1. APHASIA AND DYSARTHRIA
Presenter: Dr. Zeleke W/Y (NR-II)
Moderators: Dr. Nebiyu B (Consultant Neurologist)
Dr. Guadie B (Consultant Neurologist)
Date Aug 30,2022
3. Objective
• At the end of this lecture,we should be able to understand
Language anatomy and aphasia syndrome
Speech and speech disorder/dysarthria
4. Introduction: Historical background
• The neuroscience of language began with Paul Broca in 1861.
• He reported reduced production of one single utterance after sustained left
inferior frontal infarction.
• Over the next 50 years, several brilliant scientists followed in Broca’s steps,
including Wernicke, Lichtheim, Liepmann, Lissauer, Dejerine, Kussmaul, and
Freud.
• They detailed a host of language syndromes associated with cerebral lesions in
various locations.
5. Introduction....
• Language is a distinctive human facility for communication through symbols.
• The anatomical study of language disorders has had considerable historical
importance over the past two centuries in the development of theories of cerebral
localization in general.
• Historically, language was the first higher cortical function to be correlated with
specific sites of brain damage
• It continues to serve as a model for the practical use of a cognitive function, in the
localization of brain lesions and for the understanding of human cortical processes
in general.
6. Terminologies
Terms Definitions
Language Is a mechanism for expressing thoughts and ideas by speech (auditory symbols) by writing
(graphic symbols)by gestures and pantomime(motor symbols)
Speech Consists of words, which are articulated vocal sounds that symbolize and communicate
ideas.
Phonation The production of vocal sounds without word formation entirely a function of larynx.
Articulation Is the enunciation of words and phrases it is a function of organs and muscles innervated
by brainstem.
Vocalization The sound made by the vibration of the vocal folds, modified by workings of the vocal
tract.
6
8. ANATOMY OF THE LANGUAGE CENTERS
• The classical language centers are located in the perisylvian areas of
the language-dominant hemisphere.
• Current evidence is that language functions involve widespread neural
networks in many parts of both hemispheres.
12. Contd....
• There are three cortical levels involved in language comprehension.
• The first is the level of arrival: a function of the primary cortical reception areas.
• Language symbols are perceived, seen, or heard, without further differentiation of the impulses.
• The second level: knowing, or gnostic function
• Concerned with the recognition of impulses, formulation of engrams for recall of stimuli, and
revisualization.
• The third level: recognition of symbols in the form of words or the higher elaboration and
association of learned symbols as a function of language.
• Has greatest importance in aphasia.
13. Contd....
• Broca’s area (areas 44 and 45) also extends to the level of areas 9,46 and 47,more widely 6,8 and
10.
• Lies in the opercular and triangular portions of the inferior frontal gyrus in the dominant
hemisphere.
• It activates particular sequences of sounds to produce words and sentences is formulated in the
adjacent association cortex.
• The main function is speech production.
• It connects with other regions of the frontal lobes, including the prefrontal cortex, premotor cortex,
and SMA.
14. Contd....
• Wernicke’s area (area 22), which encompasses the posterior two-thirds of the
superior temporal gyrus in the dominant hemisphere.
• It may also includes a rim of adjacent association cortex from Brodmann’s areas 37,
39, and 40.
• It has reciprocal connections with the supramarginal gyrus and angular gyrus of the
parietal lobe, as well as with regions of the temporal lobe such as Brodmann’s area
37.
• The main function is understanding of written and spoken language.
15. Contd….
• Arcuate fasciculus is a bundle of nerve fibers that connects the temporal and parietal
lobes of the brain.
• is a subcortical white matter that connect Wernicke’ and Broca’ areas
• The ability to hear a word and then repeat it aloud requires transfer of information
across the Sylvian fissure from Wernicke’s area to Broca’s area.
• Neural representations for sounds are converted into words in Wernicke’s area, and
neural representations for words are converted back into sounds in Broca’s area.
16. Contd....
• The supramarginal gyrus
Lies between visual cortex and
posterior perisylvian language area
is concerned with visual language
functions
17. Contd....
• Exner’s center lies in the middle frontal
gyrus of the language dominant frontal
lobe very near frontal eye field.
just anterior to the primary motor
cortex for the hand
It concerned with writing language.
19. Contd....
• The perisylvian language areas are perfused by the MCA
the anterior language areas are supplied by the superior
division and
the posterior areas by the inferior division
20. APHASIA
• Derived from ancient Greek ‘’speechlessness’’.
• It is the disturbance in formulation and comprehension of language.
• This class of language disorder ranges from having difficulty
remembering words to being completely unable to speak, read or
write.
• Aphasia is usually linked to brian damage, most commonly by stroke.
21.
22. Language Examination
• Initial appraisal of language function takes place during the taking of
the history.
• It is difficult to evaluate language status in a person who has altered
mental status, inattention, agitation, or severe depression.
23. Contd....
Handedness
• The left cerebral hemisphere is dominant for language
in 99% of right-handers, and 60% to 70% of left-handers
• The remaining (30-40%) of left handers: half right hemisphere dominant and
half mixed dominance.
• The right (or nondominant) hemisphere is thought to contribute more to the
melody (prosody), rhythm, emotional expression, and accent in language.
24. Contd....
• Shifted sinistrals (anomalous dextrals) are naturally left-handed individuals forced by
parents or teachers early in life to function right-handed, primarily for writing.
• Right-handed patients (dextrals) who are left-hemisphere dominant for language
• Left-handed patients (sinistrals) who are still left-hemisphere dominant
• “Right-handed” patients who are right-hemisphere dominant: anomalous dextrals
• Left-handed patients who are right-hemisphere dominant: true sinistrals
26. • It is synonymous with polyglots.
• What is polyglots?
• A person who knows and is able to use several languages
• Require examination in all of their languages.
• Polyglots may have several centers for speech in somewhat discrete
but overlapping cortical areas.
27. • Factors that influence includes:
age of language acquisition
frequency of language use
premorbid proficiency, and
linguistic similarity between one's languages
28. • Age at acquision matters.
• Early bilingual individuals who acquired both languages by the age of 6
years had a bilateral organization of both languages.
• Late bilingual individuals who acquired a second language after the age
of 6 years had the lateralization of language function in the left
hemisphere for both languages.
29. • Which language recovers best in multilingual aphasics is variable.
• Pitres’ law states that recovery from aphasia will be best for the
language most used.
• Ribot’s rule holds that recovery will be best for the native language.
• In fact, most patients show parallel recovery in both languages
30. • Spontaneous speech
• Check for fluency vs nonfluency
• Ask the open ended questions
• Note the patient’s fluency, including phrase
length, rate, and abundance of spontaneous
speech.
31. • Comprehension
• How to assess
comprehension?
Commands it could be one
step or multiple steps
Yes/No responses:ask
question with possible Yes/No
answer
Pointing responses
• Repetition
• Patient is asked to repeat simple and
complex sentences.
• Simple tasks: counting or repearing single
words
• More complex tasks:polysyllabic words or
phrase or tongue twisters
• A popular phrase for testing repetition in
aphasia is “no ifs, ands, or buts.
32. • Naming
• It can be evaluated by:
Confrontation naming: Ask patient to name common objects in the
room, body parts, and colors pointed by the examiner.
Word list generation: Ask the patient to provide list
• E.g. name of animals, words starting with A...etc.
33. • Writing
• Ask the patient to write their name
and write a sentence.
• Through dictation or copying
• Reading
• Ask the patient to read aloud
single words, a brief passage, and
the front page of a newspaper
and test for comprehension.
34. Causes of Aphasiaa
Cerebral contusion; subdural or epidural hematoma
Cerebrovascular accident
Ictal or post-ictal deficit with focal seizures in dominant hemisphere
Mass lesions such as brain tumor, abscess, or toxoplasmosis
Inflammatory or autoimmune disorders such as multiple sclerosis or
vasculitis
Developmental disorders such as language delay or autism
Degenerative disorders such as progressive nonfluent aphasia,
semantic dementia, moderately advanced AD, and HD
35. Classification of language Disorders
• The Wernicke-Geschwind model (Boston classification) recognizes
eight aphasia syndromes:
Broca’s
Wernicke’s
Conduction
Global
Transcortical (motor, transcortical sensory or mixed) and
Anomic
36. Classification....
• Central/ perisylvian aphasia
• Due to lesions involving the
perisylvian cortical structures
• Includes: Broca’s, Wernicke’s,and
conduction
• Commonly have loss of repetition
• Paracentral/ extrasylvian aphasia
• Due to lesions surrounding the
perisylvian areas
Border zone (watershed) infarction (BZI)
• Includes: transcortical syndromes and
anomic aphasia
• Commonly have preserved repetition
38. Broca’s Aphasia
• Cause - lesions of Broca’s area and adjacent
structures in the dominant frontal lobe.
• The most common etiology is infarct in the
territory of the left MCA superior division.
• Clinically, the most salient feature of is
decreased fluency of spontaneous speech.
• Prosody is also lacking.
39. Contd….
• The resulting speech has an effortful, telegraphic quality, with a lack of grammatical
structure and a monotonous sound.
• Speech output is often better for certain overlearned, semiautomatic tasks, such as
naming the days of the week or singing familiar songs and performance is often
improved by cuing.
• Repetition is also impaired especially, phrases with a high content of function words.
• Comprehension especially reading is relatively intact in Broca’s aphasia.
• Exception: impaired comprehension of syntactically dependent structures.
40. Contd….
• Commonly associated features include dysarthria, and right hemiparesis
affecting the face and arm more than the leg.
• Visual fields are usually normal.
• Other common features are frustration and depression.
• Little Broca’s aphasia and big Broca’s aphasia.
41.
42. Wernicke’s Aphasia
• Cause - lesion of Wernicke’s area and adjacent
structures in the dominant temporoparietal lobes.
• The most common etiology is infarct in the left MCA
inferior division territory.
• Clinically, patients will have markedly impaired
comprehension.
• In severe condition, do not respond appropriately to
questions and follow virtually no commands.
43. Contd….
• Spontaneous speech has normal fluency, prosody, and grammatical structure.
• Impaired lexical function results in speech that is empty, meaningless, and full of
nonsensical paraphasic errors.
• Naming is with frequent paraphasic errors or other irrelevant responses.
• Lesions of Wernicke’s area also result in disconnection from Broca’s area, causing
impaired repetition.
• Reading and writing consist of fluent, but meaningless, paraphasic renditions.
44. Contd….
• Paraphasia: substitution of intended words with incorrect words.
• Paraphasic errors can divided in to two, including:
• A. Verbal or semantic: inappropriate substitutions of a word for one of similar
meaning
E.g. patient says ‘’ink’’ instead of ‘’pen’’ or ‘’bus’’ instead of ‘’taxi’’
• B. Literal or phonemic: inappropriate substitution of part of a word for one with a
similar sound
E.g. patient says “pish” instead of “fish” or “rot” instead of “rock.”
45. Contd….
• Commonly associated features include a contralateral visual field cut,
especially of the right upper quadrant due to involvement of the lower
(temporal) portion of the optic radiation.
• Apraxia may be present , but it can be difficult to demonstrate because of
impaired comprehension.
• Dysarthria and right hemiparesis are usually absent or very mild.
46. Contd….
• Note that: marked contrast to Broca’s aphasia, patients often appear unaware of their
deficit (anosognosia), behaving as if carrying on a normal conversation despite their
markedly abnormal speech.
• When examining the patient with Broca’s aphasia, the patient often feels frustrated,
while when examining the patient with Wernicke’s aphasia, the examiner may feel
frustrated.
• Angry or paranoid behavior may occur, this misdiagnose Wernicke’s aphasia as a
psychotic disorder.
47.
48.
49. Conduction Aphasia/Associative Aphasia
• It is due to a lesion that interrupts the conduction of
impulses between Wernicke’s and Broca’s areas.
• The lesion most often lies in the deep white matter
in the region of the supramarginal gyrus.
• Which involves the AF and other fiber tracts that run
from the posterior to the anterior language areas.
• It is usually due to an embolic occlusion of a terminal
branch of the MCA.
50. Contd….
• A patient will have normal fluency and comprehension, but impaired
repetition.
• Repetition is worst for multisyllabic words and sentences, and it is during
repetition that paraphasic errors are most apt to appear.
• Paraphasic errors (primarily literal) are common, and naming is often impaired,
which can lead to a misdiagnosis of Wernicke’s aphasia.
• Patients are aware of and try to correct the pronunciation errors.
• Patients have difficulty reading aloud and writing to dictation.
51.
52. Global aphasia/Total aphasia
• There is both nonfluency and impaired
comprehension.
• The lesion may involve both anterior and
posterior speech areas.
• It can be seen in large left MCA infarcts that
include both the superior and the inferior
divisions or Left ICA.
53. Contd....
• Most commonly a large lesion has destroyed the entire perisylvian
language center, or separate lesions have destroyed both the PIF and PST
regions.
• It can also be seen in the initial stages of large left MCA superior division
infarcts that eventually improve to become Broca’s aphasia (big Broca’s)
and in large subcortical infarcts, hemorrhages, or other lesions.
• Typically, there is both a hemiplegia and a field cut.
54.
55.
56. Transcortical aphasias
• Are syndromes in which the perisylvian
language area is preserved but disconnected
from the rest of the brain.
• The usual etiology is a BZI (watershade
infarct).
• Because the PIF and PST areas and the
connecting AF are intact, the patients are
aphasic but have a paradoxical preservation of
the ability to repeat.
57. Contd....
• Transcortical aphasias resemble Broca’s, Wernicke’s, and global
aphasias.
• Exception repetition is spared.
• Are also common in subcortical lesions, such as those involving the
basal ganglia or thalamus in the dominant hemisphere.
• In addition, transcortical aphasia is a common pattern seen during
recovery from other aphasia syndromes.
58. Transcortical Motor Aphasia
• Also known as anterior isolation syndrome.
• An analogue of Broca aphasia in which speech is
hesitant or telegraphic, comprehension is
relatively spared, but repetition is fluent.
• Lesions found in the frontal lobe, anterior to the
Broca area, in the deep frontal white matter, or in
the medial frontal region, in the vicinity of the
SMA.
• All of these lesion sites are within the ACA
territory.
59.
60. Transcortical sensory aphasia
• Also known as posterior isolation syndrome.
• An analogue of Wernicke aphasia in which fluent, paraphasic speech,
paraphasic naming, impaired auditory and reading comprehension, and
abnormal writing coexist with normal repetition.
• MCA–PCA watershed infarcts are one possible cause of this disorder.
• The PST region is isolated from the surrounding parietal, occipital, and temporal
cortex that store word associations.
61.
62. Mixed transcortical aphasia
• It is syndrome of isolation of speech area
• Is global aphasia in which the patient repeats, often echolalically, but
has no propositional speech or comprehension.
• There is intact repetition
• One possible cause is combined MCA–ACA and MCA–PCA watershed
infarcts.
63. Anomic (Amnesic, Amnestic, Nominal) Aphasia
• Deficit in naming ability with preservation of other language functions.
• Speech may be relatively empty and circumlocutory because of the
word-finding deficit.
• It is the most common but least specific type of aphasia.
• Anomia occurs with every type of aphasia so it is nonlocalizing
syndrome.
• Patients with any aphasia type, as it develops or recovers, may pass
through a stage in which anomia is the primary finding, and it may be
the most persistent deficit.
64. Contd....
• When anomic aphasia is accompanied by all four elements of
Gerstmann’s syndrome, the lesion virtually always lies in the dominant
angular gyrus.
• Dysnomia is sometimes used to refer to mild difficulty with naming.
• Patients with subtle dysnomia often have particular difficulty naming
lower-frequency words or parts of objects.
• E.g. parts of a watch or a shirt is a useful bedside test.
67. Subcortical Aphasia/Extrasylvian
• Subcortical aphasia is not a new concept; it was recognized by Lichtheim
in the 19th century.
• Language disorders that arise not from damage to the perisylvian
language areas
• It is arise from lesions involving the thalamus, caudate, putamen,
periventricular white matter, or internal capsule of the language-
dominant hemisphere.
• Usually vascular in origin.
68. Contd….
• The speech disorder is difficult to categorize in the Wernicke-Geschwind scheme and
may most resemble a TCA.
• Two types have been described: an anterior and a posterior syndrome.
• The anterior syndrome (caudate or striatocapsular aphasia):
It is characterized by slow dysarthric speech with preserved phrase length, that is,
not telegraphic, preserved comprehension, and poor naming.
It resembles a transcortical motor aphasia.
69. Contd….
• Posterior syndrome (thalamic aphasia):
Fluent speech without dysarthria, poor comprehension, and poor naming.
Resembles Wernicke’s or TCA but accompanied by a hemiplegia
• In both forms, repetition is relatively preserved, and the patients usually have an
accompanying hemiplegia.
• It is the relative preservation of repetition that indicates a link between the subcortical
and transcortical syndromes.
70. Contd….
• The mechanism by which subcortical lesions cause aphasia remains conjectural.
• But it may involve secondary dysfunction of the perisylvian language areas
because of interruption of fibers that communicate between cortical and
subcortical structures.
• Modern imaging has shown that cortical hypoperfusion is common in
subcortical aphasia.
71. Progressive primary aphasia
• It is a condition in which patients present with a progressive loss of specific language
functions with relative sparing of other cognitive domains.
• Which eventually end up severe aphasia, even mutism, or evolving into dementia.
• Occur in the context of neurodegenerative disease (usually FTD)
• Have an insidious onset and gradual progression.
• Language disturbance is the most prominent cognitive feature and remains most
prominent even after other cognitive domains become involved.
72. Contd....
• Three major PPA syndromes are recognized.
• Commonly they have atrophy in perisylvian brain regions, more
prominent in the language-dominant hemisphere .
• Progressive nonfluent aphasia:
• Most closely resembles Broca's aphasia.
• The loss of fluency is typically due to a combination of agrammatism and
articulatory deficits.
73. Contd....
• Progressive semantic dementia
• Aphasia is fluent, but lacks the paraphasic quality seen in Wernicke aphasia.
• Comprehension is impaired mainly for single words, there is no any deficit in
sound processing.
• Patients frequently repeat back the word that they do not understand
• The pattern of atrophy is highly characteristic and involves both anterior
temporal lobes, usually more so on the left.
74. Contd....
• Logopenic progressive aphasia
• Patients are typically fluent, with breaks in fluency caused by word-finding pauses.
• Phonemic paraphasic errors are common.
• Repetition and comprehension are highly dependent on the length of the stimulus,
such that longer sentences are much less likely to be understood or repeated back
accurately.
• In contrast to semantic dementia, single-word comprehension is likely to be intact
• The atrophy is most prominent in the posterior superior temporal and inferior
parietal regions.
75. Contd....
• Patients eventually develop evidence of other degenerative neurologic
disorders such as:
frontotemporal lobar degeneration (most often)
corticobasal degeneration or
progressive supranuclear palsy
76. NONDOMINANT HEMISPHERE LANGUAGE DISTURBANCES
• Affective aspects of language are impaired.
• There is loss or impairment of the rhythm and emotional elements of
language.
• Prosody refers to the melodic aspects of speech—the modulation of pitch,
volume, intonation, and inflection that convey nuances of meaning and
emotional content.
• Hyperprosody is exaggeration, hypoprosody a decrease, and aprosody an
absence of the prosodic component of speech.
77. Contd….
• Patients lose the ability to convey emotion in speech or to detect the emotion
expressed by others.
• Dysprosodic speech is flat and monotonous, without inflection or emotion.
• Dysprosody may occur with right hemisphere lesions.
• There is often difficulty processing nonliteral, context bound, complex aspects of
language, such as understanding figurative language, stories, and jokes.
78. Recovery from Aphasia
• Aphasia from acute disorders like stroke show spontanoues improvement over
days, weeks and months greatest recovery the first 3 months.
Global aphasia seen in big Broca’s usually recovers to a Broca’s aphasia.
Broca’s aphasia may recover to a TCM aphasia and, eventually, to a subtle
dysnomia.
Wernicke’s aphasia may recover to a TCS aphasia and then to a dysnomia.
• Dysnomia is the most common long-term deficit.
79. Other Syndromes Related to Aphasia
• Several important syndromes are related to the aphasic disorders of
the dominant hemisphere.
• These disorders can occur either together with aphasia or in isolation.
80. Alexia and Agraphia
• They are impairments in reading or writing ability, respectively.
• Caused by deficits in central language processing and not by simple
sensory or motor deficits.
• In patients with aphasia, agraphia is invariably present.
81. Agraphia without aphasia
• Can be seen in lesions of the inferior parietal lobule of the language-
dominant hemisphere.
• This may or may not be accompanied by the other features of
Gerstmann’s syndrome.
82. Alexia without agraphia
• It is caused by a lesion in the left occipital cortex extending to the splenium corpus
callosum, often a left PCA infarct.
• Visual information reaches the left visual field, but pathways that allow interpretation of
written language from the left visual field are interrupted
e.i. the lesions interrupt the flow of visual input in to the language network.
• The patient has a right visual field defect (right hemianopia).
• It is one of example of a disconnection syndrome.
• Patient can write, but not read even their own writing.
83. Alexia with agraphia
• It is due to lesions of the dominant inferior parietal lobule, in the
region of the angular gyrus, and lesions of the dominant posterior
middle frontal gyrus (Exner’s area).
• Alexia, which is an acquired deficit in reading, should be distinguished
from dyslexia, a developmental reading disorder.
84. Gerstmann’s Syndrome
• It consists of tetrad of
Agraphia (impaired writing)
Acalculia (impaired simple arthimetic)
right–left disorientation
finger agnosia (inability to name individual fingers)
• This syndrome is strongly localizing to the dominant inferior parietal lobule, in
the region of the angular gyrus.
85. Aphemia (Verbal Apraxia) aka pure word mutism
• Aphemia is primarily a disorder of articulation.
• This patient lost her ability to produce speech but was able to comprehend and
write fluently and have severe apraxia of speech.
• Dysarthria and facial paresis usually accompany this syndrome.
• Severe aphemia can cause muteness, with preserved writing ability.
• Lesions typically lie in or around Broca's area, involving the lowermost part of the
precentral gyrus.
86. Cortical Deafness, Pure Word Deafness
• Also known as auditory verbal agnosia.
• It is selective inabaility to comprehend the spoken word, in the absence of aphasia or defective
hearing.
• Bilateral lesions of the primary auditory cortex in Heschl’s gyrus.
• Net effect of underlying lesion is to interruption of flow of information from auditory association
cortex to the language network.
• These patients are often aware that a sound has occurred, but are unable to interpret verbal stimuli
87. Contd....
• Spontaneous writing & ability to comprehend written language are preserved, but writting
following dictation is impaired.
• Like alexia without agraphia, there is a lesion in one hemisphere and disconnection with
the other hemisphere.
• They can speak normally but cannot understand even their own speech if it is recorded
and played back to them.
• Pure word deafness is usually associated with restricted lesions in the superior temporal
gyrus.
88. AMUSIA
• Loss of musical ability, either production or comprehension, may occur in patients
with aphasia or agnosia, or acquired amusia may develop independently.
• One classification of amusia includes vocal amusia, instrumental amnesia, musical
agraphia, musical amnesia, disorders of rhythm, and receptive amusia.
• Melody and rhythm may be affected independently.
• The centers that control musical ability are largely undefined compared to the
centers that control verbal language.
89. Difference between aphasia and dysarthria
• Aphasia
• language disorder
• Dysarthria
• Speech disorder
• is the impairment of speech in
which the speech of the person is
affected
91. Anatomy and physiology of speech
• Speech consists of words, which are articulated vocal sounds that symbolize
and communicate ideas.
• Articulation is the enunciation of words and phrases it is a function of organs
and muscles innervated by brainstem.
• Speech requires the interpretation of the auditory and visual images and
association of these images with the motor centers that control expression
• Coordination between the respiratory muscles and muscles of larynx, pharynx,
soft palate, tongue and lips (vocal tract).
92. Contd....
• Three levels of motor speech function.
• the emotional level:most primitive
• the patient may respond to a painful stimulus with an “ouch,” even
though other language functions are entirely absent.
• Emotional language may be preserved when all other language functions
are lost.
• the automatic level:which is concerned with casual, automatic speech;
• E.g. the patient may be able to answer questions with words such as
“yes” and “no,” and be able to count or recite the days of the week.
93. Contd....
• The highest level is propositional, volitional, symbolic, or intellectualized
language, which is most easily disrupted and most difficult to repair.
• Language requires the use of symbols (sounds, marks, gestures) for
communication.
• Propositional language is the communication of thoughts, ideas, feelings,
and judgments using words, syntax, semantics, and rules of conversation.
94. ANATOMY AND PHYSIOLOGY OF ARTICULATION
• Sounds are produced by expired air passing through the vocal cords.
• Properly articulated speech requires coordination between the
respiratory muscles and the muscles of the vocal tract.
• Respiratory movements determine the strength and rhythm of the
voice.
95. Contd....
• Modifications in sound are produced by changes in the size and shape
of the glottis, pharynx, and mouth and by changes in the position of
the tongue, soft palate, and lips.
• The oropharynx, nasopharynx, and mouth
resonating chambers and further influence the timbre and character
of the voice.
96. Contd....
• Articulation is one of the vital bulbar functions.
• Several CNs are involved in speech production
The trigeminal nerves control the muscles of mastication and open
and close the mouth.
The facial nerves control the muscles of facial expression
The vagus nerves and glossopharyngeal nerves control the soft palate,
pharynx, and larynx.
The hypoglossal nerves control tongue movements
97. TYPES OF SPEECH SOUNDS
• Based on the place of articulation sounds can be classified in to:
Labiodental f and v
Labials (b, p, m, and w)
Linguals (t, d, l, r, and n )
Palatal (German ch and g, and the French gn)
Velar or tongue-back sounds (k, g, and ng)
uvular
98. EXAMINATION OF ARTICULATION
• Note the accuracy of pronunciation, rate of speech, resonance, and
prosody (variations in pitch, rhythm, and stress of pronunciation)
• The nonsense phrase “puhtuhkuh” or “pataka” tests all the three: labials
(puh/pa), linguals (tuh/ta), and velars (kuh/ka).
• Making patient repeat a syllable like ‘’puh’’
• Listen for abnormally slow or rapid repetition, regularity and evenness,
uniform loudness, or tremulousness.
99. Contd....
• Example in MG there is weakness and fatigueability of articulation may
be brought out by having the patient count to 100 at about one
number per second.
• Listen for the voice to become hoarse, hypernasal, slurred, or breathy.
• Disturbances of laryngeal function and of speech rhythm may be
elicited by having the patient attempt prolonged phonation, such as by
singing and holding a high “a” or “e” or “ah” sound.
100. Contd....
• Assess loudness, pitch, quality (hoarseness, breathiness), steadiness,
nasality, and duration.
• E.g. in the cerebellar dysfunction, the voice may break, waver, or
flutter excessively.
• Note whether the pitch of the voice is appropriate for the patient’s age
and sex.
101. Contd....
• Coughing requires normal vocal cord movement.
• A normal cough indicates that vocal cord innervation is intact.
• Dysphonia with a normal cough suggests laryngeal disease or a nonorganic
speech disturbance.
• The intensity of the glottic click reflects the power of vocal cord adduction.
• The glottic click may also be elicited by asking the patient to say “oh-oh” or to
make a sharp, forceful grunting sound.
102. Contd....
• Resonance is an important voice quality.
• Normal resonance depends on an adequate seal between the oropharynx and
nasopharynx (velopharyngeal competence).
• When palatal weakness causes an inadequate seal on pronouncing sounds that
require high oral pressure, the voice has a nasal quality.
• An audible nasal emission is nasal air escape that causes a snorting sound.
103. Contd....
• How to check nasal components of voice ?
• Pronouncing sounds with a nasal component (m, n, ng) as in the phrase “ming, ping,
ring, sing,” will normally produce slight condensation and fogging on the surface of
glass.
• Have the patient say a phrase with no sounds having a nasal component (“we see
three geese”).
• Clouding of the surface suggests an abnormal nasal component of the voice.
• Velopharyngeal incompetence is common in patients with cleft palate.
104. Contd....
• Neurologic disturbances of articulation may be caused by the following:
primary muscle diseases affecting the tongue, larynx, and pharynx;
neuromuscular junction disorders;
LMN disease involving either the CN nuclei or the peripheral nerves that supply
the muscles of articulation
cerebellar dysfunction
BG disease; or disturbances of the UMN control of vocalization.
105. Contd....
• Lower motor neuron disorders causing difficulty in articulation may occur in cranial
neuropathies.
• Trigeminal nerve lesions: there is little impairment of articulation unless the
involvement is bilateral.
• Seventh nerve paralysis causes difficulty in pronouncing labials and labiodentals.
• Dysarthria is noticeable only in peripheral facial palsy; the facial weakness in the
central type of facial palsy is usually too mild to interfere with articulation.
106. Contd....
• Ninth and eleventh nerves lesions: usually do not affect articulation.
• A unilateral lesion of CN X causes hypernasality.
• Hypoglossal nerve or nucleus lesion: cause impairment of all enunciation, but with
special difficulty in pronouncing lingual sounds.
• The speech is lisping in character and is clumsy and indistinct.
• Laryngeal musculature paralysis: hoarseness, and the patient may not be able to
speak above a whisper; there is particular difficulty pronouncing vowels.
107. Contd….
• The soft palate weakness: results in nasal speech (rhinolalia) caused by
inability to seal off the nasal from the oral cavity.
• There is special difficulty with the velar sounds.
• The speech resembles that of a patient with a cleft palate.
• Characteristically, b becomes m, d becomes n, and k becomes ng.
• ALS and MG are common causes of this type of speech difficulty.
108. Contd….
• Spasmodic dysphonia
• Also known as laryngeal dystonia, is a disorder in which the muscles that generate a
person's voice go into periods of spasm.
• It is also a focal dystonia characterized by a striking abnormality of voice production.
• Adductor spasmodic dysphonia: most common one
Irregular involuntary spasms of the vocal muscles cause erratic adduction of the
cords.
The voice becomes a high-pitched and choked quality that varies markedly during the
course of a sentence.
109. Contd….
• Abductor spasmodic dysphonia is the second most common
• The vocal folds cannot vibrate when they are open.
• The open position of the vocal folds also allows air to escape from the lungs during
speech.
• As a result, the voices of these individuals often sound weak, quiet, and breathy or
hoarse.
• In both types, there is often a dramatic improvement in the voice during shouting,
whispering, or singing.
110. Stuttering መንተባተብ
• Also known as stammering: refers to faulty, spasmodic, interrupted speech characterized by
involuntary hesitations in which the speaker is unable to produce the next expected sound.
• It is also a speech disorder in which the flow of speech is disrupted by involuntary repetitions and
prolongations of sounds, syllables, words, or phrases as well as involuntary silent pauses or blocks
in which the person who stutters is unable to produce sounds.
• The flow of speech is broken by pauses during which articulation is entirely arrested.
• For many people who stutter, repetition is the main concern.
111.
112. Contd....
• Stuttering implies a more severe disturbance of speech, with faltering or
interrupted speech characterized by difficulty in enunciating syllables and
joining them together.
• Interference with communication may be profound and the social
consequences severe.
• Stuttering speech is stumbling and hesitant in character, with habitual and
spasmodic repetitions of consonants or syllables, alternating with pauses.
113. Contd....
• There may be localized cramps, spasms, and tic-like contractions of the muscles
essential to articulation.
• Which results in grimaces, spasms and contractions of the muscles of the head
and extremities, and spasm and incoordination of the respiratory muscles.
• The individual may have difficulty particularly for dentals and labials
consonants.
• Often the first syllable or consonant of a word is repeated many times.
114. Contd....
• The individual may remain with his mouth open until the articulatory
spasm relaxes, then the words explode out until the breath is gone.
• He then takes another breath, and the process is repeated.
• Stuttering is markedly influenced by emotional excitement and by the
presence of strangers.
115. Contd....
• In spite of difficulty in speaking, the individual may be able to sing
without hesitation.
• There have been accomplished professional singers who stuttered
severely in ordinary speech.
• Britain’s King George VI stuttered severely, as memorably depicted in
the motion picture The King’s Speech.
116. Common etiology of stuttering
• No single, exclusive cause of developmental stuttering is known
• Commonly, it has genetic basis.
• Developmental stuttering: Seen in children who are still learning
sentence construction, especially when the child is excited and has a
lot to say or is under pressure
• Emotional distress (psychogenic stuttering)
117. Lallation
• A baby talk: the speech is childish, babbling, and characterized by a lack of precision in
pronouncing certain consonants, especially the letters r and l.
• A uvular is substituted for a lingual-palatal r.
• E.g. “broken reed” is pronounced “bwoken weed.”
• The diphthong ow or other sounds may be substituted for the l sound, or sometimes l may
be substituted for r.
• T and d may be substituted for s, g, and the k sound.
118. Contd....
• Lalling may occur because of hearing defects, mental or physical retardation, or
from psychogenic disorders.
• In lisping, the sibilants are imperfectly pronounced, and th is substituted for s; a
similar defect in articulation may be associated with partial edentulism.
• Lalling and lisping are usually because of imperfect action of the articulatory
apparatus (as in children), persistent faulty habits of articulation, imitation of
faulty patterns of articulation, poor speech training, habit, or affectation.
119. NONORGANIC (FUNCTIONAL) SPEECH DISORDERS
• Speech, but not language, disorders may occur on a nonorganic basis.
• The most common are dysphonia and aphonia.
• Psychogenic foreign accent syndrome has been reported.
• In anxiety and agitation the speech may be broken, tremulous, high-
pitched, uneven, and breathless.
120. Contd….
• The speech may be rapid and jumbled (tachyphemia or tachylalia), or there may be
lalling or mutism.
• In hysterical aphonia, there is profound speech difficulty but no disturbance of
coughing or respiration.
• Manic patients may have a rapid flow of words (pressured speech), often with an
abrupt change of subject.
• In depression speech may be slow, sometimes with mutism.
• In schizophrenia there may be hesitancy with blocking, or negativism with resulting
mutism (alalia).
121. Contd….
• Palilalia, echolalia, and perseveration are often manifestations of psychosis.
• but they can occur with organic lesions, especially of the frontal lobes.
Palilalia is the repetition of one’s own speech.
Echolalia is the meaningless repetition of heard words.
Perseveration is the persistence of one reply or one idea in response to
various questions.
122. MOTOR SPEECH DISORDERS
• They are syndromes of abnormal articulation, the motor production of speech,
without abnormalities of language.
• A patient with a motor speech disorder should be able to produce normal expressive
language in writing and to comprehend both spoken and written language.
• Include:
dysarthrias, disorders of speech articulation and apraxia of speech.
four rarer syndromes: aphemia, foreign accent syndrome, acquired stuttering, and the
opercular syndrome.
123. DYSARTHRIA
• Dysarthrias is abnormal articulation of sounds or phonemes.
• Dysarthrias are disorders of muscular control of speech affecting speed,
strength, timing, range, or accuracy of movements involving speech.
• Anarthria is total loss of ability to articulate.
• The most consistent finding in dysarthria is the distortion of consonant sounds.
124. Contd….
• Dysarthria is neurogenic, related to dysfunction of the cranial
nerves, NMJ, or muscle, corticobulbar tracts,cerebellar
connections, or BG.
• Also results from mechanical disturbances of tongue or
larynx.
• It affects not only articulation but also phonation, breathing,
or prosody (emotional tone) of speech.
125. Classification
• Age of onset: congenital/acquired
• General causes: vascular/neoplastic/traumatic/infectious
• Neuroanatomic areas involved: Cerebral/cerebellum/brainstem
• Cranial nerves involved: V, VII, IX, X, XI, XII
• Speech process involved: respiration/resonance/articulation/prosody
127. Flaccid dysarthria
• It is motor speech disorder produced by injury or malfunction of one
or more of cranial or spinal nerves.
• It reflects problems in the nuclei, axon, or NMJ that make up motor
units of final common pathways.
• Its primary deviant speech characteristic can be traced to muscular
weakness and reduced muscle tone and their effects on the speed,
range and accuracy of speech movements.
• Unlike most others dysarthria types, sometimes results from damage
confined to isolated muscle groups.
128. Contd....
• It is due lesion in the following cranial nerves.
• V, VII, IX, X, XI, XII
• Facial muscle weakness: difficulty in articulating
labials (b, p, m, w).
• Lingual weakness of tongue muscles: difficulty in
articulating linguals
• Palatal weakness: result in hyper nasality.
• It is associated with disorders involving
LMNs weakness of the bulbar muscles:
polymyositis,
myasthenia gravis, and
bulbar poliomyelitis
• The speech pattern is breathy and nasal
129.
130. Spastic dysarthria
• Motor speech disorder produced by damage to the CNS bilaterally directly or
indirectly (motor cortex or corticobulbar tracts).
• It may manifest in any or all of the rspiratory, phonatory,resonatory and
articulatory components of speech.
• Its characteristics reflect the combined effects of weakness and spasticity in a
manner that slows movement and reduces its range and force.
• Excessive muscle tone seems to be an important contributor of this disorders.
131. Contd....
• Clinical features reflects the effects of excessive muscle tone and weakness on
speech.
• The speech is harsh or “strain-strangle” in vocal quality, with reduced rate, low
pitch.
• Patient speaks with reduced excursion of the mouth as if talking with a sore tongue
or from the back of the throat.
• Patients often have the features of “pseudobulbar palsy’’ and easy laughter and
crying (emotional incontinence, pseudobulbar affect, or pathological laughter and
crying).
132.
133. Ataxic dysarthria
• It is a perceptually distiguishable motor speech disorder associated with damage to
the cerebellar control circuit.
• It may manifest in any or all the rspiratory, phonatory,resonatory and articulatory level
of speech, but it is characteristics are most evident in articulation and prosody.
• Its speech characteristics reflect the effects of incoordination and reduced muscle
tone on speech which results in slowness and inaccuracy in the force, range, timing
and direction of speech movement.
• Ataxia is an important contributor to the speech deficits of the patient in cerebellar
disease.
134. Contd....
• Ataxic dysarthria is characterized by one of two patterns:
irregular breakdowns of speech with explosions of syllables interrupted by
pauses, or a slow cadence of speech, with excessively equal stress on every
syllable.
“scanning speech”
• Slurred and drunken speech which is too soft or too explosive on different letters
with words running into one another
• Causes include cerebellar strokes, tumors, multiple sclerosis, and cerebellar
degenerations.
135.
136. Hypokinetic dysarthria
• It is motor speech disorder associated with B.G control circuit pathology.
• It may also manifest in any or all the rspiratory, phonatory,resonatory and
articulatory level of speech, but it is characteristics are most evident in voice
articulation and prosody.
• Its deviant speech characteristic reflects the effects of rigidity, reduced force and
range of motion and slow individual.
• Decreased motility or range of movement is significant contributor to this disorder.
137. Contd....
• There is decreased and monotonous loudness and pitch, rapid rate and
occasional consonant errors.
• Typically seen in PD.
138.
139. Hyperkinetic dysarthria
• It is also motor speech disorder associated with B.G control circuit
pathology.
• It may also manifest in any or all levels of components of speech, but
with prominent effects on prosody.
• Unlike most CNS based dysarthria , it can result from abnormalities of
movement at only one level of speech production.
140. Contd....
• It is characterized by marked variation in rate, loudness, and timing,
with distortion of vowels, harsh voice quality, and occasional, sudden
stoppages of speech.
• This speech pattern is seen in hyperkinetic movement disorders such
as HD and dystonia.
141.
142. Mixed dysarthria
• It involves combinations of the other five types.
• One common mixed dysarthria is a spastic-flaccid dysarthria seen in ALS.
• The ALS patient has the harsh, strain-strangle voice quality of spastic dysarthria,
combined with the breathy and hypernasal quality of flaccid dysarthria.
• MS may feature a spastic-flaccid-ataxic or spastic-ataxic mixed dysarthria, in which
slow rate or irregular breakdowns is added.
• Wilson disease can involve hypokinetic, spastic, and ataxic features.
143.
144.
145. The management
• Treatment will depend on the cause and severity of your symptoms
and the type of dysarthria.
• Speech therapy techniques for strengthening muscles, training more
precise articulations, slowing the rate of speech to increase
intelligibility, or teaching the patient to stress specific phonemes.
146. Contd....
• Devices such as
pacing boards to slow articulation
palatal lifts to reduce hypernasality
amplifiers to increase voice volume
communication boards for subjects to point to pictures, and
augmentative communication devices and computer technique for patients
who are unable to communicate in speech.
147. Contd....
• Surgical procedures such as a pharyngeal flap to reduce hypernasality
or vocal fold Teflon injection or transposition surgery to increase
loudness may help the patient to speak more intelligibly.
• In PD, most patients have elements of dysarthria and dysphonia, and
So,treatment options include speech therapy, drug treatment, DBS ,
and surgical.
148. Apraxia of Speech
• Disorder of the motor programming of articulation of sequences of phonemes,
especially consonants.
• The motor speech system makes errors in selection of consonant phonemes, in the
absence of any “weakness, slowness or incoordination” of the muscles of speech
articulation.
• Patient knows what he or she wants to say and how it should sound yet cannot
articulate it properly.
• Consonants are frequently substituted, not distorted.
149. Contd….
• The four cardinal features of apraxia of speech are:
effortful, groping, or “trial-and error” attempts at speech, with efforts
at self-correction
dysprosody
inconsistencies in articulation errors; and
difficulty with initiating utterances
150. Contd….
• How to test for speech apraxia???
Repetition of sequences of phonemes (pa/ta/ka).
Repetition of a polysyllabic word (e.g., “catastrophe” or “television”) is
especially likely to elicit apraxic errors.
Repeating the same word five times will bring out the inconsistency in
the apraxic utterances.
151. Aphemia/verbal apraxia
• Diffential for both apraxia of speech and dysarthria.
• Is a syndrome of near muteness, with normal comprehension, reading, and
writing.
• Patients are often anarthric, with no speech whatever, and then effortful,
nonfluent speech emerges.
• Aphemia is clearly a motor speech disorder rather than an aphasia, if written
language and comprehension are indeed intact
• In general, aphemia is likely to involve lesions in the vicinity of the primary motor
152. “Foreign Accent Syndrome”
• An acquired form of motor speech disorder, related to the dysarthrias.
• The patient acquires a dysfluency resembling a foreign accent, usually
after a unilateral stroke.
• Lesions may involve the motor cortex of the left hemisphere.
• The disorder can also be mixed with aphasia.
153. Acquired Stuttering
• It is uncommon motor speech disorder following acquired brain lesion.
• Involves hesitancy in producing initial phonemes, with an associated
dysrhythmia of speech.
• Most often described in patients with left hemisphere cortical strokes.
• It could also be psychogenic.
154. Opercular Syndrome/Foix-Chavany-Marie syndrome or cheiro-oral
syndrome
• It is a severe form of pseudobulbar palsy.
• There is bilateral lesions of the perisylvian cortex or subcortical connections.
• Patients become completely mute.
• These patients can follow commands involving the extremities but not the cranial
nerves.
• “Automatic-voluntary dissociation”
There is discrepancy between automatic activation of the cranial musculature and
voluntar actions.
This concept fell into disfavor around the turn of the twentieth century, in the face of more holistic schemes of brain function proposed by Sigmund Freud and Pierre Marie, only to be revitalized eventually by Norman Geschwind and others in the 1960s and subsequent decades.
Anatomy of Language
Areas
(A) Core language circuit composed
of Broca’s area, Wernicke’s area, and the arcu-
ate fasciculus. (B) Network of areas involved
in language, including interactions with
adjacent anterior and posterior association
cortex, subcortical structures, and callosal
connections to the contralateral hemisphere.
About 90% to 95% of the population is right-handed.
Cuing giving first sounds of words of naming
Conduction aphasia may evolve from Wernicke’s aphasia.
Although conduction aphasia results primarily from lesions that disrupt communication between Wernicke’s and Broca’s areas, the most severe and persistent repetition disturbance follows damage to Wernicke’s area itself.
PIF=Posteoinferofrontal area
PST=Posterosuperotemporal area
