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APHASIA

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Aphasia

Defenition
Neuronal network
cerebral dominance
Aetiology
Clinical assessment
Syndromes of aphasia
Aphasia 
=
a disorder of language rather than
speech.
Speech 
=
the articulation and phonation of
language sounds;
Principal method
of
human communication,
consisting of words
used in a structured and conventional way and
conveyed by speech,
writing,
or
gesture.
Expression of
or
the ability to express
thoughts and feelings
By
articulate sounds.
Aphasia
is
the loss of ability
to
produce
and/or
understand language.
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.
A large, complex neurocognitive network, usually
located
in the left hemisphere,
subserves the capacity
for human language
• Aphasia is defined as a disorder of language
that is acquired secondary to brain damage.
• First, aphasia is distinguished from congenital
or developmental language disorders,
called dysphasias.
• (Contrary to British usage, in the United States,
the term dysphasia applies to developmental
language disorders rather than partial or
incomplete aphasia.)
language is a complex system of
communication symbols and rules for their
use
the method of human communication, either
spoken or written, consisting of the use of
words in a structured and conventional
way
Language centers — 
The language network comprises areas of perisylvian
cortex,
including
the classical language areas
of
Broca and Wernicke.
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
Angular gyrus
Other regions of the cerebrum contribute importantly to
normal language.
These include
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.
• 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. 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
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 
Aphasia with 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
Transient episodes of aphasia may occur
(TIA),
migraine,
&
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
Fluency
Comprehension
Repetition 
Naming 
 Content 
Reading
Writing 
Nonfluent • Fluent
Dysarthric
Effortfull
Sparse
Prosody lost
Phrase length
decreased
Despp
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
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
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 should be noted.
Dysarthria vs Aphasia;
Asking them to mimic the speech disturbance can be
helpful.
A right-sided visual field disturbance
=
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.
(Barré's sign).
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.
Conduction aphasia
Good Repetition - Nominal
Good Comprehension
Poor repetition – Conduction
Fluent
Good Repetition –Trans
cortical-sensory
Poor Comprehension

Poor repetition - Wernicke


Good Repetition – Transcortical motor
Good Comprehension
Poor Repetition –Broca’s

Non Fluent
Good Repetition - Isolation
Poor Comprehension
Poor Repetition – Global
• Perisylvian aphasias
Perisylvian aphasias
Wernicke’s
Broca’s
Conduction
Good Repetition - Nominal
Good Comprehension
Poor repetition – Conduction
Fluent
Good Repetition –Trans
cortical-sensory
Poor Comprehension

Poor repetition - Wernicke


8 Anomic
• Fluent
• Good comprehension
• Good repetition
• Naming severely affected
•   A wide variety of lesions, including both dominant and
nondominant hemisphere loci, may produce anomic aphasia.
• Particularly common sources are insults to (a) the dominant
inferior parietal lobe and (b) the dominant anterior temporal
cortices.
• The latter insults have been associated with category-specific
naming deficits in which naming in different semantic categories
(e.g., living versus nonliving entities) is differentially impaired.
8 Anomic
• The angular gyrus and anterior temporal cortices are
supplied by different branches of the inferior division
of the MCA.
Anomic aphasia
(Bradley)
Spontaneous speech Fluent, some word-finding pauses,
circumlocution
Naming Impaired

Comprehension Intact

Repetition Intact

Reading Intact

Writing Intact, except for anomia

Associated signs Variable or none


Good Repetition - Nominal
Good Comprehension
Poor repetition – Conduction
Fluent
Good Repetition –Trans
cortical-sensory
Poor Comprehension

Poor repetition - Wernicke


3Conduction aphasia. 
Fluent spontaneous output
Comprehension of spoken language is relatively intact
disproportionate disruption of repetition.
. Motor and sensory disturbances are usually absent or
mild.
Conduction aphasia
Spontaneous speech Fluent, some hesitancy, literal
paraphasic errors
Naming May be moderately impaired
Comprehension Intact

Repetition Severely impaired


Reading + Inability to read aloud; some reading
comprehension
Writing Variable deficits

Associated signs + Apraxia of left limbs


+ Right hemiparesis, usually mild
+ Right hemisensory loss
+ Right hemianopia
Good Repetition - Nominal
Good Comprehension
Poor repetition – Conduction
Fluent
Good Repetition –Trans
cortical-sensory
Poor Comprehension

Poor repetition - Wernicke


5 Transcortical sensory
Severe auditory Comprehension
Repetition Good
Fluency Good
Reading aloud may be fairly preserved, whereas
reading comprehension is quite poor.
Motor deficits are generally absent,
Hemisensory deficits are common.
watershed between the posterior cerebral artery
(PCA) and MCA.
Good Repetition - Nominal
Good Comprehension
Poor repetition – Conduction
Fluent
Good Repetition –Trans
cortical-sensory
Poor Comprehension

Poor repetition - Wernicke


2 Wernickes
 Fluent, effortless, well-articulated output, almost always
contaminated with paraphasias and neologisms.
 severe disturbance of auditory comprehension
Repetition poor
In the acute phase, patients seem to be unaware of their inability
to comprehend spoken language,calmly providing
inappropriate and grossly paraphasic answers to observer’s
inquiries.
A superior homonymous quadrantanopia 
NO dramatic motor or sensory deficits, and the fluid production of
speech,  confused or psychotic rather than aphasic, and may delay
diagnosis while metabolic or psychiatric disturbances are sought
MISDIAGNOSIS
2 Wernickes
posterior third of the superior temporal gyrus (Wernicke’s
area; Brodmann area 22), an auditory association area. 
 Lesion size may vary considerably, and damage often
extends to the middle temporal gyrus and the inferior
parietal lobe 
 Wernicke’s area is supplied by the inferior division of the
MCA.
Wernicke’s
feature clinical
Spontaneous speech Fluent, with paraphasic errors
Usually not dysarthric Sometimes
logorrheic
Naming Impaired (often bizarre paraphasic misnaming
Comprehension Impaired

Repetition Impaired

Reading Impaired for comprehension, reading


aloud
Writing Well-formed, paragraphic
Associated signs ± Right hemianopia Motor, sensory
signs usually absent
Good Repetition – Transcortical motor
Good Comprehension
Poor Repetition –Broca’s

Non Fluent
Good Repetition - Isolation
Poor Comprehension
Poor Repetition – Global
Good Repetition – Transcortical motor
Good Comprehension
Poor Repetition –Broca’s

Non Fluent
Good Repetition - Isolation
Poor Comprehension
Poor Repetition – Global
 4 Transcortical motor
aphasia. 
• Nonfluent severely disrupted, nonfluent, and halting
• Comprehension good
• Repetition relatively spared
• a) prefrontal cortices and subjacent white matter
anterior or superior to Broca’s area
• Watershed area between ACA and MCA anteriorly
• Or
• (b) supplementary motor area and cingulate gyrus.
These lesions disconnect Broca’s area from limbic areas
and other sources of the drive to communicate.
• ACA
Bedside Features of Transcortical
Aphasias
Isolation Transcortical Transcortical
syndrome motor sensory
Speech Nonfluent Nonfluent Fluent
Echolalic echolalic
Naming impaired Impaired Impaired
Comprehension Impaired Intact Impaired
repetition intact intact intact

Reading Impaired + Intact Impaired


Writing Impaired + Intact Impaired
Good Repetition – Transcortical motor
Good Comprehension
Poor Repetition –Broca’s

Non Fluent
Good Repetition - Isolation
Poor Comprehension
Poor Repetition – Global
1.  Broca’s aphasia.
Nonfluent
Good comprehension relatively
Poor repetition
Telegraphic
Depression Frustration
Gesture prominent
Posterior portion of the inferior frontal gyrus
(Broca’s area; Brodmann areas 44 and 45)
superior division of the MCA.
Broca’s aphasia
Feature findings
Spontaneous speech nonfluent/mute /dysrthric/telegraphic
naming impaired
comprehension intact
repetition impaired
Reading Often impaired( third alexia)
Writing Impaired dysmorphic dysgrammatical
Associated signs Right hemiparesis
Right hemisensory loss
± Apraxia of left limbs
Aphemia

• A rare variant of Broca aphasia is aphemia, a nonfluent


syndrome in which the patient is initially mute and then
able to speak with phoneme substitutions and pauses.
• All other language functions are intact, including writing.
• This rare and usually transitory syndrome results from
small lesions of the Broca area or its subcortical white
matter or of the inferior precentral gyrus.
• Because written expression and auditory
comprehension are normal, aphemia is not a true
language disorder;
• aphemia may be equivalent to pure apraxia of
speech
Good Repetition – Transcortical motor
Good Comprehension
Poor Repetition –Broca’s

Non Fluent
Good Repetition - Isolation
Poor Comprehension
Poor Repetition – Global
 6Mixed transcortical aphasia.
• rare and remarkable condition is analogous to global aphasia,
except for preserved ability to repeat
• Fluency minimal or absent.
• Comprehension lost
• Echolalia
•  Lesions are an additive combination of those producing
transcortical motor and sensory aphasias.
• Insults anterosuperior to Broca’s area and posterosuperior to
Wernicke’s area cut off the perisylvian language zone from access
to other cortices.
•  Isolation of the speech area is a synonym for mixed transcortical
aphasia
• lesions fall in the crescentic vascular border zone among the ACA,
MCA, and PCA
Bedside Features of Transcortical
Aphasias
Isolation Transcortical Transcortical
syndrome motor sensory
Speech Nonfluent Nonfluent Fluent
Echolalic echolalic
Naming impaired Impaired Impaired
Comprehension Impaired Intact Impaired
repetition intact intact intact

Reading Impaired + Intact Impaired


Writing Impaired + Intact Impaired
Good Repetition – Transcortical motor
Good Comprehension
Poor Repetition –Broca’s

Non Fluent
Good Repetition - Isolation
Poor Comprehension
Poor Repetition – Global
7 Global
Nonfluent
comprehension lost
repetition lost
Entire left perisylvian region, encompassing Broca’s area in
the inferior frontal lobe, Wernicke’s area in the posterior
temporal lobe, and all the interposed parietofrontal
cortices.
In rare cases, separate, discrete lesions of Broca’s area
and Wernicke’s area produce global aphasia without
hemiparesis.
 ICA and MCA occlusions
Global aphasia
Feature
Spontaneous speech Mute/ nonfluent
Naming impaired
Comprehension impaired

repetition impaired

Reading impaired

writing impaired

Asociated signs Right hemiparesis/ Right hemisensory


loss /Right hemianopia
Perisylvian aphasias • Extrasylvian aphasias
 Wernicke’s • Transcortical motor
 Broca’s
• Transcortical sensory
 Conduction
• Isolation
 repetition impaired in all • Anomic
 • Repetition intact in
all 4
Alexia without agraphia (pure
alexia)
Disconnection syndrome
acquired loss of reading ability in a literate person, with
preserved ability to write spontaneously
Reading severely impaired,
spontaneous speech, repetition, and auditory
comprehension are normal.
unable to read phrases they themselves have written
Recognition of words spelled aloud and traced on the palm
is normal.  
Alexia without agraphia (pure
alexia)
Only words presented visually pose difficulty.
Patients frequently exhibit a slow, letter-by-letter reading
strategy, painstakingly recognizing and stating aloud
each letter in a word and then, from the string of spoken
letters, determining the target word.
A right homonymous hemianopia is common but not
invariable.
Disorders of color vision, including achromatopsia and
color anomia, may be present
Alexia without agraphia (pure
alexia)
•  Simultaneous lesions of the left occipital lobe and the
splenium of the corpus callosum,
• depriving the angular gyrus region critical for word
recognition of visual input from either the left or right
hemisphere
• The smallest sufficient injury is a single lesion of the paraventricular white
matter of the mesial occipitotemporal junction (the forceps major),
interrupting interhemispheric and intrahemispheric visual tracts to the
angular gyrus but sparing the corpus callosum and left occipital cortex
•  left PCA infarction, tumor, demyelinating disorders such as multiple
sclerosis (MS) or acute disseminated encephalomyelitis (ADEM),
toxoplasma or herpes encephalitis, and mitochondrial
encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
 Alexia with agraphia
Acquired illiteracy—
inability to read or write—
but relatively well-preserved oral language function.
  Speech is fluent, auditory comprehension and repetition are
intact.
Hemisensory deficits are frequent, and hemiparesis and
hemivisual disturbances are variable
A full-fledged Gerstmann’s syndrome, including dyscalculia,
dysgraphia, left–right confusion, and finger agnosia, can occur
dominant inferior parietal lobule (angular and supramarginal
gyri).
 Pure word deafness (auditory
verbal agnosia
•  Patients resemble Wernicke’s aphasics superficially .
Comprehension and repetition of spoken language are
impaired, whereas speech is fluent.
• Unlike in Wernicke’s patients, however, paraphasias are
rare and, more importantly, comprehension of written
material is intact. Writing production is also normal.
• Although uncomprehending of word sounds, patients
have intact hearing and are generally successful in
identifying meaningful nonverbal sounds such as car
horns or telephone rings. identified
 Pure word deafness (auditory
verbal agnosia
• Two types of lesions underlie pure word deafness, both
disconnecting Wernicke’s area from input from primary
auditory cortices.
• Some patients harbor bilateral superior temporal
lesions.
• A roughly equal number exhibit a single deep superior
temporal lesion in the dominant hemisphere, blocking
ipsilateral and crossing callosal auditory pathways.
Good Repetition - Nominal
Good Comprehension
Poor repetition – Conduction
Fluent
Good Repetition –Trans
cortical-sensory
Poor Comprehension

Poor repetition - Wernicke


Good Repetition – Transcortical motor
Good Comprehension
Poor Repetition –Broca’s

Non Fluent
Good Repetition - Isolation
Poor Comprehension
Poor Repetition – Global
• Poor Repetition, WBC
– Wernicke
– Broca’s
– Conduction
• Good Repetition, TIA
– Transcortical / Motor & Sensory
– Isolation
– Anomic
34 Perisyvian aphasia include all
EXCEPT

(a) Wernickes aphasia


(b) Broca’s aphasia
(c) Conduction aphasia
(d) Transcotical motor aphasia
• 34 Perisyvian aphasia include all EXCEPT

(a) Wernickes aphasia


(b) Broca’s aphasia
(c) Conduction aphasia
(d) Transcotical motor aphasia
35. Following are true of Broca’s
aphasia
(a) It is a fluent aphasia
(b) Comprehension is intact
(c) Repetition is retained
(d) Telegraphic speech
(e) Abundent paraphasia is
uncommon
• 35. Following are true of Broca’s aphasia
(a) It is a fluent aphasia
(b) Comprehension is intact
(c) Repetition is retained
(d) Telegraphic speech
(e) Abundent paraphasia is
uncommon
Brocas aphasia
• Spontaneous speech-- Nonfluent, mute, or telegraphic,
usually dysarthric
• Naming Impaired
• Comprehension- Intact (mild difficulty with complex
grammatical phrases)
• Repetition Impaired
• Reading- Often impaired (“third alexia”)
• Writing Impaired (dysmorphic, dysgrammatical)
• Associated signs- Right hemiparesis/Right hemisensory
loss/± Apraxia of left limbs
• Traditional Broca area in the posterior part of the inferior
frontal gyrus, along with damage to adjacent cortex and
subcortical white matter
• . Lesions involving the traditional Broca area (Brodmann
areas 44 and 45) resulted in difficulty initiating speech,
and lesions combining Broca area, the lower precentral
gyrus, and subcortical white matter yielded the full
syndrome of Broca aphasia
Wernickes aphasia
I cant take class tomorrow as I have to go to trivandrum
pi cat cla kumoro pi ha ko privan
Spontaneous speech Fluent, with paraphasic errors
Usually not dysarthric
Sometimes logorrheic
Naming Impaired (often bizarre paraphasic misnaming)
Comprehension Impaired
Repetition Impaired
Reading Impaired for comprehension, reading aloud
Writing Well-formed, paragraphic
Associated signs± ----- Right hemianopia
Motor, sensory signs usually absent
Wernickes aphasia
• The psychiatric manifestations of Wernicke aphasia are quite
different from those of Broca aphasia.
• Depression is less common; many
• Wernicke aphasics seem unaware of or unconcerned about their
communicative deficits.
• With time, some patients become angry or paranoid about the
inability of family members and medical staff to understand them.
• This behavior, like depression, may hinder rehabilitative efforts
Wernickes aphasia
• The lesions of patients with Wernicke aphasia usually involve the
posterior portion of the superior temporal gyrus, sometimes
extending into the inferior parietal lobule
• The exact confines of the Wernicke area have been much debated.
• Damage to the Wernicke area (Brodmann area 22) has been
reported to correlate most closely with persistent loss of
comprehension of single words, although others have found only
larger temporoparietal lesions in patients with lasting
Wernicke aphasia
• Extension of the lesion into the inferior parietal region may predict
greater involvement of reading comprehension.
• Reading comprehension is usually affected similarly to
auditory comprehension, but occasional patients show
greater deficit in one modality versus the other
• The patient usually has no hemiparesis and can grasp the pen and
write easily. Written productions are even more abnormal than oral
ones, however, in that spelling errors are also evident. Writing
samples are especially useful in the detection of mild
Wernicke aphasia.
Global Aphasia

• summation of the deficits of


Broca aphasia and Wernicke aphasia
Global Aphasia

• Spontaneous speech -Mute or nonfluent


• Naming Impaired
• Comprehension Impaired
• Repetition Impaired
• Reading Impaired
• Writing -Impaired
• Associated signs Right hemiparesis
• Right hemisensory
• lossRight hemianopia
Conduction Aphasia
• Spontaneous speech Fluent, some hesitancy, literal
paraphasic errors
• Naming- May be moderate limpaired
• Comprehension Intact
• Repetition Severely impaired
• Reading + Inability to read aloud; some reading
comprehension
• Writing Variable deficits
• Associated signs + Apraxia of left limbs+
Right hemiparesis, usually mild+
Right hemisensory loss+
Right hemianopia
• The lesions of conduction aphasia usually involve either
the superior temporal or inferior parietal regions.
• Benson and associates suggested that patients with limb
apraxia have parietal lesions, whereas those without
apraxia have temporal lesions
• Conduction aphasia may represent a stage of recovery
in patients with Wernicke aphasia in whom the damage
to the superior temporal gyrus is not complete
• Anatomical involvement of the arcuate fasciculus is
present in most, if not all, cases of conduction aphasia
Anomic Aphasia
• Spontaneous speech Fluent, some word-finding pauses,
circumlocution
• Naming Impaired
• Comprehension Intact
• Repetition Intact
• Reading Intact
• Writing Intact, except for anomia
• Associated signs Variable or none
Transcortical aphasia
• The transcortical aphasias are syndromes in which
repetition is normal, presumably because the causative
lesions do not disrupt the perisylvian language circuit
from the Wernicke area through the arcuate fasciculus to
the Broca area.
• Instead, these lesions disrupt connections from other
cortical centers into the language circuit (hence the
name “transcortical”).
• The transcortical syndromes are easiest to think of as
analogues of the syndromes of global, Broca, and
Wernicke aphasias, with intact repetition.
Mixed transcortical aphasia, or the syndrome of the
isolation of the speech area, is a global aphasia in which
the patient repeats, often echolalically,
but has no propositional speech or comprehension.
This syndrome is rare, occurring predominantly in large,
watershed infarctions of the left hemisphere
or
both hemispheres
that spare the perisylvian cortex,
or
in advanced dementias.
• Transcortical motor aphasia is an analogue of Broca aphasia in
which speech is hesitant or telegraphic, comprehension is relatively
spared, but repetition is fluent
• This syndrome occurs with lesions in the frontal lobe, anterior to the
Broca area, in the deep frontal white matter, or in the medial frontal
region, in the vicinity of the supplementary motor area.
• All of these lesion sites are within the territory of the
anterior cerebral artery, separating this syndrome from
the aphasia syndromes of the middle cerebral artery
(Broca, Wernicke, global, and conduction).
• The third transcortical syndrome,
• transcortical sensory aphasia, is an analogue of
Wernicke aphasia in which fluent,
• paraphasic speech, paraphasic naming, impaired
auditory and reading comprehension, and abnormal
writing coexist with normal repetition.
• This syndrome is relatively uncommon, occurring in
strokes of the left temporo-occipital area and in
dementias. Bedside examination findings in the
transcortical aphasias are summarized in
Pure Alexia without Agraphia

Alexia,
or
acquired inability to read,
is a form of aphasia,
=
as a linguistic blindfolding:
patients can write but cannot read their own writing.
On bedside examination,
speech,
auditory comprehension,
and
repetition are normal.
Naming may be deficient,
especially for colors

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