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1
Q

Mixed dysarthria etiologies

A

Degenerative disease (66%); Vascular (11%)

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2
Q

Neurodegenerative diseases causing mixed dysarthria

A

ALS, Multiple Sclerosis, Friedreich’s ataxia, Parkinson’s, Parkinson’s plus syndromes: Progressive Supranuclear Palsy, Multiple Systems Atrophy, Corticobasal degeneration

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3
Q

ALS mixed combo

A

Flaccid-Spastic

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4
Q

MS mixed combo

A

Spastic-Ataxic (could be all)

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5
Q

PSP mixed combo

A

Spastic-Hypokinetic (ataxic)

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6
Q

MSA mixed combo

A

Spastic-hypokinetic (ataxic)

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7
Q

Corticobasal degeneration mixed combo

A

Spastic-hypokinetic (ataxic)

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8
Q

Wilson’s disease mixed combo

A

Spastic-ataxic-hypokinetic (hyperkinetic)

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9
Q

Hepatocerebral degeneration mixed combo

A

Spastic-ataxic/hypo & hyper

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10
Q

hypoxic encephalopathy mixed combo

A

ataxic-hypokinetic-hyperkinetic

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11
Q

central pontine myelinolysis mixed combo

A

Spastic-ataxic-Unilateral UMN (hypo/hyper ?)

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12
Q

vascular mixed combo

A

Spastic-Ataxic-unilateral UMN (could be all)

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13
Q

tumor & infectious disease mixed combo

A

could be all

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14
Q

TBI and mixed combo

A

Spastic-Ataxic (could be all)

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15
Q

Parkinson’s Plus

A

Hypokinetic symptoms prominent in “mixed dysarthric conditions: PSP Progressive Supranuclear Palsy, MS Multiple Systems Atrophy, CBD Corticobasal degeneration; maybe w/ hyperkinesia, ataxia, spasticity

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16
Q

MSA

A

multiple syste atrophy; 3/100,000; onset: 50, survival ~9 years; neuronal loss in basal ganglia, substantial nigra, cerebellum, brainstem nuclei, corticospinal tracts, cerebral cortex

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17
Q

MSA-P (Parkinsonian)

A

used to be Striatonigral generation; nerve loss in basal ganglia and substantial nigra; HYPOKINETIC, maybe w/ spasticity and ataxia

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18
Q

MSA-C (cerebellar)

A

used to be olivopontocerebellar atrophy; nerve loss in cerebellar circuit (middle cerebellar peduncles, white matter, parking cells, pontine, olivary, arcuate nuclei); ATAXIC, maybe w/ spasticity and hypokinesia

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19
Q

MSA-A (autonomic)

A

used to by Shy-Drager syndrome; degeneration of motor components of autonomic and somatic CNS; Autonomic deficits: decreased blood pressure & respiration, incontinence, impotence; gait disturbance; dysarthria (ataxia, hypo, spastic) and dysphagia

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20
Q

CBD Corticobasal degeneration

A

Frontal & parietal lobe atropy, neuronal death in basal ganglia; onset: 50-70; survival: 5-15; asymmetric limb rigidity/dyskinesia, cog deficits, yes/no reversal, apraxia of speech; HYPO and SPASTIC, maybe w/ ataxic and hyper

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21
Q

Progressive supranuclear palsy PSP

A

neuroal atrophy in cortex (frontal, maybe temporal lobes), basal ganglia, thalamus, hypothalamus, subthalamus, brainstem nuclei; 1.4/100,000; more in men than women; onset: 55-70, survival: 6-7; vertical gaze paralysis, symmetric parkinsonism (rigid, bradykinesia, postural instability), personality & cog changes; dysphagia & dysarthria (hypo, spastic, ataxic)

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22
Q

Wilson’s Disease

A

impairment in processing copper; brown ring around cornea, tranquil rigidity, wing-beating tremor; med tx does not help dysarthria

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23
Q

Hepatocerebral degeneration

A

chronic liver disease; lem tremor, choreoathetosis, ataxic gait

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24
Q

Hypoxic encephalopathy

A

damage to basal ganglia, cortex, brainstem nuclei; hypo hyper spastic and ataxic dysarthria (not studied)

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25
TBI
imprecise arctic, hyper nasal, strained, mono pitch & loud, excess equal stress, repiratory incoordination; cog deficits
26
Motor Neuron Disease
ALS (UMN & LMN); Progressive bulbar palsy (LMN CRANIAL) 25%; Primary muscular atrophy (LMN Spinal) 5%; Primary lateral sclerosis (UMN only) 0.5%
27
Amyotrophic Lateral Sclerosis
aka Lou Gehrig; 5% familial, 1-5/100,000; men > women; onset: 40-70, survival ~1-5, 12+; death by respiratory failure; degeneration of UMN and LMN; unable to walk, limb wasting/atrophy, respiratory weakness, dysphagia, dysarthria (Flaccid spastic mix)
28
Multiple Sclerosis
1-2/1,000; women>men; onset: 20-40, survival: ; autoimmune disease- immune system attacks CNS white matter; scattered diverse lesions; gait disturbance, visual/sensory problems (nystagmus; trigeminal neuralgia); facial nerve weakness, cog deficits, dysarthria (50%)- ataxic/spastic (NOT scanning speech)
29
Friedreich's ataxia
spinocerebellar tract; dysarthria- ataxic w/ spastic, LMN weakness, extrapyramidal signs
30
Apraxia of Speech
impaired programming of speech movements; rarely "pure" (aphasia 72%, dysarthria 29%); Vascular (49%), degenerative disease (28%); *other signs: hyperactive stretch reflex, babinski sign
31
Apraxia of Speech: speech characteristics
consonant & vowel distortions/distorted substitutions; slow rate (inter-segment durations), abnormal prosody; NOT consistent error type/position; groping, increased errors w/ increased length, awareness of errors, automatic>propositional speech; AMRs > SMRs; errors increase w/ increased length/complexity
32
Apraxia of speech: neural basis
Broca's area (NOT surrounding MCA area); precentral gyrus of insult [Literature unclear-- both can have AOS]
33
Apraxia: areas to assess
motor speech programming; oral apraxia (command vs imitated); neuromuscular function (no dysarthria); language (no aphasia)
34
Feedforward motor control
predicting/planning; normal speaking conditions, automatic/fast/precise; neural connection from inferior frontal cortex to M1
35
Feedback motor control
observing/correcting; integrates somatosensory & auditory input w/ feedforward systems; articulatory parameters modified based on discrepancy between internal model and actual sensory state; use w/ perturbation/children; adaptive, slower, precise "enough"; helps feedforward system to learn new motor plans; neural: temper-parietal regions
36
Impaired feedfwd, intact feedback AOS hypothesis
normal speech pattern w/ bite block suggests feedback control intact, feedback used as compensations following damage to feedforward; slow rate, imprecise arctic may be due to reliance on feedback system (Jacks, 2008)
37
Motor learning for acquisition
blocked stimulus; high # trials/session; frequent feedback; performance feedback; delayed feedback
38
Motor learning for retention
random stimulus; high # trials/session; less frequent feedback; results feedback; delayed feedback
39
Traditional treatment hierarchies (AOS)
Easy to Hard (phonation- vowels- consonants- nonsense CV-CVCV-CVC syllables- real world- conversation-phone
40
Cuing
auditory; visual; tactile (faded as correct production attained)
41
The 8 Step Continuum
Integral stimulation therapy- continuum of gradually reducing sensory feedback (simultaneous production; fading simultaneous clinician; solo repetition; delayed repetition; reading words; delayed word reading; response to questions; conversation)
42
Sound Production Treatment (SPT)
Tx w/ most effectiveness in lit for AOS; target client errors; minimal pairs; response-contingent tx hierarchy used; (model/imitate-model/written cue-integral stimulation-attic place & model- sound in isolation- new target)
43
Indirect tx appraoches
rate modification; gestural intersystem reorganization; Melodic Intonation Therapy (MIT); Masked auditory feedback
44
Damage to striatum (putamen/caudate)
Basal ganglia UNDERinhibits motor cortex; results in hyperkinesia
45
Mechanisms of hyperkinesia
damage to subthalamic nucleus & damage to striatum (dis-inhibition/over-excitation of cortex); neurotransmitter dysequilibrium (among excitatory cholinergic & inhibitory dopaminergic NT)
46
Dysequilibrium among neurotransmitters
excitatory (choline) & inhibitory (dopaminergic) transmitters are involved in BG control circuit; neuroleptic drugs that modulate NTs may cause unintended imbalance in BG, hyperkinesia
47
Classification of hyperkinesias
fast/slow; rhythmic/irregular/continuous; many/few body parts; rest/static posture during voluntary movement; sleep deprivation, anxiety & heightened emotions exacerbate symptoms
48
Tremor
rhythmic, periodic movements of body part; types: resting (parkinson's), postural, kinetic (action/intention/terminal), essential
49
Essential tremor
most common movement disorder; 50% autosomal dominant; onset early adulthood; tremor in tongue, velum, pharynx, larynx; diagnosis: sustained vowel production, endoscopic visualization or VFs show periodic fluctuations 4-7; tx: reduced intensity levels, elevate pitch to change VF tension, shorter vowel duration, precede vowels w/ /h/
50
Spasms
Involuntary contractions of muscles; Myoclonus (brief twitches/jerks of body parts); tonic spasm- prolonged, continuous CRAMP
51
Palatal myoclonus
palatal tremor; rhythmic movements of velum, pharyngeal walls, laryngeal muscles; patients report ear clicks, laryngeal spasm; silent intervals due to interruption of movement, intermittent hyper nasality, voice arrest, slow voice tremor during vowel prolongation
52
Action myoclonus
clonic spasms brought about by movement; imprecise speech, inability to talk fast (patient report); slow rate, deterioration of repeated syllables w/ increased rate, decreased precision w/ increased rate
53
Dystonia
involuntary abnormal postures; generalized or focal; speech: effortful, dysphagia, distorted vowels, irregular arctic breakdowns, inappropriate silences, harsh/strained, audible inspiration, vocal tremor, loudness variations
54
Blepharospasm
eye dystonia
55
spasmodic torticollis
neck
56
oromandibular dystonia
jaw; direction/rhythm of movement altered; involuntary open/close mouth, lip purse & retraction, tongue protrusion/rotation; maybe w/ blepharospasm, facial grimacing
57
spasmodic dysphonia
(laryngeal) vocal folds; AD-ductor most common, uncontrolled tight laryngeal closure; ABductor- uncontrolled opening VFs, uncommon; tx: botox, surgical resection of RLN/modification VFs
58
Botox tx
prevents acetylcholine release at neuromuscular junction; interferes w/ nerve impulses, results in flaccid paralysis; for SD, to thyroarytenoid or lateral cricoarytenoid; post injection: 2-3 weeks breathy, aspiration compensate weak VFs, after 3 weeks: voice tx session, counseling (return for injection ~5 months)
59
Chorea
rapid, random, purposeless movements (Huntington's, sydenham's chorea, pregnancy)
60
Athetosis
slow, sinous, writhing purposeless movements (athetoid or mixed cerebral palsy, HD)
61
Huntington's disease
neurons in caudate, putamen, cortex; onset: 30-50; couse: onset- jerks, spasms in extremities, progression to chorea, athetosis, mental deterioration, death 10-20 years
62
HD Characteristics
motor: chorea, dystonia, athetosis, dyscoordination, speech, swallowing, balance, walking; Cognitive- short-term men, organization, concentration, Emotional: irritable, depressed, anxious, social withdrawal
63
Chorea speech characteristics
effortful speech, chew/swallow impair; imprecise consonants, prolonged intervals, variable rate, inappropriate silences, prolonged phonemes, phonation- loudness variations, sudden forced inspiration, voice stoppage, transient breathiness
64
HD tx
tx most effective in 1st few years; maintain best speech/voice, easy fwd prosody, DAF metronome may be helpful for pacing; cog symptoms may preclude successful tx in advanced HD
65
Tics
repeated, stereotyped patterned movements; tourette's (humming, whistling, lip smacking, echolalia, palilalia, coprolalia, coughing, grunting, throat clearing, screaming, vocal/motor tics), stuttering
66
Ballism
gross, abrupt contractions of axial muscles; flailing; ballistic
67
Hyperkinetic tx
pharmacologic (botox, indirect for tremor/seizure med); behavioral (posture, rate reduction, breathy (ADSD)/harsh (ABSD) onset); instrumental biofeedback (EMG, visual feedback of breathing patterns); bite block
68
Basal Ganglia damage/dysarthria
damage to striatum--> UNDERinhibirion of motor cortex --> HYPERkinesia; damate to substantia nigra --> OVERinhibition of mtor cortex --> HYPOkinesia
69
Basal Ganglia loops
Big: motor cortex+++striatum----globus pallidus ---- thalmaus/cortex +++ body; little loops: striatum ---- globus pallidus ---- subthalamic nucleus +++ globus pallidus --- thalamus/cortex; striatum ---- substanti nigra ---- striatum (Glutamate +, gaba -)

Motor Speech Disorders (3 decks)

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