Aphasia is language dysfunction that may involve impaired comprehension or expression of words or nonverbal equivalents of words. It results from dysfunction of the language centers in the cerebral cortex and basal ganglia or of the white matter pathways that connect them. Diagnosis is clinical, often including neuropsychologic testing, with brain imaging (CT, MRI) to identify cause. Prognosis depends on the cause and extent of damage and on patient age. There is no specific treatment, but speech therapy may promote recovery.

Language function resides predominantly in the following:

Posterosuperior temporal lobe, which contains Wernicke’s area

Adjacent inferior parietal lobe

Posteroinferior part of the frontal lobe just anterior to the motor cortex, which contains Broca’s area

Subcortical connection between those regions—usually in the left hemisphere, even in left-handed people

Damage to any part of this roughly triangular area (eg, by infarct, tumor, trauma, or degeneration) interferes with some aspect of language function. Prosody (quality of rhythm and emphasis that adds meaning to speech) is usually influenced by both hemispheres but is sometimes affected by dysfunction of the nondominant hemisphere alone.

Aphasia is distinct from developmental disorders of language and from dysfunction of the motor pathways and muscles that produce speech (dysarthria). It is broadly divided into receptive and expressive aphasia.

Receptive (sensory, fluent, or Wernicke’s) aphasia: Patients cannot comprehend words or recognize auditory, visual, or tactile symbols. It is caused by a disorder of the posterosuperior temporal gyrus of the language-dominant hemisphere (Wernicke’s area). Often, alexia (loss of the ability to read words) is also present.

Expressive (motor, nonfluent, or Broca’s) aphasia: The ability to create words is impaired, but comprehension and ability to conceptualize are relatively preserved. It is due to a disorder that affects the dominant left frontal or frontoparietal area, including Broca’s area. It often causes agraphia (loss of the ability to write) and impairs oral reading.

There are other types of aphasia (see Table 1: Function and Dysfunction of the Cerebral Lobes: Types of Aphasia), which may overlap considerably. No aphasia classification system is ideal. Describing the types of deficits is often the most precise way to describe a particular aphasia.

Table 1

Types of Aphasia

Location of Causative Lesion*
Common Causes
Speech Pattern

Lesion (usually small) anywhere in the left-hemisphere language areas
Various disorders
Anomia in oral language (leading to empty, circumlocutory, paraphasic speech) and in written language, fluent speech, good auditory and reading comprehension, normal repetition

Broca’s (nonfluent, expressive, motor)
Large lesion in the left frontal or frontoparietal area, including Broca’s area



Anomia in oral and written language, nonfluent speech (with slow, effortful production, short phrase length, impaired prosody, and reduced use of prepositions and conjunctions), good comprehension, impaired repetition, impaired writing (agraphia)

Wernicke’s (fluent, receptive, sensory)
Large lesion in the left temporoparietal area, including Wernicke’s area

Anomia in oral and written language, fluent speech (with paraphasias, a variety of grammatical forms, but often conveying little meaning), poor auditory and written comprehension, impaired repetition, errors in reading (alexia), agraphia

Subcortical lesion in the left hemisphere, often under the superior temporal gyrus or under the inferior parietal lobe


Anomia (with prominent paraphasias), otherwise fluent speech, good comprehension, impaired repetition (with frequent paraphasias), good reading comprehension

Writing unaffected

Large lesion in the left frontotemporoparietal area, including Broca’s and Wernicke’s areas



Severe anomia in oral and written language, nonfluent speech (often with sparse output), poor comprehension, impaired repetition, alexia, agraphia

Transcortical motor
Lesion in the left frontal area, excluding Broca’s and Wernicke’s areas




Similar to Broca’s aphasia except with normal repetition

Articulation often unaffected

Transcortical sensory
Lesion in the temporoparietal area, excluding Broca’s and Wernicke’s areas




Similar to Wernicke’s aphasia, except with normal repetition
*Causative lesion is in the language-dominant (usually left) hemisphere.

Symptoms and Signs

Wernicke’s aphasia: Patients speak normal words fluently, often including meaningless phonemes, but do not know their meaning or relationships. The result is a jumble of words or “word salad.” Patients are typically unaware that their speech is incomprehensible to others. A right visual field cut commonly accompanies Wernicke’s aphasia because the visual pathway is near the affected area.

Broca’s aphasia: Patients can comprehend and conceptualize relatively well, but their ability to form words is impaired. Usually, the impairment affects speech production and writing (agraphia, dysgraphia), greatly frustrating patients’ attempts to communicate. Broca’s aphasia may include anomia (inability to name objects) and impaired prosody.


Exclusion of other communication problems

Bedside and neuropsychologic testing

Brain imaging

Verbal interaction can typically identify gross aphasias. However, the clinician should try to differentiate aphasias from communication problems that stem from severe dysarthria, impaired hearing, vision (eg, when assessing reading), or motor writing ability.

Initially, Wernicke’s aphasia may be mistaken for delirium. However, Wernicke’s aphasia is a pure language disturbance without other features of delirium (eg, fluctuating level of consciousness, hallucinations, inattention).

Testing to identify specific deficits should include assessment of the following:

Spontaneous speech: Speech is assessed for fluency, number of words spoken, ability to initiate speech, presence of spontaneous errors, word-finding pauses, hesitations, and prosody.

Naming: Patients are asked to name objects. Those who have difficulty naming often use circumlocutions (eg, “what you use to tell time” for “clock”).

Repetition: Patients are asked to repeat grammatically complex phrases (eg, “no ifs, ands, or buts”).

Comprehension: Patients are asked to point to objects named by the clinician, carry out one-step and multistep commands, and answer simple and complex yes-or-no questions.

Reading and writing: Patients are asked to write spontaneously and to read aloud. Reading comprehension, spelling, and writing in response to dictation are assessed.

Formal cognitive testing by a neuropsychologist or speech and language therapist may detect finer levels of dysfunction and assist in planning treatment and assessing potential for recovery. Various formal tests for diagnosing aphasia (eg, Boston Diagnostic Aphasia Examination, Western Aphasia Battery, Boston Naming Test, Token Test, Action Naming Test) are available.

Brain imaging (eg, CT, MRI; with or without angiographic protocols) is required to characterize the lesion (eg, infarct, hemorrhage, mass). Further tests are done to determine the etiology of the lesion (eg, stroke, seizure disorder) as indicated (see Stroke (CVA): Diagnosis and see Seizure Disorders: Diagnosis ).


Recovery is influenced by cause, size and location of lesions, extent of language impairment, and, to a lesser degree, the age, education, and general health of the patient. Children < 8 yr often regain language function after severe damage to either hemisphere. After that age, most recovery occurs within the first 3 mo, but improvement continues to a variable degree up to a year.


Speech therapy

Augmentative communication devices

Effectiveness of treatment is unclear, but most clinicians think that treatment by qualified speech therapists helps and that patients treated soon after onset improve the most. Patients who cannot recover basic language skills and caregivers of such patients are sometimes able to convey messages with augmentative communication devices (eg, a book or communication

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