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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
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
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.
Components of speech
Speech is the mechanical function of one’s
ability to communicate in oral language.
 Language production
 Phonation
 Articulation
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
Brain areas involved in
Language
Exner’s area
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)
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.
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.
Language Area
Broca’s area
Wernicke’s area
Angulargyrus
Exner’s area
Reading area
AREA 22
AREA39
AREA 44
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
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
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
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
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.
Pathways of speech and language
• Arcuate fasciculus is the bridge from the Wernicke’s area
to the Broca’s area
SPEECH DISORDER
 Dysphasia
 Dysarthria
 Dysphonia
 Mutism
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
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.
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
Type of Aphasia
Fluent/Non Fluent
Receptive/Expressive
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
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
Receptive Aphasia(Fluent aphasia)
Poor speech comprehension, and production of
meaningless speech.
Fluent ,unlabored
Maintain a melodic line, voice rising and falling
normally.
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
Word classes in Broca aphasia
Mostly nouns
Some adjectives
A few verbs
Function words few or non-existent
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
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)
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
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
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

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
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
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
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
Trans cortical motoraphasia
• Nonfluent output
– Delayed initiation
– Terse, poorly
elaborated
utterances
– Incomplete
sentences
– Verbal paraphasia
• Good comprehension
• Good repetition
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)
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
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
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
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
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
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
3 Types of Paraphasias
 Literal/phonological paraphasia
 Neologistic paraphasias
 Verbal paraphasias.
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.
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.
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
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
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
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
52
Dysarthria
• Two types of dysarthria
 Congenital/Developmental
 Acquired
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
.
54
Dysarthria
7 types of dysarthria
Based on symptoms:
Flaccid dysarthria
Hypokinetic dysarthria
Spastic dysarthria
Mixed dysarthria
Ataxic dysarthria
UMN dysarthria
Hyperkinetic dysarthria
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
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
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
Hyperkinetic Dysarthria
Damage to the basal ganglia, (regulates
motor movement)
Hyperkinetic movements: unintended and
uncontrolled movements occurring either
spontaneously or when muscles contract.
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
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.
61
Dysarthria
• Evaluation:
– Obtaining neurological medical report
– Observing muscles during:
• Rest
• Sustained postures
• Action
– Checking muscle function for both:
• Non-speech movements
• Speech
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
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
Characteristics of Speech
Apraxia
Groping attempts to find the correct
articulatory position
Frequent articulation errors
Self-correcting behaviors
Variable in their abilities
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
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
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
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
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
Two main classifications of Spasmodic
dysphonia
Adductor
Abductor
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
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
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.
• 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.
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
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.
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
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. 
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
.
Assessment of Speech
 Spontaneous speech
 Comprehension
 Naming
 Repetition
 Reading
 Writing
 Calculation
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
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?
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

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.
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.
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
 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 
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
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.
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).
 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
Aphasia – Risk Factors
Uncontrollable factors
Age
Gender
Racial or ethnic background
Family history
Controllable factors
Hypertension
Diabetes
Tobacco smoking
Alcohol use
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.
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
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
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
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.
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
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
• 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.
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)
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
THE END
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.
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?
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?
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.

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Speech disorder .

  • 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
  • 6. Brain areas involved in Language Exner’s area
  • 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.
  • 10. Language Area Broca’s area Wernicke’s area Angulargyrus Exner’s area Reading area
  • 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
  • 18. SPEECH DISORDER  Dysphasia  Dysarthria  Dysphonia  Mutism
  • 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
  • 22. Type of Aphasia Fluent/Non Fluent Receptive/Expressive
  • 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
  • 45. 3 Types of Paraphasias  Literal/phonological paraphasia  Neologistic paraphasias  Verbal paraphasias.
  • 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
  • 52. 52 Dysarthria • Two types of dysarthria  Congenital/Developmental  Acquired
  • 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 .
  • 54. 54 Dysarthria 7 types of dysarthria Based on symptoms: Flaccid dysarthria Hypokinetic dysarthria Spastic dysarthria Mixed dysarthria Ataxic dysarthria UMN dysarthria Hyperkinetic dysarthria
  • 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.
  • 61. 61 Dysarthria • Evaluation: – Obtaining neurological medical report – Observing muscles during: • Rest • Sustained postures • Action – Checking muscle function for both: • Non-speech movements • Speech
  • 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
  • 70. Two main classifications of Spasmodic dysphonia Adductor Abductor
  • 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 .
  • 80. Assessment of Speech  Spontaneous speech  Comprehension  Naming  Repetition  Reading  Writing  Calculation
  • 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. 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.