Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Motor Speech Disorders > Midterm > Flashcards

Midterm Flashcards

1
Q

Flaccid dysarthria

A

weakness; LMN; breathiness, hoarseness, diplophonia, reduced maximum vowel duration (weak vocal fold); vocal flutter, short phrases, audible insiration/stridor, weak cough ; reduced tone and reflexes; hypernasality; monopitch and monoloudness; harsh voice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Spastic dysarthria

A

spasticity; bilateral UMN; strained, harsh, strangled voice, grunt @ end of expiration; slow rate; increased tone and reflexes; slow rate, mild hypernasality; increased effort/fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Ataxic dysarthria

A

incoordination; cerebellar control circuit; unsteadiness during vowel prolongation, sometimes alterations in loudness and pitch; irregular arctic breakdowns, increased errors w/ increased length, aud/visible groping for arctic posture, slow rate, sound prolongations, distorted substitutions & additions, syllable and word segmentation; irregular rate; scanning speech; harsh; dysmetria (over/under shoot)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hypokinetic dysarthria

A

rigidity, reduced ROM, poor movement scaling; reduced dopamine in basal ganglia control circuit; breathiness (sometimes aphonia) or harsh, hoarseness, reduced volume, loudness decay, vocal flutter/rapid voice tremor, reduced max vowel prolongation; rapid, blurred rate; short rushes of speech parkinsonian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Unilateral UMN dysarthria

A

variable combinations of weakness, spasticity, incoordination; unilateral UMN ; imprecise consonants, slow AMRs, harsh voice, mild hyernasality, contralateral weakness of lower face, tongue; increased tone and reflexes; increased effort/fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Apraxia of speech

A

impairment in planning, programming; left (dominant) hemisphere frontal cortex; usually co-morbid w/ nonfluenct aphasia; slow rate, prolonged speech segments, abnormal prosody, consonant and vowel distortions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Vocal flutter

A

rapid tremor like fluctuation in voice due to weakness and LMN CN X; common in ALS, hypo kinetic dysarthria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hyperkinetic dysarthria

A

essential voice tremor (esp vowel prolongation), involuntary noises & movements; vocalizations, voice interruptions, variable or excessive volume, laryngeal myoclonus, voice: horse, strained, breathy, sometimes jaw tremor or chorea; may be irregular rate; pauses/stoppages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Myoclonus

A

slow, regular voice fluctuations during vowel prolongation; “slow tremor”; palatal-pharyngeal-laryngeal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Scanning prosody

A

robotic; mono rate and pitch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Chin fasciculations

A

LMN CN VII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Dysarthria

A

“accidental articulation”; neurologically based speech disorder due to CNS/PNS abnormality; movement or muscle abnormalities (weakness/paralysis, tone de or in, incoordination, speech, range, steadiness, accuracy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Prevalence of various MSDs

A

Mixed most common (31%), hyperkinetic (21%), rest ~10% (apraxia, flaccid, spastic, hypokinetic, ataxic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Motor Speech Disorders categorized by

A

age of onset, disease progression, lesion location, pathophysiology, and/or speech characteristics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

UMN Dysarthria AKA & caused by

A

spastic dysarthria, pseudobulbar palsy; bilateral damage to UMN pathways (direct and indirect activation pathways)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

UMN Direct pathway effects

A

loss of fine, skilled, rapid movement; contralateral weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

UMN Indirect pathway effects

A

hyperactive reflexes; stretch reflexes (spasticity); clonus; increased muscle tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Non-speech symptoms UMN Dysarthria

A

dysphagia; drooling; non-speech oral movements (reduced lip retraction, reduced DDK, weak, slow, reduced tongue ROM) ; emotional lability; hyperactive reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pesudobulbar or labile affect

A

emotional lability; pathological laughing or crying; reduced threshold for emotional responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Most common spastic dysarthria etiology

A

stroke; multiple cerebral or single brainstem; corona radiate, internal capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Amyotrophic Lateral Sclerosis

A

progressive degeneration of UMNs and LMS; one presents first, eventually becomes mixed (flaccid-spastic) dysarthria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

TBI

A

can cause bilateral pyramidal/extrapyramidal system damage; widespread cordial, subcortical and brainstem damage; linear & rotational movements; diffuse axonal injury (stretched/torn axons); lacerated brain tissue, blood vessel hemorrhages; mixed dysarthria frequent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Multiple Sclerosis

A

autoimmune disorder of myelin in CNS; often mixed ataxic-spastic dysarthria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Bilaterally innervated nerves

A

CNs EXCEPT CN VII facial (lower) CN XII hypoglossal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Contra laterally innervated nerves

A

CN VII, CN XII, spinal nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Unilateral (left) UMN lesion face

A

lower right face weak, both sides of forehead wrinkle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Mechanism of hyperactive stretch reflex (spasticity)

A

indirect activation pathway inhibits stretch reflex; daman to UMN releases this inhibition, resulting in hyperactive stretch reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Alpha motor neurons

A

LMN; innervate “extrafusal” muscle fibers, causes muscle fibers to shorten

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Gamma motor neurons

A

innervate intrafusal muscle fibers (spindles); influenced by indirect activation pathway/basal ganglia/cerebellum; maintain muscle tone, stretch reflex; when fired, muscle spindle shortens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Stretch reflex

A

when muscle moved involuntarily, spindles contract, sensory neurons detect “stretch” SO alpha motor neurons fire to contract the muscle (back to original position)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Gamma motor neuron system

A

maintains normal tone by low-level alpha motor neuron firing; w/ UMN lesions, DISinhibited (overactive) so spasticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Spasticity in orofacial system

A

depends on presence of muscle spindles (jaw=high spindle density, clear stretch reflex; face/lips=none, palate, pharynx, larynx- variable)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Management of spasticity

A

medical (botox, baclofen pumps); stretching (slow, passive stretch inhibits stretch reflex, fast stretch increases tone); vibration (may reduce tone); icing (short-term reduction of tone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Unilateral UMN dysarthria

A

People experience speech system even though CN bilateral innervation; individual variation? bilateral innervation not enough?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Unilateral UMN Dysarthria Speech

A

imprecise consonants, irregular arctic breakdowns, harsh, reduced loudness, slow rate, hyper nasality, slow imprecise irregular AMRs; slurred/think speech that deteriorates w/ fatigue or stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Unilateral UMN Dysarthria non-speech

A

unilateral lingual & lower facial weakness; hemiplegia, hemiparesis, sensory deficits (limb); hyperreflexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Unilateral UMN Dysarthria etiology

A

stroke (90%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Neuronal response to ischemia

A

lack of blood/O2; neurons become swollen (edema), shrink, die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Neuronal response to axonal injury

A

cell bodies swell, lose internal components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Neuronal response to wallian degeneration

A

axons separated from cell bodies will degenerate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Neuronal response to neurofibrillary degeneration

A

clumps of neural fibers from plaques or tangles, cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Nerve regeneration?

A

in PNS, axon may regenerate if cell body survives; NOT CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Neuronal response to muscle atrophy

A

district of nerve innervating muscle may result in wasting away of muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Neuronal response to diaschisis

A

abnormal function of healthy cells because of lack of input from diseased neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Demyelinization occurs in

A

MS, Guillain-Barre, leukodystrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Astrocytes

A

react to CNS injury by forming scars in neural tissue (process aka gliosis, astrocytosis, astrogliosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Degenerative disease

A

gradual decline in neuronal function; neurons may atrophy and disappear (Parkinson’s- substantial nigra, AD- neurofibrillary tangles); chronic, progressive, diffuse; can begin w/ focal impairment (e.g. speech); clinical difference on localization, progression rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Inflammatory disease

A

infectious processes, subacute; meningitis- leptomeninges, CSF; encephalities- brain parenchyma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Toxic-metabolic disease

A

toxins result in altered neural function; e.g. vitamin deficiencies, biochemical disorders (genetic), drug toxicity, lead/mercury; Leads to edema, ischemia, demyelination; diffuse effects; acute, subacute, or chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Neoplastic disease (cancer)

A

-oma tumor of named organ; uncontrolled cell growth interrupts function of normal cells, mass lesions; focal chronic or progressive signs; CNS tumors rarely metastasize outside CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Traumatic disease

A

acute onset, improving course; PNS- focal or multifocal, CNS-TBI; penetrating vs closed head injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Vascular disease

A

CVA; acute one, focal localization, course stabilizes/improves & progress due to edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Motor plan preparation

A

left inferior frontal cortex (primary motor cortex) “brainstormer”; when damaged, poorly constructed motor plans and apraxia of speech

54
Q

Motor plan selection

A

basal ganglia “gatekeeper”; when damaged, not enough or too much inhibition of cortical motor system and hyper/hypokinetic dysarthria; helps set stage for movement

55
Q

Motor Command transmission

A

UMN system: motor cortex to brainstem “middle manager”; when damaged, reduced transmission of motor commands/failed inhibition of stretch reflex and spastic dysarthria

56
Q

Motor execution

A

“worker bee” LMN System: Brainstem to muscles; when damaged, failure to contract muscles and flaccid dysarthria

57
Q

Motor correction/coordination

A

Cerebellar control circuit “clean up crew” error corrector; when damaged, failure to correct for irregularities and ataxic dysarthria; makes sure movement goes all right

58
Q

CNS speech motor system

A

Control circuits (basal ganglia, cerebellum) and UMN system (direct and indirect activation pathways)

59
Q

PNS Motor Speech System

A

Final Common Pathway- LMN System

60
Q

Direct activation pathway

A

Sends motor commands from motor cortex to LMN system via corticbulbar tract (CN nuclei) or Corticospinal tract (spinal nerves); AKA pyramidal tract; facilitates skilled, discrete movements;

61
Q

Indirect activation pathway

A

Helps regulate muscle tone, reflexes; AKA Extrapyramidal tract; inhibits activity of direct path, maintains posture, tone, regulates reflexes, stable frame for skilled movements

62
Q

Damage to UMN leads to

A

contralateral limb weakness, loss of skilled moments or slowness, spastic muscle tone

63
Q

Corticobulbar tract

A

*Most important in speech/dysarthria; primary motor cortex –> corona radiata/internal capsule –>partial decussation and synapse on CN nuclei; mostly bilateral activation of LMN; unilateral damage to one side of cortex=minor speech difficulties

64
Q

LMN System affected indirectly through

A

reticular formation, red nucleus, vestibular nuclei, basal ganglia, cerebellum

65
Q

Damage to UMN results in spasticity by

A

releasing inhibition of the indirect activation pathway, resulting in hyperactive stretch reflex

66
Q

Damage to UMN results in (symptoms)

A

Damage to direct AND indirect pathways: muscular weakness on contralateral limb, jaw tongue, loss skilled movements, spastic muscle tone

67
Q

LMN system (peripheral speech control)

A

Final Common Pathway- peripheral mediation of ALL motor activity, last link in neural chain to movement; mediated via alpha motor neurons that innervate muscles

68
Q

Peripheral speech control

A

CN innervate muscles of phonation, resonance, articulation; spinal nerves involved in respiration; muscle ipsilaterally LMN innervated; damage=flaccid/reduced tone on affected side

69
Q

CN V Trigeminal

A

origin: pons; function: jaw movment; face, mouth, jaw sensation

70
Q

CN VII Facial

A

origin: pons; function: facial movement; hyoid elevation; stapedius reflex; salivation; lacrimation; taste

71
Q

CN IX Glossopharyngeal

A

origin: medulla; function: pharyngeal movement, pharynx and tongue sensation, taste

72
Q

CN IX Glossopharyngeal

A

origin: medulla; function: pharyngeal movement, pharynx and tongue sensation, taste

73
Q

CN X Vagus

A

Origin: medulla; Function: pharyngeal, palatal, and laryngeal movement; pharyngeal sensation; control of visceral organs

74
Q

CN XI Accessory

A

origin: medulla, spinal cord; function: shoulder and neck movement

75
Q

CN XII Hypoglossal

A

origin: medulla; function: tongue movement

76
Q

Spinal nerves for speech control

A

innervate diaphragm, intercostal muscles (rib expansion), abdominals; damage=reduces respiratory support; innervation widely distributed BUT SN3-5 damage can paralyze diaphragm

77
Q

Basal ganglia function

A

sets background for intentional moment- regulates tone, suppresses extraneous movements; involved in selection of movements, early acquisition of learned, skilled movements

78
Q

Basal ganglia mechanism

A

inhibiting or release of inhibition (disinhibiting) activity of motor cortex; dopamine and BAGA inhibit, acetylcholine excites; regulates inhibition output of basal ganglia to thalamus which contains exciting output to motor cortex

79
Q

Basal ganglia lesion to striatum

A

hyperkinetic; reduced actitation in striatum, too LITTLE inhibition from globes plaids to cortex, uncontrollable involuntary movements

80
Q

Basal ganglia lesion to substantia nigra

A

damages dopamine cells- hypo kinetic; not enough inhibition from substantial nigra to striatum, overactive sub thalamic nucleus, too much inhibition from globes plaids to thalamus and back to cortex; inability to move

81
Q

Cerebellum functions

A

error control/input and output; monitors motor output to muscles by input from somatosensory cortex & some from brainstem

82
Q

Cerebellum mechanism

A

cortex sends “efferent copy” to cerebellum as motor command sent to brainstem; spinocerebellar tracts bring sensory info on body position/movement; cerebellum compares efferent (intended) copy w/ sensory info from actual movements and sends corrective feedback to cortex or brainstem if they don’t match

83
Q

Effectiveness as treatment target

A

getting message across; adjustment to disability

84
Q

Efficiency as treatment target

A

getting message across in reasonable time; compensation for impairment

85
Q

Naturalness as treatment target

A

how did message sound? restoration of impaired function ; “cosmetic”; unilateral UMN dysarthria, unilateral VF paresis

86
Q

Compensation treatments

A

speech strategies (slow rate, over arctic); prosthetic devices (AAC, palatal lift, amplification, pacing board); speech & gesture; modification of physical environment

87
Q

Adjustment treatments

A

reduce need for lost function (planning for progressive speech loss, changing career/lifestyle) **as SLP, ID factors that limit communication and shape pragmatic decisions

88
Q

Treatment goals

A

relate symptoms to functional components and pathophysiology; target pathophysiology when possible then functional components

89
Q

Principles of motor learning in speech treatment

A

drill, specificity of training, practice schedules, speed v accuracy

90
Q

5 components of speech

A

respiration, phonation, articulation, resonance, prosody

91
Q

Motor speech exam

A

history, structural/functional exam, acoustic motor speech exam, testing connected speech, nonverbal oral apraxia, apraxia of speech, stress testing (MG), assessment of intelligibility, comprehensibility, efficiency

92
Q

Motor Speech Exam- CN VII

A

symmetry, involuntary movements, fasciculations? lip movements, puffing cheeks, ROM, affect

93
Q

Motor Speech Exam- CN V

A

jaw hang low, involuntary movements, opening mouth/resist pressure to close, clench teeth/resist close, speech movements

94
Q

Motor Speech Exam- CN XII

A

symmetry of tonge, wet, fascinations, protrusion/pressure, side to side movement, ROM

95
Q

Motor Speech Exam- CN X

A

palate hang, symmetry, ahhh, airflow on mirror from nares, resonance

96
Q

Motor Speech Exam- CN X and Spinal nerves

A

cough, glottal coup, respiration

97
Q

Reflexes

A

gag (asymmetric?); jaw jerk (if present w/ chin tap, maybe UMN disease); sucking (w/ stroke upper lip, UMN disease); snout 9tip of nose??); palmomental (elevation of ipsilateral chin w/ hand stroking, UMN)

98
Q

Acoustic Motor Speech Exam

A

/a/ phonation/resonation; /u/ resonance/nasal flutter, velopharyngeal closure (w/ nasal occlusion); DDK AMR pppp kkkk tttttt, SMR pu tu ku; connected speech (passage/convo)

99
Q

nonverbal oral apraxia testing

A

difference between command vs imitation responses; reflex (imitate) sometimes intact when volitional impaired

100
Q

Motor Speech Exam indicators of Apraxia of Speech

A

distorted arctic, substitutions, omissions, blocking, groping; AMR better than SMR; automatic better than volitional; mono > multi syllabic words

101
Q

Stress testing

A

fatigue; LMN present, test for Myasthenia Gravis; deterioration of vocal quality, resonance, arctic, w/ subsequent recovery

102
Q

Intelligibility testing

A

single word, phoneme, sentence, conversation (% words intelligible); intelligibility= # words correct/total words vs efficient intelligible words/time

103
Q

Flaccid dysarthria mechanism

A

muscular weakness & reduced tone caused by damage to final common pathway; neuronal nuclei, axons, neuromuscular junction, muscle fibers may be affected

104
Q

Flaccid dysarthria etiology

A

degenerative disease (40%) surgical trauma (20%) stroke (10%)

105
Q

Flaccid dysarthria characteristics

A

neuromuscular weakness, hypotonia, hyporeflexia, muscle atrophy, fasciculation/fibrillations

106
Q

Flaccid dysarthria (dysphonia)

A

larynx; CN X Vagus pharyngeal branch (pharyngeal, superior laryngeal- internal and external (cricothyroid, pitch and adduction), recurrent laryngeal (adduction/abduction); muscles of larynx, pharynx, soft palate), CN V Trigeminal, CN VII Facial, CN XII Hypoglossal

107
Q

Vagus CN X: Recurrent Laryngeal Nerve

A

laryngeal adduction & abduction; aspiration, dysphagia, stridor, unilateral VF paralysis; breathy, reduced volume, decreased pitch, shortened phrase

108
Q

Vagus CN X: Pharyngeal branch

A

muscles of pharynx, velum, palatoglossus (palatal elevation); asymmetric velum at rest- deviation to strong side, decreased gag reflex; hyper nasal, decreased phrase length, imprecise pressure consonants

109
Q

Trigeminal CN V mandibular branch

A

muscles of jaw, soft palate; lesion- slow/limited ROM for jaw, jaw deviated to weak side, inability to elevate jaw (imprecise bilabial and lingual arctic, slow rate of speech)

110
Q

CN VII motor branch

A

muscles of facial expression, speech production;bell’s palsy, hypotonicity, distortion labial consonants

111
Q

CN XII Hypoglossal

A

receives taste, tactile info; innervates intrinsic and extrinsic muscles of tongue; lesion- tongue movement and tone, atrophy, shrunken tongue, fasciculations, deviation to weak side,imprecise lingual and velar consonants ; mostly contralateral innervation from UMN

112
Q

Fibrillations

A

invisible spontaneous muscles contractions due to slow repetitive action potentials

113
Q

Spinal nerve damage

A

respiratory muscles, shoulder/neck to compensate for breathing, short phrases, decreased loudness, prosodic abnormality (monopitch/loud)

114
Q

Hyopkinetic dysarthria features

A

muscle rigidity, reduced foce & ROM, resting tremor

115
Q

Hypokinetic dysarthria mechanism

A

loss of dopamine cells in substantia nigra- OVER inhibits motor context (so less movement)

116
Q

Hyperkinesia mechanism

A

damage to striatum (putamen/caudate) in basal ganglia causes UNDERinibition of motor cortex

117
Q

Basal Ganglia circuitry

A

Morot cortex –> striatum input, output globus pallidus –> thalamus, cortex; little loops: striatum to Globus Paladus to Substantia Nigra to Globus Paladus; Striatum to Substantia Nigra back to Striatum

118
Q

Hypokinetic dysarthria etiology

A

degenerative disease (~90%)

119
Q

Hypokinetic dysarthria medications

A

neuroleptic med (blocking effect on dopamine receptors)

120
Q

Hypokinetic dysarthria motor characteristics

A

reduced, slow (bradykinesia) movement; rigid tone; difficulty initiating, resting tremor, reduced postural reflexes, irregular gait, masked facies

121
Q

Hypokinetic dysarthria speech characteristics

A

reduced movement, imprecise consonants, repetition of syllables, short phrase and short “rushes of speech”, rapid rate, harsh, breathy

122
Q

Parkinson’s disease treatment (med)

A

med: L-dopa dopamine replacement, levodopa- induced dyskinesia; ;

123
Q

Deep Brain Stimulation for PD

A

reduces rigidity, increases movement aplitude, reduces L-Dopa dosage; new speech problems (harsh, reduced fluency)

124
Q

Parkinson’s disease treatment (surgical)

A

surgical ablation- pallidotomy, thalamotomy (Globus pallidus, ventral lateral nucleus of thalamus), Subthalamotoy (subthalamic nucleus all symptoms);today- deep brain stimulation (globes pallidus, thalamus (VL), STN; nigral cell transsplantation- to striatum to replace dopaminergic cells (mixed outcomes)

125
Q

Parkinson’s disease treatment (behavioral)

A

rate based (Delayed auditory feedback, pacing boards, hand tapping) or aptitude-based (LVST) (intensive, high effort- PT OT Big)or pitch-limiting voice treatment

126
Q

Intra-cerebellar mechanism

A

Input goes from deep nuclei –> mossy & climbing fibers; if mossy & climbing match, Purkinje fires to cancel the correction of the movement; output goes from deep cerebellar nuclei to thalamus

127
Q

Mossy fibers

A

intended movement

128
Q

Climbing fibers

A

actual movement; primes deep cerebellar nucleus for correction by activating purkinje cell

129
Q

Ataxic dysarthria etiology

A

degenerative disease (45%), vascular (11%), demyelinating disease (10%)

130
Q

Ataxic dysarthria characteristics

A

dysmetria (over/undershoot); decomposition of movement; halting, imprecise, poorly coordinated, lacking in speed and fluidity; stumble over/slur words, difficulty coordinating breathing, slow rate improves intelligibility

131
Q

Motor characteristics of ataxia

A

broad stance/gait, unstable trunk, excessive rebound, intention/terminal tremor, hypotonia, nystagmus, oculodysmetria, normal strength of oral structures but irregular AMRs

132
Q

Speech characteristics of ataxia

A

imprecise consonants, irregular arctic breakdowns, distorted vowels, excess/equal stress, slow rate, prolonged sounds, harsh, mono pitch and loud, explosive loudness, respiratory incoordination

Motor Speech Disorders (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions