from mixed dysarthria through acquired AOS Flashcards
mixed dysarthria lesion and clinical presentations (much of what is known based on ALS)
progressive degeneration of UMNs and LMNs; weakness as prominent motor symptom; symptoms may first appear in limbs (spinal), bulbar (CNs), or mixed (brainstem and MNs)
mixed dysarthria perceptual
prolonged intervals and phonemes, inappropriate silences, flaccid + spastic effect; add’l from sheet: abnormal pitch, monopitch, harsh voice, breathy, strained, hypernasal, nasa emission, monoloudness, audible inspiration, slow rate, short phrases, reduced stress, excess and equal stress, imprecise consonants, distorted vowels, intelligibility
mixed dysarthria etiologies
degenerative (most common, esp. ALS, Friedrich’s ataxia,), demyelinating (MS), vascular, toxic-metabolic, traumatic, neoplasm, infectious or autoimmune
mixed dysarthria disease example
ALS: absence of muscle nourishment, progressive, no cure; hypoglossal MNs disproportionately affected); 1-5 years life expectancy; reduced intelligibility; especially lower lip, tongue, jaw movement, can use instrumental measures and speech characteristics as first disease markers and to separate stages of ALS (Green, Yunusova, et al.)
ataxic dysarthria lesion and clinical presentations
bilateral damage to cerebellum (and connections to thalamus and cerebral hemisphere)/cerebellar pathways in brainstem/generalized cerebellar disease; disordered contractions of agonist/antagonist muscles; lack of coordination; jerky movements; dysrhythmia, dysmetria (over-, undershooting), intention tremor, wide gait
ataxic dysarthria perceptual
imprecise consonant, articulatory breakdown, distorted vowels, excess and equal stress, prolonged phonemes and intervals, slow rate, harshness, monopitch, monoloudness, excessive loudness variation; scanning speech (choppy, out-of-sync); articulation and prosody most prominent
ataxic dysarthria etiologies
degenerative, vascular, demyelinating, cerebellar, tumors, TBI, stroke, toxicity
ataxic dysarthria disease example
Friedrich’s ataxia: autosomal recessive; loss of coordination, fatigue, vision impairment, heart condition, most common childhood onset type
roles of cerebellum
connect to cerebral cortex; auditory and proprioceptive feedback; connections to brainstem and indirect activation pathways; cooperation with basal ganglia
inputs to cerebellum and outputs from cerebellum
input from cortex, vestibular system, spinal cord, brainstem, and relay neurons in pons; output to cortex, primary motor and premotor cortex via deep cerebellar nuclei via thalamus: cortex->cerebellar cortex->relay nuclei->thalamus
Weismer, Yunusova, Bunton
instruments must be sensitive to dysarthria, tell us about the movement of speech motor systems, functional communication implications, and feasibility of implementation and interpretation
basal ganglia components and fx
caudate, putamen, globus pallidus, substantia nigra, subthalamic nucleus; integrate motor info. for complex movements, plan and execute complex movements, movement selection, motor learning, postural support/muscle tone for skilled, voluntary movement, regulate amplitude, velocity, initiation
BG effect on direct pathways (corticospinal; voluntary)
excitatory by mechanism of disinhibition (not letting gate close)
BG effect on indirect pathways
inhibits unwanted movements (tics, tremors, etc.)
hypokinetic and hyperkinetic
hypo: too much inhibition; not enough excitation; not enough inhibition; too much excitation
hypokinetic dysarthria lesions and clinical presentations
not enough direct pathway excitation; damage to basal ganglia (substantia nigra) and fiber tracts; neurotransmitter imbalance; reduced movements; muscle rigidity, resting tremor, bradykinesia, hypokinesia, postural instability, acceleration of speech, walk (much of this from PD)
hypokinetic dysarthria perceptual
monopitch/monoloud/reduced stress contrasts, imprecise consonants, breathy, reduced vocal intensity, fast rate, short rushes of speech; add’l from sheet: harshness, variable rate, inappropriate silence, repeated phonemes/syllables
hypokinetic dsyarthria etiologies
degenerative, vascular, trauma, infectious, virus, stroke, antipsychotic, dementia
hypokinetic dysarthria disease example
PD (majority): dopaminergic neurons loss in substantia nigra; resting tremor, slow movements, rigid, masked face, usually later in life, progression between 5-15 years
hyperkinetic dysarthria lesion and clinical presentations
basal ganglia lesion (esp. caudate/putamen); abnormal, rhythmic, or irregular involuntary movements (hyperkinesia): myoclonus–single jerk, tics, tremor, dyskinesia, athetosis–writhing, ballism–fast/irregular/gross, chorea–rapid/involuntary/purposeless, dystonia–abnormal posture from excessive muscle contraction
hyperkinetic dysarthria perceptual
inappropriate silences, voice stoppages, prolonged intervals, excessive loudness variation or alternating loudness, irregular articulation, vowel distortions, imprecise consonants, strained, harsh, transient breathiness, audible inspiration; prosody and rate (+ interruptions) most noticeable
hyperkinetic dsyarthria etiologies
degenerative, Huntington’s Chorea, dystonia, toxic, medication, tumors
hyperkinetic dysarthria subtypes
chorea (rapid, random movements); dystonia (slow, sustained movements)
hyperkinetic dysarthria disease example
Huntington’s Chorea: inherited, degenerative, abnormal movements, often starts in 40s, survival 15 yrs., caudate nucleus atrophy
