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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
Mixed spastic-flaccid Dysarthria essential assessment
**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
26
Unilateral UMN lesion
common after unilateral stroke --> symptoms on opposite side of lesion - contralateral weakness (unilateral innervation) - no weakness (bilateral innervation) - structures @ rest --> asymmetrical
27
Unilateral UMN lesion motor assessment
- unilateral lower face and tongue weakness - decreased ROM - slow oral mvmets - drooling
28
Unilateral UMN lesion essential assessment
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
29
What is the cerebellum
maintaining, modulating, controlling movement - receives info from and projects info to all levels of the brain - part of indirect system (posture/coordination/balance)
30
Ataxic Dysarthria | cerebellum
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
31
Mixed ataxic-spastic Dysarthria - multiple sclerosis
- 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
32
Mixed ataxic-spastic Dysarthria - Friedreich's Ataxia
- 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
33
extrapyramidal level
- 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
basal ganglia is made up of 5 clusters of neurons
*caudate nucleus *putamen *globus pallidus - claustrum - amygdaloid nucleus *most important for speech
35
striatum
def: largest component of basal ganglia (extrapyramidal level --> white matter) decision caudate nucleus and putamen
36
lenticular nucleus
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
role of extrapyramidal chemicals
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
3 types of extrapyramidal chemicals
- 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
function of extrapyramidal system
*indirect system (multiple synapses, indirect neural route) - posture, tone - facilitates all movement - regulates gross body movement think basal ganglia
40
hypo vs hyper
hypo - too little hyper - too much
41
extrapyramidal level - hypokinetic Dysarthria
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
hypokinetic Dysarthria etiology
- idiopathic - stroke - trauma - infection - carbon monoxide poisoning
43
hypokinetic Dysarthria global changes (idiopathic PD)
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
akinetic
loss of spontaneous movement seen in idiopathic PD
45
bradykinetic
slowness of movement and speed (or progressive hesitations/halts) as movements are continued seen in idiopathic PD
46
cogwheel phenomenon
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
festination
short rapid gait like shuffling seen in idiopathic PD
48
palilalia
moving very quickly --> in speech repeating phrases very rapidly so speech blurs together seen in idiopathic PD
49
hypokinetic Dysarthria nonverbal changes due to high tone (idiopathic PD)
- masked face --> decreased expression and blinking; appears passive/depressed - paucity of gestures - decreased swallows with accumulation of salvia (drooling)
50
hypokinetic Dysarthria essential assessment (idiopathic PD)
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
dyskinesia
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
late stage hypokinetic symptoms
- paucity of speech - social isolation
53
stages of progressive disease for hypokinetic Dysarthria
early: - education, counseling, behavioral middle: - counseling and behavioral late: - AAC - maintenance -counseling
54
t/f bilateral deep brain stimulation improves motor functions while possibly worsening speech and swallowing
t
55
What are the structures of the extrapyramidal level of concern for hypokinetic and hyperkinetic dysarthria?
basal ganglia, substantia nigra, subthalamic nucleus
56
what’s another extrapyramidal structure that we've discussed? The dysarthria tied to it? (cerebellum)
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
Which structure produces dopamine?
substantia nigra produces dopamine, decrease (hypo) in dopamine can cause masked face, paucity in motor function; too much will increase(hyper)
58
akinetic
loss spontaneous movement
59
bradykinetic
slowness of movement and speed (or progressive hesitations/halts) as movements are continued | seen in PD
60
etiology and global changes of multiple system atrophy (MSA) --> shy dager and OPCA type of parkinson's plus syndrome
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
etiology and global changes of progressive supranuclear palsy type of parkinson's plus syndrome
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
Atypical global changes for parkinson's plus
- 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
Motor assessment for MSA and PSP these are parkinson's plus
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
Essential assessments for MSA and PSP these are parkinson's plus
**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
palatal myoclonus definition specific symptom of OPCA
palatal myoclonus --> quick tic like movement in soft palate --> patient hears clicking with speaking due to soft palate and PPW moving apart
66
what is pseudobulbar palsy
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
t/f high muscle tone - spasticity - hypertonia all mean the same thing
true; seen in bilateral spastic Dysarthria
68
define clonus
clonus: involuntary, rhythmic, contractions and relaxation global changes seen with bilateral spastic Dysarthria
69
differential diagnosis LMN lesion vs Bilateral UMN damage - changes in cognition
70
differential diagnosis LMN lesion vs Bilateral UMN damage - changes in motor control
71
differential diagnosis LMN lesion vs Bilateral UMN damage - changes in laryngeal valve
72
differential diagnosis LMN lesion vs Bilateral UMN damage - changes in velar valve
73
differential diagnosis LMN lesion vs Bilateral UMN damage - changes in lip and tongue
74
What is anterior corticospinal tract
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
T/F Following decussation somatotopic organization is preserved
True
76
T/F if lesion occurs ABOVE decussation some weakness will be seen on anterior corticospinal tract
True
77
describe cerebellum
- recevies info from and project info to process motor coordination - part of indirect system - filters out excess impulses - balance, muscle tone, equilibrium
78
define vermis
space where RH and LH join
79
ataxic gait vs festinating gait
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
UMN White Matter Fibers Association
Association: interconnect cortical regions in same hemisphere
81
UMN White Matter Fibers Commissural
Commissural: interconnect corresponding cortical regions of opposite hemispheres
82
UMN White Matter Fibers Projection
Projection: transmit info from cortex to bulbar and spinal nuclei

Motor Speech (3 decks)

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