Approach to the patient with

aphasia
 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.
 NEUROANATOMY
• A large, complex neurocognitive network,
usually located in the left hemisphere,
subserves the capacity for human language
 Language centers
• The language network comprises areas of perisylvian cortex,
including the classical language areas of Broca and Wernicke.
• 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, several
frontal and temporal lobe regions that support sentence-level
processing, and vast regions of temporal, occipital, and parietal cortex
that support knowledge of words and their meanings.
• Although it is likely that subcortical nuclei make a contribution to normal
language performance, evidence from perfusion imaging indicates that
aphasic syndromes associated with ischemic subcortical lesions are often
accompanied by perfusion defects that involve cortical language regions.
• 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.
 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.
• A smaller proportion of left-handed individuals,
variably estimated between 31 to 70 percent,
have left-sided language dominance.
• 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.
• 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.
• 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.
 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:
 ETIOLOGIES
• 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.
• Other structural causes include hemorrhagic stroke;
neoplasm; cerebral abscess, encephalitis, or other central
nervous system infections; and traumatic brain injury.
• Multiple sclerosis and acute disseminated
encephalomyelitis are uncommon but reported causes of
aphasia
 ETIOLOGIES
• Transient episodes of aphasia may occur with
transient cerebral ischemia (TIA), migraine, and
seizures.
• 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.
• 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
• 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.
– The aphasia may be the presenting symptom in 40 percent of Landau-
Kleffner cases
• 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 
 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."
 Nonfluent speech…
• 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.
– 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").
 Comprehension
• 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.
 Comprehension
• The Token test is a structured evaluation of
auditory comprehension.
• 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. 
 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.
 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.
• The Aachen aphasia test appears useful in distinguishing
between Broca- and Wernicke-type aphasias.
• 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
Other neurologic examination features
• The language examination is best interpreted in the context of
the entire neurologic examination.
• 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.
• The diagnosis of aphasia should be usually made only in the
setting of an otherwise intact sensorium.
• 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.
• 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
 Broca's aphasia
• Classically localized to lesions affecting the frontal lobe, Broca's
aphasia is characterized by nonfluency with sparse output and
agrammatism.
• 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.
• 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.
• 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.
• 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.
• Patients often try repeatedly to correct their errors.
• Written language may be similarly affected.
• 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.
• There is often no other accompanying neurologic deficit.
 Global aphasia
• A global aphasia includes deficits in all language functions.
• 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.
– 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
 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.
• 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.
• When associated with lesions in the mesial frontal lobe,
patients may demonstrate apathy and lateralized frontal
release signs.
• 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) 
 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.
• This syndrome has been produced by lesions adjacent
to Wernicke's area in the temporal-occipital or
parietal-occipital areas (eg, angular gyrus).
• 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 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.
– 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, 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.
• 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
 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.
• 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.
 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.
• 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.
 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 FTD) and have an insidious
onset and gradual progression.
• 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.
• Three major PPA syndromes are recognized .
• All three syndromes are associated with atrophy in perisylvian brain regions,
more prominent in the language-dominant (usually left) hemisphere
 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.
• Atrophy may be visible on magnetic resonance
imaging (MRI) and involves the anterior insula
and premotor regions
 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.
 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.
• The atrophy is most prominent in the posterior superior
temporal and inferior parietal regions
 DIAGNOSIS
• All patients with a newly identified aphasia should undergo
a structural brain scan, usually magnetic resonance imaging
(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.
• 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.
• 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.
 CONDITIONS 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.
• 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.
• Hypophonia is often present in akinetic mutism, but not in
aphasia.
• These patients may exhibit signs of catatonia (waxy flexibility).
• However, a nonfluent aphasia may also accompany frontal
lobe lesions.
• 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
• 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
• Patients with schizophrenia may have abnormal speech content that can
include neologisms, and can be difficult to distinguish from fluent aphasia.
– 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 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.
• Semantic and phonemic paraphasic errors are common with aphasia but
rarely occur in schizophrenic speech.
• While fluent aphasia is associated with aberrant production of grammatical
affixes and function words (paragrammatism) schizophrenic language is not
associated with a morphological disturbance.
• Persistent patient examination can usually reveal intact verbal comprehension
in the individual with schizophrenia.
• 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.
• 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.
• Recognizing the presence of apraxia of speech may alter the
therapeutic approach used by the speech therapist.
 Prognosis and treatment
• Aphasia is a loss of ability to produce or understand
language.
• The most common cause of aphasia is cerebrovascular
disease, particularly cerebral infarction.
• Aphasia complicates 15 to 38 percent of ischemic
strokes.
• Other structural pathologies (infection, trauma,
neoplasm) and certain neurodegenerative diseases
(primary progressive aphasia) can also cause aphasia.
• Aphasia can be a devastating condition and is one of the most feared consequences
of cerebral infarction and other brain injuries.
• Although quality of life in patients with aphasia is difficult to measure directly, the
disruption in communication with its likely effects on employment status and social
networks suggests that its impact can be profound.
• Caregivers of stroke survivors are likely to experience more stress when caring for a
family member with, rather than without, aphasia.
• Comprehension deficits can also limit rehabilitation efforts targeting other poststroke
deficits such as hemiparesis.
• Patients with poststroke aphasia have greater morbidity and mortality than stroke
patients without aphasia.
• While most, if not all, patients with poststroke aphasia have some functional
recovery, residual deficits are common.
• Unfortunately, there is limited evidence that therapeutic interventions are effective.
 PROGNOSIS
• Recovery from aphasia is influenced by lesion
location and type of aphasia.
• As an example, large lesions in the left
hemisphere with global aphasia have a much
poorer recovery than small, subcortical lesions
with anomia.
• The prognosis for aphasia recovery depends in large part upon the
underlying etiology.
• This has been best studied in cerebrovascular disease.
• Most patients with poststroke aphasia improve to some extent.
• Most improvement occurs within the first few months and plateaus
after one year.
• The severity of the initial aphasia strongly correlates with the long-
term deficit; those with milder degrees of aphasia at onset are the
most likely to recover completely.*1
• Patients with significant aphasia may benefit from intensive
treatment regimens even after the period of spontaneous recovery.
• Diffusion and perfusion magnetic resonance
imaging (MRI) studies demonstrate that early
recovery after stroke (in the first few days and
weeks) is related to reperfusion of language areas.
• Functional neuroimaging studies suggest that
subsequent improvement is associated with
increased activation of contiguous areas in the
perisylvian language areas as well as homologous
brain regions in the right hemisphere.
• Patients with aphasia resulting from right-hemisphere lesions
often have less severe permanent language deficits, likely as a
consequence of incomplete language lateralization in these
individuals
• While there is some evidence to suggest that left-handed
individuals with left-hemisphere stroke and women have less
complete lateralization of language dominance than right-
handed individuals and men, neither handedness nor gender
have consistently been shown to impact recovery from
poststroke aphasia.
• Similarly, increased age has not been consistently shown to
influence prognosis.
 MANAGEMENT
• The underlying cause of the aphasia should be treated specifically.
• Aphasia resulting from an intraparenchymal mass or hematoma,
or from an extra-axial mass or fluid collection, may improve
dramatically with removal of the offending mass.
• In CNS tumors, treatment of edema with steroids may result in
rapid improvement, but worsening of the neoplastic disease is
likely to be accompanied by recurrence of aphasia.
• Episodes of aphasia resulting from epileptic seizures should
resolve with adequate anticonvulsant therapy.
• The treatment of acquired epileptic aphasia (Landau-Kleffner
syndrome) is problematic, and children with this disease may be
left with permanent linguistic dysfunction, particularly auditory
comprehension defects
 Speech and language therapy
• Aphasia may resolve spontaneously, especially when it is caused by a
small ischemic lesion, but in most cases, a speech-language pathologist is
consulted to assist the patient in recovering linguistic abilities and to train
the patient and family members in alternative strategies for
communication.
• The available data from clinical trials offer weak support for this
approach, but no single technique has emerged as more effective than
others.
• Challenges in studying the use of speech and language therapy include
the heterogeneity of aphasia syndromes, the wide variety and lack of
standardized techniques employed in speech and language therapy, as
well as the fact that many patients improve spontaneously.
• The actual speech-language rehabilitation technique may not matter as
much as the actual number of sessions and intensity of therapy.
• One review of 10 studies of 864 patients with poststroke aphasia found
that intense (in excess of two hours per week) speech and language
therapy over a short period of time was more effective than less intense
therapy provided over a longer period of time.
– However, a subsequent randomized study in 116 patients found that in the
subacute setting, patients who received two hours of therapy per week had similar
recoveries compared with those who received five hours of therapy a week.
• Study results have also differed as to whether similar or disparate benefits
are expected from professional therapists versus community-based
programs or trained family members.
• While some have found that language therapy works best when
administered early after stroke, others have found that, after adjusting for
the effects of early spontaneous recovery, similar gains can be attained
when speech therapy is administered in more chronic stages
• Newer language therapy techniques that are being studied
include the use of computer-assisted techniques, as well as so-
called constraint-induced aphasia therapy (CIAT; high-intensity
therapy that restricts the use of nonverbal communication).
• In one study of 27 patients with chronic poststroke aphasia, CIAT
produced benefits both when used alone and when combined
with memantine .
• Developments are also being made in the application of
augmentative and alternative communication devices.
• The recent development of smartphones, tablet computers, and
similar devices has led to the availability of downloadable
applications for therapy and communication.
 Pharmacologic approaches
• The rationale behind pharmacologic treatment
of aphasia involves replacing depleted
neurotransmitters, enhancing neuroplasticity,
and improving cerebral blood flow.
• No pharmacologic intervention has been proven
to result unequivocally in long-term benefit.
• Examples of clinical trials of medications in
patients with poststroke aphasia include the
following:
• Bromocriptine was studied in a randomized,
double-blind trial in 38 patients with a
poststroke nonfluent aphasia.
• After 16 weeks of treatment, there was no
difference in the recovery of language function
between active and placebo-treated groups.
• This negative result was concurrent with the
results of a previous randomized study.
• Amphetamine in conjunction with speech/language therapy
(10 sessions over five weeks) appeared to improve language
more than therapy alone in a randomized, double-blind study
in 21 poststroke aphasia patients.
• The between-group differences appeared to be maintained at
the six-week and six-month assessments but were no longer
significant after six months.
• A 2003 systematic review of the use of amphetamines in
poststroke rehabilitation concluded that the aggregated results
of small studies supported future research of this treatment
approach, but not their use in routine clinical practice
• Piracetam was studied in 24 stroke patients with
aphasia.
• After six weeks of treatment, the piracetam-treated
group appeared to make greater gains in language
function on certain subtest areas compared with the
placebo-treated group.
• A meta-analysis of prior studies of piracetam in acute
stroke concluded that there was weak evidence of
piracetam's efficacy in the treatment of poststroke
aphasia.
• The acetylcholinesterase inhibitors donepezil
and galantamine have shown promise in open-
label studies in patients with poststroke
aphasia.
• There is some evidence that donepezil and
other acetylcholinesterase inhibitors may be
efficacious in vascular dementia and also in
aphasia resulting from neurodegenerative
dementia.
• Memantine (10 mg twice daily) was studied
along with CIAT in 27 patients with chronic
poststroke aphasia in a randomized, controlled,
parallel-group study.
• Memantine treatment was associated with a
sustained benefit at 48 weeks on measures of
aphasia and communication.
• The benefit of drug treatment appeared to be
augmented by CIAT.
• Depression often develops in patients with chronic or progressive
aphasias and may impair aphasia recovery.
• Psychotherapy or pharmacologic management may improve the
outcome in these patients.
• However, a six-month clinical trial of the monoamine oxidase inhibitor, 
moclobemide, in 90 unselected patients with poststroke aphasia did
not find that treatment was associated with greater improvement of
the aphasia compared with placebo treatment.
• The use of prophylactic antidepressant medications is not supported in
patients with poststroke aphasia or aphasia of other etiologies.
• It seems reasonable, however, to monitor such patients for the
development of depression and institute treatment if depression does
emerge.
 Transcranial magnetic or electrical
stimulation
• Applied to the contralateral, unaffected cerebral
hemisphere, transcranial magnetic stimulation
(TMS) is believed to suppress its activity, and as a
result, the tonic inhibition of the affected
hemisphere.
• While uncontrolled reports in a small number of
patients with poststroke aphasia and a limited
number of small controlled trials report evidence of
efficacy, further study of this modality is required. *
• An alternative approach applies a weak polarizing electric current to the
cortex using electrodes applied to the skull.
• In one study, this modality was applied to 10 patients with chronic stroke-
induced aphasia and appeared to induce enhanced naming accuracy.
• In another nonrandomized study in eight patients with chronic poststroke
aphasia, cortical stimulation applied via surgically implanted electrodes
appeared to augment the effect of speech and language therapy.
• A futility study of anodal transcranial direct stimulation in 74 aphasic
patients indicated nonfutility of treatment versus sham treatment and
paves the way for further research on the technique.
• This treatment is also being evaluated in patients with primary
progressive aphasia