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motor speech disorders > through spastic dysarthria > Flashcards

through spastic dysarthria Flashcards

1
Q

motor speech disorder

A

affects motor control of speech neurologically (not musculoskeletal): dysarthria and apraxia

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2
Q

dysarthria

A

abnormalities in parameters of speech mechanism (respiratory, laryngeal, nasal, oral tract, articulators)–execution, movement disorder

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3
Q

apraxia

A

planning/programming impairment

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4
Q

dysarthria types (Mayo clinic)

A

flaccid + spastic (brainstem: F: brainstem MN or nerves to muscles; S:fiber tracts between cortex and MN); ataxic (cerebellum); hypokinetic, hyperkinetic (basal ganglia); mixed (Duffy adds unilateral UMN)

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5
Q

gold standard of dysarthria classification

A

DAB perceptual (clustering)

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6
Q

cortical areas for planning and programming speech

A

primary motor cortex, lateral premotor cortex, supplementary motor cortex, Broca’s, parietal lobe of dom. hemisphere, right hem.

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7
Q

control/monitoring circuits for speech

A

cerebellum (coordination, tone, sequencing, motor learning, adjustment) and basal ganglia (posture, tone, inhibitory, coordination, planning/executing/refining/regulating movement)

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8
Q

direct activation pathways (pyramidal)

A

corticospinal, corticobulbar (support skilled movement; alpha MN)

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9
Q

indirect activation pathways (extrapyramidal)

A

corticoreticular (reflex, posture, tone, subsconscious, facilitate pyramidal; support skilled movement, gamma MN)

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10
Q

peripheral pathways

A

final common pathway: LMN of cranial and spinal nerves (damage leads to weakness, paralysis, fasciculations, fibrillations)

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11
Q

motor end plate

A

specialized post-synaptic area in neuromuscular junction of PNS important for activating muscle

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12
Q

bundles of axons travel together in ___ and ___

A

tracts (CNS–synapse with other neurons); nerves (PNS–nerves transmitting to muscles or from sensory organs)

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13
Q

cell body, axon, synapse diseases associated with dysarthria

A

ALS; MS/Guillain Barre; myasthenia gravis

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14
Q

cortical motor areas

A

prim. motor cortex; supp. motor area; premotor area; Broca’s; left insula; right insula

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15
Q

cortical sensory areas

A

prim. sensory, visual, auditory cortices

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16
Q

cerebellar damage

A

hypotonia, intention tremor, dysmetria, decomposition of movement, ataxia

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17
Q

basal ganglia damage

A

hypokinesia (Parkinson’s), muscle rigidity, resting tremor, bradykinesia

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18
Q

important cranial and (spinal) nerves for speech

A

V, VII, X, XII + IX/XI with X, (respiration)

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19
Q

UMN contralateral vs. bilateral

A

corticospinal; corticobulbar (esp. head and neck); EXCEPTIONS: CN VII–upper face receives bilateral corticobulbar/UMN input and lower face receives contralateral UMN; CN XII–receives mostly contralateral corticobulbar

20
Q

UMN and LMN damage

A

spasticity, weakness, hyper-reflexia; hypotonicity, atrophy, hyporeflexia, weakness (voluntary and automatic), fasciculations

21
Q

direct pathway damage

A

weakness and loss of skilled movement, hyporeflexia, Babinski, decreased muscle tone

22
Q

indirect pathway damage

A

spasticity, clonus, hyperactive stretch reflexes, increased muscle tone

23
Q

unilateral UMN vs. LMN damage

A

UMN: spastic paresis of contralateral genioglossus=reduced ROM, no fasciculations, tongue deviates to opposite side of lesion; LMN: flaccid paresis or low muscle tone with atrophy, reduced ROM, fasciculations, tongue deviates to side of lesion

24
Q

MSD eval consists of

A

background/hx; oral mech/DDK/nonverbal oral apraxia/AOS; resp.-laryng. integrity; articulation; auditory-perceptual characteristics and intelligibility

25
Q

AMR vs. SMR

A

repetition of single syllable (alternating motion rate) vs. syllable sequence (sequential motion rate); both should be 5-7x/sec. for adults

26
Q

Can you use DDK rate (syll./sec.) to make inferences about speed or regularity of tongue movement for speech?

A

No

27
Q

low tech manometer used to

A

assess breath support (cup with straw)

28
Q

vowel prolongation (normal)

A

about 8 seconds

29
Q

things to look for in articulation

A

precision, rate and rhythm, coordination, intelligibility (perceptual), instrumental

30
Q

cognitive linguistic load in assessing speech from low cog. ling. load to high

A

non-speech–monologue–conversation

31
Q

intelligibility vs. comprehensibility

A

degree to which listener understands acoustic signal (fx impairment: adequate for communication?); intelligibility PLUS other contributing contextual information (disability: impact on daily life)

32
Q

ways to test intelligibility

A

interval scaling/percent estimates; PCC (children); transcription; Direct Magnitude Estimation (weird scale thing–more for research, requires modulus, more for global severity measures, better with groups), Visual Analog Scale, published tests

33
Q

considerations for instrumental testing

A

sensitivity to dysarthria, relevance to fx comm., measure reflective of movement characteristics, feasibility of application and interpretation

34
Q

key perceptual components

A

pitch, loudness, voice quality, respiration, prosody, articulation, overall impressions

35
Q

Have instrumental studies validated a straightforward relationship between phys. deficits and preceptual labels?

A

No

36
Q

flaccid dysarthria lesion and clinical presentations

A

LMN damage (motor unit of fcp, brainstem to spinal cord and muscles): cell body, cranial nerves, axons, neuromuscular juncture, muscle fiber; hypotonia, weakness/paralysis/atrophy, fasciculations, no reflexes, drooping/drooling in oral mech.

37
Q

flaccid dysarthria perceptual

A

phonatory incompetence (breathy, short inhalations, stridor), resonatory incompetence (hypernasal, nasal emission), phonatory-prosodic insufficiency (monopitch, monoloud), imprecise consonants; add’l from sheet: harsh voice, audible inspiration, slow rate, short phrases

38
Q

flaccid dysarthria acoustics

A

greater VOT variability (resp. incompetence), reduced formant transitions

39
Q

flaccid dysarthria etiologies

A

progressive bulbar palsy, polio, Guillain-Barre, Bell’s palsy, muscular dystrophy, trauma, tumor, brainstem stroke, myasthenia gravis

40
Q

spastic dysarthria lesion and clinical presentations

A

bilateral UMN damage (MN in cerebral cortex, axons, up to but not including LMN synapse); hypertonia (spasticity), pathologic reflexes, no fasciculations

41
Q

spastic dysarthria pyramidal vs. extrapyramidal damage

A

fine, skilled movements, hypotonia, weakness (more distal), hyporeflexia, Babinski present; increased tone, spasticity, clonus, hyperactive reflexes

42
Q

spastic dysarthria perceptual

A

prosodic excess (slow rate, reduced stress, effortful), artic.-resonatory incompetence, prosodic insufficiency (monopitch, monoloud), phonatory stenosis (strained-strangled); add’l from sheet: abnormal pitch, pitch breaks, breathy, harsh, hypernasal, short phrases, excess and equal stress, distorted vowels, imprecise consonants

43
Q

spastic dysarthria acoustics

A

shorter VOT, slow speaking rate

44
Q

spastic dysarthria etiologies

A

stroke (if bilateral), primary lateral sclerosis, TBI, tumor, cerebral palsy, multiple sclerosis (autoimmune, myelin damage/demyelination)

45
Q

corticospinal tract crosses at the

A

medulla

46
Q

flaccid dysarthria disease example

A

myasthenia gravis: autoimmune, more women (and younger) than men

47
Q

spastic dysarthria disease example

A

cerebral palsy, multiple sclerosis (autoimmune, demyelinating, more women than men)

motor speech disorders (3 decks)

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