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Neuro Rehab 2 > Cerebellar Disorders > Flashcards

Cerebellar Disorders Flashcards

1
Q

what are 6 cerebellar functions

A
  1. coordinate range, velocity, and strength of ms contractions to produce steady, volitional mvmts and postures
  2. equilibrium in conjunction w vestib and sensory systems
  3. ms tone regulation
  4. eye-head coordination
  5. coordinating ms for speech production
  6. error-based motor learning and adaptation
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2
Q

what is the cerebellum’s role in error-based motor learning and adaptation

A

implicit memories and procedural memories
- feed forward (ex: how to ride a bike)

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3
Q

describe the cerebellum’s process for complex computations

A

takes in sensory inputs and compares to environment, to visual input, to vestib input, and intended motor plan
-> then makes real time adjustments to maintain balance and have smooth motor patterns

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4
Q

how does the cerebellum communicate with other regions of the brain

A

3 main, large axonal bundles running through peduncles

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5
Q

what is the role of deep cerebellar nuclei

A

send efferent signals and adjustments to motor mvmts

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6
Q

what are the 3 pairs of deep cerebellar nuclei

A

fastigial
interposed
dentate

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7
Q

what are the 3 functional zones

A

spinocerebellar
cerebrocerebellar
vestibulocerebellar

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8
Q

what functional zones are the 3 deep cerebellar nuclei located in

A

fastigial & interposed = spino
dentate = cerebro

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9
Q

what is the general function of fastigial and interposed nuclei

A

motor execution

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10
Q

where is the fastigial nuclei located specifically

A

in vermis of spinocerebellums

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11
Q

where does fastigial nuclei receive signals from

A

vermis and cerebellar afferents which carry vestib, prox somatosensory (trunk & postural ms), auditory, & visual info
- aka medial descending systems

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12
Q

where are efferents from fastigial nuclei sent

A

vestib nuclei and reticular formation

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13
Q

what are the functions of the fastigial nuclei and what is the main one (4)

A

postural ms tone **
upright postural control
locomotion
gaze and eye mvmts

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14
Q

what are 5 s/sx of a lesion to the fastigial nuclei

A

poor balance
ataxic gait
- truncal ataxia/instability
falls
hypotonia
oculomotor deficits

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15
Q

what nuclei compose the interposed nuclei and where are they located

A

emboliform and globose nuclei

lateral spinocerebellum

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16
Q

what can truncal ataxia manifest as

A

instability
rocking back and forth

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17
Q

where does the interposed nuclei receive signals from

A

spinocerebellar tract, prox somatosensory, (limbs and periphery), auditory and visual pathways
- aka lateral descending systems

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18
Q

where are efferents from interposed nuclei sent

A

red nucleus of rubrospinal tract

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19
Q

what are the functions of the interposed nuclei (2)

A

control agonist-antagonist firing
coordinated limb mvmts

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20
Q

what are 7 s/sx of a lesion on the interposed nuclei

A

imbalance
ataxic gait
intention tremor
rebound phenomenon
dysdiadochokinesia
dysmetria
dysarthria

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21
Q

where does the dentate nuclei receive afferent inputs from

A

cerebral cortex (motor, premotor, prefrontal, sensory, visual, auditory cortices) via pontine nuclei
- aka areas 4 & 6

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22
Q

where are efferent signals sent from the dentate nuclei

A

red nucleus and ventrolateral thalamic nucleus

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23
Q

what are the functions of the dentate nuclei (4) and what is the main one

A

motor planning**
complex, multi joint mvmt
visually guided mvmt
sensorimotor error adjust

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24
Q

what are 5 s/sx of a lesion on the dentate nuclei

A

dysdiadochokinesia, dysmetria, dyssynergia (decomposition of mvmt), poor visuomotor coordination

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25
Q

where are vestibular nuclei located and what is consideration of this

A

in brainstem (medulla) so technically not cerebellar nuclei

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26
Q

where are signals to vestibulocerebellum received from

A

afferents from vestib and visual areas

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27
Q

where are efferent signals from vestibulocerebellum sent to

A

efferents to medial and lateral vestib nuclei (start of vestibulospinal pathways)

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28
Q

what are the functions of the vestibulocerebellum (4) and what are the main ones

A

posture and balance** control
coordinate eye** and head mvmt
VOR
gaze stability

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29
Q

what are 4 s/sx of a lesion on the vestibulocerebellum

A

ataxia w vertigo & nystagmus
unable use vestib info to control eye mvmts during head rotation (VOR)
poor coordinated mvmt of trunk and limbs in standing and w walking
imbalance and dec postural control

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30
Q

what is the function of the cerebellar peduncles

A

information super highways
- connects cerebellum to rest of brain

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30
Q

what is an important consideration in how the peduncles sit in relation to brain

A

form walls to 4th ventricle
- makes cerebellum vulnerable to changes in. ICP and hydrocephalus

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31
Q

what is the blood supply for the cerebellum and where does each go

A

SCA -> ant lobe
PICA -> post lobe
AICA -> vent ant and post lobes, flocculonodular lobe

all 3 arise from vertebrobasilar arteries

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32
Q

what is the most common blood supply syndrome of the cerebellum

A

PICA
- SCA and AICA are rare

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33
Q

how does the cytoarchitecture vary in the cerebellum and what are the 2 main components

A

fairly uniform

purkinje cells
climbing/mossy fibers

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34
Q

what is the role of purkinje cells

A

axons project to one of deep cerebellar nuclei
- carries output of cerebellar cortex

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35
Q

what is the general function of climbing and mossy fibers

A

modulate activity of purkinje cells

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36
Q

climbing vs mossy fibers

A

climbing
- produce large complex spikes in purkinje cells
- not modulated by sensory or motor activity
- more involved in feed forward programs

mossy
- synapse w granule cells then eventually purkinje cells
- highly modulated by sensory stim and motor activity (relay info like direction, velocity, duration, magnitude of mvmt and sensory stim)
- more involved w ongoing motor activity and making adjustments

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37
Q

what are non-motor cerebellar functions and what is responsible for this

A

memory, cog, attention, executive function, spatial cog

interconnections w pre-frontal cortex

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38
Q

what type of syndrome do you see more marked cog dysfunction

A

when post lobes of cerebellum are affected bilaterally (PICA infarct)

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39
Q

how do effects present for unilateral lesions and why

A

ipsilateral effects

d/t uncrossed or double crossing of efferents to cerebrum, vestib nuclei, and red nucleus

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40
Q

what are 7 common s/sx of cerebellar lesions

A
  1. ataxia (uncoordinated mvmt)
  2. dec balance and postural instability
  3. dysarthria
  4. nystagmus, vertigo, ocular motor dysfunction
  5. hypotonia
  6. n/v
  7. asthenia (generalized weakness)
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41
Q

what are 4 examples of hereditary etiology for cerebellar disorders

A
  1. autosomal dominant
    - spinocerebellar ataxia
    - episodic ataxia
  2. autosomal recessive
    - Friedrich’s ataxia
  3. x-linked disorders
    - mitochrondrial dz
    - fragile-x syndrome
  4. vit E deficiency -> poor cerebellar fxn
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42
Q

what are 5 acquired etiologies for cerebellar disorders

A

MS
CVA, TBI, brain tumor
toxicity - EtOH, heavy metal, drugs
infectious process
-> can cause abscesses or inflammation
idiopathic - slow degen

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43
Q

what is an autosomal dominant etiology for cerebellar disorders

A

spinocerebellar ataxia

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44
Q

what is an autosomal recessive etiology for cerebellar disorders

A

friedrich’s ataxia

45
Q

what are x-linked etiologies for cerebellar disorders

A

mitochondrial dz
fragile-x syndrome

46
Q

what is spinocerebellar ataxia characterized by

A

ataxia and dystonia, dysarthria, opthalmoplegia (extraocular eye ms), poor hand control, spasticity, neuropathy

47
Q

how can effects of spinocerebellar ataxia present

A

purely cerebellar or extracerebellar effects (SC degen)

48
Q

prognosis and course of dz for spinocerebellar ataxia

A

manifests 30-50s
normal to shortened lifespan

leads to cerebellar atrophy - slow progressing and no med intervention available

49
Q

what is Friedrich’s ataxia

A

degen of SC, peripheral n., and cerebellum
-> more severe presentation than spinocerebellar atrophy

50
Q

what are the first signs of Friedrich’s ataxia

A

ataxic gait
then UE and trunk involvement

51
Q

what are 4 s/sx of Friedrich’s ataxia

A

loss of proprioception and vibration sense
- d/t peripheral n. and SC involvement
hyporefleia
dysarthria
(+) Babinski

52
Q

what are 4 secondary complications is Friedrich’s ataxia associated with

A

cardiac abnormalities
hearing loss
vision loss
progressive MSK degen

53
Q

course and prognosis of Friedrich’s ataxia

A

onset 5-15yo
wc bound w/i 10-20yo
shorter life span (may survive 60s-70s)

54
Q

what is mitochondrial dz

A

lack of energy/power, results in weakness and neuro-degen w particular impacts on cells in cerebellum

55
Q

what is the prominent clinical feature of mitochondrial dz

A

cerebellar ataxia

56
Q

course of dz in mitrochrondrial dz

A

typical onset in young adulthood
progressive

57
Q

what is fragile-x syndrome often a differential dx for

A

children showing signs of developmental delay

58
Q

what is fragile-x syndrome? what will pts often have difficulty w and why

A

inherited form of intellectual disability

difficulty w motor learning, cog, and coordination
-> alterations in structure and plasticity of synapses on purkinje cells

59
Q

what is ataxia w vitamin E deficiency (AVED) characterized by (6)

A

dysarthria
proprioceptive loss
loss of balance
titubation (involuntary mvmt of head)
dystonia
retinitis pigmentosa (pigment affected)

60
Q

course of AVED and prognosis/treatment

A

manifests in late childhood -> early teens
many individuals wc bound if untreated

treatable w vit E supplementation
- can halt or improve sx

61
Q

how common is a cerebellar artery stroke in general

A

very rare - 5%

62
Q

what are 4 s/sx of a PICA stroke

A

vertigo
ataxia
nystagmus
unsteadiness

63
Q

what are 4 s/sx of a SCA stroke

A

dysmetria of UE (ipsi)
unsteadiness
dysarthria
nystagmus

64
Q

what are 3 s/sx of an AICA stroke (pons involvement)

A

dysmetria
vestib signs
facial sensory loss

65
Q

what is a common sx of all cerebellar artery strokes and what is the concern w this

A

swelling
-> compression of 4th ventricle
—> hydrocephalus from obstructing CSF flow

66
Q

what are 4 s/sx of edema and compression of the posterior fossa d/t a cerebellar artery stroke and what is the concern

A
  1. compromises respiratory centers in brainstem
  2. brainstem herniation
  3. CN VI palsy
  4. abnormal pupil reactions

can be lethal

67
Q

how does cerebellar stroke treatment compare to cerebral strokes

A

very similar

68
Q

why are there poorer prognoses w cerebellar strokes

A

rapid inc in pressure in area that isn’t forgiving

69
Q

what are indications for poor prognoses in cerebellar strokes

A

damage to cerebellar nuclei and/or output pathways, superior cerebellar peduncles

SCA lesion, hemorrhagic, extracerebellar damage

70
Q

what is the pathophys of EtOH toxicity which causes cerebellar dysfunction

A

alteration in GABA receptor dependent neurotransmission
- EtOH inc GABA release in purkinje cells and interneurons, inc tonic inhibition of interneurons, dec excitatory output of deep cerebellar nuclei
—> cerebellar dysfunction and ataxia

higher affinity for vermis and vermis is more vulnerable to changes
-> see more trunk and LE ataxia

71
Q

how does EtOH create long term cerebellar dysfunction

A

EtOH induced cerebellar damage can persist even after complete abstinence d/t neuronal and mitochondrial damage

72
Q

what component of the cerebellum is especially vulnerable to toxicity

A

purkinje cells

73
Q

what is a common secondary complication of long term EtOH toxicity

A

thiamine deficiency
- wernicke’s encephalopathy
- korsakoff’s syndrome **

korsakoff common in EtOH abuse
- memory loss, ataxia, vision changes

74
Q

what are other common toxicities other than EtOH which can lead to cerebellar disorders (7)

A

thiamine deficiency
anti-epileptics
amioderone
chemo
cocaine, heroin
environmental toxins
hyperthermia

75
Q

what is multisystem atrophy (MSA)

A

sporadic neurodegen dz of undetermined etiology w adult onset
- death w/i 6-10yo

76
Q

what are 2 main types of manifestations of MSA

A

autonomic dysfunction
motor dysfunction

can see neuropsych sx

77
Q

what are 3 s/sx of autonomic dysfunction in MSA

A

GU dysfunction
- urinary retention, incontinence/constipation
ED
OH

78
Q

what are s/sx of motor dysfunction in MSA

A

parkinsonism and/or cerebellar dysfxn
- gait ataxia
- dysarthria
- intention tremor
- oculomotor dysfunction

79
Q

what are the 2 subtypes of MSA

A

MSA-P (predominant parkinsonism)
MSA-C (predominant cerebellar)

80
Q

what is the treatment for MSA

A

levodopa

81
Q

why do we check CN function in a PT exam for a cerebellar disorder

A

CN can be impacted by loss of communication w cerebellum

82
Q

what are components of the BSF exam that are esp important in cerebellar disorders

A

coordination
- non-equilibrium tests (dysmetria, dyssynergia, dysdiadochokinesia, rebound, intention tremor)
- equilibrium tests

CN function

oculomotor function
- smooth pursuits, saccades

vestib screening tests: VOR, VORc

83
Q

what are 8 non-equilibrium tests

A

finger to nose
finger to finger
finger opposition
forearm pron/sup
rebound test
heel to shin
drawing a circle
hand or feet tapping

84
Q

what are 8 equilibrium/balance tests

A

standing w narrow BOS
perturbations
romberg
tandem stance & walk
walk on heels or toes
figure 8
start and stop on command
walk sideways, around obstacles

85
Q

what is a dz specific standardized measure of ataxia

A

Friedrich ataxia rating scale

86
Q

what are 3 standardized measures of ataxia and what does the literature say

A

ICARS - most detailed
SARA - excludes oculomotor
BARS - shortest, includes all domains

ICARS is preferred d/t high correlation w disability scale

87
Q

what are 12 PT interventions for ataxia

A

PNF: RI, COI, SR
Frenkel exercises
mCIMT
endurance training
trunk stabilization/strengthening
axial and/or limb weighting
balance training
BWSTT and overground gait training
vestib habituation exercises
biofeedback
cooling
VR

88
Q

when selecting a PT intervention for ataxia, what should you consider

A

nature of lesion
compensatory vs restorative strategies

89
Q

how should PT interventions for ataxia be prescribed and progressed

A

work on specific and target mvmts
-» then inc speed

90
Q

when is axial and/or limb weighting appropriate and why

A

great compensatory strategy
- will see deterioration if remove wt

91
Q

when is biofeedback used as an intervention in ataxia

A

to get a more precise ms response
(don’t fully understand mechanism)

92
Q

what are 3 strategies to improve function in someone w ataxia

A
  1. use external constraints to provide steadiness and enable practice of tasks otherwise too difficult
    -> walking in parallel bars
  2. practice actions involving production of rapid initial burst of agonist activity
    -> jumping, jogging, throwing a ball
  3. practice tasks that require predictive timing
    -> hand eye coordination, bouncing a ball, hitting a baseball
93
Q

what is a strategy to improve functional balance in ataxia

A

train everyday actions in standing w narrow BOS and no arm support

94
Q

what are strategies to inc prox strength w low ms tone and truncal ataxia

A

pushups against wall for UE WB-ing
pulling activities w weighted objects or resistance

95
Q

what are strategies to improve UE control in cerebellar disorders

A

UE exercises in sitting and standing
picking up and placing activities

start arms close to body -> progress by inc reaching distance

96
Q

what are strategies to improve dynamic stability of trunk and limbs in cerebellar disorders

A

activities rely on balance control
- tandem walking
- walking in narrow spaces
- walking on different surfaces

gradually inc mvmt complexity/dual task and speed

97
Q

what are strategies to improve intersegmental control and coordination in cerebellar disorders

A

WBing exercises for LE involving repetitive flex and ext over fixed feet
- repetitive STS
- repetitive squats
- step ups/down
- heel raises

vary wt resistance or body wt, additional wts in vests

98
Q

what are strategies to provide practice controlling agonist/antagonist ms activity

A

performance of smooth mvmts
various amps and speeds
stopping and starting at various points in range and at various mvmt speeds

99
Q

what are things to consider in creating practice environment which enables person to develop more control/accuracy during practice

A

support condition
timing constraints
environmental context

100
Q

what are ataxia balance crutches

A

forearm crutches
maintain contact simultaneously
helps to prevent lateral displacement & sway

101
Q

what is important to emphasize if PNF is used as an intervention in cerebellar disorders

A

emphasize timing of agonist/antagonist, strengthening

102
Q

what are frenkel exercises and what does the literature say

A

AROM exercises, can help to improve coordination bc of focus on smoothness of mvtms

no evidence of benefits in literature

103
Q

why does limb weighting work when it is on the patient

A

inc proprioceptive and spinocerebellar inputs that can help the cerebellum adjust mvmt and get better motor output

104
Q

what outcomes were seen w limb weighting

A

short term improvement of performance but may cause worsening of sx when removed or not used

good compensatory method for short term use w ADLs

105
Q

what does evidence say about axial weighting

A

encouraging findings, mechanism poorly understood

106
Q

how does cooling work as a PT intervention

A

can dec cerebellar intention tremor
- via improved nerve conduction velocity, inc ms stiffness

107
Q

what does the evidence say about the use of biofeedback (visual or auditory) in MS

A

improve gait parameters
- inc in gait speed and stride

108
Q

when do you choose compensatory methods to dec cerebellar ataxia

A

degen or progressive conditions
early in rehab to promote safety and independence w functional tasks

109
Q

what are compensatory strategies that can be used in cerebellar disorders (6)

A

use of visual/verbal cues
dec speed of mvmt
inc BOS - use of UE in sitting
weighting
cooling
AD for amb

110
Q

when do you choose restorative approaches and promote recovery in cerebellar disorders

A

stable, non-progressive insults or lesions

111
Q

what are restorative strategies that can be used in cerebellar disorders (8)

A

balance/equilibrium activities
frenkels
PNF
strength/endurance training
mCIMT
vestib retraining
VR
BWSTT and overground gait training
obstacle courses
- narrow paths, head turns, change directions

Neuro Rehab 2 (48 decks)

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