Version May 2024
INTRODUCTION — Language is a distinctive human facility for communication through symbols. Aphasia is the loss of ability to produce and/or understand language. This usually manifests as a difficulty speaking or understanding spoken language, but reading and writing are also usually impacted. Aphasia can also impact the use of manual sign language and Braille.
This topic reviews the clinical assessment of aphasia, the major aphasia syndromes, and an initial approach to diagnostic evaluation and management. Specific conditions that cause aphasia are discussed in detail separately (see appropriate topic reviews). Other aspects of the neurologic examination, as well as the prognosis and treatment of aphasia, are discussed separately. (See "The detailed neurologic examination in adults" and "The mental status examination in adults" and "Aphasia: Prognosis and treatment".)
NEUROANATOMY — A large, complex neurocognitive network, usually located in the left hemisphere, subserves the capacity for human language [1].
Language centers — The language network comprises areas of perisylvian cortex, including the classical language areas of Broca and Wernicke. While these are not anatomically discrete areas, important neural networks subserving critical language function have been identified:
●Broca's area or Brodmann area 44 in the posterior inferior frontal gyrus innervates adjacent motor neurons subserving the mouth and larynx, and controls the output of spoken language.
●Wernicke's area or Brodmann area 22, comprising the posterior two-thirds of the superior temporal gyrus, receives information from the auditory cortex and accesses a network of cortical associations to assign word meanings.
●The angular gyrus in the inferior parietal lobule is adjacent to visual receptive areas and subserves the perception of written language, as well as other language-processing functions.
Other regions of the cerebrum contribute importantly to normal language. These include the insula, which is integral to normal articulation [2], several frontal and temporal lobe regions that support sentence-level processing [3], and vast regions of temporal, occipital, and parietal cortex that support knowledge of words and their meanings [4-6].
Although it is likely that subcortical nuclei make a contribution to normal language performance [7,8], evidence from perfusion imaging indicates that aphasic syndromes associated with ischemic subcortical lesions are often accompanied by perfusion defects that involve cortical language regions [9,10]. The fact that these subcortical aphasias have been associated with a better prognosis than cortical varieties may be explained by their tendency to resolve with restoration of cortical perfusion.
While the classic Wernicke-Lichtheim model described here maintains its utility for clinicians seeking a rudimentary understanding of aphasia, advances in methodology for aphasia assessment and brain imaging have permitted the development of a dual-stream model for the neuroanatomy of language [11]. This model consists of a ventral stream and a dorsal stream. The ventral stream is rooted in the bilateral temporal lobes and is important for mappings from auditory input to meanings. Integrity of regions and the connections within this stream are crucial for normal auditory comprehension. The dorsal stream is unilaterally organized and includes chiefly frontal lobe areas associated with speech production and a region in the temporoparietal junction. Integrity of these regions and connections among them are essential for fluent speech, as they provide auditory and proprioceptive feedback.
Finally, there is increasing evidence that cerebellar lesions may result in linguistic deficits, including grammatical disturbances [12-15].
Cerebral dominance — Most individuals are left-hemisphere dominant for language function. Cerebral dominance is influenced by handedness; of the 90 to 95 percent of people who are right handed, more than 95 percent have left-sided language dominance [16]. A smaller proportion of left-handed individuals, variably estimated between 31 to 70 percent, have left-sided language dominance [17,18].
Patients with right-sided language dominance tend to have less severe and less enduring aphasia after right-sided brain injury, suggesting that language lateralization is incomplete in these individuals. The presence of bilateral representation of language function in certain individuals is further supported by functional neuroimaging studies, as well as in studies of Wada testing performed in patients prior to epilepsy surgery. Such studies indicate that language networks are not as strongly lateralized in women compared with men, and in left-handed versus right-handed individuals [7,12,17,19,20].
Abnormalities of the left cerebral hemisphere that are present during development may result in atypical hemispheric dominance. A substantial left-hemisphere injury in childhood (before the age of six years) is likely to be associated with a shift in at least some language functions to the right [21]. Atypical language dominance is also noted to be more common in patients with temporal lobe epilepsy, particularly when the pathology is most prominent in the left side [22-24].
ETIOLOGIES — Any insult or pathologic process that results in damage or dysfunction of the language network may cause aphasia. The presentation of the aphasia varies according to the underlying cause:
●Aphasia that has an acute or subacute presentation with relatively fixed deficits is likely due to structural disease. The most common etiology is ischemic stroke [25]. Other structural causes include hemorrhagic stroke; neoplasm; cerebral abscess, encephalitis, or other central nervous system infections; and traumatic brain injury [26]. Multiple sclerosis and acute disseminated encephalomyelitis are uncommon but reported causes of aphasia [27-29].
●Transient episodes of aphasia may occur with transient cerebral ischemia (TIA), migraine, and seizures [30,31]. The presence of aphasia during a TIA is one risk factor that identifies an individual at relatively high risk of stroke in the next few days and weeks [32,33]. In seizures, aphasia may be either an ictal phenomenon (eg, brief speech arrest at onset of a complex partial or secondary generalized seizure) or a postictal manifestation [34-37]. (See "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults" and "Definition, etiology, and clinical manifestations of transient ischemic attack" and "Focal epilepsy: Causes and clinical features".)
●A progressive aphasia can be a manifestation of neurodegenerative disease. In children, certain forms of epilepsy (such as Landau-Kleffner syndrome and epilepsy with continuous spike-and-waves during slow-wave sleep) are associated with a progressive loss of previously attained language function [38]. The aphasia may be the presenting symptom in 40 percent of Landau-Kleffner cases [39] (see "Epilepsy syndromes in children", section on 'Developmental and epileptic encephalopathy with spike-wave activation in sleep (DEE-SWAS)').
Primary progressive aphasia (PPA) and semantic dementia are syndromes that occur in older adults and most commonly represent frontotemporal degeneration, or, less commonly, Alzheimer disease, Creutzfeldt-Jakob disease, or another form of neurodegenerative dementia [40-43]. (See "Frontotemporal dementia: Clinical features and diagnosis" and "Clinical features and diagnosis of Alzheimer disease", section on 'Atypical presentations'.)
CLINICAL ASSESSMENT — Aphasias are classically subdivided based on observed vascular syndromes, cerebral infarction being the most common etiology of aphasia. These are categorized as fluent or nonfluent aphasias, and then are further subdivided according to observed deficits in content, repetition, naming, comprehension, reading, and writing.
Fluency — Fluency is usually assessed qualitatively by listening to the patient's spontaneous speech. Nonfluent speech has the following characteristics:
●Sparse output, with a decreased number of words per minute.
●Shortened phrases, typically five words or fewer.
●Agrammatism, characterized by the omission or substitution of function words (eg, prepositions, articles, conjunctions) or suffixes (eg, "ed" for past events). This type of speech pattern is the most specific feature of dysfluency and often referred to as "telegraphic."
●Effortfulness, with hesitations and a disruption of the normal melodic rhythm. Occasionally, patients with normal speech melody and little effort in spontaneous speech will exhibit word-finding pauses that make the assessment of fluency more difficult; however, these patients should be classified as fluent.
●A breakdown of speech praxis, the ability to coordinate the articulatory movements required for comprehensible speech [44]. This may be tested by asking the patient to repeatedly pronounce the syllables, /pa/, /ta/, and /ka/ (individually) and then to link the three together into a sequence /pa-ta-ka/. Another approach is to ask the patient to repeat the word "catastrophe" or "artillery" as many times as possible in 5 or 10 seconds.
The best objective measure of fluency is to record the patient's speech, count the number of words or morphemes in a group of utterances, and take the mean. However, even this may vary considerably in a given patient depending on the emotional valence and complexity of the conversational topic.
Content — Language errors during spontaneous or tested speech should be noted. Patients with Wernicke's aphasia, for example, make paraphasic errors and neologisms. Paraphasic errors are usually either whole-word (semantic) substitutions (eg, "chair" for "table") or phonemic (literal) substitutions (eg, "cable" for "table"). Neologisms are entirely new nonwords. Patients are often unaware of their paraphasic errors.
Repetition — Repetition is tested by asking the patient to repeat phrases of increasing complexity. "Serial speech," consisting of over-learned sequences (such as "one, two, three" or "A, B, C") is preserved in all but the most severe cases. This should be followed by short sentences using high-frequency words ("She did it" and "This is it"), then longer utterances with less frequent words ("They heard him speak on the radio last night"), and finally, complex, low-frequency phrases ("hopping hippopotamus"; "Methodist Episcopal"; "No ifs, ands, or buts").
Naming — When testing naming, patients are asked to give the names of real objects available to the examiner, such as "key," "buttonhole," "eyebrow," and "knuckles." Words used less frequently are more difficult for the aphasic patient to retrieve and constitute a more sensitive test for anomia. Photographs or line drawings may also be used to assess anomia. The retrieval of verbs is generally best tested by using pictures.
In addition to confrontational naming, word retrieval and production may be tested by asking the patient to "name by definition," ie, the examiner provides a definition of an object or action, and the patient provides the appropriate name.
Comprehension — Comprehension is evaluated by giving a sequence of commands, beginning with one-step, midline commands ("Close your eyes" or "Stick out your tongue"), and progressing to multistep commands and those involving the extremities ("Show me two fingers"; "Close your eyes and point to the window"; "Stand up, turn around, clap two times, and sit down").
Commands that require a body part to cross the midline (eg, "Touch your right ear with your left thumb") are more complex than those that do not. Commands involving increasingly complex grammatical structures can also be used (eg, "Touch the coin with the pencil"; "With the comb, touch the coin"). More complex questions (eg, "Does a stone sink in water?"; "Do you put on your shoes before your socks?") and those using complex grammatical structures such as passive voice or possessive (eg, "Is my aunt's uncle a man or a woman?"; "If a lion was killed by a tiger, which one is still alive?") can elicit comprehension deficits in those who can follow simple commands.
The Token test is a structured evaluation of auditory comprehension [45]. A series of commands involving 20 tokens of different shapes, size, and color is presented in increasing complexity from "touch the small red square" to "put the large green circle under the small yellow square, before you touch the white circle."
Impaired comprehension may be due to failure of speech sound discrimination, word recognition, auditory working memory, or syntactic structure building. Word recognition can be tested by asking the patient to point to items that are plainly visible or accessible. "Two-way" naming deficits, in which the patient can neither name an item nor point to it on command (despite being able to repeat the name) represent abnormal word comprehension; this is a characteristic feature of semantic dementia, a form of frontotemporal lobar dementia. (See "Frontotemporal dementia: Clinical features and diagnosis", section on 'Semantic variant PPA'.)
Reading — Patients are asked to read aloud from a newspaper or from a list of single words. There may be dissociations in the ability to read regularly spelled words, irregular words, or pronounceable nonwords. Reading comprehension may be tested with written commands (eg, "Fold this paper in half and put it on the table") or with a written word-picture matching test.
Writing — The patient is asked to write a sentence spontaneously. It may also be useful to dictate material to the patient, particularly for testing of regularly spelled words, irregular words, and pronounceable nonwords. The patient can also be asked to write names of objects or actions in response to pictures. Accuracy with written naming may be dissociated from spoken naming [46].
Other language assessments — Bedside examination is sufficient in most cases to assess aphasia. Validated scales such as the Boston diagnostic aphasia examination and Western aphasia battery are often used in clinical studies and as part of neuropsychologic test batteries [47]. The Aachen aphasia test appears useful in distinguishing between Broca- and Wernicke-type aphasias [48].
Although not specific for aphasia, verbal fluency tasks provide a means for rapid assessment of word knowledge and verbal executive function and are useful in the assessment of semantic memory in neurodegenerative disease. (See "Frontotemporal dementia: Clinical features and diagnosis", section on 'Semantic variant PPA' and "Clinical features and diagnosis of Alzheimer disease", section on 'Cardinal symptoms'.)
Other neurologic examination features — The language examination is best interpreted in the context of the entire neurologic examination. (See "The detailed neurologic examination in adults".)
A broad mental status examination that includes the assessment of level of consciousness, attention, memory, praxis, executive function, and visuospatial abilities is important to avoid mistaking aphasia for other conditions causing mental status changes and vice versa. (See "The mental status examination in adults".)
The diagnosis of aphasia should be usually made only in the setting of an otherwise intact sensorium. (See 'Conditions mistaken for aphasia' below.)
Hearing should be specifically tested; if abnormal, this must be taken into account when interpreting the examination of comprehension and repetition.
Dysarthria may be present and should be noted. In the setting of the examination, it is usually easy to distinguish dysarthria from aphasia; however, when obtaining historical information from patients and observers about a past episode of speech disturbance it can be surprisingly challenging. Asking them to mimic the speech disturbance can be helpful.
The presence or absence of other neurologic deficits contributes to localization and underlying etiology.
●A right-sided visual field disturbance suggests a left-hemisphere lesion of the optic tract, lateral geniculate nucleus, optic radiations, or posterior cortices. (See "Homonymous hemianopia".)
●A right hemiparesis with spasticity, abnormal reflexes, and a Babinski sign is common in the setting of nonfluent aphasias. At times, weakness will be very subtle, consisting only of a facial weakness and/or a pronator drift.
●Cerebellar findings, such as dysmetria and dysdiadochokinesia, are not commonly caused by lesions that result in aphasia, but cases have been reported in which aphasia seemed to result from cerebellar damage.
●Hemianesthesia suggests a parietal lobe or thalamic lesion. Fluent aphasia is more commonly associated with sensory deficits. Sensory deficits from parietal lobe lesions may include failure of two-point discrimination, astereognosis, and agraphesthesia. These may be difficult to reliably test in the patient with aphasia.
APHASIA SYNDROMES — Based on the assessment of language as described above, it should be possible to classify the aphasia according to one of the classic language syndromes listed in the table (table 1).
Although modern aphasiology is increasingly viewing the language faculty according to more complex models, the Wernicke-Lichtheim model and this classification scheme maintains clinical utility, as these syndromes are at least to some degree associated with neuroanatomic localization, etiology, and prognosis [49]. As an example, in one study of 325 patients with aphasia resulting from cerebral infarction, 95 percent of patients had magnetic resonance imaging (MRI) lesions that corresponded to their clinical syndrome [50]. Limitations of this model include that it does not formally consider basic linguistic elements such as phonology (the sound pattern of language), morphology (the combination of language's smallest meaningful units), syntax (the structure of sentences), semantics (the relationship of language to meaning), and pragmatics (nuances of articulation and discourse).
Broca's aphasia — Classically localized to lesions affecting the frontal lobe, Broca's aphasia is characterized by nonfluency with sparse output and agrammatism (see 'Fluency' above) [49,50]. Repetition is also impaired. Comprehension is relatively spared but is usually not completely normal, particularly for grammatically complex speech. Writing is generally affected in proportion to speech. The association between Broca's aphasia and Broca's area is most consistently observed in acute rather than chronic stroke [51].
There is often an associated right hemiparesis and oral apraxia reflecting injury to contiguous structures in the motor and supplementary motor areas.
Wernicke's aphasia — Wernicke's aphasia is a fluent aphasia with markedly impaired comprehension [49]. In its classic form, speech is voluminous but meaningless, containing paraphasic errors and neologisms. This is often described as "word salad." The speech usually retains normal cadence and intonation. Comprehension and production of written language is similarly impaired. The patient appears unaware of the deficit.
Associated with lesions in the posterior superior temporal gyrus (Wernicke's area), there is typically no motor deficit with this syndrome [49,52]. However, a right superior visual field defect may be present.
Conduction aphasia — Conduction aphasia refers to a syndrome of fluent aphasia with impaired repetition, frequent paraphasic errors (usually phonemic), but relatively preserved comprehension [49]. Patients often try repeatedly to correct their errors. Written language may be similarly affected [53].
This syndrome may be observed during recovery from a Wernicke's aphasia and also with lesions in the supramarginal gyrus or deep parietal white matter [37,50,53,54]. There is often no other accompanying neurologic deficit.
Global aphasia — A global aphasia includes deficits in all language functions [49]. Patients are often mute or produce only nonword utterances. They cannot follow commands, although they may respond to the intonation or expression of the speech.
Because this syndrome is usually associated with extensive perisylvian injury affecting both Broca's and Wernicke's areas, patients generally have a right hemiparesis and often a right visual field deficit [49,50]. However, case reports of global aphasia without hemiparesis have been reported in the setting of encephalitis, selective lesions involving both Broca's and Wernicke's areas, and as a late manifestation of degenerative dementia [55,56].
Transcortical motor aphasia — Characterized by a nonfluent speech output, with good comprehension and repetition, patients with this type of aphasia appear to have difficulty initiating speech, as well as completing a thought. Writing is disrupted proportionately. This can occur during recovery from a Broca's aphasia or as a primary deficit [57].
This syndrome has been described in infarcts involving the anterior cerebral artery and/or the anterior-middle cerebral artery watershed that damage the supplementary motor area and/or connections to the frontal perisylvian speech area [49,50,58,59]. It may also occur in patients recovering from a Broca's aphasia. When associated with lesions in the mesial frontal lobe, patients may demonstrate apathy and lateralized frontal release signs [59]. By contrast, when associated with damage in the supplementary motor area, patients appear to make a great effort to speak, and may also demonstrate right-sided long tract signs (weakness, hyperreflexia, Babinski sign) [27].
Transcortical sensory aphasia — This is a fluent aphasia with frequent paraphasic errors and impaired comprehension that appears similar to a Wernicke's aphasia. One difference is intact repetition that can take the form of echolalia. Patients can often read aloud (sometimes with errors), but without comprehension. Among other theories, this syndrome has been interpreted as representing a disconnection between phonological processing, which remains intact, and lexical-semantic decoding, which is impaired [60].
This syndrome has been produced by lesions adjacent to Wernicke's area in the temporal-occipital or parietal-occipital areas (eg, angular gyrus) [50,61]. This can be a watershed zone between middle and posterior cerebral artery territories. Consistent with this localization, patients generally have no motor deficits, but may have lateralized sensory or visual field deficits (inferior quadrantanopia or hemianopia).
Transcortical mixed aphasia — Patients with a transcortical mixed aphasia have all features of a global aphasia except that repetition is spared. They have little to no spontaneous verbal speech, but may repeat what has just been said [62]. When given the start of a common phrase, they are sometimes able to repeat and then finish it on their own. Comprehension of written and spoken language is severely impaired.
Produced by injury to the anterior and posterior watershed area or by multifocal cerebral emboli [50,62,63], there are often other neurologic deficits. Depending on the clinical setting, this syndrome can occur in the setting of bihemispheric watershed damage that produces bilateral spastic quadriparesis ("man in a barrel" syndrome) and/or visual field loss.
Anomic aphasia — While anomia is a common feature of most aphasia syndromes, an isolated deficit of anomia can also occur. Patients with anomic aphasia cannot name (or write) the word for a particular item. Often, they can state the meaning and retrieve words related to the one for which they are searching. Spontaneous speech is characterized by pauses, circumlocution (substitution of related words or phrases), and occasional paraphasic errors, but is otherwise fluent with intact repetition and sentence comprehension [26,64].
Associated lesions in different anatomic sites have been described, including the basal temporal lobe, the anterior inferior temporal lobe, the temporo-parieto-occipital junction, and the inferior parietal lobe [26,50,64].
Aphasia-related disorders — Pure word deafness, alexia without agraphia, and pure word mutism are not technically disturbances in language, but are related to aphasia.
Pure word deafness — This is a rare syndrome. Patients can comprehend written but not spoken language [65,66]. Spontaneous speech is usually normal, sometimes with paraphasic errors. Repetition is often preserved. The general neurologic examination is normal. Pure word deafness is usually associated with restricted lesions in the superior temporal gyrus [67].
Alexia without agraphia — Patients with this syndrome can write, but not read. Their ability to understand and produce oral speech remains intact. Lesions producing this deficit are in the left occipital lobe and extend to the splenium of the corpus callosum (eg, left posterior cerebral artery occlusion) [28,29]. The patient has a right visual field defect. Visual information reaches the left visual field, but pathways that allow interpretation of written language from the left visual field are interrupted.
Pure word mutism — Also known as aphemia, pure word mutism produces deficits in the production of oral speech with retention of auditory comprehension as well as the ability to write. Dysarthria and facial paresis usually accompany this syndrome. Lesions typically lie in or around Broca's area, involving the lowermost part of the precentral gyrus [68-70].
PROGRESSIVE APHASIAS — The syndromes outlined above occur primarily in the context of focal brain damage (eg, stroke or trauma).
By contrast, syndromes of primary progressive aphasia (PPA) occur in the context of neurodegenerative disease (usually frontotemporal dementia) and have an insidious onset and gradual progression [71-73]. In patients with one of these syndromes, language disturbance is the most prominent cognitive feature and remains most prominent even after other cognitive domains become involved. Individuals with PPA often remain independent with complex nonverbal activities for several years [73].
Three major PPA syndromes are recognized [73,74]. All three syndromes are associated with atrophy in perisylvian brain regions, more prominent in the language-dominant (usually left) hemisphere [74]. These are described briefly here and in more detail separately:
●Progressive nonfluent aphasia – The aphasia most closely resembles Broca's aphasia, in that the patient is nonfluent and comprehension is relatively spared. The loss of fluency is typically due to a combination of agrammatism and articulatory deficits. (See "Frontotemporal dementia: Clinical features and diagnosis", section on 'Nonfluent variant PPA'.)
Atrophy may be visible on MRI and involves the anterior insula and premotor regions [73,75]. (See "Frontotemporal dementia: Clinical features and diagnosis", section on 'Neuroimaging'.)
●Progressive semantic dementia – The aphasia is fluent, but lacks the paraphasic quality seen in Wernicke aphasia. Comprehension is impaired mainly for single words, but not due to any deficit in sound processing. Patients frequently repeat back the word that they do not understand (eg, "What is a hamburger?" or "I don't know what coughing means"). Surface dyslexia, loss of the ability to read low-frequency, irregularly spelled words (eg, "yacht," "colonel"), is commonly observed. The pattern of atrophy is highly characteristic and involves both anterior temporal lobes, usually more so on the left [73,75]. (See "Frontotemporal dementia: Clinical features and diagnosis", section on 'Neuroimaging'.)
●Logopenic progressive aphasia – Patients are typically fluent, with breaks in fluency caused by word-finding pauses. Phonemic paraphasic errors are common. Repetition and comprehension are highly dependent on the length of the stimulus, such that longer sentences are much less likely to be understood or repeated back accurately. In contrast to semantic dementia, single-word comprehension is likely to be intact. (See "Frontotemporal dementia: Clinical features and diagnosis", section on 'Logopenic variant PPA'.)
The atrophy is most prominent in the posterior superior temporal and inferior parietal regions [73-75]. (See "Frontotemporal dementia: Clinical features and diagnosis", section on 'Neuroimaging'.)
CONDITIONS MISTAKEN FOR APHASIA — A number of conditions may either obscure or be mistaken for aphasia.
●Patient with metabolic encephalopathy or delirium may have difficulty naming and fail to follow commands. Paraphasic errors, while relatively uncommon, may occur in an agitated delirium. This condition may be recognized by fluctuating attention and level of consciousness, along with agitation, hallucinations, and/or asterixis. Other focal neurologic signs that can accompany fluent aphasia (eg, visual field deficits) are generally absent in patients with metabolic encephalopathy. (See "Acute toxic-metabolic encephalopathy in adults".)
●Akinetic mutism can result from lesions of the mesial frontal region. Patients demonstrate a paucity of speech output and poor response to commands that may suggest aphasia. Observation of bilaterally decreased motor responses, not restricted to speech, helps identify akinetic mutism [76,77]. Hypophonia is often present in akinetic mutism, but not in aphasia [78]. These patients may exhibit signs of catatonia (waxy flexibility). However, a nonfluent aphasia may also accompany frontal lobe lesions. (See 'Broca's aphasia' above and 'Transcortical motor aphasia' above.)
●Patients who are depressed may be reluctant to converse and be examined, and may therefore appear to have comprehension or naming difficulties. Flattened affect, poor eye contact, and other evidence of withdrawal are important to note in this regard (see "Unipolar depression in adults: Assessment and diagnosis"). Contributing to potential diagnostic confusion is the fact that many patients with chronic aphasia are depressed; clinicians should consider that both conditions may be contributing to the clinical picture [79-81]. (See "Aphasia: Prognosis and treatment".)
●Patients with schizophrenia may have abnormal speech content that can include neologisms, and can be difficult to distinguish from fluent aphasia [82-84]. Listening carefully to the speech content can help distinguish the two. An underlying theme or preoccupation is often discernible in the disorganized speech of a schizophrenic patient, but not in the patient with aphasia. The jargon output of a fluent aphasia seems accidental rather than volitional, while the neologisms produced by schizophrenic patients often seem to be "made up" and inflected in a manner appropriate for their context [85,86]. Semantic and phonemic paraphasic errors are common with aphasia but rarely occur in schizophrenic speech [82]. While fluent aphasia is associated with aberrant production of grammatical affixes and function words (paragrammatism) [25], schizophrenic language is not associated with a morphological disturbance [85]. Persistent patient examination can usually reveal intact verbal comprehension in the individual with schizophrenia. (See "Schizophrenia in adults: Clinical features, assessment, and diagnosis".)
●Dysarthria is usually easy to distinguish from aphasia in the setting of a fixed deficit; however, when obtaining historical information from patients and observers about an episode of speech disturbance, it can be challenging. The term "garbled speech," for example, can be applied to either condition. Asking them to mimic the speech disturbance they experienced or witnessed can be helpful.
●Apraxia of speech is a motor speech disorder characterized by slow, effortful speech that has an abnormal rhythm and articulation errors. This can be difficult to distinguish from Broca's aphasia, and the two conditions commonly occur together, presumably because the anatomic basis for the conditions are contiguous [87,88]. One MRI study of stroke patients identified as having isolated apraxia of speech (without aphasia) found that lesions in the left premotor and motor cortex were most common [89]. Recognizing the presence of apraxia of speech may alter the therapeutic approach used by the speech therapist [90,91].
DIAGNOSIS — All patients with a newly identified aphasia should undergo a structural brain scan, usually MRI. If the presentation is abrupt, suggesting an acute cerebrovascular event, or if there are other findings that suggest an intracranial mass lesion, the examination may be urgent. The presence of an ischemic stroke should trigger further evaluation (see "Overview of the evaluation of stroke"). Other identified structural brain lesions will usually also warrant further testing.
Episodes of transient aphasia should prompt investigation of possible seizures or transient cerebral ischemia (TIA). Electroencephalography (EEG) and/or cerebrovascular imaging may be helpful in such patients. Prolonged EEG monitoring may be required to detect active seizure activity in some patients with aphasic status epilepticus [92]. (See "Initial evaluation and management of transient ischemic attack and minor ischemic stroke" and "Evaluation and management of the first seizure in adults".)
Aphasia with an insidious onset and gradual progression, especially in middle-aged or older adults, suggests neurodegenerative disease (ie, primary progressive aphasia [PPA]) but a slowly growing mass lesion should be excluded in these patients as well.
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Aphasia (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Definition – Aphasia is the loss of ability to produce and/or understand written and/or spoken language.
●Neuroanatomy – Left-hemisphere language dominance is present in more than 95 percent of individuals. (See 'Cerebral dominance' above.)
The neural network subserving language function is increasingly recognized to be a large and complex system involving regions throughout the cerebral hemisphere and possibly the cerebellum as well. Important language centers lie in the perisylvian region of the dominant hemisphere. (See 'Language centers' above.)
●Etiologies – Ischemic stroke is the most common cause of aphasia; however, any structural brain pathology and certain neurodegenerative conditions can also produce aphasia. (See 'Etiologies' above.)
●Syndromes – Aphasias are classified into specific syndromes according to observed deficits in fluency, content, repetition, naming, comprehension, reading, and writing (table 1). These syndromes have been associated in many cases with a specific neuroanatomic localization. (See 'Clinical assessment' above and 'Aphasia syndromes' above.)
●Differential diagnosis – Aphasias may be confused clinically with delirium, as well as acute and chronic psychiatric conditions. However, a careful clinical examination can usually distinguish these. (See 'Conditions mistaken for aphasia' above.)
●Evaluation – All patients with aphasia should have a neuroimaging study. The acuity of the presentation dictates the urgency of the testing. Patients with episodic aphasia should be additionally evaluated for seizures and transient cerebral ischemia (TIA). (See 'Diagnosis' above.)
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