Dysarthria is a term associated with a group of neurological diseases caused by lesions in the PNS or CNS.

1. DYSARTHRIA
AYJNIHH
1

2.  Dysarthria is a term associated with a group of neurological diseases
caused by lesions in the PNS or CNS.
Different speech perturbations are associated to the type and location
of the lesions, which are correlated with both: the kind of dysarthrias and
the brain damage.
The speech is one of the mechanisms that are more sensitive to lesions in
the PNS or CNS due to the precise coordination and timing required for
normal speech production.
2

3. The movements can also be impaired in different
ways:
•The muscle can move too far enough (overshoot)
•The muscles can’t move all the way to target (undershoot)
•Move in wrong direction
•Move with too little strength
•Move with poor timing
•Involuntary movements
3

4. Rosenbek & Lapointe (1985) described dysarthria as a group of
related motor speech resulting from disturbed muscular
control over the speech mechanism.
This disturbed muscular control can result in difficulties in,
•Respiration
•Phonation
•Resonance
•Articulation
•Prosody
4

5. Darley (1983) provides a good summary of dysarthria,
“Dysarthria refers to group of disorders involving any
or all of the basic motor speech processes-
respiration, phonation and prosody resulting from
disturbances in muscular control due to damage to the
CNS or PNS. And is always evidenced by some degree
of weakness, slowness, in coordination or alteration of
muscle tone of speech apparatus”
5

6. CLASSIFICATION SYSTEMS OF DYSARTHRIA:
Cauder (1967) gave classification as central and peripheral dysarthria
based on the level of lesion:
 Central- spastic, dyskinetic & ataxicCentral- spastic, dyskinetic & ataxic
 Peripheral- myopathic, myopathic neural & LMN typePeripheral- myopathic, myopathic neural & LMN type
6

7. TYPES EXAMPLES
Age of onset Congenital/Acquired
General cause Vascular/ Neoplastic/ Traumatic/
Infectious
Disease process Multiple sclerosis/ Myasthenia Gravis
Neuro anatomic area involved Cerebral/ Cerebellar/ Brain stem
Cranial nerves involved V, VII, IX, X, XI, XII
Speech process involved Respiration, resonance, articulation,
resonance-prosody
Speech valves involved Respiratory, laryngeal, pharyngeal, velar,
lingual, dental, labial
Speech events involve Neural, muscular, structural
Perceptual characteristic Pitch, loudness, voice quality,
respiration, prosody, articulation, general
impression
Darley, Aronson & Brown (1975)Darley, Aronson & Brown (1975)
7

8. Darley, Aronson & Brown (1969, 1975) identified 8Darley, Aronson & Brown (1969, 1975) identified 8
types of Dysarthriatypes of Dysarthria
Type Localization Neuro motor basis
Flaccid LMN (final common
pathway, motor unit)
Weakness
Spastic B/L UMN (direct &
indirect activation
pathway)
Spasticity
Ataxic Cerebellum (cerebellar
control circuit)
In coordination
Hypokinetic Basal ganglia control
circuit (Extrapyramidal)
Rigidity/ reduced range of
movement
Hyperkinetic Basal ganglia control
circuit (Extrapyramidal)
Involuntary movements
Unilateral UMN Unilateral UMN Weakness/ ?incoordination
Mixed More than one More than one
8

9. FLACCIDFLACCID
DYSARTHRIDYSARTHRI
AA
9

10. •Flaccid dysarthria is a perceptually distinguishable motor
speech disorder produced by injury or malfunction of one or
more of the cranial or spinal nerves.
•It reflects problems in the nuclei, axons, or neuromuscular
junctions that make up the motor units of the final common
pathway (FCP) and it may manifest in any or all of the
respiratory, phonatory, resonatory and articulatory
components of speech.
• Its primary deviant speech characteristics can be traced to
muscular weakness and reduced muscle tone and their effects
on the speed, range and accuracy of speech movements.
•The primary weakness as an explanation for the speech
characteristics of this disorder leads to its designation as
flaccid dysarthria.
10

11. •Unlike most other dysarthria types, flaccid dysarthria
sometimes results from damage confined to isolated muscle
groups.
•As a result, it is justifiable to think of subtypes of the
disorder, each characterized by speech abnormalities
attributable to unilateral or bilateral damage to a specific
cranial or spinal nerve or combination of cranial or spinal
nerves.
• Accurate identification of the cranial or spinal nerve source
for the deviant speech features can help localize the
offending lesion that, in flaccid dysarthria, will always be
somewhere between the brain stem or spinal cord and muscles
of speech.
11

12. Etiologies of Flaccid DysarthriaEtiologies of Flaccid Dysarthria
• Traumatic (33%)
• Surgical (28%)
•Nonsurgical (6%)
•Neuropathies of undetermined origin (27%)
• Muscle disease (8%)
•Tumor (6%)
•Myasthenia gravis (6%)
•Degenerative (6%)
•Vascular (5%)
12

13.
NEUROMUSCULAR DEFICITS ASSOCIATED
WITH FLACCID DYSARTHRIA.
Direction Rhythm Rate Range Force Tone
Individual
Movements
Repetitive
Movements
Individual
Movements
Repetitive
Movements
Individual
Movements
Repetitive
Movements
Individual
Movements
Muscle
tone
Normal Regular Normal Normal Reduced Reduced Weak Reduced
13

14. Flaccid dysarthria due to lesion in the following cranial nerves:
Trigeminal (Vth) nerve:
In patients with unilateral mandibular branch
lesions
•The jaw may deviate to the weak side when opened, and the partly opened
jaw may be pushed easily to the weak side by the examiner.
•The degree of masseter or temporalis contraction felt on palpation when
the patient bites down may be decreased on the weak side.
•With bilateral weakness, the jaw may hang open at rest.
• The patient may be unable to close it or may move it slowly or with
reduced range.
•The patient may be unable to resist the examiner’s attempts to open or
close the jaw and may be unable to clench the teeth strongly enough for
normal masseter or temporalis contraction to be felt. 14

15. •Patient complaints that may relate to jaw weakness include chewing
difficulty, drooling, and overt recognition that the jaw is difficult to close
or move.
•If sensory branches to speech structures are affected, the patient may
complain of decreased face, cheek, tongue, teeth or palate sensation.
•This can be assessed while the patients’ eyes are closed by asking them to
indicate when they detect touch or pressure applied to the affected areas.
•Decreased sensation of undetermined origin in one or more of the
peripheral branches of the Vth nerve is often referred to as trigeminal
sensory neuropathy.
•Viral etiology is common, but association with diabetes, sarcoidosis, and
connective tissue disease has also been noted.
•Facial numbness is occasionally a presenting symptom in multiple sclerosis
(Regli, 1981).
15

16. Facial (VIIth) nerve:
•The visible effects of unilateral VIIth nerve lesions can be striking.
•At rest, the affected side sags and is hypotonic.
• The forehead may be unwrinkled, the eyebrow drooped, and the eye open
and unblinking.
•The tip of the nose and corner of the mouth may be drawn toward the
unaffected side.
•Drooling on the affected side may occur.
•The nasolabial fold is often flattened and the nasal ala may be immobile
during respiration.
•During smiling the face will retract more toward the intact side.
16

17. •Food may stand between the teeth and cheek on the weak side because of
buccinators weakness.
•With milder weakness, asymmetry may be apparent only with use, as in
voluntary retraction, pursing, and cheek puffing, with or without resistance
from the examiner.
•Reduced or absent movement will be observable during voluntary,
emotional, and reflexive activities.
•Fasciculations and atrophy may be apparent on the affected side.
17

18. •Bilateral VIIth nerve lesions are less common than
unilateral lesions.
•With bilateral lesions, the effects of weakness are on both sides, but may
be less striking visually because of the symmetric appearance.
•At rest, the mouth may be lax and the space between the upper and lower
lips wider than normal.
•During reflexive smiling the mouth may not pull upward, giving the smile a
“transverse” appearance.
•The patient may be unable to retract, purse, or puff the cheeks, or the
seal on puffing may be overcome easily by the examiner.
18

19. Glossopharyngeal (IXth) nerve:
•The IXth nerve is assessed clinically by examining the gag reflex,
particularly asymmetry in the ease with which the reflex is elicited.
• A reduced gag may implicate the sensory or motor components of the
reflex, the sensory component if the patient reports decreased sensation
in the area.
• However, a normal gag can be present after intracranial section of the
IXth nerve suggesting that the Xth nerve is also involved in pharyngeal
function.
•Therefore, the gag reflex may not be a reliable test for IXth nerve
function (Clinical Examinations in Neurology, 1991).
19

20.
•It is clear, however, that the IXth nerve may be implicated in patients
with dysphagia, with lesion to the nerve presumably affecting
pharyngeal elevation during the pharyngeal phase of swallowing.
Some individuals with IXth nerve lesions develop brief
attacks of severe pain that begin in the throat and
radiate down the neck to the back of the lower jaw.
Pain can be triggered by swallowing or tongue protrusion.
This condition is known as glossopharyngeal neuralgia.
20

21. Vagus (Xth) Nerve:
Unilateral pharyngeal branch lesions are manifested by the
following;
•The soft palate hangs lower on the side of the lesion.
•It pulls toward the nonparalyzed side on phonation.
•A palate that hangs low at rest but elevates symmetrically.
•If palatal asymmetry on phonation is ambiguous, the clinician should look
for a levator “dimple” representing the point of maximum contraction of
the levator veli palatini muscle. If it is centered, the palate may not be
weak; if it is displaced to one side, the palate is probably weak on the
opposite side.
21

22. •The gag reflex may be diminished on the weak side.
•In bilateral lesions the palate will hang low in the pharynx at rest and
move minimally or not at all during phonation.
• The gag reflex may be difficult to elicit or absent.
•And nasal regurgitation may occur during swallowing.
22

23. Accessory (XIth) nerve:
•Lesions of the spinal portion of the XIth nerve reduce shoulder elevation
on the side of the lesion and weaken head-turning to the side opposite to
the lesion.
•Such lesions do not generally affect speech.
• If bilateral weakness causes significant shoulder weakness and head
drooping, then respiration, phonation, and resonance may be indirectly and
mildly affected by the postural deficit.
23

24. Hypoglossal (XIIth) nerve:
•In unilateral hypoglossal lesions the tongue may be atrophic and shrunken
on the weak side.
• Fasciculations may be apparent.
• The tongue will deviate to the weak side on protrusion because the action
of the unaffected genioglossus muscle is unopposed.
•The ability to curl the tip of the tongue to the weak side inside the mouth
will be diminished as will be ability to push the tongue onto the cheek
against resistance.
24

25. •Voluntary tongue lateralization within the mouth occasionally yields
paradoxic results, with ability to push the tongue into the cheek on the
weak side sometimes appearing normal.
•They may complain that the tongue feels “heavy” or “thick”, or that it
doesn’t move well for eating and speaking.
•Drooling complaints may be related to lingual weakness.
25

26. Spinal nerve lesions:
Nonspeech oral and respiratory mechanisms:
•Compromised respiratory nerve function can result in rapid shallow
breathing.
•Flaring of the nasal alae and use of upper chest and shoulder neck
muscles to elevate and enlarge the rib cage suggest respiratory
compromise.
•Thoracic expansion may be visibly restricted during inhalation and
patients may be unable to hold their breath for more than a few
seconds.
•They may be unable to generate or sustain subglottal air pressure
sufficient to support speech.
26

27. Level Direct, acoustic, and physiologic observations
Respiratory
Laryngeal/Respiratory
Velopharyngeal
Lingual
Reduced vital capacity
Termination of speech at larger than normal lung volumes
Larger than normal inspiratory & rib cage volumes
Abnormal chest wall movements*
Neck and glossopharyngeal breathing*
Vocal cord immobility/sluggishness
Incomplete glottal closure
Abnormal vocal cord frequency and amplitude perturbations
Increased airflow rate
Increased inspiratory volume*
Increased breaths per minute *
Reduced pause frequency & duration*
Reduced speech duration/syllables per breath group*
Reduced range & Variability of f0
High amplitude of f0 with reduced energy of harmonics
Reduced format intensity & definition
Increased high-frequency spectral energy (noise)
(including findings from studies of Velopharyngeal incompetence associated with cleft palate)
Reduced/absent palatal movement
Reduced/absent pharyngeal-wall movement
Increased nasal air flow
Decreased energy in f0
Increased frequency of f0
Reduced pitch range
Increased format bandwidth
Reduced overall intensity & intensity range
Extra resonances
Antiresonances
Reduced Sustained lingual force
27

28. SPASTICSPASTIC
DYSARTHRIADYSARTHRIA
28

29. •Spastic dysarthria is a perceptually distinguishable motor speech disorder
produced by damage to the direct and indirect activation pathways of the
central nervous system (CNS), bilaterally.
•It may manifest in any or all of the respiratory, phonatory, resonatory,
and articulatory components of speech, but it is generally not confined to a
single component.
•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 (spasticity) seems to be an important contributor
to the distinguishing features of the disorder, hence its designation as
spastic dysarthria.
• The correct identification of spastic dysarthria can aid the diagnosis of
neurologic disease and may help localize the sites of the lesions to the CNS
motor pathways.
29

30. The clinical features of spastic dysarthria reflect the
effects of excessive muscle tone and weakness on speech.
Flaccid dysarthria: weakness alone
Spastic dysarthria: effects of excessive muscle tone and
weakness
30

31. Direction Rhythm Rate Range Force Tone
Individual
Movements
Repetitive
Movements
Individual
Movements
Repetitive
Movements
Individual
Movements
Repetitive
Movements
Individual
Movements
Muscle
tone
Normal Regular Slow Slow Reduced
(Weak)
Reduced biased Reduced Excessive
Neuromuscular deficits associated with spastic dysarthria.
31

32.
ETIOLOGIES OF SPASTIC DYSARTHRIA
• Vascular (31%)
•Degenerative (30%)
•Traumatic (12%)
• Undetermined (12%)
•Demyelination (6%)
•Tumor (4%)
•Multiple causes (3%)
•Infectious (1%)
32

33. Speech component Acoustic or physiologic observation
Respiratory (or respiratory/laryngeal)
(based on studies of spastic cerebral palsy)
Reduced:
Inhalatory & exhalatory volumes (shallow breathing)
Respiratory intake
Vital capacity
Rate of amplitude variations
Poor visuomotor tracking with respiratory movements
Laryngeal Decreased:
Vocal cord abduction during respiration Fundamental frequency variability Hyperadduction of true & false cords
during speech Poor visuomotor tracking with pitch variations.
Velopharyngeal Increased pharyngeal constriction
Slow, sluggish Velopharyngeal movement Incomplete Velopharyngeal closure.
Articulatory/rate/prosody Reduced:
Completeness if articulatory contacts
Completeness of consonant clusters
Speed and range of tongue movement
Range of jaw movement
Acceleration & deceleration of articulators
Tongue strength
Articulatory effort for final word stress
Frequency & intensity increases for initial word stress
SPL contrasts in consonants
Voice-onset-time for stops
Amplitude of release bursts for stops
Overall speech rate
Increased:
Syllable & word durations
Duration of nonphonated intervals
Spirantization during stops
Prolonged phonemes
Slow phoneme-to-phoneme transitions
Centralization of vowel formants
Voicing of voiceless stops
33

34. Ataxic
Dysarthri
a
34

35. •Ataxic Dysarthria is a perceptually distinguishable motor speech
disorder associated with damage to the cerebellar control circuit.
•It may be manifest in any or all the respiratory, phonatory,
resonatory, and articulatory levels of speech, but its characteristics
are most evident in articulation and prosody.
• Its speech characteristics reflect the effects of incoordination and
reduced muscle tone on speech, the products of which are slowness and
inaccuracy in the force, range, timing, and direction of speech
movements.
•Ataxia is an important contributor to the speech deficits of patients
with cerebellar disease, hence the disorder's designation as ataxic
dysarthria.
•The identification of ataxic dysarthria can aid the diagnosis of
neurologic disease and may assist lesion localization because its
presence is so strongly associated with cerebellar dysfunction.
35

36. Common clinical signs of cerebellar disease:
Midline zone (vermis, flocculonodular lobe, fastigial nuclei)
Disordered stance and gait
Truncal titubation
Rotated or tilted head postures
Ocular motor abnormalities
Dysarthria
Lateral hemispheric zone (hemispheres, dentate, and interposed nuclei)
Hypotonia
Dysmetria
Dysdiadochokinesis
Ataxia
Tremor
Ocular motor abnormalities
Dysarthria
36

37. ETIOLOGIES OF ATAXIC DYSARTHRIA
• Degenerative (34%)
• Vascular (16%)
• Demyelinating (15%)
• Undetermined (14%)
•Toxic/metabolic (7%)
• Traumatic (6%)
• Inflammatory (5%)
•Tumor (3%)
•Multiple (1%)
37

38. Nonspeech oral mechanism:
•The oral mechanism is often normal.
•That is, the size, strength and symmetry of the jaw, face, tongue, and
palate may be normal at rest, during emotional expression, and during
sustained postures.
•The gag reflex is usually normal and pathologic oral reflexes are generally
absent.
•Drooling is uncommon and the reflexive swallow is usually normal on casual
observation.
38

39. •Non speech AMRs of the jaw, lips, and tongue may be irregular.
• This is usually most apparent on lateral wiggling of the tongue or
retraction and pursing of the lips; judgements that nonspeech AMRs are
irregular should be interpreted cautiously and only after observing many
normal individuals, because normal performance is frequently somewhat
irregular on these tasks.
• It is more relevant to observe the direction and smoothness of jaw and
lip movements during connected speech and speech AMRs for evidence of
dysmetria;
• Irregular movement during speech are often observable, are not
frequently observed in normal speakers, and are more relevant to the
speech diagnosis than nonspeech AMRs.
39

40. Direction Rhythm Rate Range Force Tone
Individual
Movements
Repetitive
Movements
Individual
Movements
Repetitive
Movements
Individual
Movements
Repetitive
Movements
Individual
Movements
Muscle
tone
Inaccurate Irregular Slow Slow Excessive
to normal
Excessive
to normal
Normal to
excessive
Reduced
Neuromuscular deficits associated with ataxic dysarthria.
40

41. Primary distinguishing speech and speech-related findings in ataxic
dysarthria:
Perceptual
Phonation-respiration
Excessive loudness variations
Articulation-prosody
Irregular articulatory breakdowns
Irregular AMRs
Distorted vowels
Excess and equal stress
Prolonged phonemes
Physical
Dysmetric jaws, face, and tongue AMRs
Patient complaints
“Drunk”/intoxicated speech
Stumble over words
Bites tongue/cheek when speaking or eating.
Speech deteriorates with alcohol
Poor coordination of breathing with speech.
41

42. Speech component Acoustic or physiologic observation
Respiratory/laryngeal Abnormal and paradoxical rib cage and abdominal movements
Reduced vital capacity (probably secondary to incoordination)
Poor visuomotor tracking with respiratory movements
Poor visuomotor tracking with f
Increased variability of f and intensity during vowel prolongation and AMRS
Articulation, rate,
& prosody
Reduced rate:
Increased syllabus duration
Increased duration of formant transitions
Longer voice onset time (but sometimes shorter)
Lengthened consonant clusters & vowel nuclei slow AMRs
Disproportionate lengtheningof lax/unstressed vowels
Difficulty initiating purposeful movement
Slow lip, tongue, & jaw movements
Increased variability, inconsistency, or instability of:
Segment durations
Rate
Intensity
AMR rate & intensity
F0
Range & velocity of articulatory movements, especially AMRs
increased instability of force & static position control in lip,
tongue, & jaw on nonspeech tasks
Inconsistent reduction of base word (first syllable) duration
with increases in number of syllabus in words
Inconsistent velophayngeal closure
Other
Breakdown in rhythmic EMG patterns in articulatory muscles
during syllable repetition
Poor visuomotor tracking with lower lip & jaw movements on
nonspeech tasks
Occasional failure o articulatory contact for consonants.
42

43. HypokineticHypokinetic
DysarthriaDysarthria
43

44.
•Hypokinetic dysarthria is a perpetually distinguishable motor speech
disorder associated with basal ganglia control circuit pathology.
•It may be manifest in any or all of the respiratory, phonatory, resonatory
and articulatory levels of speech, but its characteristics are most evident
in voice, articulation, and prosody.
•Its deviant speech characteristics reflect the effects of rigidity,
reduced force and range of movement, and slow individual but sometimes
fast repetitive movements on speech.
•Decreased mobility or range of movement is a significant contributor to
the disorder, hence its designation as hypokinetic dysarthria.
44

45. •Hypokinetic dysarthria is the only dysarthria in which a prominent
perceptual characteristic may be rapid speech rate.
• Its identification can aid neurologic diagnosis and localization.
•Its presence is strongly associated with basal ganglia pathology and is
often tied to a depletion of, or functional reduction in the effect of the
neurotransmitter, dopamine, on the activities of the basal ganglia.
Parkinson’s disease is the prototypic disease associated with hypokinetic
dysarthria.
45

46. •the clinical features of hypokinetic dysarthria reflect the effects on
speech of aberrations in the maintenance of proper background tone and
supportive neuromuscular activity on which the quick discrete, phasic
movements of speech are superimposed.
•the disorder helps to illustrate the role of the basal ganglia control circuit
in providing an adequate neuromuscular environment for voluntary motor
activity.
• hypokinetic speech may give the impression that the movements and
resultant sounds are “all there” but have been attenuated in their range or
amplitude as well as their ability to vary with normal flexibility and speed.
46

47. Primary deficits Examples
Resting tremor Head
Limb
Pill-rolling
Jaw, lip, tongue
Rigidity Resistance to passive stretch in all directions through full range of movement
Paucity of movement
Bradykinesia/
Hypohinesia
Slow initiation & speed of movements
“Freezing”
Akinesia Festinating gait
Reduced:
Armswing during walking
Limb gestures during speech
Eye blinking
Head movement:
accompanying vertical & horizontal eye movement
Frequency of swallowing
Micrograhia
Masked facies
Postural
abnormalities
Stopped posture (flexed head & trunk)
Poor adjustment to tilting or falling
Difficulty turning in bed
Difficulty going from sitting to standing.
CLINICAL CHARACTERISTICS OF BASAL GANGLIA CONTROL CIRCUIT DISORDERS
ASSOCIATED WITH HYPOKINETIC DYSARTHRIA
Common nonspeech clinical signs of parkinsonism:
47

48. ETIOLOGIES OF HYPOKINETIC DYSARTHRIAETIOLOGIES OF HYPOKINETIC DYSARTHRIA
•Degenerative (75%)
•Vascular (10%)
•Undetermined (6%)
•Toxic/metabolic (3%)
•Traumatic (2%)
•Multiple (2%)
•Infectious (1%)
48

49. Nonspeech oral Mechanism:Nonspeech oral Mechanism:
•The face may be unblinking and unsmiling, masked or expressionless at
rest and lack animation during nonverbal social interaction.
•Movements of the eyes and face, hands, arms and trunk that normally
accompany speech and complement the emotions and indirect meanings
conveyed through prosody may be attenuated.
•Chest and abdominal movements during quiet breathing may appear
reduced or nonexistent, and they may remain reduced in excursion when
the patient attempts to breathe deeply.
49

50. •As the eyes may blink infrequently, so may the patient swallow
infrequently, perhaps another reflection of rigidity or reduced
automatic movements.
•This may lead to excessive saliva accumulation and drooling. When
moving the eyes to look to the side or up or down, the normal
tendency for head turning to accompany the gaze may be absent.
•A tremor or tremulousness of the jaw and lips may be apparent at
rest or during sustained mouth opening or lip retraction.
•Similarly, the tongue is often strikingly tremulous on protrusion or at
rest within the mouth.
•The lips (particularly upper) may appear tight or immobile at rest and
during movement, including speech.
50

51. •The size, strength, and symmetry of the jaw, face and tongue may b
normal, often surprisingly so given their limited movement during speech.
•Nonspeech alternating motion rates (AMRs) of the jaw, lips, and tongue
may be slowly initiated and completed, or rapid and markedly restricted in
range.
•The overall impression derived during casual observation and formal oral
mechanism examination is one of a lack of vigor or animation in the absence
of a degree of weakness that might explain it.
• At rest, as well as during social interaction and speech, the patient’s
facial affect appears restricted. “flat”. Unemotional, and sometimes
depressed. These impressions may not accurately reflect the patients’
inner emotional state. Unfortunately, but predictably, their speech usually
faithfully mirrors their nonverbal behaviors.
51

52. Direction Rhythm Rate Range Force Tone
Individual
Movements
Repetitive
Movements
Individual
Movements
Repetitive
Movements
Individual
Movements
Repetitive
Movements
Individual
Movements
Muscle
tone
Normal Regular Slow fast Reduced Very
Reduced
Reduced Excessive
NEUROMUSCULAR DEFICITS ASSOCIATED WITHNEUROMUSCULAR DEFICITS ASSOCIATED WITH
HYPOKINETIC DYSARTHRIA.HYPOKINETIC DYSARTHRIA.
52

53. Speech component Acoustic or physiologic observation
Respiratory
(or respiratory/laryngeal)
Reduced:
Vital capacity
Amplitude of chest wall movements
Airflow volume during vowel prolongation
Intraoral pressure during AMRs
Syllabus per breath group
Maximum vowel duration
Increased:
Respiratory rate
Latency to begin exhalation
Latency to initiate phonation after exhalation initiated Irregular breathing patterns
Paradoxic rib cage & abdominal movements
Difficulty altering automatic patterns for speech.
Laryngeal Bowed vocal cords in spite of solid, nonflaccid appearance
Tremulousness if arytenoid cartilages
Asymmetry of laryngeal structures & movements during phonation, especially in hemiparkinsonism
Ventricular foid movement during phonation
Decreased:
Intensity
Pitch & loudness variability
Speed to initiate phonation
Intensity peaks across syllabus
Increased glottal resistance
Laryngealizaton
Increased shimmer
Continuous voicing in segments with voiceless
consonants
Voiceless transitions from vowels to following consonants
Poor pitch control for visuomotor tracking
53

54. Velopharyngeal
Speech component
Articulatory/rate/prosody
Increased nasal airflow during nonnasal target productions Reduced velocity & degree of velar movement during speech
Abnormal spread of nasalization across syllables
Acoustic or physiologic observation
Reduced:
Amplitude & velocity of lip movements
Amplitude & duration of lip muscle action
potentials
Jaw stability during vowel prolongation
Tongue endurance & strength
Spectrographic acoustic contrast & detail
Speech rate
Ability to increase rate on request
First & second format transition rates (=
Slowness of movement)
Syllable boundary durational differences
Between separate & compound nouns f0,
intensity & articulatory effort increases to signal
stress
Variation in syllable duration.
Increased or accelerated:
Connected speech & AMR rates
Rate variability
Frequency & duration of pauses during connected
speech
Articulatory undershoot of lip & velum
Lip rigidity/stiffness
Poor maintenance of temporal reciprocity
between jaw depressors and elevators
Poor visuomotor tracking with jaw and lip
movements
Abnormal jaw and lip tremor at rest, during
sustained postures, & active & passive
movement.
54

55. HyperkineticHyperkinetic
DysarthriaDysarthria
55

56. •Hyperkinetic dysarthria is a perceptually distinguishable motor speech
disorder that is most often associated with diseases of the basal ganglia
control circuit.
•It may be manifest in any or all of the respiratory, phonatory, resonatory,
and articulatory levels of speech, and it often has prominent effects on
prosody.
•Unlike most central nervous system (CNS) based dysarthrias, it can result
from abnormalities of movement at only one level of speech production,
sometimes only a few muscles at that level.
•Its deviant speech characteristics are the product of abnormal, rhythmic
or irregular and unpredictable, rapid or slow involuntary movements.
56

57. •Involuntary movements are the theme that ties together the
manifestations of the disorder, but there is considerable variability in
their form and locus.
•This heterogeneity could justify a formal division of the disorder
into subtypes under the broad heading of hyper kinetic dysarthrias.
57

58. Designation Speed Rhythmicity Anatomic substrate
Dyskinesia Fast or slow Irregular or rhythmic Basal ganglia control circuit
Myoclonus Fast or slow Irregular or rhythmic Cortex to spinal cord
Palatopharyngo-
laryngeal
Slow Regular Brain stem (Guillain Mollaret triangle)
Action Fast Irregular Basal ganglia or cerebellar control circuit
Tics Fast Irregular but patterned Basal ganglia control circuit
Chorea Fast Irregular Basal ganglia control circuit
Ballism Fast Irregular Area of subthalamic nucleus
Athetosis Slow Irregular Basal ganglia control circuit
Dystonia Slow Irregular/sustained Basal ganglia control circuit
Spasmodic dysphonia Slow Irregular/sustained Basal ganglia control circuit
Spasmodic torticollis Slow Irregular/sustained ? Basal ganglia control circuit
Spasm Slow or fast Irregular ? Basal ganglia control Circuit
Hemifacial spasm Fast Irregular Facial nucleus Cerebellopontine angle,
facial canal
Essential tremor Slow or fast Rhythmic ? Striatum
Organic voice Slow Rhythmic Cerebellar control circuit
Spasmodic dysphonia Slow Rhythmic ?
Other *
Fasciculations Fast Irregular LMN
Synkinesis Fast or Slow Irregular LMN
Facial myokymia Intermediate Rhythmic LMN
GORIES OF ABNORMAL MOVEMENT ASSOCIATED WITH HYPERKINETIC DYSAGORIES OF ABNORMAL MOVEMENT ASSOCIATED WITH HYPERKINETIC DYSA
58

59. CHORECHORE
AA
59

60. Nonspeech oral mechanism in patients with chorea:
•The jaw, face, tongue and palate are usually normal in size, strength and
symmetry.
•The gag reflex is often normal.
•Pathologic oral reflexes may not be present.
• Drooling is occasionally observed, and chewing and swallowing difficulties
are not uncommon.
•The most striking abnormality is motor unsteadiness and often easily
observed choreiform movements.
• At rest or during attempts to maintain lip retraction and rounding, mouth
opening, or tongue protrusion, quick unpredictable, involuntary movements
may occur
60

61. Primary distinguishing speech and speech related findings in the hyperkinetic dysarthria of chorea
____________________________________________________________________
Perceptual
Phonation/respiration Sudden forced inspiration,
expiration, voice stoppages,
transient breathiness,
strained-harsh voice quality,
excess loudness variations
Resonance Hypernasility (intermittent)
Articulation Distortions and irregular breakdowns, slow
and irregular AMRs
Prosody Prolonged intervals and phonemes,
variable rate, inappropriate silences,
excessive-inefficient-variable patterns
of stress
Physical Quick, unpatterned involuntary
head/neck, jaw, face, tongue,
palate, pharyngeal, laryngeal,
thoracic-abdominal movements
at rest, during sustained
postures and movement
Dysphagia
Patient Complaints Effortful speech, inability to “get
speech out,” involuntary
orofacial movements
Chewing and swallowing
problems 61

62. DYSTONIA
62

63. Nonspeech oral mechanism in patients with Dystonia:
•As in chorea, the oral mechanism is often normal in size, strength, and
symmetry, and reflexes may be normal.
•Drooling may occur, and chewing and swallowing complaints are common.
Patients frequently complain that food gets stuck in the throat or that
chewing is difficult because of jaw or tongue movements (Golper and
others, 1983).
•The striking features of the nonspeech oral mechanism exam are most
evident at rest or during attempts to maintain steady facial postures.
63

64. •Affected neck muscles may cause elevation of the larynx; torsion of the
neck may be marked in patients with torticollis.
•As in chorea, recognition of dystonia is most difficult when movements are
sublet or when cognitive or other motor deficits make valid observations
difficult.
•Patients may use sensory tricks to inhibit dystonic movements, and it is
important to ask if they are aware of such tricks when they do not use
them spontaneously.
•These often involve pressure or light touch to the jaw, cheek, or back of
the neck: some patients will hold a pipe in the mouth because it inhibits
jaw, lip or tongue dystonias.
In some cases, the non speech oral mechanism examination may be entirely
normal, dystonic movements being triggered only by speech. There is a
tendency for such patients to have very focal dystonic movements that
may involve only the jaw, tongue, pharynx, larynx or respiratory muscles. 64

65. Primary distinguishing speech and speech related findings in the hyperkinetic dysarthria of dystonia:
Perceptual
Phonation- respiration Strained-harsh voice quality, voice
stoppages, audible inspiration,
excess loudness variations,
alternation loudness, voice tremor
Resonance Hypernasility
Articulation Distorted vowels, irregular
articulatory breakdowns, slow
irregular AMRs
Prosody Inappropriate silences, excess
loudness variations,
excessive-inefficient-variable
patters of stress
Physical Relatively slow, waxing and
waning head-neck, jaw, face,
tongue, palate, pharyngeal,
laryngeal, thoracic-abdominal
movements
Present at rent, during sustained
postures and movement, but
sometimes only during speech
Improvement with “sensory tricks”
Dysphagia
PatienT complaints Effortful speech, inability to “get
speech out, “involuntary
orofacial movements
“Tricks” that improve speech
temporarily
Chewing and swallowing
problems (food “sticks” in throat)
65

66. MYOCLONUS
66

67. NONSPEECH ORAL MECHAMISM IN PATIENTS WITH
HYPERKINETIC DYSARTHRIA ASSOCIATED WITH
PALATOPHARYNGOLARYNGEAL MYOCLONUS (PM):
•Palatopharyngolaryngeal myoclonus is present at rest, during sustained
postures and movement, and during sleep.
•In some cases, the eyeballs, diaphragm, tongue, lips and jaw are also
involved.
•The most common finding in PM is abrupt, rhythmic, beating-like elevation
of the soft palate at a rate of 60 to 240 per minute.
•Pharyngeal contractions also may be apparent and, because of activity of
the tensor veli palatini, may produce opening and closing of the Eustachian
tube with an associated clicking sound that sometimes can be heard by
ohers (Aronson, 1990).
•Deuschl and others (1990) reported that these “earclicks” were a very
frequent complaint in patients with idiopathic PM and were rare in
symptomatic PM. 67

68. •Myoclonic movements of the larynx can sometimes be seen on the external
surface of the neck, and patients may complain of a clicking sensation in
the larynx or a sensation of laryngeal spasm (aronson, 1990).
•It is important to distinguish myoclonic movements in the external neck
from carotid pulses, which are usually slower and do not visibly displace the
laryngeal cartilages.
•Myoclonic movements of the lips and even the nares are sometimes
present.
•Apparent lingual myoclonus may be seen, but lingual jerks may be
secondary to laryngeal myoclonus.
68

69. Perceptual
phonation-respiration Often no apparent abnormality.
Momentary voice arrests during contextual speech
when severe
Voice arrests or myoclonic beats at
60 to 240 Hz during vowel prolongation
Resonance Usually normal, but occasional intermittent
hypernasality
Articulation-prosody Usually normal, but brief silent intervals if
myoclonus interrupts inhalation or initiation of
exhalation, phonation, or articulation
Physical Myoclonic movements of palate, pharynx, and
larynx and sometimes lips, nares, tongue and
respiratory muscles
Laryngeal/pharyngeal myoclonus sometimes
observable beneath neck surface
Patient Complaints Earclicks
Patient often unaware of myoclonic movements and
usually doesn’t complain of speech difficulty
Primary distinguishing speech and speech-related findings in the
hyperkinetic dysarthria of Palatopharyngolaryngeal myoclonus:
69

70. Perceptual
Phonation- respiration Occasional adductor voice arrests
Articulation-prosody Slow rate, decreased precision with increased rate
Marked deterioration of AMR regularity with
increased rate
Physical Normal at rest unless other neuromuscular
deficits present
Quick, gross, or fine jerky movements of
orofacial muscles during speech-especially
lips-worsening with increased rate
Patient complaints Awareness of imprecise speech and inability or
reluctance to speak at normal or rapid rates
Primary distinguishing speech and speech related findings
in the hyperkinetic dysarthria of action myoclonus:
70

71. TREMO
R
71

72. ORAL MECHANISUM IN HYPERKINETIC DYSARTHRIA
ASSOCIATED WITH ORGANIC VOICE TREMOR:
•Lingual tremor may be apparent at rent or on protrusion in patients
with organic voice tremor.
• When present during phonation, it may represent genuine lingual
tremor or be secondary to vertical oscillations of the larynx.
•Tremorous movements of the jaw and lips are often apparent at rest,
during sustained postures, and during vowel prolongation
72

73. •Palatal and pharyngeal tremor and often obvious during sustained
“ah”, synchronous with the perceived voice tremor.
•Fiberscopic observation of the larynx may reveal rhythmic vertical
laryngeal movements, and adductor and abductor oscillation of the
vocal folds, synchronous with perceived voice tremor (Aronson, 1990;
Tomoda and others, 1987).
•Vertical oscillations of the larynx also can often be seen on the
external neck during vowel prolongation.
73

74. Primary distinguishing speech and speech related findings
in the hyperkinetic dysarthria of organic voice tremor:
Perceptual
Phonation-respiration Quavering, rhythmic, waxing and waning tremor,
most evident on vowel prolongation at a rate
of approx. 4 to 7 Hz.
Voice arrests may occur in severe forms but may
disappear if pitch is raised
Articulation Usually normal, but rate may be slowed
Prosody Normal pitch and loudness variability may be
restricted or altered by the voice tremor
Physical Rhythmic, vertical laryngeal movements and
adductor and abductor oscillations of the vocal
cords synchronous with voice tremor
Tremor of jaw, lips, tongue and palate/pharynx,
may be present, especially during phonation.
Lingual and jaw tremor may be secondary to
laryngeal tremor
Patient complaints Shaky or jerky voice
Worse with fatigue or anxiety
Improves with alcohol
Frequent family history of tremor
74

75. MIXED
DYSARTHRIA
75

76. •Imposing functional and anatomic divisions on the nervous system
helps our attempts to understand the brain’s operations.
•It also establishes a framework for localizing and categorizing
nervous system diseases.
• Unfortunately, no rule of nature obligates neurologic disease to
restrict itself to the division we impose upon it.
• As a result, the effects of neurologic disease can be “mixed” and
spread across two or more divisions of the nervous system.
•Mixed dysarthrias represent a heterogeneous group of speech
disorders and neurologic diseases.
•Virtually any combination of two or more of the pure dysarthria
types is possible, and in any particular mix any one of the components
may predominate.
76

77. Dysarthria
Disease Flaccid Spastic Ataxic Hypokinetic Hyperkinetic UUMN
Degenerative ALS ++ ++ ? - - -
MS + +/++ +/++ + + +
Friedreich’s ataxia ? + ++ ++ - -
PSP - ++ + ++ - -
Shy-Drager syndrome + +/++ ++ ++ - -
Striatonigral
degeneration*
- +/? - ++ +/? -
Corticobasal
degeneration*
- +/++ + +/++ ? ?
Toxic-metabolic
Wilson’s Disease
- +/++ +/++ ++ - -
Hepatocerebral
degeneration*
- +/++ +/++ +/++ +/++ -
Hypoxic - ? +/++ +/++ +/++ -
Types of dysarthria that may be present in
neurologic diseases that can produce mixes dysarthrias:
77

78. Goals of Assessment/ Examination :
 Description and problem detection: which characterizes
the features of speech, represents the data base upon
which diagnostic & treatment decisions are made. The
bases of description derive from- patient’s history and
description of the problem; OPM examination; perceptual
characteristics of speech and results of slandered clinical
tests; and acoustic and physiologic analysis of speech.
 Establishing diagnosis possibilities
 Establishing diagnosis
 Establishing implications for localization and disease
diagnosis: when motor sp disorder is identified, its
implications for neurologic localization should be
addressed explicitly, especially if the referral source is
unfamiliar with the method of classification.
78

79.  Specifying severity: it can be estimated. This
estimate is imp for 3 reasons–
 1)subjective or objective measures of severity can
be matched against the patient's complaints which
may suggestive of psychogenic contribution to the
disorder,
 2)it influences prognosis and management decision
making;

 3)baseline data against which future changes can be
compared.
79

80. General guidelines:
Motor speech examination has 3 essential components.
1.History
2.Identification of salient speech features
3. Identification confirmatory signs
With this information diagnosis is made, recommendations
are formulated,& results communicated to the patient,
referring physician, and others.
1. History:
Rowland,1989– 90% of Neurogenic diagnosis depends on the
patient’s history.
2. Salient features: are those features that contribute most
directly and influentially to diagnosis. They include the
speech characteristics themselves and their presumed
neuromuscluar substrates.
80

81. According to Darley, Aronson, and Brown (1975): 6 salient
features that influence speech production. (shown in table
below)
Feature Abnormality associated with motor speech disorder.
Strength Reduced, usually consistently but sometime
progressively
Speed Reduced or variable ( inc in hypokinetic)
Range Reduced or variable (excessive in hyperkinetic)
Steadiness Unsteady, either rhythmic or arhythmic
Tone Increased, decreased, or variable
Accuracy Inaccurate, either consistently or inconsistently
81

82. 3. Confirmatory signs: are additional clues about the
location of pathology. In the context of speech examination,
they are signs other than deviant speech characteristics
and salient neuromuscular features that characterize them
that help confirm the speech diagnosis.
Confirmatory signs can be found in speech or nonspeech
muscles such as– in speech– atrophy, reduced tone,
fasciculations, poorly inhibited laughter or crying, reduced
normal reflexes or presence of pathologic reflexes, and
strength of the cough.
Confirmatory signs confirms or support conclusions about the
nature of a speech disorder, but a particular motor speech
diagnosis does not require that confirmatory signs be
present.
Confirmatory signs from nonspeech motor system come from
observations of gait and station, direct muscles
observation, muscles stretch reflexes etc.
82

83. Motor Speech Examination:
1.During nonspeech activates
In general, it provides information about the size strength,
symmetry, range, tone, steadiness, speed, & accuracy of
orofacial movts, particularly the jaw, face, tongue & palate.
The observations are primarily visual and tactual, but also rely
on auditory information. The observations are done at rest,
during sustained pastures, during movts, and reflexes.
a. The face at rest – observer symmetry, expressions are
present or not, involuntary movts, etc
b. The face during sustained pastures– observation of symmetry,
range of movts, strengths and tone, and ability to maintain
sustained posture. Sustained postures includes: retraction of
lip; rounding or pursing of the lips; puffing of cheeks;&
sustained mouth opening.
83

84. c. Face during movements
d. The Jaw at rest– observe symmetry, quick and slow
involuntary movts. such as clenching, opening or pulling
to one side, or tremor like up & down movts.
e. The Jaw during sustained posture– observed during
sustained facial posture tasks like mouth opening.
f. the jaw during movts– during SMR and AMR
g. The tongue at rest
h. The tongue during sustained postures– protrusion,
resisting pressure to push it inward with tongue blade,
lateralizing to cheek; lateralizing outside the mouth.
i. The tongue during movts– rapid side to side movts
j. The velopharynx during movts— during production of /ah/
k. Respiration-- respiratory adequacy can be observed
during quite breathing and a few nonspeech
84

85. l. reflexes– can provide confirmatory clues about the
neuropathology and its location in CNS verses PNS. 1.gag or
pharyngeal reflex: by stroking the back of the tongue,
posterior pharyngeal wall. 2.jaw jerk: it is primitive reflex, if
present then indicative of pathologic. for testing it patient
should be relaxed, with the lips parted and the jaw about
the halfway open. A tongue blade ( or fingertip) is placed on
the patient’s chin and the blade is then tapped with reflex
hammer or a finger of other hand.
m. Sucking reflex
n. Snout reflex
85

86. 2.Tasks for speech assessments
Following tasks are designed to isolate as well as possible
respiratory-phonatory, velopharyngeal, and the
articualatory sys for independent assessment:
a. Vowel prolongation – observe for pitch, loudness and
voice quality
b. Alternate motion rate (AMR)—speed and regularity of
reciprocal movts of the jaw, lips, & anterior and posterior
tongue, also for precise articulatory movts. Inability to
sustain AMR more than few seconds reflects
inadequacies at the respiratory-phonatory or
velopahryngeal levels. AMR for /p/, /t/ &/k/ usually can
be 5 to 7 repetition per sec. for /k/ is slower than /p/ and
/t/.
c. Sequential motor rate (SMR)– ability to move quickly from
one articulatory position to another. sequencing for SMR
is heavy &, for this reason they r useful when apraxia of
speech is suspected.
86

87. d. Contextual speech– most useful task for evaluating the
integrated function of all components of speech,and each
primary valves. It includes narrative, conversational speech
as well as reading aloud a standard paragraph.
e. Stress testing.
Published testes:
FDA by Enderby, (1983): relies 9 points rating scale provide to
patient’s applied information and observation of all
structures and function. And speech.
Assessment of intelligibility in dysarthric speakers (ADIS): by
Yarkston and Beukalman 1981. : this is probably the most
widely used standardized test for measuring intelligibility,
speaking rate, and communication efficiency in dysarthrics.
It quantifies intelligibility of single words & sentences &
provides an estimate of communication efficiency by
examining the rate of intelligible words per min in
sentences.
87

88. 88