1. Speech disorders
DR. SUBODH KUMAR MAHTO,
DEPT. OF MEDICINE
PGIMER,DR.RML HOSPITAL.
NEW Delhi
DR. SUBODH KUMAR MAHTO,
DEPT. OF MEDICINE
PGIMER,DR.RML HOSPITAL.
NEW Delhi
2. Overview
Definitions
Components of speech
Anatomy and Areas of language in brain
Pathway of language in brain
Types of speech and language disorders
Aphasia syndromes
Approach to aphasia
3. Definitions
Phonation is the production of vocal sounds
without word formation.
Speech consists of words which are articulate
vocal sounds that symbolize and communicate
ideas.
Articulation is the enunciation of words and
functions, it is a function of organs and muscles
innervated by the brainstem.
Language is a mechanism for expressing
thoughts and ideas by speech, by writing or by
gestures and actions.
4. Components of speech
Speech is the mechanical function of one’s
ability to communicate in oral language.
Language production
Phonation
Articulation
5. Speech and Hemispherical Dominance
Speech is the function of cerebral
hemisphere.
In right handedness, 90% of human have
left hemispherical dominance.
10% have left handedness, 7 out of these
10% have left hemispherical dominance 3
out of the 10% have right hemispherical
dominance
97% of human have left hemispherical
dominance.
3% have right hemispherical dominance.
Speech is a function of Left hemisphere
7. Anatomy of speech function
4 main language areas
Situated, in most persons, in the left
cerebral hemisphere
The entire language zone that
encompasses these areas is perisylvian,
i.e., it borders the sylvian fissure.
Two language areas
Receptive Language(central language
zone)
Executive Language(Production
zone)
8. Receptive Language
The main receptive area, subserving the perception
of spoken and probably of internal language, occupies
the posterior-posterosuperior temporal area (the
posterior portion of area 22) and Heschl’s gyri (areas
41 and 42). The posterior part of area 22 in the planum
temporale is referred to as Wernicke’s area
A second receptive area, subserving the perception
of written language, occupies the angular gyrus (area
39) in the inferior parietal lobule, anterior to the visual
receptive areas. The supramarginal gyrus, which lies
between these auditory and visual language “centers,”
and the inferior temporal region, just anterior to the
visual association cortex, are probably part of this
central language zone as well.
9. Executive Language(Production zone)
Broca’s area
Concerned with motor aspects of speech.
Situated at the posterior end of the inferior
frontal convolution (Brodman’s areas 44 and
45).
Exner’s writing area
Situated in the posterior part of the second
frontal convolution
Integrated with the motor apparatus for the
muscles of thehand.
12. Broca’s area
The motor area for
spoken speech is
situated in the
posterior part of the
left inferior frontal
gyrus.
Paul Broca, a French
Surgeon, described it
in 1865 .
This area is
neuroanatomically
described as the
13. Wernicke’s area
The auditory
comprehension of
spoken speech takes
place in the posterior
end of the superior
temporal gyrus.
Karl Wernicke, a
German neurologist,
identified it and
described the pathway
connection to Broca’s
area via the arcuate
fasciculus.
This area is
14. Conduction Area
• A deep, white matter
tract, connecting the
Wernicke’s area to
the Broca’s area, also
called arcuate
fasciculus.
• Damage to the
arcuate fasciculus
leads to conduction
aphasia: repetition
deficits arise following
damage to the
15. Exner’s area
It is an area of the brain
just above Broca’s area
and anterior to the
primary motor control
area. It is the area for
writing, close to the area
for hand movement.
Damage to it results in
agraphia.
This area is neuro
anatomically described
16. Reading area
It is an area of the brain just
medial to the left occipital lobe
and in the splenium of the
corpus callosum.
It is the centre for reading. It
recieves impulses from the eye
and transmits them to the
association area for analysis
by red matter, then passes it
on to the arcuate fasciculus.
A lesion here causes pure
word blindness.
This area is neuroanatomically
described as Brodmann area
17.
17. Pathways of speech and language
• Arcuate fasciculus is the bridge from the Wernicke’s area
to the Broca’s area
19. Dysphasia
Group of language disorders in which
there is impairment of the power of
expression by speech, writing, or
signs, or impairment of the power of
comprehension of spoken or written
language.
More severe forms of dysphasia are
called aphasia
20. Wide variation in classification
schemes
Influential ones in history of aphasiology:
Wernicke-Lichtheim 1881, 1885
Head 1926
Goldstein 1948
Luria 1966
Benson 1979
Benson & Ardila 1996
Damasio 1998
But ..
All recognize just a small number of basic
syndromes
Most of the variation in classification
schemes is just terminological.
21. Damasio’s Classification
• Wernicke’s aphasia
• Broca’s aphasia
• Conduction aphasia
• Transcortical sensory aphasia
• Transcortical motor aphasia
• Global aphasia
• Anomic aphasia
• Alexia
• Pure word deafness
• Atypical aphasias
23. Classification of Aphasias
Three broad categories:
Nonfluent aphasias – there are difficulties in
articulating but relatively good auditory verbal
comprehension (e.g., Broca’s severe, Broca’s
mild)
Fluent aphasias – fluent speech but difficulties
either in auditory verbal comprehension or in the
repetition of words, phrases, or sentences spoken
by others (e.g., Wernicke’s or sensory aphasia;
Anomic)
Pure” aphasias – there are selective impairments
in reading, writing, or the recognition of words
24. Expressive Aphasia(Non Fluent )
Caused by damage to inferior left frontal lobe
Disruption of normal speech production
Slow, laborious, Non fluent aphasia
Difficulty in saying little words with grammatical
meaning
25. Receptive Aphasia(Fluent aphasia)
Poor speech comprehension, and production of
meaningless speech.
Fluent ,unlabored
Maintain a melodic line, voice rising and falling
normally.
26. Characteristics of Broca Aphasia
Non-fluent speech
Decrease verbal output
to less than 10
words/min, increased
effort in production of
speech
Poorly articulated
Consists of short
phrases
Produced with effort
Mostly nouns and other
content words
Deficiency or absence of
inflectional affixes
Absent or deficient
syntactic structure
27. Word classes in Broca aphasia
Mostly nouns
Some adjectives
A few verbs
Function words few or non-existent
28. Comprehension in Broca’s aphasia
Generally good
More or less impaired for syntactically
complex sentences
Difficulty in comprehending the same
words that are omitted in speech
production
Also, difficulty with repetition of these
words
Difficulty understanding relational
words
29. Subtypes of Broca aphasia
Type I
little Broca aphasia
Milder defects
Less extensive damage
Better prognosis
Type II
Symptoms worse
More extensive damage.
Most commonly involed the left inferior
frontal gyrus(area 44)
30. Wernicke’s Aphasia
Impaired comprehension
Fluent verbal output
Output of words may
reach up to 200
words/min, Effortless
speech
Augmented verbal output
Extra syllables at ends
of words
Extra words at ends of
phrases
Extra phrases at ends
of sentences
Augmentations usually
nonsensical
Syntax otherwise not too
bad
31. Areas of damage in Wernicke’s
aphasia
Always involved:
Posteriorsuperiortemporal gyrus
The classical core of Wernicke’s area
Usually also involved:
More of superiortemporal gyrus
middle temporal gyrus
Temporal plane
Often also involved:
Angulargyrus
Supramarginal gyrus
Temporal-occipital junction area
32. Subtypes of Wernicke aphasia
Type I
Damage is more anterior
Phonological recognition most affected
“Word deafness”
Type II
Damage is more posterior, incl. angular
gyrus
More word-blindness than word-deafness.
I.e alexia
33. Conduction Aphasia
Relatively uncommon.
Spontaneous speech
is fluent.
Considerable word
finding difficulty .
Preserved auditory
comprehension.
Significant difficulty
with repetition .
Self correction with
Numerous pauses.
Lesion: Left superior
temporal area,
supramarginal gyrus
34. Global aphasia
Severe impairment in all
modalities Speaking,
listening, reading and
writing Severely impaired
auditory comprehension.
Involve both broca,s and
wernicke,s area
Very limited speech output.
Only few understandable
utterances.
Caused by massive Fronto-
tempero-parietal
lesion,Complete occlusion
35. Extra-Sylvian Aphasic Syndromes
“Extra-Sylvian” (“Transcortical”)
Extrasylvian motor aphasia
Type I
Type II
Extrasylvian sensory aphasia
Sometimes just called ‘anomic
aphasia’
Type I
Type II
36. Trans cortical Aphasic Syndromes
In all perisylvian syndromes, repetition is
faulty
In all extra-sylvian aphasic syndromes,
repetition is intact
“Aphasia without repetition disturbance
almost invariably indicates pathology outside
the perisylvian region
37. Trans cortical motoraphasia
• Nonfluent output
– Delayed initiation
– Terse, poorly
elaborated
utterances
– Incomplete
sentences
– Verbal paraphasia
• Good comprehension
• Good repetition
38. Trans cortical motoraphasia, Type I
Left dorso lateral prefrontal damage
Anterior and superior to Broca’s area
Non-fluent output, but repetition good
Articulation is normal
Difficulty following commands
Understand command but do not respond
Damage anterior and superior to Broca’s
area( Brodmann,s area) 45, 46, and/or part of
area 9)
39. Trans cortical motoraphasia, Type II
Damage to supplementary motor area
Occlusion of left anterior cerebral artery
Non-fluent output, but good repetition
Difficulty initiating speech
Perhaps a purely motor disorder that does not
involve basic language functions
40. Trans cortical sensory aphasia
Speech is fluent
Good repetition
Comprehension is
impaired
Naming is impaired
Paraphasia is frequent
Semantic substitutions
Neologisms
Echolalia (patients repeat
words of examiner)
Pointing is impaired
Two subtypes
41. Trans cortical sensory aphasia, Type
I
Damage to temporal-parietal-occipital
junction area
I.e., lower angular gyrus and upper area
37
Fluent spontaneous output
Poor comprehension
Naming strongly impaired
Semantic paraphasia
42. Trans cortical sensory aphasia, Type
II
Damage to upper angular gyrus
Fluent output
Variable ability to comprehend speech
Naming strongly impaired
Few semantic paraphasias
Repetition excellent
Many circumlocutions
43. Anomic aphasia
• Perhaps part of a
continuum with
extrasylvian sensory
aphasia
• Comprehension is good
in many cases
– Unlike extrasylvian
sensory aphasia
• Production and
repetition are good
• Cannot be reliably
localized
– Many different areas of
damage can result in
naming difficulty
• Left middle and
44. Paraphasia
Loses the ability of speaking correctly
Substitutes one word for another
Changes words and sentences in an
inappropriate way
Speech is fluent but is error-prone, e.g.
'treen' instead of 'train‘
Often develops after a stroke or brain
injury
46. Literal/phonological paraphasia
More than half of the spoken word is said
correctly.
saying pun instead of spun.
May occur in Receptive aphasia
and Sensory Transcortical Aphasia.
Neologistic
Spoken word that is said less than half
correct.
Occasionally the word is not said correctly at
all,
Example Balenti for Banana.
47. Verbal paraphasia
Word is substituted for the target word.
A common example is saying dog instead of
cat.
Semantic paraphasia - The substituted word is
related to the intended word
Remote paraphasia - The substituted word is,
at most, distantly related to the intended word.
48. 28/02/2006
Summary of Aphasias
Type of
Aphasia
Spontaneous
speech
Paraphasias Comprehension Repetition Naming
Broca’s Nonfluent - Good Poor Poor
Global Nonfluent - Poor Poor Poor
Transcortical
motor
Nonfluent - Good Good Poor
Wernicke’s
Aphasia
Fluent + Poor Poor Poor
Transcortical
sensory
Fluent + Poor Good Poor
Conduction Fluent + Good Poor Poor
Anomic Fluent + Good Good Poor
49. The Dysarthrias
A group of impairments that may affect the
speed, range, direction, strength, and timing of
motor movements.
A hallmark of dysarthria speech: errors are
consistent
Errors are distortions and omission of sounds
No difficulty with initiation of sound
Results from paralysis, weakness, or
discoordination of speech muscles
Not a language disorder but rather a difficulty
in motor speech control
Global characteristic: weak muscular function
Can affect: respiration, phonation, articulation,
50. 50
Motorspeech system:
The brain
Pathways in the central and peripheral nervous
systems
Muscles and structures of respiration
The larynx
The articulators
Muscle movement depends:
Motor planning and programming in the cerebral
cortex
Motor plan refined by different cerebral areas
(e.g., the force and speech of muscle contraction
are modified, muscles are coordinated with each
other)
51. 51
Dysarthria
Dysarthria: breakdown or disruption
somewhere in this chain of events.
Muscles cannot contract with full strength, or are
not coordinated with each other
Results in a breakdown in articulation.
Different etiologies include:
Stroke
Traumatic Brain Injury
Degenerative Neurological Disease
Brain Tumors
Infections
53. Developmental Dysarthria
Present at birth
Usually occurs along with known disturbance to
neuromotor functioning
Can be caused by pre-, peri-, or post-natal
damage to the nervous system
Most common types:
-spastic
-dyskinetic
.
55. 55
Flaccid Dysarthria
Damage to peripheral nervous system
Muscles: flaccid, or lose tone, lose normal
muscular stretch reflex that maintains muscle
tone.
Characterized by hypotonia (weak muscle tone)
which results in weakness or paralysis of the
affected muscle
Speech characteristics include shallow
breathing, breathy voice, aphonia (no voice),
reduced pitch and loudness, monotone,
hypernasality, and imprecise articulation
Etiologies
Bell’s Palsy, myasthenia gravis, and muscular
56. 56
Spastic Dysarthria
Damage to central nervous system nerve tracts
or cerebral areas that control muscles of the
speech production system.
Muscles: spasticity, or increased muscle tone
because of an unregulated stretch reflex arc.
Characterized by hypertonia (stiff and rigid
muscles) commonly caused by stroke
Speech movements are difficult and speech is
characterized as slow with jerky, imprecise
articulation and reduction in the rapidly
alternating movements of speech
57. 57
Ataxic Dysarthria
Damage to cerebellum or nerve tracts
communicating with cerebellum
Ataxia: incoordination
The speech of ataxic dysarthria is often
described as sound “drunk”
Characterized by a combination of hypotonia
(reduced tone) and ataxia resulting in problems
in the accuracy, timing, and direction of
movement
Speech movements are jerky and imprecise
58. 58
Hyperkinetic Dysarthria
Damage to the basal ganglia, (regulates
motor movement)
Hyperkinetic movements: unintended and
uncontrolled movements occurring either
spontaneously or when muscles contract.
59. 59
Hypokinetic Dysarthria
Damage to basal ganglia
Muscles: hypokinetic with reduced in
range, strength, and force of movement
because of excessive rigidity.
Excessive muscular rigidity: high levels of
muscle tone
60. 60
Mixed Dysarthria
Combination of any of the other types of
dysarthrias
Associated with degenerative neurological
diseases such as Amyotrophic Lateral Sclerosis.
Multiple levels or areas of the nervous system
damaged or disrupted at the same time.
62. Speech Apraxia
Disorder of motor placement and sequencing
that’s unrelated to muscle weakness, slowness,
or paralysis,not arise due to patients failure to
understand the nature of task.
When speech muscle groups are affected, it
is called apraxia of speech
Speech difficulties are not the result of
muscle weakness or slowness (dysarthria) or of
linguistic processing (aphasia)
Broca,s aphasia and conduction aphasia are
commonly involved.
63. 63
Speech Apraxia
In true apraxia of speech, no inherent weakness
of muscles
Apraxia of speech can co-occur with:
Oral apraxia - disruption in the ability to
purposely move oral structures
Limb apraxia - disruption in the ability to
purposely move limbs on command
64. Characteristics of Speech
Apraxia
Groping attempts to find the correct
articulatory position
Frequent articulation errors
Self-correcting behaviors
Variable in their abilities
65. 65
Speech Apraxia
Individuals often recognize their errors
Attempt to correct them resulting in “groping”
Individuals often report: ‘they know what they
want to say, but can’t say it’
May be able to write it down or give descriptions
66. 66
Speech Apraxia
The errors: variable
Sometimes may say a word correctly and other
times not
More errors on consonants than vowels.
Automatic speech is better
67. Dysphonia.
Dysphonia is a syndrome dominated by
sustained muscle contractions frequently
causing twisting and repetitive movements, or
abnormal postures that may be sustained or
intermittent
Spasmodic Dysphonia is a focal (isolated)
dysphonia that involves one small group of
muscles in one area of the body: the larynx
Most dysphonias are “action induced” e.g.,
larynx is normal at rest, not during speaking
68. Spasmodic dysphonia
Spasmodic dysphonia is one of the most
frequently misdiagnosed conditions in
speech-language pathology
Psychogenic or organic?
Cause is unknown
Focal dysphonia involving uncontrollable
spasms in the muscles for voicing
Basal ganglia malfunctioning
69. Onset is usually gradual
Average age of onset is between 30 and 50
More common in females than in males
Some cases are hereditary (gene on
chromosome 9)
Often diagnosed following respiratory tract
infections, laryngeal damage due to injury, and
vocal overuse
Symptoms worsen under stressful conditions
and while talking on the phone
71. AdductorSpasmodic Dysphonia
Most common form
Involuntary muscle spasms cause the vocal
folds to slam together
Stiffness of vocal folds
Tight, strained, strangled or “over pressurized”
voice (Stemple, 2000)
Prolongation of vowel sounds
Words are cut off or difficult to initiate due to
spasms
Stuttering like symptoms
Most evident in vowels, liquids, glides
72. AbductorSpasmodic Dysphonia
Spasms in the PCA
Abrupt, discontinuous escapes of air
Inability of the TVF to close for voicing results in
a whispered voice quality
Voiceless consonants are prolonged
/s/, /h/, /k/ before open vowel sound
Difficulty coordinating speaking and breathing
73. Approach to a patient with aphasia
• Historic time course aids in the differential
diagnosis of aphasia.
• Is the patient right or left handed
• Education status of patient
• Mother tongue of patient
• Is patient deaf or not
• Sudden-onset or rapid progression implies stroke
or other vascular cause.
• A slowly progressive course leads to consideration
of degenerative, neoplastic, or neuro-
immunological causes.
74. • History
A sudden onset of aphasia in an otherwise healthy
adult is most likely to be vascular (ischaemic
stroke or intracerebral haemorrhage), although
tumour, infection, or other lesion limited to a single
vascular territory will often mimic the stroke
syndrome.
Considerations of pace of onset and coincident
disease may broaden the differential diagnosis as
to the cause.
75. Rapid onset with poor nutrition will lead to suspicion
of Wernicke's encephalopathy where it mimics
aphasia.
Rapid-onset fluent aphasia with severe impairments
in word meaning should be treated as herpes
encephalitis until proven otherwise.
Aphasia due to seizure or migraine may appear in
patients with history of epilepsy or migraine
headaches.
Progression of aphasia over several weeks raises
76. Weight loss can be a sign of cancer or
nutritional deficiency, raising the suspicion for
tumor or Wernicke's encephalopathy.
Impairment of language over at least 2 years
followed by the onset of other cognitive or
behavioral deficits suggests a
neurodegenerative disorder, such as
Alzheimer's disease or primary progressive
aphasia.
77. General examination
Fever or tachycardia may signal infectious cause
such as herpes encephalitis or brain abscess.
Neck stiffness occurs with meningoencephalitis or
subarachnoid haemorrhage.
Depressed, apathetic, or manic affect is common
after stroke or in dementia.
Cardiac arrhythmia, carotid bruit, and peripheral
pulse deficit suggest ischaemic stroke, CNS Lyme
disease, or carotid stenosis.
Traumatic aphasia may be accompanied by typical
findings of head injury such as bruises, fractures,
bleeding, or watery nasal discharge (CSF
78. Neurological examination
Neurological deficits may indicate the relative
extent of damage to the brain.
Stance and gait may be affected by truncal rigidity
or haemiparesis of the leg.
Sensory deficits on the right often accompany
aphasia due to left parietal or thalamic lesions of
any cause.
Several aspects of language are tested to
distinguish between various aphasia syndromes,
which are associated with particular vascular
territories.
79. How is Aphasia Identified
Assessment of speech and language
disturbances – important component
Assessment and treatment completed by
interdisciplinary team of professionals using a
holistic approach
Evaluation goals will address:
Presence or absence of aphasia
Type or syndrome of aphasia
Most beneficial treatment plan
Prognosis for recovery
Referrals to other professional as needed
.
81. Fluency
speech output may be nonfluent
hesitations
stops and starts
slow and effortful production
absence of normal pitch and stress
variation
Ability to speak in full sentences Or
patient is able to talk only in phrases
82. Comprehension
The ability to understand spoken language
Complex process that involves
being able to segment the sounds heard into
meaningful phonemes
understanding the meaning of words within the
sentence
retaining the message in memory long enough to
understand it and formulate a response
Whether patient can hear and understand speech?
Tested by asking the patient to obey a command.
Ask the patient to show the tongue, close eyes, lift
a limb.
Fluency is preserved or not.
Speech whether fluent without hesitations?
Is it incessant, rapid and uninterrupted?
83. Naming
Process of knowing and retrieving the label for an
object, picture, or concept
Complex process
recognize the object
retrieve the semantic label for the object
develop the phonological form for the label
program the speech movements needed to say
the word
Examples
Pen, Match box.
saying the wrong name
saying a word that is phonologically or
semantically similar
using a nonsense word
84. Repetition
Being able to repeat words or phrases requires
good connecting pathways between Wernicke’s
area and Broca’s area
Broca’s area is important for the programming
and movements for speech production.
Wernicke’s area is critical for processing and
understanding auditory information.
Patient is asked to repeat a simple sentence
It has to be clearly stated by the examiner
Eg: Today is Wednesday, the August 17th, 2009.
See whether the patient is able to repeat what
you say .
Hearing is usually normal in these patients.
85. Reading and Writing
Whether answers a written question
Whether obeys commands which are
written down.
Ask the patients to read aloud.
Ask the patients to write name.
Ask the patients to draw picture, or
do small calculation.
86. Simplified flow chart forunderstanding various
aphasias
Comprehension
Yes No
Fluency and
Repetition
Fluency and
Repetition
F+, R–
(Conduction)
F–, R–
(Broca’s)
F+, R–
(Wernicke’s)
F–, R+
(TCM)
F+, R+
(TCS)
TCM:Transcortical Motor; TSC:Transcortical Sensory
87. Evaluation of cognition will help distinguish
aphasia from more diffuse disorders such as
dementia, in which there is derangement of:
Attention span
Visuospatial skills
Recent and remote memory
Executive functions
Social behaviour
88. Upper motor neuron and cranial nerve findings may
evidence causes of both vascular and nonvascular
aphasia.
Upper motor neuron facial weakness often
accompanies stroke.
Multiple sclerosis and the tauopathies that cause
progressive nonfluent aphasia can cause central
(upper motor neuron) cranial nerve dysfunction.
Other cranial nerve deficits should raise suspicion
for a systemic aetiology of aphasia (e.g., infection
89. Ophthalmic signs such as ptosis, meiosis, visual
field cuts, or ophthalmoplegia may also occur.
Unilateral ptosis and meiosis are signs of carotid
dissection as a cause of stroke.
Ophthalmoplegia is associated with Wernicke's
encephalopathy and tauopathies
(neurodegeneration resulting from tau protein
neurofibrillary tangles) that can cause progressive
nonfluent aphasia.
An internuclear ophthalmoplegia suggests multiple
sclerosis.
90. Lower motor neuron deficits generally are features of
aphasia of nonvascular etiology:
Lyme disease
Carcinomatous or lymphomatous meningitis
Sarcoidosis
Aphasia dysarthria motor neuron disease
(amyotrophic lateral sclerosis/frontotemporal
dementia).
91. Cause of aphasia
Multiple strokes or multiple lesions in multiple
sclerosis
Sarcoidosis
Neoplastic disease
Trauma
Wernicke's encephalopathy
Some rare degenerative diseases.
Infectious diseases
Tumors
Exposure to toxins or poisons
Hydrocephalus
92. Aphasia – Risk Factors
Uncontrollable factors
Age
Gender
Racial or ethnic background
Family history
Controllable factors
Hypertension
Diabetes
Tobacco smoking
Alcohol use
93. Imaging
CT head : The initial investigation for suspected stroke, and widely
available.
MRI with and without contrast
Essential for a broader differential diagnosis, including demyelinating
disease, cancer, and infections.
Positron emission tomography (PET) or single photon emission CT
(SPECT)
Focal hypoperfusion or hypometabolism can also be helpful in
distinguishing subtypes of primary progressive aphasia from each other
and from other degenerative conditions.
Specialised cardiac and vascular studies may be helpful in evaluation of
aphasia
* Echocardiogram *Bubble study
* Carotid Doppler
* Magnetic resonance angiography of neck/circle of Willis may identify
occlusion.
CXR and CT chest may be diagnostic of hilar lymphadenopathy raising
suspicion of sarcoidosis as aetiology of aphasia.
94. Ancillary studies
Lumbar puncture : Essential if an infectious cause is
suspected on the basis of fever, tachycardia, nausea, or
leukocytosis.
CSF can also be useful in diagnosing neoplastic causes,
multiple sclerosis, and other neuroimmunological causes.
CSF evidence of amyloidosis may provide additional evidence
favouring diagnosis of Alzheimer's disease.
Electroencephalography (EEG) :Critical if seizure is the
suspected cause. Can also be helpful in diagnosing herpes
encephalitis and Creutzfeldt-Jakob disease.
Neuropsychological testing : Sometimes necessary to
differentiate aphasia from dementia.
Electromyography May reveal lower motor neuron lesions
associated with amyotrophic lateral sclerosis.
Serum thiamine is requested if Wernicke's encephalopathy is
suspected
95. How is Aphasia Treated
Prognostic Indicators
Factors that predict or determine which clients
will benefit from therapy
Include:
Site, type, and size of brain injury
Time post onset (TPO)
Type and severity of aphasia
Handedness
Age
Pre-injury status
96. Designing Treatment Plans
• Teamwork involving a neurologist, psychologist,
speech therapist, social worker, linguist,
relatives and colleagues of patients.
• Interactive process aimed at improving their
functioning in the real world.
• Treatment strategies: the client’s compensatory
strategies
Self-directed
Clinician-directed
• Treatment approaches: target the specific deficits
and the underlying processes that produce the
errors
• When designing treatment plan, consider
evidence-based practice (interventions that have
been studied and proven effective in a controlled
97. Treatment Strategies forBroca’s
Aphasia
• Melodic Intonation Therapy
Best candidates are patients whose
Auditory comprehension is better than
their verbal expression and verbal
expression is severely impaired
• Response Elaboration Training (RET)
Designed for nonfluent aphasia patents in
order to increase the length and information
content of verbal responses.
98. Wernicke’s Aphasia
• Promoting Aphasics’ Communicative
Effectiveness
– Therapist and client take turns conveying
information to each other participating equally
as senders and receivers of messages.
– There is an exchange of new information.
– Therapist can model communication options.
– Any Communication channel is acceptable:
visual, gestural, graphic, verbal
– Barrier Activities useful in PACE therapy
99. Promoting Aphasics’ Communicative
Effectiveness, PACE Therapy
PACE therapy is a type of Functional Communication
Therapy (FCT)
purpose: emphasis on Pragmatic aspect of
communication and information involving a RANGE
OF COMMUNICAITON INTENTIONS, such as
informing, requesting, questioning, negating
primary objective of traditional therapy has been
to stimulate (Schuell) or restoration of patient’s
language function across 4 modalities
leads to isolated modality practice
Goals are written to address Activities of Daily
Living (ADL) using COMMUNICATION, not the
motor skills of performing the tasks
100. • Drug therapy
Randomized controlled trials with dopamine
agonist (bromocriptine), piracetam, donepezil
have shown weak evidence in favour of mild
efficacy particularly in non-fluent aphasias.
• Transcranial magnetic stimulation (TMS)
Reported to be useful in a few case reports of
chronic global aphasia.
101. Measuring Outcomes
Carryover of test scores to real-world
communication is the standard for
effectiveness of treatment
Outcomes: functional communication
improvements with intervention
Instruments to measure outcomes:
Communication Abilities of Daily Living,
Second Edition (CADL-2)
Functional Independence Measures (FIMS)
ASHA Functional Assessment of
Communication Skills (ASHA-FACS)
102. Aphasia Recovery
Better recovery in brain trauma vs. stroke
Left handed show better recovery vs. right
Highest recovery in 1st
3 months post
damage
Broca’s Aphasia highest rate of recovery
Therapy- melodic intonation
104. Case 1
• A 60 yr old man, known case of diabetes mellitus
for 10 yrs, was brought to the hospital as he
suddenly developed difficulty in speaking
properly. On examination there was no motor
weakness except mild motor aphasia. He had
normal comprehension, telegraphic speech with
good repetition.
• Q : What type of aphasia is he suffering from?
• Q : Localize the area and the arterial supply of
that area.
105. Case 2
• A 35 yr old man was brought to the hospital with
history of gradual onset speech defect and
vomiting for past 3 months. On examination he
had features of raised ICT.
• Q : What is the possible diagnosis?
106. Case 3
• A 50 yr old right handed man was brought to
the hospital with speech defect. On
examination he was aphasic and CECT of brain
showed lesion in right hemisphere.
• Q : What type of aphasia is he suffering from?
107. Case 4
• An accountant from Delhi came to the hospital
with complaints of difficulty in performing his
job and inability to write properly. He was also
unable to name the different fingers and had
right left confusion.
• Q : What is the diagnosis?
• Q : Localize the area involved.
Editor's Notes
1.Fluency: In aphasia, speech output may be nonfluent with hesitations and stops and starts, slow and effortful production, and the absence of normal pitch and stress variation. Problems with fluency usually give a good indication to where the site of lesion is in the brain.