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CommDis2 SLP405

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