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Med Neuro Block 3 > Cerebellar Disorders > Flashcards

Cerebellar Disorders Flashcards

1
Q

Functions of the cerebellum:

A

To make movements of the extremities, trunk and eyes as smooth as possible by continually making small corrections.

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2
Q

How does the cerebellum achieve movements

A

Achieved through coordinated contraction/relaxation of agonist & antagonist muscles

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3
Q

Inputs to cerebellum come from which areas

A

sensory (proprioception) pathways from spinal cord, cortex, brainstem

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4
Q

How does motor information from cord get to cerebellum

A

–> ventral spino cerebellar tract —>superio rcerebellar peduncle–> cerebellum

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5
Q

Visual,sensory,motor information from cortex get to cerebellum how?

A

pontine nuclei–>middle cerebellar peduncle –>cerebellum

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6
Q

How does Proprioceptive information from limbs get to crebellum

A

–>fasiculus gracilis/cuneatus–> spinocerebellar tract and cuneo cerebellar tract –> interior cerebellar peduncle –>cerebellum

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7
Q

How does there cerebellum cause movement (the path)?

A

VL thalamus–> primary motor&supplementary motor cortex–> ventral&lateral corticospinal tract–> movement

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8
Q

Tract cerebellum takes to get head/eye control and posture

A

Cerebellum–> vestibular nuclei–> head/eye control&posture

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9
Q

how does cerebellum cause unconsious motor control?

A

Cerebellum –> medullary&pontine reticular formation–> medullary&pontine reticulospinal tract –>unconscious motor control

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10
Q

Deficits are_______ to the lesion due to ‘doublecrossing’ or because fibers remain ipsilateral

A

ipsilateral

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11
Q

Deficits are ipsilateral to the lesion due to _________or because fibers remain ipsilateral

A

‘doublecrossing’

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12
Q

Acute lesions to cerebellum are accompanied by

A

nausea/vomiting due to vertigo and ataxic on finger to nose or heel to shin

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13
Q

Cerebellar lesion symptoms resulting in nausea/vomiting can mimic what?

A

vestibular dysfunction… similar but

these pts are not necessarily ataxic on finger to nose or heel to shin

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14
Q

Ataxia =

A

uncoordinated muscle movement; errors in speed, range, force, timing

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15
Q

uncoordinated muscle movement; errors in speed, range, force, timing

A

Ataxia

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16
Q

Truncal ataxia =

A

wide-based, unsteady gait or difficulty sitting up; “drunklike”; localizes to lesion of
vermis

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17
Q

wide-based, unsteady gait or difficulty sitting up; “drunklike”; localizes to lesion of ______

A

vermis, this is truncal ataxia

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18
Q

Romberg test=

A

ask patient to stand in place, feet together and close eyes, if she or hee needs to step to stabilize, then deficit could be due cerebellar, proprioceptive, or vestibular
dysfunction; not specific to cerebellar disorders

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19
Q

Romber test is specific to cerebellar disorders

A

false

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20
Q

difficulty coordinating an extremity; manifests as dysmetria & dysrhythmia;
lesion of ipsilateral lateral hemispheres

A

Appendicular Ataxia

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21
Q

Appendicular Ataxia

A

difficulty coordinating an extremity; manifests as dysmetria & dysrhythmia;
lesion of ipsilateral lateral hemispheres

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22
Q

What are 6 signs of Appendicular Ataxia

A 
Dysmetria
Dysrhythmia
Finger-nose-finger test
heel-to-shin test
Finger tapping
Dysdiadochokinesia
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23
Q

overshoot/undershoot of a body part (limb) during movement toward a target

A

Dysmetria =

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24
Q

Dysmetria =

A

overshoot/undershoot of a body part (limb) during movement toward a target
–seen in appendicular ataxia

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25
Q

Dysrhythmia =

A

abnormal rhythm and timing of movement

–for appendicular ataxia

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26
Q

abnormal rhythm and timing of movement

A

Dysrhythmia

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27
Q

Finger-nose-finger test—

A

alternating between touching nose and examiner’s finger;
abnormal if patient’s finger shakes as it approaches target (either nose or finger)
–for appendicular ataxia

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28
Q

Finger tapping—

A

watch amplitude, rhythm, speed; cerebellar disorders cause abnormal rhythm, slowed speed, and varying amplitude

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29
Q

During finger tapping… cerebellar disorders cause ______rhythm,______ speed, and______ amplitude

A

abnormal
slowed
varying

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30
Q

Dysdiadochokinesia =

A

abnormal speed/rhythm when tapping hand with

palm/dorsum alternatively

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31
Q

abnormal speed/rhythm when tapping hand with

palm/dorsum alternatively

A

Dysdiadochokinesia

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32
Q

involuntary, rhythmic oscillation of a body part

A

tremor

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33
Q

Postural tremor =

A

tremor that occurs when a limb is held in a particular position (eg. open hands held extended); lesion of ipsilateral lateral hemisphere

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34
Q

tremor that occurs when a limb is held in a particular position (eg. open hands held extended); lesion of ipsilateral lateral hemisphere

A

Postural tremor

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35
Q

Action/intention tremor =

A

tremor that occurs when limb is in motion; lesion of ipsilateral lateral hemisphere

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36
Q

tremor that occurs when limb is in motion; lesion of ipsilateral lateral hemisphere

A

Action/intention tremor

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37
Q

Action/intention tremor occurs when limb is in motion; lesion is on _______ side

A

ispliateral hemisphre

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38
Q

Titubation =

A

tremor of trunk or head; lesion of vermis

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39
Q

Lesion in the vermis results in

A

titubation

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40
Q

Ocular dysmetria =

A

overshoot or undershoot of the eyes as patient focuses on a target; lesion of flocculonodular lobe (part of lateral hemispheres)

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41
Q

overshoot or undershoot of the eyes as patient focuses on a target; lesion of flocculonodular lobe (part of lateral hemispheres)

A

Ocular Dysmetria

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42
Q

Lesion of flocculonodular lobe results in

A

Ocular dysmetria–overshoot or undershoot of patient focusing on target

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43
Q

Flocculonodular lobe is in which part of hemisphere

A

lateral

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44
Q

Saccades =

A

quick, voluntary movement of eyes onto target; mediated by cortex—frontal & parietal eye fields

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45
Q

quick, voluntary movement of eyes onto target; mediated by cortex—frontal & parietal eye fields

A

Saccades

46
Q

Slow eye movements =

A

involuntary movement of eyes mediated by cerebellum, vestibular nuclei & pathways, and extraocular motor nuclei

47
Q

involuntary movement of eyes mediated by cerebellum, vestibular nuclei & pathways, and extraocular motor nuclei

A

Slow eye movements

48
Q

Nystagmus =

A

rhythmic oscillations of the eyes; mediated by cortex; is an attempt by the cortex to correct abnormal signal to brain b/c of deficit of slow eye movements

49
Q

mediated by cortex; is an attempt by the cortex to correct abnormal signal to brain b/c of deficit of slow eye movements

A

Nystagmus

50
Q

Named after fast-beating phase of eye movements; eg. “right beating nystagmus”—fast phase of eye movements are to the______ & slow phase of eye movements to ____

A

right

left

51
Q

Nystagmus is due to

A

Due to a deficit of the slow eye movement system

52
Q

If nystagmus is acute in onset, can be accompanied by

A

vertigo, nausea, vomiting

53
Q

Lesion of ________ can cause vertical, horizontal, or rotatory nystagmus

A

vermis/flocculonodular lobe

54
Q

Pure vertical nystagmus

A

ALWAYS caused by CNS lesion (ie brainstem or cerebellar injury) direction-changing nystagmus in central

55
Q

A horxontal or rotary nystagmus could be causes by:

A

a central or peripheral nervous system lesion

56
Q

R beating horizontal nystagmus on R gaze, upgaze, downgaze –>

A

L VOR or L vestibular nuclear lesion (lesion could be central or peripheral with horizontal nystagmus)

57
Q

R beating horizontal nystagmus on R gaze, L beating horizontal nystagmus on left gaze, verticle nystagmus on upgaze–>

A

likely to be cerebellum or one of it’s pathways

58
Q

Slow saccades =

A

slowness in eye movements when trying to quickly look at target

59
Q

Scanning (or ataxic) speech =

A

slow, effortful speech with difficulty articulating; lesion of lateral hemispheres

60
Q

slow, effortful speech with difficulty articulating; lesion of lateral hemispheres

A

Scanning (or ataxic) speech

61
Q

Hypotonia of ipsilateral limb results in

A

b/c cerebellum influences corticospinal tracts; pt falls to weak side (ipsilateral to lesion)

62
Q

Lateral hemispheres of cerebellar are in charge of

A

motor planning for extremities

63
Q

Motor pathway lateral hemisferes influence

A

LCST

64
Q

If Lateral hemispheres are lesioned we see

A

Appendicular ataxia

65
Q

Intermediate hemisphere is in charge of

A

distal limb coordination

66
Q

Motor pathway intermediate hemisphere influences

A

LCST, rubrospinal tract

67
Q

Lesion in intermediate hemisphere results in

A

Appendicular ataxia

68
Q

Region of the cerebellum responsible for proximal limb

A

Vermis

69
Q

trunk coordination and balace and vestibuloocular reflexes

A

Floculonodular lobe

70
Q

Vermis influences which motor pathway

A

VCST, reticulospinal tract, vestibulospinal tract

71
Q

Flocculonodular lobe influences which motor pathway

A

Medial longitudinal fasciculus

72
Q

If the vermis is lesioned we see

A

truncal ataxia

73
Q

If the flocculonodular lobe is lesioned we see

A

Nystagmus/slow saccades

74
Q

Differential diagnosis for cerebellar dysfunction: vestibular dysnfunction

A

Vestibular dysfunction (also causes vertigo, difficulty walking, N/V, nystagmus); but usually no dysmetria or ataxia on finger to nose or heel to shin

75
Q

Differential diagnosis for cerebellar dysfunction: corticospinal tract dysfunction

A

Corticospinal tract dysfunction—also causes hypotonia & weakness can be mistaken for ataxia

76
Q

Differential diagnosis for cerebellar dysfunction: impaired proprioception

A

Impaired proprioception—these pts have a sensory ataxia (proprioceptive loss in feet makes walking difficult)

77
Q

Clinical deduction for cerebellar disorders:

A

• Determine if process is acute (ie. occurred over minutes to hours) or chronic (slowly over many
days to weeks)
• Localize lesion

78
Q 
Cerebellar stroke (ischemic or hemorrhagic)
 Alcohol intoxication 
Drug overdose (eg. phenytoin)
 Multiple sclerosis
....examples of
A

Acute

79
Q

Essential tremor
Spinocerebellar ataxia
Tumor (eg. astrocytoma)
Chronic alcoholism

A

Chronic

80
Q

Pathogenesis of cerebellar stroke

A

the main arteries supplying blood (SCA, PICA, AICA) become diseased due to atherosclerosis; more commonly, the penetrating arteries from these arteries undergo arteriolosclerosis (thickening of vessels) from chronic HTN & other vascular risk factors (diabetes, smoking, high cholesterol)–> blood flow compromised –> ischemic stroke; or severe spike in blood pressure causes brittle vessel to rupturehemorrhagic stroke

81
Q

Symptoms and onset of cerebellar stoke can be:

A

acute or sudden; may be felt right away and improve over weeks

82
Q

Symtpoms of cerebellar stroke

A

inability to walk, frequent falls, nausea, vomit, vertigo

83
Q

Signs of cerebellar stroke

A

dysmetria of ipsilateral arm/leg on finger-to-nose and heel-to-shin, mild ipsilateral dysdiadochokinesia,mild dysarthria, horizontal and verticle nystagmus

84
Q

dysmetria of ipsilateral arm/leg on finger-to-nose and heel-to-shin, mild ipsilateral dysdiadochokinesia,mild dysarthria, horizontal and verticle nystagmus

A

signs of cerebellar stroke

85
Q

Localization of cerebellar stroke

A

ips cerebellar hemisphere (lateral and flocculonodular lobes) and vermis

86
Q

What risks do we look for cerebellar stoke?

A

HTN, smoking, diabetes, high cholesterol

87
Q

One of the most common causes of ataxia

A

Alchohol intoxication

88
Q

What are the acute symptoms of alcohol ataxia

A

inability to walk with frequent falls, no ‘checking’ of loss of balance, slurred speech;
caused by cerebellar neuronal dysfunction

89
Q

Chronic symptoms of alcohol intoxication

A

: ataxia with walking/maintaining balance, difficulty with finger dexterity; caused by
Purkinje cell destruction & subsequent atrophy of vermis

90
Q

Signs of alcohol ataxia

A

difficulty walking/tandem gait, dysarthria, dysmetria of limbs, nystagmus

91
Q

what is the localization of alcohol intoxication

A

cerebellar vermis

92
Q

The most common movement disorder

A

essential tumor

93
Q

Essential tumor characteristics

  • characteristic of tremor
  • genetic pattern
  • ect
A

Usually symmetric, bilateral, postural or action tremor that is persistent & visible; no other cause found;
autosomal dominant in 50% of patients; involves arms/hands, voice, head; chronic neurodegenerative
disorder; gradual loss of Purkinje cells

94
Q

Signs of essential tumor

A

dysmetria, ataxic gait, head titubation

95
Q

Localization of essential tumor

A

cerebellar hemispheres & vermis

96
Q

Spinocerebellar ataxia is a group of ________ disorders caused by ___________ and _________

A

Group of autosomal dominant ataxic disorders caused by degeneration of afferent & efferent cerebellar pathways & destruction of Purkinje cells

97
Q

Spinocerebellar ataxia is caused by a gene mutation which is:

A

each caused by a gene mutation resulting in a CAG triplet repeat expansion at different genetic loci

98
Q

What symptoms do we see with spinocerebellar ataxia

-3 qualities

A

Slowly progressive ataxia of limbs/trunk, scanning speech, slowed saccades

99
Q

Most cause profound cerebellar atrophy

A

Spinocerebellar ataxia

100
Q

Higher morbidity & mortality than essential tremor

A

spinocerebellar ataxia

101
Q

Localization of essential tumor

A

entire cerebellum

102
Q

Most common childhood primary brain tumor

A

Astrocytoma

103
Q

Astrocytoma is a low grade tumor comprised of ________

A

A low grade tumor composed of astrocytes (a type of glial cell & hemce a glioma)

104
Q

Localization: tumor usually grows in

A

cerebellar hemisphere

105
Q

Slowly progressive ipsilateral limb/truncal ataxia, scanning speech, nystagmus due to tumor
compressing on adjacent cerebellar parenchyma

A

Astrocytoma

106
Q

Astrocytoma is slowly progressive _______ limb/truk ataxia

A

ipsilateral

107
Q

nystagmus due to astrocytoma tumor

compressing on

A

adjacent cerebellar parenchyma

108
Q

An astrocytoma show signs of increased intracranial pressure which cause:

A

—morning headaches, blurred vision,

may culminate in nausea/vomiting, difficulty concentrating in school

109
Q

An autoimmune/inflammatory disorder affecting CNS white matter

A

Mutliple sclerosis

110
Q

MS is more common in ____________ and each lesion is reffered to as _________

A

Predilection for young (25-40’s), white females • Each lesion is referred to as a ‘plaque’

111
Q 
In MS affects on:
optic nerves
Cerebral white matter regions
Cerebellar white matter
Medial longitudinal fasciculus
spinal cord
A

Optic nerves–sudden vision loss
cerebral white matter–all descending/ascending cortex
cerebrellar white matter–especially middle cerebellar peduncle
Medial long fasciculus–white matter that mediates eye movements and if lesioned causes internucuer opthalmoplegia

112
Q

How does MS affect the spinal cord

A

resluts in complete or incomplete spinal cord lesion in transverse section affecting ascending/descending tracts–called transverse myelitis

Med Neuro Block 3 (9 decks)

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