migraine accounts for 20 % of all headache. The rest 10 percent of headache comprises of sinusitis and ocular causes of headache. Contrary to popular belief ocular causes of headache comprises of only 2 % of all cases of headache.
What is the difference between migraine and tension headache?
However, there is a significant distinction between the two. Tension headaches are probably the most common of these two, generally prolonged and may last months to years, like a cap or band on head, while migraine headaches are episodic, hemi cranial, associated with nausea, vomiting, blurred vision, photophobia or phonophobia with rarely neurological signs. Many patients usually have tension headaches between their migraines.
What is epilepsy?
A neurological disorder that causes seizures or unusual sensations and behaviours.
How would you know if you have epilepsy?
Seizures are the basic indicator of epilepsy. They vary widely: Staring straight ahead, repetitive swallowing, and lapsing into complete immobility for a few seconds characterize absence (petit mal) seizures, which can recur many times in a day, to tonic clonic seizures with loss of consciousness, to confusion with automatism as in complex partial seizures.
What are the main types of seizures?
The different types of generalized seizures are: absence seizures (formerly known as petit mal), complex partial seizures, tonic-clonic or convulsive seizures (formerly known as grand mal)., atonic seizures (also known as drop attacks)., clonic seizures. Or tonic seizures.
What are tonic clonic seizures?
These seizures typically initiate abruptly with either a focal or generalized onset. A prodrome (which, in this case, is a vague sense of impending seizure) may also be present before the seizure begins. The seizure itself includes both tonic and clonic contractions, with tonic contractions usually preceding clonic contractions. After these series of contractions, there is an extended postictal state where the person is unresponsive and commonly sleeping with loud snoring. There is usually pronounced confusion upon awakening.
What is a tonic seizure?
A tonic seizure is a sudden, short-lived episode of unusual electrical activity in the brain that causes muscles to stiffen. An individual who experiences a tonic seizure is unable to control body movements and loses consciousness during the event.
How long does a tonic seizure last?
In the tonic stage of the seizure, your muscles stiffen, you lose consciousness, and you may fall down. The clonic stage consists of rapid muscle contractions, sometimes called convulsions. Tonic-clonic seizures usually last 1­–3 minutes. If the seizure lasts longer than five minutes, it’s a medical emergency.
What are myoclonic seizures?
Myoclonic seizures are characterized by brief, jerking spasms of a muscle or muscle group. They often occur with atonic seizures, which cause sudden muscle limpness.
What causes juvenile myoclonic epilepsy?
The exact cause of Juvenile Myoclonic Epilepsy is not known as is the case with other types of epilepsy. Some of the risk factors which increase the likelihood of developing JME. Children suffering from childhood absence epilepsy are more at a risk for developing juvenile myoclonic epilepsy.
WHAT IS benign childhood epilepsy?
Benign Rolandic epilepsy is also called benign childhood epilepsy with centrotemporal spikes. This refers to a pattern of brain waves it often creates on an electroencephalogram (EEG). With this condition, seizures affect the face and sometimes the body. As a result, the disorder causes problems for some children. It almost always disappears, though, by adolescence.
What is absence seizure?
Absence seizures are typically brief occurrences that may be mistaken for daydreaming. Learn more about the symptoms at the Epilepsy Foundation. Sometimes confused with daydreaming, this type of brief seizure causes cause lapses in awareness or staring.
What is a simple partial seizure?
A simple partial seizure is the most localized type, with a discharge that is predominantly one-sided or presents localized features without loss of consciousness.
What is complex partial seizure?
A complex partial seizure is associated with disease of the temporal lobe and characterized by varying degrees of impairment of consciousness, automatism like smacking of lips and hand movements?
What are the signs of a partial seizure?
Not everyone will experience all symptoms of partial onset seizures. Partial-onset seizure symptoms may include: Abnormal stiffness of the arm and/or leg. Illusions and hallucinations. Déjà vu or jamais vu. Fear/anxiety. Lip smacking, chewing, or swallowing movements. Loss of consciousness.
What is frontal lobe related seizures?
Frontal lobe seizures often last less than 30 seconds. In some cases, recovery is immediate. Signs and symptoms of frontal lobe seizures might include: Head and eye movement to one side. Complete or partial unresponsiveness or difficulty speaking. Explosive screams, including profanities, or laughter. Abnormal body posturing, such as one arm extending while the other flexes, as if the person is posing like a fencer. Repetitive movements, such as rocking, bicycle pedalling or pelvic thrusting. They may mimic hysterical behaviour and can therefore be missed.
The frontal lobe is the largest lobe and gives rise to seizures with distinctive features depending on the area of the frontal lobe involved. Motor features are prominent and motor seizure types seen range from focal hyperkinetic seizures with pelvic thrusting and bipedal kicking or pedalling to focal bilateral motor seizures with asymmetric tonic posturing. Frontal lobe seizures may begin with a brief aura, even when seizures occur from sleep. Seizures are typically brief, and can have prominent vocalization, bizarre Behavior, urinary incontinence, and head and eye deviation. Frontal lobe seizures may be exclusively nocturnal and often cluster. The ictal EEG may not show ictal patterns or may be obscured by movement artifact. When awareness is impaired, frontal focal impaired awareness seizures can be difficult to distinguish from absence seizures. Nocturnal frontal lobe seizures can be mistaken for parasomnias, however: Frontal lobe seizures are usually brief events (< 2 minutes), with stereotyped features seen from seizure to seizure and preserved awareness. Parasomnias are usually longer in duration (> 10 minutes), have variable features from event to event and are characterized by a confusional state with the patient having no memory of the event afterwards. In parasomnias, clustering is rare and the common non-REM parasomnias typically occur 1-2 hours after falling asleep, in the first cycle of deep slow wave sleep. Nocturnal frontal lobe seizures typically occur throughout the night, and more frequently within half an hour of falling asleep or awakening. Frontal lobe seizures may be mis-diagnosed as non-epileptic seizures as there may be bilateral motor phenomena with preserved awareness, and the ictal EEG can be normal.
What are subtypes of frontal lobe seizures?
Primary sensorimotor cortex related seizures, seizures are focal motor seizures characterized by localized clonic, tonic-clonic, tonic or myoclonic activity. They may exhibit features of a Jacksonian march where unilateral tonic-clonic movements start in one muscle group and spread systematically to adjacent groups reflecting the spread of ictal activity through the motor cortex according to the homunculus. There may be focal somatosensory features alone, such as unilateral tingling, or in combination with motor features. Negative motor features such as focal atonic features may also occur.
Supplementary sensorimotor cortex related seizures, seizures are focal bilateral motor seizures characterized by an abrupt onset and offset of asymmetric tonic posturing, lasting 10-40 seconds with minimal postictal confusion. Asymmetric posturing of the upper limbs occurs, with extension of the upper limb contralateral to the hemisphere of seizure onset and flexion of the ipsilateral upper limb. Loud vocalization or speech arrest can occur at seizure onset. The head and eyes are often turned to the side contralateral to the hemisphere of seizure onset. There may be a focal somatosensory seizure prior to onset of the motor features.
The supplementary sensorimotor area is highly connected to other brain regions and asymmetric posturing may be seen in seizures from other regions through rapid spread to the supplementary sensorimotor area.
In Orbitofrontal cortex type of frontal lobe related seizures, impaired awareness, initial repetitive automatisms, olfactory hallucinations and illusions and autonomic features may be seen.
In Frontopolar cortex type of frontal lobe related seizures, they may be characterized by forced thoughts, impaired awareness, ipsilateral head and eye version with possible progression to contralateral version, autonomic features and axial tonic-clonic movements resulting in falls.
In Dorsolateral frontal cortex originating frontal lobe related seizures, in the dominant hemisphere, a seizure occurring in or near Broca’s area can result in aphasia or dysphasia in a patient who is otherwise awake and responsive. Motor features occur, most commonly tonic features, and are accompanied by contralateral head and eye version. Forced thoughts may be described.
In Cingulate cortex originating frontal lobe related seizures, seizures are characterized by automatisms at onset with impaired awareness, emotion/mood and autonomic features. Focal emotional seizures with laughter (gelastic seizures) may occur.
In Fronto-parietal operculum originating seizures, seizures are characterized by facial (mouth and tongue) clonic movements (which may be unilateral), laryngeal symptoms, articulation difficulty, swallowing or chewing movements and hyper-salivation. Autonomic (e.g. epigastric, urogenital, gastrointestinal, cardiovascular or respiratory) and emotional (e.g. fear) features are common. Gustatory hallucinations are particularly common.
What is temporal lobe related seizure?
Temporal lobe seizures begin in the temporal lobes of your brain, which process emotions and are important for short-term memory. Some symptoms of a temporal lobe seizure may be related to these functions, including having odd feelings — such as euphoria, deja vu or fear abnormal sensations or hallucinations.
Temporal lobe seizures are characterized by behavioural arrest and impaired awareness. Automatisms are common during the seizure, and include oral and/or manual automatisms. There may sensory (auditory), emotional (fear), cognitive (deja vu) or autonomic features (epigastric sensation, tachycardia, colour change) prior to onset of impaired awareness. Postictal confusion typically occurs.
Specific features suggest seizure onset in the dominant or non-dominant temporal lobe (see hemispheric lateralization). Ictal speech, spitting, vomiting, drinking, urge to urinate and automatisms with preserved consciousness suggest seizure onset in the non-dominant temporal lobe. Postictal speech disturbance suggests a dominant temporal lobe seizure. Upper limb dystonia is a useful lateralizing feature, lateralizing the seizure to the contralateral hemisphere. Conversely, manual automatisms usually occur on the ipsilateral side.
In infants, temporal seizures may be subtle and manifest with pallor, apnoea and behavioural arrest. There may be earlier and more marked motor manifestations including tonic seizures and epileptic spasms, which may reflect different patterns of spread in the developing brain.
Temporal focal impaired awareness seizures can have similar features to frontal focal impaired awareness seizures, however impaired awareness seizures of temporal origin tend to have a slower onset and progression, and postictal confusion is more pronounced.
Temporal focal impaired awareness seizures need to be distinguished from absence seizures. While both may have automatisms, temporal lobe seizures are typically longer (> 30 seconds), associated with pallor, and followed by postictal confusion.
What are subtypes of temporal lobe related seizures?
Seizures that arise in the mesial temporal lobe may be characterized by distinctive seizure onset features such as an autonomic seizure with rising epigastric sensation or abdominal discomfort, or cognitive seizure with deja vu/jamais vu, or emotional seizure with fear. Unpleasant olfactory and gustatory sensory seizures may also occur. These focal seizure types may occur in isolation or may be followed by the onset of behavioural arrest with slowly progressive impairment of awareness and oral (chewing, lip-smacking, swallowing, tongue movements) and manual automatisms. Autonomic phenomena (pallor, flushing, tachycardia) are common. Upper limb automatisms may be unilateral and may lateralize the seizure to the ipsilateral hemisphere. Unilateral pupillary dilatation can occur, and can also lateralize the seizure to the ipsilateral hemisphere. Contralateral upper limb dystonia may develop and head and eye version to the contralateral side can occur. Whilst seizures tend to have a longer duration than for lateral temporal lobe seizures, evolution to a focal to bilateral tonic-clonic seizure is uncommon.
Lateral temporal lobe seizures may have an initial focal seizure with auditory or vertiginous features. The focal sensory auditory seizure is usually a basic sound such as buzzing or ringing (rather than formed speech). If the sound is heard in only one ear it suggests the seizure is in the contralateral hemisphere. In comparison to mesial temporal lobe seizures, lateral temporal seizures are of shorter duration, and the onset of impaired awareness is an earlier feature (the initial aware phase is not as prolonged). Lateral temporal lobe seizures may spread and motor features such as contralateral upper limb dystonia, facial twitching or grimacing, and head and eye version may occur. Evolution to a focal to bilateral tonic-clonic seizure is more common than in mesial temporal lobe seizures.
What is parietal lobe related seizures?
Seizures with onset in the parietal lobe may be difficult to diagnose, especially in children, because of the subjective nature of the experience that occurs. Positive and/or negative sensory features occur. Typically, paraesthesia is reported but disorientation, complex visual hallucinations, vertiginous and visual illusions and disturbance of body image (somatic illusion) can occur. Receptive language impairment can occur with dominant hemisphere involvement. Ipsilateral or contralateral rotatory body movements can occur. There is often involvement of other lobes as the seizure spreads.
What are subtypes of parietal lobe related seizures?
Seizures onset with contralateral (or rarely ipsilateral or bilateral) focal somatosensory seizure, most commonly paraesthesias with tingling and/or numbness. There may be prickling, tickling, crawling or electric-shock sensations in the affected body part. The sensory abnormality may spread sequentially along a body part as the seizure spreads on the cortex according to the sensory homunculus (Jacksonian march), when this occurs motor activity in the affected body part commonly follows. Less common sensory features include pain and thermal perceptions (such as sensations of burning or cold).
Seizures may be characterized by body image distortions with feelings of movement (e.g. floating) or altered posture (e.g. twisting movement) in a stationary limb. Somatic illusions such as feeling of a body part being enlarged (macrosomatognosia), shrunken (microsomatognosia) or absent (asomatognosia), or elongated (hyperschematica) or shortened (hyposchematica) may also occur. Distal body parts and the tongue are more commonly affected.
Focal cognitive seizures are seen, followed by a feeling of inability to move which may spread sequentially through body parts in a Jacksonian march (ictal paralysis), this may be followed by clonic jerking in affected body parts.
Focal cognitive seizures are seen with visual illusions including macropsia (objects in a section of the visual field appear larger) or micropsia (objects appear smaller). Versie eye movements (typically contralateral) or epileptic nystagmus may be seen. If nystagmus is seen, this is typically with the fast component to the side contralateral to the hemisphere of seizure onset with the slow component returning to the ipsilateral side. Eye movements typically occur with retained awareness, and may be accompanied by head or trunk version. Complex visual hallucinations may occur.
Seizures arising in the non-dominant hemisphere may be characterized by sexual sensations affecting the genitalia. The subsequent phase of the seizure may be accompanied by sexualized Behavior.
Focal cognitive seizures are seen characterized by language impairment with difficulties reading, calculating and writing.
Seizures are characterized by facial (mouth and tongue) clonic movements (which may be unilateral), laryngeal symptoms, articulation difficulty, swallowing or chewing movements and hyper-salivation. Autonomic (e.g. epigastric, urogenital, gastrointestinal, cardiovascular or respiratory) and emotional (e.g. fear) features are common. Gustatory hallucinations are particularly common.
What is occipital lobe related seizures?
Seizures arising in the occipital lobe are characterized by focal sensory visual seizures that are subjective experiences, leading to difficulty in diagnosis in young children. Oculomotor features may also occur such as forced eye closure, eyelid fluttering, eye deviation and nystagmus. There is often involvement of other lobes as the seizure spreads.
Seizures in Primary visual cortex area result in focal sensory visual seizures, these may be positive visual phenomena (typically multi-coloured shapes such as circles, flashes), or negative phenomena such as loss of a part of a visual field or blindness (amaurosis). Bilateral loss of vision may occur and this may be in the form of a black-out or a white-out. More complex formed visual images, considered focal cognitive seizures, are not seen in seizures arising in this area. The visual phenomenon is seen in the contralateral visual field to the hemisphere of seizure onset. If positive visual phenomena occur in a part of the visual field, the person may be seen to look in that direction during the seizure. It can be helpful to ask a young child to draw what they see during their seizure. Focal visual sensory seizures are usually brief (< 2 minutes) which can assist in distinguishing them from migraine aura (5-15 minutes).
What are subtypes of occipital lobe related seizure?
Seizures in Extra-striate cortex area is associated with more complex formed visual hallucinations such as pictures of people, animals or scenes. These are considered focal cognitive seizures.
In Parieto-occipital junction seizures Epileptic nystagmus may be seen. If nystagmus is seen, this is typically with the fast component to the side contralateral to the hemisphere of seizure onset and the slow component returning to the ipsilateral side. Eye movements typically occur with retained awareness, and may be accompanied by head or trunk version. There may also be eyelid flutter or forced eyelid closure.
Occipital seizures arising In Inferior to the calcarine fissure area tend to spread to the temporal lobe producing a focal impaired awareness seizure.
Occipital seizures arising in Superior to the calcarine fissure area can spread to the parietal lobe, front-parietal operculum or frontal lobes. Focal atonic motor seizures can occur if the seizure spreads rapidly to frontal regions.
What are pre – seizure symptoms?
Symptoms that indicate a seizure is in progress include: losing consciousness, which is followed by confusion. having uncontrollable muscle spasms. drooling or frothing at the mouth. falling. having a strange taste in your mouth. clenching your teeth. biting your tongue.
What are the most common symptoms of mild seizures?
Seizure signs and symptoms may include: Temporary confusion. A staring spell. Uncontrollable jerking movements of the arms and legs. Loss of consciousness or awareness. Cognitive or emotional symptoms, such as fear, anxiety or deja vu.
What is pre – seizure behaviour?
Abnormal behaviour possibly lasting for several hours fear, nervousness, disorientation, attention seeking.
What medicines cause seizures?
Common Causes of Drug-Induced Seizures. Of the 386 cases evaluated that were related to poisoning or drug intoxication in which seizures occurred, the leading causes were the following in order of frequency: bupropion, diphenhydramine, tricyclic antidepressants, tramadol, amphetamines, isoniazid, and venlafaxine.
What is aging?
The most common change in the cardiovascular system is stiffening …leading to hypertension. Your bones, joints and muscles. With age, bones tend to shrink in size and density, weakening them …resulting in fractures. Age-related structural changes in the large intestine can result in more constipation. Your bladder may become less elastic as you age, resulting in the frequent micturition. You can’t do much prevent aging. Prevent fall, take a supplement and have a healthy life style.
What is it like living with mental disorders for patients, relatives and caregivers?
Above we have discussed in summary the main psychiatric disorders. Not only do these disorders create havoc in the lives of those suffering from them but the caretakers and family members are also affected markedly. Let us therefore consider what it is like living with these conditions. Since these disorders affect behaviour of the patients sometimes the relatives are bewildered as to why the patient is behaving oddly, sometimes wickedly. It is even difficult to fathom if the change in behaviour is of sudden onset as opposed to personality disorders, retardation, ADHD or autism where the behaviour is of long standing. A previously stable person becomes unstable, a previously shy person shows disinhibition. For example, a previously nice old man suddenly has increased libido and becomes a sexual predator molesting his old wife or young women in the household. It might happen in dementia. What then? Or a stable successful businessman suddenly goes off in a spending binge, spending money on cars and not needed articles. It might happen in mania. How to go about it? It is extremely essential that these behaviours be understood in terms of illnesses by the relatives so that they can cope with them and thereby be treated or such unexplained behaviours can result in chaos in the life of the family.
What does it mean to live with anxiety and depression?
For the patient living with the symptoms of anxiety and depression means altering your entire schedule to fit the needs of your illness. No longer do circumstances dictate what your day will be like, anxiety and depression are now your blueprints. Either of these illnesses decides whether you will be sociable or a recluse as you complete your tasks.
For the relatives of patient suffering from anxiety like panic disorder, it is essential to understand that patient is avoiding exposure to anxiety proving situations and due to illness and not due to any character flaw in him. So, support to the patient is essential along with the treatment.
What it’s like living with depression?
For the patient living with depression feels like you’re in a dark hole with nowhere to go. Living with anxiety makes you feel like you’re losing your mind. Depression takes away all of your motivation and drive to do anything, but anxiety makes you want to constantly do that activity.
For the relatives it might feel quite difficult to fathom why a rich businessman suddenly feels that he is a pauper and must sell his house to meet his expense. The relatives at times react by showing the person his money, gold and other assets to no avail. Business decisions takes during depression might be contrary to what the person might have done if normal. If the person is in an executive post, like being the leader of an organisation or a country, the decision taken during depression might affect the fate of the organisation or the country.
How to live with obsessive compulsive neurotic patient?
For the doctor, when a person with OCPD approaches you with a problem, it seems such a grand waste of time as such a person repeats all his activity again and again. To empathise is important but you must also inform the person about his mental condition leading to his behaviour. The problem is that he understands it but has no choice.
For the family dealing with people who have OCPD can be especially difficult if you focus purely on their weaknesses, or on the parts of their personality that truly bothers you. But there are some aspects of OCPD that are actually the traits of a conscientious person. For example, the person with OCPD appreciates the value of hard work and is willing to put in intense effort to reach a goal. A person with OCPD may be careful with money, have strong morals or religious values, and have the capability to focus attention on one idea or detail for a long time. These strengths can come in handy in the academic world, in other employment sectors, and even in some social environments. Capitalize on these strengths, and point them out to the person with OCPD when possible.
How to live with bipolar disorder?
For the patient suffering from BD he must build structure into your life. Developing and sticking to a daily schedule can help stabilize the mood swings of bipolar disorder. Include set times for sleeping, eating, socializing, exercising, working, and relaxing. Try to maintain a regular pattern of activity even through emotional ups and downs.
For the relatives suffering from bipolar disorder, two things are of utmost importance. One is to manage indiscrete reckless behaviour during times of mania by treatment and to help him/her avoid any suicidal attempt by the patient during times of depressive phase. For example, patient may want to needlessly buy a Mercedes car in times of mania thinking he is the king, and sell his gold in times of depression, thinking he is a pauper. The key is to prevent such untoward incidents.
How to support a loved one with schizophrenia?
Tips for supporting a loved one’s schizophrenia treatment, is religious adherence to treatment as the patient might be suspicious of medications. Go for long acting medications if needed. It is unusual for paranoid patients to attack caregivers but not unknown. So, such event must be anticipated and help be at hand. Till medication helps, it is important not to confront or augment the psychotic delusion.
How to live with personality disorder?
Personality disorders can vary greatly between individuals, something that can complicate a diagnosis. Personality disorders are grouped into clusters with similar disorders based on the types of behaviours patients exhibit. These are commonly sorted into groups:
Cluster A disorders involve eccentric thoughts and behaviours. These include paranoid, schizoid and schizotypal personalities.
Cluster B disorders involve amplified thoughts and actions. Disorders in this group range from the aloof antisocial patient to the narcissist.
Cluster C disorders are based in fear. Obsessive-compulsive disorder and dependent or avoidant behaviours are commonly found in this classification.
Consistent unusual behaviours that make it difficult to relate to others. Bouts of irregular, alarming or alienating activity. Emotional instability paired with intense personal relationships. Dramatic, overly emotional displays aimed at drawing attention. Fear of relationships or fears in life that justify odd behaviours. Chronic avoidance, anxiousness or extreme shyness. Understanding is the key since these disorders are lifelong personality habits and not easily amenable to treatment,
How to live with an alcoholic?
Living with an addict for the relatives can be a living hell: unpredictable and dangerous, yet sometimes exciting and romantic. We never know when we’ll be blamed or accused. We can’t dependably plan social events. As the addict becomes more irresponsible, we pick up the slack and do more, often becoming the sole functioning parent or even the sole provider. We’re unable to lean on our partner for comfort or support. Meanwhile, we rescue him or her from disasters, medical emergencies, accidents, or jail, make excuses for no-shows at work and family gatherings, and patch up damaged property, relationships, and self-inflicted mishaps. We may also endure financial hardship, criminality, domestic violence, or infidelity due to the addict’s behaviour. We worry, feel angry, afraid, and alone. We hide our private lives from friends, co-workers, and even family to cover up the problems created by addiction or alcoholism. Our shame isn’t warranted; nonetheless, we feel responsible for the addict’s actions. Our self-esteem deteriorates from the addict’s lies, verbal abuse, and blame. Our sense of safety and trust erodes as our isolation and despair grow. Many of the feeling’s partners experience are the same, regardless of the type of addiction. Alcoholism is considered a disease. Like other addiction, it’s a compulsion that worsens over time. Alcoholics drink to ease their emotional pain and emptiness. Some try to control their drinking and may be able to stop for a while, but once alcohol dependency takes hold, most find it impossible to drink like non-alcoholic. When they try to curb their drinking, they eventually end up drinking more than they intend despite their best efforts not to. No matter what they say, they aren’t drinking because of you, nor because they’re immoral or lack willpower. They drink because they have a disease and an addiction. They deny this reality and rationalize or blame their drinking on anything or anyone else. Denial is the hallmark of addiction.
When should a person be considered an alcoholic?
The following parameters should be considered. When an alcoholic drinks alcohol in greater amounts or for a longer period than was intended. Has a persistent desire or has made failed attempts to reduce or control drinking? Spends great time in activities to obtain or use alcohol or to recover from its effects. Has a strong desire to drink alcohol. Fails to meet obligations at work, school, or home due to recurrent drinking. Drinks despite the recurrent social or interpersonal problems caused or worsened as a result. Stops or reduces important activities due to drinking. Drinks when it’s physically hazardous to do so. Drinks despite a recurrent physical or psychological problem caused or worsened as a result. Develops tolerance (needs increased amounts to achieve desired effect). Has withdrawal symptoms from disuse, such as tremor, insomnia, nausea, anxiety, agitation. Alcoholism is a family disease. It’s said that at least five other people experience the effects of each drinker’s alcoholism, coined “second-hand drinking” by Lisa Frederiksen. We try to control the situation, the drinking, and the alcoholic. If you live with an alcoholic, you’re affected most, and children severely suffer because of their vulnerability and lack of maturity, especially if their mother or both parents are addicts.
Alcoholics have two patterns of drinking. One is drinking daily from morning to night in binges followed by abstinence, or, two daily drinking in large amounts without abstinence. Both are dangerous.
It’s painful to helplessly watch someone we love slowly destroy him- or herself, our hopes and dreams, and our family. We feel frustrated and resentful from repeatedly believing the addict’s broken promises and from trying to control an uncontrollable situation. This is our denial.
In time, we become as obsessed with the alcoholic as he or she is with alcohol. We may look for him or her in bars, count his or her drinks, pour out booze, or search for bottles. As it says in Al-Anonymous- Understanding Ourselves, “All our thinking becomes directed at what the alcoholic is doing or not doing and how to get the drinker to stop drinking.” Without help, our co-dependency follows the same downward trajectory of alcoholism.
There is hope, and there is help for the addict and for co-dependent family members. The first step is to learn as much as you can about alcoholism and co-dependency. Many of the things we do to help an addict or alcoholic are counterproductive and actually can make things worse.

How must a relative trying to deal with an addict, act?
It is important and useful to have some guidelines when you’re dealing with an addicted person. To help you in this crisis situation, here are some Do’s and Don’ts.
Don’t: Such patients are plausible and may ask for loan of money. Don’t comply. They will abuse your loan on their addiction.
Do: Maintain your own balance and integrity. Don’t let the addicted person draw you into using drugs or alcohol with him/her. Also, don’t let him convince you that you’re wrong for seeing the problem.
Don’t: Expect results just by asking him/her to quit. It will seldom (if ever) do any good to say, “If you loved me, you’d quit.” The compulsion to get more alcohol or drugs is bigger than he is and it’s usually bigger than his love for his family. It’s just flat-out overwhelming. If you accept this, you can get started on the solution.
Do: Find a rehab program for your loved one. If you have any choice in the matter, ask plenty of questions before selecting one. Find out exactly how the program works, ask if you can talk to someone who has completed the program. The program should make sense to you.
Don’t: The National Institute on Drug Abuse recommends a program of longer than three months that for a better chance of sobriety. Addiction seldom occurs overnight and there is plenty of destruction of life skills along the way. It takes time to rebuild a life.
Do: If humanly possible, stand by the addicted person in your life. Sometimes, especially when there are kids, it’s vital to remove yourself and the children from the situation. If you can, let the addicted person know that you support him and his recovery. The drugs have already convinced him that he is worthless so when he has support, there is a greater chance he can turn things around during rehab.
Don’t: Put yourself in a situation where you can be abused mentally or physically. If you are vulnerable due to size, emotional state or other reason, find your own support. Family, counsellors, ministers, even law enforcement can and should be utilized. You might feel ashamed or embarrassed about being in this situation. That’s completely natural. You must speak out for your own protection. You can’t help anyone if you are beaten down or ill yourself.
Do: Insist on rehab as the right answer for addiction. Families with an addicted loved one live in terror of the phone call that tells them that their addicted loved one is dead or has been jailed. Find an effective rehab program and make this the only solution you will accept—not promises that she will “cut down,” “wean herself off,” or “only do it one more time.”
Don’t: Expect that the person will immediately take off for rehab when you first approach him. You may have to intervene. Either find a professional interventionist who has successfully gotten many people to rehab or get together with all your family and the addict’s close friends and cut off all means of escape. If some have been providing money or shelter, they must agree that rehab is the only option. There must be no way out other than going to rehab.
Do: If you are going to stage an intervention, it must be done from caring and love. Criticism or blame will only push the person further into his uncomfortable guilt. Drugs are already his solution for this guilt.
Don’t: Assume that his going to rehab means that everything has been resolved. He will need your love, guidance, and support during rehab and afterward as he establishes a new, sober life for himself. Help him move back into life in a step-by-step manner, maintaining your support.
What treatment are available for an addict?
Above all consider specialised treatment. Alcoholic anonymous participation gives good results. Treatment with baclofen, disulfiram or naltrexone is available for alcoholics. For alcohol deaddiction, my personal belief is that baclofen gives good results in binge drinking and otherwise gives abstinence in about 20 % of cases. Used correctly, disulfiram can give good results in alcohol abuse in over 50 % of patents.
Heroin use is a big problem and such patients somehow tends to get themselves and their family members including care givers in a soup. One must be careful as such patients for theft, or robbery. Those doctors providing buprenorphine treatment to heroin addicts must comply with state laws. Overzealous attempts to try to help such patients without understanding laws of the land can lead to legal trouble for the doctors concerned.
Addictions are covered later in the book.
What is biofeedback?
Biofeedback a process whereby electronic monitoring of a normally automatic bodily function is used to train someone to acquire voluntary control of that function.
What can be the aetiology of anxiety and its management?
Everyone periodically experiences fear and anxiety. Fear is an emotional, physical, and behavioural response to an immediately recognizable external threat (e.g., an intruder, a car spinning on ice). Anxiety is a distressing, unpleasant emotional state of nervousness and uneasiness; its causes are less clear. Anxiety is less tied to the exact timing of a threat; it can be anticipatory before a threat, persist after a threat has passed, or occur without an identifiable threat. Anxiety is often accompanied by physical changes and behaviours similar to those caused by fear.
Some degree of anxiety is adaptive; it can help people prepare, practice, and rehearse so that their functioning is improved and can help them be appropriately cautious in potentially dangerous situations. However, beyond a certain level, anxiety causes dysfunction and undue distress. At this point, it is maladaptive and considered a disorder.
Anxiety occurs in a wide range of physical and mental disorders, but it is the predominant symptom of several. Anxiety disorders are more common than any other class of psychiatric disorder. However, they often are not recognized and consequently not treated. Left untreated, chronic, maladaptive anxiety can contribute to or interfere with treatment of some general medical disorders.
The causes of anxiety disorders are not fully known, but both psychiatric and general medical factors are involved. Many people develop anxiety disorders without any identifiable antecedent triggers. Anxiety can be a response to environmental stressors, such as the ending of a significant relationship or exposure to a life-threatening disaster.
What medical disorders can directly cause anxiety?
Hyperthyroidism, Pheochromocytoma, Hyperadrenocorticism, Heart failure, Arrhythmias, Asthma, COPD.
What drugs can cause anxiety?
Other causes include use of drugs; effects of corticosteroids, cocaine, amphetamines, and even caffeine can mimic anxiety disorders. Withdrawal from alcohol, sedatives, and some illicit drugs can also cause anxiety.
What can be the result of anxiety?
Anxiety can arise suddenly, as in panic, or gradually over many minutes, hours, or even days. Anxiety may last from a few seconds to years; longer duration is more characteristic of anxiety disorders. Anxiety ranges from barely noticeable qualms to complete panic. The ability to tolerate a given level of anxiety varies from person to person.
Anxiety disorders can be so distressing and disruptive that depression may result. Alternatively, an anxiety disorder and a depressive disorder may coexist, or depression may develop first, with symptoms and signs of an anxiety disorder occurring later.
Deciding when anxiety is so dominant or severe that it constitutes a disorder depends on several variables, and physicians differ at what point they make the diagnosis. Physicians must first use history, physical examination, and appropriate laboratory tests to determine whether anxiety is due to a general medical disorder or drug. They must also determine whether anxiety is better accounted for by another mental disorder
A family history of anxiety disorders (except acute and posttraumatic stress disorders) helps in making the diagnosis because some patients appear to inherit a predisposition to the same anxiety disorders that their relatives have, as well as a general susceptibility to other anxiety disorders. However, some patients appear to acquire the same disorders as their relatives through learned behaviour.
How is anxiety treated?
Treatments vary for the different anxiety disorders, but typically involve a combination of psychotherapy specific for the disorder and drug treatment. The most common drug classes used are the benzodiazepines and SSRIs.
What is the management of OCD?
OCD is a chronic illness that usually can be treated in an outpatient setting. The mainstays of treatment of OCD include the use of serotoninergic antidepressant medications, particular forms of behaviour therapy (exposure and response prevention and some forms of CBT), education and family interventions, and, in extremely refractory cases, neurosurgery.
How is panic disorder treated?
Treatment for panic disorder focuses on reducing or eliminating your symptoms. This is achieved through therapy with a qualified professional and in some cases, medication. Therapy typically involves cognitive-behavioural therapy (CBT). This therapy teaches you to change your thoughts and actions so that you can understand your attacks and manage your fear.
Medications used to treat panic disorder can include selective serotonin reuptake inhibitors (SSRIs), SSRIs prescribed for panic disorder may include: fluoxetine, paroxetine, sertraline and serotonin-norepinephrine reuptake inhibitors (SNRIs), benzodiazepines like diazepam or clonazepam. In addition to these treatments, there are a number of steps that you can take at home to reduce your symptoms. Examples include: maintaining a regular schedule, exercising on a regular basis, getting enough sleep, avoiding the use of stimulants such as caffeine
What is the treatment of phobias?
Pharmacotherapy recommendations differ for SAD and specific phobias. As a general rule, while both medication and psychotherapy are first-line treatment for SAD, pharmacotherapy is not first-line treatment for specific phobia.
What is the treatment for Social anxiety disorder (social phobia)?
At present, three drugs are approved by the US Food and Drug Administration (FDA) for the treatment of social anxiety disorder, as follows: The selective serotonin reuptake inhibitors (SSRIs) paroxetine and sertraline. The selective serotonin/norepinephrine reuptake inhibitor (SNRI) venlafaxine. The SSRIs escitalopram, fluoxetine, and fluvoxamine. The monoamine oxidase inhibitor (MAOI) phenelzine is rarely used to fear of interactions.
Treatment of social anxiety disorder should be initiated with an SSRI, along with benzodiazepines, titrated to the minimum effective dosage. If the response is partial or non-existent at 6 weeks, the dosage may be increased; this may be done every 2 weeks until the maximum dose is reached.
Long-term treatment data from double-blind, randomized controlled trials addressing social anxiety disorder show that continuing SSRI or venlafaxine therapy for up to 6 months can result in increased treatment response rates. Long-term treatment data on clonazepam are limited but support the long-term efficacy of this drug.
What is the treatment for specific phobias?
As a general rule, pharmacotherapy is not first-line treatment for specific phobia.
To date, no controlled studies have demonstrated the efficacy of psychopharmacologic intervention for specific phobias. Clinical lore suggests that as-needed administration of a short-acting benzodiazepine might be useful for temporary anxiety relief in specific situations (e.g., right before boarding a plane, for patients with a fear of flying).
What is the treatment for Agoraphobia?
Agoraphobia, specifically the panic symptoms, responds to treatment with SSRIs (e.g., escitalopram, citalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline), [and some benzodiazepines (e.g., alprazolam, lorazepam, diazepam, and clonazepam.
What is the drug treatment of depression?
Drugs used for treatment of depression include the following: Selective serotonin reuptake inhibitors (SSRIs), Serotonin/norepinephrine reuptake inhibitors (SNRIs), Atypical antidepressants, Tricyclic antidepressants (TCAs).
My take is that if there are no contraindications one must start with tricyclics as they give the best results. Their side effects have been over emphasised by the compliant journals. Switch to SNRI if no response. Can use SSRI in case of side effects to the tricyclics. Continue for a duration of 6 months or more or as individually dictated and then taper off.
SSRIs have the advantage of ease of dosing and low toxicity in overdose. SSRIs are greatly preferred over the other classes of antidepressants for the treatment of children and adolescents, and they are also the first-line medications for late-onset depression. This recommendation is supported by the 2011 APA guideline. So, in children and elderly, use SSRIs.
The serotonin-deficient variety of depression is characterised more by feelings of misery as opposed to flatness and lack of drive (the dopamine variety).
How to manage psychotic symptoms?
Anti-psychotic medications have been most effective in easing symptoms. The addition of lithium or anticonvulsants as mood stabilizers to this combination can be beneficial for those with bipolar disorder. Electroconvulsive therapy (ECT) is a very rapid and effective treatment for psychotic depression and catatonic psychosis.
I start with conventional antipsychotics like haloperidol, and switch to risperidone or trifluoperazine after stabilisation for a duration of a month or more. The dose should be adjusted to minimal dose that can keep the symptoms from appearing. The duration will depend on diagnosis. Schizophrenia which presented with the duration of more than six months may require indefinite treatment, while shizophreniform psychosis or brief psychotic disorder may require even lesser duration of treatment. All must be individualised. A high risk of relapse patient will require a longer duration of treatment
What are additional Therapies for Depression?
Transcranial magnetic stimulation (TMS) has been approved by the FDA for the treatment of major depressive disorder when one class of antidepressant has failed.
Vagus nerve stimulation (VNS) has been approved by the FDA for use in adult patients who have failed to respond to at least 4 adequate medication and/or ECT treatment regimens. The device requires surgical implantation.
Deep brain stimulation (DBS) appears to be a safe and effective long-term treatment for treatment-resistant depression. Experience with this invasive technique is limited, however, and the method remains experimental.
How is Treatment-Resistant Depression managed?
In one third to two thirds of cases of depression, patients fail to remit with first-line therapy
Assessment of patients with treatment-resistant depression should include consideration of the following, accuracy of diagnosis and possible comorbid medical conditions, adequacy of medication dose and duration of treatment, as well as adherence to treatment regimen, possible comorbid psychiatric conditions (e.g., substance abuse, anxiety disorders, personality disorders).
Assuming that the assessment of the diagnosis is correct, there are no significant complicating diagnoses, and the current treatment has been at a therapeutic dose for a sufficient amount of time, possible interventions for persistent symptoms can include the following. • Increasing the medication dose to the maximum tolerated, • Augmenting the current medication with another antidepressant, • Changing to a different antidepressant, • Adding psychotherapy or more intensive care if not already completed, • Considering the use of ECT
The Sequenced Treatment Alternatives to Relieve Depression (STARD) trial, the largest open-label trial to date, examined various strategies for treatment-resistant depression. The STARD trial showed that in patients who did not respond to an initial SSRI (citalopram), switching to another SSRI antidepressant, changing medication class, and switching to CBT were all equally effective treatments. Achieving remission, rather than partial response, was the best predictor of a better long-term prognosis.
The AHRQ found conflicting evidence regarding the differences between second-generation antidepressants for treatment-resistant depression. A good-quality study revealed no substantial differences in the effectiveness of sustained-release bupropion, sertraline, and sustained-release venlafaxine; however, fair-quality studies indicated a trend toward greater effectiveness with venlafaxine than with citalopram, fluoxetine, or paroxetine.
My take is dothiepin should be the starting drug, followed by switch to imipramine and if no response to imipramine to be changed to venlafaxine in dose of 150 mg/d
Augmentation combinations can include the following: • Bright-light therapy plus any antidepressant, • Buspirone (BuSpar) plus a TCA or SSRI, • Lithium plus any antidepressant
• Methylphenidate (Ritalin) or dextroamphetamine (Dexedrine) plus any antidepressant other than an MAOI, • TCA plus an SSRI, • Triiodothyronine (Cytomel) plus any antidepressant
The STARD trial found that augmentation of an SSRI with bupropion and augmentation with buspirone were equally effective after a lack of response to the SSRI. Aripiprazole (Abilify) is the first drug approved by the FDA for adjunctive treatment in major depressive disorder and the first drug to receive FDA approval for use in treatment-resistant depression. What is a medical ECT? Electroconvulsive therapy (ECT) is a medical treatment most commonly used in patients with severe major depression or bipolar disorder that has not responded to other treatments. ECT involves a brief electrical stimulation of the brain while the patient is under anaesthesia. How effective is ECT? Studies show that electroconvulsive therapy (ECT) is helpful 70% to 90% of the time, but each person’s experience is unique. The degree of improvement. The treatments may bring a full recovery, a partial recovery, or in some cases, no benefit at all. How does electroconvulsive therapy (ECT) work? Electroconvulsive therapy (ECT) is a procedure, done under general anaesthesia, in which small electric currents are passed through the brain, intentionally triggering a brief seizure. ECT seems to cause changes in brain chemistry that can quickly reverse symptoms of certain mental health conditions. What are indications for ECT? Indications for continuation ECT include a history of ECT-responsive illness, patient preference, resistance or intolerance to medications alone, and ability of the patient (or surrogate consenter) to provide informed consent and adhere to the treatment plan. What are the contraindications of ECT therapy? Due to the physiologic changes associated with ECT, the list of contraindications includes recent MI, heart failure, recent stroke, elevated ICP, aneurysm/AVM at risk of rupture, pheochromocytoma, severe HTN, and cervical spine instability, most of which are only relative. What are the long-term effects of ECT? Effects on memory One of the main reasons ECT is considered a controversial therapy concerns the purported effects of the therapy on memory. ECT may cause both retrograde amnesia (the loss of memories that existed prior to treatment) and anterograde amnesia (loss of memories formed after treatment). What are the immediate negative side effects of ECT? The main side effects associated with ECT are described below: Muscle soreness. A patient’s muscles may feel sore after they have undergone ECT, although this is usually caused by the administration of muscle relaxants rather than activity in the muscles during therapy. What is the success rate of ECT? ECT is delivered in a series of six to 12 sessions, usually three times a week. Treatment may be either inpatient or outpatient, depending on the patient’s situation. The good news — ECT has been found to have an 86 percent success rate for severe depression. What is Paediatric Depression? Increasingly, paediatric patients with depression have been treated with SSRIs or CBT. Fluoxetine is the only medication currently approved by the FDA for the treatment of depression in children. There are few studies on the use of medications for paediatric patients with major depressive disorder, and some of those that have been performed have methodologic problems. Additionally, very few pharmacokinetic studies have been performed in children, and most of those have focused on the effects of TCAs. In adolescents, suicidality associated with antidepressants is an important issue. What are the dangers in treating paediatrics patients for depression? The clinician needs to inform parents and patients about adverse effects, dose, timing of therapeutic effect, and danger of overdose, particularly with TCAs, before initiating pharmacologic treatment. Parents should take responsibility for medication storage and administration, especially with younger children and children at risk for suicide. What are the guidelines for treating paediatric depression? The guideline is as follows: • For mild depression, CBT or interpersonal psychotherapy is recommended first • For pharmacologic therapy, SSRIs are the first-line choice • If there is no response to the SSRI, switch to a second SSRI. How do you treat resistant depression in paediatric population? In the Treatment of SSRI-Resistant Depression in Adolescents, patients who did not respond to an initial SSRI and were switched to combination therapy with CBT plus either another SSRI or venlafaxine had no better response than switching medications alone. However, a switch to any second medication provided a good response, and each of the medications provided a similar response. The use of SSRIs as first-line medications in paediatric patients is supported by reports that these agents are effective in this population and have a relatively safe adverse-effect profile and very low lethality after overdose; in addition, SSRIs offer the convenience of once-daily administration. Several studies have reported a 70-90% response rate to SSRIs in adolescents with major depressive disorder. Children and adolescents with major depressive disorder responded significantly more frequently to fluoxetine (58%) than to placebo (32%), according to Emslie et al in an 8-week double-blind study. However, only 31% of children achieved full remission. A possible explanation for the partial response in these young patients is that the effective treatment may involve variation in dose or length of treatment. Also, the ideal treatment likely involves a combination of pharmacologic and psychosocial interventions. Except for lower initial doses, the administration of SSRIs in children and adolescents is similar to the treatment regimens used for adult patients. The clinician should treat patients with adequate and tolerable doses for at least 4 weeks. At 4 weeks, if the patient has not shown even minimal improvement, the clinician should consider increasing the dose. If, at this time, the patient shows improvement, the dose can be continued for at least 6 weeks. However, if no improvement is apparent at 6 weeks, other treatment strategies should be considered. Is there a relationship between antidepressants and suicidality in youths? In October 2003, the FDA issued a public health advisory regarding reports of suicidality in paediatric patients being treated with antidepressant medications for major depressive disorder. This advisory reported suicidality (both ideation and attempts) in clinical trials of various antidepressant drugs in paediatric patients. The FDA asked that additional studies be performed, because suicidality occurred in both treated and untreated patients with major depression and, thus, could not be definitively linked to drug treatment. In September 2004, the results of an FDA analysis suggested that the risk of emergent suicidality in children and adolescents taking SSRIs was real. The FDA advisors recommended the following: • A black-box warning label should be placed on all antidepressants, indicating that they increase the risk of suicidal thinking and behaviour (suicidality) • A patient information sheet (“Medication Guide”) should be provided to the patient and the patient’s caregiver with every prescription • The results of controlled paediatric trials of depression should be included in the labelling for antidepressant drugs. So, what are the recommendations when treating paediatric depression? Given the possibility of increased suicidality, the FDA recommended that physicians who prescribe antidepressants to paediatric patients provide close monitoring in these cases. Close monitoring includes at least weekly face-to-face contact with patients or their family members or caregivers during the first 4 weeks of treatment; visits every other week for the next 4 weeks; visit at 12 weeks; and then visits as clinically indicated beyond 12 weeks. Additional contact by telephone may be appropriate between office visits. Some studies have shown that the FDA warnings regarding suicide in children on antidepressants may have had the unintended result of a decrease in the rates of diagnosis and treatment of depression, as well as dosing adjustments by physicians and an increase in suicidality. It has also been noted that monitoring of these patients did not increase following the warnings. TCAs are no longer considered the first-line treatment for paediatric patients with depressive disorders; however, individual cases may respond better to TCAs than to other medications. TCAs may also be useful for those with comorbid attention deficit hyperactivity disorder (ADHD), enuresis, and narcolepsy, as well as for augmentation strategies. What tests must be done before treating paediatric depression with TCAs? The TCAs require a baseline electrocardiogram (ECG), resting blood pressure, and pulse rate. Because of the potential of the TCAs to induce a fatal overdose, the clinician must carefully determine the exact amount of medication to be prescribed. Plasma levels should be monitored to measure compliance and to avoid toxicity. In addition, weight should be frequently documented. No laboratory tests are currently indicated before or during the administration of the SSRIs. No other tests are indicated in a healthy child before starting antidepressants. How should depression during Pregnancy be treated? Although avoiding the use of medication during pregnancy is preferable, the benefits of prompt medical treatment of major depressive disorder may often outweigh the risks of exposure of the foetus to an antidepressant. One meta-analysis found that the possible risks of untreated peripartum depression include increased risk of preterm birth, low birth weight, slower head growth, and intrauterine growth restriction. There is no clear evidence that available antidepressants are teratogenic. APA guidelines support psychotherapy as the first choice of therapy for pregnant women with mild depression. In severe depression during pregnancy, especially in cases of psychosis, agitation, or severe retardation, electroconvulsive therapy may be the safest and quickest treatment option. One randomized, double-blind study found that bright-white-light therapy was significantly more effective than placebo for depression during pregnancy. Conflicting evidence exists regarding the use of SSRIs during pregnancy and an increased risk of persistent pulmonary hypertension of the new-born (PPHN). An initial Public Health Advisory in 2006 was based on a single retrospective study. Since then, studies have yielded conflicting findings, with 3 trials suggesting risk and 3 trials finding no risk of PPHN associated with antidepressants. In a December 2011 review, the FDA concluded that, given the conflicting results from different studies, it is premature to reach any conclusion about a possible link between SSRI use in pregnancy and PPHN. The FDA advises health care professionals not to alter their current clinical practice of treating depression during pregnancy and to report any adverse events to the FDA MedWatch program. What are the risks to infants whose mothers were on antidepressants? A further possible risk for infants born to women taking SSRIs is neonatal withdrawal symptoms, which includes high-pitched crying, tremors, and disturbed sleep. In one study, 30% of neonates exposed to SSRIs in utero developed withdrawal symptoms, typically peaking within 2 days of birth but sometimes as long as 4 days after birth. These investigators recommended monitoring exposed neonates for as long as 48 hours after birth. What is postpartum Depression? Principles of treatment of postpartum major depressive disorder are the same as for depression during any other time of life. Earlier initiation of treatment is associated with better prognosis. Patients with postpartum depression should be assessed for danger to herself or to her children, as well as for other symptoms such as psychosis or substance abuse. Most antidepressants probably can be used safely during breast-feeding; however, this has not been studied thoroughly, and the same risk-benefit considerations should be applied as when treating depression during pregnancy. Postpartum blues are typically mild and resolve spontaneously; no specific treatment is required, other than support and reassurance. For first episodes of depression in postpartum women, 6-12 months of treatment is recommended. For women with recurrent major depression following pregnancy, long-term maintenance treatment with an antidepressant is indicated. How to go about antidepressants and Breast-feeding? Most antidepressants probably can be used safely during breast-feeding; however, this has not been studied thoroughly, and the same risk-benefit considerations should be applied as when treating depression during pregnancy. Women who plan to breast-feed must be informed that antidepressants, like all psychotropic medications, are secreted into breast milk. Concentrations in breast milk vary widely. Data on the use of TCAs, fluoxetine (Prozac), sertraline (Zoloft), and paroxetine (Paxil) during breast-feeding are encouraging, and serum antidepressant levels in the breast-fed infant are either low or undetectable. Reports of toxicity in breast-fed infants are rare, although the long-term effects of exposure to trace amounts of medication are not known. Are special precautions necessary while using antidepressants in the Elderly? Geriatric psychopharmacology follows the tenet of “start low, go slow, but go.” This is based on the belief that elderly patients respond to such agents more slowly than younger patients and the fact that older patients tend to have a higher rate of side effects and adverse events from drug-drug or drug-disease interactions. Most classes of medications have been associated with an increased risk of falls in elderly patients, especially the frail elderly. Furthermore, results from a study by Andreescu et al suggest that high levels of worry in elderly patients with depression were associated with slower response to pharmacotherapy and earlier recurrence. Start antidepressant medications at a lower dose (often, half the usual dose) in the elderly, and titrate more slowly than in younger adults. Furthermore, customary practice is to give the elderly patient a longer trial (12 wk. vs customary 6-8 wk.) before increasing the dose, changing the medication, or labelling it a failure. However, the need to wait 12 weeks remains a point of controversy and is undergoing more research. In the elderly, drug-drug interactions are a concern with particular SSRIs because polypharmacy is common in this age group. Of the SSRIs, the likelihood of drug-drug interaction is highest with fluoxetine, paroxetine, and fluvoxamine. The specific interactions of these medications and medications commonly used in the elderly (e.g., certain antibiotics, warfarin) are well established and available in many reference books. SSRIs should be used in the elderly only with consideration by a physician familiar with these types of medications. The SSRIs that offer a lower likelihood of drug-drug interactions include escitalopram, citalopram, and sertraline. These medications should be used as first-line treatment in the elderly or in patients where drug-drug interaction is a concern. Gastrointestinal side effects, including nausea, which can lead to weight loss, can be a problem in the elderly with use of SSRIs. Often, the nausea is short-lived, but when it is not, further options should be evaluated. When to hospitalize in depression? If suicidality is present, hospitalization with the patient’s consent or via emergency commitment should be undertaken unless there are clear-cut means to ensure the patient’s safety while outpatient treatment is begun. A child who is suicidal or has made an attempt at suicide should be admitted to a protected environment until all medical and social services can be employed. In addition to suicidal or homicidal ideation, indications for psychiatric hospitalization include the following: Severe depression, Gross disorganization, Inability to care for self (i.e., inability to provide basic needs such as eating, drinking, and other activities of daily living) and failing medical status due to depression. What is fatal insomnia, (FI)? Fatal insomnia is a typically hereditary prion disorder causing difficulty sleeping, motor dysfunction, and death. FI, a very rare disease, usually results from an autosomal dominant mutation, but several sporadic cases have been identified. Average age at onset is 40 yr. (ranging from the late 30s to the early 60s). Common early symptoms include difficulty falling asleep and intermittent motor dysfunction (eg, myoclonus, spastic paresis). This stage can last for months but eventually progresses to severe insomnia, myoclonus, sympathetic hyperactivity (eg, hypertension, tachycardia, hyperthermia, sweating), and dementia. Death occurs in an average of 13 mo. FI should be considered in patients with motor dysfunction, sleep disturbances, and a family history. Genetic testing can confirm the diagnosis. What Complications can arise during treatment for Depression with SSRIs? Clinically significant hyponatremia may develop in elderly patients taking SSRIs. In addition to older age, risk factors include the following, • Female gender• Smoking • Low body weight • Tumours • Respiratory or CNS illnesses • Previous episodes of hyponatremia • Concomitant use of other medications (particularly diuretics) • Antidepressant-induced hyponatremia occurs through the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), resulting in an euvolemic hyponatremia with low serum and high urine osmolarities. The hyponatremia generally starts within 1 month after starting the medication, and it reverses within a month after discontinuing the medication. Monitoring the sodium level in the elderly for at least 1 month after commencing an SSRI is suggested. Although SSRIs do not have the same risk of cardiac arrhythmia as is present with TCAs, arrhythmia risk is especially pertinent in overdose. In addition, suicide risk must always be considered, especially when treating a child or adolescent with mood disorder. Suicidality A small number of case reports have described a putative association between SSRI administration and increased suicidality (perhaps linked to behavioural activation or akathisia). However, although such phenomena may have occurred in a small number of cases, several studies suggest that SSRIs, like other antidepressants, generally reduce the risk of suicide in adult patients who are depressed. Stroke A large-scale study that followed more than 80,000 women aged 54-79 found that women who suffer depression and use antidepressants face an increased risk of stroke. The hazard ratio for stroke was 1.29 for women with a history of depression. Withdrawal symptoms Abrupt discontinuation of SSRIs that have shorter half-lives, such as paroxetine, may induce withdrawal symptoms, some of which may mimic a recurrence of a depressive episode (e.g., tiredness, irritability, severe somatic symptoms). The withdrawal symptoms can appear after as few as 6-8 weeks of SSRI treatment. In addition to causing rebound depression, paroxetine discontinuation can also cause cholinergic rebound. Moreover, relapse may occur earlier after rapid withdrawal (< 15 days) than after more gradual withdrawal (≥ 15 days). Interactions with other drugs Awareness of possible interactions with other medications is important. To varying degrees, but especially for fluvoxamine, the SSRIs inhibit the metabolism of several medications that are metabolized by the diverse clusters of hepatic cytochromes P-450 isoenzymes (e.g., TCAs, neuroleptics, antiarrhythmics, benzodiazepines, carbamazepine, theophylline, warfarin, terfenadine [removed from United States market]). This inhibition results in higher plasma levels of those agents. In addition, interactions of SSRIs with other serotonergic medications, particularly MAOIs, may induce the serotonergic syndrome, marked by agitation, confusion, and hyperthermia. SSRIs also have a high rate of protein binding, which can lead to increased therapeutic or toxic effects of other protein-bound medications. MAOIs should not be administered less than 5 weeks after discontinuation of fluoxetine and less than 2 weeks after discontinuation of other SSRIs. Also, the clinician should not prescribe SSRIs within 2 weeks after stopping the MAOIs. What Complications can arise during treatment for Depression with Tricyclic antidepressants? The adverse effects of TCAs, which result largely from their anticholinergic and antihistaminic properties, include the following: • Sedation, • Confusion, • Dry mouth, • Orthostasis, • Constipation, • Urinary retention, • Sexual dysfunction, • Weight gain Caution should be used in patients with cardiac conduction abnormalities. Bupropion is associated with a risk of seizure at doses above 450 mg a day, especially in patients with a history of seizure or epileptic disorders. This risk appears much lower in the sustained-release bupropion preparations. Mirtazapine is a potent antagonist at 5-HT2, 5-HT3, alpha2-, and histamine (H1) receptors and, thus, can be very sedating and frequently causes weight gain. Adverse effects such as drowsiness may tend to improve over time and with higher doses. Trazodone is very sedating and usually is used as a sleep aid in small doses (i.e., 25 to 50 mg) rather than as an antidepressant. What is mania? Mania is a mental illness marked by periods of great excitement or euphoria, delusions, and overactivity. Many people suffering from mania do not think anything is wrong. What does Mania feel like? Because manic episodes can cause great elation or great irritability, manic episodes can be perceived as pleasant or unpleasant. For some with a grandiose, elated mood, a manic episode is a pleasurable experience. They feel very good about themselves and engage in pleasurable behaviour, like spending money or having sex. What are the physical signs of mania? A mixed episode of bipolar disorder features symptoms of both mania or hypomania and depression. Common signs of a mixed episode include depression combined with agitation, irritability, anxiety, insomnia, distractibility, and racing thoughts. What can cause mania? Various triggers have been associated with switching from euthymic or depressed states into mania. One common trigger of mania is antidepressant therapy. Studies show that the risk of switching while on an antidepressant is between 6-69 percent. What are signs of mixed mania in bipolar disorder? A mixed episode of bipolar disorder features symptoms of both mania or hypomania and depression. Common signs of a mixed episode include depression combined with agitation, irritability, anxiety, insomnia, distractibility, and racing thoughts. What medications trigger mania? Drugs That Might Cause Mania (Excessive Elation) are isoniazid, corticosteroids, Methylphenidate (Ritalin) or amphetamine, recreational drugs like cocaine or phencyclidine (PCP), Levothyroxine and antidepressants. How to treat bipolar disorder in pregnancy? Both treated and untreated women with bipolar disorder were at greater risk of adverse pregnancy outcomes than women without mental illness. It is important to remember the potential consequences of bipolar relapse in pregnancy and the puerperium: a woman’s mental state may preclude her from caring for herself or for her child adequately and this may lead to offspring being removed from maternal care. Given the current status it is clear that prophylactic treatment with psychotropic drugs should be actively encouraged for all pregnant women with bipolar disorder. What are the symptoms of hypomania? Effected people tend to overestimate their capabilities. They feel inflated self-esteem or grandiosity. Increased alcohol consumption. They fail to see the obvious risks involved in their ventures. Making lots of plans. What is the difference between mania and hypomania? As nouns the difference between mania and hypomania. is that mania is violent derangement of mind; madness; insanity while hypomania is (medicine) a mild form of mania, especially the phase of several mood disorders characterized by euphoria or hyperactivity. What drugs are used for Mania? For acute mania, the following medications are commonly prescribed: lithium, Depakote (divalproex), Tegretol (carbamazepine), Trileptal (oxcarbazepine), and antipsychotic medications such as Zyprexa (olanzapine) or Seroquel (quetiapine). After how many episodes of bipolar I can be diagnosed? In order to be diagnosed with bipolar I, you must have had at least one manic episode that may have been preceded or followed by hypomanic or depressive episodes. What is bipolar ll. In the case of bipolar II, you must have had at least one major depressive episode and at least one hypomanic episode, but never experienced a manic episode. What is alcohol withdrawal? Alcohol withdrawal is physical symptoms and emotions you have if you drink heavily or frequently and suddenly stop drinking. You are most likely to have withdrawal problems 1 to 7 days after your last drink, or if you drink much less alcohol than you usually drink. What is the cause? If you abuse alcohol, you may have withdrawal if: You decide to stop drinking. You are in a place where you can’t drink alcohol, such as at a hospital, treatment centre, or jail. What are the symptoms? The effects of alcohol withdrawal vary greatly. Most people with mild to moderate alcohol dependence have one or more of these symptoms: Headache, dizziness, nausea and vomiting, shaking, sweating, restlessness, seizures, increased heart rate or blood pressure, trouble sleeping or concentrating, strong desire to drink to relieve the symptoms of withdrawal. Some people who are dependent on alcohol have a life-threatening condition called delirium tremens (DTs) when they stop drinking alcohol. This is a medical emergency. The symptoms may include, confusion, hallucinations, agitation, seizures, memory problems, fever, very high heart rate and blood pressure. How is it diagnosed? Your healthcare provider will review your symptoms, examine you, and ask about your medical history and memory. You may have one or more of these tests: urine and blood tests to check for the level of alcohol and other drugs in your body blood tests to find out how your liver and kidneys are working X-rays to check for broken bones from a fall or other health problems. How is it treated? If you abuse or are dependent on alcohol, you must first admit that you have a problem. Some people know they have an alcohol problem but deny that they need help to stop drinking. When you can admit that you have problem and admit you need help, call your healthcare provider. Many people who abuse or are dependent on alcohol have trouble admitting that they have a problem. Others may then have to confront those who abuse or are dependent on alcohol about the need for treatment. Detoxification: Detoxification is also known as “drying out.” It means that you stop using alcohol completely. Detoxification can be done as an outpatient, or in a hospital or drug treatment facility. Which choice is best for you depends on how much and how long you have been drinking? It also depends on other medical problems that you may have. Treatment for withdrawal symptoms may include: anti-anxiety medicines, blood pressure medicine Anticonvulsants, vitamins, intravenous (IV) fluids. Detoxification may take 3 to 4 days. Long-Term Treatment: After detoxification, treatment may include social, medical, and psychological therapies. Social treatment involves family members and focuses on problems at home and at work. To discourage you from drinking again, your healthcare provider may prescribe medicines. These medicines work best as one part of a full treatment program. Disulfiram (Antabuse) will make you feel sick if you drink alcohol after you take the medicine. Knowing that you will have this reaction can discourage you from drinking. Naltrexone or acamprosate can help stop drinking by reducing the craving for alcohol. Psychological therapy often involves: Group therapy to understand alcohol dependence and why people drink. Strategies to help people learn ways to limit the amount of alcohol they drink. Cognitive behaviour therapies are helpful for people trying to manage situations and triggers which may tempt them to abuse alcohol. Self-help support groups such as Alcoholics Anonymous (AA) and Rational Recovery can be helpful. AA looks at alcohol abuse and dependence as a disease. RR looks at alcohol abuse and dependence as a choice. At local chapter meetings you can meet others and get support to help you avoid alcohol. Meetings are open to anyone who has a drinking problem and wants to become and stay sober. Al-Anon meetings can help support families of people who abuse alcohol. How long will the effects last? The severe shakes and hallucinations of delirium tremens (DTs) may last 1 to 5 days. Alcohol has long-lasting effects. It can take weeks or months before you feel more clear-headed, less depressed, less anxious, and have more energy. DTs can be fatal if not treated. How can I take care of myself? If you abuse or are dependent on alcohol, the most important thing you can do is to admit the problem and ask for help. If you decide to stop drinking alcohol or are in a situation in which you cannot drink (such as in a hospital), ask for medical help. You may not need hospital treatment for withdrawal symptoms, but you should be where someone can get help for you if you need it. While you are being treated for withdrawal: Follow advice for treatment of any other medical problems. Talk with family and friends. Consider joining a support group in your area. Ask for help at home and work when the load is too great to handle. Find ways to relax, for example take up a hobby, listen to music, watch movies, take walks. Try deep breathing exercises when you feel stressed. Try to get at least 7 to 9 hours of sleep each night. Eat a healthy diet. Limit caffeine. If you smoke, quit. Don’t use alcohol or drugs. Exercise according to your healthcare provider’s instructions. . To help prevent problems, tell your healthcare provider and pharmacist about all the medicines, natural remedies, vitamins, and other supplements that you take. What can be done to help prevent alcohol withdrawal? If you are physically dependent on alcohol, you will have withdrawal symptoms when you quit drinking. Seek treatment so that you can withdraw safely and with much less discomfort. What is amnesia? Amnesia is partial or total inability to recall past experiences. It may result from traumatic brain injury, degeneration, metabolic disorders, seizure disorders, or psychologic disturbances. Diagnosis is clinical but often includes neuropsychologic testing and brain imaging (e.g., CT, MRI). Treatment is directed at the cause. What happens in the brain in amnesia? Processing of memories involves registration (taking in new information), encoding (forming associations, time stamps, and other processes necessary for retrieval), and retrieval. Deficits in any of these steps can cause amnesia. Amnesia, by definition, results from impairment of memory functions, not impairment of other functions (e.g., attention, motivation, reasoning, language), which may cause similar symptoms. What is the working classification of amnesia? Amnesia can be classified as follows: Retrograde: Amnesia for events before the causative event Anterograde: Inability to store new memories after the causative event Global: Amnesia for information related to all senses and past times Sense-specific: Amnesia for events processed by one sense—e.g., an agnosia Amnesia may be transient (as occurs after brain trauma), fixed (as occurs after a serious event such as encephalitis, global ischemia, or cardiac arrest), or progressive (as occurs with degenerative dementias, such as Alzheimer’s disease). Memory deficits more commonly involve facts (declarative memory) and, less commonly, skills (procedural memory). What are the causes of amnesia? Amnesia can result from diffuse cerebral impairment, bilateral lesions, or multifocal injuries that impair memory-storage areas in the cerebral hemispheres. Predominant pathways for declarative memory are located along the medial Para hippocampal region and hippocampus as well as in the inferomedial temporal lobes, orbital surface of the frontal lobes (basal forebrain), and diencephalon (which contains the thalamus and hypothalamus). Of these structures, the hippocampal gyri, hypothalamus, nuclei of the basal forebrain, and dorsomedial thalamic nuclei are critical. The amygdaloid nucleus contributes emotional amplifications to memory. The thalamic intralaminar nuclei and brain stem reticular formation stimulate the imprinting of memories. Bilateral damage to the mediodorsal nuclei of the thalamus severely impairs recent memory and the ability to form new memories; the most common causes are Thiamine deficiency, Hypothalamic tumours, vertebrobasilar ischemia. Other causes of amnesia, include the following: Bilateral damage to the medial temporal lobes (especially the hippocampus) Degenerative dementias Severe brain trauma Global brain anoxia or ischemia Alcoholic-nutritional disorders (e.g., Wernicke’s encephalopathy, Korsakoff’s psychosis—see Drug Use and Dependence: Wernicke’s Encephalopathy and see Drug Use and Dependence: Korsakoff’s Psychosis) Various drug intoxications (e.g., chronic solvent sniffing, amphotericin B or lithium toxicity) Posttraumatic amnesias for the periods immediately before and after concussion or more severe head trauma seem to result from medial temporal lobe injury. More severe injuries may affect larger areas of memory storage and recall, as can many diffuse cerebral disorders that cause dementia. Psychologic disturbances of memory result from extreme psychologic trauma or stress (see Dissociative Disorders: Dissociative Amnesia). With aging, many people gradually develop noticeable problems with memory, often first for names, then for events, and occasionally for spatial relationships. This widely experienced so-called benign senescent forgetfulness has no proven relationship to dementia, although some similarities are hard to overlook. People who have a subjective memory problem, who do worse on objective memory tests, but who otherwise have intact cognition and daily function may have amnestic mild cognitive impairment (amnestic MCI). People with amnestic MCI are more likely to develop Alzheimer’s disease than age-matched people without memory problems. How do you diagnose amnesia? Simple bedside tests (e.g., 3-item recall, location of objects previously hidden in the room) and formal tests (e.g., word list learning tests such as the California Verbal Learning Test and the Buschke Selective Reminding Test) can help identify verbal memory loss. Assessment of nonverbal memory is more difficult but may include recall of visual designs or a series of tones. Clinical findings usually suggest causes and any necessary tests. How do you manage amnesia? Any underlying disorder or psychologic cause must be treated. However, some patients with acute amnesia improve spontaneously. Certain disorders that cause amnesia (e.g., Alzheimer’s disease, Korsakoff’s psychosis, herpes encephalitis) can be treated; however, treatment of the underlying disorder may or may not lessen the amnesia. If it does not, no specific measures can hasten recovery or improve the outcome. What is Transient Global Amnesia (TGA)? Transient global amnesia is disturbed memory typically caused by vascular or ischemic lesions in the brain. Diagnosis is primarily clinical but includes laboratory tests and CT, MRI, or both to evaluate central circulation. The amnesia typically remits spontaneously but may recur. There is no specific treatment, but underlying abnormalities are corrected. What are the causes of TGA? Transient global amnesia is typically caused by ischemia (eg, due to atherosclerosis, thrombosis, or thromboembolism) that transiently affects the posteromedial thalamus or hippocampus bilaterally, but this amnesia can be caused by seizure activity or migraines. A distinct benign form of transient global amnesia can follow excessive alcohol ingestion, moderately large sedative doses of barbiturates, use of several illicit drugs, or sometimes relatively small doses of benzodiazepines (especially midazolam and triazolam What are the Symptoms and Signs of TGA? Patients present with acute global amnesic confusion that usually lasts 6 to 12 h but may last from 30 min to 24 h (rarely). Patients have a retrograde memory deficit that can extend back for several years; they are often disoriented to time and place but usually not to personal identity. Anterograde memory is less disturbed. Many patients are anxious or agitated and may repeatedly ask questions about transpiring events. Language function, attention, visual-spatial skills, and social skills are retained. Impairments gradually resolve as the episode subsides. The benign transient amnesia after substance ingestion is distinct because it is selectively retrograde (i.e., for events during and preceding intoxication), relates specifically to drug-accompanied events, does not cause confusion (once acute intoxication resolves), and recurs only if similar amounts of the same drug are ingested. Diagnosis is primarily clinical. Neurologic examination typically does not detect any abnormalities other than disturbed memory. Brain ischemia must be ruled out (see Stroke (CVA): Diagnosis). Laboratory tests should include CBC, coagulation tests, and evaluation for hypercoagulable states. CT, MRI, or both, with or without angiographic protocols, are done. EEG usually shows nonspecific abnormalities and is unnecessary unless a seizure is suspected or episodes recur. Prognosis is good. Symptoms typically last < 24 h. As the disorder resolves, the amnesia lessens, but memory for events during the attack may be lost. Usually, episodes do not recur, unless the cause is seizures or migraines. Overall lifetime recurrence rate is about 5 to 25%. No specific treatment is indicated. What is Asperger syndrome and its management? Asperger syndrome is a pervasive developmental disorder. Children who have it do not develop normally in several basic areas: They behave oddly at times and have trouble with social skills. They may not want to interact with others or may have trouble doing so. They may not be able to understand body language or use gestures to communicate. They are obsessed with specific topics and become like little professors about those topics. Asperger syndrome is also called an autistic spectrum disorder because it is a mild form of autism. Autism is a disorder in which children have communication and social problems. What is the cause of Asperger syndrome? The cause of this disorder is unknown. It may be caused by problems during birth. The fathers of children with this disorder may also have intense and limited interests, a rigid style, and be awkward or timid with other people. Brain scans show that the structure or shape of certain parts of the brain is different in children with Asperger syndrome. This disorder sometimes runs in families. There may be certain genes linked to Asperger syndrome. About 1 in 10,000 children are diagnosed with Asperger syndrome. Boys have it 4 times as often as girls. Most children are diagnosed between the ages of 5 and 9. What are the symptoms Asperger syndrome? The language and self-help skills of children with Asperger syndrome develop normally. They show normal curiosity about their surroundings. Most parents of children with Asperger syndrome notice problems by the child’s third birthday. Children with this disorder: have a hard time making eye contact and using facial expressions and hand gestures when talking to other people. may be clumsy and uncoordinated, or have awkward postures and gestures. are very self-focused. They will often have long-winded, one-sided conversations, and not notice if others respond. They may seem uncaring about other people’s feelings. may not understand humour and may have a hard time understanding the social cues of others. may speak very fast, or in a monotone, “robotic” voice. They often have a very formal way of speaking. are obsessed with one or two subjects, such as trains, sports statistics, or spiders. They become experts about their interest and talk all the time about facts related to these subjects. may get very upset at the slightest change in routine. are very sensitive to certain sounds, textures, tastes, and smells. may take longer than most children to learn to walk, catch a ball, or ride a bike. People with this disorder do not relate well to others in large groups, but they may do fine in smaller groups or one-to-one. They can be very attached to friends and family. How is Asperger syndrome diagnosed? Not all children with Asperger syndrome have the same symptoms. The healthcare provider will examine and observe your child and ask about symptoms, medical history, and the family history of any medical and mental problems. A psychologist can test your child’s intelligence, social, and communication skills. A psychiatrist may evaluate your child to see if medicine might help his or her symptoms. How is Asperger syndrome treated? There is no one best treatment for all children with Asperger syndrome. Before you decide on your child’s treatment, find out what your options are. Learn as much as you can and make your choice for your child’s treatment based on your child’s needs. A good treatment program will: build on the child’s interests offer a predictable schedule teach tasks as a series of simple steps actively hold the child’s attention in highly structured activities provide regular evaluation of educational and behavioural goals Usually children are placed in public schools and the school district pays for all needed services. These will include working with a speech therapist, occupational therapist, school psychologist, social worker, school nurse, or aide. You may want to visit public schools in your area to see the type of program they offer to special needs children. By law, public schools must prepare and carry out a teaching plan. This plan is designed to help children in a special education program to learn specific skills. The list of skills is known as the child’s Individualized Education Program (IEP). The IEP is an agreement between the school and the family about the child’s goals. Parents play an important part in creating the program, as they know their child and his or her needs best. If your child is under 3 years of age and has special needs, check into early intervention programs. A cognitive behavioural therapist can help the child learn to manage stress, and cut back on obsessive interests and repetitive routines. Treatment includes doing activities at home as well as at school. Behavioural therapy can also be done in the home by parents. The first step is to choose a skill to work on. You need to make sure the child can succeed. When your child succeeds, reward the behaviour. When they are rewarded, they start to understand what you want them to do. A reward follows a behaviour and increases the chances that the behaviour will be repeated. Be sure that the reward you use is something your child wants, and that it works for the behaviour you are trying to change. Some things that have been found to work well for children with Asperger syndrome are food, hugs, massage, being lifted or swung in the air, TV, videos, music, and reading books. It is important to show your child that interacting with people is fun and that communicating with people leads to good things (rewards). Give your child lots of supervised opportunities to practice communication and social skills. Sometimes medicine can help. Mood- or behaviour-altering drugs can improve behaviours that may cause self-injury or greatly interfere with school or social ability. These medicines must be prescribed by a doctor experienced with their use in children with this disorder. There is no medicine that will take away the symptoms of Asperger syndrome. Parents often learn of new or alternative treatments through friends or the media. Your provider can help you decide if these treatments could help or harm your child. How long will the effects of Asperger syndrome last? Asperger syndrome is a lifelong condition. Treatment helps. People with this disorder can have good relationships, hold jobs, and lead happy and productive lives. What are behavioural emergencies (BE)? Patients who are experiencing severe changes in mood, thoughts, or behaviour or severe, potentially life-threatening drug adverse effects need urgent assessment and treatment. Non- specialists are often the first care providers for outpatients and inpatients on medical units, but whenever possible, such cases should also be evaluated by a psychiatrist. When a patient’s mood, thoughts, or behaviour is highly unusual or disorganized, assessment must first determine whether the patient is a -Threat to self -Threat to others The threat to self can include inability to care for self (leading to self-neglect) or suicidal behaviour Self-neglect is a particular concern for patients with psychotic disorders, dementia, or substance abuse because their ability to obtain food, clothing, and appropriate protection from the elements is impaired. Patients posing a threat to others include those who are actively violent, those who appear belligerent and hostile (i.e., potentially violent), and those who do not appear threatening to the examiner and staff members but express intent to harm another person (e.g., spouse, neighbour, public figure). What are the causes of behavioural emergencies? Aggressive, violent patients are often psychotic and have diagnoses such as polysubstance abuse, schizophrenia, delusional disorder, or acute mania. Other causes include physical disorders that cause acute delirium and intoxication with alcohol or other substances, particularly methamphetamine, cocaine, and sometimes phencyclidine. How are behavioural emergencies evaluated? Management typically occurs simultaneously with evaluation, particularly evaluation for a possible physical disorder, it is a mistake to assume that the cause of abnormal behaviour is a mental disorder or intoxication, even in patients who have a known psychiatric diagnosis or an odour of alcohol. Because patients are often unable or unwilling to provide a clear history, other collateral sources of information (e.g., family members, friends, caseworkers, medical records) must be identified and consulted immediately. How must BE patients be approached? Actively violent patients must first be restrained by Physical means, Drugs (chemical restraint), or Both Such interventions are done to prevent harm to patients and others and to allow evaluation of the cause of the behaviour (e.g., by taking vital signs and doing blood tests). Close monitoring, sometimes involving constant observation by a trained sitter, is required. Although clinicians must be aware of legal issues regarding involuntary treatment such issues must not delay potentially lifesaving interventions. Potentially violent patients require measures to defuse the situation. Measures that may help reduce agitation and aggressiveness include Moving patients to a calm, quiet environment (e.g., a seclusion room, when available) Removing objects that could be used to inflict harm to self or others Expressing sympathetic concern for patients and their complaints Responding in a confident yet supportive manner Speaking directly—mentioning that patients seem angry or upset, asking them if they intend to hurt someone—acknowledges their feelings and may elicit information; it does not make them more likely to act out. Counterproductive measures include arguing about the validity of patients’ fears and complaints Issuing threats (e.g., to call police, to commit them), speaking in a condescending manner, attempting to deceive patients (e.g., hiding drugs in food, promising them they will not be restrained), When hostile, aggressive patients are interviewed, staff safety must be considered. Most hospitals have a policy to search for weapons (manually, with metal detectors, or both) on patients presenting with disordered behaviour. Patients who are hostile but not yet violent typically do not assault staff members randomly; rather, they assault staff members who anger or appear threatening to them. Doors to rooms should be left open and staff members should avoid positioning themselves between patients and the door so that patients do not feel trapped or threatened; it is preferable that patients run out than assault staff members. Staff members may also avoid appearing threatening by sitting on the same level as patients. Staff members may avoid angering patients by not responding to their hostility in kind, with loud, angry remarks or arguing. If patients nonetheless become increasingly agitated and violence appears impending, staff members should simply leave the room and summon sufficient additional staff to provide a show of force, which sometimes deters patients. Typically, at least 4 or 5 people should be present (some preferably young and male). However, the team should not bring restraints into the room unless they are definitely to be applied; seeing restraints may further agitate patients. Verbal threats must be taken seriously. In most states, when a patient expresses the intention to harm a particular person, the evaluating physician is required to warn the intended victim and to notify a specified law enforcement agency. Specific requirements vary by state. Typically, state regulations also require reporting of suspected abuse of children, the elderly, and spouses. How must the patients of behavioural emergency be restrained? Use of physical restraints is controversial and should be considered only when other methods have failed and a patient continues to pose a significant risk of harm to self or others. Restraints may be needed to hold the patient long enough to administer drugs, do a complete assessment, or both. Because restraints are applied without the patient’s consent, certain legal and ethical issues should be considered First, adequate staff are assembled in the room, and patients are informed that restraints must be applied. Patients are encouraged to cooperate to avoid a struggle. However, once the clinician has determined that restraints are necessary, there is no negotiation, and patients are told that restraints will be applied whether or not they agree. Some actually understand and appreciate having external limits on their behaviour. In preparation for applying restraints, one person is assigned to each extremity and another to the patient’s head. Then, each person simultaneously grasps their assigned extremity and places the patient supine on the bed; one physically fit person can typically control a single extremity of even large, violent patients (provided all extremities are grasped at the same time). However, an additional person is needed to apply the restraints. Rarely, upright patients who are extremely combative may first need to be sandwiched between 2 mattresses. Leather restraints are preferred. One restraint is applied to each ankle and wrist and attached to the bed frame, not the rail. Restraints are not applied around the chest, neck, or head, and gags (e.g., to prevent spitting and swearing) are forbidden. Patients who remain combative in restraints (e.g., attempting to upset the stretcher, bite, or spit) require chemical restraint. Use of physical restraints should be considered a last resort, when other steps have not sufficiently controlled aggressive, potentially violent behaviour. When restraints are needed for such a situation, they are legal in all states as long as their use is properly ordered and documented in the patient’s medical record. Restraints have the advantage of being immediately removable, whereas drugs may alter symptoms enough or in a way that delays assessment. Hospital accreditation standards require that patients in restraints be continuously observed by a trained sitter. Immediately after restraints have been applied, the patient must be monitored for signs of injury; circulation, range of motion, nutrition and hydration, vital signs, hygiene, and elimination are also monitored. Physical and mental comfort and readiness for discontinuation of restraints as appropriate are also assessed. These assessments should be done every 15 min. What can be the complications of restraints? Agitated or violent people brought to the hospital by police are almost always in restraints (e.g., handcuffs). Occasionally, young, healthy people have died in police restraints before or shortly after hospital arrival. The cause is often unclear but probably involves some combination of overexertion with subsequent metabolic derangement and hyperthermia, drug use, aspiration of stomach contents into the respiratory system, embolism in people left in restraints for a long time, and occasionally serious underlying medical disorders. Death is more likely if people are restrained in the hobble position, with one or both wrists shackled to the ankles behind their back; this type of restraint may cause asphyxia and should be avoided. Because of these complications, violent patients presenting in police custody should be evaluated promptly and thoroughly and not dismissed as mere socio behavioural problems. What is the treatment of BE? Antipsychotics (typically a conventional antipsychotic, but a 2nd-generation drug may be used) Haloperidol in 1–10 mg po, IM (deltoid). (1–2.5 mg for mild agitation and for frail or older patients; 2.5–5 mg for moderate agitation; 5–10 mg for severe agitation). The drug is usually required only if psychosis is clear. What is breath holding spells (BHS)? A breath-holding spell is an episode in which the child stops breathing involuntarily and loses consciousness for a short period immediately after a frightening or emotionally upsetting event or after a painful experience. Breath-holding spells occur in 5% of otherwise healthy children. They usually begin in the first year of life and peak at age 2. They disappear by age 4 in 50% of children and by age 8 in about 83% of children. The remainder may continue to have spells into adulthood. There are 2 forms of breath-holding spells: What are types of BHS? Cyanotic form: This form is the most common and often occurs as part of a temper tantrum or in response to a scolding or other upsetting event. Pallid form: This form typically follows a painful experience, such as falling and banging the head, but can follow frightening or startling events. Both forms are involuntary and readily distinguished from uncommon brief periods of voluntary breath-holding by stubborn children, who invariably resume normal breathing after getting what they want or after becoming uncomfortable when they fail to get what they want. What is the pathophysiology of breath holding spells? During a cyanotic breath-holding spell, children hold their breath (without necessarily being aware they are doing so) until they lose consciousness. Typically, the child cries out, exhales, and stops breathing. Shortly afterward, the child begins to turn blue and unconsciousness ensues. A brief seizure may occur. After a few seconds, breathing resumes and normal skin colour and consciousness return. It may be possible to interrupt a spell by placing a cold rag on the child’s face at onset. Despite the spell’s frightening nature, parents must try to avoid reinforcing the initiating behaviour. As the child recovers, parents should continue to enforce household rules. Distracting the child and avoiding situations that lead to tantrums are good strategies. Cyanotic breath-holding has been found to respond to iron therapy, even in the absence of anaemia, and to treatment for obstructive sleep pane (when present). During a pallid breath-holding spell, vagal stimulation severely slows the heart rate. The child stops breathing, rapidly loses consciousness, and becomes pale and limp. If the spell lasts more than a few seconds, muscle tone increases, and a seizure and incontinence may occur. After the spell, the heart speeds up again, breathing restarts, and consciousness returns without any treatment. Because this form is rare, further diagnostic evaluation and treatment may be needed if the spells occur often. Simultaneous ECG and EEG can help to differentiate cardiac and neurologic causes. What are brief psychotic disorders and how to manage them? Brief psychotic disorder consists of delusions, hallucinations, or other psychotic symptoms for at least 1 day but < 1 mo., with eventual return to normal premorbid functioning. It is typically caused by severe stress in susceptible people. Brief psychotic disorder is uncommon. Pre-existing personality disorders (e.g., paranoid, histrionic, narcissistic, schizotypal, borderline) predispose to its development. A major stressor, such as loss of a loved one, may precipitate the disorder. The disorder causes at least one psychotic symptom: Delusions, Hallucinations, disorganized speech and Grossly disorganized or catatonic behaviour. This disorder is not diagnosed if a psychotic mood disorder, a schizoaffective disorder, schizophrenia, a physical disorder, or an adverse drug effect (prescribed or illicit) better accounts for the symptoms. Differentiating between brief psychotic disorder and schizophrenia in a patient without any prior psychotic symptoms is based on duration of symptoms; if the duration exceeds 1 mo., the patient no longer meets required diagnostic criteria for brief psychotic disorder. Treatment is similar to that of an acute exacerbation of schizophrenia; supervision and short-term treatment with antipsychotics may be required. What is Catatonia And its management? Catatonia, is a distinct and heterogeneous neuropsychiatric syndrome, with both motoric and behavioural signs. It may be hypokinetic, hyperkinetic, or mixed and includes volitional signs, such as mutism, negativism, and automatic obedience. It was formerly relegated to a schizophrenia subtype, or considered extinct after the advent of modern psychopharmacology. Renewed interest and emerging systematic data have highlighted the frequency and pattern of catatonic presentations in psychiatric and medical settings, including in critical illness. Treatment is with lorazepam and ECTs. What is cognitive therapy? Cognitive therapy is a very active and direct type of therapy that works by changing negative thoughts that cause emotional distress. Although there are many kinds of cognitive therapy that go by different names, they all focus on your thoughts and beliefs as a primary cause of your symptoms. This type of therapy works well in treating depression, anxiety, and panic disorders. What is the theory behind this therapy? Experts who study and use cognitive therapy believe that depression is caused by: your negative outlook and thoughts about events, the future, and yourself negative core beliefs you developed over time and through events in your early life For example, your spouse may be mildly upset with you, or your boss may say he wants to see you. If you link self-defeating beliefs with a negative view of reality, you may leap to the conclusion that your spouse no longer loves you or your boss is about to fire you. How do your beliefs affect your thoughts? If you have the belief that you should be perfect and never make mistakes, you will probably be very critical of yourself, even over the most minor matters. You may tend to blame yourself for everything. You may think you are a failure in everything you do. Even a simple mistake can lead to negative thoughts that leave you feeling hopeless and awful. The goal of cognitive therapy is to break this cycle by stopping these negative thinking habits and replacing them with more realistic ones. You and your therapist will work as a team to test the logic of your thoughts. For example, your therapist may help you examine your belief that you should be perfect. Is it reasonable to expect that of yourself? What has been the result of that belief? What is likely to be the result of it in the future? What are the steps in cognitive therapy? Test your personal beliefs and the way you think about events, yourself, and the future. Become familiar with your negative thought patterns so you are aware of them when they occur. Do the homework you and your therapist agree on. Cognitive therapy is a team effort. Keep the momentum going once you have made changes in your thinking habits. Read books on cognitive therapy. Go in for booster sessions with your therapist. Changing negative attitudes and beliefs takes a lot of work but it can be done. Cognitive therapy can change. What is psychotherapy and how does it work? Psychotherapy is a collaborative treatment based on the relationship between an individual and a psychologist. Grounded in dialogue, it provides a supportive environment that allows you to talk openly with someone who’s objective, neutral and non-judgmental. What is the difference between psychotherapy and therapy? Psychotherapy, like counselling, is based on a healing relationship between a health care provider and client. Psychotherapy, or therapy for short, also takes place over a series of meetings, though often it has a longer duration than counselling. Some people participate in therapy off and on over several years. What are the types of psychology therapy? Approaches to psychotherapy fall into five broad categories: Psychoanalysis and psychodynamic therapies. This approach focuses on changing problematic behaviours, feelings, and thoughts by discovering their unconscious meanings and motivations. Behavior therapy. What are the different types of mental therapy? Types of Mental Health Therapy are: individual, group, and pharmacological (drug). Different types of individual therapies include: psychoanalytical, behavioural, cognitive, and cognitive-behavioural. Differing types of group therapies include family therapy and psychodrama. How is psychotherapy used to treat depression? Psychotherapy helps people with depression: Understand the behaviours, emotions, and ideas that contribute to his or her depression. Understand and identify the life problems or events — like a major illness, a death in the family. Help to restructure ways of thinking, negative attributes and attitudes someone has about himself. How effective is Gestalt therapy? The result revealed that there was a significant difference in the level of self-awareness before and after gestalt therapy. Hence, the study concluded that gestalt therapy is found to be an effective therapy in improving the level of self-awareness among the patients with Schizophrenia. What are the different types of counselling approaches? Types of counselling include educational, career, marriage and family, mental health and substance abuse counselling. Within these specialties, different counselling approaches can be taken, including cognitive therapy, psychotherapy, existential counselling, person-cantered therapy and rational emotive Behavior therapy. What are the personality traits of a physical therapist? Part of the therapist’s job is to temper the patient’s nerves, often through demonstrating the behaviour necessary to make it through therapy. Individuals, who maintain control of difficult sessions with empathy, tenderness and a sense of humour, are among the most successful therapists. What is placebo? Placebo a medicine or procedure prescribed for the psychological benefit to the patient rather than for any physiological effect. Why do placebos work? Placebos are used in clinical double-blind testing to determine the effectiveness of new medications. Doctors may give a placebo to a patient in pain to test if they’re a hypochondriac. Patients and clinicians may not be informed about who is receiving a placebo, with the goal of preventing the placebo effect or clinician bias. What are the advantages of placebos? The body has powerful, natural recuperative abilities and a placebo could help facilitate this. Acts as a psychological boost, that a person’s positive attitude may be important in recovery from illness. What is the purpose of a placebo? The purpose of a placebo is to evaluate the patient’s and doctor’s “participation” in any therapeutic effect, as separate from the medicine alone. How effective are placebos? Placebos aren’t always effective. Research indicates that they are more likely to be effective when patients are suffering from symptoms such as fatigue, itching, and pain—sensations that the brain can modulate and perceive differently depending on the situation. What is a Nocebo? A nocebo effect is said to occur when negative expectations of the patient regarding a treatment cause the treatment to have a more negative effect than it otherwise would have. For example, when a patient anticipates a side effect of a medication, they can suffer that effect even if the “medication” is actually an inert substance. The complementary concept, the placebo effect, is said to occur when positive expectations improve an outcome. Both placebo and nocebo effects are presumably psychogenic, but they can induce measurable changes in the body. One article that reviewed 31 studies on nocebo effects reported a wide range of symptoms that could manifest as nocebo effects including nausea, stomach pains, itching, bloating, depression, sleep problems, loss of appetite, sexual dysfunction and severe hypotension. What is the difference between placebo and nocebo? Placebo is when a positive effect is seen in the study group when giving a known “non-effector” (meaning it is a substance already established as having no effect), whereas nocebo is an aggravation of symptoms or negative effect seen in the study group when giving a known “non-effector”. What is placebo surgery? Placebo surgery is a sham surgery (placebo surgery) is a faked surgical intervention that omits the step thought to be therapeutically necessary. What is a placebo procedure? Common placebos procedures include inert tablets (like sugar pills), inert injections (like saline), sham surgery, and other procedures. What is a placebo investigation?? Placebo investigation in an investigation that helps patient believe that investigation has been done. placebo effect is proportional to the elaborateness of the rituals surrounding it, the investigators expressed confidence and enthusiasm for the procedure, and a patient’s belief that it will help. What is the process of meditation? The Process of Meditation. In focused attention techniques, it is bringing back the attention to the single object of focus – be it the breath, a mantra, a chakra, feelings of loving-kindness, or anything else (external or internal, actual or imagined). In open monitoring types of meditation (like mindfulness). What is mindfulness? Mindfulness is a mental state achieved by focusing one’s awareness on the present moment, while calmly acknowledging and accepting one’s feelings, thoughts, and bodily sensations, used as a therapeutic technique. What is the difference between meditation and mindfulness? The difference between meditation and mindfulness is that meditation is more focused on self-realisation and inner experience, whereas mindfulness is an attitude—the practice of focusing your attention on the present moment without distraction or reactivity. Why is meditation beneficial? Meditation is the practice of clearing your mind to gain the benefits of a calm, relaxed state. This practice is meant to foster better concentration, positive energy, and the clarity that can allow you to view the world around you with a more serene attitude. It can Boosts immune system, lowers blood pressure, Eases inflammation, reduces heart risk, Increases Gray matter. What are the benefits of mindfulness? Mindfulness improves well-being. Increasing your capacity for mindfulness supports many attitudes that contribute to a satisfied life. Being mindful makes it easier to savour the pleasures in life as they occur, helps you become fully engaged in activities, and creates a greater capacity to deal with adverse events. What are the best meditation techniques? This is one of the best meditation techniques for beginners. Ancient, powerful and effective, by simply watching your breath, you give your mind something to focus on in a relaxed way. Get yourself in a comfortable position, close your eyes and begin to observe the sensations of breathing. What is neuroplasticity and how does it help? It’s an oft-repeated idea that blind people can compensate for their lack of sight with enhanced hearing or other abilities. The musical talents of Stevie Wonder and Ray Charles, both blinded at an early age, are cited as examples of blindness conferring an advantage in other areas. Then there’s the superhero Daredevil, who is blind but uses his heightened remaining senses to fight crime. It is commonly assumed that the improvement in the remaining senses is a result of learned behaviour; in the absence of vision, blind people pay attention to auditory cues and learn how to use them more efficiently. But there is mounting evidence that people missing one sense don’t just learn to use the others better. The brain adapts to the loss by giving itself a makeover. If one sense is lost, the areas of the brain normally devoted to handling that sensory information do not go unused — they get rewired and put to work processing other senses. A new study provides evidence of this rewiring in the brains of deaf people. The study, published in The Journal of Neuroscience, shows people who are born deaf use areas of the brain typically devoted to processing sound to instead process touch and vision. Perhaps more interestingly, the researchers found this neural reorganization affects how deaf individuals perceive sensory stimuli, making them susceptible to a perceptual illusion that hearing people do not experience. These new findings are part of the growing research on neuroplasticity, the ability of our brains to change with experience. A large body of evidence shows when the brain is deprived of input in one sensory modality, it is capable of reorganizing itself to support and augment other senses, a phenomenon known as cross-modal neuroplasticity. What are tremors? Tremor, an involuntary, rhythmic, oscillatory movement of a body part, is the most common movement disorder encountered in clinical practice. Rest tremors occur in a body part that is relaxed and completely supported against gravity. Action tremors occur with voluntary contraction of a muscle and can be further subdivided into postural, isometric, and kinetic tremors. All persons have low-amplitude, high-frequency physiologic tremors at rest and during action that are not reported as symptomatic. The most common pathologic tremor is essential tremor. In one-half of cases, it is transmitted in an autosomal dominant fashion, and it affects 0.4 to 6 percent of the population. More than 70 percent of patients with Parkinson disease have tremor as the presenting feature. This tremor is typically asymmetric, occurs at rest, and becomes less prominent with voluntary movement. Features consistent with psychogenic tremor are abrupt onset, spontaneous remission, changing tremor characteristics, and extinction with distraction. Other types of tremor are cerebellar, dystonic, drug- or metabolic-induced, and orthostatic. The first step in the evaluation of a patient with tremor is to categorize the tremor based on its activation condition, topographic distribution, and frequency. The diagnosis of tremor is based on clinical information obtained from a thorough history and physical examination. For particularly difficult cases, single-photon emission computed tomography to visualize the integrity of the dopaminergic pathways in the brain may be useful to diagnose Parkinson disease. Tremor is an involuntary, rhythmic, oscillatory movement of a body part. It is the most common movement disorder encountered in clinical practice.1–3 There is no diagnostic standard to distinguish among common types of tremor, which can make the evaluation challenging. However, establishing the underlying cause is important because prognosis and specific treatment plans vary considerably. History and physical examination can provide a great deal of certainty in diagnosis. The most common tremor in patients presenting to primary care physicians is enhanced physiologic tremor, followed by essential tremor and parkinsonian tremor.1,3–6 All tremors are more common in older age. A comprehensive review of medications (prescribed and over-the-counter), with specific attention to medications started proximal to the onset of tremor, is important in patients with new-onset tremor. The diagnosis of tremor is based on clinical information obtained from a thorough history and physical examination. A rest tremor is usually caused by parkinsonism. Tremor in children is potentially serious; patients should be promptly referred to a neurologist. For particularly difficult tremor cases, single-photon emission computed tomography to visualize the integrity of the dopaminergic pathways in the brain may be useful to diagnose Parkinson disease. What are essential tremors? The most common pathologic tremor is essential tremor. In one-half of cases, it is transmitted in an autosomal dominant fashion, and it affects 0.4 to 6 percent of the population.4,8 Careful history reveals that patients with essential tremor have it in early adulthood (or sooner), but most patients do not seek help for it until 70 years of age because of its progressive nature. Despite being sometimes called “benign essential tremor,” essential tremor often causes severe social embarrassment, and up to 25 percent of those afflicted retire early or modify their career path. Essential tremor is an action tremor, usually postural, but kinetic and even sporadic rest tremors have also been described. It is most obvious in the wrists and hands when patients hold their arms in front of themselves (resisting gravity); however, essential tremor can also affect the head, lower extremities, and voice. It is generally bilateral, is present with a variety of tasks, and interferes with activities of daily living.1,5 In a series of 200 Italian patients referred to a neurologist for evaluation of tremor, 15 percent had uncommon clinical features that included postural, action, rest, orthostatic, and writing tremors, and 10 percent had tongue or facial dyskinesia. Diagnostic criteria have been proposed, but none have been accepted universally. Persons with essential tremor typically have no other neurologic findings; therefore, it is often considered a diagnosis of exclusion. If the tremor responds to a therapeutic trial of alcohol consumption (two drinks per day), the diagnosis of essential tremor is assured. What are Parkinson’s tremors? Parkinsonism is a clinical syndrome characterized by tremor, bradykinesia, rigidity, and postural instability. Many patients will also have micrographic, shuffling gait, masked facies, and an abnormal heel-to-toe test.10,14–16 Causes of parkinsonism include brainstem infarction, multiple system atrophy, and medications that block or deplete dopamine, such as methyldopa, metoclopramide (Reglan), haloperidol, and risperidone (Risperdal).9,10 Idiopathic Parkinson disease is a chronic neurodegenerative disorder; its prevalence increases with age. It is the most common cause of parkinsonism. More than 70 percent of patients with Parkinson disease have tremor as the presenting feature. The classic parkinsonian tremor begins as a low-frequency, pill-rolling motion of the fingers, progressing to forearm pronation/supination and elbow flexion/extension. It is typically asymmetric, occurs at rest, and becomes less prominent with voluntary movement. Although rest tremor is one of the diagnostic criteria for Parkinson disease, most patients exhibit a combination of action and rest tremors. What are enhanced physiological tremors? A physiologic tremor is present in all persons. It is a low-amplitude, high-frequency tremor at rest and during action that is not reported as symptomatic. This tremor can be enhanced by anxiety, stress, and certain medications and metabolic conditions. Patients with a tremor that comes and goes with anxiety, medication use, caffeine intake, or fatigue do not need further testing.1,8 What are drug and metabolite induced tremors? Dozens of medications can cause or exacerbate tremor. Patients with new-onset tremor should have a comprehensive medication review with specific attention to medications (prescribed and over-the-counter) started proximal to the onset of tremor.8 Medications particularly prone to inducing or exacerbating tremor are those that stimulate the sympathetic nervous system (e.g., amphetamines, terbutaline, pseudoephedrine) and psychoactive medications (e.g., tricyclic antidepressants, haloperidol, fluoxetine . When medication review reveals a likely culprit, a trial off of this medication should be attempted. What are cerebellar tremors? The classic cerebellar tremor presents as a disabling, low-frequency, slow intention or postural tremor, and is typically caused by multiple sclerosis with cerebellar plaques, stroke, or brainstem tumours. Other neurologic signs include dysmetria (overshoot on finger-to-nose testing), dyssynergia (abnormal heel-to-shin testing and/or ataxia), and hypotonia. What are psychogenic tremors? Differentiation of organic from psychogenic tremor can be difficult. Features consistent with psychogenic tremor are abrupt onset, spontaneous remission, changing tremor characteristics, and extinction with distraction. Often, there is an associated stressful life event. Based on clinical experience, the prevalence of psychogenic tremor is thought to be high, but there are no precise estimates. What are tremors in children? The diagnosis of tremor in children is poorly understood. A variety of genetic conditions are associated with tremor in children, including spinal muscular atrophy, mitochondrial diseases, Huntington disease, and fragile X syndrome. Brain tumours, hydrocephalus, nutritional deficiencies (e.g., vitamin B12), heavy metal poisoning, prescription medications, pyruvate carboxylase deficiency, and homocystinuria can also cause tremor in children. Tremor in children is potentially serious; patients should be promptly referred to a neurologist. What is the treatment of tremors? Most types of tremor cannot be cured, and a mild tremor usually requires no treatment. If the shaking is impacting everyday life, however, many treatments are available. For essential tremor, a doctor may prescribe beta-blockers, such as propranolol, metoprolol, or nadolol. A doctor may also recommend anti-seizure medication, such as primidone. Parkinson’s disease treatments disease-specific drugs, such as levodopa and carbidopa, to manage advanced cases. What is delirium? The essential features of delirium include disturbances of consciousness, attention, cognition, and perception. The disturbance develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day. Following are the DSM-IV criteria for delirium (1): • Disturbance of consciousness (i.e., reduced clarity of awareness of the environment) with reduced ability to focus, sustain, or shift attention. • A change in cognition (such as memory deficit, disorientation, language disturbance) or the development of a perceptual disturbance that is not better accounted for by a pre-existing, established, or evolving dementia. • The disturbance develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day. What are other commonly associated features of delirium? Dysarthria is a frequent speech and language disturbance, and dysnomia (i.e., impaired ability to name objects), dysgraphia (i.e., impaired ability to write), or even frank aphasia may be observed. Perceptual disturbances may include misinterpretations, illusions, or hallucinations. For example, the patient may see the nurse mixing intravenous solutions and conclude the nurse is trying to poison him or her (misinterpretation); the folds of the bedclothes may appear to be animate objects (illusion); or the patient may see a group of people around the bed when no one is actually there (hallucination). Although visual misperceptions and hallucinations are most common in delirium, auditory, tactile, gustatory, and olfactory misperceptions or hallucinations can also occur. Misperceptions range from simple and uniform to highly complex. A patient with delirium may have a delusional conviction of the reality of a hallucination and exhibit emotional and behavioural responses consistent with the hallucination’s content. Other commonly associated features of delirium include disturbances of sleep, psychomotor activity, and emotion. Disturbances in the sleep-wake cycle observed in delirium include daytime sleepiness, night-time agitation, and disturbances in sleep continuity. In some cases, complete reversal of the night-day sleep-wake cycle or fragmentation of the circadian sleep-wake pattern can occur. What are subtypes of delirium? Delirium is often accompanied by disturbed psychomotor activity. Two subtypes of delirium are seen based on psychomotor activity and arousal levels. These delirium subtypes included the “hyperactive” (or agitated, hyperalert) subtype and the “hypoactive” (lethargic, hypo alert) subtype. Others have included a “mixed” delirium subtype with alternating features of both. Ross et al. (4) suggested that the hyperactive form is more often characterized by hallucinations, delusions, agitation, and disorientation, while the hypoactive form is characterized by confusion and sedation and is less often accompanied by hallucinations, delusions, or illusions. Comparable levels of cognitive impairment have been observed with both motor subtypes. The delirious individual may also exhibit emotional disturbances, such as anxiety, fear, depression, irritability, anger, euphoria, and apathy. There may be affective lability, with rapid and unpredictable shifts from one emotional state to another. How must delirium be managed? Haloperidol may be administered orally, intramuscularly, or intravenously and may cause fewer extrapyramidal symptoms when administered intravenously. Haloperidol can be initiated in the range of 1–2 mg every 2–4 hours as needed (0.25–0.50 mg every 4 hours as needed for elderly patients), with titration to higher doses for patients who continue to be agitated. For patients who require multiple bolus doses of antipsychotic medications, continuous intravenous infusions of antipsychotic medication may be useful (e.g., haloperidol bolus, 10 mg i.v., followed by continuous intravenous infusion of 5–10 mg/hour; lower doses may be required for elderly patients). For patients who require a more rapid onset of action, droperidol, either alone or followed by haloperidol, can be considered. Benzodiazepine treatment as a monotherapy is generally reserved for delirium caused by withdrawal of alcohol or sedative-hypnotics. Patients with delirium who can tolerate only lower doses of antipsychotic medications may benefit from the combination of a benzodiazepine and antipsychotic medication. Cholinergic such as physostigmine may be useful in delirium known to be caused specifically by anticholinergic medications. Paralysis, sedation, and mechanical ventilation may be required for agitated patients with delirium and hypercatabolic conditions. Palliative treatment with opiates may be needed by patients with delirium for whom pain is an aggravating factor. Multivitamin replacement should be given to patients with delirium for whom there is the possibility of B vitamin deficiencies (e.g., those who are alcoholic or malnourished). What is the prognosis of delirium? While the majority of patients recover fully, delirium may progress to stupor, coma, seizures, or death, particularly if untreated. Full recovery is less likely in the elderly, with estimated rates of full recovery by the time of discharge varying from 4% to 40%. Persistent cognitive deficits are also quite common in elderly patients recovering from delirium, although such deficits may be due to pre-existing dementia that was not fully appreciated. What is dementia, and its types? Dementia is chronic, global, usually irreversible deterioration of cognition. Diagnosis is clinical; laboratory and imaging tests are used to identify treatable causes. Treatment is supportive. Cholinesterase inhibitors can sometimes temporarily improve cognitive function. Dementia may occur at any age but affects primarily the elderly (about 5% of those aged 65 to 74 and 40% of those > 85). It accounts for more than half of nursing home admissions. At least 5 million people in the US have dementia. What are the types of dementia? The most common types of dementia are Alzheimer’s disease, vascular dementia, Lewy body dementia, frontotemporal dementias, and HIV-associated dementia. Dementia also occurs in patients with Parkinson’s disease, Huntington’s disease, progressive supranuclear palsy, Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome, other prion disorders, and neurosyphilis. Patients can have > 1 type (mixed dementia). Some structural brain disorders (eg, normal-pressure hydrocephalus, subdural hematoma), metabolic disorders (eg, hypothyroidism, vitamin B12 deficiency), and toxins (eg, lead) cause a slow deterioration of cognition that may resolve with treatment. This impairment is sometimes called reversible dementia, but some experts restrict the term dementia to irreversible cognitive deterioration. Depression may mimic dementia (and was formerly called pseudodementia); the 2 disorders often coexist. However, depression may be the first manifestation of dementia. Changes in cognition, including memory, occur with aging, but they are not dementia. The elderly has a relative deficiency in recall, particularly in speed of recall, compared with recall during their youth. However, this change does not affect daily function. Mild cognitive impairment is more severe than age-associated memory impairment; memory is impaired compared with that of age-matched controls, but other cognitive domains and daily function are not affected. Up to 50% of patients with mild cognitive impairment develop dementia within 3 yr. Any disorder may exacerbate cognitive deficits in patients with dementia. Delirium often occurs in patients with dementia. Drugs, particularly benzodiazepines and anticholinergics (eg, some tricyclic antidepressants, antihistamines, antipsychotics, benztropine), may temporarily cause or worsen symptoms of dementia, as may alcohol, even in moderate amounts. New or progressive renal or liver failure may reduce drug clearance and cause drug toxicity after years of taking a stable drug dose (eg, of propranolol). What are the symptoms of dementia? Dementia impairs cognition globally. Onset is gradual, although family members may suddenly notice deficits (eg, when function becomes impaired). Often, loss of short-term memory is the first sign. Although symptoms exist in a continuum, they can be divided into early, intermediate, and late. Personality changes and behavioural disturbances may develop early or late. Motor and other focal neurologic deficits occur at different stages, depending on the type of dementia; they occur early in vascular dementia and late in Alzheimer’s disease. Incidence of seizures is somewhat increased during all stages. Psychosis—hallucinations, delusions, or paranoia—occurs in about 10% of patients with dementia, although a higher percentage may experience these symptoms temporarily. What happens in early stage of dementia? Recent memory is impaired; learning and retaining new information become difficult. Language problems (especially with word finding), mood swings, and personality changes develop. Patients may have progressive difficulty with independent activities of daily living (eg, balancing their check book, finding their way around, remembering where they put things). Abstract thinking, insight, or judgment may be impaired. Patients may respond to loss of independence and memory with irritability, hostility, and agitation. Functional ability may be further limited by the following: Agnosia: Impaired ability to identify objects despite intact sensory function (see Function and Dysfunction of the Cerebral Lobes: Agnosia) Apraxia: Impaired ability to do previously learned motor activities despite intact motor function (see Function and Dysfunction of the Cerebral Lobes: Apraxia) Aphasia: Impaired ability to comprehend or use language (see Function and Dysfunction of the Cerebral Lobes: Aphasia) Although early dementia may not compromise sociability, family members may report strange behaviour accompanied by emotional lability. What happens in intermediate stage of dementia? Patients become unable to learn and recall new information. Memory of remote events is reduced but not totally lost. Patients may require help with basic activities of daily living (eg, bathing, eating, dressing, toileting). Personality changes may progress. Patients may become irritable, anxious, self-centred, inflexible, or angry more easily, or they may become more passive, with a flat affect, depression, indecisiveness, lack of spontaneity, or general withdrawal from social situations. Behavior disorders may develop: Patients may wander or become suddenly and inappropriately agitated, hostile, uncooperative, or physically aggressive. By this stage, patients have lost all sense of time and place because they cannot effectively use normal environmental and social cues. Patients often get lost; they may be unable to find their own bedroom or bathroom. They remain ambulatory but are at risk of falls or accidents secondary to confusion. Altered sensation or perception may culminate in psychosis with hallucinations and paranoid and persecutory delusions. Sleep patterns are often disorganized. What happens in late stage of dementia? Patients cannot walk, feed themselves, or do any other activities of daily living; they may become incontinent. Recent and remote memory is completely lost. Patients may be unable to swallow. They are at risk of undernutrition, pneumonia (especially due to aspiration), and pressure ulcers. Because they depend completely on others for care, placement in a long-term care facility often becomes necessary. Eventually, patients become mute. Because such patients cannot relate any symptoms to a physician and because elderly patients often have no febrile or leukocytic response to infection, a physician must rely on experience and acumen whenever a patient appears ill. End-stage dementia results in coma and death, usually due to infection. What is the differential diagnosis of dementia? Dementia must be distinguished from the following: Delirium: Distinguishing between dementia and delirium is crucial (because delirium is usually reversible with prompt treatment) but can be difficult. Attention is assessed first. If a patient is inattentive, the diagnosis is likely to be delirium, although advanced dementia also severely impairs attention. Other features that suggest delirium rather than dementia (eg, duration of cognitive impairment—see Table 1: Delirium and Dementia: Differences Between Delirium and Dementia) are determined by the history, physical examination, and tests for specific causes.
Age-associated memory impairment: This impairment is not severe enough to affect daily function. If affected people are given enough time to learn new information, their intellectual performance is good.
Mild cognitive impairment: Memory is impaired, but other cognitive domains and daily function are not affected.
Dementia of depression: This cognitive disturbance resolves with treatment of depression. Depressed older patients may experience cognitive decline, but unlike patients with dementia, they tend to exaggerate their memory loss and rarely forget important current events or personal matters. Neurologic examinations are normal except for signs of psychomotor slowing. When tested, patients with depression make little effort to respond, but those with dementia often try hard but respond incorrectly. When depression and dementia coexist, treating depression does not fully restore cognition.
What tests must be employed to screen dementia?
Clinical criteria: The best screening test for dementia is a short-term memory test (eg, registering 3 objects and recalling them after 5 min); patients with dementia forget simple information within 3 to 5 min. Another test assesses the ability to name objects within categories (eg, lists of animals, plants, or pieces of furniture). Patients with dementia struggle to name a few; those without dementia easily name many.
In addition to loss of short-term memory, diagnosis of dementia requires at least one of the following cognitive deficits: Aphasia, Apraxia, Agnosia
Impaired ability to plan, organize, sequence, or think abstractly (executive dysfunction)
Each cognitive deficit must substantially impair function and represent a significant decline from a previous level of functioning. Also, the deficits must not occur only during delirium.
The Mini-Mental Status Examination is often used. When delirium is absent, the presence of multiple deficits, particularly in patients with an average or a higher level of education, suggests dementia.
History and physical examination should then focus on signs of treatable disorders that cause cognitive impairment (eg, vitamin B12 deficiency, neurosyphilis, hypothyroidism, depression.
Laboratory testing: Tests should include thyroid-stimulating hormone and vitamin B12 levels. Routine CBC and liver function tests are sometimes recommended, but yield is very low. If clinical findings suggest a specific disorder, other tests (eg, for HIV or syphilis) are indicated. Lumbar puncture is rarely needed but should be considered if a chronic infection or neurosyphilis is suspected. Other tests may be used to exclude causes of delirium.
Neuroimaging: CT or MRI should be done in the initial evaluation of dementia or after any sudden change in cognition or mental status. Neuroimaging can identify potentially reversible structural disorders (eg, normal-pressure hydrocephalus, brain tumors, subdural hematoma) and certain metabolic disorders (eg, Hallervorden-Spatz disease, Wilson’s disease). Occasionally, EEG is useful (eg, to evaluate episodic lapses in attention or bizarre behaviour). Functional MRI or single-photon emission CT can provide information about cerebral perfusion patterns and help with differential diagnosis (eg, in differentiating Alzheimer’s disease from frontotemporal dementia and Lewy body dementia).
What measures must the caregivers take in cases of dementia?
Dementia is usually progressive. However, progression rate varies widely and depends on the cause. Dementia shortens life expectancy, but survival estimates vary.
Treatment is directed at-
Measures to ensure safety
Provision of appropriate stimulation, activities, and cues for orientation
Elimination of drugs with sedating or anticholinergic effects
Possibly cholinesterase inhibitors
Assistance for caregivers
Arrangements for end-of-life care
Patient safety: Occupational and physical therapists can evaluate the home for safety; the goals are to prevent accidents (particularly falls), to manage behaviour disorders, and to plan for change as dementia progresses.
How well patients’ function in various settings (i.e., kitchen, automobile) should be evaluated using simulations. If patients have deficits and remain in the same environment, protective measures (eg, hiding knives, unplugging the stove, removing the car, confiscating car keys) may be required. Some states require physicians to notify the Department of Motor Vehicles of patients with dementia because, at some point, such patients can no longer drive safely. If patients wander, signal monitoring systems can be installed, or patients can be registered in the Safe Return program. Information is available from the Alzheimer’s Association. Ultimately, assistance (eg, housekeepers, home health aides) or a change of environment (living facilities without stairs, assisted-living facility, skilled nursing facility) may be indicated. Patient’s dress can have an inscribed caregivers phone number to be used in case the patient wanders away and lands with police and is unable to tell his phone number.
Environmental measures: Patients with mild to moderate dementia usually function best in familiar surroundings. Whether at home or in an institution, the environment should be designed to help preserve feelings of self-control and personal dignity by providing the following:
Frequent reinforcement of orientation
A bright, cheerful, familiar environment
Minimal new stimulation
Regular, low-stress activities
Large calendars and clocks and a routine for daily activities can help with orientation; medical staff members can wear large name tags and repeatedly introduce themselves. Changes in surroundings, routines, or people should be explained to patients precisely and simply, omitting nonessential procedures. Patients require time to adjust and become familiar with the changes. Telling patients about what is going to happen (eg, about a bath or feeding) may avert resistance or violent reactions. Frequent visits by staff members and familiar people encourage patients to remain social.
The room should be reasonably bright and contain sensory stimuli (eg, radio, television, night-light) to help patients remain oriented and focus their attention. Quiet, dark, private rooms should be avoided.
Activities can help patients function better; those related to interests before dementia began are good choices. Activities should be enjoyable, provide some stimulation, but not involve too many choices or challenges. Exercise to reduce restlessness, improve balance, and maintain cardiovascular tone should be done daily. Exercise can also help improve sleep and manage Behavior disorders. Occupational therapy and music therapy help maintain fine motor control and provides nonverbal stimulation. Group therapy (eg, reminiscence therapy, socialization activities) may help maintain conversational and interpersonal skills.
What is the treatment of dementia?
Drugs: Eliminating or limiting drugs with CNS activity often improves function. Sedating and anticholinergic drugs, which tend to worsen dementia, should be avoided. The cholinesterase inhibitors donepezil, rivastigmine, and galantamine (see Delirium and Dementia: Treatment) are somewhat effective in improving cognitive function in patients with Alzheimer’s disease or Lewy body dementia and may be useful in other forms of dementia. These drugs inhibit acetylcholinesterase, increasing the acetylcholine level in the brain.
Memantine, an NMDA (N-methyl-d-aspartate) antagonist, may help slow progression of moderate to severe dementia and can be used with a cholinesterase inhibitor.
Other drugs (eg, antipsychotics) have been used to control behaviour disorders (see Delirium and Dementia: Drugs). Patients with dementia and signs of depression should be treated with nonanticholinergic antidepressants, preferably SSRIs.
How must be the caregivers in family be assisted in dementia?
Caregiver assistance: Immediate family members are largely responsible for care of a patient with dementia. Nurses and social workers can teach them and other caregivers how to best meet the patient’s needs (eg, how to deal with daily care and handle financial issues); teaching should be ongoing. Other resources (eg, support groups, educational materials, Internet web sites) are available.
Caregivers may experience substantial stress. Stress may be caused by worry about protecting the patient and by frustration, exhaustion, anger, and resentment from having to do so much to care for someone. Health care practitioners should watch for early symptoms of caregiver stress and burnout and, when needed, suggest support services (eg, social worker, nutritionist, nurse, home health aide). If a patient with dementia has an unusual injury, the possibility of elder abuse should be investigated.
What are the legal issues in dementia?
Because insight and judgment deteriorate in patients with dementia, appointment of a family member, guardian, or lawyer to oversee finances may be necessary. Early in dementia, before the patient is incapacitated, the patient’s wishes about care should be clarified, and financial and legal arrangements (eg, durable power of attorney, durable power of attorney for health care) should be made. When these documents are signed, the patient’s capacity should be evaluated, and evaluation results recorded (see also Medicolegal Issues: Capacity (Competence) and Incapacity). Decisions about artificial feeding and treatment of acute disorders are best made before the need develops. In advanced dementia, palliative measures may be more appropriate than highly aggressive interventions or hospital care.
What is Alzheimer’s Disease?
Alzheimer’s disease causes progressive cognitive deterioration and is characterized by senile plaques, β-amyloid deposits, and neurofibrillary tangles in the cerebral cortex and subcortical Gray matter.
Alzheimer’s disease is the most common cause of dementia; it accounts for > 65% of dementias in the elderly. The disease is twice as common among women as among men, partly because women have a longer life expectancy. Alzheimer’s disease affects about 4% of people aged 65 to 74 and 30% of those > 85. Prevalence in industrialized countries is expected to increase as the proportion of the elderly increases.
Most cases are sporadic, with late onset (≥ 60 yr.) and unclear aetiology. However, about 5 to 15% are familial; half of these cases have an early (presenile) onset (< 60 yr.) and are typically related to specific genetic mutations. What is the pathology of Alzheimer’s dementia? At least 5 distinct genetic loci, located on chromosomes 1, 12, 14, 19, and 21, influence initiation and progression of Alzheimer’s disease. Mutations in genes for the amyloid precursor protein, presenilin I, and presenilin II may lead to autosomal dominant forms of Alzheimer’s disease, typically with presenile onset. In affected patients, the processing of amyloid precursor protein is altered, leading to deposition and fibrillar aggregation of β-amyloid. β-Amyloid may lead to neuronal death and formation of neurofibrillary tangles and senile plaques, which consist of degenerated axonal or dendritic processes, astrocytes, and glial cells around an amyloid core. Other genetic determinants include the apolipoprotein (apo) E alleles (ε). Apo E proteins influence β-amyloid deposition, cytoskeletal integrity, and efficiency of neuronal repair. Risk of Alzheimer’s disease is substantially increased in people with 2 ε4 alleles and may be decreased in those who have the ε2 allele. Variants in SORL1 may also be involved; they are more common among people with late-onset Alzheimer’s disease. These variants may cause the gene to malfunction, possibly resulting in increased production of β-amyloid. What are the Symptoms and Signs of Alzheimer’s dementia? Symptoms and signs of Alzheimer’s disease are similar to those of other dementias, with early, intermediate, and late stages. Loss of short-term memory is often the first sign. Cognitive deficits tend to involve multiple functions. The disease progresses gradually but may plateau for periods of time. Behavior disorders (eg, wandering, agitation, yelling, persecutory ideation) are common Generally, diagnosis is similar to that of other dementias. Clinical criteria (including a thorough history and standard neurologic examination) are 85% accurate in establishing the diagnosis and differentiating Alzheimer’s disease from other forms of dementia, such as vascular dementia and Lewy body dementia. Traditional diagnostic criteria for Alzheimer’s disease include all of the following: Dementia established clinically and documented by a formal mental status examination Deficits in ≥ 2 areas of cognition Gradual onset and progressive worsening of memory and other cognitive functions No disturbance of consciousness Onset after age 40, most often after age 65 No systemic or brain disorders that could account for the progressive deficits in memory and cognition However, deviations from these criteria do not exclude a diagnosis of Alzheimer’s disease, particularly because patients may have mixed dementia. What is the difference between Alzheimer’s Disease and Lewy Body Dementia? Alzheimer’s Disease has senile plaques, neurofibrillary tangles, and β-amyloid deposits in the cerebral cortex and subcortical Gray matter, affects twice as many women, Familial in 5–15% cases , Parkinsonian symptoms Very rare, occurring late in the disease, Hallucinations Occur in about 20% of patients, usually when disease is moderately advanced while Lewy Body Dementia they are in neurons of the cortex, Affects twice as many men, Inheritance, Rarely familial, Parkinsonian symptoms- Prominent, obvious early in the disease with Axial rigidity and unstable gait, Hallucinations Common Occur in about 80%, usually when disease is early, Most commonly, visual Alzheimer’s disease and Lewy body dementia (LBD) are both types of dementia. They have several similarities, but there are also some clear differences between the two diseases. LBD: Lewy body dementia is the second most common type of dementia, with an estimated 1.4 million Americans diagnosed. Alzheimer’s: Alzheimer’s disease is the most prevalent type of dementia. There are more than 5.5 million Americans with Alzheimer’s disease. Cause LBD: As the name suggests, Lewy body dementia is believed to be caused by the build-up of Lewy body proteins in the brain. Alzheimer’s: Alzheimer’s is characterized by amyloid plaques and neurofibrillary tangles in the brain. Researchers are still seeking answers as to what exactly triggers these brain changes in both LBD and Alzheimer’s, but they have identified nine specific risk factors that they believe play a role in triggering many cases of dementia.2 The good news about these factors is that they are one we can at least partially control. Cognition LBD: Symptoms and memory can vary significantly in LBD, such that on one day your grandmother might not recognize you and the next day, she can recall the names of each of her grandchildren. Alzheimer’s: While cognition can vary somewhat in Alzheimer’s, typically the person’s ability to think and use his memory gradually declines over time. In Alzheimer’s symptoms, there is not usually a big variance from one day to the next. Physical Movement LBD: Often, one of the early symptoms of LBD is difficulty walking, a decrease in balance and ability to control physical movements. These symptoms are similar to Parkinson’s disease.3 Frequent falling is also common early in LBD. Alzheimer’s: Physical deterioration usually does not occur in Alzheimer’s until the disease has significantly progressed, unless the individual has other diseases or illnesses. Facial Expressions LBD: Some people who have LBD display a flat affect, where their faces show very little emotion.3 This is another symptom that may present early in the disease and overlaps with Parkinson’s. Alzheimer’s: While facial expressions often decrease as the disease progresses, this often doesn’t develop until the middle to later stages of Alzheimer’s. Visual Hallucinations LBD: Visual hallucinations, where people see things that aren’t actually there, are quite common in LBD. These hallucinations typically occur earlier in the progression of LBD. Alzheimer’s: Hallucinations do occur in Alzheimer’s, but are generally not as prevalent as in LBD.4 They also tend to occur in the later stages of Alzheimer’s disease, as compared to the earlier stages of LBD. REM Sleep Behavior Disorder LBD: People with LBD sometimes experience REM sleep Behavior disorder, a dysfunction where they physically act out the situations in their dreams. Some research suggests that REM sleep behaviour disorder can be one of the earlier predictors of LBD.5 Alzheimer’s: REM sleep behaviour disorder is not typically present in Alzheimer’s, although other types of sleep disturbances may occur. Sensitivity to Antipsychotics LBD: People with LBD have a very high risk of serious side effects if antipsychotic medications are given to them. According to the Lewy Body Dementia Association, “It is estimated that a high percentage of [dementia with Lewy bodies] DLB patients exhibit worsening parkinsonism, sedation, immobility, or even neuroleptic malignant syndrome (NMS) after exposure to antipsychotics. NMS is a rare, life-threatening medical emergency characterized by fever, generalized rigidity and breakdown of muscle tissue that can cause renal failure and death. The heightened risk of NMS in DLB mandates that typical or traditional antipsychotics (such as haloperidol, fluphenazine or thioridazine) should be avoided. Atypical antipsychotics have been available for treating mental illness for 25 years and may be safer to use in patients with DLB, but only with extreme caution. Patients with Parkinson’s disease dementia (PDD) appear to have a lower risk of an adverse reaction to an antipsychotic, but all patients with LBD should be carefully managed with any antipsychotic drug.” Alzheimer’s: While anyone who takes an antipsychotic medication has a small risk of developing neuroleptic malignant syndrome, individuals with Alzheimer’s are not nearly as prone to developing the extreme sensitivity to antipsychotic medications that people with LBD demonstrate. Disease Progression LBD: According to research conducted by James E. Galvin, MD, MPH and other researchers at the Washington University School of Medicine, the median survival time for those in the study with LBD is 78 years old, and survival after onset of Lewy body dementia was 7.3 years. Alzheimer’s: In the above-referenced study, the median survival time for participants with Alzheimer’s was 84.6 years old, and the survival rate after the beginning of symptoms was 8.4 years. It has been suggested that the difference in the disease progression between LBD and Alzheimer’s can partially be explained by the increase in falls, and therefore injuries and hospitalizations, in those with LBD. Gender LBD: Men have a higher chance of developing LBD than women do. Alzheimer’s: Women have a higher chance of developing Alzheimer’s. Prognosis Although progression rate varies, cognitive decline is inevitable. Average survival from time of diagnosis is 7 yr., although this figure is debated. Average survival from the time patients can no longer walk is about 6 mo. Treatment Generally, similar to that of other dementias Possibly cholinesterase inhibitors and memantine General treatment is the same as that of all dementias (see Delirium and Dementia: Treatment). Cholinesterase inhibitors modestly improve cognitive function and memory in some patients. Four are available; generally, donepezil, rivastigmine, and galantamine are equally effective, but tacrine is rarely used because of its hepatotoxicity. Donepezil is a first-line drug because it has once/day dosing and is well-tolerated. The recommended dose is 5 mg once/day for 4 to 6 wk., then increased to 10 mg once/day. Treatment should be continued if functional improvement is apparent after several months, but otherwise it should be stopped. The most common adverse effects are GI (eg, nausea, diarrhoea). Rarely, dizziness and cardiac arrhythmias occur. Adverse effects can be minimized by increasing the dose gradually (see Table 6: Delirium and Dementia: Drugs for Alzheimer’s Disease). Memantine, an N-methyl-d-aspartate receptor antagonist, appears to slow the progression of Alzheimer’s disease. The dose is 5 mg po once/day, which is increased to 10 mg po bid over about 4 wk. For patients with renal insufficiency, the dose should be reduced or the drug should be avoided. Memantine can be used with a cholinesterase inhibitor. Efficacy of high-dose vitamin E (1000 IU po once/day or bid), selegiline, NSAIDs, Ginkgo biloba extracts, and statins is unclear. Oestrogen therapy does not appear useful in prevention or treatment and may be harmful. Prevention Preliminary, observational evidence suggests that risk of Alzheimer’s disease may be decreased by the following: Continuing to do challenging mental activities (eg, learning new skills, doing crossword puzzles) well into old age Exercising Controlling hypertension Lowering cholesterol levels Consuming a diet rich in ω-3 fatty acids and low in saturated fats Drinking alcohol in modest amounts However, there is no convincing evidence that people who do not drink alcohol should start drinking to prevent Alzheimer’s disease. What is Vascular Dementia? Vascular dementia is acute or chronic cognitive deterioration due to diffuse or focal cerebral infarction that is most often related to cerebrovascular disease. Vascular dementia is the 2nd most common cause of dementia among the elderly. It is more common among men and usually begins after age 70. It occurs more often in people who have vascular risk factors (eg, hypertension, diabetes mellitus, hyperlipidaemia, smoking) and in those who have had several strokes. Many people have both vascular dementia and Alzheimer’s disease. Vascular dementia occurs when multiple small cerebral infarcts (or sometimes haemorrhages) cause enough neuronal or axonal loss to impair brain function. What are the types of vascular dementia? Vascular dementias include the following: Lacunar disease: Small blood vessels are affected. Multi-infarct dementia: Medium-sized blood vessels are affected. Strategic single-infarct dementia: A single infarct occurs in a crucial area of the brain (eg, angular gyrus, thalamus). Binswanger’s dementia (subcortical arteriosclerotic encephalopathy): This uncommon variant of small-vessel dementia is associated with severe, poorly controlled hypertension and systemic vascular disease. It involves multiple lacunar infarcts in deep hemispheric white and Gray matter. What are the Symptoms and Signs of vascular dementia? Symptoms and signs are similar to those of other dementias. However, because infarction is the cause, vascular dementia tends to progress in discrete steps; each episode is accompanied by intellectual decline, sometimes followed by modest recovery. As the disease progresses, focal neurologic deficits often develop: Exaggeration of deep tendon reflexes Extensor plantar response Gait abnormalities Weakness of an extremity Hemiplegia’s Pseudobulbar palsy with pathologic laughing and crying Other signs of extrapyramidal dysfunction However, because small-vessel ischemic damage tends to cause small, incremental deficits, the decline appears to be gradual. Cognitive loss may be focal. For example, short-term memory may be less affected than in other dementias. Patients with partial aphasia may be more aware of their deficits; thus, depression may be more common than in other dementias. How do you diagnose vascular dementia? Generally similar to diagnosis of other dementias Diagnosis is similar to that of other dementias (see Delirium and Dementia: Diagnosis). If focal signs or evidence of cerebrovascular disease is present, a thorough evaluation for stroke should be done ( CT and MRI may show bilateral multiple infarcts in the dominant hemisphere and limbic structures, multiple lacunar strokes, or periventricular white-matter lesions extending into the deep white matter. In Binswanger’s dementia, imaging shows leukoencephalopathy in the cerebrum semiovale adjacent to the cortex, often with multiple lacunae affecting structures deep in the Gray matter (eg, basal ganglia, thalamic nuclei). Low-Density Periventricular Changes in Deep White Matter What is the prognosis of vascular dementia? The 5-yr mortality rate is 61%, which is higher than that for most forms of dementia, presumably because other atherosclerotic disorders coexist. What is the treatment of vascular dementia? Generally similar to treatment of other dementias Generally, treatment is the same as that of other dementias. However, vascular dementia may be preventable, and its progression may be slowed by BP control, cholesterol-lowering therapy, regulation of plasma glucose (90 to 150 mg/dL), and smoking cessation. The efficacy of cholinesterase inhibitors and memantine is uncertain. However, because many patients also have Alzheimer’s disease, these drugs may have some benefit. Adjunctive drugs for depression, psychosis, and sleep disorders are useful. What is Lewy Body (LB) Dementia? Lewy body dementia is chronic cognitive deterioration characterized by cellular inclusions called Lewy bodies in the cytoplasm of cortical neurons. Lewy body dementia is the 3rd most common dementia. Age of onset is typically > 60.
What is pathology of LB dementia?
Lewy bodies are spherical, eosinophilic, neuronal cytoplasmic inclusions composed of aggregates of α-synuclein, a synaptic protein. They occur in the cortex of some patients with primary Lewy body dementia. Neurotransmitter levels and neuronal pathways between the striatum and the neocortex are abnormal.
Lewy bodies also occur in the substantia nigral of patients with Parkinson’s disease, and patients with Parkinson’s disease may develop Lewy body dementia. Thus, some experts think that Parkinson’s disease and Lewy body dementia may be part of a more generalized synucleopathy affecting the central and peripheral nervous systems (see Movement and Cerebellar Disorders: Parkinson’s Disease). Lewy bodies sometimes occur in patients with Alzheimer’s disease, and patients with Lewy body dementia may have neuritic plaques and neurofibrillary tangles. Lewy body dementia, Parkinson’s disease, and Alzheimer’s disease overlap considerably.
What are the clinical features of LB dementia?
Initial cognitive deterioration resembles that of other dementias (see Delirium and Dementia: Symptoms and Signs). Extrapyramidal symptoms occur. However, unlike in Parkinson’s disease, in Lewy body dementia, cognitive and extrapyramidal symptoms usually begin within 1 yr. of each other. Also, the extrapyramidal symptoms differ from those of Parkinson’s disease: In Lewy body dementia, tremor does not occur early, rigidity of axial muscles with gait instability occurs early, and deficits tend to be symmetric. Repeated falls are common.
Fluctuating cognitive function is a relatively specific feature of Lewy body dementia. Periods of being alert, coherent, and oriented may alternate with periods of being confused and unresponsive to questions, usually over a period of days to weeks but sometimes during the same interview. Memory is impaired, but the impairment appears to result more from deficits in alertness and attention than in memory acquisition; thus, short-term recall is affected less than digit span memory (ability to repeat 7 digits forward and 5 backward). Patients may stare into space for long periods. Excessive daytime drowsiness is common. Visuospatial and vasoconstriction abilities (tested by block design, clock drawing, or figure copying) are affected more than other cognitive deficits. Thus, Lewy body dementia may be difficult to distinguish from delirium, and all patients presenting with these symptoms and signs should be evaluated for delirium.
Visual hallucinations are common and often threatening, unlike the benign hallucinations of Parkinson’s disease. Auditory, olfactory, and tactile hallucinations are less common. Delusions occur in 50 to 65% of patients and are often complex and bizarre, compared with the simple persecutory ideation common in Alzheimer’s disease.
Autonomic dysfunction is common, and unexplained syncope may result. Autonomic dysfunction may occur simultaneously with or after onset of cognitive deficits. Extreme sensitivity to antipsychotics is typical. Many patients have rapid eye movement (REM) sleep Behavior disorder, a parasomnia characterized by vivid dreams without the usual physiologic paralysis of skeletal muscles during REM sleep. As a result, dreams may be acted out, sometimes injuring the bed partner.
How do you diagnose LB dementia?
Diagnosis is considered probable if 2 of 3 features—fluctuations in cognition, visual hallucinations, and parkinsonism—are present and possible if only one is present. Supportive evidence consists of repeated falls, syncope, and sensitivity to antipsychotics. Overlap of symptoms in Lewy body dementia and Parkinson’s disease may complicate diagnosis. When motor deficits (eg, tremor, bradykinesia, rigidity) precede and are more severe than cognitive impairment, Parkinson’s disease is usually diagnosed. When early cognitive impairment and behavioural disturbances predominate, Lewy body dementia is usually diagnosed.
CT and MRI show no characteristic changes but are helpful initially in ruling out other causes of dementia.
What is the treatment of LB dementia?
Treatment is generally supportive. Rivastigmine 1.5 mg po bid, titrated upward as needed to 6 mg bid, may improve cognition. Other cholinesterase inhibitors may also be useful. In about half of patients, extrapyramidal symptoms respond to antiparkinsonian drugs (see Movement and Cerebellar Disorders: Treatment), but psychiatric symptoms may worsen. If such drugs are needed, levodopa is preferred. Traditional antipsychotics, even at very low doses, tend to acutely worsen extrapyramidal symptoms and are best avoided. How to manage dementia with LB?
Recurrent visual hallucinations are a core feature of dementia with Lewy bodies (DLB). While the spectrum of behavioural and psychological symptoms of dementia in DLB is broader than psychosis alone—also including anxiety, depression, apathy, and agitation—hallucinations and delusions (i.e., psychosis) are common in patients with DLB and are a key issue in living with the disease
Delusions are an important determinant of quality of life (QoL) in DLB as assessed by both patients and caregivers] Behavioural disturbances are associated with depression in DLB caregivers and are major contributors to caregiver distress and strain. Although research is lacking with regard to the determinants of institutionalization in DLB, Parkinson’s disease (PD) studies show that psychosis is the main risk factor for nursing home placement.
The management of hallucinations and delusions in DLB is challenging, however. Antipsychotics have risks in patients with DLB. “Severe neuroleptic sensitivity” is a suggestive feature in DLB clinical diagnostic criteria, in part based on research showing that 81% of patients with DLB who received typical antipsychotics had adverse reactions, one-half of which were severe. Atypical antipsychotics received a black-box warning from the US Food and Drug Administration (FDA) in 2005 due to an increased risk of death in patients with dementia-related behavioural disturbances. This warning was extended to typical antipsychotics in 2008. Studies demonstrate an increased risk of death in patients with dementia who are treated with antipsychotics in both the short and long term.
The benefits of antipsychotics in DLB are uncertain, but few alternatives exist. A meta-analysis of pharmacologic strategies for the closely related Lewy body dementias (LBDs) (i.e., both DLB and PD dementia [PDD]) found few studies of antipsychotic agents in these conditions. In the small studies cited, often with limited methodologic rigor, there was no evidence for efficacy and also a limited ability to exclude potentially beneficial effects. When considering PDD with psychosis, a Movement Disorder Society evidence-based medicine review concluded that clozapine was “efficacious” and had an acceptable risk with specialized monitoring; quetiapine was considered “investigational” given a lack of supporting evidence; and olanzapine was characterized as “unlikely efficacious” and as having “unacceptable risk” given clearly demonstrated worsening of motor function.
Clinicians, patients, and families are often left wondering what to do, particularly when hallucinations and delusions are distressing or when they contribute to behaviours that put patients and family members at risk. In this scenario, lack of treatment evidence is unsatisfying and untenable; something has to be tried
The approach to antipsychotic use in patients with DLB starts with avoidance. Addressing underlying medical conditions and weaning medications that may exacerbate hallucinations and delusions are important first steps. Evidence from PDD suggests that treating systemic illness, adjusting medications, and monitoring over weeks may preclude the need for antipsychotic therapy in the short term in as many as two-thirds of patients, though one-half of these patients required antipsychotic medication on long-term follow-up. When discontinuing medications, the approach favoured in PDD with psychosis is also relevant in DLB: start by discontinuing medications with anticholinergic properties, including tricyclic antidepressants and bladder antispasmodics. Sequential consideration is then given to discontinuing amantadine, monoamine oxidase B inhibitors, and dopamine agonists (all of which are less commonly used in DLB than in PD). Finally, if needed and tolerated, wean levodopa/carbidopa to the dose that best balances cognitive/behavioural and motor effects.
While robust evidence for a beneficial effect of cholinesterase inhibitors on hallucinations and delusions is lacking, there is some evidence that these medications may help people with DLB and improve psychiatric symptoms in those with PDD. Thus, cholinesterase inhibitors can be tried for overall benefit with a hoped-for impact on hallucinations and delusions.
What is the prognosis of LB dementia?
In Lewy body dementia progresses, prognosis is poor.
What is HIV-Associated Dementia?
HIV-associated dementia is chronic cognitive deterioration due to brain infection by HIV.
HIV-associated dementia (AIDS dementia complex) may occur in the late stages of HIV infection. Unlike almost all other forms of dementia, it tends to occur in younger people. Purely HIV-associated dementia is caused by neuronal damage by the HIV virus. However, in patients with HIV infection, dementia may result from other infections, such as secondary infection with JC virus causing progressive multifocal leukoencephalopathy. Other opportunistic infections (eg, fungal, bacterial, viral, protozoan) may also contribute.
What is pathology of HIV-Associated Dementia?
In purely HIV-associated dementia, subcortical pathologic changes result when infected macrophages or microglial cells infiltrate into the deep Gray matter (ie, basal ganglia, thalamus) and white matter.
Prevalence of dementia in late-stage HIV infection ranges from 7 to 27%, but 30 to 40% may have milder forms. Incidence is inversely proportional to CD4+ count.
What are Symptoms and Signs of HIV-Associated Dementia?
Symptoms and signs may be similar to those of other dementias (see Delirium and Dementia: Symptoms and Signs). Early manifestations include slowed thinking and expression, difficulty concentrating, and apathy; insight is preserved, and manifestations of depression are few. Motor movements are slowed; ataxia and weakness may be evident. Abnormal neurologic signs may include paraparesis, lower-extremity spasticity, ataxia, and extensor-plantar responses. Mania or psychosis is sometimes present.
How do you Diagnose HIV-Associated Dementia?
Generally similar to initial diagnosis of other dementias
Prompt evaluation, including MRI, when deterioration is acute
Generally, diagnosis of dementia in patients with HIV infection is similar to that of other dementias (see Delirium and Dementia: Diagnosis). However, when patients present with an acute change in cognitive function, the cause must be identified as soon as possible.
CT or MRI should be done to check for signs of CNS infection (eg, toxoplasmosis). MRI is more useful than CT because it can exclude other CNS causes of dementia (eg, progressive multifocal leukoencephalopathy, cerebral lymphoma). Late-stage findings of HIV dementia may include diffuse nonenhancing white matter hyperintensities, cerebral atrophy, and ventricular enlargement. If no contraindication is identified by neuroimaging, lumbar puncture is done to rule out infection.
What is the prognosis of HIV-Associated Dementia?
Patients with HIV infection and untreated dementia have a worse prognosis (average life expectancy of 6 mo.) than those without dementia.
What is the Treatment of HIV-Associated Dementia?
Highly active antiretroviral therapy
The primary treatment is highly active antiretroviral therapy, which increases CD4+ counts and improves cognitive function. Supportive measures are similar to those for other dementias
What is Frontotemporal (FTD)Dementia?
Frontotemporal dementia (FTD) refers to sporadic and hereditary disorders that affect the frontal and temporal lobes, including Pick’s disease.
What is the pathology of FTD?
FTD accounts for up to 10% of dementias. Age at onset is typically younger (age 55 to 65) than in Alzheimer’s disease. FTDs affect men and women about equally. Pick’s disease is a variant of FTD, which may be pathologically characterized by severe atrophy, neuronal loss, gliosis, and presence of abnormal neurons (Pick cells) containing inclusions (Pick bodies).
About half of FTDs are inherited; most mutations involve chromosome 17q21-22 and result in abnormalities of the microtubule-binding tau protein; thus, FTDs are considered tauopathies. Some experts classify supranuclear palsy and Corticobasal degeneration with FTDs because they share similar pathology and gene mutations affecting the tau protein. Symptoms, gene mutations, and pathologic changes may not correspond to each other. For example, the same mutation causes FTD symptoms in one family member but symptoms of Corticobasal degeneration in another, and Pick’s cells may be absent in patients with typical symptoms of Pick’s disease.
What are the clinical features of FTD?
Generally, FTD affects personality, behaviour, and usually language function (syntax and fluency) more and memory less than does Alzheimer’s disease. Abstract thinking and attention (maintaining and shifting) are impaired; responses are disorganized. Orientation is preserved, but retrieval of information may be impaired. Motor skills are generally preserved. Patients have difficulty sequencing tasks, although visual-spatial and constructional tasks are affected less.
Frontal release signs (grasp, root, suck, snout, and palmomental reflexes and glabellar sign—see Approach to the Neurologic Patient: Reflexes) appear late in the disease but also occur in other dementias. Some patients develop motor neuron disease with generalized muscle atrophy, weakness, fasciculations, bulbar symptoms (eg, dysphagia, dysphonia, difficulty chewing), and increased risk of aspiration pneumonia and early death.
Frontal variant FTD: Social behaviour and personality change because the orbitobasal frontal lobe is affected. Patients become impulsive and lose their social inhibitions (eg, they may shoplift); they neglect personal hygiene. Some have Klüver-Bucy syndrome, which involves emotional blunting, hypersexual activity, hyperorality (eg, bulimia, sucking and smacking of lips), and visual agnosias. Impersistence (impaired concentration), inertia, and mental rigidity appear.
Behavior becomes repetitive and stereotyped (eg, patients may walk to the same location every day). Patients may pick up and manipulate random objects for no reason (called utilization behaviour). Verbal output is reduced; echolalia, perseveration (inappropriate repetition of a response), and eventually mutism occurs.
Primary progressive aphasia: Language function deteriorates because of asymmetric (worse on left) anterolateral temporal lobe atrophy; the hippocampus and memory are relatively spared. Most patients present with difficulty finding words. Attention (eg, digit span) may be severely impaired. Many patients have aphasia, with decreased fluency and difficulty comprehending language; hesitancy in speech production and dysarthria are also common. In some patients, aphasia is the only symptom for ≥ 10 yr.; in others, global deficits develop within a few years.
Semantic dementia is a type of primary progressive aphasia. When the left side of the brain is affected most, the ability to comprehend words is progressively lost. Speech is fluent but lacks meaning; a generic or related term may be used instead of the specific name of an object. When the right side is affected most, patients have progressive anomia (inability to name objects) and prosopagnosia (inability to recognize familiar faces). They cannot remember topographic relationships. Some patients with semantic dementia also have Alzheimer’s disease.
How to Diagnose FTD?
Diagnosis is suggested by typical clinical findings. As for other dementias, cognitive deficits are evaluated (see Delirium and Dementia: Diagnosis). CT and MRI are done to determine location and extent of brain atrophy and to exclude other possible causes (eg, brain tumors, abscesses, stroke). FTDs are characterized by severely atrophic, sometimes paper-thin gyri in the temporal and frontal lobes. However, MRI or CT may not show these changes until late in FTD. Thus, FTDs and Alzheimer’s disease can usually be differentiated more easily by clinical criteria. For example, primary progressive aphasia differs from Alzheimer’s disease in that memory and visuospatial function are preserved and syntax and fluency are impaired.
What is the Prognosis of FTD?
FTDs usually progress gradually, but progression rate varies; if symptoms are limited to speech and language, progression to general dementia may be slower.
What is the treatment of FTD?
There is no specific treatment. Treatment is generally supportive
What is Normal–Pressure Hydrocephalus (NPH)?
Normal-pressure hydrocephalus is characterized by gait disturbance, urinary incontinence, dementia, enlarged brain ventricles, and normal or slightly elevated CSF pressure.
Normal-pressure hydrocephalus is thought to result from a defect in CSF resorption in arachnoid granulations. This disorder accounts for up to 6% of dementias.
What are the Symptoms and Signs of NPH?
Most commonly, the gait disturbance is nonspecific unsteadiness and impaired balance, although a magnetic gait (the feet appear to stick to the floor) is considered the characteristic gait disturbance. Dementia may not occur until late in the disorder. The most common early symptoms of dementia are disturbances of executive function and attention; memory tends to become impaired later.
How to diagnose NPH?
-Clinical evaluation
-Neuroimaging
-Sometimes removal of CSF
The classic symptoms (gait disturbance, urinary incontinence, and dementia), even combined, are nonspecific for normal-pressure hydrocephalus, particularly in the elderly. For example, some forms of vascular dementia can cause dementia, gait disturbance, and, less commonly, urinary incontinence. Brain imaging may show ventricular enlargement disproportionate to cortical atrophy; this finding is nonspecific but may support the diagnosis of normal-pressure hydrocephalus.
Lumbar puncture with removal of 20 to 30 mL of CSF can be done as a diagnostic trial. Improvement in gait, continence, and cognition after removal helps confirm the diagnosis, but improvement may not be evident until several hours after removal.
What is the Treatment of NPH?
Ventriculoperitoneal shunting is useful for patients with acceptable surgical risks. Improvements after lumbar puncture to remove CSF, done during diagnosis, may predict the response to shunting. In several case series (but in no randomized trials), patients improved substantially, typically in gait, continence, and daily functioning, after shunting; improvement in cognition was less common.
What is Behavioural variant Frontotemporal Dementia (bvFTD) and how to manage it?
Unfortunately, accurate identification of Behavioural variant Frontotemporal Dementia (bvFTD) can be difficult for clinicians, including primary care physicians, geriatricians, general psychiatrists and general neurologists, who do not specialize in the assessment of neurodegenerative syndromes. bvFTD is a neurodegenerative disorder caused by focal degeneration of the frontal and anterior temporal lobes; it has an incidence and prevalence similar to Alzheimer’s disease (AD) among young-onset patients. bvFTD is often mistaken for AD or other conditions including psychiatric disorders, such as late-onset schizophrenia, atypical psychosis and depression. Alternatively, though non-specialist clinicians have become more aware of bvFTD as an entity, they may erroneously interpret their patients’ symptoms as indicating bvFTD when the patient has another neurologic or psychiatric disorder. Patients with AD presenting with agitation and aggression, which occur frequently in AD, can be diagnosed as bvFTD due to the difficulty of delineating the whole symptom profile necessary for differential diagnosis. The resulting confusion and social upheaval for the patient and their family can be highly distressing. The diagnosis of bvFTD relies upon subjective behavioural features, including behavioural disinhibition, apathy or loss of interest, loss of sympathy or empathy, compulsive stereotypic behaviour and dietary changes. Treatment is on lines of dementia.
What is Sundowning and how to manage it?
Sundowning is a term used about the changes in behaviour that occur in the evening, around dusk. Some people who have been diagnosed with dementia experience a growing sense of agitation or anxiety at this time.
Practical tips on preventing sundowning • Follow a routine during the day that contains activities the person enjoys • Going outside for a walk or visiting some shops is good exercise • Limit the person’s intake of caffeinated drinks: tea, coffee and colas. Consider stopping the person from drinking alcohol altogether. Caffeine-free tea, coffee and cola is available, as is alcohol-free beer and wine • Try and limit the person’s naps during the day to encourage them to sleep well at night instead • Close the curtains and turn the lights on before dusk begins, to ease the transition into night-time • If possible, cover mirrors or glass doors. Reflections can be confusing for someone with dementia • Once you are in for the evening, speak in short sentences and give simple instructions to the person, to try and limit their confusion • Avoid large meals in the evening as this can be disrupt sleep patterns • Introduce an evening routine with activities the person enjoys, such as watching a favourite programme, listening to music, stroking a pet etc. Try to keep television or radio stations set to something calming and relatively quiet however. Sudden loud noises or people shouting can be distressing for a person with dementia.
How about the problem of treatment of opioid addiction in Punjab with buprenorphine?
The medicine buprenorphine is a derivative of opioid and is far more potent than morphine and is a longer lasting pain reliever. Pharmaceutical experts don’t rule out the use of a combination of the medicine for recreational purposes and it has been used intravenously by addicts. That is why, under the State Drug Policy-2017, the government regulates the sale of buprenorphine along with five other drugs. The medicine cannot be dispensed for more than seven days in a single visit. Additionally, it can be sold at only at designated de-addiction centres.
While the Punjab Government was going gaga about buprenorphine weaning addicts away from ‘chitta’, the state’s Food and Drug Administration (FDA) was grappling with an important question: How much does this habit-forming drug sell? The FDA through its field staff started collecting data regarding its sale from all the de-addiction centres. The outcome was baffling.
It was found that six crore tablets had been dispensed in a year; of these, 4.5 crore had been given in the government sector and 1.6 crore in the private sector. The report on this was kept a closely guarded secret for several months before it was reported in The Tribune. “We are replacing one addiction with the another,” an official closely monitoring everything said.
However, a major breakthrough came last year when, acting on a tip-off, a drug inspector in Ludhiana found a cache of 1.6 lakh tablets (a combination of buprenorphine and naloxone) stocked with a wholesaler, Oracle Laboratories. It was then that the lid over the illegal sale of this medicine blew off. As per the instructions of the DCGI, the highly habit-forming de-addiction drug, can only be supplied directly to de-addiction centres by the manufacturer. Hoarding it was illegal.
Later, it emerged during the investigation that the network was much bigger than what the state had imagined. The medicine was being manufactured in pharmaceutical factories in Gujarat and Uttarakhand and making way into Punjab through courier companies, AC buses and railway parcel systems.
From Ludhiana, the drug was not just being supplied within the state, it was being sent to de-addiction centres in Delhi, Haryana and Rajasthan as well.
Not only did it turn out to be a case of illegal procurement, storage and dispensation of the medicine, tests also confirmed that the medicine being manufactured didn’t meet the standards. The amount of salt in the tablets was much lesser than what was mentioned on the strip. However, owner of Oracle Laboratories increased government’s problem further when he said that his company was not the only one indulging in this practice. “There are at least 15 companies in Punjab that are doing the same thing, but no action has been taken against them,” Vikas Bansal, director of the company said, alleging he was being singled out.
When it comes to salt variation in the medicine, Oracle is not the lone defaulter. Punjab Government is investigating three big manufacturers whose de-addiction drug buprenorphine was found to contain 17-25 per cent more salt than allowed, while one had below the dose given on the label.
The three companies include Rusan Pharma (Addnok-N) that operates from Uttarakhand, Maan Pharmaceuticals (Cizdol-N), Gujarat and SBS Biotech (QTRUGS), Haryana. The state government has written to their respective states. Earlier fearing that a bigger dose can vitiate the entire de-addiction programme, the state government had even recommended suspension of sale of the medicine from the three drug companies.
De-addiction has emerged as a big business proposition in the state and besides companies, de-addiction centres are also indulging in illegal activities. Some of the centres have been found doing business at a scale which is not humanly possible without indulging in unlawful activities.
A reality check revealed that a Tarn Taran centre employing just one doctor dispensed 50 lakh tablets of buprenorphine in just six months. The FDA expressed fear that such centres were acting as bulk sale points of the medicine. The state government chose to act against a few but spared big fish, like the centre in Tarn Taran.
The situation is such that even at the top level the government has faced allegations of helping one player monopolise the buprenorphine business.
Even psychiatrists have said that they are not being allowed to prescribe the medicine because the government wants only a few favourites to control the market.
However, the mess in drug de-addiction programme has shaken the highest quarters at the government. Even the CM, who had hailed the free flow of de-addiction drug in January, was soon instructing all the deputy commissioners “to check misuse of buprenorphine tablets by unscrupulous elements.”
Taking queue from the Ludhiana raid, FDA Punjab started visiting several transport and courier companies and railway authorities to sensitise them about how they were being taken for a ride by unscrupulous elements. The situation slipping out of hand on the ground forced the FDA to issue new guidelines regarding transportation of de-addiction medicine. As per the revised guidelines, the medicine can be sent only through India Post’s Speed Post and not by any other mode of transportation. Besides asking Gujarat and Uttarakhand governments to investigate the three companies involved in illegal sale of the medicine in Punjab, the state FDA has also taken up the matter with Drug Controller General of India to tighten the noose around the companies creating menace in the state by violating the instructions.
What about management of dystonia?
Dystonia are sustained involuntary muscle contractions, often distorting body posture. Dystonia can be primary or secondary, and they can be generalized, focal, or segmental. Diagnosis is clinical. Treatment of generalized dystonia is often with a combination of anticholinergic drugs, muscle relaxants, and benzodiazepines. Treatment of focal or segmental dystonia is often with botulinum toxin; more generalized or refractory cases may benefit from surgery.
What are the causes of dystonia?
Dystonia may be primary (idiopathic) or secondary to degenerative or metabolic CNS disorders (eg, Wilson’s disease, Hallervorden-Spatz disease, various lipidoses, multiple sclerosis, cerebral palsy, stroke, brain hypoxia) or drugs (most often phenothiazines, thioxanthenes, butyrophenones, and antiemetics).
Generalized dystonia (dystonia musculorum deformans):
This rare dystonia is progressive and characterized by movements that result in sustained, often bizarre postures. It is often hereditary, usually as an autosomal dominant disorder with partial penetrance; asymptomatic siblings of patients often have a forme fruste of the disorder. The causative gene is usually DYT1, causing DYT1 dystonia.
Symptoms usually begin in childhood with inversion and plantar fixation of the foot while walking. The dystonia may affect only the trunk or a leg but sometimes affects the whole body. Patients with the most severe form may become twisted into grotesque fixed postures and ultimately confined to a wheelchair. Symptoms that begin during adulthood usually affect only the face or arms. Mental function is usually preserved.
Focal dystonia:
These dystonia’s affect a single body part. They typically start in a person’s 30s or 40s and affect women more often. Initially, spasms may be periodic, occurring randomly or during stress; they are triggered by certain movements of the affected body part and disappear during rest. Over days, weeks, or many years, spasms may progress; they may be triggered by movements of unaffected body parts and may continue during rest. Eventually, the affected body part remains distorted, sometimes in a painful position, resulting in severe disability. Symptoms vary depending on the specific muscles involved.
Occupational dystonia consists of focal dystonic spasms initiated by performing skilled acts (eg, writer’s or typist’s cramp, the yips in golfers).
Spasmodic dystonia consists of a strained, hoarse, or creaky voice due to abnormal involuntary contraction of laryngeal muscles.
Torticollis begins with a pulling sensation followed by sustained torsion and deviation of the head and neck. The cause is often unknown but, in some cases, is probably genetic. In early stages, it can be voluntarily overcome. Patients may discover sensory or tactile tricks that make the spasm stop, such as touching the face on the side contralateral to the deviation. Torticollis can also be caused by dopamine -blocking drugs (eg, haloperidol).
Segmental dystonia: These dystonia affect ≥ 2 contiguous body parts.
Meige’s disease (blepharospasm-oromandibular dystonia) consists of involuntary blinking, jaw grinding, and grimacing, usually beginning in late middle age. It may mimic the buccal-lingual-facial movements of tardive dyskinesia.
How to diagnose dystonia?
Diagnosis is clinical.
What is the Treatment of dystonia?
For generalized dystonia, anticholinergics, muscle relaxants, or both.
For focal dystonia, botulinum toxin.
Treatment is often unsatisfactory. For generalized dystonia, a high-dose anticholinergic drug (trihexyphenidyl 2 to 10 mg po tid, benztropine 3 to 15 mg po once/day) is most commonly used, often with a muscle relaxant (usually baclofen), a benzodiazepine (eg, clonazepam), or both. Generalized dystonia that is severe or does not respond to drugs may be treated with deep brain stimulation of the globus pallidus interna, which requires surgery.
For focal or segmental dystonia or for generalized dystonia that severely affects specific body parts, the treatment of choice is purified botulinum toxin type A. injected into the affected muscles by an experienced practitioner. Botulinum toxin weakens muscular contractions, but it does not alter the abnormal neural stimulus. Toxin injection is particularly effective for blepharospasm and torticollis. Dosage varies greatly. Treatments must be repeated every 3 to 6 mo.
What is Erectile dysfunction (ED)?
Erectile dysfunction (ED) is the inability to attain or sustain an erection satisfactory for sexual intercourse. Most erectile dysfunction is related to vascular, neurologic, psychologic, and hormonal disorders; drug use can also be a cause. Evaluation typically includes screening for underlying disorders and measuring testosterone levels. Treatment options include oral phosphodiesterase inhibitors or apomorphine, intraurethral or intracorneal prostaglandins, mechanical pump devices, and surgical implants.
The term impotence has been replaced by the term erectile dysfunction. In the US, at least 10 to 20 million men > 18 are affected. The prevalence of partial or complete ED is about 50% in men 40 to 70 and increases with aging. However, many men can be successfully treated.
What are types of ED?
Primary ED (ie, the man has never been able to attain or sustain erections) is rare and is almost always due to psychologic factors (guilt, fear of intimacy, depression, severe anxiety) or clinically obvious anatomic abnormalities. Most often, ED is secondary (i.e., a man who previously could attain and sustain erections no longer can). Over 80% of secondary ED cases have an organic ethology. However, in many men with organic disease, ED leads to secondary psychologic difficulties that compound the problem. Psychologic factors must be considered in every case.
What are causes of ED?
Psychologic causes may relate to performance anxiety, stress, or a mood disorder (particularly depression). ED may be situational, involving a particular place, time, or partner.
The major organic causes of ED are vascular and neurologic disorders, often stemming from atherosclerosis and diabetes. Complications of surgery, usually prostate surgery, are another common cause. Other causes include hormonal disorders, drugs, and structural disorders of the penis (eg, Peyronie’s disease).
The most common vascular cause is atherosclerosis of penile arteries, often secondary to diabetes. Atherosclerosis and aging decrease the capacity for dilation of arterial blood vessels and smooth muscle relaxation, limiting the amount of blood that can enter the penis. Inadequate impedance of venous outflow (venous leaks) may cause ED or, more commonly, failure to maintain tumescence as long as desired. Venous leaks make it difficult for blood to remain in the penis during erection, so erections occur but cannot be sustained. Priapism, particularly as in sickle cell disease, may damage penile vasculature and lead to ED.
Stroke, partial complex seizures, multiple sclerosis, peripheral and autonomic neuropathies, and spinal cord injuries are among the neurologic causes. Diabetic neuropathy and surgical injury are particularly common causes.
Any endocrinopathy associated with testosterone deficiency (hypogonadism) may decrease libido and cause ED. However, erectile function only rarely improves with normalization of serum testosterone levels.
What are drugs causing ED?
Numerous drug causes are possible. Alcohol can cause temporary ED.
Commonly Used Drugs That Can Cause Erectile Dysfunction are Antihypertensives, β-Blockers, clonidine, loop diuretics, (probably), spironolactone, thiazide diuretics, Alcohol, anxiolytics, cocaine, monoamine oxidase inhibitors, opioids, SSRIs, tricyclic antidepressants, Amphetamines, antiandrogens, anticancer drugs, anticholinergics, cimetidine, Oestrogens AND onadotropin-releasing hormone.
Of men who have undergone transurethral resection of the prostate, up to 40% can experience problems with erections for reasons that are not clear. ED is more common after more extensive prostatic resection (eg, radical prostatectomy). Prolonged perineal pressure (as occurs during bicycle riding) can cause temporary ED.
How to do a Clinical evaluation of ED?
Evaluation should include history of drug and alcohol use, smoking, diabetes, hypertension, and atherosclerosis and symptoms of vascular, hormonal, neurologic, and psychologic disorders. It is vital to screen for depression, which may not always be apparent. Satisfaction with sexual relationships should also be explored. Partner sexual dysfunction (eg, atrophic vaginitis, depression) must be considered and evaluated.
Examination is focused on the genitals and extragenital signs of hormonal, neurologic, and vascular disorders. Genitals are examined for anomalies, signs of hypogonadism, and fibrous bands or plaques (Peyronie’s disease). Poor rectal tone, perineal sensation, or abnormal anal wink or bulbocavernosus reflexes may indicate neurologic dysfunction. Diminished peripheral pulses suggest vascular dysfunction.
A psychologic cause should be suspected in young healthy men with abrupt onset of ED, particularly if onset is associated with a specific emotional event or if the dysfunction occurs only in certain settings. A history of ED with spontaneous improvement also suggests psychologic origin (psychogenic ED). Men with psychogenic ED usually have normal nocturnal erections and erections upon awakening, whereas men with organic ED often do not.
How is ED investigated?
Laboratory assessment should include measurement of testosterone level; if the level is low or low-normal, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) should be measured (see Male Reproductive Endocrinology and Related Disorders: Diagnosis of primary and secondary hypogonadism). Evaluation for occult diabetes, dyslipidaemias, hyperprolactinemia, thyroid disease, and Cushing’s syndrome should be done based on clinical suspicion.
A penile pressure–brachial pressure index (systolic BP in the penis divided by systolic BP in the arm) < 0.6 indicates impaired blood flow to the penis, but this test is seldom done in general clinical practice. Additional invasive or provocative penile tests include duplex ultrasonography before and after injection of a vasoactive drug and cavernosography or cavernosometry; these tests can be considered in some patients, such as those with posttraumatic erectile dysfunction or before penile reconstructive surgery (eg, for Peyronie’s disease).
What is the Treatment of ED?
Treatment of cause
Usually an oral phosphodiesterase inhibitor
Sometimes a mechanical device or an intracavernosal or intraurethral prostaglandin
Underlying organic disorders require appropriate treatment. Drugs that are temporally related to onset of ED should be stopped or switched. Depression may require treatment. For all patients, reassurance and education (including of the patient’s partner whenever possible) are important.
For further therapy, non-invasive methods (mechanical devices and drugs) are tried first. All drugs and devices should be tried ≥ 5 times before being considered ineffective.
Mechanical devices: Men who can develop but not sustain an erection may use a constriction ring. As soon as erection occurs, a metal or elastic ring or a leather band with snaps (sold by prescription in pharmacies or OTC in sex paraphernalia stores as a “cock ring”) is placed around the base of the penis, preventing venous outflow. If the man cannot develop an erection, a vacuum device can draw blood into the penis, after which the band or ring is placed at the base of the penis to retain the erection. Bruising of the penis, coldness of the tip of the penis, and lack of spontaneity are some drawbacks to this modality. A constriction ring and vacuum devices might also be useful adjuncts for patients who do not respond satisfactorily to drug therapy.
Drugs: The primary drugs for ED are oral phosphodiesterase inhibitors,
Oral phosphodiesterase inhibitors selectively inhibit cyclic guanosine monophosphate (cGMP)–specific phosphodiesterase type 5 (PDE5), the predominant phosphodiesterase isoform in the penis. These drugs include sildenafil, vardenafil, and tadalafil. By increasing cGMP, these drugs enhance the nitric oxide release essential for normal erection. Although vardenafil and tadalafil are more elective for the penile vasculature than sildenafil, adverse effects of these drugs are similar. Although no clinical trials directly compare the drugs, all 3 appear to be equally effective (60 to 75%). Sildenafil dose is 50 mg, although most men respond best to 100 mg. Tadalafil has a significantly longer duration of action (24 to 48 h) than sildenafil and vardenafil (about 4 to 6 h), which might lead to more convenient dosing. The usual dosage for tadalafil and vardenafil is 5 to 20 mg. All PDE5 inhibitors are generally taken at least 1 h before sexual intercourse. Dosing frequency should not be ≤ 24 h for sildenafil and vardenafil and not ≤ 48 h for tadalafil.
All PDE5 inhibitors cause direct coronary vasodilation and potentiate the hypotensive effects of other nitrates, including those used to treat cardiovascular disease as well as recreational amyl nitrate (“poppers”). Thus, all nitrates are contraindicated for 24 h after the administration of any PDE5 inhibitor. Other adverse effects of PDE5 inhibitors include flushing, visual abnormalities, and headache. Sildenafil and vardenafil may cause abnormal colour perception. Tadalafil use has been linked with myalgias. Some users of PDE5 inhibitors have rarely developed anterior ischemic optic neuropathy, but whether there is a causal relationship is unclear. Vardenafil should be administered cautiously and at lower initial dosages to patients receiving α-blockers, such as prazosin, doxazosin, and tamsulosin, because of the risk of prolonged hypotension. One study showed that sildenafil may be safely administered with doxazosin. Apomorphine increases erectile neurogenic signals by CNS mechanisms. It appears to be only moderately effective and can cause nausea, somnolence, and hypotension. Alprostadil (the prostaglandin PGE1), given via intraurethral insertion or intracavernosal injection, can produce erections with a mean duration of about 60 min. It causes priapism (see Symptoms of Genitourinary Disorders: Priapism) in ≤ 1% and penile pain in about 10%. The intracavernosal dose is adjusted by the physician to minimize priapism; the patient can then self-inject at home. Priapism is less common with intraurethral therapy, but intraurethral therapy is much less effective (50 to 60%) than intracavernosal injection, the most effective pharmacotherapy for erectile dysfunction (80 to 90%). Combination therapy with a PDE5 inhibitor and alprostadil may be useful for some patients who fail to respond to oral PDE5 inhibitors alone.
Surgery: For patients who do not respond to drug therapy, invasive treatment options include implantation of a penile prosthesis. Prostheses can be rigid plastic rods or hydraulically operated devices. Both involve the risks of general anaesthesia, infection, and prosthetic malfunction.
What is drug dependence?
A single definition for drug dependence is elusive. Concepts that aid in defining drug dependence are tolerance and psychologic and physical dependence.
Tolerance describes the need to progressively increase the drug dose to produce the effect originally achieved with smaller doses.
Psychologic dependence includes feelings of satisfaction and a desire to repeat the drug experience or to avoid the discontent of not having it. This anticipation of effect is a powerful factor in the chronic use of psychoactive drugs and, with some drugs, may be the only obvious reason for intense craving and compulsive use. Craving and compulsion to use a drug lead to using it in larger amounts, more frequently, or over a longer period than was intended when use began. Psychologic dependence involves giving up social, occupational, or recreational activities because of drug use, as well as persistent use despite knowing that the drug is likely causing a physical or mental problem. Drugs that cause psychologic dependence often have ≥ 1 of the following effects:
Reduced anxiety and tension
Elation, euphoria, or other pleasurable mood changes
Feelings of increased mental and physical ability
Altered sensory perception
Changes in behaviour
Drugs that because psychologic dependence include marijuana, amphetamine, 3,4-methylenedioxymethamphetamine (MDMA), and hallucinogens, such as lysergic acid diethylamide (LSD), mescaline, and psilocybin.
Physical dependence is manifested by a withdrawal (abstinence) syndrome, in which untoward physical effects occur when the drug is stopped or when its effect is counteracted by a specific antagonist. Drugs that because strong physical dependence include heroin, alcohol, benzodiazepines, and cocaine. Abstinence syndromes are drug-specific or drug class–specific and may vary considerably based on the amount and frequency of use and on patient characteristics, which may affect how patients experience withdrawal.
What is addiction?
Addiction, a concept without a consistent, universally accepted definition, is used here to refer to compulsive use and overwhelming involvement with a drug, including spending an increasing amount of time obtaining the drug, using the drug, or recovering from its effects. It may occur without physical dependence. Addiction implies the risk of harm and the need to stop drug use, regardless of whether the addict understands and agrees.
What is drug abuse?
Drug abuse is definable only in terms of societal disapproval. Drug abuse may involve the following:
Experimental and recreational use of drugs, which is usually illegal
Unsanctioned or illegal use of psychoactive drugs to relieve problems or symptoms
Use of drugs because of dependence or the need to prevent withdrawal.
What is illicit drug use?
Illicit drug use, although usually considered abuse simply because it is illegal, does not always involve dependence. Use of legal substances, such as alcohol and prescription drugs, may involve dependence and abuse. Abuse of prescription and illegal drugs cuts across all socioeconomic groups.
What is recreational drug use?
Recreational drug use has increasingly become a part of Western culture, although in general, it is not sanctioned by society. Some users apparently are unharmed; they tend to use drugs episodically in relatively small doses, precluding clinical toxicity and development of tolerance and physical dependence. Many recreational drugs (e.g., crude opium, alcohol, marijuana, caffeine, hallucinogenic mushrooms, coca leaf) are “natural” (i.e., close to plant origin); they contain a mixture of relatively low concentrations of psychoactive compounds and are not isolated psychoactive compounds. Recreational drugs are most often taken orally or inhaled. Taking these drugs by injection makes it harder to predict and control desired and unwanted effects.

Intoxication refers to development of a reversible substance-specific syndrome of mental and behavioural changes that may involve altered perception, euphoria, cognitive impairment, impaired judgment, impaired physical and social functioning, mood lability, belligerence, or a combination. Taken to the extreme, intoxication can lead to overdose, significant morbidity, and risk of death.
What are narcotics?

Narcotics and scheduled drugs: Narcotics are drugs that cause insensibility or stupor (narcosis), but the term is typically restricted to drugs that bind to opiate receptors: opium, opium derivatives, and their semisynthetic and synthetic analogues. However, the US government classifies cocaine as a narcotic, even though it does not bind at opiate receptors or have morphine -like effects. Many narcotics (specifically opioids) are used therapeutically to induce anaesthesia and to relieve pain, cough, and diarrhoea. The morphine -like effects of opioids are welcomed in most clinical situations but contribute to the attractiveness of narcotics for abuse.
What is schedule of drugs?
In India as well as US, the Drug Abuse Prevention and Control Acts and subsequent modifications require the pharmaceutical industry to maintain physical security of and strict record keeping for certain classes of drugs .Controlled substances are divided into 5 schedules (or classes) on the basis of their potential for abuse, accepted medical use, and accepted safety under medical supervision. The schedule classification determines how a substance must be controlled.
Schedule I: These substances have a high potential for abuse, no accredited medical use, and a lack of accepted safety. They can be used only under government-approved research conditions.
Schedule II to IV: Going from schedule II to IV, these drugs have progressively less potential for abuse. They have an accredited medical use.
Schedule V: These substances are least likely to be abused. Some Schedule V drugs do not require a prescription.
State schedules may vary from federal schedules.
Some Examples of Controlled Substances
Cannabis, GHB, heroin, LSD, MDMA, some opioids, psilocybin
Amphetamines, barbiturates (short-acting), cocaine, hydrocodone, methadone
, methylphenidate, morphine, other strong opioid agonists, phencyclidine
Anabolic steroids, barbiturates (intermediate-acting), buprenorphine, dihydrocodeine, ketamine
Barbiturates (long-acting), benzodiazepines, chloral hydrate, meprobamate, pentazocine, propoxyphene, zolpidem
Cough suppressants containing small amounts of codeine
*Cannot be prescribed. GHB = gamma hydroxybutyrate; LSD = lysergic acid diethylamide; MDMA = methylenedioxymethamphetamine.
What are the principals of treatments of Addiction in general?
Both pharmacotherapy and behavioural treatment are required to relieve the symptoms of addictive disorders
At the clinical level, the theoretical model of addiction is similar to that of an infectious disease such as tuberculosis. The development of addiction depends on the interaction of agent, host and environment
For example, high drug availability and low price (agent) would increase the risk, but genetic factors (host) or opportunities for other pleasures in life (environment) could offset the increased risk. Treatment approaches must also address all of these variables.
All have in common the activation of brain reward pathways that have evolved to ensure survival, which largely explains the compelling nature of drug reward. The activation of the reward system produces reinforcement of drug acquisition behaviours and associations between environmental cues that signal the arrival of drug effects or drug withdrawal symptoms as drugs disappear from the body through metabolism. The environmental stimuli that become neurologically associated with drug effects are variable and may include persons, places and situations. Treatment approaches, therefore, have attempted to diminish the strength of these conditioned reflexes that lead to relapse and facilitate the development of new memories that produce natural rewards. In this paper, pharmacological approaches that reduce aversive effects of drug cessation, reduce drug reward or reduce drug desire or craving will be discussed. Behavioural approaches are also necessary in combination with medication, but will not be discussed here.
The modern definition of addiction emphasizes uncontrolled drug use rather than tolerance and physiological dependence as essential features of the disorder. It is generally recognized that addiction has strong hereditary influences and once established, it behaves as a chronic brain disorder with relapses and remissions over the long term The diagnostic criteria, which are signs of compulsive drug seeking, are the same for all drug categories (ethanol, opioids, stimulants, sedatives, nicotine and cannabinoids), even though the mechanisms for activating the reward system are quite different.
The clinical data fit best when addiction is considered to be a syndrome characterized by compulsive drug-seeking behaviour that impairs psychosocial functioning or health. Even after detoxification and long periods of abstinence, relapse frequently occurs despite sincere efforts to avoid further drug use. People or situations previously associated with drug use elicit involuntary reactions and may provoke relapse
If tolerance and withdrawal symptoms were the only elements of addictive illness, treatment would simply consist of detoxification, a process that allows the body to cleanse itself while receiving descending doses of a medication that reduces withdrawal symptoms. If drug taking does not resume, homeostatic mechanisms will gradually readapt to the absence of the drug and tolerance will be diminished or lost. We now know that detoxification is, at best, a first step in treatment and that simply achieving a drug-free state is not the most significant accomplishment. The more difficult aspect is the prevention of relapse to drug-taking behaviour.
What are usual symptoms of drug withdrawal?
It is unfortunate that the majority of drug-dependent persons are merely treated with detoxification and little or no long-term follow-up the withdrawal syndrome from opiate addiction can be very uncomfortable, but it is not life-threatening unless the patient has pre-existing medical problems. The symptoms consist of sweating, muscle aches, cramps, nausea, diarrhoea, vomiting, lachrymation, rhinorrhoea, tremors, tachycardia and other signs of autonomic nervous system hyperactivity. The discomfort has been compared to a bad case of the flu.
How to treat cocaine addiction?
Stimulant (cocaine and amphetamine) withdrawal does not usually require medication, but rapid return to drug use is frequent. A medication that reduces stimulant withdrawal symptoms such as modafinil may reduce relapse. The withdrawal syndrome from stimulants such as cocaine and amphetamine consist of hypersomnia, hyperphagia, bradycardia and a number of depressive symptoms that usually resolve over several days. Interestingly, cocaine withdrawal symptoms appear to be predictive of treatment outcome. They found that more withdrawal symptoms in subjects at the start of treatment accurately predicted poorer outcome following treatment. Given these findings, the pharmacological reversal of cocaine withdrawal symptoms with agents such as modafinil may improve clinical outcome
How to treat alcohol addiction?
In the treatment of patients dependent on alcohol or other sedatives, appropriate detoxification is critical because the sedative withdrawal syndrome is potentially life-threatening. Benzodiazepines effectively suppress the sedative withdrawal syndrome, and with proper attention to electrolytes and vitamins, the vast majority of patients can be safely eased into the alcohol-abstinent state in preparation for a long-term rehabilitation programme.
Until 1995, disulfiram was the only medication available to prevent relapse to uncontrolled drinking in detoxified alcoholics. This medication blocks the metabolism of alcohol, causing the accumulation of acetaldehyde, a noxious by-product. The resulting acetaldehyde reaction is so unpleasant that it effectively prevents patients from consuming any alcohol. Disulfiram has a place in the pharmacopoeia of medications for alcoholism but its usefulness is limited. Despite treatment contracts and even legal coercion, most alcoholics will not take disulfiram regularly and randomized clinical trials have not shown disulfiram to be efficacious.
Acamprosate, a medication that appears to decrease the desire for alcohol, was developed in Europe and has been available in the USA since 2004. Acamprosate appears to reduce the long-lasting neuronal hyperexcitability that follows chronic alcohol use. The mechanisms are unclear but may include alterations in glutamate receptor gene expression. This medication suppresses the intake of alcohol in rats and, as with naltrexone, activity in the animal model predicts clinical efficacy. In double-blind studies, acamprosate has been shown to increase the likelihood of continuous abstinence in alcoholics and to shorten the period of drinking if the patient slips and consumes some alcohol.
The opiate receptor antagonist naltrexone has been reported in several clinical trials to reduce alcohol craving (O’Brien 2005) as well as alcohol reward. Human laboratory studies of alcohol priming in non-treatment-seeking alcoholics demonstrated a reduction in alcohol craving and alcohol drinking in spite of the alcohol priming drink in participants who were not seeking treatment
Preclinical data have also shown an effect of alcohol on serotonergic systems. This has motivated trials using medications affecting that system. Ritanserin, a 5-hydroxytryptamine-2 (5-HT2) receptor antagonist, was found to be no more effective than placebo in the treatment of alcoholism. Ondansetron, a 5-HT3 antagonist, was found to reduce drinking in early-onset alcoholics both alone (Johnson et al. 2000) and in combination with naltrexone.
How to treat nicotine addiction?
Symptoms of nicotine withdrawal can be diminished by nicotine replacement therapy through chewing gum, patch or nasal spray. Nicotine gum and nicotine patch do not achieve the peak plasma levels seen with cigarettes, and thus they do not produce the same magnitude of nicotine’s pleasant effects. Comparisons with placebo treatment show large benefits for nicotine replacement at six weeks, but the advantage diminishes with time. The administration of nicotine as a patch, gum or nasal spray can also be used as a maintenance treatment for extended periods as is the case with methadone. The levels obtained via a nicotine patch usually do not produce the pleasant responses achieved through smoking and there are usually no withdrawal symptoms on stopping the patch. Theoretically, smokers should be able to switch their nicotine dependence from administration via smoking to nicotine delivered by patch, chewing gum or nasal spray. Although some smokers continue to chew nicotine gum for many months after giving up cigarettes, most discontinue nicotine replacement after a few weeks. The tendency to relapse may be strong, and thus it is important to teach patients behavioural techniques to resist the urge to smoke. Clinical serendipity played a role in the discovery of bupropion as an effective treatment of nicotine dependence. Originally used as an antidepressant, bupropion was found to significantly improve abstinence rates in smokers whether or not they were depressed. The mechanism is unclear, but one effect of bupropion is the relief of negative affect in recently abstinent smokers. A very recent medication that applies the partial agonist principle in the treatment of tobacco use disorder is varenicline. This is an α4 β2 nicotinic receptor partial agonist that has been reported to relieve cigarette craving and to result in a significantly higher rate of abstinence at 52 weeks (23%) than placebo (10.3%) or bupropion (14.6%)
How to treat marijuana addiction?
Heavy marijuana users also develop a physical dependence and may present for treatment when they are unable to stop daily use on their own. The symptoms consist of irritability, anxiety, marijuana craving, decreased quality and quantity of sleep and decreased food intake. Various medications have been used to alleviate these symptoms and some clinicians have reported success with dronabinol, the oral form of delta-9-tetrahydrocannabinol.
How to treat opiate addiction?
For opiate detoxification, methadone is not always available due to legal limitations and buprenorphine may be undesirable because it is a partial opiate agonist. Clonidine, an α2-agonist, reverses opiate withdrawal by acting on auto receptors producing presynaptic inhibition of locus coeruleus activity. This effectively reduces the large adrenergic component of opioid withdrawal
How to treat heroin addiction?
The use of heroin or other opiates purchased on the street for the purpose of obtaining a ‘high’ has a significant risk of producing addiction. Detoxification is not applicable to those opioid-dependent patients who prefer transition to maintenance using methadone or buprenorphine. Methadone has a slow onset by the oral route. It is a long-acting μ-opiate receptor agonist that largely prevents reward or euphoria if the patient ‘slips’ and takes a dose of an opiate. The mechanism for preventing euphoria is based on cross-tolerance in which tolerance (insensitivity) acquired by the use of one drug in a category conveys tolerance to all drugs in that category. Of course, the maintenance dose of methadone must be adjusted to the purity of heroin on the street. A dose of heroin significantly higher in opioid equivalents than the maintenance dose of methadone would override the cross-tolerance effect. Patients can be maintained for many years on a properly adjusted dose of methadone. Craving for opioids is diminished or absent, and patients are able to engage in constructive activities. Cognition and alertness are not impaired, and complex tasks including higher education can be accomplished Currently, approximately 200,000 former opiate addicts are being maintained on methadone in the USA. Those with significant psychosocial problems require counselling or psychotherapy in addition to the medication.
As a partial agonist, buprenorphine produces limited opiate effects, and thus overdose is rare except when combined with benzodiazepines. Owing to its high affinity for the μ-receptor, buprenorphine effectively prevents access to the receptor by other opiates and opioids, thus reducing the likelihood that other opioids will be used. Patients treated with buprenorphine become physiologically dependent on it, as is the case with methadone, but if buprenorphine is stopped, withdrawal symptoms are quite mild. A limitation of buprenorphine is the ceiling on opiate agonist effects giving a maximal efficacy equivalent to approximately 40—50 mg of methadone. Addicts using large doses of street heroin may find that buprenorphine is not sufficiently potent to block withdrawal or drug craving.
What are the uses of naltrexone?
Advances in understanding how opioids interact with opiate receptors to produce their pharmacological effects led to the development of specific antagonists that have high affinity for these receptors, but do not activate the chain of cellular events producing opioid drug effects. Naltrexone is an antagonist that has great affinity for μ-opiate receptors and significant but less affinity for ∂- and κ-opiate receptors. Unlike methadone, it has no agonist effects, so there are no opioid calming or other subjective effects. When first introduced, naltrexone was thought to be an ideal medication for heroin addiction because it occupied opiate receptors and blocked the effects of subsequent heroin injections. Experience has shown that most heroin addicts prefer methadone because it provides mild opioid-reinforcing effects that are absent in naltrexone. Thus, naltrexone has been used very little except for white-collar opiate addicts such as physicians, nurses and former addicts released from prison on probation. The effects of blocking opiate receptors probably depend on the degree of tonic activation of the endogenous opioid system. Some normal volunteers given naltrexone experience nausea and dysphoria, while others experience no reaction. Although long-term blockade of opiate receptors might be expected to produce impairment of neuroendocrine function, remarkably few effects have been noted even in patients who have taken naltrexone daily for several years.
In 2006, a slow-release (depot) injectable preparation of naltrexone was given FDA approval and made available for prescription. Paradoxically, it was approved only for alcoholism because it was discovered in animal models that alcohol activated endogenous opioids. Subsequent work has clearly shown that endogenous opioids are involved in alcohol reinforcement. This was a discovery in an animal model that led directly to a completely novel treatment for alcoholism in humans. Such translational examples give hope that knowledge gained from basic research will eventually lead to new and better treatments. In 1983, clinical trials began and it was found that blocking opiate receptors with naltrexone significantly reduced relapse to clinically significant drinking
Of course, the depot form of naltrexone is also effective for the treatment of opioid addiction), and clinical trials are underway that will eventually lead to FDA approval for that indication in addition to alcoholism. Thus, opiate receptor antagonists have been found to be effective in the treatment of both opiate addiction (blocking external opiates) and alcoholism (blocking endogenous opioids). The availability of a depot form is expected to significantly improve the adherence to medication for this treatment method.
What is the genetic influence on addiction?
The evidence for genetic influence on vulnerability to addiction is strong, but as with other complex psychiatric disorders, gene association studies based on diagnosis have not identified consistent susceptibility genes. Diagnosis in psychiatry still depends on behaviour rather than biomarkers. Recently, a sub-category of alcoholism based on a functional allele of the gene for the μ-opiate receptor has been studied as a candidate gene for an alcoholism endophenotype. The critical functional observation is an increased stimulation effect from alcohol in carriers of this gene. Recent reports of significantly improved treatment results in alcoholic patients selected on the basis of this genetic variant have raised the exciting prospect of alcoholism treatment guided by genomic testing
Taken together, the various lines of evidence suggest that alcohol activates the endogenous opioid system and this activation is exaggerated in carriers of this genetic variant. The proposed circuitry involves β-endorphin neurons that modulate ventral tegmental GABA neurons inhibiting dopamine (DA) neurons. Alcohol causes a release of β-endorphin that inhibits GABA neurons, thus releasing DA neurons from inhibition and allowing dopaminergic stimulation. This mechanism is supported by micro dialysis studies showing that the alcohol-induced DA increase is blocked by naltrexone.
There are different mechanisms whereby medications can block or diminish the euphoria produced by drugs of abuse. Antagonist treatment prevents the addictive agent from effective binding to brain receptors that mediate the euphoric response. This is best illustrated by naltrexone treatment in opiate dependence, since the mechanism of opiate euphoria results from the stimulation of μ-opiate receptors. The mechanism of stimulant euphoria is not well understood, so it has been more difficult to develop medications to block this essential clinical phenomenon. Nicotine replacement therapy for smokers can reduce the pleasure of smoking by a cross-tolerance mechanism similar to that of methadone for heroin euphoria.
What is the prognosis of addictive disorders?
Medications that target addiction phenomena, such as euphoria, withdrawal and craving, are being developed as adjunctive treatments that may significantly improve clinical outcome. When viewed in comparison with other chronic diseases, the current treatments for addiction are reasonably successful. Long-term treatment is accompanied by improvements in physical status, as well as in mental, social and occupational functions. Treatment is usually not curative. As is the case with other chronic diseases, when the treatment is ended, relapse eventually occurs in most cases.
What are the causes of death in addiction?
The mortality rates are approximately 1% to 3% per year and increase with more frequent use the causes of death are overdose, infections, suicide, and trauma.
What is hypoglycaemia?
Hypoglycaemia unrelated to exogenous insulin therapy is an uncommon clinical syndrome characterized by low plasma glucose level, symptomatic sympathetic nervous system stimulation, and CNS dysfunction. Many drugs and disorders cause it. Diagnosis requires blood tests done at the time of symptoms or during a 72-h fast. Treatment is provision of glucose combined with treatment of the underlying disorder.
Most commonly, symptomatic hypoglycaemia is a complication of drug treatment of diabetes mellitus (DM). Oral antihyperglycemics or insulin may be involved.
What are the causes of hypoglycaemia?
Causes of physiologic hypoglycaemia can be classified as
Reactive (postprandial) or fasting
Insulin-mediated or non–insulin-mediated
Drug-induced or nondrug-induced
Insulin-mediated causes include exogenous administration of insulin or an insulin secretagogue and insulin-secreting tumours (insulinomas). A helpful practical classification is based on clinical status: whether hypoglycaemia occurs in patients who appear healthy or ill. Within these categories, causes of hypoglycaemia can be divided into drug-induced and other causes. Pseudo hypoglycaemia occurs when processing of blood specimens in untreated test tubes is delayed and cells, such as RBCs and leukocytes (especially if increased, as in leukaemia or polycythaemia), consume glucose. Factitious hypoglycaemia is true hypoglycaemia induced by nontherapeutic administration of sulfonylureas or insulin.
The surge in autonomic activity in response to low plasma glucose causes sweating, nausea, warmth, anxiety, tremulousness, palpitations, and possibly hunger and paraesthesia. Insufficient glucose supply to the brain causes headache, blurred or double vision, confusion, difficulty speaking, seizures, and coma. In controlled settings, autonomic symptoms begin at or beneath a plasma glucose level of about 60 mg/dL (3.33 mmol/L), whereas CNS symptoms occur at or below a glucose level of about 50 mg/dL (2.78 mmol/L). However, symptoms suggestive of hypoglycaemia are far more common than the condition itself. Most people with glucose levels at these thresholds have no symptoms, and most people with symptoms suggestive of hypoglycaemia have normal glucose concentrations.
What is the treatment of hypoglycaemia?
Immediate treatment of hypoglycaemia involves provision of glucose. Patients able to eat or drink can drink juices, sucrose water, or glucose solutions; eat candy or other foods; or chew on glucose tablets when symptoms occur. Infants and younger children may be given 10% dextrose solution 2 to 5 mL/kg IV bolus. Adults and older children unable to eat or drink can be given glucagon 0.5 (< 20 kg) or 1 mg (≥ 20 kg) SC or IM or 50% dextrose 50 to 100 mL IV bolus, with or without a continuous infusion of 5 to 10% dextrose solution sufficient to resolve symptoms. The efficacy of glucagon depends on the size of hepatic glycogen stores; glucagon has little effect on plasma glucose in patients who have been fasting or who are hypoglycemic for long periods. How to assess and treat hyponatremia? Hyponatremia is decrease in serum Na concentration < 136 mEq/L caused by an excess of water relative to solute. Common causes include diuretic use, diarrhoea, heart failure, and renal disease. Clinical manifestations are primarily neurologic (due to an osmotic shift of water into brain cells causing oedema), especially in acute hyponatremia, and include headache, confusion, and stupor; seizures and coma may occur. Diagnosis is by measuring serum Na. Serum and urine electrolytes and osmolality help determine the cause. Treatment involves restricting water intake and promoting its loss, replacing any Na deficit, and treating the cause. Hyponatremia reflects an excess of total body water (TBW) relative to total body Na content. Because total body Na content is reflected by ECF volume status, hyponatremia must be considered along with status of the ECF volume: hypovolemia, euvolemia, and hypervolemia (see Table 1: Electrolyte Disorders: Principal Causes of Hyponatremia). Note that the ECF volume is not the same as effective plasma volume. For example, decreased effective plasma volume may occur with decreased ECF volume, but it may also occur with an increased ECF volume (eg, in heart failure, hypoalbuminemia, or capillary leak syndrome). What are the principal Causes of Hyponatremia? Hypovolemic hyponatremia Decreased TBW and Na, with a relatively greater decrease in Na GI losses Diarrheal Vomiting 3rd-space losses Burns Pancreatitis Peritonitis Rhabdomyolysis Small-bowel obstruction Renal losses Diuretics Mineralocorticoid deficiency Osmotic diuresis (glucose, urea, mannitol Salt-losing nephropathies (eg, interstitial nephritis, medullary cystic disease, partial urinary tract obstruction, polycystic kidney disease) Euvolemic hyponatremia Increased TBW with near-normal total body Na Drugs Diuretics, barbiturates, carbamazepine, chlorpropamide, clofibrate, opioids, tolbutamide, vincristine, Possibly cyclophosphamide, NSAIDs, oxytocin Disorders Adrenal insufficiency as in Addison’s disease, Hypothyroidism, Syndrome of inappropriate ADH secretion, Increased intake of fluids Primary polydipsia States that increase nonosmotic release of ADH Emotional stress Pain Postoperative states Hypervolemic hyponatremia Increased total body Na with a relatively greater increase in TBW Extrarenal disorders Cirrhosis Heart failure Renal disorders Acute kidney dysfunction Chronic kidney disease Nephrotic syndrome What is Syndrome of Inappropriate ADH Secretion-a cause of hyponatremia? The syndrome of inappropriate ADH secretion (SIADH) is attributed to excessive ADH release. It is defined as less-than-maximally-dilute urine in the presence of plasma hypo-osmolality (hyponatremia) without volume depletion or overload, emotional stress, pain, diuretics, or other drugs that stimulate ADH secretion in patients with normal cardiac, hepatic, renal, adrenal, and thyroid function. SIADH is associated with myriad disorders Disorders Associated with Syndrome of Inappropriate ADH Secretion are – Cancer of CNS, Duodenum, Lung, Lymphoma, Pancreas CNS disorders Acute intermittent porphyria Acute psychosis Brain abscess Encephalitis Guillain-Barré syndrome Head trauma Meningitis Stroke Subdural or subarachnoid haemorrhage Endocrine disorders Addison’s disease Hypopituitarism Hypothyroidism Pulmonary disorders and treatments Aspergillosis Lung abscess Pneumonia Positive-pressure breathing TB Surgery What are the Symptoms and Signs of hyponatremia? Symptoms mainly involve CNS dysfunction. However, when hyponatremia is accompanied by disturbances in total body Na content, signs of ECF volume depletion or overload also occur (see Fluid Metabolism: Volume Overload). In general, older chronically ill patients with hyponatremia develop more symptoms than younger otherwise healthy patients. Symptoms are also more severe with faster-onset hyponatremia. Symptoms generally occur when the effective plasma osmolality falls to < 240 mOsm/kg. Symptoms can be subtle and consist mainly of changes in mental status, including altered personality, lethargy, and confusion. As the serum Na falls to < 115 mEq/L, stupor, neuromuscular hyperexcitability, hyperreflexia, seizures, coma, and death can result. Severe cerebral enema may occur in premenopausal women with acute hyponatremia, perhaps because oestrogen and progesterone inhibit brain Na+, K+-ATPase and decrease solute extrusion from brain cells. Sequelae include hypothalamic and posterior pituitary infarction and occasionally brain stem herniation. How to diagnose hyponatremia? 1.Serum and urine electrolytes and osmolality 2.Clinical assessment of volume status Hyponatremia is occasionally suspected in patients who have neurologic abnormalities and are at risk. However, because findings are nonspecific, hyponatremia is often recognized only after serum electrolyte measurement. Identification of the cause: Identifying the cause can be complex. The history sometimes suggests a cause (eg, significant fluid loss due to vomiting or diarrhoea, renal disease, compulsive fluid ingestion, intake of drugs that stimulate ADH release or enhance ADH action). The volume status, particularly the presence of obvious volume depletion or overload, suggests certain causes. Overtly hypervolemic patients usually have a readily recognizable condition, such as heart failure or hepatic or renal disease. Euvolemic patients and patients with equivocal volume status require more laboratory testing to identify a cause. What is the Treatment of hyponatremia? 1.When hypovolemic, 0.9% saline 2.When hypervolemic, fluid restriction and sometimes a diuretic 3.When euvolemic, treatment of cause 4.Rarely cautious correction with hypertonic (3%) saline Rapid correction of hyponatremia, even mild hyponatremia, risks neurologic complications -Osmotic demyelination syndrome). Except possibly in the first few hours of treatment of severe hyponatremia, Na should be corrected no faster than 0.5 mEq/L/h. Even with severe hyponatremia, increase in serum Na concentration should not exceed 10 mEq/L over the first 24 h. Mild hyponatremia: Mild, asymptomatic hyponatremia (ie, serum Na > 120 mEq/L) requires restraint because small adjustments are generally sufficient. In diuretic-induced hyponatremia, elimination of the diuretic may be enough; some patients need some Na or K replacement. Similarly, when mild hyponatremia results from inappropriate hypotonic parenteral fluid administration in patients with impaired water excretion, merely altering fluid therapy may suffice.
Severe hyponatremia: Severe hyponatremia (serum Na < 109 mEq/L; effective osmolality 14 mEq/L/8 h) and neurologic symptoms start to develop, it is critical to prevent further serum Na increases by stopping hypertonic fluids. In such cases, inducing hyponatremia with hypotonic fluid may mitigate the development of permanent neurologic damage. What is hypothyroidism? Hypothyroidism is thyroid hormone deficiency. It is diagnosed by clinical features such as a typical facies, hoarse slow speech, and dry skin and by low levels of thyroid hormones. Management includes treatment of the cause and administration of thyroxine. Hypothyroidism occurs at any age but is particularly common among the elderly. It occurs in close to 10% of women and 6% of men > 65. Although typically easy to diagnose in younger adults, it may be subtle and manifest atypically in the elderly.
What are types of hypothyroidism?
Primary hypothyroidism: Primary hypothyroidism is due to disease in the thyroid; thyroid-stimulating hormone (TSH) is increased. The most common cause is autoimmune. It usually results from Hashimoto’s thyroiditis and is often associated with a firm goitre or, later in the disease process, with a shrunken fibrotic thyroid with little or no function. The 2nd most common cause is post-therapeutic hypothyroidism, especially after radioactive iodine therapy or surgery for hyperthyroidism or goitre. Hypothyroidism during overtreatment with propylthiouracil, methimazole’, and iodide abates after therapy is stopped.
Secondary hypothyroidism: Secondary hypothyroidism occurs when the hypothalamus produces insufficient thyrotropin-releasing hormone (TRH) or the pituitary produces insufficient TSH. Sometimes, deficient TSH secretion due to deficient TRH secretion is termed tertiary hypothyroidism.
What are symptoms and signs of hypothyroidism?
Symptoms and signs of primary hypothyroidism are often subtle and insidious. Symptoms may include cold intolerance, constipation, forgetfulness, and personality changes. Modest weight gain is largely the result of fluid retention and decreased metabolism. Paraesthesia of the hands and feet are common, often due to carpal-tarsal tunnel syndrome caused by deposition of proteinaceous ground substance in the ligaments around the wrist and ankle. Women with hypothyroidism may develop menorrhagia or secondary amenorrhea.
The facial expression is dull; the voice is hoarse and speech is slow; facial puffiness and periorbital swelling occur due to infiltration with the mucopolysaccharides hyaluronic acid and chondroitin sulphate; eyelids droop because of decreased adrenergic drive; hair is sparse, coarse, and dry; and the skin is coarse, dry, scaly, and thick. The relaxation phase of deep tendon reflexes is slowed. Hypothermia is common. Dementia or frank psychosis (myxoedema madness) may occur.
Carotenemia is common, particularly notable on the palms and soles, caused by deposition of carotene in the lipid-rich epidermal layers Deposition of proteinaceous ground substance in the tongue may cause macroglossia. A decrease in both thyroid hormone and adrenergic stimulation causes bradycardia. The heart may appear to be enlarged on examination and imaging, partly because of dilation but chiefly because of pericardial effusion. Pleural or abdominal effusions also may be noted. The pericardial and pleural effusions develop slowly and only rarely cause respiratory or hemodynamic distress.
Elderly patients have significantly fewer symptoms than do younger adults, and complaints are often subtle and vague. Many elderly patients with hypothyroidism present with nonspecific geriatric syndromes—confusion, anorexia, weight loss, falling, incontinence, and decreased mobility. Musculoskeletal symptoms (especially arthralgias) occur often, but arthritis is rare. Muscular aches and weakness, often mimicking polymyalgia rheumatica or polymyositis, and an elevated CK level may occur. In the elderly, hypothyroidism may mimic dementia or parkinsonism.
Although secondary hypothyroidism is uncommon, its causes often affect other endocrine organs controlled by the hypothalamic-pituitary axis. In a woman with hypothyroidism, indications of secondary hypothyroidism are a history of amenorrhea rather than menorrhagia and some suggestive differences on physical examination. Secondary hypothyroidism is characterized by skin and hair that are dry but not very coarse, skin depigmentation, only minimal macroglossia, atrophic breasts, and low BP. Also, the heart is small, and serous pericardial effusions do not occur. Hypoglycaemia is common because of concomitant adrenal insufficiency or growth hormone deficiency.
Myxoedema coma is a life-threatening complication of hypothyroidism, usually occurring in patients with a long history of hypothyroidism. Its characteristics include coma with extreme hypothermia (temperature 24° to 32.2° C), areflexia, seizures, and respiratory depression with CO2 retention. Severe hypothermia may be missed unless low-reading thermometers are used. Rapid diagnosis based on clinical judgment, history, and physical examination is imperative, because death is likely without rapid treatment. Precipitating factors include illness, infection, trauma, drugs that suppress the CNS, and exposure to cold.
How to Diagnose hypothyroidism?
1.TSH
2.Free thyroxine (T4)
Serum TSH is the most sensitive test, and screening of selected populations is warranted (see Thyroid Disorders: Laboratory Testing of Thyroid Function). In primary hypothyroidism, there is no feedback inhibition of the intact pituitary, and serum TSH is always elevated, whereas serum free T4 is low. In secondary hypothyroidism, free T4 and serum TSH are low (sometimes TSH is normal but with decreased bioactivity).
What is the Treatment of hypothyroidism?
l-Thyroxine, adjusted until TSH levels are in mid normal range
Various thyroid hormone preparations are available for replacement therapy, including synthetic preparations of T4 (l-thyroxine), T3 (liothyronine), combinations of the 2 synthetic hormones, and desiccated animal thyroid extract. L-Thyroxine is preferred; the usual maintenance dose is 75 to 150 μg po once/day, depending on age, body mass index, and absorption (for paediatric doses, see Endocrine Disorders in Children: Treatment). The starting dose in young or middle-aged patients who are otherwise healthy can be 100 μg or 1.7 μg/kg po once/day.
However, in the elderly and in patients with heart disease, therapy is begun with low doses, usually 25 μg once/day.
Key Points
Primary hypothyroidism is most common; it is due to disease in the thyroid, and TSH levels are high.
Secondary hypothyroidism is less common; it is due to pituitary or hypothalamic disease, and TSH levels are low.
Symptoms develop insidiously and typically include cold intolerance, constipation, and cognitive and/or personality changes; later, the face becomes puffy and the facial expression dull.
Myxoedema coma is a life-threatening complication that requires rapid diagnosis and treatment.
Free thyroxine (T4) level is always low, but T3 may remain normal early in some disorders.
Serum TSH is the best diagnostic test, and screening is warranted in select populations (eg, the elderly) because the disease is so subtle and insidious.
Oral T4 (L-thyroxine) is the preferred treatment and is given in the lowest dose that restores serum TSH levels to the midnormal range.
What is Subclinical Hypothyroidism?
Subclinical hypothyroidism is elevated serum TSH in patients with absent or minimal symptoms of hypothyroidism and normal serum levels of free T4.
Subclinical thyroid dysfunction is relatively common; it occurs in more than 15% of elderly women and 10% of elderly men, particularly in those with underlying Hashimoto’s thyroiditis.
How should subclinical hypothyroidism be treated?
In patients with serum TSH > 10 mU/L, there is a high likelihood of progression to overt hypothyroidism with low serum levels of free T4 in the next 10 yr. These patients are also more likely to have hypercholesterolemia and atherosclerosis. They should be treated with l-thyroxine, even if they are asymptomatic. For patients with TSH levels between 4.5 and 10 mU/L, a trial of l-thyroxine is reasonable if symptoms of early hypothyroidism (eg, fatigue, depression) are present. l-Thyroxine therapy is also indicated in pregnant women and in women who plan to become pregnant to avoid deleterious effects of hypothyroidism on the pregnancy and foetal development. Patients should have annual measurement of serum TSH and free T4 to assess progress of the condition if untreated or to adjust the l-thyroxine dosage.
What is Irritable bowel syndrome (IBS)?
Irritable bowel syndrome (IBS) is characterized by abdominal discomfort or pain that is accompanied by at least two of the following: relief by defecation, change in frequency of stool, or change in consistency of stool. The cause is unknown, and the pathophysiology is incompletely understood. Diagnosis is clinical. Treatment is symptomatic, consisting of dietary management and drugs, including anticholinergics and agents active at serotonin receptors.
Hormonal fluctuations affect bowel functions in women. Rectal sensitivity is increased during menses but not during other phases of the menstrual cycle. The effects of sex steroids on GI transit are subtle. The role of small-bowel bacterial overgrowth in IBS is controversial.
What are Symptoms and Signs of IBS?
IBS tends to begin in the teens and 20s, causing bouts of symptoms that recur at irregular periods. Onset in late adult life is less common but not rare. Symptoms rarely rouse the sleeping patient. Symptoms are often triggered by food, particularly fats, or by stress.
Patients have abdominal discomfort, which varies considerably but is often located in the lower quadrant, steady or cramping in nature, and relieved by defecation. In addition, abdominal discomfort is temporally associated with alterations in stool frequency (increased in diarrhoea-predominant IBS and decreased in constipation-predominant IBS) and consistency (i.e., loose or lumpy and hard). Pain or discomfort related to defecation is likely to be of bowel origin; that associated with exercise, movement, urination, or menstruation usually has a different cause. Although bowel patterns are relatively consistent in most patients, it is not unusual for patients to alternate between constipation and diarrhoea. Patients may also have symptoms of abnormal stool passage (straining, urgency, or feeling of incomplete evacuation), pass mucus, or complain of bloating or abdominal distention. Many patients also have symptoms of dyspepsia. Extra-intestinal symptoms (e.g., fatigue, fibromyalgia, sleep disturbances, chronic headaches) are common.
How Is IBS diagnosed?
Diagnosis is based on characteristic bowel patterns, time and character of pain, and exclusion of other disease processes through physical examination and routine diagnostic tests. Diagnostic testing should be more intensive when the following red flags are present either at initial presentation or at any time after diagnosis: older age, fever, weight loss, rectal bleeding, vomiting. Because patients with IBS can develop organic conditions, testing for other conditions should also be considered in patients who develop alarm symptoms or markedly different symptoms during the course of IBS. Common illnesses that may be confused with IBS include lactose intolerance, drug-induced diarrhoea, post-cholecystectomy diarrhoea, laxative abuse, parasitic diseases (e.g., giardiasis), eosinophilic gastritis or enteritis, microscopic colitis, and early inflammatory bowel disease. However, uninflamed colonic diverticula do not cause symptoms, and their presence should not be considered explanatory.
The Rome criteria are standardized symptom-based criteria for diagnosing IBS. The Rome criteria require the presence of abdominal pain or discomfort for at least 3 days/mo. in the last 3 mo. along with ≥2 of the following: (1.) improvement with defecation, (2) onset (of each episode of discomfort) associated with a change in frequency of defecation, or (3) change in consistency of stool.
What is the Treatment of IBS?
• Support and understanding
• Normal diet, avoiding gas-producing and diarrhoea-producing foods
• Increased fibre intake constipation
• Loperamide for diarrhoea
• Possibly tricyclic antidepressants
Diet: In general, a normal diet should be followed. Meals should not be overly large, and eating should be slow and paced. Patients with abdominal distention and increased flatulence may benefit from reducing or eliminating beans, cabbage, and other foods containing fermentable carbohydrates. Reduced intake of sweeteners (e.g., sorbitol, mannitol, fructose), which are constituents of natural and processed foods (e.g., apple and grape juice, bananas, nuts, and raisins), may alleviate flatulence, bloating, and diarrhoea. Patients with evidence of lactose intolerance should reduce their intake of milk and dairy products. A low-fat diet may reduce postprandial abdominal symptoms.
Dietary fibre supplements may soften stool and improve the ease of evacuation. A bland bulk-producing agent may be used (e.g., raw bran, starting with 15 mL [1 tbsp] with each meal, supplemented with increased fluid intake). Alternatively, psyllium hydrophilic mucilloid with two glasses of water may be used. However, excessive use of fibre can lead to bloating and diarrhoea, so fibre doses must be individualized. Occasionally, flatulence may be reduced by switching to a synthetic fibre preparation (eg, methylcellulose).
Drug therapy: Drug therapy is directed toward the dominant symptoms. Anticholinergic drugs (e.g., hyoscyamine 0.125 mg po 30 to 60 min before meals) may be used for their antispasmodic effects.
Serotonin receptor modulation may be of benefit. Tegaserod, a 5HT4 agonist, stimulates motility and alleviates constipation. In 2007, tegaserod was withdrawn from the market because, in clinical trials, it slightly increased the incidence of cardiovascular ischemic events (ie, MI, unstable angina pectoris, stroke) compared with placebo. Tegaserod has since been reintroduced under a restricted program. The chloride channel activator lubiprostone may help patients with constipation.
In patients with diarrhoea, oral diphenoxylate 2.5 to 5 mg or loperamide 2 to 4 mg may be given before meals. The dose of loperamide should be titrated upward to reduce diarrhoea while avoiding constipation. For many patients, tricyclic antidepressants (TCAs) help relieve symptoms of diarrhoea, abdominal pain, and bloating. These drugs are thought to reduce pain by down-regulating the activity of spinal cord and cortical afferent pathways arriving from the intestine. Secondary amine TCAs (e.g., nortriptyline, desipramine) are often better tolerated than parent tertiary amines (eg, amitriptyline, imipramine, doxepin) because of fewer anticholinergic, sedating antihistaminic, and α-adrenergic adverse effects. Treatment should begin with a very low dose of a TCA (e.g., desipramine 10 to 25 mg once/day at bedtime), increasing as necessary and tolerated up to about 100 to 150 mg once/day. SSRIs are also useful, particularly for patients with anxiety or an affective disorder, but may exacerbate diarrhoea
Preliminary data suggest that certain probiotics (e.g., Bifidobacterium infantis) alleviate IBS symptoms, particularly bloating. The beneficial effects of probiotics are not generic to the entire species but specific to certain strains. Certain aromatic oils (carminatives) can relax smooth muscle and relieve pain caused by cramps in some patients. Peppermint oil is the most commonly used agent in this class.
Psychologic therapies: Cognitive-behavioural therapy, standard psychotherapy, and hypnotherapy may help some IBS patients.
What is migraine in general?
Migraines are severe, recurring, and painful headaches. They can be preceded or accompanied by sensory warning signs and other symptoms.
The extreme pain that migraines cause can last for hours or even days.
According to the American Migraine Association, they affect 36 million Americans, or approximately 12 percent of the population.
Migraines can follow an aura of sensory disturbances followed by a severe headache that often appears on one side of the head. They tend to affect people aged 15 to 55 years.
Fast facts on migraines:
Some people who experience migraines can clearly identify triggers or factors that cause the headaches, such as allergies, light, and stress.
Some people get a warning symptom before the start of the migraine headache.
Many people with migraine can prevent a full-blown attack by recognizing and acting upon the warning signs.
Over-the-counter (OTC) medications can eliminate or reduce pain, and specific medications can help some people with migraine.
People who have severe attacks can take preventive medicines.
What are Triggers of migraine?
The cause of migraines is not yet known.
It is suspected that they result from abnormal activity in the brain. This can affect the way nerves communicate as well as the chemicals and blood vessels in the brain. Genetics may make someone more sensitive to the triggers that can cause migraines.
However, the following triggers are likely to set off migraines:
Hormonal changes: Women may experience migraine symptoms during menstruation, due to changing hormone levels.
Emotional triggers: Stress, depression, anxiety, excitement, and shock can trigger a migraine.
Physical causes: Tiredness and insufficient sleep, shoulder or neck tension, poor posture, and physical overexertion have all been linked to migraines. Low blood sugar and jet lag can also act as triggers.
Triggers in the diet: Alcohol and caffeine can contribute to triggering migraines. Some specific foods can also have this effect, including chocolate, cheese, citrus fruits, and foods containing the additive tyramine. Irregular mealtimes and dehydration have also been named as potential triggers.
Medications: Some sleeping pills, hormone replacement therapy (HRT) medications, and the combined contraceptive pill have all been named as possible triggers.
Triggers in the environment: Flickering screens, strong smells, second-hand smoke, and loud noises can set off a migraine. Stuffy rooms, temperature changes, and bright lights are also possible triggers.
What is Treatment of migraine?
There is currently no single cure for migraines. Treatment is aimed at preventing a full-blown attack, and alleviating the symptoms that occur.
The treatment of migraine symptoms focuses on avoiding triggers, controlling symptoms, and taking medicine.
Medications
Most of the drugs effective as prophylactics against migraines (as opposed to abortive drugs) are well-known to psychiatrists, including amitriptyline, nortriptyline, Depakote (divalproex sodium), Neurontin (gabapentin), and Topamax (topiramate). Effective non-psychiatric prophylactic agents include the beta blockers propranolol and atenolol, and the ACE inhibitor verapamil. This is a good list to keep in mind such as when you are choosing something for a depressed patient with migraines (go with the tricyclics) or for a migraine patient with bipolar disorder (the obvious choice would be Depakote).
What are the Types of migraine?
There are two main types of migraine. This classification depends on whether the individual experiences any disturbances of the senses leading up to a migraine. These are known as auras.
Migraine with aura
This picture is an illustration of what a person experiencing migraine with aura might see.
For many people with migraine, the auras act as a warning, telling them that a headache is soon to come. The effects of an aura can include:
confusing thoughts or experiences
the perception of strange, sparkling or flashing lights
zig-zagging lines in the visual field
blind spots or blank patches in the vision
pins and needles in an arm or leg
difficulty speaking
stiffness in the shoulders, neck, or limbs
unpleasant smells
If the following symptoms are unusual for the person with migraine, they should not be ignored:
an unusually severe headache
visual disturbance
loss of sensation
difficulties with speech
When migraines with aura affect vision, the patient may see things that are not there, such as transparent strings of objects. They may also not see parts of the object in front of them or even feel as if part of their field of vision appears, disappears, and then comes back again.
People experiencing an aura may describe the visual disturbance as similar to the sensation that follows being exposed to a very bright camera flash.
Migraine without aura
More commonly, a person will experience a migraine without any sensory disturbance leading up to the attack. Between 70 and 90 percent of migraines occur without an aura.
Other types
There are other types of migraine related to specific syndromes or triggers, including:
Chronic migraine: This refers to any migraine that triggers attacks on over 15 days of the month.
Menstrual migraine: This is when the attacks occur in a pattern connected to the menstrual cycle.
Hemiplegic migraine: This causes weakness on one side of the body for a temporary period.
Abdominal migraine: This is a syndrome that connects migraine attacks to irregular function in the gut and abdomen. It mainly occurs in children under 14 years of age,
Migraine with brainstem aura: This is a rare type of migraine that can trigger severe neurological symptoms, such as affected speech.
What are the Symptoms of migraine?
Symptoms of migraine can start a while before the headache, immediately before the headache, during the headache, and after the headache. Although not all migraines are the same, typical symptoms include:
moderate to severe pain, usually confined to one side of the head but capable of occurring on either side of the head
severe, throbbing, or pulsing pain
increasing pain during physical activity or when straining
inability to perform regular activities due to pain
feeling sick and physically vomiting
increased sensitivity to light and sound, relieved by lying quietly in a darkened room
Some people experience other symptoms such as sweating, temperature changes, stomach ache, and diarrhoea.
Migraine vs headache
It is important to know the difference between a migraine attack and a headache.
Headaches can vary a great deal in how long they last, how severe they are, and why they happen. They may not occur in a recognizable pattern as migraine attacks do.
Migraine attacks will present as moderate-to-severe headaches on one side of the head that occur with other symptoms, such as nausea and vomiting. Migraine and non-migraine headaches are different and can indicate different causes.
To help identify a migraine headache, it can be useful to keep a diary of symptoms noting the time of onset, any triggers, the duration of the headaches, any noticeable signs or auras leading up to a migraine attack, and any other symptoms.
The International Headache Society recommends the “5, 4, 3, 2, 1” criteria to diagnose migraines without aura.
This stands for:
5 or more attacks with a duration of 4 hours to 3 days
At least two of the following qualities: Occurring on one side of the head, a pulsating quality, moderate-to-severe pain, and aggravation by routine physical activity
At least one additional symptom, such as nausea, vomiting, sensitivity to light, or sensitivity to sound.
What is tension headache?
Tension headaches are dull pain, tightness, or pressure around your forehead or the back of your head and neck. Some people say it feels like a clamp squeezing the skull. Often called stress headaches, they’re the most common type for adults.
What are types of tension headache?
There are two types:
Episodic tension headaches happen less than 15 days per month.
Chronic tension headaches happen more than 15 days a month.
These headaches can last from 30 minutes to a few days. The episodic kind usually starts gradually, often in the middle of the day.
Chronic ones come and go over a longer period of time. The pain may get stronger or ease up throughout the day, but it’s almost always there.
How to Help Headache Pain
Although your head hurts, tension headaches usually don’t keep you from your daily activities, and they don’t affect your vision, balance, or strength.
Who Gets tension headaches?
Up to 80% of adults in the U.S. get them from time to time. About 3% have chronic daily tension headaches. Women are twice as likely to get them as men.
Most people with episodic tension headaches have them no more than once or twice a month, but they can happen more often.
Many people with the chronic type have usually had them for more than 60-90 days.
What Are the Symptoms?
A few common ones include:
Mild to moderate pain or pressure in the front, top, or sides of the head
Headache that starts later in the day
Trouble sleeping
Feeling very tired
Irritability
Trouble focusing
Mild sensitivity to light or noise
Muscle aches
Unlike migraine headaches, you won’t have other nerve symptoms, such as muscle weakness or blurred vision. And they don’t usually cause severe sensitivity to light or noise, stomach pain, nausea, or vomiting.
What is the Treatment of chronic tension headache?
Usually it is associated with depressive disorder and responds well to antidepressants like dothiepin or amitriptyline.
What are cluster headaches?
Cluster headaches are simply speaking a cluster of migraine attacks jumbled together. Cluster headaches are comparatively rare and are described as an excruciating “boring” pain, often over one eye, lasting from 15 minutes to several hours. They may occur several times per day or night.
What is the treatment of chronic cluster headache?
The most common preventative treatments are, Verapamil prescribed for cluster headache as research has shown that a daily dose can be effective, Methysergide is effective in episodic (short term bouts) of cluster headache, Lithium at a low dose can be effective although again this will need careful monitoring, Corticosteroids are also given, hyperbaric oxygen is also used.
What is the best treatment for acute cluster headaches?
The oxygen options. 100% oxygen is pure oxygen that is inhaled, delivered through a face mask. The treatment is quick, effective, and safe when used to address the pain of cluster headaches but has not been proven effective in treating traditional migraine. Inhaled oxygen therapy has been used to treat cluster headaches for more than 50 years. Treatment with combination of ergot alkaloids and paracetamol helps. Triptans may be used.
Why Psychiatrists have a major role in headache treatment?
Just because most patients of tension headache which is chronic have an underlying depressive disorder and respond to antidepressants. Also, many patients of migraine have some element of chronic tension headache and respond to antidepressants. Besides most headaches say 95 % do not have a structural problem in the brain and are functional. Now who is better equipped to treat functional disorders. Psychiatrist it is!
We know that headaches are common in the general population, but they are particularly common among patients with psychiatric problems. Patients with depression have a 46% lifetime prevalence of migraine, while bipolar patients have a 51% prevalence. Patients with migraines have triple the risk of developing depression than patients without migraines.
There’s a tendency among no specialists to view tension-type headaches as being a waste-basket category for anything that is not a migraine, but in reality, these headaches have fairly specific diagnostic criteria.
More important is for psychiatrists to know something about the controversy surrounding the safety of combining triptans with SSRIs. In 2006, the FDA issued an alert that combining triptans with either SSRIs or SNRIs can cause serotonin syndrome. The agency said this was based on 27 cases gathered over five years. The announcement was met widely with scepticism, because millions of patients had been combining triptans with SSRIs over the years and serotonin syndrome had rarely, if ever, been reported in the literature. Despite requests, the FDA has not made details of these 27 cases of supposed serotonin syndrome public, and a recent review concluded that “withholding these medications due to fears of serotonin syndrome is difficult to justify”
Other techniques that have some empirical support for relief of chronic headaches include standard progressive muscle relaxation exercises and acupuncture.
What are Physical disorders mimicking mental disorders?
Numerous physical disorders cause symptoms mimicking specific mental disorders. Other physical disorders may not mimic specific mental syndromes but instead change mood and energy.
Following is the list of diseases causing Confusion, delirium, disorientation in a patient
Cerebral arteritis, including that caused by SLE, CNS infection (eg, encephalitis, meningitis, toxoplasmosis), Complex partial seizures, Dehydration, Drug overdose, including prescription drug overdose, Electrolyte abnormalities, Fever, Hypoglycaemia, Hypothermia, Hypothyroidism, Hypoxia, Liver failure, Mass lesion (eg, tumour, hematoma), Renal failure, Sepsis, Thyroid disorders, Vascular infarct, Vitamin deficiency.
Following is the list of diseases causing Cognitive impairment, behavioural instability
Alzheimer’s and other dementias, HIV/AIDS, Lyme disease, Mass lesion, Multiple sclerosis, Neurosyphilis, Parkinson’s disease, Subdural hematoma, SLE, Thyroid disorders, Vascular infarct, Vitamin deficiency, Delusions, Multiple sclerosis, Polysubstance abuse, Seizure disorders,
Following is the list of diseases causing Depression
Brain tumour, Cancer treatments, including interferon, Cushing’s syndrome, Dementia, Diabetes mellitus, Hypothyroidism, Multiple sclerosis, Sarcoidosis, Euphoria,
Following is the list of diseases causing mania
Brain tumour, Multiple sclerosis, Polysubstance abuse, isoniazid use.
Following is the list of diseases causing Hallucinations
Encephalitis, Mass lesion, Migraine, Seizure disorders.
Following is the list of diseases causing Insomnia
Circadian rhythm disorders, Dyspnoea or hypoxia, Gastroesophageal reflux disease (GERD), Hyperthyroidism, Periodic leg movement disorder or restless legs syndrome, Pain syndromes
Following is the list of diseases causing Irritability
Multiple sclerosis, Vitamin B12 deficiency,
Following is the list of diseases causing Memory impairment
Hypothyroidism, Multiple sclerosis, SLE, Vitamin deficiency
Following is the list of diseases causing Mood symptoms
HIV/AIDS, Multiple sclerosis,
Following is the list of diseases causing Personality change
Mass lesion, Multiple sclerosis, Seizure disorders, SLE,
Following is the list of diseases causing Psychosis (eg, hallucinations)
Brain tumour, Dementia, Electrolyte abnormalities, Migraine, Multiple sclerosis, Polysubstance abuse, Sarcoidosis,
Following is the list of diseases causing Sensory loss
SLE, Syphilis
*In addition, numerous drugs and toxins may cause mental symptoms.
Many drugs cause mental symptoms;
the most common drug causes are CNS-active drugs (eg, anticonvulsants, antidepressants, antipsychotics, sedative/hypnotics, stimulants) Anticholinergics (eg, antihistamines), Corticosteroids
Numerous other therapeutic drugs and drug classes have also been implicated; they include some classes that may not ordinarily be considered (eg, antibiotics, antihypertensives). Drugs of abuse, particularly alcohol, amphetamines, cocaine, hallucinogens, and phencyclidine (PCP), particularly in overdose, are also frequent causes of mental symptoms. Withdrawal from alcohol, barbiturates, or benzodiazepines may cause mental symptoms (eg, anxiety) in addition to symptoms of physical withdrawal.
In addition to the problem of causing mental symptoms, patients with a mental disorder may develop a physical disorder (eg, meningitis, diabetic ketoacidosis) that causes new or worsened mental symptoms. Thus, a clinician should not assume that all mental symptoms in patients with a known mental disorder are due to that disorder. The clinician may need to be proactive in addressing possible physical causes for mental symptoms, especially in patients unable to describe their physical health because they have psychosis or dementia.
Patients presenting for psychiatric care occasionally have undiagnosed physical disorders (including substance abuse, diabetes, and hypothyroidism) that are not the cause of their mental symptoms but nonetheless require evaluation and treatment.
There are seven common physical disorders that often co-occur, or are linked to an increase risk of mental health conditions. They are 1. Endometriosis 2. Eczema 3. Fibromyalgia 4. Irritable Bowel Syndrome (IBS) 5. Lupus 6. Acne 7. Chronic Fatigue Syndrome
What is faith healing?
Faith healing is the practice of prayer and gestures (such as laying on of hands) that are believed by some to elicit divine intervention in spiritual and physical healing, especially the Hindu, and Christian practice.
What to do for tardive dyskinesia?
Tardive dyskinesia is a side effect of antipsychotic medications. These drugs are used to treat schizophrenia and other mental health disorders.
TD causes stiff, jerky movements of your face and body that you can’t control. You might blink your eyes, stick out your tongue, or wave your arms without meaning to do so.
Antipsychotic medications that can cause tardive dyskinesia include antipsychotics like:
• Haloperidol (Haldol)
• Fluphenazine
• Risperidone (Risperdal)
• Olanzapine (Zyprexa)
Your chances of getting TD go up the longer you take an antipsychotic medicine.
Some drugs that treat nausea, reflux, and other stomach problems can also cause TD if you take them for more than 3 months. These include:
• Metoclopramide (Reglan)
• Prochlorperazine (Compazine)
What to do for benzodiazepine addiction?
Anxiolytics and sedatives (hypnotics) include benzodiazepines, barbiturates, and related drugs. High doses can cause stupor and respiratory depression, which is managed with intubation and mechanical ventilation. Chronic users may have a withdrawal syndrome of agitation and seizures, so dependence is managed by slow tapering with or without substitution (ie, with pentobarbital or phenobarbital).
The therapeutic benefit of anxiolytics and sedatives is well-established, but their value in alleviating stress and anxiety is also probably the reason that they are abused so frequently. Abused anxiolytics and sedatives include benzodiazepines, barbiturates, and other drugs taken to promote sleep.
Patients taking high doses of sedatives frequently have difficulty thinking, slow speech and comprehension (with some dysarthria), poor memory, faulty judgment, narrowed attention span, and emotional lability. In susceptible patients, psychologic dependence on the drug may develop rapidly. The extent of physical dependence is related to dose and duration of use; eg, pentobarbital 200 mg/day taken for many months may not induce significant tolerance, but 300 mg/day for > 3 mo. or 500 to 600 mg/day for 1 mo. may induce a withdrawal syndrome when the drug is stopped. Tolerance and tachyphylaxis develop irregularly and incompletely; thus, considerable behavioural, mood, and cognitive disturbances persist, even in regular users, depending on the dosage and the drug’s pharmacodynamic effects. Some cross-tolerance exists between alcohol and barbiturates and nonbarbiturate anxiolytics and sedatives, including benzodiazepines. (Barbiturates and alcohol are strikingly similar in the dependence, withdrawal symptoms, and chronic intoxication they cause.)
Pregnancy: Prolonged use of barbiturates during pregnancy can cause withdrawal in the neonate
Toxicity or overdose: The signs of progressive anxiolytic and sedative intoxication are depression of superficial reflexes, fine lateral-gaze nystagmus, slightly decreased alertness with coarse or rapid nystagmus, ataxia, slurred speech, and postural unsteadiness.
Increasing toxicity can cause nystagmus on forward gaze, miosis, somnolence, marked ataxia with falling, confusion, stupor, respiratory depression, and, ultimately, death. Overdose of a benzodiazepine rarely causes hypotension, and these drugs do not cause arrhythmias.
Withdrawal: When intake of therapeutic doses of anxiolytics and sedatives is stopped or reduced below a critical level, a self-limited mild withdrawal syndrome can ensue. After only a few weeks, attempts to stop using the drug can exacerbate insomnia and result in restlessness, disturbing dreams, frequent awakening, and feelings of tension in the early morning.
Withdrawal from benzodiazepines is rarely life threatening. Symptoms can include tachypnoea, tachycardia, tremulousness, hyperreflexia, confusion, and seizures. Onset may be slow because the drugs remain in the body a long time. Withdrawal may be most severe in patients who used drugs with rapid absorption and a quick decline in serum levels (e.g., alprazolam, lorazepam, triazolam). Many people who misuse benzodiazepines have been or are heavy users of alcohol, and a delayed benzodiazepine withdrawal syndrome may complicate alcohol withdrawal.
Withdrawal from barbiturates taken in large doses causes an abrupt, potentially life-threatening withdrawal syndrome similar to delirium tremens. Occasionally, even after properly managed withdrawal over 1 to 2 wk., a seizure occurs. Without treatment, withdrawal of a short-acting barbiturate causes the following:
Treatment
Airway protection
Flumazenil to be considered
Urine alkalinisation for barbiturates
Toxicity or overdose: Acute intoxication generally requires nothing more than observation, although the airway and respirations should be carefully assessed. If ingestion was within 1 h, the gag reflex is preserved, and the patient can protect the airway, 50 g of activated charcoal may be given to reduce further absorption; however, this intervention has not been shown to reduce morbidity or mortality. Occasionally, intubation and mechanical ventilation are required.
The benzodiazepine receptor antagonist flumazenil can reverse severe sedation secondary
to benzodiazepine overdose. Dose is 0.2 mg IV given over 30 sec; 0.3 mg may be given after 30 sec, followed by 0.5 mg q 1 min to total 3 mg. However, its clinical usefulness is not well-defined because most people who overdose on benzodiazepines recover with only supportive care, and occasionally flumazenil precipitates seizures. Contraindications to flumazenil include long-term benzodiazepine use (because flumazenil may precipitate withdrawal), an underlying seizure disorder, presence of twitching or other motor abnormalities, a concomitant epileptogenic drug overdose (especially of tricyclic antidepressants), and cardiac arrhythmias. If barbiturate overdose is diagnosed, urine should be alkalinized to increase excretion. Withdrawal and detoxification: Severe acute withdrawal requires hospitalization, preferably in an ICU, and use of appropriate doses of IV benzodiazepines.
What is schizophrenia in general?
Schizophrenia is characterized by psychosis (loss of contact with reality), hallucinations (false perceptions), delusions (false beliefs), disorganized speech and behaviour, flattened affect (restricted range of emotions), cognitive deficits (impaired reasoning and problem solving), and occupational and social dysfunction. The cause is unknown, but evidence for a genetic component is strong. Symptoms usually begin in adolescence or early adulthood. One or more episodes of symptoms must last ≥ 6 months before the diagnosis is made. Treatment consists of drug therapy, psychotherapy, and rehabilitation.
What is prevalence of schizophrenia?

Worldwide, the prevalence of schizophrenia is about 1%. The rate is comparable among men and women and relatively constant cross-culturally. The rate is higher among lower socioeconomic classes in urban areas, perhaps because its disabling effects lead to unemployment and poverty. Similarly, a higher prevalence among single people may reflect the effect of illness or illness precursors on social functioning. The average age at onset is 18 yrs. in men and 25 yrs. in women. Onset is rare in childhood, but early-adolescent onset or late-life onset (when it is sometimes called paraphrenia) may occur.
What are the causes of schizophrenia?
Although its specific cause is unknown, schizophrenia has a biologic basis, as evidenced by alterations in brain structure (eg, enlarged cerebral ventricles, decreased size of the anterior hippocampus and other brain regions) and by changes in neurotransmitters, especially altered activity of dopamine and glutamate. Some experts suggest that schizophrenia occurs in people with neurodevelopmental vulnerabilities and that the onset, remission, and recurrence of symptoms are the result of interactions between these enduring vulnerabilities and environmental stressors.
Neurodevelopmental vulnerability: Vulnerability may result from genetic predisposition; intrauterine, birth, or postnatal complications; or viral CNS infections. Maternal exposure to famine and influenza during the 2nd trimester of pregnancy, birth weight 6 mg, dose-dependent prolactin elevation, or metabolic syndrome.
What are the issues in treatment of schizophrenia?
Treatment is with antipsychotics. Older psychiatrists prefer first generation antipsychotics like haloperidol and trifluoperazine. Haloperidol in doses of 5-15 mg/d. Trifluoperazine in dose of 15 mg/d. Side effects are EPS (common) and tardive dyskinesia(rare). Newer psychiatrists prefer olanzapine. Olanzapine 10–20 mg po at bedtime 15 mg po at bedtime Most common adverse effects: Somnolence, metabolic syndrome, and dizziness
Newer SGAs are very similar to each other in efficacy but differ in adverse effects, so drug choice is based on individual response and on other drug characteristics. For example, olanzapine, which has a relatively high rate of sedation, may be prescribed for patients with prominent agitation or insomnia; fewer sedating drugs might be preferred for patients with lethargy. A 4- to 8-wk trial is usually required to assess efficacy. After acute symptoms have stabilized, maintenance treatment is initiated; for it, the lowest dose that prevents symptom recurrence is used. Risperidone is the only SGA available in a long-acting injectable formulation.?
Weight gain, hyperlipidaemia, and elevated risk of type 2 diabetes are the major adverse effects of SGAs (SGA = Second-generation antipsychotic). Thus, before treatment with SGAs is begun, all patients should be screened for risk factors, including personal or family history of diabetes, weight, waist circumference, BP, and fasting plasma glucose and lipid profile. Those found to have or be at significant risk of metabolic syndrome may be better treated with ziprasidone or aripiprazole than the other SGAs. Patient and family education regarding symptoms and signs of diabetes, including polyuria, polydipsia, weight loss, and diabetic ketoacidosis (nausea, vomiting, dehydration, rapid respiration, clouding of sensorium), should be provided. In addition, nutritional and physical activity counselling should be provided to all patients when they start taking an SGA. All patients taking an SGA require periodic monitoring of weight, body mass index, and fasting plasma glucose and referral for specialty evaluation if they develop hyperlipidaemia or type 2 diabetes.
What is rehabilitation in schizophrenia?
Psychosocial skill training and vocational rehabilitation programs help many patients work, shop, and care for themselves; manage a household; get along with others; and work with mental health care practitioners. Supported employment, in which patients are placed in a competitive work setting and provided with an on-site job coach to promote adaptation to work, may be particularly valuable. In time, the job coach acts only as a backup for problem solving or for communication with employers.
When to hospitalise in schizophrenia?
Hospitalization or crisis care in a hospital alternative may be required during severe relapses, and involuntary hospitalization may be necessary if patients pose a danger to themselves or others. Despite the best rehabilitation and community support services, a small percentage of patients, particularly those with severe cognitive deficits and those poorly responsive to drug therapy, require long-term institutional or other supportive care.
How to interpret violence among mentally ill patients?
While researchers are beginning to understand more about factors linking violence and mental illness, much more research needs to be done to identify individuals at risk.
For years, substance use has been known as a key factor mediating the intersection of mental illness and violence against self and others, but drugs and alcohol may be the more significant partner in that interaction.
Only a small proportion of violent crime is committed by people with mental illness, but the role of substance abuse is important.
Mania, acute use of substances, stress, and sleep deprivation can all activate this system in the brain for violence maladaptively, but use of substances also perturbs that already complex system.
Alcohol, for example, is a stimulant and a depressant, two responses that are regulated independently of each other.
On the stimulant side, binge drinking keeps the alcohol level up to maintain activation, he said. Binge drinkers who haven’t developed dependence and don’t otherwise drink heavily are the people in whom alcohol does the most spectacular harm—they’re more likely to have fights, accidents, and suicidal behaviour than people who drink and get drunk every day.
Suicide attempts that are mainly premeditated and based on feelings of hopelessness still require a component of impulsivity. With severe depression, a small increase in impulsivity can be decisive.

What is substance-induced mood disorder (SIMD)?
When taking a drug or stopping a drug causes days or weeks of mood changes, the problem is called substance-induced mood disorder. Many medicines and illegal drugs can cause you to be depressed. The drugs make you feel sad, uninterested in daily events, and hopeless. You may also get manic symptoms. When you are manic you are overexcited, have too much energy, and have difficulty controlling your actions.
It is not substance-induced if you were depressed or manic before you started using the drug and the drug makes it worse.
What is the most common substance induced mood disorder?
When overall harm to society and the drug user are considered together, alcohol is by far the most damaging (despite being legal more often than the other drugs.
What is the cause of substance induced mood disorder?
Many drugs change the way brain cells communicate with each other. Drugs can change the amounts of chemical messengers, called neurotransmitters, in your nervous system. Having the right balance of these chemical messengers in your nerves and brain is important for good mood. Two important neurotransmitters are dopamine and serotonin. Too little or too much of these chemicals can cause mood problems. Many drugs and medicines change how dopamine and serotonin work. This can upset the balance of these chemicals.
Frequent or daily use of some drugs can cause mood problems. Withdrawal (stopping use of some drugs) can cause mood problems for up to 4 weeks after you quit.
Drugs and medicines that can cause mood problems while you are using them are:
amphetamines such as speed, Ritalin, and Dexedrine decongestants such as pseudoephedrine (Sudafed) heart and high blood pressure medicines, inhalants such as gasoline and spray paint, antianxiety medicines such as clonazepam
Drugs that can cause mood problems while you use them and during withdrawal are:
alcohol (beer, wine, or hard liquor) cocaine, hallucinogens such as LSD and hallucinogenic mushrooms , marijuana, sedatives and antianxiety medicines such as diazepam (Valium), clonazepam lorazepam (Ativan), and alprazolam , narcotics such as heroin, and pain medicines such as morphine, codeine, Percocet, and tramadol , steroid medicines, Other prescription medicines can cause mood problems. Some of these are antidepressants, birth control pills, steroids, some antibiotics, certain acne medicines, and medicines for high blood pressure.
What are the symptoms of SIMD??
You may have the symptoms of depression or mania, or you may cycle between the two. The symptoms may come when you are using drugs or in the month after you stop.
How is SIMD diagnosed?
Your healthcare provider or a mental health professional can tell you if your symptoms are substance-induced mood disorder. He or she will ask about your symptoms and your drug or alcohol use. You may be asked to have some lab tests to rule out medical problems such as hormone imbalances. There are blood and urine tests to check for substance abuse.
How is SIMD treated?
If you have been abusing drugs, go to a substance abuse therapist or program for help with stopping and handling withdrawal symptoms. Do not suddenly stop using drugs without professional help. Stopping some drugs abruptly can be very dangerous, and may even result in death.
Substance-induced mood disorder can be treated with either group or individual psychotherapy. Therapy in a group with other people having substance abuse problems is often very helpful. In some cases, medicines for depression or anxiety may help you to stop substance abuse. Discuss the options with your healthcare provider or therapist.
Most towns and cities have chapters of Alcoholics Anonymous (AA) and Narcotics Anonymous (NA). Look for these in your community.
Claims have been made that certain herbal and dietary products help people avoid a return to substance abuse. No herb or dietary supplement has been proven to consistently or completely stop substance abuse. Supplements are not tested or standardized and may vary in strength and effects. They may have side effects and are not always safe.
Learning ways to relax may help. Yoga and meditation may also be helpful. You may want to talk with your healthcare provider about using these methods along with medicines and psychotherapy.
How long will the effects of SIMD last?
Substance-induced mood disorder usually lasts as long as you continue substance abuse, or until you have gone a month or more without abusing substances. The treatments listed above most often will help you to remain free of drug use.
How can I take care of myself from SIMD?
If you have been abusing drugs, go to a substance abuse program or skilled mental health professional for help with stopping the substance abuse and handling the withdrawal symptoms.

What is chronic pain?
Chronic pain is pain that persists or recurs for > 3 mo., persists > 1 mo. after resolution of an acute tissue injury, or accompanies a nonhealing lesion. Causes include chronic disorders (e.g., cancer, arthritis, diabetes) and injuries (e.g., herniated disk, torn ligament), and many primary pain disorders (e.g., neuropathic pain, fibromyalgia, chronic headache). Various drugs and psychologic treatments are used.
Chronic pain often leads to vegetative signs (e.g., lassitude, sleep disturbance, decreased appetite, loss of taste for food, weight loss, diminished libido, constipation), which develop gradually; depression may develop. Patients may become inactive, withdraw socially, and become preoccupied with physical health. Psychologic and social impairment may be severe, causing virtual lack of function.
How to evaluate chronic pain?
Evaluation for organic cause initially and if symptoms change
An organic cause should always be sought—even if a prominent psychologic contribution to the pain is likely. Physical processes associated with the pain should be evaluated appropriately and characterized. However, once a full evaluation is done, repeating tests in the absence of new findings is not useful. The best approach is often to stop testing and focus on relieving pain and restoring function.
The effect of pain on the patient’s life should be evaluated; evaluation by an occupational therapist may be necessary. Formal psychiatric evaluation should be considered if a coexisting psychiatric disorder (eg, major depression) is suspected as cause or effect.
How to treat chronic pain?
Often treatment of chronic pain involves multimodal therapy (e.g., analgesics, physical methods, psychologic treatments)
Specific causes should be treated. Early, aggressive treatment of acute pain is always preferable and may limit or prevent sensitization and remodelling and hence prevent progression to chronic pain.
Drugs or physical methods may be used. Psychologic and behavioural treatments are usually helpful. Many patients who have marked functional impairment or who do not respond to a reasonable attempt at management by their physician benefit from the multidisciplinary approach available at a pain clinic.
Many patients prefer to have their pain treated at home, even though an institution may offer more advanced modalities of pain management. Also, pain control may be compromised by certain practices in institutions; for example, they restrict visiting hours, use of televisions and radios (which provide useful distraction), and use of heating pads (for fear of thermal injury).
Analgesics include NSAIDs, opioids, and adjuvant analgesics One or more drugs may be appropriate. Adjuvant analgesics are most commonly used for neuropathic pain.
For persistent, moderate-to-severe pain that impairs function, opioids should be considered after determining the following:
What conventional treatment practice is?
Whether other treatments are reasonable
Whether the patient has an unusually high risk of adverse effects from an opioid
Whether the patient is likely to be a responsible drug user
Prescription drug abuse may be a problem, and physicians should not offer long-term opioid therapy unless they can assess risk of abuse, monitor patients appropriately, and respond reasonably to problematic drug use. As pain lessens, patients usually need help reducing use of opioids. If depression coexists with pain, antidepressants should be used.
Depending on the condition, trigger point injection, joint or spinal injections, nerve blocks, or neuraxial infusion may be appropriate.
Many patients benefit from physical therapy or occupational therapy. Spray-and-stretch techniques can relieve myofascial trigger points. Some patients require an orthosis. Spinal cord stimulation may be appropriate.
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Are there some treatments for depression that are not antidepressants?

TMS
A recent study on a kind of therapy called transcranial magnetic stimulation (TMS), which uses magnetic pulses to alleviate depression, showed that after a year of treatment, 68% of adult patients had improved depression symptoms and 45% had complete remission. Currently, TMS is used among patients who do not respond well to antidepressants, but some experts think the therapy could one day be used as a first-line treatment. In TMS, a large magnet is placed on the left side of a patient’s head, and magnetic pulses stimulate the under-active areas of the patient’s brain that are involved in mood regulation. The patient is awake the entire time, and there are few reported side effects aside from headaches in some. Other research published in August showed TMS could also have positive benefits for memory.
Acupuncture
Acupuncture is becoming an increasingly mainstream way in the U.S. to treat a wide variety of ailments from chronic pain to anxiety
Exercise
Scientists are increasingly showing that exercise improves mental health. For instance, Jasper Smits a psychologist with a clinic in Dallas has long recommended that therapists use exercise therapy for people who are not responding to other forms of treatments. In 2012, a clinical trial of heart failure patients found that regular exercise help alleviate depressive symptoms. It’s believed that exercise increases hormones like serotonin and dopamine in the brain, subsequently making people feel better.
Exposure therapy
For depression symptoms that may be related to other mental health issues like phobias and obsessive-compulsive disorder, exposure therapy can help patients become more accustomed to and comfortable with things that used to bring them fear and anxiety. For example, if someone is afraid of flying, they my build up to taking an actual trip on a plane by starting with simply looking at images of airplanes.
Mindfulness
Plenty of research supports meditation as a possible treatment for depression and anxiety. The mechanism is not entirely understood, but if a person can be acutely aware of what is happening in the present moment, the thought it is that they can relax and gain more focus. As TIME reported in January, many cognitive therapists have started recommending it for patients as a way to deal with their anxiety and depression since it can mitigate stress.
Eye Movement Desensitization Reprocessing (EMDR)
According to the Anxiety and Depression Association of America, eye movement desensitization and reprocessing, or EMDR, “seems to have a direct effect on the way that the brain processes information… It helps a person see disturbing material in a less distressing way.” It’s still considered a fairly new type of therapy. As a patient goes through an unpleasant memory, they may watch moving lights, listen to tones and feel taps on their palm. It’s primarily used to treat PTSD, and still needs a lot more efficacy evidence. EMDR has had its share of controversy among researchers who question whether it really works.
Electric shock treatment
Also known as electroconvulsive therapy (ECT), shock treatment is fairly common treatment in which electric currents are passed through the brain and trigger seizures. It’s believed that the shocks interfere with brain chemistry that might be out of orders. ECT is considered much safer today than it was in the past–which too high doses were given resulting in negative side effects like memory loss and physical injury.
Cognitive behavioural therapy
People are likely familiar with cognitive behavioural therapy, which is a talk therapy usually recommend for patients with moderate to severe depression. The idea behind cognitive behavioural therapy is to help patients understand the events or emotions behind their current status, and figure out ways to mitigate how they’re feeling day-to-day. Some recent research has suggested that cognitive therapy can work even if it’s not necessarily done face to face. In 2012, a study compared face-to-face therapy to therapy done over the phone and found that phone therapy was just as effective, and patients were more likely to stick with it. Some therapists will even do sessions via video chat, like Skype.
What is new about catatonia?
Despite the official tie of catatonia to schizophrenia in the classification, in textbooks and in clinical teaching, young clinicians in the 1970s identified catatonia to be common among patients with mood disorders, especially in the excited states of mania. By 1980, the acute onset of fever, rigidity and autonomic signs was recognized as a toxic response to neuroleptics in the “neuroleptic malignant syndrome” (NMS). The syndrome was first related to malignant hyperthermia (MH), but treatments for MH failed to bring relief. Comparisons of NMS to the malignant form of catatonia (MC) found the two to be indistinguishable. When the treatments for MC were applied, NMS resolved. NMS is now considered and treated as a variant of catatonia.
Excited states of delirious mania next met catatonia symptom criteria for which treatments for catatonia are effective. Delirious mania is a catatonia variant.
Children and adolescents with autism spectrum disorders exhibit many signs of catatonia. Their repetitive self-injurious behaviour (SIB) is a feature among the negativism, posturing, staring and mutism common to these patients. Although the use of ECT in adolescents, especially those with neurodevelopmental defects, was considered risky and unethical, treatment trials found that the catatonia features, including SIB, resolved. The latest reports find the children to be very tolerant of benzodiazepines and, for effective treatment, high doses are needed. SIB is considered a sign of catatonia.
Patients with tics diagnosed as suffering from Gilles de la Tourette syndrome meet the criteria for catatonia. These patients respond to ECT, suggesting that systematic studies of catatonia are warranted.
Today, a fashionable syndrome of anti-N-methyl-D-aspartate receptor encephalitis is sweeping the United States today. The detailed descriptions find that more than 70% of the patients meet the criteria for catatonia. Enthusiasts drive the discussion to unproven intravenous immunoglobulin (IVIG) replacement therapy, and to the search for ovarian tumours, but once the association with catatonia is recognized and its effective treatments applied, the syndrome will be seen as a treatable form of catatonia, much as NMS and SIB are now recognized.
When the presence of two or more catatonia signs for more than 24 h points to catatonia, a reduction of 50% or more in catatonia signs after an intravenous dose of a barbiturate or benzodiazepine verifies the syndrome. The test is reported positive in 50–80% of the patients who meet clinical signs of catatonia. Excluding such a test is arbitrary and is equivalent to excluding the findings in an electroencephalogram for a seizure disorder or a serologic test for syphilis.
The new proposal calls for the recognition of catatonia as a defined syndrome with a single numeric code and with four types for descriptive purposes: an inhibited form described as the Kahlbaum syndrome, an excited form of delirious mania, a malignant form that includes the neuroleptic malignant syndrome and a form associated with systemic illnesses.
More than 135 years after its birth, catatonia is now recognized as an identifiable and treatable syndrome. Its characteristics are well defined, a simple test verifies the diagnosis and the treatments of high-dose benzodiazepines and ECT are remarkably effective and safe. Catatonia warrants the proposed separation from schizophrenia and establishment as an independent syndrome in the classification of psychiatric illnesses with a single numeric code.
What is therapeutic recreation?
Therapeutic recreation uses leisure activities like games and crafts to improve health and well-being.
How to manage common sleep problems?
Some of the most common problems are:
Bruxism
Bruxism is grinding, gnashing, or clenching your teeth during sleep or in situations that make you feel anxious or tense. It can be mild and happen only once in a while, or it may be violent and happen often. Bruxism most often occurs in the early part of the night. You may not be aware that you have bruxism until your teeth or jaws are damaged. People who have bruxism are also more likely to snore and develop sleep apnoea.
Hypersomnia is excessive daytime sleepiness or prolonged night-time sleep. Hypersomnia is not feeling tired or sluggish during the day because you haven’t gotten a normal amount of sleep. If you have hypersomnia, you feel very drowsy during the day and have an overwhelming urge to fall asleep, even after getting enough sleep at night. You often doze, nap, or fall asleep in situations where you need or want to be awake and alert. Other symptoms may include irritability, mild depression, trouble concentrating, and memory loss.
Jet Lag
Jet lag is caused by flying to different time zones. Our bodies work on a 24-hour cycle of “circadian rhythms” that control body temperature, hunger, and when we sleep and wake. When traveling to a new time zone, our circadian rhythms are slow to adjust. They may remain on their original schedule for several days. This results in our bodies telling us it is time to sleep, when it’s actually the middle of the afternoon, or it makes us want to stay awake when it is late at night. West-to-east trips require one day of recovery for each time zone crossed; east-to-west journeys require one day for each one and a half time zones crossed.
Kleine-Levin syndrome is a rare disorder that causes you to be extremely drowsy off and on. You may sleep up to 20 hours per day. Other symptoms include eating too much, being irritable, feeling disoriented, lacking energy, and being very sensitive to noise. The disorder usually starts in the late teens and is 4 times more common in men than in women. Symptoms may last for days to weeks, disappear, and then come back.
People with narcolepsy have sudden, uncontrollable urges to sleep. They may fall asleep unexpectedly for several minutes to an hour at a time, sometimes while driving. The body relaxes so completely and so suddenly that they may fall to the floor. They awaken refreshed but may fall asleep again in another hour or two.
Nightmares are scary dreams filled with monsters or frightening events. Most people have nightmares occasionally, usually in the early morning hours. Nightmares may be the result of taking certain medicines such as antidepressants, antihistamines, or sleeping pills. They may also be a sign of post-traumatic stress disorder (PTSD) or panic disorder.
Night terrors are fairly common in children, but are unusual in adults. Night terrors usually occur within 2 hours of bedtime and last from 10 to 30 minutes. During a night terror, you may:
be agitated and restless but cannot be awakened or comforted
sit up, possibly screaming or talking wildly
not respond even though your eyes are wide open and staring.
In the morning, you cannot remember what happened. Night terrors are harmless and each episode will end of its own accord in deep sleep.
If you have restless legs syndrome (RLS), you have aching, twitching, tingling, burning, or prickling sensations in the lower leg muscles when you lie in bed or sometimes when you are sitting. Staying asleep is a problem as well. Things like rubbing your legs, getting up and walking around, or taking a hot shower usually offer only temporary relief. The sensations return when you go back to bed. The discomfort and sleeplessness that accompany RLS may distress you and cause depression. RLS is more common in people over 65.
Adults with sleep apnoea repeatedly stop breathing for more than 10 seconds while they sleep. During normal sleep, throat muscles relax. Nasal blockage, a large tongue, or obesity may block your airway. This blockage stops the movement of air and the amount of oxygen in your blood drops. The drop in oxygen causes the brain to send a signal for you to wake up so that you open up the airway in your throat and start breathing again. If you have sleep apnoea, this cycle may repeat as often as 50 or more times an hour. Generally, you will not remember waking up but you may be very sleepy the next day.
Sleep talking is speaking or making sounds while you sleep, usually for no more than 30 seconds. You seldom remember what you said or even that you were talking. Sleep talking is not usually considered a medical problem; however, it can be frustrating if it keeps a bed partner awake.
Somnambulism (Sleepwalking)
Sleepwalking is a tendency to wander during deep sleep. Sleepwalking usually occurs during the second or third hour of night-time sleep. While sleepwalking:
you cannot be awakened no matter what you do
your eyes are open, but staring blankly
you are not as well coordinated as when awake
you may do things such as dressing and undressing, opening and closing doors, or turning lights on and off
Sleepwalking most often occurs in children 4 to 15 years old. It tends to run in families and occurs more often in boys.
Most sleep disorders can be successfully treated or controlled once properly diagnosed.

How to manage dystonia?
Dystonia are sustained involuntary muscle contractions, often distorting body posture. Dystonia can be primary or secondary, and they can be generalized, focal, or segmental. Diagnosis is clinical. Treatment of generalized dystonia is often with a combination of anticholinergic drugs, muscle relaxants, and benzodiazepines. Treatment of focal or segmental dystonia is often with botulinum toxin; more generalized or refractory cases may benefit from surgery.
Dystonia may be primary (idiopathic) or secondary to degenerative or metabolic CNS disorders (eg, Wilson’s disease, Hallervorden-Spatz disease, various lipidoses, multiple sclerosis, cerebral palsy, stroke, brain hypoxia) or drugs (most often phenothiazines, thioxanthenes, butyrophenones, and antiemetics).
Generalized dystonia (dystonia musculorum deformans): This rare dystonia is progressive and characterized by movements that result in sustained, often bizarre postures. It is often hereditary, usually as an autosomal dominant disorder with partial penetrance; asymptomatic siblings of patients often have a forme fruste of the disorder. The causative gene is usually DYT1, causing DYT1 dystonia.
Symptoms usually begin in childhood with inversion and plantar fixation of the foot while walking. The dystonia may affect only the trunk or a leg but sometimes affects the whole body. Patients with the most severe form may become twisted into grotesque fixed postures and ultimately confined to a wheelchair. Symptoms that begin during adulthood usually affect only the face or arms. Mental function is usually preserved.
Focal dystonia: These dystonia’s affect a single body part. They typically start in a person’s 30s or 40s and affect women more often. Initially, spasms may be periodic, occurring randomly or during stress; they are triggered by certain movements of the affected body part and disappear during rest. Over days, weeks, or many years, spasms may progress; they may be triggered by movements of unaffected body parts and may continue during rest. Eventually, the affected body part remains distorted, sometimes in a painful position, resulting in severe disability. Symptoms vary depending on the specific muscles involved.
Occupational dystonia consists of focal dystonic spasms initiated by performing skilled acts (eg, writer’s or typist’s cramp, the yips in golfers).
Spasmodic dystonia consists of a strained, hoarse, or creaky voice due to abnormal involuntary contraction of laryngeal muscles.
Torticollis begins with a pulling sensation followed by sustained torsion and deviation of the head and neck. The cause is often unknown but, in some cases, is probably genetic. In early stages, it can be voluntarily overcome. Patients may discover sensory or tactile tricks that make the spasm stop, such as touching the face on the side contralateral to the deviation. Torticollis can also be caused by dopamine -blocking drugs (eg, haloperidol).
Segmental dystonia: These dystonia affect ≥ 2 contiguous body parts.
Meige’s disease (blepharospasm-oromandibular dystonia) consists of involuntary blinking, jaw grinding, and grimacing, usually beginning in late middle age. It may mimic the buccal-lingual-facial movements of tardive dyskinesia.
Diagnosis
Diagnosis is clinical.
Treatment
For generalized dystonia, anticholinergics, muscle relaxants, or both
For focal dystonia, botulinum toxin Treatment is often unsatisfactory.
For generalized dystonia, a high-dose anticholinergic drug (trihexyphenidyl 2 to 10 mg po tid, benztropine 3 to 15 mg po once/day) is most commonly used, often with a muscle relaxant (usually baclofen), a benzodiazepine (eg, clonazepam), or both. Generalized dystonia that is severe or does not respond to drugs may be treated with deep brain stimulation of the globus pallidus interna, which requires surgery.
For focal or segmental dystonia or for generalized dystonia that severely affects specific body parts, the treatment of choice is purified botulinum toxin type A injected into the affected muscles by an experienced practitioner. Botulinum toxin weakens muscular contractions, but it does not alter the abnormal neural stimulus. Toxin injection is particularly effective for blepharospasm and torticollis. Dosage varies greatly. Treatments must be repeated every 3 to 6 mo.
How to go about managing Somatoform Disorders?

Somatoform Disorders, is a condition that occur when individuals express emotional distress indirectly as physical symptoms even when no physical pathology exists.
Two important conclusions follow:

1. Significant emotional distress is being overlooked
   Individuals will very often seek medical attention for emotional distress not via direct psychiatric complaints but rather indirectly, through somatoform symptoms. ese patients are most often not identified as emotionally distressed, and their underlying suffering goes unidentified, unaddressed, and untreated.
2. Physical symptoms are being unnecessarily treated
   A very significant proportion of individuals seeking primary medical care (about one in every five patients) have physical symptoms that are not caused by general medical conditions. Yet, the majority of those individuals will be diagnosed as suffering primarily physical ailments and receive treatments that are not directed at the cause of the symptoms. ese treatments are often harmless, and in some cases may even indirectly and non-specifically help the individual. But in a significant percentage of cases, these treatments will be wasteful or even harmful. Misdirected therapies may be costly, may cause iatrogenic illness, and will distract proper attention away from the person’s underlying distress.
   What is cognitive therapy?
   Cognitive therapy is a very active and direct type of therapy that works by changing negative thoughts that cause emotional distress. Although there are many kinds of cognitive therapy that go by different names, they all focus on your thoughts and beliefs as a primary cause of your symptoms.
   This type of therapy works well in treating depression, anxiety, and panic disorders.
   What is the theory behind cognitive therapy?
   Experts who study and use cognitive therapy believe that depression is caused by:
   your negative outlook and thoughts about events, the future, and yourself
   negative core beliefs you developed over time and through events in your early life
   For example, your spouse may be mildly upset with you, or your boss may say he wants to see you. If you link self-defeating beliefs with a negative view of reality, you may leap to the conclusion that your spouse no longer loves you or your boss is about to fire you.
   How do your beliefs affect your thoughts?
   If you have the belief that you should be perfect and never make mistakes, you will probably be very critical of yourself, even over the most minor matters. You may tend to blame yourself for everything. You may think you are a failure in everything you do. Even a simple mistake can lead to negative thoughts that leave you feeling hopeless and awful.
   The goal of cognitive therapy is to break this cycle by stopping these negative thinking habits and replacing them with more realistic ones. You and your therapist will work as a team to test the logic of your thoughts. For example, your therapist may help you examine your belief that you should be perfect. Is it reasonable to expect that of yourself? What has been the result of that belief? What is likely to be the result of it in the future?
   What are the steps in cognitive therapy?
   Test your personal beliefs and the way you think about events, yourself, and the future.
   Become familiar with your negative thought patterns so you are aware of them when they occur.
   Do the homework you and your therapist agree on. Cognitive therapy is a team effort.
   Keep the momentum going once you have made changes in your thinking habits. Read books on cognitive therapy. Go in for booster sessions with your therapist.
   Changing negative attitudes and beliefs takes a lot of work but it can be done. Cognitive therapy can change.
   What are types of suicidal behaviours?
   So many different types of behaviours are sometimes referred to as suicide attempts. The lack of clarity and agreement about what to call different types of suicidal behaviours is a problem clinically and in clinical research. But there is a difference between an Actual Attempt, an Interrupted Event, an Aborted Attempt, and Preparatory Acts/Behaviour.
   Suicide attempt
   The Columbia Suicide History Form (Oquendo et al., 2013) did us a valuable service by providing definitions of different behaviours. These definitions are also used in the Columbia – Suicide Severity Rating Scale (C-SSRS) which is now routinely used in antidepressant clinical trials.
   Actual Attempt
   An Actual Attempt is defined as a potentially self-injurious act committed with at least some intent to die (which does not have to be explicit) as a result of act.
   Interrupted Attempt
   If a person intends to start a suicidal behaviour, but someone or something stops the person from STARTING the act, this should be called an Interrupted Attempt. What this means is that if someone or something had not stopped the person, an Actual Attempt would have occurred.
   Note: If the person starts the suicidal act (e.g., takes a single pill in an attempt to overdose), and is then stopped by someone, this should be called an Actual Attempt.
   Here are some examples of what would constitute an Interrupted Attempt:
   – A person opens a bottle of pills and is ready to take them in order to kill herself, but someone comes into the room.
   – A person is standing at the edge of the roof with the intention to jump, but someone grabs him and prevents him from jumping.
   The C-SSRS suggests the following question to ask about Interrupted Attempts:
   Has there been a time when you started to do something to end your life but someone or something stopped you before you actually did anything?
   Some persons who have an Interrupted Attempt are known to take precautions in a subsequent suicide attempt to not be interrupted and die by suicide in that subsequent event.
   Aborted Attempt
   If a person starts a suicidal behaviour, but stops himself or herself before starting to carry out any potentially lethal behaviour, this should be called an Aborted Attempt.
   Preparatory Acts or Behaviour
   These are any acts that are directly in preparation for making a suicide attempt. Acts or preparation towards imminently making a suicide attempt. Examples: buying pills, writing a suicide note, giving one’s belongings away.

What to do in case of suicidal patient?
A health care practitioner who foresees the likelihood of suicide in a patient is, in most jurisdictions, required to inform an empowered agency to intervene. Failure to do so can result in criminal and civil actions. Such patients should not be left alone until they are in a secure environment. They should be transported to a secure environment (often a psychiatric facility) by trained professionals (e.g., ambulance, police), never by family members or friends.
Any suicidal act, regardless of whether it is a gesture or an attempt, must be taken seriously. Every person with a serious self-injury should be evaluated and treated for the physical injury. If an overdose of a potentially lethal drug is confirmed, immediate steps are taken to prevent absorption and expedite excretion, administer any available antidote, and provide supportive treatment
Initial assessment can be done by any health care practitioner trained in the assessment and management of suicidal behaviour. However, all patients require psychiatric assessment as soon as possible. A decision must be made as to whether patients need to be admitted and whether involuntary commitment or restraint is necessary. Patients with a psychotic disorder, delirium, or epilepsy and some with severe depression and an unresolved crisis should be admitted to a psychiatric unit.
After a suicide attempt, the patient may deny any problems because the severe depression that led to the suicidal act may be followed by a short-lived mood elevation. Nonetheless, the risk of later, completed suicide is high unless the patient’s problems are resolved.
Psychiatric assessment identifies some of the problems that contributed to the attempt and helps the physician plan appropriate treatment. It consists of the following:
Establishing rapport
Understanding the suicide attempt, its background, the events preceding it, and the circumstances in which it occurred
Appreciating the current difficulties and problems
Thoroughly understanding personal and family relationships, which are often pertinent to the suicide attempt
Fully assessing the patient’s mental state, with particular emphasis on recognizing depression, anxiety, agitation, panic attacks, severe insomnia, other mental disorders, and alcohol or drug abuse (many of these problems require specific treatment in addition to crisis intervention)
Interviewing close family members and friends
Contacting the family physician
What are self-Harming Behaviours?
What does it mean to self-harm? Self-harm means injuring your body deliberately in a way that leaves marks or causes damage. It may also be called self-injury, self-mutilation, self-inflicted violence, self-destructive behaviour, and self-abuse. Self-harm does not mean that you want to die. You may hurt yourself, even though you want to live. Examples of self-harm include:
• cutting, biting, or scratching yourself until your skin is broken and bleeds
• head banging or hitting yourself hard enough to cause bruises
• burning your skin using heat, chemicals, or cigarettes
• pulling hair from your scalp or eyebrows
• pulling off your fingernails or toenails
• picking at scabs continually until you bleed and the sore does not heal
• putting foreign objects under your skin
• swallowing poisons
Why do people self-harm?
If you deliberately harm yourself, you may be trying to:
• distract you from something that you feel you cannot stand
• express feelings you can’t put into words
• help you feel in control
• make you feel something, instead of feeling numb
• release stress and tension
• relieve guilt or get revenge by punishing yourself
The sense of relief you may get does not last long. The next time you are faced with intense emotions or emotional numbness, you are likely to self-harm again to escape and feel better. If your self-harm, you may be at a higher risk for suicide due to acting on impulse and the danger of certain self-harm behaviours.
How are self-harming behaviours (SHB)treated?
The following can help reduce symptoms:
• medicines, especially for symptoms of anxiety, panic, depression, or obsessive thoughts
• treatment for any alcohol or drug abuse problems
Many cases are Borderline personality disorder and keep doing self-harm repeatedly. May improve with mood stabilizers and or quetiapine.
One type of therapy that may help is dialectical behaviour therapy (DBT). DBT teaches you to manage unbearable situations in a healthy way instead of harming yourself. DBT teaches you how to deal with stress, regulate your feelings, and to validate your feelings. Many mental health centres and therapists provide DBT. Your therapist can help you learn safer, alternative ways to communicate, self-soothe, and cope. Journaling, art therapy, relaxation techniques, and physical exercise may be useful to replace self-harm behaviours.
What is a psychological autopsy and how can it help?
The Psychological Autopsy (PA) has become a best practice post-mortem procedure. Psychological autopsy is an oral examination of a deceased person’s family, friends, colleagues, and acquaintances to determine the deceased person’s state of mind at the time of death and whether suicide can be ruled as the official cause. It is designed to produce critical information that can help identify suicidal risk factors.
What are the signs and symptoms of Parkinson’s disease?
Some people with Parkinson’s will first notice a sense of weakness, difficulty walking, and stiff muscles. Others may notice a tremor of the head or hands. Early symptoms of Parkinson’s disease are usually mild and generally occur gradually.
What are the causes of Parkinson’s disease?
Though it is known that Parkinson’s disease is caused due to the death of dopamine secreting neurons in the brain, the exact cause of this damage is still unknown. It is believed that environment and genetics play a role. Certain medications, toxins and other diseases can produce symptoms, similar to Parkinson’s disease, and then it is known as secondary Parkinsonism, which may be reversible.
What is the difference between Parkinson’s dementia and Alzheimer’s dementia?
Therefore, patients with Parkinson’s who develop dementia may develop Alzheimer’s dementia as well. The main difference between Parkinson’s Disease dementia and Lewy Body dementia is a bit arbitrary. If motor symptoms come first, by at least a year, and dementia develops later, the convention is to call it Parkinson’s Disease dementia.
What are the end stages of Parkinson’s Disease?
There is progressive worsening of symptoms despite of drug therapy. Tremor increases gradually, and in the later stages there may be action tremor. Unsteadiness in walking or turning, resulting in falls, become more pronounced as. Dementia and depression occur in a large number of patients.
What is the treatment of Parkinson’s disease?
Drug which can pass through to the brain and readily get converted to dopamine. Helps in managing Parkinson’s disease.
Levodopa.
Catechol-O-methyltransferase (COMT) inhibitors: Inhibits the action of catechol-O-methyl transferase an enzyme which is involved in degrading neurotransmitters.
Entacapone. Tolcapone. Opicapone. Nitecapone.
Dopamine agonists: Activates dopamine receptors and helps in managing the disease.
Bromocriptine. Pergolide. Pramipexole. Ropinirole
MAO-B inhibitors: Increases the amount of dopamine in the basal ganglia by inhibiting the activity an enzyme that breaks down dopamine.
What procedures can be used in treatment of Parkinson disease?
Deep brain stimulation: Surgical procedure to treat motor symptoms such as stiffness, slowed movement, tremor, rigidity and walking problems.
Carbidopa/Levodopa enteral suspension: The drug is delivered to the small intestine through a tube in the stomach through a keyhole made through surgery.
Thalamotomy: Destruction of a part of the thalamus to help alleviate movement disorders.
Pallidotomy: Pallidotomy is destruction of the globus pallidus, the part of the brain responsible for symptoms of Parkinson’s disease.
What are Indications for EEG in psychiatric practice?
Epilepsy–the propensity for recurrent, unprovoked seizures is a clinical diagnosis made based upon history-taking from the patient, family and/or other observer of suspected events. The physical examination may further support or refute the diagnosis of epilepsy. EEG is not required to make a diagnosis of epilepsy and treatment can and should be initiated without EEG in patients who are experiencing recurrent, unprovoked seizures. Single EEG may be normal in a case of epilepsy.
EEG can differentiate whether a patient has juvenile myoclonic epilepsy which shows generalised spike and wave abnormality or generalised tonic clonic seizures which may or may not show generalized spikes or focal spikes or slow waves. So many of JME patients are mistreated without using valproate in absence of this cheap and reliable investigation
If focal spikes are seen from temporal region it is diagnostic of temporal lobe epilepsy and carbamazepine or phenytoin will give good results.
Frontal intermittent delta activity may be diagnostic of brain tumour as EEG record from frontal region usually has beta activity.
EEG is diagnostic of absence seizure which shows bursts of synchronous and symmetrical spike and wave abnormality. This type of seizure needs ethosuximide or valproic acid.
An urgent EEG is indicated in all unconscious patients suspected of non-convulsive status epilepticus or subclinical seizures. This includes comatose or obtunded inpatients of unclear aetiology especially those in whom seizures preceded the onset of coma.
EEGs obtained after a first unprovoked seizure might offer insights into recurrence risk and/or the need for further neuroimaging. First episode seizure with recurrent E.G. abnormalities must be treated with drugs.
EEG obtained periodically helps the patient’s compliance with medication.
EEG obtained periodically helps the clinician track the epileptic disorder in absence of over seizure especially in JME patients.
In children or adults with epilepsy which fails to respond to standard treatments and/or seizures and progressive neurologic problems, EEG may be warranted but this should be obtained through a neurologic consultation since such a consultation is needed to fully evaluate and assess such patients.
EEG is needed to declare a patient brain dead.
EEG may be recorded while giving ECT under general anaesthesia to prove that a person has had a convulsion as sub convulsive dose is not effective.
Anxiety disorders and depressive disorders all show loss of normal alpha in awake state and a preponderance of beta activity seen all over. Hysterical seizure patients and tension headache patient will show such beta activity which can give an indicator to the diagnosis.
24 Hour EEG monitoring or video EEG or sleep deprived EEG further adds to the yield.
Furthermore, is an inexpensive non-invasive investigation which satisfies the urge of headache patients to get investigated without exposing them to radiation. A sort of placebo investigation in anxiety and headaches of benign treatable causes. Don’t make mistakes. It helps.
What is alcohol withdrawal (AW)?
Alcohol withdrawal is physical symptoms and emotions you have if you drink heavily or frequently and suddenly stop drinking. You are most likely to have withdrawal problems 1 to 7 days after your last drink, or if you drink much less alcohol than you usually drink.
What is the cause of AW?
If you abuse alcohol, you may have withdrawal if:
You decide to stop drinking.
You are in a place where you can’t drink alcohol, such as at a hospital, treatment centre, or jail.
What is the symptoms AW?
The effects of alcohol withdrawal vary greatly. Most people with mild to moderate alcohol dependence have one or more of these symptoms:
Headache, dizziness, nausea and vomiting, shaking, sweating, restlessness, seizures, increased heart rate or blood pressure, trouble sleeping or concentrating, strong desire to drink to relieve the symptoms of withdrawal.
Some people who are dependent on alcohol have a life-threatening condition called delirium tremens (DTs) when they stop drinking alcohol. This is a medical emergency. The symptoms may include: confusion, hallucinations, agitation, seizures, memory problems, fever, very high heart rate and blood pressure.
How is AW investigated?
After a review your symptoms, examination, and memory, one or more of these tests may be done.
urine and blood tests to check for the level of alcohol and other drugs in your body
blood tests to find out how your liver and kidneys are working
X-rays to check for broken bones from a fall or other health problems.
How is AW treated?
If you abuse or are dependent on alcohol, you must first admit that you have a problem. Some people know they have an alcohol problem but deny that they need help to stop drinking. When you can admit that you have problem and admit you need help, call your healthcare provider.
Many people who abuse or are dependent on alcohol have trouble admitting that they have a problem. Others may then have to confront those who abuse or are dependent on alcohol about the need for treatment.
Detoxification is also known as “drying out.” It means that you stop using alcohol completely. Detoxification can be done as an outpatient, or in a hospital or drug treatment facility. Which choice is best for you depends on how much and how long you have been drinking? It also depends on other medical problems that you may have.
Treatment for withdrawal symptoms may include:
Anti-anxiety medicines
Blood pressure medicine
Anticonvulsants
Vitamins
Intravenous (IV) fluids.
Detoxification may take 3 to 4 days.
Long-Term Treatment:
After detoxification, treatment may include social, medical, and psychological therapies.
Social treatment involves family members and focuses on problems at home and at work.
To discourage you from drinking again, your healthcare provider may prescribe medicines. These medicines work best as one part of a full treatment program.
Disulfiram (Antabuse) will make you feel sick if you drink alcohol after you take the medicine. Knowing that you will have this reaction can discourage you from drinking.
Naltrexone (Neltima) or acamprosate (Acamprol) can help stop drinking by reducing the craving for alcohol.
Psychological therapy often involves:
Group therapy to understand alcohol dependence and why people drink.
Strategies to help people learn ways to limit the amount of alcohol they drink.
Cognitive behaviour therapies are helpful for people trying to manage situations and triggers which may tempt them to abuse alcohol.
Self-help support groups such as Alcoholics Anonymous (AA) and Rational Recovery can be helpful. AA looks at alcohol abuse and dependence as a disease. RR looks at alcohol abuse and dependence as a choice. At local chapter meetings you can meet others and get support to help you avoid alcohol. Meetings are open to anyone who has a drinking problem and wants to become and stay sober. Al-Anon meetings can help support families of people who abuse alcohol.
How long will the effects of AW last?
The severe shakes and hallucinations of delirium tremens (DTs) may last 1 to 5 days. Alcohol has long-lasting effects. It can take weeks or months before you feel more clear-headed, less depressed, less anxious, and have more energy. DTs can be fatal if not treated.
What are psychoactive drugs?
Mood-altering drugs—also called psychoactive drugs—are drugs that can change or affect the way a person thinks, feels, or acts. These drugs usually have physical effects as well, but what sets them apart from other drugs is that they work on the mind and the senses. Most of these drugs work on the central nervous system (CNS).
Psychoactive drugs can be classified as
CNS depressants
Opiates
CNS stimulants
hallucinogens
Cannabis
Solvents and inhalants
CNS Depressants
These are drugs that act on the central nervous system, producing feelings of relaxation, and can lead to intoxication. These drugs lower blood pressure, respiration, and heart rate. In large doses, depressant drugs may lower these body functions to the point of death.
Examples of depressants include alcohol (e.g., beer, wine, spirits, coolers), benzodiazepines (minor tranquillizers or sleep medications), barbiturates
Opiates
These drugs were originally derived from the Asian poppy, but many drugs in this class are now produced by the pharmaceutical industry. These drugs are often prescribed by physicians and used under medical supervision to relieve and manage pain. Opiates can produce surges of pleasure followed by stupor. They also produce nausea, constipation, and slow breathing to a point where it may stop. Opiates have high addiction potential and can produce physical dependence at a prescribed dose.
Examples of opiates include morphine, codeine, heroin and various prescription pain relief medications (e.g., OxyContin)
CNS Stimulants
These drugs act on the brain and the body to cause a variety of effects, including increased blood pressure, heart, and respiration rates; raised blood sugar levels; increased energy and alertness; and decreased appetite.
Examples of stimulants include cocaine (including crack), amphetamines (e.g., Benzedrine, speed, crystal met, amphetamine), diet pills, nicotine—tobacco products, caffeine—coffee, tea, chocolate, colas, methylphenidate (Ritalin), Methylenedioxymethamphetamine (MDMA – Ecstasy) ** a stimulant with hallucinogenic properties.
Hallucinogens
Sometimes referred to as “psychedelics,” these drugs act on the brain, intensifying all senses, dramatically affecting perception, and creating disorientation. Hallucinogens raise the heart rate and sensory activity and muddle perceptions of reality.
Examples of hallucinogens include lysergic acid diethylamide (LSD, acid), psilocybin (magic mushrooms), mescaline (peyote),
Cannabis
Cannabis products are considered in a classification of their own because they act like a hallucinogen, but also produce depressant effects. Cannabis effects include relaxation and slowed response time, as well as memory and concentration problems.
Examples of cannabis products include marijuana, hash, hash oil, synthesized THC medicinal product (e.g., Marinol), cannabis-based medicinal product (e.g., Sativex)
Solvents and Inhalants
Solvents and inhalants are found in household and commercial products. They are used by pouring the product into a bag and inhaling. Effects range from effects similar to being intoxicated to serious and unpredictable results such as seizures, convulsions, brain damage, heart failure, and death.
Examples of solvents and inhalants include Gas, paint thinner, aerosols, plastic cement.

What are psychobiotics?
If depression is a downstream collection of symptoms, and inflammation, oxidative stress, and mitochondrial dysfunction are driving these symptoms, what is at the source? It appears, from data in animals and humans, that disruption to our gut ecology may be a major player, and the microbiome has stepped to the forefront of cutting-edge psychiatric research.
Enter psychobiotics: “a live organism that, when ingested in adequate amounts, produces a health benefit in patients suffering from psychiatric illness.” A review by Dinan et al. encompasses the clinical basis for the use of probiotics in mental health with reference to animal studies in which behavioural changes resulted from exposure to bacterial strains such as bifidobacterium and lactobacillus. In placebo-controlled trials in humans, measures of anxiety, chronic fatigue, and depression and anxiety associated with irritable bowel syndrome.
The therapeutic clinical applications of probiotics have been limited to a handful of strains out of the more than 7000 at last count. It appears that colonization is not an expected outcome of probiotic supplementation, and that genomic communication between bacteria and immune receptors may account for anti-inflammatory effects.
What are the investigations in a case of seizures?
After a seizure, symptoms and medical history are reviewed. Several tests to determine the cause of your seizure are done and it is evaluated how likely it is that you’ll have another seizure. Recurrence of seizure is an important point that guides whether treatment is to be continued for long.
Tests may include a neurological exam includes your Behavior, motor abilities and mental function to determine if you have a problem with your brain and nervous system.
Blood sample are done to check for signs of infections, genetic conditions, blood sugar levels or electrolyte imbalances.
If an infection is suspected as the cause of a seizure, you may need to have a sample of cerebrospinal fluid removed for testing.
An electroencephalogram (EEG) is an investigation where electrodes are attached to your scalp with a paste-like substance. The electrodes record the electrical activity of your brain, which shows up as wavy lines on an EEG recording. The wavy lines show alpha activity dominant posteriorly in a normal subject. In a case of epilepsy, either spike or wave are seen or spikes are seen or slow waves are seen, either localized or in a generalized pattern. Spike and wave pattern, or spikes are hard signs of epilepsy while slow waves seen in an awake patient may be considered as a soft sign of epilepsy. The EEG may reveal a pattern that tells whether a seizure is likely to occur again. EEG testing may also help your doctor exclude other conditions that mimic epilepsy as a reason for your seizure. Depending on the details of your seizures, this test may be done as an outpatient in the clinic, overnight at home with an ambulatory device or over a few nights in the hospital.
A CT scan uses X-rays to obtain cross-sectional images of your brain. CT scans can reveal abnormalities in your brain that might cause a seizure, such as tumors, bleeding and cysts.
An MRI scan uses powerful magnets and radio waves to create a detailed view of your brain. Your doctor may be able to detect lesions or abnormalities in your brain that could lead to seizures.
A PET scan uses a small amount of low-dose radioactive material that’s injected into a vein to help visualize active areas of the brain and detect abnormalities.
A SPECT test uses a small amount of low-dose radioactive material that’s injected into a vein to create a detailed, 3-D map of the blood flow activity in your brain that happens during a seizure. Doctors also may conduct a form of a SPECT test called subtraction ictal SPECT co registered to MRI (SISCOM), which may provide even more-detailed results
What is the Treatment is a case of seizure?
Treatment for seizures often involves the use of anti-seizure medications. Several options exist for anti-seizure medications. The goal is to find the medicine that works best for you and that causes the fewest side effects.
The drug of choice is ethosuximide for absences along with valproic acid. Complex partial seizures do well with carbamazepine and phenytoin. Generalised tonic clonic seizures are treated with carbamazepine or sodium valproate. Juvenile myoclonic seizures are well controlled with sodium valproate. Resistant seizures with kindling may need phenobarbitone. Recently levetiracetam and lamotrigine are also coming up. The duration of treatment is three years to life time. Periodic assessments by EEG are mandatory in JME and other seizures like absences.
Rarely used treatment modalism may include Device placement in Vagus nerve stimulation, Deep brain stimulation and surgery.
Not everyone who has one seizure will have another one, and because a seizure can be an isolated incident, your doctor may not decide to start treatment until you’ve had more than one.
The optimal goal in seizure treatment is to find the best possible therapy to stop seizures, with the fewest side effects.
Surgery and other therapies If anti-seizure medications aren’t effective, other treatments may be an option:
Surgery. The goal of surgery is to stop seizures from happening. Surgeons locate and remove the area of your brain where seizures begin. Surgery works best for people who have seizures that always originate in the same place in their brains.
Vagus nerve stimulation. A device implanted underneath the skin of your chest stimulates the Vagus nerve in your neck, sending signals to your brain that inhibit seizures. With Vagus nerve stimulation, you may still need to take medication, but you may be able to lower the dose.
Responsive neurostimulation. During responsive neurostimulation, a device implanted on the surface of your brain or within brain tissue can detect seizure activity and deliver an electrical stimulation to the detected area to stop the seizure.
Deep brain stimulation. Doctors implant electrodes within certain areas of your brain to produce electrical impulses that regulate abnormal brain activity. The electrodes attach to a pacemaker-like device placed under the skin of your chest, which controls the amount of stimulation produced.
Dietary therapy. Following a diet that’s high in fat and low in carbohydrates, known as a ketogenic diet, can improve seizure control. Variations on a high-fat, low-carbohydrate diet, such as the low glycaemic index and modified Atkins diets, though less effective, aren’t as restrictive as the ketogenic diet and may provide benefit.
What is the status of Pregnancy and seizures?
Women who’ve had previous seizures typically are able to have healthy pregnancies. Birth defects related to certain medications can sometimes occur.
In particular, valproic acid — one possible medication for generalized seizures — has been associated with cognitive deficits and neural tube defects, such as spina bifida. The American Academy of Neurology recommends that women avoid using valproic acid during pregnancy because of risks to the baby. Discuss these risks with your doctor. Because of the risk of birth defects and because pregnancy can alter medication levels, preconception planning is particularly important for women who’ve had seizures.
In some cases, it may be appropriate to change the dose of seizure medication before or during pregnancy. Medications may be switched in rare cases.
What about interactions of Contraception and anti-seizure medications?
Some anti-seizure medications can alter the effectiveness of birth control (oral contraceptive) medication.
What should be advise to the patients of epilepsy about Personal safety?
Seizures don’t usually result in serious injury, but if you have recurrent seizures, injury is a possibility. These steps can help you avoid injury during a seizure:
Take care near water. Don’t swim alone or relax in a boat without someone nearby.
Wear a helmet for protection during activities such as bike riding or sports participation.
Take showers instead of baths, unless someone is near you.
Modify your furnishings. Pad sharp corners, buy furniture with rounded edges and choose chairs that have arms to keep you from falling off the chair. Consider carpet with thick padding to protect you if you do fall.
Display seizure first-aid tips in a place where people can easily see them. Include any important phone numbers there, too.
What is Seizure first aid?
It’s helpful to know what to do if you witness someone having a seizure. If you’re at risk of having seizures in the future, pass this information along to family, friends and co-workers so that they know what to do if you have a seizure.
To help someone during a seizure, take these steps:
Carefully roll the person onto one side
Place something soft under his or her head
Loosen tight neckwear
Avoid putting your fingers or other objects in the person’s mouth
Don’t try to restrain someone having a seizure
Clear away dangerous objects, if the person is moving
Stay with the person until medical personnel arrive
Observe the person closely so that you can provide details on what happened
Time the seizure
Stay calm

Why seizures, epileptic or non-epileptic, are seen in psychiatry OPDs?
Convention has it that seizures are seen in psychiatric OPD. Hysterical seizures, or conversion reaction are routinely seen in psychiatric settings. So epileptic patients are also referred to psychiatric OPDs. Beside epilepsy usually does not have a structural basis. In the absence of structural basis, they are therefore clubbed as functional disorders and hence referred to psychiatry. Noteworthy it is that EEG machine was discovered by a psychiatrist. Most psychiatric departments in medical college have an EEG Machine. Also, psychiatric problems such as depression, anxiety, and psychosis especially psychosis like epileptic psychosis are more common among persons with epilepsy than among the general population. Therefore, psychiatrists who help manage these problems can play a very significant role in the treatment of persons with epilepsy.
Are dying patients optimistic?
In the first phase of the study, Gray and his colleagues analysed the blog posts of terminally ill patients with cancer or amyotrophic lateral sclerosis (ALS), which the patients had kept on their own, independent of the study. (They had to have written at least ten posts over a three-month period and died during this time.) Gray compared these posts to blog posts written by healthy people who were asked to imagine that they had been diagnosed with untreatable cancer, and that they had created a blog for which they should write a single entry about the experience.
The results showed that the terminally ill patients’ words were more positive on average than the ones written by the non-patients. For example, one patient wrote: “I may not have much more than a few weeks left on this earth, I’ll be spending it with the people I love — doing the things I’ve missed. Thank you all for everything you’ve given me on the way. All I can say is that despite my current condition, I’ve enjoyed a life with far more than most.”
So, perceptions can be faulty. Poor people are not necessarily sad and dying patients not necessarily pessimistic?
List some famous people with mental illness!
Leonardo da Vinci (1452-1519), Da Vinci was known to have kept complicated journals where he wrote upside-down and backwards. He also had dyslexia. 2. Michelangelo (1475-1564), Known for his incredible art, Michelangelo also suffered from obsessive-compulsive disorder (OCD)., 3. Isaac Newton (1643-1727), The scientist who explained gravity and had the Laws of Motion named after himself, Isaac Newton was known to have suffered from bipolar disorder and possible depression. 4. Beethoven (1770-1827), While Beethoven is well-known for being a deaf composer and coming up with masterpieces such as Fur Elise, he also suffered from bipolar disorder and depression., 5. Edgar Allan Poe (1809-1849), Though this is no surprise, the father of the American short-story suffered from depression and alcoholism. , 6. Abraham Lincoln (1809-1865), The 16th president of the United States suffered from depression and anxiety attacks., 7. Charles Darwin (1809-1882), The creator of the Theory of Evolution suffered from obsessive-compulsive disorder (OCD—-to — 31. Princess Diana, 32Robin Williams – Depression,33. Michael Phelps – ADHD, 34. Ben Affleck – Alcoholism, 35. Jonty Rhodes-seizures etc.
So, you can see that mental disorders do not preclude a person from soaring great hights. In fact, they can sometimes be a boon in disguise.

What is transcranial magnetic stimulation (TCMS)?
Current treatment options for depression, including drugs and brain stimulation procedures such as electroconvulsive therapy (ECT) or transcranial magnetic stimulation (TMS) are effective but some time is needed before their effect kicks in. US researchers have now discovered that low field magnetic stimulation (LFMS) is just as effective and improves symptoms immediately.
Scientists from Harvard University (Boston) and Weill Cornell Medical College (New York) reported in “Biological Psychiatry” that they discovered the properties accidentally while carrying out an imaging study in healthy volunteers. Further analyses led the physicians to the parameters that seemed to cause the antidepressant effects.
“LFMS is unlike any current treatment. It uses magnetic fields that are a fraction of the strength but at higher frequency than the electromagnetic fields used in TMS and ECT,” explained lead author Michael Rohan from Harvard University.
In order to apply the procedure, the researchers developed a portable device, which was tested in a double-blind trial on 63 subjects with depression or bipolar disorders. When the patients received real LFMS, an immediate and substantial improvement in mood was observed compared to the control group. There were no side effects.
Thus, future use of low field magnetic stimulation in the treatment of depression is conceivable
What is artificial intelligence (AI)?
Artificial Intelligence (AI) is increasingly being used in many sectors but its applicability in the medical industry is still in its nascent stages, with several research programmes under way to test the efficacy of machine learning in clinical settings.
How can AI be of use to the healthcare industry?
AI can help fill the gaps when you need to examine a lot of data and there is a shortage of human expertise. Mostly, the problems where AI can be useful are routine and common. Medical imaging is generally a good example since you have large datasets to work with and the information that is gathered is not always uniform.
Do you believe AI can work with specialists to help them arrive at a diagnosis?
Human-computer interaction is an important part of our research. It is about how we communicate the model’s prediction in a way that is understandable to the doctors so that they can make use of that information. The output of an AI model is just one out of many pieces of information a doctor has to synthesise to make a decision for the patient.
In many ways, it is like a thermometer. Before thermometers, someone would just feel your forehead and say you are ‘kind of warm but not sure how warm’. But now you have a tool that tells you a precise reading of temperature. While you still may have to figure out other things, the information gives you a better way of quantitating what’s happening in a disease process in an individual. Similarly, in medical imaging, you don’t make a diagnosis based on the model’s prediction alone but that information can also help you arrive at a decision when presented with other factors.
What was your research programme using machine to detect diabetic retinopathy?
The first version of the model we trained was in partnership with a couple of hospitals in Tamil Nadu and a healthcare provider in the US. The model was as accurate as a general eye doctor. We improved on that and now the models are as accurate as a retina specialist. So, the accuracy level has been fairly high.
A lot of the challenges are more around understanding how to implement a system like this in a real-world setting than training the model itself. If you have the right kind of data and if you get doctors to agree on what the state of disease is, you can train a good model. The question is how you implement that system in a hospital.
Is there a scope for full-scale rollout of these models in the foreseeable future?
Besides regulatory approval, you need to figure out how patients are referred and managed following their screening. Currently, we are working live with an Indian eyecare hospital with a regulatory-approved model that is being used at a smaller scale. However, enrolling these programmes and then carefully rolling them out can take time, maybe to the order of years. It is still early stages, but we are looking forward to talking with our partners in India to see how we can make it work. But there is potential for full-scale implementation in the future.
What is the future in psychiatry?
The CBS News website reports that it is the Défense Advanced Research Projects Agency (DARPA) that is behind the “plans for a cutting-edge technology-based research program to develop a tiny, implanted chip in the skull to treat psychiatric disorders such as anxiety, PTSD and major depression,” with the aim of finding “new, more effective treatment options for veterans and service members with such debilitating conditions.” This project, named the “Systems-Based Neurotechnology for Emerging Therapies (SUBNETS), will study what exactly goes wrong with brain networks in people with certain psychiatric disorders.”

Till hundred years back who could think that mental disorders would be so amenably, treatable. Anti-psychiatry groups still don’t accept the scientific advancements. So, hundred year from now we might see a situation where brain computer interphase is used in education, diagnosis, therapy, treatment, forensic investigation etc.

In the end a Joke-
Welcome to the Psychiatric Hotline.
If you are obsessive-compulsive, please press 1 repeatedly.
If you are co-dependent, please ask someone to press 2.
If you have multiple personalities, please press 3, 4, 5, and 6.
If you are paranoid-delusional, we know who you are and what you want. Just stay on the line so we can trace the call.
If you are schizophrenic, listen carefully and a little voice will tell you which number to press.
If you are depressed, it doesn’t matter which number you press. No one will answer.
If you are delusional and occasionally hallucinate, please be aware that the thing you are holding on the side of your head is alive and about to bite off your ear.