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5.CD2-MotorSpDis2
CommDis2 SLP405
| Question | Answer |
|---|---|
| Types of brain damage | Brainstem (dysphagia, dysarthria). Lang. dom. (L) hemisphere (aphasia, apraxia, dysarthria). Visuospatial (R) hemisphere (prosody, humor). Diffuse vs focal. |
| Describing motor speech disorders | Age of onset. Chronic, congentital, progressive. Severity. ELMS (etiology, lesion site, motor signs, speech characteristics. |
| Motor speech etiologies VITAMIN_D | Vascular. Infection. Trauma. Anoxia. Metabolic/toxic. Ideopathic. Neoplasms (new growth). Degenerative disease (PD, HD, MS, CBD, ALS) |
| Types of dysarthria (5) | Flaccid. Spastic. Ataxic. Hypokinetic. Hyperkinetic. |
| E: Flaccid | Degenerative (ALS), 40%; Traumatic, 22%; Vascular (brain stem stroke), 9%; Muscle disease (muscular dystrophy), 9%; Myasthenia gravis, 4%; Demyelinating, 2% (Guillain-Barre) |
| E: Ataxic | 50% Degenerative: Hereditary (Friedreich's). Non-hereditary (MS). 20% Vascular and tumor (cerebellopontine angle tumors, acoustic neuroma) |
| E: Spastic | Degenerative (ALS, PSP), 60%; Vascular 17%; Ideopathic 10%; Congenital (CP), 8%; Traumatic (4%); Demyelinating (MS), 1% |
| E: Hypokinetic | 75% degenerative (PD, PSP, Shy Drager). 10% vascular. 3% toxic/metabolic. 2% traumatic. |
| E: Hyperkinetic | Toxic/metabolic (drugs). 5-6% of dysarthrias (rarest). Degenerative (rapid cognitive, motor and speech declines). |
| L: Flaccid | LMN: cranial nerves, cranial/spinal nuclei, axons, neuro muscular junction, muscle fiber |
| L: Ataxic | Cerebellum |
| L: Spastic | UMN (white matter): dysfunction of direct & indirect activation pathways (DAP & IAP) affecting final common path (FCP) (Insalaco, lecture). Cerebral cortex, internal capsule, peduncles, brain stem (Murdoch, 2011). |
| L: Hypokinetic | Dopamine loss to the basal ganglia: caudate (HD), putamen, subthalamic nucleus, substantia nigra (PD), globus pallidus |
| L: Hyperkinetic | Basal ganglia: Caudate (HD) |
| M: Flaccid | Paralysis. Fasciculations. Reduced reflexes. |
| M: Ataxic | Gait and limb ataxia, essential tremor, nystagmus, hypotonia, dysmetria, dysdiadochokinesia, intention tremor, possible lower face weakness |
| M: Spastic | Spasticity - overactive muscle contraction in reaction to being stretched. Hypertonic, hyperreflexive bulbar muscles. Impaired voluntary muscle movement. Facial and lingual weakness (UMN). Pathological reflexes (Babinski). No atrophy. |
| M: Hypokinetic | Difficulty with larger movements (facial, vocal dynamics). |
| M: Hyperkinetic | Bizarre, abnormal, involuntary movement (overexcitation of sensorimotor cortex): orofacial, head, respiratory. |
| S: Flaccid | Hypernasality. Breathiness. Nasal emission. Audible inspiration. Short phrases. |
| S: Ataxic | excess and equal stress, irregular breakdowns, distorted vowels, prolonged phonemes, excess loudness variations |
| S: Spastic | Slow rate (104wpm reading), short phrases, effortful speech. Fatigue with speaking. Hypernasality (less than flaccid dysarthria). Strained-strangle voice. Pitch breaks. Imprecise consonants. Low pitch. |
| S: Hypokinetic | Rapid rate (reduced vowel space). Light articulatory contacts. Soft, trailing, weak voice. No emotion. |
| S: Hyperkinetic | Bizarre, irregular (not weak) voice, voice stoppages, excessive prosody, pitch breaks. Difficulty coordinating voiced/unvoiced consonants, open/closed syllables. |
| Acoustic evaluation | 1) Instrumentation of phonation : Voice/Speech deviance, DDK (Computerized Speech Lab). 2) Instrumentation of resonance: Nasalance (Nasal and non-nasal sentences, nasometer) |
| Perceptual evaluation | Counting (1-2-3-4…), word intelligibility, AIDS (Yorkston & Beukelman), phonetic intelligibility test (Kent, 1989, JSHD), Grandfather or Rainbow passage |
| Physiological evaluation | respiration, phonation and resonance -add articulation: strength, speed, range, steadiness, tone, accuracy. CN examination, Subglottal pressure, Airflow (simple water manometer), Lung volume (Spirometer) NSOMs, DDK/AMRs, and SMRs. |
| Dys Tx - Respiraory | Inspire to high lung lung volume. Initiate speech at top of breath cycle. Keep utterance short. Phrasing - break at natural points |
| Dys Tx - Laryngeal | often difficult to obtain improvements in prosody, loudness |
| Dys Tx - V-P incompetence | Consider prosthesis, palatal lift. V-P closure will not likely improve as a result of speech tx. When possible, improve intra-oral pressure for voiceless consonants |
| Dys TX - Speech rate | Usually already speaking at slow rate. Try slowing speech for effect. May allow longer phonation time for each phoneme. Model slow rate and phrasing |
| General goals for Dysarthria (Yorkston et al.; Rosenbek et al.) | Maximize: effectiveness, efficiency, naturalness. Unlikely to achieve prior level of communication. Reduce level of impairment/strengthen a weakness (flaccid only). Compensate (includes non-speech supports) Reduce demands - eg change lifestyle |
| Motor learning principles | |
| DAP Origin/destination | Cerebral Cortex (corticospinal; corticobulbar) TO cranial and spinal nerve nuclei. |
| DAP Function | Direct voluntary, skilled movements |
| DAP Lesion signs | Weakness and loss of skilled movement/dexterity. Hyporeflexia. Hypotonia (decreased tone) |
| IAP Origin/destination | Cerebral Cortex (corticoreticular; corticorubral; reticulospinal; rubrospinal; vestibulospinal; tectospinal) TO cranial and spinal nerve nuclei |
| IAP Function | Control posture, tone, and movements supportive of voluntary movement |
| IAP Lesion signs | Spasticity. Clonus. Hyperactive Stretch Reflexes. Babinski Sign. Hypotonia (increase tone). Decorate or decerebrate posture. |
Created by:
ashea01
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