Published on

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

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide


  2. 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. 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. 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. 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. 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. 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. 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
  10. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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
  29. 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. 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. 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. 32.   ETIOLOGIES OF SPASTIC DYSARTHRIA • Vascular (31%) •Degenerative (30%) •Traumatic (12%) • Undetermined (12%) •Demyelination (6%) •Tumor (4%) •Multiple causes (3%) •Infectious (1%) 32
  33. 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. 34. Ataxic Dysarthri a 34
  35. 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. 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. 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. 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. 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. 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. 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. 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. 43. HypokineticHypokinetic DysarthriaDysarthria 43
  44. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 55. HyperkineticHyperkinetic DysarthriaDysarthria 55
  56. 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. 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. 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. 59. CHORECHORE AA 59
  60. 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. 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. 62. DYSTONIA 62
  63. 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. 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. 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. 66. MYOCLONUS 66
  67. 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. 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. 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. 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. 71. TREMO R 71
  72. 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. 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. 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
  76. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 88