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Motor Speech > benchmark 2 > Flashcards

benchmark 2 Flashcards

1
Q

T/F Vestibular-reticular level does not have direct impact on speech

A

True its part of the autonomic system (respiration, swallowing, etc) - limbic level affect motivation, emotion, arousal, engagement –> effect on treatment

part of CNS

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2
Q

Spastic Dysarthria - UMN level

What are the tracts?

A

cortical-pyramidal tracts

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3
Q

direct vs indirect systems

A

direct: skilled mvmt, faster, single synapse –> pyramidal tract

indirect: slow mvmt like balance posture, coordination, multiple synapses - extrapyramidal tract (white matter)

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4
Q

decussation

A

90% crosses over at medulla; 10% still supplies same side (anterior corticospinal tract)

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5
Q

ipsilateral vs contralateral

A

Contralateral = occurs on other side
Ipsilateral = occurs on the same side

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6
Q

gray vs white matter

A

gray: neuronal cell bodies, vary in complexity –> spinal cord (reflex arc), brainstem (respiration) - cortical (complex) (LMN is gray matter)

white matter: axons, major descending pathways - send motor signal (effernet) to body (UMN is white matter)

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7
Q

UMN lesion

A

damage to white matter; spastic paralysis, exaggerated stretch reflexes - atrophy with prolonged disuse

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8
Q

corticospinal fibers vs corticobulbar fibers

A

part of UMN lesion –> damage to white matter

corticospinal: 1 axon from cortex to spinal nucleus —> innervates spinal motor neurons
corticobulbar: 1 axon from cortex to brainstem –> innervates cranial nuclei of CNS

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9
Q

UMN White Matter Fibers

A

Association: interconnect cortical regions in same hemisphere

Commissural: interconnect corresponding cortical regions of opposite hemispheres

Projection: transmit info from cortex to bulbar and spinal nuclei

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10
Q

UMN Lesion to direct system

A
  • UM lesions usually affect both direct and indirect tracts b/c they are close in proximity
  • impairment to rapid, discrete, skilled mvmt and rapid reflexes
  • reduced ROM and force of motion
  • rapid muscle fatigue
  • increased deliberate attention to do skilled tasks
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11
Q

lesion to indirect system

A

impaired control of slow movements

damage = high tone, extra tightness
*rapid muscle fatigue

requires deliberate attention to:
- maintain posture
-regulate tone
- fine tune force and ROM
- allow preset of muscle to desired length
- control balance
- control speed of movement

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12
Q

damage ABOVE decussation of pyramidal system (including unilateral and bilateral damage)

A

symptoms will be on contralateral side

bilateral damage: paralysis and paresis; spastic over entire body –> entire face

unilateral damage: upper face will not be impaired –> it will only affect one side of lower face

If lesion occurs AFTER decussation —> no damage to anterior corticopinal tract (10% remaining on side of origination)

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13
Q

spastic dysarthria - bilateral UMN lesion

etiology

A
  • CVA
  • tumor
  • TBI
  • polio
  • ALS
  • infection like meningitis
  • infantile CP (usually from stroke)
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14
Q

spastic dysarthria - bilateral UMN lesion

global changes –> think hypertonia and reflexes

A

Spasticity: imbalance b/w excitatory and inhibatory signals

Hypertonia: high muscle tone
- weakness with increased resistance to passive movement
- movment pattern weakenss (not individual muscles)
- lmited ROM
- clonus: involuntary, rhythmic, contractions and relaxation

Reflexes –>
- dimisnh initially
- hyperreflexia: increases over time
- re-emergence of developmental reflexes (biting, rooting, etc)

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15
Q

spastic dysarthria - bilateral UMN lesion

motor assessment

A

Lack of coordination of subsystem
- rapid, shallow breathing
- no laryngeal pathology –> limited ROM in VFs, slow vibrations/hyperADDuction
- decrease ROM
- slow oral movements

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16
Q

spastic dysarthria - bilateral UMN lesion

essential assessment

A

Conversational Speech
- reduced loudness, short breath groups
- strained-strangled voice, low pitch
- slow speech
- elongated sounds –> initiated and terminated slowly
- voiceless –> voiced

AMR/SMR
- slow but rhythmic

Prolonged vowels
- short duration
- rough
- strain-strangled
- low pitch

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17
Q

t/f spastic dysarthria and UMN lesion are the synonyms

A

true

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18
Q

spastic Dysarthria —> bilateral damamge vs unilateral damamge

A

Bilateral:
- pseudobulbar palsy –> fake CN weakness –> spastic Dysarthria symptoms can appear similar to flaccid dysartehria
- emotional lability with pseudobulbar cry
- neurological smile –> involuntary, spastic excessive smile

Unilateral:
- minimal deficits

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19
Q

Therapy for spastic Dysarthria –> ID problem, hypothesis goal

A

avoid fatigue –> no artic drilling
- problem: hyperfunction to attempt to cover for what they can not do
- hypothesis: intelligibility gets better when they use effortless speech –> hypertonicity is reduced, effort will decrease
- goal: reducing effort in subsystems improves speech –> improve speech clarity, reduce tone and effort in speech subsystems

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20
Q

Mixed spastic-flaccid Dysarthria etiolgoy

A

aka ALS and PLS

  • idiopathic
  • viral agents suspected
  • 10% are genetic
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21
Q

what is ALS

A

Mixed spastic-flaccid Dysarthria

motor neuron disease, degenration of UMN and LMN; rapid disease progression

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22
Q

what is PLS

A

Mixed spastic-flaccid Dysarthria

slower progression than ALS

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23
Q

Mixed spastic-flaccid Dysarthria global changes

A
  • emotional lability
  • all-pervading weakness
  • decreased ROM
  • begins more distal and spastic –> dissolves to flaccid
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24
Q

Mixed spastic-flaccid Dysarthria motor assessment

A
  • difficulty taking deep breath
  • severely reduced ROM
  • atrophy/fasciculation/weakness
  • either decrease in reflexes or hyperactive reflexes
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25
Q

Mixed spastic-flaccid Dysarthria essential assessment

A

**conversational speech (fatigue)

  • reduced loudness, short breath groups
  • stridor, weak, excess/equal stress
  • overriding hypernasality
  • distortions/imprecision

AMR/SMR
- hypernasal
- slow
- decreased ROM
- fatigue

Prolonged vowels
- short duration
- breathy

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26
Q

Unilateral UMN lesion

A

common after unilateral stroke –> symptoms on opposite side of lesion
- contralateral weakness (unilateral innervation)
- no weakness (bilateral innervation)
- structures @ rest –> asymmetrical

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27
Q

Unilateral UMN lesion motor assessment

A
  • unilateral lower face and tongue weakness
  • decreased ROM
  • slow oral mvmets
  • drooling
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28
Q

Unilateral UMN lesion essential assessment

A

may be no change or mild spastic symptoms

“conversational speech:
- reduced loudness, short breath groups
- rough, strained, wet
- imprecise consonants, irregular articulatory breakdown

AMR/SMR: slow, imprecise, irregular
prolonged vowels: short duration

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29
Q

What is the cerebellum

A

maintaining, modulating, controlling movement
- receives info from and projects info to all levels of the brain
- part of indirect system (posture/coordination/balance)

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30
Q

Ataxic Dysarthria

cerebellum

A

bilateral cerebellar CVA: balance and coordination deficits

*irregular, inaccurate mvmt
- intention/terminal tremor
- decreased motor steadiness
- slow mvmt
- over/under shoot target
- decreased coordination
- hypotonia

*prosody:
- primary speech deviation is dysprosody
- unnatural speech
- lack of consistency in errors
*hallmarked by articulatory breakdowns

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31
Q

Mixed ataxic-spastic Dysarthria - multiple sclerosis

A
  • CNS demyelinating disease
  • onset 30-40s; mostly women
  • pervasive weakness/decreased coordination
  • ataxic gait
  • intention tremor
  • visual loss/diplopia
    *incoordination of speech subsystems
    *conversational speech may be normal
  • bursts of loudness
  • rough, reduced pitch
  • slow speech
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32
Q

Mixed ataxic-spastic Dysarthria - Friedreich’s Ataxia

A
  • autosomal recessive transmission linked to gene FXN
  • change in cognition (dementia)
  • sensorineural deafness
  • gait ataxia
  • slowly spreads from trunk to arms
  • loss of sensation in extremities
  • scoliosis

*lack of coordination of subsystems
- bursts of loudness
- rough, breathy, strain-strangled, stridor
- inappropriate pitch
- reduced distinction between voiced and voiceless sounds
- prolonged phonemes, intervals and silences
- irregular changes in pitch and loudness

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33
Q

extrapyramidal level

A
  • center of brain in both hemispheres
  • indirect motor system (slow movement/coordination)
  • both hypokinetic and hyperkinetic

made up of 3 clusters of neurons:
- basal ganglia
- substantia nigra
- subthalamic nucleus

34
Q

basal ganglia is made up of 5 clusters of neurons

A

*caudate nucleus
*putamen
*globus pallidus
- claustrum
- amygdaloid nucleus

*most important for speech

35
Q

striatum

A

def: largest component of basal ganglia (extrapyramidal level –> white matter) decision

caudate nucleus and putamen

36
Q

lenticular nucleus

A

def: important for the motor system but also plays a role in cognitive functions, including working memory, executive function, reward

putamen and globus pallidus

37
Q

role of extrapyramidal chemicals

A

secrete chemicals –> too high or too low can cause unwanted changes

the chemicals allow these structures to communicate with each other:
- basal ganglia
- substantia nigra
- subthalamic nucleus
- cortex, brainstem

38
Q

3 types of extrapyramidal chemicals

A
  • noradrenaline –> pons, allow for smooth movements
  • dopamine –> substantia nigra; allows for mvmt with freedom and ease (power steering of car); decreased associated with hypokinesia and PD
  • acetylcholine –> myoneural junctions; primary neurotransmitter for PNS; important for CNS too
39
Q

function of extrapyramidal system

A

*indirect system (multiple synapses, indirect neural route)

  • posture, tone
  • facilitates all movement
  • regulates gross body movement

think basal ganglia

40
Q

hypo vs hyper

A

hypo - too little
hyper - too much

41
Q

extrapyramidal level - hypokinetic Dysarthria

A

idiopathic PD = 80%
-caused by degeneration of substantia nigra = decrease in dopamine
-changes in cognition can occur in ~50% of patients
-early onset all symptoms are about the same –> differential diagnosis occurs later in disease

Parkinson-plus syndrome (mixed hypokinetic Dysarthria) = 20%; progressive quicker than idiopathic PD
- multplie system athropy (shy drager, OPCD)
- progressive supranuclear palsy
- secondary parkinsons (non-progressive)

42
Q

hypokinetic Dysarthria etiology

A
  • idiopathic
  • stroke
  • trauma
  • infection
  • carbon monoxide poisoning
43
Q

hypokinetic Dysarthria global changes (idiopathic PD)

A

Increased tone with paucity of movement:
- asymmetry with flexion (starts on one side eventually becoming bilateral with one side weaker)
- reduced strength, ROM, accuracy
- bowed VFs (weak breathy)
- rigidity

Variable speed (fast or slow)
- false starts and arrests of mvmt
- festination –> rapid, small steps
- palilalia –> involuntary repetition of words or phrases during speech
- short rushes of speech (fast artic with slow production)

Rest tremor (goes away when limb moves):
- reduced steadiness lips, tongue, jaw, larynx, diaphragm
- pill rolling –> thumb moves against index finger, goes away when hand moves

44
Q

akinetic

A

loss of spontaneous movement

seen in idiopathic PD

45
Q

bradykinetic

A

slowness of movement and speed (or progressive hesitations/halts) as movements are continued

seen in idiopathic PD

46
Q

cogwheel phenomenon

A

rhythmic resistance to passive movement (2-7 Hz)

Clinically, it is characterized by muscular stiffness throughout the range of passive movement in both extension and flexion

seen in idiopathic PD

47
Q

festination

A

short rapid gait like shuffling

seen in idiopathic PD

48
Q

palilalia

A

moving very quickly –> in speech repeating phrases very rapidly so speech blurs together

seen in idiopathic PD

49
Q

hypokinetic Dysarthria nonverbal changes due to high tone (idiopathic PD)

A
  • masked face –> decreased expression and blinking; appears passive/depressed
  • paucity of gestures
  • decreased swallows with accumulation of salvia (drooling)
50
Q

hypokinetic Dysarthria essential assessment (idiopathic PD)

A

conversational speech
reduced loudness and variable rate of artic

respiration –> reduced loudness, short breath groups, fading
phonation –> breathy, low pitch, monopitch
resonance –> no change
articulation –> variable rate, inappropriate sliences, palilalia, false starts/arrests
AMR/SMR –> variable, hard to predict

51
Q

dyskinesia

A

involuntary movement in body

seen in idiopathic PD with medical Rx of Sinemet
- gives patients more freedom of movement instead of feeling frozen
- off period –> decrease body mvmt, increase speech
- on period –> when dopamine takes effect; increase body mvmt, decrease speech

52
Q

late stage hypokinetic symptoms

A
  • paucity of speech
  • social isolation
53
Q

stages of progressive disease for hypokinetic Dysarthria

A

early:
- education, counseling, behavioral

middle:
- counseling and behavioral

late:
- AAC
- maintenance
-counseling

54
Q

t/f bilateral deep brain stimulation improves motor functions while possibly worsening speech and swallowing

A

t

55
Q

What are the structures of the extrapyramidal level of concern for hypokinetic and hyperkinetic dysarthria?

A

basal ganglia, substantia nigra, subthalamic nucleus

56
Q

what’s another extrapyramidal structure that we’ve discussed? The dysarthria tied to it? (cerebellum)

A

The main components of the extrapyramidal motor system are the nuclei of the basal ganglia. Other structures which are involved include cerebellum and brainstem

57
Q

Which structure produces dopamine?

A

substantia nigra produces dopamine, decrease (hypo) in dopamine can cause masked face, paucity in motor function; too much will increase(hyper)

58
Q

akinetic

A

loss spontaneous movement

59
Q

bradykinetic

A

slowness of movement and speed (or progressive hesitations/halts) as movements are continued

seen in PD

60
Q

etiology and global changes of multiple system atrophy (MSA) –> shy dager and OPCA

type of parkinson’s plus syndrome

A

etiology and global changes:
shy-drager: undetermined; drop in BP when standing
olivopontocerebellar degeneration (OPCA): unknown, possibly genetic; dementia

overall global change:
- similar to idiopathic PD
- rapid progression
- does not respond well t meds

61
Q

etiology and global changes of progressive supranuclear palsy

type of parkinson’s plus syndrome

A

etiology and global changes:
- idiopathic deterioration of brain cells; mood and cognitive changes; doll’s eyes

overall global change:
- similar to idiopathic PD
- rapid progression
- does not respond well t meds

62
Q

Atypical global changes for parkinson’s plus

A
  • Dysarthria is more severe in PSP and MSA than in PD
  • quicker progression
  • poor response to treatment
    early cognitive involvement
  • early problems with gait and balance
63
Q

Motor assessment for MSA and PSP

these are parkinson’s plus

A

chest - loss of automatic movement, increased rigidity, irregular swallowing

larynx - rigidity, slow VF movement

no change in velopharynx

lips, tongue, jaw: rigidity, decrease ROM

64
Q

Essential assessments for MSA and PSP these are parkinson’s plus

A

**conversational speech

respiration - reduced loudness
phonation: monopitch
resonance: MSA no change; PSP hypernasality
articulation: shorts rushes of speech, variable rate, palilalia

specific symptoms for shy-drager: laryngeal stridor
specific symptoms for OPCA: palatal myoclonus (clicking)
specific symptom for PSP: hypernasal and doll eye’s

65
Q

palatal myoclonus definition

specific symptom of OPCA

A

palatal myoclonus –> quick tic like movement in soft palate –> patient hears clicking with speaking due to soft palate and PPW moving apart

66
Q

what is pseudobulbar palsy

A

bilateral UMN lesion –> spastic Dysarthria can appear to have similar symptoms as flaccid Dysarthria

pseudo= fake
bulbar = CN
palsy = weakness

uncontrollable laugh or neurological smile

67
Q

t/f high muscle tone - spasticity - hypertonia all mean the same thing

A

true; seen in bilateral spastic Dysarthria

68
Q

define clonus

A

clonus: involuntary, rhythmic, contractions and relaxation

global changes seen with bilateral spastic Dysarthria

69
Q

differential diagnosis LMN lesion vs Bilateral UMN damage - changes in cognition

A
70
Q

differential diagnosis LMN lesion vs Bilateral UMN damage - changes in motor control

A
71
Q

differential diagnosis LMN lesion vs Bilateral UMN damage - changes in laryngeal valve

A
72
Q

differential diagnosis LMN lesion vs Bilateral UMN damage - changes in velar valve

A
73
Q

differential diagnosis LMN lesion vs Bilateral UMN damage - changes in lip and tongue

A
74
Q

What is anterior corticospinal tract

A

The 10% of the axon fibers that do not cross over at the medulla (decussation)

If lesion occurs after decussation —> no damage to anterior corticospinal tract

75
Q

T/F

Following decussation somatotopic organization is preserved

A

True

76
Q

T/F if lesion occurs ABOVE decussation some weakness will be seen on anterior corticospinal tract

A

True

77
Q

describe cerebellum

A
  • recevies info from and project info to process motor coordination
  • part of indirect system
  • filters out excess impulses
  • balance, muscle tone, equilibrium
78
Q

define vermis

A

space where RH and LH join

79
Q

ataxic gait vs festinating gait

A

ataxic (cerebellar) gait –> described as clumsy, staggering movements with a wide-based gait

Festinating Gait –> aka Parkinsonian Gait; rigidity and bradykinesia; walks with slow little steps also may have difficulty initiating steps.

80
Q

UMN White Matter Fibers

Association

A

Association: interconnect cortical regions in same hemisphere

81
Q

UMN White Matter Fibers

Commissural

A

Commissural: interconnect corresponding cortical regions of opposite hemispheres

82
Q

UMN White Matter Fibers

Projection

A

Projection: transmit info from cortex to bulbar and spinal nuclei

Motor Speech (3 decks)

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