This document provides an overview of aphasia and aphasia syndromes. It defines aphasia as an acquired language disorder resulting from brain damage. The major aphasia syndromes discussed are Broca's aphasia (nonfluent speech with relatively preserved comprehension), Wernicke's aphasia (fluent but meaningless speech with impaired comprehension), global aphasia (combination of Broca's and Wernicke's deficits), conduction aphasia (impaired repetition with otherwise intact language), and pure word deafness (isolated auditory comprehension deficit). Each syndrome is characterized by its pattern of impaired and preserved language functions as well as its associated neurological deficits and lesion location.

1. APHAISA AND APHASIA SYNDROMES

2. INTRODUCTION
 Language has provided the foundation of human
civilization and learning.
 analysis of the patterns of abnormality in the language
has practical usefulness in neurological diagnosis.
 Historically, language was the first higher cortical
function to be correlated with specific sites of brain
damage.
 Aphasia is defined as a disorder of language that is
acquired secondary to brain damage. [Alexander and
Benson (1997)].
 First, aphasia is distinguished from congenital or
developmental language disorders, called dysphasia's.

3.  aphasia is a disorder of language rather than speech.
 language is a complex system of communication
symbols and rules for their use.
 Speech is the articulation and phonation of
language sounds.
 speech disorders include
 dysarthria,
 dysphonia (voice disorders),
 stuttering,
 speech apraxia.
 Dysarthrias are disorders of articulation of single
sounds.
 Dysarthria may result from mechanical disturbance of
the tongue or larynx or from neurological disorders.

4. Apraxia of speech
 syndrome of misarticulation of phonemes, especially
consonant sounds.
 Dysarthria - certain phonemes are consistently distorted.
 apraxia of speech - inconsistent distortions and
substitutions of phonemes.
 The disorder is called an apraxia because there is no
primary motor deficit in articulation of individual
phonemes.
 speech-apraxic patients produce inconsistent articulatory
errors, usually worse on the initial phonemes of a word
and with polysyllabic utterances.

5. LINGUISTIC COMPONENTS
 Phonemes are the smallest meaning-carrying sounds.
 morphology is the use of appropriate word endings and
connector words.
 semantics refers to word meanings.
 lexicon is the internal dictionary.
 syntax is the grammatical construction of phrases and
sentences.
 Discourse refers to the use of these elements to create
organized and logical expression of thoughts.
 Pragmatics refers to the proper use of speech and
language in a conversational setting including pausing
while others are speaking, taking turns properly, and
responding to questions

6. NEURO ANATOMICAL BASIS
• Reception and processing of spoken language
• Auditory cortex, Heschl’s gyrus, [ superior temporal
gyrus].
• Wernicke’s area or Brodmann’s area 22 [ posterior
part of the left superior temporal gyrus ]
• Via the arcuate fasciculus
• Broca’s area in the posterior inferior frontal gyrus.
• Adjacent motor cortex, subserving the mouth and
larynx
• Brainstem cranial nerve nuclei.

8.  The inferior parietal lobule, especially the supra marginal
gyrus,
 involved in phoneme processing in language
comprehension.
 phoneme production for repetition and speech.
 Reading
 requires the perception of visual language stimuli by the
occipital cortex.
 followed by processing into auditory language information,
via the heteromodal association cortex of the angular gyrus.
 Writing
 involves the activation of motor neurons projecting to the
arm and hand.
 In addition, other cortical centers involved in cognitive
processes project into the primary language cortex,
influencing the content of language.

9. ROLE OF SUBCORTICAL STRUCTURES
 Thalamus:
 relay for the reticular activating system.
 appears to alert the language cortex.
 lesions of the dominant thalamus frequently
produce fluent aphasia.
 Nuclei of the basal ganglia
 Especially the caudate nucleus and putamen,
participate in expressive speech.

10.  In right-handed people, and in a majority of left-handers,
clinical syndromes of aphasia result from left hemisphere
lesions.
 Rarely, aphasia may result from a right hemisphere lesion
in a right-handed patient, a phenomenon called crossed
aphasia.
 In left-handed persons, language disorders are usually
similar to those of right-handed persons with similar
lesions, but occasional cases present with atypical
syndromes.

11.  In right-handed aphasics
 left hemisphere lesion in 99% of the cases
 the other 1% are crossed aphasics.
 In left-handed aphasics
 60% had lesions of the left hemisphere.
 40% had lesions of the right hemisphere.
 There may be a degree of mixed dominance for language
in non-right-handed individuals.
 Aphasia may tend to be less severe in left handers and
recovery better.
 just a family history of left handedness in a right-handed
aphasic may predict better recovery.

12. SYMPTOMS AND DIFFERENTIAL DIAGNOSIS OF
DISORDERED LANGUAGE
Muteness - a total loss of speech:
 May represent severe aphasia.
 Severe form of dysarthria.
 Frontal lobe dysfunction with akinetic mutism.
 Severe extrapyramidal system dysfunction, as in parkinson
disease.
 Non- neurological disorders of the larynx and pharynx.
 Psychogenic syndromes, such as catatonia.
 A good rule of thumb is that if the patient can write or type
and the language form and content are normal, the
disorder is probably not aphasic in origin.

13. Hesitant speech:
 symptom of aphasia,
 symptom of dysarthria or stuttering,
 psychogenic disorder
 rule of thumb is that if one can transcribe the utterances
of a hesitant speaker into normal language, the patient is
not aphasic.
Anomia:
 inability to produce a specific name.
 generally a reliable indicator of language disorder.
 it may also reflect memory loss.

14. Paraphasic speech:
 refers to the presence of errors in the patient’s speech output.
 literal or phonemic errors: involving substitution of an
incorrect sound (e.g., shoon for spoon),
 verbal or semantic errors: involving substitution of an
incorrect word (e.g., fork for spoon).
Perseveration:
 The inappropriate repetition of a previous response.
Neologisms:
 aphasic utterances involve non existent word forms.
 A pattern of paraphasic errors and neologisms that so
contaminate speech that the meaning cannot be
discerned is called jargon speech.

15. Fluent, paraphasic speech:
 differential diagnosis here involves
 Aphasia,
 Psychosis,
 Acute encephalopathy or delirium,
 Dementia.
 Aphasic patients are usually not confused or
inappropriate in behavior.
 they do not appear agitated or misuse objects, with
occasional exceptions.
 By contrast, most psychotic patients speak in an easily
understood, grammatically appropriate manner, but their
behavior and speech content are abnormal.
 Only rarely do schizophrenics speak in “clang
association” or “word salad” speech.

16. BEDSIDE LANGUAGE EXAMINATION
 A wealth of information
about language
function can be
obtained during the
clinical interview.
 D. Frank Benson and
Norman Geschwind
popularized a bedside
language examination
of six parts, updated by
Alexander and Benson
(1997).

17. Spontaneous speech:
 Fluent speech flows rapidly and effortlessly.
 Non fluent speech is uttered in single words or short phrases,
with frequent pauses and hesitations.
 1st observe the elementary characteristics such as
 initiation difficulty,
 articulation,
 phonation or voice volume,
 rate of speech,
 prosody or melodic intonation of speech,
 phrase length.
 2nd the content of speech utterances should be
analyzed in terms of the presence of word-finding
pauses, circumlocutions, and errors such as literal
and verbal paraphasias and neologisms.

18. Naming:
 tested by asking the patient to name objects, object
parts, pictures, colors, or body parts to
confrontation.
 A few items from each category should be tested.
 Proper names of persons are often affected
severely.
 The examiner should ensure that the patient
recognizes the items or people that he or she
cannot name.

19. Auditory comprehension:
 Is tested by asking the patient to follow a series of
commands of one, two, and three steps.
 An example of a one-step command is “stick out your
tongue”.
 a two-step command is “hold up your left thumb and close
your eyes.”
 Successful following of commands ensures adequate
comprehension but not vise versa.

20.  The patient must hear the command, understand
the language the examiner speaks, and possess
the motor ability to execute it, including the absence
of apraxia.
 Because apraxia is difficult to exclude with
confidence, it is advisable to test comprehension by
tasks that do not require a motor act, such as yes-
no questions

21. Repetition:
 Dysarthric patients have difficulty with rapid sequences of
consonants.
 Aphasics have special difficulty with grammatically
complex sentences.
 Often, aphasics can repeat familiar phrases much better
than unfamiliar ones.
Reading:
 Should be tested both aloud and for comprehension.
 The examiner should carry a few printed commands to
facilitate a rapid comparison of auditory to reading
comprehension.
 Examiner must have some idea of the patient’s pre
morbid reading ability

22. Writing:
 The element of the bedside examination most often
omitted.
 A writing specimen may be the most sensitive
indicator of mild aphasia, and it provides a
permanent record for future comparison.
 Spontaneous writing, such as a sentence describing
why the patient has come for examination, is
especially sensitive for the detection of language
difficulty.
 When spontaneous writing fails, writing to dictation
and copying should be tested.

23.  Finally, combine the results of the bedside
language examination with those of the rest of the
neurological examination.
 These “associated signs” help to classify the type
of aphasia and to localize the responsible brain
lesion

24. DIFFERENTIAL DIAGNOSIS OF
APHASIC SYNDROMES

25. BROCA’S APHASIA
 Paul Broca, the French physician described in 1861.
 The speech pattern is non fluent.
 If the maximum sentence length is fewer than seven
words, then the patient is nonfluent.
 Patient speaks hesitantly, often producing the principal,
meaning-containing nouns and verbs but omitting small
grammatical words.
 An example is “wife come hospital.”

26.  “Agrammatism” or “telegraphic speech”.
 They make many phonemic errors, with substitution of
phonemes usually differing only slightly from the correct
target.
 Naming is deficient, but the patient often manifests a “tip of
the tongue” phenomenon.
 Auditory comprehension seems intact.
 Repetition is hesitant in these patients, resembling their
spontaneous speech.
 Reading is often impaired despite relatively preserved
auditory comprehension

27.  Benson termed this reading difficulty of Broca aphasics
the “third alexia,” in distinction to the two classical
types of alexia.
 Writing is virtually always deficient in Broca aphasics.
 Associated neurological deficits of Broca aphasia include
 right hemiparesis,
 hemisensory loss,
 apraxia of the oral apparatus and the nonparalyzed left
limbs.
 An important clinical feature of Broca aphasia is its
frequent association with depression.
 The lesions site - Broca area in the posterior part of the
inferior frontal gyrus.

28.  In CT scan analyses at the Boston Veterans
Administration Medical Center, lesions combining
Broca area, the lower pre central gyrus, and sub
cortical white matter yielded the full syndrome of
Broca aphasia.
 In studies by the same group, damage to two
subcortical white matter sites the rostral sub callosal
fasciculus deep to the Broca area and the
periventricular white matter adjacent to the body of
the left lateral ventricles - were required to cause
permanent non fluency.

31. APHEMIA
 A rare variant of Broca aphasia.
 Non fluent syndrome.
 Patient is initially mute and then able to speak with
phoneme substitutions and pauses.
 All other language functions are intact, including writing.
 usually transitory syndrome
 results from small lesions of the Broca area or its sub
cortical white matter or of the inferior pre central
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.

32. WERNICKE APHASIA
 syndrome opposite to Broca aphasia.
 expressive speech is fluent.
 The speech pattern is effortless and sometimes even
excessively fluent (logorrhea).
 Neurolinguists refer to this pattern as
paragrammatism.
 In milder cases, the intended meaning of an utterance
may be discerned.
 Naming is deficient, often with bizarre, paraphasic
substitutions for the correct name.

33.  Auditory comprehension is impaired, sometimes even
for simple nonsense questions.
 Repetition is impaired.
 Reading comprehension is usually affected similarly to
auditory comprehension, but occasional patients show
greater deficit in one modality versus the other.
 Writing is also impaired.
 The patient usually has no hemiparesis and can grasp
the pen.
 Written productions are even more abnormal than oral
ones.
 Writing samples are especially useful in the detection of
mild Wernicke aphasia.

34.  Associated signs are limited in Wernicke aphasia.
 most patients have no elementary motor or sensory
deficits.
 partial or complete right homonymous hemianopia
may be present.
 The psychiatric manifestations of Wernicke aphasia
are quite different.
 Some patients become angry or paranoid about the
inability of family members and medical staff to
understand them.

35.  Lesion site - posterior portion of the superior
temporal gyrus, sometimes extending into the
inferior parietal lobule.
 Extension of the lesion into the inferior parietal
region may predict greater involvement of reading
comprehension.
 In terms of vascular anatomy, the Wernicke area
lies within the territory of the inferior division of
the left middle cerebral artery.

39. PURE WORD DEAFNESS
 Isolated loss of auditory comprehension and
repetition, without any abnormality of speech,
naming, reading, or writing.
 Hearing for pure tones and for nonverbal noises, such
as animal cries, is intact.
 Classically, the anatomical substrate is a bilateral
lesion, isolating Wernicke’s area from the primary
auditory cortex, in the bilateral Heschl’s gyri.

40.  Pure word deafness is thus an example of a
“disconnection syndrome,”
 deficit results from loss of white matter connections
rather than of gray matter language centers.
 Some cases are d/t unilateral, left temporal lesions.

41. GLOBAL APHASIA
 summation of the deficits of Broca aphasia and Wernicke
aphasia.
 Speech is nonfluent or mute, but comprehension is also
poor, as are naming, repetition, reading, and writing.
 Most patients have dense right hemiparesis, hemisensory
loss, and often hemianopia.

42.  Lesion site:
 Inferior frontal and superior temporal regions, and
often much of the parietal lobe in between.
 Left middle cerebral artery territory.
 Recovery in global aphasia may be prolonged.
 Global aphasics may recover more during the
second 6 months than during the first 6 months
after a stroke.

44. CONDUCTION APHASIA
 Characterized by its striking deficit in repetition.
 Most patients have relatively normal spontaneous speech,
although some make literal paraphasic errors and hesitate
frequently for self-correction.
 Auditory comprehension is preserved.
 Naming may be impaired.
 Reading and writing are somewhat variable, but reading
aloud may share some of the same difficulty as repeating.

45.  Associated deficits include
 hemianopia in some patients
 right-sided sensory loss may be present
 right hemiparesis is usually mild or absent.
 Some patients have limb apraxia, creating a
misimpression that comprehension is impaired.
 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.

46.  Wernicke originally postulated that a lesion disconnecting
the Wernicke and Broca areas would produce this
syndrome.
 Geschwind later pointed to the arcuate fasciculus, a
white matter tract traveling from the deep temporal lobe,
around the sylvian fissure to the frontal lobe, as the site
of disconnection.
 Anatomical involvement of the arcuate fasciculus is
present in most, if not all, cases of conduction aphasia.

48. ANOMIC APHASIA
 Naming or access to the internal lexicon, is the
principal deficit.
 Spontaneous speech is normal except for the
pauses produced by the inability to name.
 Comprehension, repetition, reading, and writing are
intact, except for the same word-finding difficulty in
written productions.
 less specific in localization than other aphasic
syndromes.

49.  Isolated, severe anomia may indicate focal left hemisphere
pathology.
 Inability to produce nouns → temporal lobe lesions
 Inability to produce verbs → frontal lobe lesions
 Alexander and Benson (1997) refer to the angular gyrus as
the site of lesions producing anomic aphasia.
 but lesions there usually produce other deficits, including
alexia and the four elements of Gerstmann syndrome.

50.  Anomia is also seen with
 mass lesions elsewhere in the brain,
 diffuse degenerative disorders, such as Alzheimer disease.
 Anomic aphasia is also a common stage in the
recovery of many aphasic syndromes.
 Anomic aphasia thus serves as an indicator of left
hemisphere or diffuse brain disease, but it has only
limited localizing value.

52. TRANS CORTICAL APHASIA’S
 Syndromes in which repetition is normal.
 causative lesions do not disrupt the peri sylvian language
circuit.
 lesions disrupt connections from other cortical centers into
the language circuit
 hence the name “transcortical” .

53. Mixed transcortical aphasia:
 Global aphasia in which the patient repeats, often
echolalically, but has no propositional speech or
comprehension.
 Occurring predominantly in large, watershed infarctions
of the left hemisphere or both hemispheres that spare
the perisylvian cortex or in advanced dementias.
Trans cortical sensory aphasia:
 Is an analogue of wernike aphasia but repetition is
fluent.
 occurring in strokes of the left temporo-occipital area
and in dementias

54. Trans cortical motor aphasia:
 Is an analogue of Broca aphasia but repetition is
fluent.
 Occurs with lesions in the
frontal lobe, anterior to the Broca area,
deep frontal white matter,
medial frontal region,
vicinity of the supplementary motor area.
 All of these lesion sites are within the territory of the
anterior cerebral artery.

56. SUB CORTICAL APHASIAS
 Defined by lesion localization in the basal ganglia or
deep cerebral white matter.
 two major groups:
 Aphasia with thalamic lesions
 Aphasia with lesions of the subcortical white matter and
basal ganglia.

57. Aphasia with thalamic lesions
 Left thalamic hemorrhages
 frequently produce a Wernicke like fluent aphasia.
 better comprehension than cortical Wernicke aphasia.
 fluctuating or “dichotomous” state has been described.
 consists of alternating alert state and a drowsy state.
 some have attributed thalamic aphasia to pressure on
adjacent structures and secondary effects on the cortex.

58.  Thalamic aphasia also occurs with
 small ischemic lesions
 Involving paramedian or anterior nuclei of the
thalamus
 in the territory of the tubero thalamic artery
 indicate that the thalamus and its connections
play a definite role in language function.
 Thalamic aphasia can occur even with a right
thalamic lesion in a left handed patient.

59. LESIONS OF THE LEFT BASAL GANGLIA AND DEEP
WHITE MATTER
 first described in basal ganglia hemorrhages, especially those
involving the putamen.
 most commonly involve global or Wernicke like aphasia.
 ischemic strokes have provided better localizing information.
 posterior sub cortical aphasia syndrome
 Involving the posterior putamen and deep temporal
white matter [temporal isthmus].
 Fluent, paraphasic speech and impaired comprehension
resembling Wernicke aphasia

60.  Anterior sub cortical aphasia syndrome:
 lesion is an infarct involving the anterior
putamen, caudate nucleus, and anterior limb of
the internal capsule.
 dysarthria, decreased fluency, mildly impaired
repetition, and mild comprehension disturbance.
 closely resembles Broca aphasia, but with
greater dysarthria and less language
dysfunction.

61. o Larger sub cortical lesions involving both the anterior and
posterior lesion sites produce global aphasia.
o basal ganglia lesions affect language, both directly and
indirectly, via decreased activation of cortical language
areas
o In summary,
 sub cortical lesions do produce aphasia
 less commonly than cortical lesions
 language characteristics of sub cortical aphasias are
often atypical.

62. PURE ALEXIA WITHOUT AGRAPHIA
 Alexia is an acquired inability to read.
 pure alexia without agraphia - described by the French
neurologist Dejerine in 1892.
 Characterized by “linguistic blindfolding”
 Patients can write but cannot read their own writing.
 Spontaneous speech, auditory comprehension, and repetition
are normal.
 Naming may be deficient, especially for colors.

63.  Associated deficits include a right hemianopia or right upper
quadrant defect in nearly all patients.
 Frequently, a deficit of short term memory.
 There is usually no hemiparesis or sensory loss.
 nearly always a stroke in the territory of the left posterior
cerebral artery, with infarction of the medial occipital lobe,
often the splenium of the corpus callosum and medial
temporal lobe.
 Dejerine postulated a disconnection between the intact right
visual cortex and left hemisphere language centers,
particularly the angular gyrus.

66. ALEXIA WITH AGRAPHIA
 described by Dejerine in 1891.
 Is an acquired illiteracy, in which a previously educated
patient is rendered unable to read or write.
 Spantanous speech, naming, auditory comprehension,
and repetition are largely intact.
 but many cases manifest a fluent, paraphasic speech
pattern with impaired naming.
 This syndrome thus overlaps with Wernicke aphasia.

67.  Associated deficits include right hemi anopia and
elements of Gerstmann syndrome.
 The lesions typically involve the inferior parietal
lobule, especially the angular gyrus.
 Etiologies include strokes in the territory of the
angular branch of the left middle cerebral artery or
mass lesions in the same region.

69. Aphasic Alexia:
 many patients with aphasia have associated reading
disturbance.
 These are “third alexia” syndrome of Broca’s aphasia and
the reading deficit of Wernicke’s aphasia.
Agraphia:
 Like reading, writing may be affected either in isolation
(pure agraphia) or in association with aphasia (aphasic
agraphia).
 In addition, writing can be impaired by motor disorders, by
apraxia and by visuospatial deficits.
 Isolated agraphia has been described with left frontal or
parietal lesions.

70. LANGUAGE IN RIGHT HEMISPHERE
DISORDERS
 Left-handed patients→ right hemisphere language
dominance → aphasia from right hemisphere lesions.
 Right-handed patients → become aphasic after right
hemisphere strokes → crossed aphasia.
 Right-handed persons → left hemisphere dominance →
subtly altered language function after right hemisphere
damage → aprosodia.
.

71. Aprosodia
 Fundamental mechanisms of speech are undisturbed.
 Affective aspects of language are impaired.
 Normal prosody or emotional intonation of speech is lost.
 Motor aprosodia
 involves loss of expressive emotion with preservation of
emotional comprehension.
 sensory aprosodia
 Involves loss of comprehension of affective language.
 also called affective agnosia.
 In other words, right hemisphere-damaged patients
understand what is said, but not how it is said.

72. LANGUAGE IN DEMENTING DISEASES
Alzheimer disease (AD):
 Patients with early AD have anomic aphasia.
 In later stages, language functions become more
obviously impaired.
 Reading and writing the last learned language
functions are among the first to decline.
 Auditory comprehension later becomes deficient,
whereas repetition and articulation remain normal.

73.  The language profile may then resemble that of
transcortical sensory or Wernicke aphasia.
 In terminal stages, speech is reduced to the expression of
simple biological wants. eventually, even muteness can
develop.
Primary progressive aphasia (PPA):
 Varient of fronto temporal dementia (FTD).
 Fronto temporal dementia is now divided into four
subgroups:
 behavioral variant FTD
 progressive nonfluent aphasia
 semantic dementia
 logopenic primary progressive aphasia.

74. progressive non fluent aphasia:
 Broca-like pattern of aphasia involving
agrammatism and apraxia of speech.
 Usually reflects a “tauopathy”.
 Mutations in familial cases found in the tau gene on
Ch 17.

75. Semantic dementia:
 progressive fluent aphasia with impaired naming and
loss of understanding of even single words.
 In reading, they may have a surface alexia pattern.
 Not a tauopathy
 Progranulin mutation on Ch 17 with production of an
abnormal protein called TDP-43.
Logopenic primary progressive aphasia:
 involves anomia and some repetition difficulty, with
intact single word comprehension.

76.  MRI - different patterns of atrophy.
 Progressive non fluent aphasia → left frontal and insular
atrophy.
 Semantic dementia → bilateral anterior temporal
atrophy.
 Logopenic progressive aphasia → posterior temporal and
inferior parietal atrophy.
 Cortico basal degeneration can also present with language
abnormalities.
 Isolated aphasia secondary to Creutzfeldt–Jakob disease
have been reported, but these usually progress to dementia
over a period of months.

77. INVESTIGATION OF THE APHASIC PATIENT
 The bedside language examination is useful in forming a
preliminary impression of the type of aphasia and the
localization of the causative lesion.
 large number of standardized aphasia test batteries have
been published.
 They have the advantage of quantitation and standardization,
permitting comparison over time.
 most helpful battery is the Boston Diagnostic Aphasia
Examination, or its Canadian adaptation, the Western
Aphasia Battery.

78.  Further diagnosis of the aphasic patient rests on the
confirmation of a brain lesion by neuro imaging.
 MRI is the better modality than CT.
 In preparation for epilepsy surgery, the Wada test, or
infusion of amobarbital through an arterial catheter, is
useful in the determination of language dominance.
 Single-photon emission CT (SPECT), PET, and
functional MRI are contributing greatly to the study of
language.

79.  fMRI study showed
 Hypo metabolism in the language cortex shortly after
an ischemic insult.
 followed by increased activation of homologous areas
in the contra lateral hemisphere.
 then a shift back to the more normal pattern of left
hemisphere activation.

80. DIFFERENTIAL DIAGNOSIS
1. Ischemic strokes:
 bedside aphasia examination is helpful in delineating the
vascular territory affected.
 Wernicke aphasia → inferior division of the left MCA.
 Global aphasia → left MCA stem / ICA.
 Trans cortical motor aphasia → left ACA territory.
 pure alexia without agraphia → left PCA territory.
2. Hemorrhagic strokes:
 most commonly the basal ganglionic hemorrhages.
 Recovery was better with hemorragic strokes.
.

81. 3. Traumatic brain injury:
 Cerebral contusions, depressed skull fractures, and
hematomas of the intra cerebral, subdural, and epidural
spaces all cause aphasia when they disrupt or compress left
hemisphere language structures.
4. Tumors of the left hemisphere:
 onset of the aphasia is gradual.
 other cognitive deficits may be associated because of
edema and mass effect.
5. Degenerative diseases:
 Alzheimer disease / FTD
 Cortico basal degeneration

82. 6. Infections:
 Brain abscesses can mimic tumors in every respect.
 Chronic infections, such as tuberculosis or syphilis, can
result in focal abnormalities.
 Herpes simplex encephalitis has a predilection for the
temporal lobe and orbital frontal cortex and aphasia can be
an early symptom.
 AIDS - Opportunistic infections / AIDS dementia complex.
7. Seizures:
 Associated with aphasia in children as part of the Landau–
Kleffner syndrome or in adults as either an ictal or post ictal
Todd phenomenon.
 Epileptic aphasia is important to recognize because
anticonvulsant drug therapy can prevent the episodes.

83. 8. Migraine:
 Another transitory cause of aphasia.
 Wernicke aphasia may be seen in a migraine attack,
usually with complete recovery over a few hours.
9. Psychogenic:
 often associated with stuttering or stammering.

84. RECOVERY AND REHABILITATION OF APHASIA
 Patients with aphasia from acute disorders, such as
stroke, generally show spontaneous improvement over
days, weeks and months.
 In general, the greatest recovery occurs during the first
3 months, but improvement may continue over a
prolonged period, especially in young patients and in
global aphasics
 The aphasia type often changes during recovery.
 Global aphasia evolves into Broca aphasia, and
Wernicke aphasia into conduction or anomic aphasia.

85.  Language recovery may be mediated by shifting of
functions to the right hemisphere or to adjacent left
hemisphere regions.
 aphasia recovers best when left hemisphere areas,
recover function.
 Right hemisphere activation seems to be a “second best”
type of recovery.
 Speech therapy, provided by speech-language
pathologists, attempts to facilitate language recovery by a
variety of techniques.

86.  Repeated practice in articulation and comprehension tasks has
traditionally been used to stimulate improvement.
 Other techniques include
 melodic intonation therapy → which uses melody to
involve the right hemisphere in speech production.
 visual action therapy → which uses gestural expression.
 Two other therapeutic techniques are
 functional communication therapy →takes advantage of
extra linguistic communication
 cVIC or Lingraphica → a computer program originally
developed for primate communication.

87.  Speech therapy has remained somewhat controversial,
but evidence of efficacy is actually better for speech
therapy than for many drugs.
 A new approach to language rehabilitation is the use of
pharmacological agents to improve speech.
 first reported that the dopaminergic drug
bromocriptine promotes spontaneous speech output
in transcortical motor aphasia.
 Stimulant drugs are also being tested in aphasia
rehabilitation.

88.  Finally, stimulation techniques such as trans cranial
magnetic stimulation and direct cortical stimulation
are being applied to patients with aphasia.
 These techniques await validation by larger clinical trials.