AUTHOR AND EDITOR INFORMATION

Section 1 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

INTRODUCTION

Section 2 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

Background

Aphasia is an acquired disorder of language due to brain damage. Aphasia does not include (1) developmental disorders of language, often called dysphasia in the United States; (2) purely motor speech disorders, limited to articulation of speech via the oral-motor apparatus, referred to as stuttering, dysarthria, and apraxia of speech; or (3) disorders of language that are secondary to primary thought disorders, such as schizophrenia.

Encompassed under the term aphasia are selective, acquired disorders of reading (alexia) or writing (agraphia). Closely related to aphasia are the family of disorders called apraxias (disorders of learned or skilled movements), agnosias (disorders of recognition), acalculias (disorders of calculation ability), and more global neurobehavioral deficits such as dementia and delirium. Such related syndromes may coexist with aphasia or exist independently.

Pathophysiology

Aphasia may occur secondary to brain injury or degeneration and involves the left cerebral hemisphere to a greater extent than the right. Language function lateralizes to the left hemisphere in 96-99% of right-handed people and 60% of left-handed people. Of the remaining left-handed people, about one half have mixed hemisphere language dominance, and about one half have right hemisphere dominance. Left-handed individuals may develop aphasia after a lesion of either hemisphere, but the syndromes from left hemisphere injury may be milder or more selective than those seen in right-handed people. 

Most aphasias and related disorders are due to stroke, head injury, cerebral tumors, or degenerative diseases. The neuroanatomic substrate of language comprehension and production is complex, including auditory input and language decoding in the superior temporal lobe, analysis in the parietal lobe, and expression in the frontal lobe, descending via the corticobulbar tracts to the internal capsule and brainstem, with modulatory effects of the basal ganglia and the cerebellum. Aphasia syndromes have been described, based on patterns of abnormal language expression, repetition, and comprehension. These syndromes have been roughly correlated with specific left hemisphere locations, though there are clearly overlaps and individual differences that make the aphasia syndromes limited in their reliability. Patients may lose the ability to produce speech, to comprehend speech, to repeat, and to hear and read words in many nuanced ways.

Frequency

United States

Data on incidence of aphasia in the United States are limited. Aphasia occurs in a variety of cerebrovascular, traumatic, and degenerative conditions. Stroke is likely the most common cause of aphasia, and it has been estimated that about 20% of stroke patients develop aphasia. More than 700,000 strokes occur in the United States each year, and approximately 170,000 new cases of aphasia every year are related to stroke. The number of patients with language disorders secondary to traumatic brain injury, brain tumors, and other brain lesions such as arteriovenous malformations is not precisely known. Patients with neurodegenerative disorders such as Alzheimer disease and frontotemporal dementia frequently manifest language deficits. The prevalence of Alzheimer disease in the United States is approximately 5 million cases.

Mortality/Morbidity

Aphasia is a condition, not a disease; therefore, it has no attributable mortality rate.

Race

No reliable data exist on the incidence of aphasia in different racial groups. Within disease entities, however, such differences are well known. In stroke, for example, African Americans have almost a 2 times higher incidence as compared with whites. In addition, specific types of stroke, such as cerebral hemorrhage, lacunar infarctions, and intracranial artery stenoses, are known to be more common in blacks than whites. One might therefore surmise that poststroke aphasias would be more common in African Americans.

Sex

Not enough data are available to evaluate differences in the incidence and clinical features of aphasia in men and women. Some studies suggest a lower incidence of aphasia in women because they may have more bilaterality of language function. Differences may also exist in aphasia type, with more women than men developing Wernicke aphasia.

Age

Age may be an important factor in recovery. Some studies suggest that recovery from aphasia due to a stroke is less favorable in patients older than age 70 than in younger patients. However, at any age, recovery of various degrees can occur, even at times remote from the brain injury.

CLINICAL

Section 3 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

History

Because patients with aphasia sometimes cannot provide a complete history, the clinical information obtained about the cause may depend on the acumen of those around the patient. Medical personnel without neurologic training may misdiagnose aphasia as confusion.

Aphasia develops abruptly in patients with a stroke or head injury. Patients with neurodegenerative diseases or mass lesions may develop aphasia insidiously, over weeks, months, or even years. "Neighborhood signs" suggestive of deficits of adjacent cortical areas, or of fiber tracts running near language areas, should be elicited. These signs include difficulties with vision, especially hemianopia; deficits of motor or sensory function; or related neurobehavioral deficits such as alexia, agraphia, acalculia, or apraxia. Patients should be asked about any indications of subtle seizures, such as staring spells or automatisms, or previous aphasic episodes.

A history of headache, acute or chronic, may be important to the diagnosis of underlying conditions such as brain tumors or arteriovenous malformations. The patient should be asked about any history of memory impairment or of difficulty performing activities of daily living at home, because language dysfunction may be part of a more generalized neurodegenerative condition such as dementia (especially Alzheimer disease or frontotemporal dementia). The patient's handedness should be recorded, as should a history of hypertension, previous brain hemorrhage, cardiac disease, carotid or intracranial vascular disease, or amyloid angiopathy.

• Anatomic considerations: Although all of the syndromes described later in this section have clinical and historical validity, they also have numerous limitations.
• • One-to-one mapping of lesions to deficits is often difficult. Many parts of both hemispheres contribute to the production and comprehension of speech. Individual differences also confuse the correlation of structure with function.
  • Patients who have had a stroke may evolve from one type of aphasia to another as they recover. The time of evaluation of the patient is therefore important in the syndrome diagnosis.
  • Patients with large tumors may have mild disease because the lesions grow slowly, allowing adjacent tissues to compensate.
  • In patients with severe congenital abnormalities, symptoms may develop in an anomalous fashion, and they have mild or no aphasia. Factors affecting the severity of findings include handedness, initial severity of the illness, time since onset, etiology, nature of the underlying vascular lesion (if any), and patient's age.
  • Status of the contralateral hemisphere is also important for diagnosis and for estimating prognosis for recovery.
• Aphasia syndromes
• • Many specific aphasic syndromes have been reported. Classic nosology of the perisylvian aphasias includes Broca, Wernicke, conduction, and global aphasias. The nonperisylvian aphasias include anomic, transcortical motor, transcortical sensory, and mixed transcortical, sometimes called the isolation of the speech area syndrome. Other more specific language syndromes include aphemia, alexia with and without agraphia, and pure word deafness. Subcortical aphasia syndromes are defined more by the anatomy of the lesion than by the language characteristics.
  • The syndromes are broad phenotypes that may accompany different types of brain dysfunction, but they are useful because they provide a terminology to permit clinicians to communicate with one another regarding the patient. The presentations of the types of aphasia vary and overlap considerably, but recent studies of both stroke patients and of normal subjects undergoing functional brain imaging have supported the general classification of aphasia syndromes.
  • Of the aphasia types mentioned, the most common and most widely appreciated are the cortical aphasias, including Broca, Wernicke, and conduction aphasias.
  • Specific information should be obtained, including the patient's reading and writing ability, the time frame of symptom onset, any word-finding difficulty, and underlying problems (eg, previous stroke, chronic difficulty with memory).

Physical

Bedside evaluation of language

Careful assessment of language function with an evaluation of neighborhood signs is important in the diagnosis of the localization and cause of aphasia. Neighborhood signs are often, but not invariably, seen; they are specific to the individual aphasic syndromes and are a great help in localization.

Although bedside examination can usually reveal the type of aphasia, formal cognitive testing by a neuropsychologist or speech/language therapist may be important to determine fine levels of dysfunction, to plan therapy, and to assess the patient's potential for recovery. Neuropsychologists and speech/language therapists commonly administer classical language tests, including the Boston Diagnostic Aphasia Examination, the Western Aphasia Battery, the Boston Naming Test, the Token Test, and the Action Naming Test.

This assessment must be broad enough to detect subtle disorders of language in patients in whom aphasia is suspected. Each component of language should be tested individually and thoroughly. Components of bedside language examination include assessments of spontaneous speech, naming, repetition, comprehension, reading, and writing. 

• Spontaneous speech should be assessed for fluency (ease and rapidity of producing words), amount of speech (number of words produced), initiation of speech, the presence of spontaneous paraphasic errors (semantic or phonemic), word-finding pauses, hesitations or circumlocutions, and prosody. Semantic or verbal paraphasias are substitutions of incorrect words (eg, "fork" for "spoon"), whereas phonemic or literal paraphasias are substitution of incorrect sounds or phonemes (eg, "poon" for "spoon"). These aspects of expressive language are helpful in the diagnosis of aphasia. Dysarthria (consistent mispronunciation of phonemes), apraxia of speech (inconsistent phoneme errors, often at the beginning of a word), and abnormalities of prosody (the emotional intonation of speech, often abnormal with right hemisphere disorders) should also be noted.
• Some patients initially perform well during the beginning of an examination, and a deficit becomes apparent only with prolonged testing. Hence, a cursory examination, as in a surgeon's progress note, may be inadequate to detect aphasia.
• Confrontation naming is tested with several items involving objects (ring, pen, watch, glasses, paper clip), object parts (watchband, winding stem, crystal), body parts (thumb, palm of the hand, wrist, elbow), and colors. Some naming disorders are particular to the class of items.
• The letter-fluency task requires the patient to generate words beginning with particular letters—as many as possible in 1 minute. Often the letters F, A, or S are used because good normal values for these letters are available. A similar test is the animal naming test of the Boston Diagnostic Aphasia Examination, in which the patient is asked to produce as many animal names as possible in 1 minute. The result of such tests may be considered a measure of frontal lobe function but not language function; however, the outcome may provide a rough measure of the number of words spoken spontaneously. The production of fewer than 8 words beginning with the letter F in 1 minute, excluding proper names and their derivatives, is abnormal. Abnormality signifies frontal dysfunction, and aphasia may or may not be present. This test result is often abnormal in dementing illnesses.
• In a condition called optic aphasia (originally described by Freud), patients cannot name objects presented visually, especially on cards, but their performance improves when the items are presented as real objects that may be rotated, and they do better still if the items are presented in a tactile modality or if the definition of the object is given. Only with experience can an examiner understand that the production of a name with hesitation or pause is an aphasic error; some patients are adept at compensating for such errors.
• Realistic bedside evaluation might include 6-8 items, including some hard words. The American Academy of Neurology produces cards with the National Institutes of Health (NIH) Stroke Scale that contain pictures illustrating a small number of hard words. The items on the NIH stroke scale are superior to the words on inventories such as the Mini-Mental State Examination (MMSE) for naming, and the test is also extremely easy to administer.
• Anomia can reflect diverse pathologies. A patient with Alzheimer disease may be unable to name an object because he or she has lost semantic information about it and no longer recognizes the object or its use. Patients who have had a stroke may likely have damage of a cognitive subsystem but the remaining aspects of language are preserved. For example, a patient may recognize an object and know exactly what it is and what it is used for, but he or she may be unable to name the object.
• A patient who can point to the object (a real object or a picture of it from among choices) or who can write the name of the object if he or she cannot say it might be said to have an inability to access the lexical form (ie, a retrieval deficit) but not a complete loss of semantic information about the object.
• A patient with optic aphasia cannot name objects presented visually, but he or she can name them in response to the definition or to auditory or tactile cues. Such patients probably have visual agnosia that becomes apparent on language testing.
• Assessment of language production should include oral and written modalities.
• Abnormal repetition is the hallmark of the perisylvian aphasias, the classic aphasias associated with lesions near the sylvian fissure. Perisylvian aphasias include Broca, Wernicke, conduction, and global aphasias.
• Preservation of repetition is a major distinguishing feature in nonperisylvian aphasias, including anomic aphasia, the transcortical aphasias, and some subcortical or thalamic aphasias. Repetition should be tested for simple and complex sentences. 
• Comprehension should be assessed in the oral and written modalities, with both simple and grammatically complex items and with sentences containing at least 2 clauses. Asking patients to perform 1- and 2-part commands is an adequate means to assess comprehension.
• Reading and spelling should be assessed with oral and written productions. Spelling can be assessed with phonologically regular and irregular words. Writing should be assessed for apraxia, writing quality, spelling, grammar, and quantity, as well as for the accuracy of the productions.
• The patient's performance should be interpreted in light of his or her entire mental status examination. The types of errors, such as omission of functor words (eg, a, the) and telegraphic writing or speech (see Broca aphasia below) should be noted. Patients may be unable to read because of nonlinguistic cognitive dysfunction. For example, in neglect dyslexia, which is usually due to a right hemispheric lesion, patients may fail to attend to and read the left side of a word or sentence.
• Silent reading may be more effective than oral reading and can be deduced by means of thorough comprehension tests. This condition is common in patients with conduction aphasia and occasionally occurs in patients with Wernicke aphasia. A surprising observation is that some patients with conduction aphasia have been known to read and understand novels.

Physical findings of aphasias

•  Broca aphasia
• • This aphasia contains a number of distinct components that occur in various combinations. In the complete syndrome, patients present with a nonfluent aphasia. They speak haltingly, without intonation, and have difficulty producing spontaneous speech, naming, and repeating. They may initially be mute, and their articulation may be impaired. Patients are often hypophonic. Comprehension is relatively spared, though it is not normal. Phrases are short and may be telegraphic or agrammatic, including major nouns and verbs but no functor words (articles, adjectives, adverbs, or conjunctions).
  • Patients have telegraphic speech and agrammatism. Naming of actions is typically worse than naming of objects.
  • A writing deficit usually parallels the phonologic deficit.
  • Repetition is abnormal and often consists of omission of functor words. Patients almost always have syntactic and comprehension deficits. Comprehension of passive constructions and of complex syntactic constructions, such as dependent clauses, may be abnormal. Neighborhood signs include buccofacial or limb apraxia and right hemiparesis involving the face and arm more than the leg.
  • Buccofacial apraxia can be tested by asking the patient to pantomime blowing a kiss or blowing out a match. Speech therapists may observe oral apraxia and difficulty swallowing. Limb apraxia may also accompany Broca aphasia, but it is most commonly caused by a large lesion including additional areas in the parietal or frontal lobes. Depression is extremely frequent because patients typically have great awareness of their deficits and patients with left hemispheric involvement may experience a catastrophic reaction.
  • Reading is often more affected than auditory comprehension. Patients may make semantic errors (eg, reading "symphony" when the word is "concert"), which is one of the components of deep dyslexia. Patients may lose the ability to sound out words (they can no longer map graphemes to phonemes) but may be able to read frequent, previously learned, highly imageable words by recognition (they could read "tree" but not "proscription").
  • Typically, the lesions in Broca aphasia are localized to the dorsolateral frontal cortex (the posterior two thirds of the inferior frontal gyrus operculum), though some cases have associated lesions in the anterior parietal cortex and lateral striate and periventricular white matter. Frontal subcortical connections, such as the subcallosal fasciculus, are important for speech initiation and may disrupt thalamofrontocortical connections. Alexander et al argued that the full syndrome would not occur without involvement of the underlying white matter tracts.¹
  • Studies involving functional imaging, including positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) suggest that separate modules within the left inferior frontal gyrus subserve different aspects of speech, including semantic, syntactic, and phonologic functions. Complete Broca aphasia occurs with a large lesion destructive of the whole area, whereas partial syndromes occur with smaller lesions. On the receptive side, comprehension of complex sentences with embedded clauses requires activation of the left frontal cortex of the Broca area.
  • Recovery from Broca aphasia may occur over months and sometimes years. Patients may progress in the nosology of Broca aphasia and may develop anomic aphasia or become normal over time.
  • Broca area aphasia, also called a baby-Broca lesion, occurs with a lesion limited to area 44 (the frontal operculum). This aphasia includes what has been called aphemia, cortical dumbness, anarthria, and subcortical motor aphasia. The condition is also closely tied to what speech/language pathologists call apraxia of speech. This condition affects production of phonemes and may not be a true language disorder or aphasia. Aphemia often improves rapidly. A similar syndrome can occur with a lesion limited to the lower prerolandic fissure. Patients may be mute, or they may express themselves in slow, effortful language with normal or nearly normal language and syntax. Foreign-accent syndrome is a variant of aphemia, involving damage to the motor speech outflow mechanism. Foreign accent syndrome is more of a cortical dysarthria, akin to acquired stuttering, than a true aphasia.
• Wernicke aphasia
• • Patients with Wernicke aphasia have fluent language expression, but the speech sounds empty because it does not convey meaning. There may be fluent phrases without nouns and verbs containing nonexistent word forms (neologisms). The patient's speech and writing may include paraphasic errors with sound substitutions (phonemic paraphasias), word substitutions (semantic paraphasias), hesitations, pauses, and circumlocutions. Grammar is better preserved than it is in Broca aphasia. This abnormal speech output is called paragrammatic, as compared to the agrammatic output of Broca aphasia.
  • Naming and repetition are typically impaired, but the most significant problem is the abnormal language comprehension. Although reading impairment often parallels the auditory comprehension deficit, patients occasionally have preserved oral reading or even reading comprehension. This is important in establishing communication with the patient. Written expression is abnormal; unlike patients with Broca aphasia, these patients can write fluently, but their word choice and spelling are usually very abnormal. In mild Wernicke aphasia, abnormal spelling in written productions may be a clue to the deficit. In acute stroke with Wernicke aphasia, patients may seem confused in addition to their language deficits, and they may even appear psychotic.
  • Patients with Wernicke aphasia are not always aware of their deficits, and over time they may become frustrated that others do not understand them. Some patients become overtly paranoid about their failure to communicate. Patients with Wernicke aphasia may recognize their errors if the mistakes are presented to them offline (eg, on an audio tape).
  • The lesion is variable but usually involves the posterior one-third of the superior temporal gyrus. Involvement of deep temporal white matter, the middle or inferior temporal gyri, or the inferior parietal lobule may predict a lesser degree of recovery. Wernicke aphasia is most typically associated with embolic strokes affecting the inferior division of the middle cerebral artery, supplying the temporal cortex and sparing the frontal, motor cortex. Recovery also depends on the size of the lesion, the amount of the traditional Wernicke area that is destroyed, the age of the patient, and the status of the contralateral hemisphere. Recovery can be complete or the aphasia can progress to conduction or anomic aphasia.
  • Similar or identical lesions can produce different syndromes of aphasia at different points in the disease process. Neighborhood signs should be sought to help in localization. In Wernicke aphasia, neighborhood signs include a superior quadrantanopsia due to involvement of optic radiations, limb apraxia due to involvement of the inferior parietal lobule or its connections to the premotor cortices, finger agnosia, acalculia, or agraphia (components of the Gerstmann syndrome) due to involvement of the angular gyrus. The key neighborhood sign is a negative one; patients with Wernicke aphasia usually have absence of hemiparesis.  
  • Research has debated the category specificity of semantic, naming, and language deficits.² For example, lesions of the fusiform or occipital gyrus may be more likely to cause an inability to name living things or highly imageable words, perhaps due to the proximity to the visual areas. Lesions of the temporal lobes are more likely to affect the naming of tools or inanimate objects, whereas frontal lesions may specifically impair verb naming.
• Conduction aphasia
• • Language output is fluent, though some patients make phonemic errors in speech and pause to correct them, giving the speech a somewhat halting quality. This attempt to correct errors is called conduit d'approche. Naming may or may not be impaired. Repetition impairment is the hallmark of conduction aphasia. Careful studies have shown the ability of patients with aphasia to correct their tape-recorded speech, suggesting an offline ability to monitor output in some cases. Auditory comprehension is typically normal in conduction aphasia. Oral reading and writing abilities are variable. Patients with conduction aphasia may have normal comprehension of written language; cases of patients with conduction aphasia who are able to read novels have been reported.
  • The classic disconnection hypothesis, originally formulated by Wernicke and more recently adopted by Geschwind³, highlights the importance of the arcuate fasciculus connecting the temporal and frontal language cortices, thereby connecting comprehension with speech-output centers. A disconnection between these centers results in the inability to repeat in the setting of intact comprehension and verbal fluency. Other theories of conduction aphasia include a deficit of auditory-verbal short-term (immediate) memory. 
  • The supramarginal gyrus is often affected in conduction aphasia, though disruption of the subcortical connections in the arcuate fasciculus may also be important. Research has implicated the supramarginal gyrus in the decoding of phonemes in receptive language and presumably their translation into oral expression. Recovery is usually good, but residual semantic and phonologic difficulties may remain.
  • Neighborhood signs include superior quadrantanopsia, if the lesion undercuts the parietal lobe, and limb apraxia, which is typically more disabling and less often diagnosed than the aphasia itself. Temporal lobe lesions that do not totally damage the Wernicke area may result in conduction aphasia, and such cases do not have associated apraxia, whereas patients with left parietal lesions often have associated limb apraxia. 
• Global aphasia 
• • In this type of aphasia, the patient has deficits in all aspects of language: spontaneous speech, naming, repetition, auditory comprehension, reading, and writing. The deficits need not be total. They may be due to strokes, tumors, dementia, or other causes.
  • Global aphasia is commonly seen in patients with large infarctions of the left cerebral hemisphere typically involving the occlusion of the internal carotid or middle cerebral artery and resulting in a large, wedge-shaped infarction of the frontal, temporal, parietal, and deep portions of the middle cerebral artery territory. Right hemiplegia (face and arm worse than the leg) is the rule, as is right homonymous hemianopsia. Limb apraxia is common. Some patients have a catastrophic reaction, described by Kurt Goldstein as an emotional meltdown when the patient is asked to perform language tasks; this phenomenon is likely related to depression.
  • Global aphasia rarely occurs with right hemispheric lesions (also called crossed aphasia). About one fifth of left-handed people and 1% of right-handed people have global aphasia after mirror-image lesions of the homologous cortex of the right hemisphere; in this case, left homonymous hemianopsia and left hemiplegia are expected.
  • Global aphasia rarely occurs without hemiparesis. In such cases, dual lesions in the left cerebral hemisphere are expected; these spare the motor areas but affect both anterior and posterior perisylvian language areas. Although multiple strokes could produce such a clinical picture, in practice, the possibility of tumors should be considered with such multiple lesions. In cases of aphasia without hemiparesis, a thalamic lesion should also be considered in the differential diagnosis.
  • Although global aphasia is often considered a devastating injury, gradations of global aphasia exist. Many patients with poststroke global aphasia evolve toward Broca aphasia, or mixed nonfluent aphasia, with improvement in language comprehension over time. Many patients with global aphasia are proficient at making their needs understood without spoken or written speech. Prosody, inflection, pointing, and expressions of approval or disapproval are some of the ways in which patients with global aphasia may communicate successfully.
  • These patients sharply contrast patients with right hemispheric lesions whose language may appear normal, but the nonlinguistic aspect of language expression is lost, including the prosody or emotional aspect of language expression and the ability to understand humor or sarcasm in the speech of others. Patients with such right-hemisphere syndromes are less aware of their deficits than patients with aphasia and may be less responsive to rehabilitation.
  • Factors affecting the prognosis may include the nature of the underlying injury (eg, dementia, tumor, stroke), the age of the patient, area of infarction (if present), the health of the remaining brain, and the availability of rehabilitation services.
  • Recovery in the first 6 months generally outpaces later recovery; however, some patients can recover function years after the initial injury. In one study of patients with global aphasia, more improvement occurred during the second 6 months after the injury than during the first 6 months.
• Pure word deafness 
• • Patients with pure word deafness cannot comprehend spoken language, but they are not deaf. Their verbal output and reading comprehension are said to be intact, but most published cases have shown some degree of fluent, paraphasic speech.
  • The condition can occur because of damage to the superior temporal (Heschl) gyrus bilaterally, but cases have been described with unilateral, left temporal lesions. Disconnection theory proposes that inputs from both Heschl gyri are cut off from input into the left hemisphere Wernicke area where sounds are decoded into language.
  • Pure word deafness should be differentiated from cortical deafness, in which both language and nonlinguistic sounds are affected, and also from auditory nonverbal agnosia. Patients with cortical deafness may appear deaf, but they often have some sparing of pure-tone hearing, especially as recovery occurs. Auditory nonverbal agnosia involves failure of recognition of familiar sounds, such as the moo of a cow or the ringing of a bell. A related disorder is phonagnosia, in which familiar voices are not recognized. All of these cortical auditory deficits (pure word deafness, cortical deafness, auditory nonverbal agnosia, and phonagnosia) usually reflect bilateral temporal lobe lesions.
• Transcortical aphasias 
• • The term transcortical aphasia was originally chosen by Lichtheim to indicate aphasias related not to primary lesions of the language cortex but to connected areas of the association cortex, which he called the area of concepts. By definition, patients with transcortical aphasia can repeat, but they have difficulty naming or producing spontaneous speech or understanding spoken speech. Patients with transcortical motor aphasia can comprehend speech but have diminished speech output and an inability to name items. Sometimes they speak only in single words, after a delay, or in a soft voice. Transcortical motor aphasia involves a deficit in the initiation of speech, reduced phrase length, and abnormal grammar. Mutism may be present initially. Repetition of overlearned phrases may be unimpaired. These patients resemble those with Broca aphasia, except that they can repeat fluently. In some patients, a stroke in the anterior cerebral artery territory is the cause, and leg greater than arm weakness, shoulder greater than hand weakness, and often an involuntary grasp response, are associated findings.
  • In transcortical sensory aphasia, patients can produce fluent speech, but it is often empty and paraphasic. Patients also have a severe deficit in comprehension of speech. Their naming is often abnormal, and they lose semantic associations of speech. In general, they act much like patients with Wernicke aphasia, except they can repeat. This type of aphasia is typically seen in advancing Alzheimer disease and other progressive dementias, but it is also seen occasionally in patients with stroke, typically those with bilateral lesions in the parieto-occipital cortex or a lesion in the left temporo-occipital cortex.
  • Mixed transcortical aphasia, also called the syndrome of isolation of the speech area, involves ability to repeat but not to produce spontaneous speech or comprehend language. Patients may repeat in an echolalic fashion, and they may complete common phrases begun by the examiner. This syndrome resembles global aphasia, except for the preserved repetition.
• Anomic aphasia
• • Patients with anomic aphasia present with fluent speech, intact or mostly intact repetition, intact auditory comprehension, reading, and writing, but an inability to name objects and body parts. Anomic aphasia may follow recovery from another type of aphasia. Anomic aphasia can be an initial presentation of an aphasia syndrome, and it warrants its own aphasia syndrome.
  • Anomic aphasia is less specific in lesion localization than the other syndromes mentioned previously. Anomia may occur with lesions in the dorsolateral frontal cortex, temporal or temporo-occipital cortex, or thalamus. Tumors of the left temporal lobe may present with anomic aphasia. This aphasia type is also the typical language deficit in patients with early Alzheimer disease.
• Subcortical aphasias
• • Broca reported lesions of the deep basal ganglia with cortical lesions in his original autopsy report of his famous patient, Tan-tan. More controversial than that association is whether a basal ganglia lesion by itself can cause aphasia.
  • A series of reports in the early 1980s associated lesions of the head of the caudate nucleus, anterior putamen, and anterior limb of the internal capsule with a nonfluent aphasia syndrome, often with dysarthria and with better repetition and comprehension than typically seen with Broca aphasia.^{4, 5, 6, 7} This syndrome has been called the anterior subcortical aphasia syndrome. When the lesion extends into the temporal isthmus area, subcortical versions of Wernicke and even global aphasia can occur. It should be clear that the diagnosis of subcortical aphasia is based more on the imaging of a subcortical lesion than on the specific language characteristics of the aphasia syndrome. 
  • In some cases, MRIs have revealed cortical lesions in patients with aphasia whose CT scans demonstrated only subcortical lesions. Blood-flow imaging has shown flow abnormalities in the cortex of patients whose MRIs depicted only lesions in the basal ganglia. Such diminished flow may partly reflect cortical ischemia and partly reflect a reduced perfusion of functionally connected areas called diaschisis.
  • Weiller et al examined patients with striatocapsular lesions, some with aphasia or neglect, and some without. On MRI, lesions in both groups were similar. However, patients with aphasia and neglect had low blood flow in the cortex, suggesting that cortical ischemia may also be important in some subcortical aphasias.⁸
•  Thalamic aphasias
• • Thalamic aphasia, like the subcortical aphasia syndromes, is defined by the anatomic documentation of a lesion in the thalamus rather than by the specific language characteristics of the aphasia syndrome. Patients with thalamic aphasia usually present with fluent language disorders, often without hemiparesis. Associated findings include anomia, jargon speech, semantic paraphasic errors, intact repetition, and relatively preserved comprehension. Such patients may also manifest an acute affective syndrome with abulia or severe depression.  
  • Thalamic aphasia was initially described in patients with left thalamic hemorrhage. The first author reported a left-handed patient with a right thalamic hemorrhage, indicating that language dominance extends down to thalamic level. In hemorrhage, of course, the language disorder possibly results from mass effect or pressure on adjacent structures rather than on the specific focus of the hemorrhage. More recent cases of thalamic aphasia secondary to ischemic stroke have solidified the evidence that the thalamus is important to language function. The vascular lesion that affects the anterior thalamus is a small-vessel disease affecting the polar artery of the thalamus. The lesion is easily seen on CT scans or MRIs. Crosson et al argued persuasively for the importance of pulvinar and other posterior structures in language, but their data were based on stimulation rather than lesion ablation.⁹ Pulvinar strokes causing aphasia are exceedingly rare because of the vascular anatomy of the thalamus. In his book, Crosson discusses the possible role of the ventral lateral nucleus in atypical aphasias.
  • Lesions of the white matter between the thalamus and the temporal lobe, the temporal isthmus, or the temporal stalk do occur and may produce aphasia due to deafferentation of the overlying temporal lobe. These aphasias closely resemble Wernicke aphasia.
  • Most strokes causing aphasia occur in the anterior nucleus of the thalamus. In patients with thalamic strokes in the distribution of the paramedian artery, CT scans show butterfly-shaped lesions in the bilateral dorsomedial nuclei (ie, posterior thalamus). Such patients may have amnesia like patients with anterior nuclear lesions, but they usually do not have aphasia.
• Pure alexia without agraphia
• • Pure alexia is known by a variety of names, including alexia without agraphia, posterior alexia, and letter-by-letter alexia. Patients with pure alexia have normal expressive speech, normal naming (except for color anomia [inability to name colors] in some), normal repetition, normal auditory comprehension, and even normal ability to write. Their alexia is a relatively pure deficit. Patients may be able to write a sentence, then be unable to read it. They have no difficulty spelling aloud and no difficulty in recognizing words spelled to them aloud or spelled in tactile fashion on the palm of the hand.
  • Neighborhood signs useful in the diagnosis of pure alexia include a contralateral (right) superior quadrantanopsia or hemianopia and color anomia. The syndrome is almost always associated with a stroke in the territory of the left posterior cerebral artery. The lesion may also involve the splenium of the corpus callosum and the medial temporal lobe. 
  • Dejerine first described this syndrome in 1892.¹⁰ He described a disconnection between the intact right occipital cortex (and intact left visual field) and the left hemisphere language area, such that letter strings seen in the right occipital lobe cannot be decoded into language in the left hemisphere. By the same disconnection mechanism, perceived colors cannot be associated with their color names, the phenomenon called color anomia. The patient can perceive and match the colors themselves, and he or she can also name colors in the abstract (eg, the color of the inside of a watermelon). One problem with the disconnection theory is that many patients with pure alexia can name single letters, and as they improve, they read letter by letter. A competing theory of pure alexia posits a decreased capacity for visual immediate memory or the loss of the ability to perceive a word at a glance.
• Alexia with agraphia
• • Alexia with agraphia is also known as the angular gyrus syndrome and central alexia. It is, in effect, an acquired illiteracy; patients lose their previously acquired reading and writing skills. Most lose spelling and the ability to understand words spelled to them. Many patients have fluent, paraphasic speech, unlike the preserved speech of pure alexia without agraphia, but auditory comprehension is much superior to reading comprehension. The lesion usually involves the angular gyrus area in the left inferior parietal lobule.
  • Closely related to the pure alexia with agraphia syndrome is the Gerstmann syndrome. Gerstmann syndrome refers to the simultaneous occurrence of agraphia, acalculia, right-left confusion, and finger agnosia. Alexia, though not originally a cardinal feature of the Gerstmann syndrome, is often associated.
  • Modern authors such as Benton have questioned the validity of the Gerstmann syndrome.^{11, 12} Some patients may have one or more of the deficits without the others. Stimulation studies in epileptic patients, however, have reproduced combinations of these deficits with stimulation in the angular gyrus area, confirming the association of the key elements of the Gerstmann syndrome.
• Right hemisphere language disorders
• • Right hemisphere contributions to language are numerous, and recent research has led to a better understanding of right hemisphere functions related to communication. The right hemisphere can maintain an extensive vocabulary and read at the word and phrase level. Higher functions of right hemisphere speech, subserved in part by right frontal and temporal lobes, include the comprehension of metaphor, sarcasm, and humor, as well as the emotional prosody of speech, ie, the extralinguistic aspects of human communication. Patients with right hemisphere lesions may understand words but fail to understand the emotional context of a conversation or the facial expressions and tones of voice that convey meaning in normal communication. In addition, they may fail to observe normal turn-taking and other pragmatic aspects of a conversation. In patients with normal speech and language comprehension, these deficits can be disabling in a social context. Patients with right hemisphere lesions may have a problem with discourse and have difficulty stringing together several sentences into a spoken paragraph with a beginning, middle, and end as a storyteller or lecturer would do.

Causes

Aphasia is a symptom and not a disease; it can occur in a variety of types of brain injury and pathology.

• In stroke, the deficit is usually sudden and obvious.
• In substantial head trauma, the deficits may be unrecognized. Exceptions involve hemorrhages or traumatic contusions directly disrupting the left hemisphere language cortex, which may then resemble stroke syndromes.
• Language disorders in dementia take a variety of forms. In dementia, the language problem may be insidious and may require elicitation with the assistance of an experienced physician, speech/language pathologist, or neuropsychologist. Some dementias, such as frontotemporal dementia, primary progressive aphasia, or Pick disease, have aphasia syndromes that closely resemble the aphasic stroke syndromes described above. Both nonfluent, Broca-like syndromes and fluent, Wernicke-like or anomic syndromes have been described. The nonfluent syndromes more commonly represent non-Alzheimer dementias (frontotemporal dementia), whereas fluent aphasias often develop in the course of Alzheimer disease. These usually begin with an anomic pattern, then progress to Wernicke or transcortical aphasia syndromes. In most cases, the associated memory deficits, as well as right hemisphere disorders and frontal dysexecutive syndromes make clear the more widespread nature of the dementing illness.
• In multiple sclerosis and Parkinson disease, no language abnormality is usually present. Dysarthric speech patterns are common in both disorders.
• A rare cause of aphasia in children is the Landau-Kleffner syndrome, a syndrome of acquired epileptic aphasia.
• • Symptoms begin in childhood and progress; electroencephalographic (EEG) findings confirm the diagnosis.
  • The syndrome is treatable; however, in some patients, the seizures are controlled more than the aphasia is.
• Aphasia is diagnosed based on language examination and the localization of a lesion in the left hemisphere or thalamus. Careful mental status and language examination is always important to diagnosis.

DIFFERENTIALS

Section 4 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

Other Problems to be Considered

Developmental disorder
Encephalopathy/delirium
Locked-in state (due to central pontine myelinolysis)
Mutism
Psychiatric disease

WORKUP

Section 5 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

Lab Studies

• The diagnosis of aphasia is based on physical examination and detailed mental state examination.
• Aphasia is a sign as much as it is a clinical problem. Therefore, the laboratory tests required depend on the underlying pathophysiology.

Imaging Studies

• Neuroimaging is required to localize and diagnose the cause of aphasia. CT scanning and MRI are the mainstays of neuroimaging.
• CT effectively demonstrates acute bleeds and most strokes older than 48 hours; however, it may miss strokes less than 48 hours old.
• MRI with diffusion-weighted imaging detects strokes as early as an hour after onset. New imaging sequences such as the T2* or gradient echo imaging are sensitive to detection of hemorrhage, an early limitation of MRI technology. 
• Contrast enhancement may be required to demonstrate tumors by both CT and MRI.
• Thin sections through the temporal lobes can demonstrate hippocampal atrophy or sclerosis, which are common in epilepsy and dementia. Coronal imaging on MRI is especially helpful in the detection of asymmetric hippocampal atrophy.
• At a time when gross atrophy of the tissue is hard to detect, PET and SPECT may be helpful in detecting hypometabolism or reduced cerebral blood flow, respectively, in dementing illnesses. These techniques are also useful in localization of epileptic foci.
• Functional MRI is increasingly being used in the study of normal activation of language structures in normal subjects. Early research is also aimed at discovering the patterns of recovery after neurologic injury such as a stroke with aphasia.

Other Tests

• EEG is important in patients with suspected seizures.
• Neuropsychological testing and speech therapy evaluation are helpful for guiding therapy for aphasia.

TREATMENT

Section 6 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

Medical Care

The treatment of a patient with aphasia depends on the cause of the aphasia syndrome. Acute stroke treatment for the aphasic patient may help alleviate the deficit. Surgery for a subdural hematoma or brain tumor may be beneficial. In infections such as Herpes simplex encephalitis, antiviral therapy may help the patient recover.

Speech and language therapy is the mainstay of care for patients with aphasia. The timing and nature of the interventions for aphasia vary widely. Blinded studies are limited, and recovery of some degree is the norm, but several studies have indicated that speech and language therapy does improve clinical outcomes in patients with aphasia. Patients' difficulties vary, and individualized programs are often important. 

• Psychological support is important. Careful diagnosis and help with the difficulties found in patients with aphasia are of value.
• Special techniques exist to treat patients with articulatory problems, agrammatism, lack of syntax, and lack of intonation ability. In general, experts agree on the importance of speech therapy in aphasia.
• Medical treatment of aphasia is considered experimental; dopaminergic, cholinergic, and stimulant drugs have been tried, but no clear benefit has been shown in large trials.
• Small-scale clinical trials of treatments for aphasia have been reviewed. Of great interest is whether the combination of medical therapy and speech therapy is of greater benefit than that of speech therapy alone.

Consultations

• Speech and language therapist
• Neuropsychologist

FOLLOW-UP

Section 7 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

Prognosis

• The prognosis for life in a patient with aphasia depends on the cause of the aphasia. A left hemisphere glioblastoma may be associated with a very short life expectancy, whereas a minor stroke may have an excellent prognosis. It is the underlying pathology, not the aphasia itself, that determines prognosis. 
• The prognosis for language recovery varies depending on the size and nature of the lesion and the age and overall health of the patient.
• • In general, patients with preserved receptive language functions are better candidates for rehabilitation than are those with impaired comprehension.
  • The potential for functional recovery from primarily expressive aphasia (ie, Broca aphasia) after a stroke is excellent.
  • The potential for recovery from a Wernicke-type aphasia due to a stroke is not as good as that for Broca aphasia.
  • The potential for recovery from aphasia due to an untreatable tumor or neurodegenerative disease is poor.

Patient Education

• Family members may benefit from education regarding language impairment to care for affected patients.
• The National Aphasia Association provides a variety of educational materials.

REFERENCES

Section 8 of 8

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

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Article Last Updated: Feb 5, 2008