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Aphasia Clinical Presentation

  • Author: Howard S Kirshner, MD; Chief Editor: Jasvinder Chawla, MD, MBA  more...
 
Updated: Feb 19, 2016
 

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 and the history provided by family members. 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. Rarely, aphasia is caused by herpes simplex encephalitis, a treatable condition but one that offers only a short window for diagnosis. Clues to the diagnosis include a history of fever, seizures, headache, and behavior changes.

A history of headache, acute or chronic, may also 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 (a cause of lobar intracerebral hemorrhage in older patients).

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 slowly growing tumors may have mild disease because the lesions grow slowly, allowing adjacent tissues to compensate for functional deficits.

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. Patients with severe, left hemisphere injury at a young age may have no residual language deficits.

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 and the localizations of specific language functions.

Of the aphasia types mentioned, the most common and most widely appreciated are the cortical aphasias, including Broca, Wernicke, conduction, and global 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).

Next

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 language testing batteries, 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. For example, patients with Broca aphasia and frontal lobe lesions often have more problems with verb naming, and those with temporal lobe lesions and Wernicke or anomic aphasia have more difficulty with noun naming.[3]

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 in adult native English speakers. Abnormality signifies frontal dysfunction, and aphasia may or may not be present. This test result is often abnormal in dementing illnesses or among patients with frontal dysfunction of any etiology. Category fluency such as animal or fruit naming in one minute also has well-established normal values and is less precisely a measure of frontal lobe function than is letter fluency.

For some rare syndromes, patients should be tested with objects presented both in the visual and tactile modalities. 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 palpated, or if the definition of the object is given.

Complete assessment of language production should include oral and written modalities. 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.

Assessment should indicate repetition testing. 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.

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 should always be assessed as part of language examination. Patients with alexia with agraphia and alexia without agraphia have different anatomic lesions, the former associated with left parietal lesions, the latter with left occipital lesions, usually a stroke in the left posterior cerebral artery territory. Spelling aloud, writing, and spelling words aloud to the patient are all preserved in patients with alexia without agraphia, but not in alexia with agraphia.

Assessing a patient with phonologically regular but complex words (eg, "furniture") and irregular words (eg, "yacht") can be useful to determine if a preexisting dyslexia is present, and, occasionally, whether or not an unusual aphasia syndrome (deep vs surface alexia) is present.

Writing should be assessed for quality, spelling, grammar, and quantity, as well as for the accuracy of the productions. In addition, patients should be tested for apraxia. Apraxia refers to the inability to understand or use tools (such as a pencil or pen) correctly in the absence of a primary motor deficit, and can occur in patients with or without aphasia. Thus, apractic agraphia should be differentiated from aphasic agraphia.

The patient's performance should be interpreted in light of the 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 or write the left side of a word or sentence.

Silent reading may be more effective than oral reading and can be deduced by means of comprehension tests. This condition is common in patients with conduction aphasia and occasionally occurs in patients with Wernicke aphasia.

Physical findings of aphasias

Broca aphasia

This aphasia syndrome 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, also called 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, often 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 are typically aware of their deficits; in extreme form, this is associated with a complete withdrawal, termed by Kurt Goldstein the catastrophic reaction.

Reading is often more affected than auditory comprehension. Patients may make semantic errors (eg, reading "symphony" when the word is "concert"), 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.[4]

Kreisler et al have attempted to relate specific components of the common aphasia syndromes with neurologic localization. The authors investigated 107 patients with a standard aphasia battery and looked at 69 predetermined areas of interest. They found an analysis to identify 67-94% of patients. They found the following:[5]

  • Nonfluent aphasias depended on frontal or putamenal lesions (mutism, low fluency).
  • Repetition depended on insula-external capsule lesions and posterior internal capsule rather than the classically described arcuate fasciculus.
  • Comprehension depended on posterior lesions of the temporal gyri or inferior frontal gyrus.
  • Phonemic paraphasias depend on external capsule lesions extending to the posterior temporal lobe or internal capsule.
  • Verbal paraphasias depended upon temporal or caudate lesions.
  • Perseveration depended upon caudate lesions.

Note that these localizations largely confirm teachings about aphasia that have been in circulation since the writings of Broca and Wernicke, and others, in the 19th century.

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 syndrome occurs with a large lesion destructive of the whole area, whereas partial syndromes occur with smaller lesions. In fact, patients with large left perisylvian lesions often have global aphasia in the early days and weeks after their strokes, and they slowly evolve into Broca aphasia. Patients with isolated Broca area lesions may have Broca aphasia on the first day of their stroke. On the receptive side, comprehension of complex sentences with embedded clauses requires activation of the left frontal cortex of the Broca area, and this task is usually deficient in patients with Broca aphasia.

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, especially multiconsonant words, and may not represent 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 productions, 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 their speech sounds empty and 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.

In studies by Naeser and colleagues[6] , destruction of Wernicke area predicted lasting loss of comprehension, and recent, acute studies by Hillis and colleagues[7] have found single word comprehension deficits to correlate with hypoperfusion of Wernicke area. 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 no hemiparesis.

Research has debated the category specificity of semantic, naming, and language deficits.[8] 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

This classical aphasia type is less common than Broca, Wernicke, or global 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 Geschwind,[9] highlights the importance of the arcuate fasciculus connecting the temporal and frontal language cortices, thereby connecting comprehension with speech-output centers. By this theory, 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 or “inner speech.”

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. Kreisler et al, in the work cited, could not confirm the roles of the arcuate fasciculus or supramarginal gyrus as classically described.[5]

Neighborhood signs in conduction aphasia 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. Global aphasia may result from 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.

Patients with large, left hemisphere lesions and global aphasia are vastly different from patients with large, 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 to primary lesions not involving the language cortex but rather 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 may be relatively unimpaired, distinguishing these patients from those with Broca aphasia who cannot repeat fluently. In some patients, a stroke in the anterior cerebral artery territory is the cause; 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, which used computed tomography (CT) as the primary neuroimaging modality, 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.[10, 11, 12, 13] 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. 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. Weiller also found that among patients with identical vascular syndromes, those who had strokes due to atrial fibrillation typically had aphasia and neglect, whereas those who had strokes due to large vessel stenosis did not. They attributed the finding to the ability of patients with chronic low flow due to large vessel stenosis to develop collaterals, whereas those with a sudden occlusion due to an embolus could not do so.[14]

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 or tuberothalamic artery of the thalamus. The lesion is easily seen on CT scans or MRIs. Lesions in the anterior thalamus also affect memory. 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.[15]

Pulvinar strokes causing aphasia are exceedingly rare because of the vascular anatomy of the thalamus. Lesions of the paramedian thalamus (thalamoperforating artery), especially if bilateral (some patients have a single artery, sometimes called the artery of Percheron, supplying both sides), cause deficits in memory and language. In his book , Crosson discusses the possible role of the ventral lateral nucleus in atypical aphasias, but usually this vascular territory (inferolateral arteries) involves a pure sensory stroke, while the posterior choroidal artery territory mainly involves the lateral geniculate body, causing an isolated hemianopia.

Lesions of the white matter between the thalamus and the temporal lobe, the temporal isthmus, or temporal stalk may produce aphasia due to deafferentation of the overlying temporal lobe. These aphasias closely resemble Wernicke aphasia. As mentioned above, however, the cases reported have not entirely excluded cortical involvement or hypometabolism as a cause of the syndrome.

Pure alexia without agraphia

Pure alexia is known by a variety of names, including alexia without agraphia, posterior alexia, and literal or letter-by-letter alexia. Patients with pure alexia have normal expressive speech, normal naming (except in some cases for color anomia or inability to name colors), 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. Patients may be able to read individual letters, then laboriously piece them together and say the words (letter-by-letter alexia).

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, postulating a disconnection between the right occipital cortex (and intact left visual field) and the left hemisphere language area, such that visual information cannot be decoded into language in the left hemisphere.[16] Later contributors recognized that the posterior left hemisphere has a word-form recognition area that, if damaged, prevents patients from reading words at a glance, as normal readers do. Nearly a century later, Geschwind[9] and then Damasio[10] refined the disconnection hypothesis of pure alexia. Cognitive neuropsychologists and behavioral neurologists have recognized the concept of damage to the orthographic recognition areas in the left occipital lobe.

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. This syndrome was also described by Dejerine.

Closely related to the pure alexia with agraphia syndrome is the Gerstmann syndrome. Gerstmann brought together the 4 deficits of agraphia, acalculia, right-left confusion, and finger agnosia and associated them with lesions of the dominant parietal lobe. 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.[17, 18] 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.

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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 aphasic syndromes that closely resemble the aphasic stroke syndromes described above, except that they begin gradually and progressively worsen. If aphasia is the sole deficit over a 2-year period, the term primary progressive aphasia can be used, though many of these patients develop other cognitive deficits over time.

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, primary progressive nonfluent aphasia), whereas fluent aphasias often develop in the course of Alzheimer disease. A variant is semantic dementia, in which the patient not only cannot name items, but the very meaning of words is lost. These patients cannot define common words. Most fluent cases of primary progressive aphasia 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.[19]

In multiple sclerosis and Parkinson disease, no language abnormality is usually present, though patients with Parkinson disease can develop language deficits along with dementia. The disease corticobasal degeneration often involves a nonfluent aphasia, sometimes meeting criteria for primary progressive aphasia before the motor deficits of limb apraxia and Parkinsonism begin. Dysarthric speech patterns are common in both multiple sclerosis and Parkinson disease.

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.

A rare but important condition not to overlook is herpes simplex encephalitis. The aphasia in herpes simplex encephalitis may mimic Wernicke aphasia mimicking a stroke deficit, but often with associated confusion. The disease usually resents with confusion, fever, headache, and seizures. Over time, the MRI usually shows a classic insula-sparing lesion, involving one or both temporal lobes. Early treatment with antiviral agents is crucial to prevent further injury until the diagnosis can be confirmed, usually by PCR testing of spinal fluid.

Aphasia is diagnosed based on language examination and the localization of a lesion in the left hemisphere. Careful mental status and language examination is always important to diagnosis.

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Contributor Information and Disclosures
Author

Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Neurological Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Jasvinder Chawla, MD, MBA Chief of Neurology, Hines Veterans Affairs Hospital; Professor of Neurology, Loyola University Medical Center

Jasvinder Chawla, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Joseph Quinn, MD, MD Assistant Professor, Department of Neurology, Portland VA Medical Center, Oregon Health Sciences University

Joseph Quinn, MD, MD is a member of the following medical societies: American Academy of Neurology, Society for Neuroscience, Society for Pediatric Radiology

Disclosure: Nothing to disclose.

References
  1. Reuters Health. Verbal training during rTMS may improve chronic aphasia. Medscape Medical News. November 25, 2014. [Full Text].

  2. Wang CP, Hsieh CY, Tsai PY, Wang CT, Lin FG, Chan RC. Efficacy of synchronous verbal training during repetitive transcranial magnetic stimulation in patients with chronic aphasia. Stroke. 2014 Dec. 45(12):3656-62. [Medline].

  3. Conroy P, Scowcroft J. Decreasing cues for a dynamic list of noun and verb naming targets: A case-series aphasia therapy study. Neuropsychol Rehabil. 2012 Jan 16. [Medline].

  4. Alexander MP, Naeser MA, Palumbo C. Broca's area aphasias: aphasia after lesions including the frontal operculum. Neurology. 1990 Feb. 40(2):353-62. [Medline].

  5. Kreisler A, Godefroy O, Delmaire C, et al. The anatomy of aphasia revisited. Neurology. 2000 Mar 14. 54(5):1117-23. [Medline].

  6. Naeser MA, Helm-Estabrooks N, Haas G, et al. Relationship between lesion extent in 'Wernicke's area' on computed tomographic scan and predicting recovery of comprehension in Wernicke's aphasia. Arch Neurol. 1987 Jan. 44(1):73-82. [Medline].

  7. Hillis AE, Gold L, Kannan V, et al. Site of the ischemic penumbra as a predictor of potential for recovery of functions. Neurology. 2008 Jul 15. 71(3):184-9. [Medline].

  8. Caramazza A. Minding the facts: a comment on Thompson-Schill et al.'s "A neural basis for category and modality specificity of semantic knowledge". Neuropsychologia. 2000. 38(7):944-9. [Medline].

  9. Geschwind N. Disconnexion syndromes in animals and man. I. Brain. 1965 Jun. 88(2):237-94. [Medline].

  10. Damasio AR, Damasio H. The anatomic basis of pure alexia. Neurology. 1983 Dec. 33(12):1573-83. [Medline].

  11. Naeser MA, Alexander MP, Helm-Estabrooks N, et al. Aphasia with predominantly subcortical lesion sites: description of three capsular/putaminal aphasia syndromes. Arch Neurol. 1982 Jan. 39(1):2-14. [Medline].

  12. Fromm D, Holland AL, Swindell CS, et al. Various consequences of subcortical stroke. Prospective study of 16 consecutive cases. Arch Neurol. 1985 Oct. 42(10):943-50. [Medline].

  13. Alexander MP, Naeser MA, Palumbo CL. Correlations of subcortical CT lesion sites and aphasia profiles. Brain. 1987 Aug. 110 (Pt 4):961-91. [Medline].

  14. Weiller C, Willmes K, Reiche W, et al. The case of aphasia or neglect after striatocapsular infarction. Brain. 1993 Dec. 116 (Pt 6):1509-25. [Medline].

  15. Crosson B. Subcortical Functions in Language and Memory. New York, NY: Guilford; 1992.

  16. Dejerine J. Contribution a l'etude anatomo-pathologique et clinique des differentes varieties de cecite verbales. Memoires Societe Biologie. 1892. 4:61-90.

  17. Benton AL. The fiction of the Gerstmann syndrome. J Neurol Neurosurg Psychiatry. 1961. 24:961-991.

  18. Benton AL. Gerstmann's syndrome. Arch Neurol. 1992 May. 49(5):445-7. [Medline].

  19. Thompson CK, Cho S, Price C, Wieneke C, Bonakdarpour B, Rogalski E, et al. Semantic interference during object naming in agrammatic and logopenic primary progressive aphasia (PPA). Brain Lang. 2012 Jan 12. [Medline].

  20. Lidzba K, Staudt M, Zieske F, Schwilling E, Ackermann H. Prestroke/poststroke fMRI in aphasia: Perilesional hemodynamic activation and language recovery. Neurology. 2012 Jan 11. [Medline].

  21. Berthier ML, Green C, Lara JP, Higueras C, Barbancho MA, Dávila G, et al. Memantine and constraint-induced aphasia therapy in chronic poststroke aphasia. Ann Neurol. 2009 May. 65(5):577-85. [Medline].

  22. Alexander MP, Benson DF, Stuss DT. Frontal lobes and language. Brain Lang. 1989 Nov. 37(4):656-91. [Medline].

  23. Alexander MP, Hiltbrunner B, Fischer RS. Distributed anatomy of transcortical sensory aphasia. Arch Neurol. 1989 Aug. 46(8):885-92. [Medline].

  24. Anderson P. Famous Faces Give Insight to Primary Progressive Aphasia. Available at http://www.medscape.com/viewarticle/809445. Accessed: August 22, 2013.

  25. Appell J, Kertesz A, Fisman M. A study of language functioning in Alzheimer patients. Brain Lang. 1982 Sep. 17(1):73-91. [Medline].

  26. Auerbach SH, Allard T, Naeser M, et al. Pure word deafness. Analysis of a case with bilateral lesions and a defect at the prephonemic level. Brain. 1982 Jun. 105:271-300. [Medline].

  27. Bakar M, Kirshner HS, Wertz RT. Crossed aphasia. Functional brain imaging with PET or SPECT. Arch Neurol. 1996 Oct. 53(10):1026-32. [Medline].

  28. Benson DF, Ardila A. Aphasia. A clinical perspective. First ed. New York: Oxford University Press; 1996. 1: 1-441.

  29. Benton AL, Hamsher K De S, Varney NR, et al. Contributions to Neuropsychological Assessment. New York: Oxford University Press; 1983.

  30. Benton AL, Hamsher KD. Multilingual Aphasia Examination. Iowa City, IA: AJA Associates; 1989.

  31. Bhogal SK, Teasell R, Speechley M. Intensity of aphasia therapy, impact on recovery. Stroke. 2003 Apr. 34(4):987-93. [Medline].

  32. Boatman D, Gordon B, Hart J, et al. Transcortical sensory aphasia: revisited and revised. Brain. 2000 Aug. 123 (Pt 8):1634-42. [Medline].

  33. Bookheimer S. Functional MRI of language: new approaches to understanding the cortical organization of semantic processing. Annu Rev Neurosci. 2002. 25:151-88. [Medline].

  34. Bowers D, Bauer RM, Heilman KM. The nonverbal affect lexicon: theoretical perspectives from neuropsychological studies of affect perception. Neuropsychology. 1993. 7:433-44.

  35. Broca P. Remarques sur le siege de la faculte du language articule, suivies d'une observation d'aphemie. Bull Soc Anat Paris. 1861. 2:330-57.

  36. Catani M, Jones DK, ffytche DH. Perisylvian language networks of the human brain. Ann Neurol. 2005 Jan. 57(1):8-16. [Medline].

  37. Catani M, Mesulam M. The arcuate fasciculus and the disconnection theme in language and aphasia: history and current state. Cortex. 2008 Sep. 44(8):953-61. [Medline].

  38. Cummings JL, Benson F, Hill MA, et al. Aphasia in dementia of the Alzheimer type. Neurology. 1985 Mar. 35(3):394-7. [Medline].

  39. Damasio AR. Aphasia. N Engl J Med. 1992 Feb 20. 326(8):531-9. [Medline].

  40. de Boissezon X, Peran P, de Boysson C, et al. Pharmacotherapy of aphasia: myth or reality?. Brain Lang. 2007 Jul. 102(1):114-25. [Medline].

  41. De Renzi E, Vignolo LA. The token test: A sensitive test to detect receptive disturbances in aphasics. Brain. 1962 Dec. 85:665-78. [Medline].

  42. DeWitt LD, Grek AJ, Buonanno FS, et al. MRI and the study of aphasia. Neurology. 1985 Jun. 35(6):861-5. [Medline].

  43. Freedman M, Alexander MP, Naeser MA. Anatomic basis of transcortical motor aphasia. Neurology. 1984 Apr. 34(4):409-17. [Medline].

  44. Freund CS. Uber optische Aphasie und Seelenblindheit. Archiv Psychiatrie Nervenkrankheiten. 1889. 20:276-97.

  45. Gefen T, Wieneke C, Martersteck A, Whitney K, Weintraub S, Mesulam MM, et al. Naming vs knowing faces in primary progressive aphasia: A tale of 2 hemispheres. Neurology. 2013 Aug 13. 81(7):658-64. [Medline].

  46. Goodglass H, Kaplan E. The Assessment of Aphasia and Related Disorders. Philadelphia, PA: Lea and Febiger; 1972.

  47. Goodglass H, Wingfield A, Hyde MR, et al. Category specific dissociations in naming and recognition by aphasic patients. Cortex. 1986 Mar. 22(1):87-102. [Medline].

  48. Hall DA, Anderson CA, Filley CM, et al. A French accent after corpus callosum infarct. Neurology. 2003 May 13. 60(9):1551-2. [Medline].

  49. Hillis AE. Aphasia: progress in the last quarter of a century. Neurology. 2007 Jul 10. 69(2):200-13. [Medline].

  50. Jacobs DH, Shuren J, Gold M, et al. Physostigmine pharmacotherapy for anomia. Neurocase. 1996. 2:83-92.

  51. Kaplan E, Goodglass H, Weintraub S. The Boston Naming Test. Philadelphia, PA: Lea and Febiger; 1978.

  52. Kertesz A. Western Aphasia Battery. London, Ontario: University of Western Ontario Press; 1980.

  53. Kertesz A, Sheppard A. The epidemiology of aphasic and cognitive impairment in stroke: age, sex, aphasia type and laterality differences. Brain. 1981 Mar. 104:117-28. [Medline].

  54. Kirshner HS. Behavioral neurology. Practical science of mind and brain. 1. 2. Boston. Butterworth Heinemann. 2002. 1-474.

  55. Kirshner HS. 1-532. Handbook of neurological speech and language disorders. First ed. New York: Marcel Dekker, Inc; 1995.

  56. Kirshner HS, Alexander M, Lorch MP, et al. Continuum: Disorders of speech and language. Baltimore MD: Lippincott Williams & Wilkins CONTINUUM.; 1999.

  57. Kirshner HS, Casey PF, Henson J, et al. Behavioural features and lesion localization in Wernicke's aphasia. Aphasiology. 1989. 3:169-176.

  58. Kirshner HS, Hughes T, Fakhoury T, et al. Aphasia secondary to partial status epilepticus of the basal temporal language area. Neurology. 1995 Aug. 45(8):1616-8. [Medline].

  59. Kirshner HS, Kistler KH. Aphasia after right thalamic hemorrhage. Arch Neurol. 1982 Oct. 39(10):667-9. [Medline].

  60. Kirshner HS, Tanridag O, Thurman L, et al. Progressive aphasia without dementia: two cases with focal spongiform degeneration. Ann Neurol. 1987 Oct. 22(4):527-32. [Medline].

  61. Lazar RM, Antoniello D. Variability in recovery from aphasia. Curr Neurol Neurosci Rep. 2008 Nov. 8(6):497-502. [Medline].

  62. Love T, Swinney D, Walenski M, et al. How left inferior frontal cortex participates in syntactic processing: Evidence from aphasia. Brain Lang. 2008 Dec. 107(3):203-19. [Medline].

  63. Mariën P, Paghera B, De Deyn PP, et al. Adult crossed aphasia in dextrals revisited. Cortex. 2004 Feb. 40(1):41-74. [Medline].

  64. Martin PI, Naeser MA, Theoret H, et al. Transcranial magnetic stimulation as a complementary treatment for aphasia. Semin Speech Lang. 2004 May. 25(2):181-91. [Medline].

  65. Mega MS, Alexander MP. Subcortical aphasia: the core profile of capsulostriatal infarction. Neurology. 1994 Oct. 44(10):1824-9. [Medline].

  66. Mesulam MM. Primary progressive aphasia. Ann Neurol. 2001 Apr. 49(4):425-32. [Medline].

  67. Morris HH, Luders H, Lesser RP, et al. Transient neuropsychological abnormalities (including Gerstmann's syndrome) during cortical stimulation. Neurology. 1984 Jul. 34(7):877-83. [Medline].

  68. Nicholas M, Obler L, Albert M, et al. Lexical retrieval in healthy aging. Cortex. 1985 Dec. 21(4):595-606. [Medline].

  69. Nishio S, Takemura N, Ikai Y, et al. Sensory aphasia after closed head injury. J Clin Neurosci. 2004 May. 11(4):442-4. [Medline].

  70. Ojemann G, Ojemann J, Lettich E, et al. Cortical language localization in left, dominant hemisphere. An electrical stimulation mapping investigation in 117 patients. 1989. J Neurosurg. 2008 Feb. 108(2):411-21. [Medline].

  71. Price CJ, Wise RJ, Watson JD, et al. Brain activity during reading. The effects of exposure duration and task. Brain. 1994 Dec. 117 (Pt 6):1255-69. [Medline].

  72. Robey RR. A meta-analysis of clinical outcomes in the treatment of aphasia. J Speech Lang Hear Res. 1998 Feb. 41(1):172-87. [Medline].

  73. Schiff HB, Alexander MP, Naeser MA, et al. Aphemia. Clinical-anatomic correlations. Arch Neurol. 1983 Nov. 40(12):720-7. [Medline].

  74. Shuren JE, Hammond CS, Maher LM, et al. Attention and anosognosia: the case of a jargonaphasic patient with unawareness of language deficit. Neurology. 1995 Feb. 45(2):376-8. [Medline].

  75. Tanridag O, Kirshner HS. Language disorders in stroke syndromes of the dominant capsulostriatum-- a clinical review. Aphasiology. 1987. 1:107-117.

  76. Thompson C. Functional neuroimaging: applications for studying aphasia. LaPointe LL eds. Aphasia and related neurogenic language disorders. 3rd ed. New York: Thieme; 2005. 19-39.

  77. Thompson CK, den Ouden DB. Neuroimaging and recovery of language in aphasia. Curr Neurol Neurosci Rep. 2008 Nov. 8(6):475-83. [Medline].

  78. Wertz RT, Weiss DG, Aten JL, et al. Comparison of clinic, home, and deferred language treatment for aphasia. A Veterans Administration Cooperative Study. Arch Neurol. 1986 Jul. 43(7):653-8. [Medline].

  79. Yang ZH, Zhao XQ, Wang CX, et al. Neuroanatomic correlation of the post-stroke aphasias studied with imaging. Neurol Res. 2008 May. 30(4):356-60. [Medline].

 
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