Dementia

Dr. Prithika Chary discusses how simple investigations can be used to make a differential diagnosis of dementia and with the help of two cases explains the approach taken to diagnose and treat such patients.

The DSM – IV criteria for definition of the dementia syndrome are multiple cognitive deficits, including memory impairment and at least one of the following :

Aphasia – problems with both expressive and receptive language

Apraxia – inability to carry our purposeful movements even though there is no motor or sensory impairment

Agnosia – failure to recognise, especially people

Decreased need for sleep

Additionally the cognitive deficits are severe enough to interfere with occupational and/or social functioning, and represent decline from previously higher function.

Neurodegenerative dementias

These are the commonest types of primary dementia and include Alzhiemers Disease, Lewy body dementia, Parkinson’s disease dementia, frontotemporal dementias and prion diseases. Most of them are protienopathies where an accumulation of misfolded proteins leads to neuronal loss, neuroinflammation and glial reaction.

Vascular dementia

This is due to microcirculation disturbances and is often included with the primary dementias. Evaluation of these patients involve several clinical tests of cognitive function and laboratory and neuroimaging studies to further confirm diagnosis. An important goal is to identify the few dementias which are treatable.

These include:

Hypothyroidism

Hypercalcaemia

Hypoglycaemia

Nutritional deficiencies of vitamin B12 and folic acid

Kidney and liver disorders

Infections including HIV and Neurosyphilis

Investigations indicated are:

The MMSE ( MiniMentalStateExamination) is used as a screening tool but has a cultural bias and may not work in all communities

There are a number of rating scales and they measure various domains of function- Cognitive, Functional, Staging of Dementia, Behavioural, Global

Laboratory investigations include:

Thyroid profile

Renal profile

Liver function tests

Lipid profile

B12 and folic acid levels

Serum calcium, Vitamin D3

HIV and VDRL

Advanced investigations include:

1 Complete neurological examination

2 Detailed neuropsychological evaluation

3 Screening for neuropsychiatric comorbidities like depression, anxiety

4 ApoE 4 levels if available

5 EEG, Lumbar puncture are useful to exclude dementia due to Jakob Creutzfeldt disease

6 MRI + MRA of the brain helps diagnose vascular dementia, Alzhiemers dementia, Frontotemporal dementia, and other causes of cognitive dysfunction like Normal Pressure Hydrocephalus, Chronic subdural haematoma, Slow growing brain tumours like Meningiomas, etc

7 The FDG PET scan of the brain can be diagnostic with specific deficits in Alzhiemers disease and helps confirm the diagnosis. In comparison with CT, MRI and SPECT, PET is expensive, seldom accessible and time consuming. Consequently, PET is not routinely used in the diagnostic workup for Alzheimer’s disease (AD). However, PET images may provide useful differential diagnostic information, such as parietal lobe changes in AD, when CT and MRI scans fail to provide sufficient information.

Case vignettes

Case one

A 70-year old college-educated female, bank employee complains of progressive short term memory loss over the past 2 years. Neurological physical examination normal. Routine laboratory investigations show hypothyroidism (under treatment) and dyslipidaemia, but is otherwise normal.

MMSE 28/30, detailed neuropsychological examination mild memory impairments

Clock face drawing and animal naming (15) were normal

Neuroimaging not contributory

Does she have Dementia? If yes, what stage? If no, why do you say so? What is the diagnosis? What will be your plan for follow up?

Answer: She has MCI or mild cognitive impairment

MCI can be considered to be early dementia and can progress to Alzhiemers disease especially in the presence of additional risk factors like smoking, head injury, social isolation, age and genetics.

She will need periodic followup once in 6-12 months with neuropsychological testing to observe progressive cognitive decline which may necessitate interventions to slow the progression of dementia. This includes diet, exercise, risk factor modification of hypertension, use of supplements, and cognitive interventions. Symptom modification with cholinesterase inhibitors and memantine and management of neuropsychiatric comorbidity is present is indicated if the deterioration in cognitive function is significant.

Case two

An 80-year old female, retired school teacher, living alone complains of poor appetite, lack of interest in performing daily tasks, is poorly groomed, hypertensive (well controlled) on amlodipine and statins and aspirin is brought with complaints of loss of weight, paranoia and intermittent mental confusion.

MMSE 24/30, Poorly groomed, poor hygiene, apathetic, motor and verbal sluggishness, no neurological lateralising deficit

Labs, MRI normal

Cognitive and neuropsychological evaluation shows depression and moderate memory impairment

No language deficit though spontaneous speech output is low

Clock face drawing – disinterested and uncooperative; animal naming needed to be coaxed but names 10

What is your diagnosis? How will you manage this patient?

Answer: This is pseudodementia due to loneliness and depression

Memory impairments without definite cognitive decline with disinterest in environment and grooming and personal ADL occurs frequently in depression. Treatment of depression- improving social interactions and providing help for ADL improved her to being more verbal, well groomed, alert and oriented

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