1. APHASIA --------------- OUTLINE
What is aphasia?
• Communication process
Does the patient have aphasia ?
• If so, where is the lesion?
• What kind of aphasia is this?
• What is the etiology?
Is it important to diagnose
aphasia?
• Localization
• Treatment
• Prognosis
• Functional state of the patient
4. APHASIA
– Acquired disorder of language due to brain damage. In form of impaired
ability to use or comprehend words.
Aphasia is an acquired communication disorder that impairs a person's ability to process language.
Aphasia impairs the ability to speak and understand others, and most people with aphasia experience
difficulty reading and writing.
This class of language disorder ranges from having difficulty remembering words to being completely
unable to speak, read, or write.
Encompassed under the term aphasia are selective, acquired disorders of reading (alexia) or writing
(agraphia).
• Aphasia causes problems with any or all of the following
communications abilities: speaking, listening, reading, and
writing.
5. • Aphasia does not include:
• Developmental disorders of
language, often called dysphasia
in the united states.
• Purely motor speech
disorders, limited to articulation
of speech via the oral-motor
apparatus, referred to as
stuttering, dysarthria, and verbal
apraxia.
• Disorders of language that are
secondary to primary thought
disorders, such as schizophrenia.
• Does not affect intelligence.
6. Communication
• Communication is a multidimensional dynamic process
that allows human beings to interact with their
environment.
• Through communication, people are able to express
thoughts, needs, and emotions. Communication is a
complex process that involves
cerebration, cognition, hearing, speech production, and
motor coordination.
• Evaluation of a communication disorder includes
consideration of all aspects of the normal communication
process
7. Language
• Language is the transformation of thoughts into
meaningful symbols communicated by speech, writing, or
gestures.
8. Anatomical basis of language
• Language is a higher cortical function lateralize to
the dominant hemisphere ( left) supplied by
MCA which is branch of anterior circulation (ICA).
9. Dominant hemisphere
• Language lateralize to the dominant hemisphere:
o80% of people are right handed.
o 96-99% of right handed people in the left hemi sphere.
o 60% of left handed people also lateralize to the left
o 25% of left handed shows right dominancy.
o the remaining are mixed dominancy.
10. Dominant hemisphere
• Many naturally left-handed children are trained to
use the right hand for writing
– in determining handedness, one must ask which hand is
preferred for throwing a ball
– threading a needle, sewing
– using a tennis racket or hammer
– which eye is used for sighting a target with a rifle or other
instrument.
• Pharmacological methods: injecting anesthetic in left
carotid artery and observe if aphasia occur
17. Analysis of language and definitions
• Language: complex system of communication symbols
and rules for their use.
• Speech: the articulation and phonation of language
sounds.
• Motor speech disorders:
– Dysarthrias: disorder of articulation of single
sounds, consistent.
– Dysphonia: voice disorder
– Stuttering
– Apraxia of speech: misarticulation of phonemes,especially
consonant sounds. inconsistent distortions and substitutions
of phonemes.
18. Analysis of language and definitions ,,,,,,Cont.....
• Paraphrasia: presence of errors in the patient’s speech output.
– Semantic: substitution of an incorrect word from same group (e.g., “fork” for
“spoon”).
– Phonemic: involving substitution of an incorrect sound (e.g., “shoon” for “spoon”)
• Syntax: the grammatical construction of phrases and sentences.
• Pragmatic : proper use of speech and language in a
conversational setting, including pausing while others are
speaking, taking turns properly, and responding to questions.
• morphology is the use of appropriate word endings and
connector words for tenses, possessives, and singular versus
plural
19. Analysis of language and definitions ,,,,,Cont.....
• Neologisms: involve nonexistent word forms
• Jargon speech: A pattern of paraphasic errors and
neologisms that so contaminate speech that the meaning
cannot be discerned.
• word salad: normal speech morphology, normal sentence
structure but incoherent content.
• Telegraphic: often producing the principal, meaning-
containing nouns and verbs but omitting small grammatical
words and morphemes.
20. Pathogenesis and etiology of aphasia
• Vascular lesions:
– Ischemic strokes, the most common cause of aphasia.
– The clinical features of the aphasia are of crucial importance to
the vascular diagnosis.
– hemorrhagic strokes an important cause of aphasia, most
commonly the basal ganglionic hemorrhages associated with
hypertension.
– AVM, drugs, may cause hemorrhages
– amyloid angiopathy.
– cerebral vasculitis.
21. Pathogenesis and etiology of aphasia
• Traumatic brain injury
– Cerebral contusions
– depressed skull fractures
– hematomas of the intracerebral, subdural, and epidural spaces
– Gunshot wounds produce focal aphasic syndromes
• Tumors of the left hemisphere
– The onset of the aphasia is gradual, and edema and mass effect
may result in other cognitive deficits.
– Enlarging tumor may be difficult to distinguish from a diffuse
encephalopathy or early dementia.
22. Pathogenesis and etiology of aphasia
• Infections of the nervous system
– Brain abscesses can mimic tumors and present with aphasia
– 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
manifestation, along with headache, confusion, fever, and
seizures.
• Aphasia often is a permanent sequel in survivors of herpes encephalitis.
– AIDS: either the AIDS dementia complex or the opportunistic
infections.
23. Pathogenesis and etiology of aphasia
• degenerative central nervous system diseases
– Alzheimer’s disease may be more common in familial cases and may
predict poor prognosis.
– dialysis dementia syndrome: started with stuttering followed
by true aphasia and dementia
• Seizures:
– Epileptic aphasia is important to recognize because anticonvulsant drug
therapy can prevent the episodes
25. Broca Aphasia
• speech pattern:
– Effortful, difficulty initiating speech
– Non fluent
– Hesitant
– telegraphic speech. An example is “wife come hospital.”
• deficiency, particularly in the comprehension of complex syntax.
• Third alexia: Reading often is impaired
• Writing: right hand could be paralyzed, left hand apraxia
• Associated neurological deficits
– right hemiparesis, hemisensory loss,
– apraxia of the oral apparatus and the nonparalyzed left limbs
• frequent association with depression
– Typically they are aware of and frustrated by their deficits.
26. Broca Aphasia
• Lesion:
– Traditional Broca Area” Brodmann’s 44&45”
– left frontoparietal lesions
– territory of the upper division of the left middle cerebral artery
29. Wernicke’s Aphasia
• the opposite of Broca’s aphasia in that expressive
speech is fluent but comprehension is impaired.
• speech pattern:
– Effortless
– excessively fluent (logorrhea).
– Paragrammatism:
• speaker of a foreign language would notice nothing a miss, but a listener
who shares the patient’s language detects speech empty of
meaning, containing verbal paraphasias, neologisms, and jargon
productions.
• Naming is deficient, often with bizarre, paraphasic
substitutions for the correct name
• patients show greater deficit in one modality than
in the other.
30. Wernicke’s Aphasia
• Writing samples are especially useful in the detection of
mild Wernicke’s aphasia.
• Associated signs are limited in Wernicke’s aphasia
– Most have no elementary motor or sensory deficits
– right homonymous hemianopia may be present.
• Depression is less common; many Wernicke’s aphasics seem
unaware of or unconcerned about their communicative deficits.
• The lesions
– posterior portion of the superior temporal gyrus, sometimes extending
into the inferior parietal lobule.
– Damage to Wernicke’s area (Brodmann’s area 22)
– Wernicke’s area lies within the territory of the inferior division of the left
middle cerebral artery.
33. Global Aphasia
• summation of the deficits of Broca’s aphasia and
Wernicke’s aphasia.
• Speech is nonfluent or mute, but comprehension also is
poor, as are naming, repetition, reading, and writing.
• Most patients have dense right
hemiparesis, hemisensory loss, and often hemianopia.
35. Conduction Aphasia
• striking deficit of repetition.
• relatively normal spontaneous speech, although
some make literal paraphasic errors and hesitate
frequently for self-correction.
• Naming may be impaired, but auditory
comprehension is preserved.
• Associated deficits:
– right-sided sensory loss may be present
• involvement of the arcuate fasciculus
37. Anomic Aphasia
• aphasic syndromes in which naming, or access to the
internal lexicon, is the principal deficit.
• Spontaneous speech except for 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
• Anomic aphasia thus serves as an indicator of left
hemisphere or diffuse brain disease.
39. Transcortical
• repetition is normal
• presumably because the causative lesions do not disrupt the perisylvian
language circuit from Wernicke’s area through the arcuate fasciculus to
Broca’s area.
• Three types:
1.Isolation syndrome:
• global aphasia in which the patient repeats, often echolalically
• occurring predominantly with large Watershed infarctions of the left hemisphere or
both hemispheres that spare the perisylvian cortex, or in advanced dementias.
2. Transcortical motor aphasia:
• analog of Broca’s, speech is hesitant or telegraphic, comprehension is relatively
spared, but repetition is fluent.
• deep frontal white matter, or in the medial frontal region, in territory of ANTERIOR
CEREBRAL ARTERY.
3. Transcortical sensory aphasia:
• analog of Wernicke’s aphasia, repetition intact
• occurring with strokes of the left temporo-occipital area and in dementias.
42. Disconnection syndromes:
loss of integration among deferent lobes due to lesion affecting the connecting pathways that leads to
disorganized normal function.
• Intrahemespheric disconnection
1. Conduction (also called "central") aphasia.
2. Buccal Lingual and Sympathetic apraxia in Broca's aphasia. Destruction of the link
between left and right motor association cortices causes an apraxia of commanded
movements of the left hand and weakness of right brachiofacial weakness, apraxia
of tongue and lips.
3. Pure word deafness.
• Interhemespheric disconnection
1.alexia without agraphia
2.Left side apraxia
3.Agenesis of corpus callosum: right and left visual fields can’t
match presented objects
44. Gerstmann’s syndrome
• Angular gyrus as
the site of
lesions
• Consist of :
• Alexia
• Agraphia
• Right Left
Disorientation
• Acalculia
• Finger Agnosia
45. Clinical Evaluation of Aphasia
History
– Onset, Frequency, Duration
• Strokes are characterized by the abrupt onset of a neurological deficit in
a patient with vascular risk factors.
• precise temporal profile is important
– Most embolic strokes are sudden and maximal at onset, whereas
thrombotic strokes typically wax and wane or increase in steps.
– The sudden onset of Wernicke’s aphasia nearly always indicates an
embolus to the inferior division of the left middle cerebral artery.
• Global aphasia may be caused by an embolus to the middle cerebral
artery stem, thrombosis of the internal carotid artery, or even a
hemorrhage into the deep basal ganglia.
– deficits tend to worsen gradually over minutes to hours, in contrast with
the sudden or stepwise onset of ischemic strokes.
• Cont,,,,,,
46. Clinical Evaluation of Aphasia ,,,,,,, CONT
History
– Baseline: difficulty in articulation, vision, hearing,
intelligence, education and literacy” reading and writing”,
psychological diseases, memory deficit- dementia
– Progression- improved , slowly progressed
– Associated symptoms
– Etiological factors: DM, Hypertension, AF, AIDS, Fever,
vomiting, Trauma
– Associated symptoms: other neurological symptoms
“ headache, loss of vision, weakness and motor deficit,
sensory loss, epilepsy, cognitive defects”
47. Clinical Evaluation of Aphasia ,,,,,,,,, CONT
Examination:
• Examination of Other Cortical Functions
o Consciousness
o Cognitive Function
o Mental Status and Memory
o Orientation
o Alertness; Attention and Concentration
o Judgment and reasoning
o Thought Contents
o Complete Neurological Exam
o aimed to localize the lesion “ Associated Deficit”
o aimed to define the etiology.
– Psychiatric evaluation: acute encephalopathy or delirium
• accompanying behavioral disturbances, such as agitation, hallucinations, drowsiness, or
excitement, and cognitive difficulties, such as disorientation, memory loss, or delusional thinking
– language assessment:
o Bedside Language Examination
o cont,,,
48. Clinical Evaluation of Aphasia ,,,,,,,,, CONT
Examination:
– Content of speech
– Paraphrasia
– telegraphic speech
– conjunctions and proposition use, syntax, and morphology of speech.
– Neologism
– Jargon of speech
– Word salad
– Assess pragmatism
– Other Useful Tests
• For neurologists, the most helpful battery is the Boston Diagnostic Aphasia Examination
• the Western Aphasia Battery.
– Both tests provide subtest information analogous to that obtained with the bedside
examination, and therefore meaningful to neurologists, as well as aphasia syndrome classification.
– clinical systemic examination
• clues to etiology
– AF
– Hypertension and DM
– Atherosclerosis
– Signs increased intra cranial pressure –papilloedema, brain metastasis
– AIDS
– evidence of trauma
– self injury and loss of sphenctric control –epilepsy
• Cont,,,,,
49. Clinical Evaluation of Aphasia ,,,,,,,, CONT
Diagnostics:
– CBC and Chemistry Panel, PT, PTT, INR –May give clue to etiology and
benefit in differentiating aphasia from
– ECG
– IMAGING:
• CT W/WO CONTRAST
• MRI
• PET AND SPECT – Academic
– EEG
– Carotid Doppler and MRA
• Referrals
– Neurology
– Speech-language pathologists
• Follow-up examinations also are helpful
– the evolution of a neurological deficit over time is the most important
clue to the specific disease process.
• Cont,,,,,,
50. Bedside Language
Examination
D. Frank Benson and Norman, updated by Alexander and Benson (1997)
51. 1. Spontaneous speech
• elicited by asking the patient to describe the weather or
the reason for coming to the doctor.
• Counting or listing days of the week.
• Signs:
– Fluency: Fluent speech flows rapidly and effortlessly; nonfluent
speech is uttered in single words or short phrases, with frequent
pauses and hesitations.
– initiation difficulty
– word-finding difficulties
– pauses
52. 2. Naming
• asking the patient to name a few items in each of
thee following category
– objects
– Object parts
– Colors
– Body parts
– Pictures
– Proper names of persons
• The examiner should ask questions to be sure that the patient recognizes
the items or people that he or she cannot name.
53. 3. Auditory comprehension
• follow a series of commands of one, two, and three steps.
• one-step command is “Stick out your tongue”
• two-step command is “Hold up your left thumb and close your eyes.”
• The responses to nonsense questions (e.g., “Do you vomit every day?”)
quickly establish whether the patient comprehends.
– Successful following of commands ensures adequate comprehension, at least
at this simple level.
– failure to follow commands does not automatically establish a loss of
comprehension. 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, or by commands that require
only a pointing response.
54. 4. Repetition
• aphasic persons have special difficulty with
grammatically complex sentences.
• grammatically complex sentences; “no ifs, ands, or buts” is
especially challenging for aphasics.
– aphasics can repeat familiar or “high-probability” phrases much better
than unfamiliar ones.
– whispering a phrase in the patient’s ear, as in a hearing test, may help
cue the patient to attempt repetition.
55. 5. Reading
• examiner must have some idea of the patient’s previous
reading ability.
– Reading should be tested both aloud and for comprehension.
– The examiner should carry a few printed commands to facilitate
a rapid comparison of auditory and reading comprehension.
56. 6. writing
• Spontaneous writing, such as a sentence
describing why the patient has come for
examination, is especially sensitive for the
detection of language difficulty.
writing to dictation and copying should be tested.
– A writing specimen may be the most sensitive indicator of mild
aphasia, and it provides a permanent record for future
comparison.
• look for spelling errors, structural errors, and apraxia.
57. RECOVERY AND REHABILITATION OF
THE PATIENT WITH APHASIA
• The sudden onset of aphasia would be expected to
cause great apprehension, but except for cases of pure or
almost pure motor disorders of speech, most patients
show remarkably little concern.
58. RECOVERY AND REHABILITATION OF
THE PATIENT WITH APHASIA
• After stroke – If symptoms last longer than two or three months,
complete recovery is unlikely
– People continue to improve over a period of time
– Slow process for both patient and FAMILY
– Need to learn compensatory strategies for communicating
• Global aphasia recovery occur after 6 months
• The aphasia type often changes during recovery: Global aphasia
evolves into Broca’s aphasia, and Wernicke’s aphasia into
conduction or anomic aphasia.
• Language recovery may be mediated by shifting of functions to
the right hemisphere or to adjacent left hemisphere regions.
59. RECOVERY AND REHABILITATION OF
THE PATIENT WITH APHASIA
• Whether contemporary methods of speech
therapy accomplish more than can be accounted
for by spontaneous recovery is still uncertain.
• Most aphasic disorders are caused by vascular
disease and trauma, and they are nearly always
accompanied by some degree of spontaneous
improvement in the days, weeks, and months that
follow the stroke or accident.
60. Communication with aphasic Do’s and Don’ts
• Keep your voice at a normal level and emphasize key words
• Augment speech with gesture and visual aids when
possible
• Repeat statements when necessary
• Do not attempt to finish the patients statement for them
61. Communication with aphasic Do’s and Don’ts
• Talk to the person as an adult NOT as a child
• Minimize or eliminate background noise
• Make sure you have the person’s attention before
communicating
• Encourage and use all modes of communication
– Speech/writing/drawing/yes-no responses
62. Communication with aphasic Do’s and Don’ts
• Give them time to talk and permit a reasonable amount of
time to respond
• Accept all communication attempts
• Keep your own communication simple but adult
• Simplify sentence structure and reduce your rate of speech
63. References
– Neurology – Bradly
– Neurology –Lindsay
– Harison
– Neuroanatomy –Snell
– National Aphasia Association
