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Med Neuro Block 3 > Cerebellar Disorders > Flashcards

Cerebellar Disorders Flashcards

1
Q

What is the function of the cerebellum?

A
  • To make movements of the extremities, trunk and eyes as smooth as possible by continually making small corrections
    • coordinated contraction/relaxation of agonist & antagonist muscles
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2
Q

What are the inputs of the cerebellum?

A
  • **Inputs: **sensory (proprioception) pathways from spinal cord, cortex, brainstem
  1. Motor information from cord ⇒ ventral spinocerebellar tract ⇒ superior cerebellar peduncle ⇒ cerebellum
  2. Visual, sensory, motor information from cortex ⇒ pontine nuclei ⇒ middle cerebellar peduncle ⇒ cerebellum
  3. Proprioceptive information from limbs ⇒ fasciculus gracilis/ cuneatus ⇒ dorsal spinocerebellar tract & cuneocerebellar tract ⇒ inferior cerebellar peduncle ⇒ cerebellum
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3
Q

What are the outputs from the cerebellum?

A
  • Outputs: brainstem (that then project back to extremities/trunk & eyes), thalamus
  1. Cerebellum ⇒ VL thalamus ⇒ primary motor & supplementary motor cortex ⇒ ventral & lateral corticospinal tract ⇒ movement
  2. Cerebellum ⇒ vestibular nuclei ⇒ head/eye control & posture
  3. Cerebellum ⇒ medullary & pontine reticular formation ⇒ medullary & pontine reticulospinal tract ⇒ unconscious motor control
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4
Q

Cerebellar deficits are ___________ to the lesion

A

ipsilateral

  • due to:
    • ‘doublecrossing’ or
    • fibers remain ipsilateral
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5
Q

Acute lesions accompanied by nausea/vomiting due to _______.

A

vertigo

  • vestibular dysfunction similar
    • pts are not necessarily ataxic on finger to nose or heel to shin
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6
Q

Ataxia

A

uncoordinated muscle movement

  • errors in speed, range, force, timing
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7
Q

**Truncal ataxia **

A

wide-based, unsteady gait or difficulty sitting up

  • localizes to lesion of vermis
    • “drunk-like”
  • Walk patient—normal walk & tandem walk
  • Romberg test
    1. ask patient to stand in place, feet together & close eyes
    2. if s/he needs to step to stabilize, then deficit could be due cerebellar, proprioceptive, or vestibular dysfunction
    3. not specific to cerebellar disorders
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8
Q

Appendicular ataxia:

A

difficulty coordinating an extremity

  • manifests as dysmetria & dysrhythmia
  • lesion of ipsilateral lateral hemispheres
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9
Q

Appendicular ataxia:

  1. Dysmetria:
  2. Dysrhythmia:
  3. Finger-nose-finger test:
  4. Heel-to-shin test:
  5. Finger tapping:
  6. Dysdiadochokinesia:
A
  1. **Dysmetria **= overshoot/undershoot of a body part (limb) during movement toward a target
  2. Dysrhythmia = abnormal rhythm and timing of movement
  3. Finger-nose-finger test—alternating between touching nose and examiner’s finger
    • abnormal if patient’s finger shakes as it approaches target (either nose or finger)
  4. Heel-to-shin test—guiding heel along shin when supine
    • abnormal if heel shakes
  5. Finger tapping—watch amplitude, rhythm, speed
    • cerebellar disorders cause abnormal rhythm, slowed speed, and varying amplitude
  6. Dysdiadochokinesia = abnormal speed/rhythm when tapping hand with palm/dorsum alternatively
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10
Q

Tremor:

  • Postural Tremor:
  • Action/Intention tremor:
  • Titubation:
A

involuntary, rhythmic oscillation of a body part

  • Postural tremor = tremor that occurs when a limb is held in a particular position (eg. open hands held extended)
    • lesion of ipsilateral lateral hemisphere
  • Action/intention tremor = tremor that occurs when limb is in motion
    • lesion of ipsilateral lateral hemisphere
  • Titubation = tremor of trunk or head
    • lesion of vermis
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11
Q

Ocular dysmetria:

A

**overshoot or undershoot of the eyes as patient focuses on a target **

  • lesion of flocculonodular lobe
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12
Q

Eye movements:

  • Saccades:
  • Slow eye movements:
A

Eye movements:

  • **Saccades: **quick, voluntary movement of eyes onto target
    • mediated by cortex—frontal & parietal eye fields
  • **Slow eye movements: **involuntary movement of eyes
    • mediated by cerebellum, vestibular nuclei & pathways, and extraocular motor nuclei
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13
Q

Nystagmus:

A

rhythmic oscillations of the eyes

  • mediated by cortex
  • an attempt by the cortex to correct abnormal signal to brain
  • deficit of slow eye movements
  • fast-beating phase of eye movements:
    • “right beating nystagmus”—fast phase of eye movements are to the right & slow phase of eye movements to left
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14
Q
  1. What causes a pure vertical nystagmus?
  2. What causes a direction-changing nystagmus?
  3. What causes a horizontal or rotary nystagmus?
A
  1. Pure vertical nystagmus:
    • ALWAYS CNS lesion
  2. Direction-changing nystagmus:
    • CNS lesion
  3. Horizontal or rotatory nystagmus:
    • CNS or PNS lesion
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15
Q

Lesion of vermis/flocculonodular lobe can cause _______, _________, or ______ nystagmus

A

vertical, horizontal, or rotatory

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16
Q
  1. R beating horizontal nystagmus on R gaze, upgaze, downgaze ⇒
  2. R beating horizontal nystagmus on R gaze, L beating horizontal nystagmus on left gaze, vertical nystagmus on upgaze ⇒
A
  1. L VOR or L vestibular nuclear lesion
    • lesion could be CNS or PNS w/ horizontal nystagmus
  2. lesion is likely to be cerebellum or one of its pathways
17
Q
  • Slow saccades:
  • Scanning (ataxic) speech:
  • Hypotonia of ipsilateral limb:
  • Impaired VOR Suppression:
A
  • **Slow saccades: **slowness in eye movements when trying to quickly look at target
  • Scanning (or ataxic) speech: slow, effortful speech with difficulty articulating
    • lesion of lateral hemispheres
  • **Hypotonia of ipsilateral limb: **b/c cerebellum influences corticospinal tracts
    • pt falls to weak side (ipsilateral to lesion)
  • Impaired VOR suppression:
    • ​L VOR activated (i.e. head moving left) ⇒ moves eyes to the right
    • if you want to move head to L and eyes to L ⇒ need to suppress VOR
      • done by the L cerebellum (L flocculonodular)
    • L cerebellar lesion ⇒ no L VOR suppression ⇒ **cannot track movements moving R to L **
18
Q

Lateral Hemispheres:

  • Function:
  • Motor pathway influenced:
  • Deficit if Lesioned:
A
  • **Function: **Motor planning for extremities
  • Motor pathway influenced: LCST
  • **Deficit if lesioned: **Appendicular ataxia
19
Q

Intermediate hemispheres:

  • Function:
  • Motor pathway influenced:
  • Deficit if Lesioned:
A
  • **Function: **Distal limb coordination
  • **Motor pathway influenced: **LCST, rubrospinal tract
  • **Deficit if lesioned: **Appendicular ataxia
20
Q
  1. **Vermis **
    • Function:
    • Motor pathway influenced:
    • Deficit if Lesioned:
  2. Flocculonodular lobe
    • Function:
    • Motor pathway influenced:
    • Deficit if Lesioned:
A
  1. **Vermis **
    • Function: Proximal limb & trunk coordination
    • Motor pathway influenced: VCST, reticulospinal tract, vestibulospinal tract
    • Deficit if Lesioned: Truncal ataxia
  2. Flocculonodular lobe
    • Function: Balance & vestibuloocular reflexes
    • Motor pathway influenced: Medial longitudinal fasciculus
    • Deficit if Lesioned: Nystagmus/slow saccades
21
Q

Differential diagnosis for cerebellar dysfunction:

A
  • Vestibular dysfunction
    • also causes vertigo, difficulty walking, N/V, nystagmus
    • usually no dysmetria or ataxia on finger to nose or heel to shin
  • Corticospinal tract dysfunction
    • ​also causes hypotonia & weakness
    • can be mistaken for ataxia
  • Impaired proprioception
    • these pts have a sensory ataxia
    • Ex: proprioceptive loss in feet makes walking difficult
22
Q

Acute causes for cerebellar dysfunctions:

A
  1. Cerebellar stroke (ischemic or hemorrhagic)
  2. Alcohol intoxication
  3. Drug overdose (eg. phenytoin)
  4. Multiple sclerosis
23
Q

Chronic causes for cerebellar dysfunctions:

A
  1. Essential tremor
  2. Spinocerebellar ataxia
  3. Tumor (eg. astrocytoma)
  4. Chronic alcoholism
24
Q

What can cause a cerebellar stroke?

A

Pathogenesis:

  • main arteries supplying blood: SCA, PICA, AICA
    • diseased due to atherosclerosis
  • penetrating arteries from the main arteries undergo arteriolosclerosis ⇒ blood flow compromised ⇒ ischemic stroke
    • ​from chronic HTN & other vascular risk factors (diabetes, smoking, high cholesterol)
  • severe spike in blood pressure causes brittle vessel to rupture ⇒ hemorrhagic stroke
25
Q

What are some clinical signs & symptoms you expect to see from a cerebellar stroke? How would you localize them?

A
  • Sudden/acute onset
    • within seconds to minutes
    • improves over weeks
  • Symptoms
    • inability to walk and frequent falls, nausea, vomiting, vertigo
  • Signs
    • dysmetria of ipsilateral arm/leg on finger-to-nose & heel-to-shin
    • mild ipsilateral dysdiadochokinesia
    • mild dysarthria
    • horizontal & vertical nystagmus
  • Localization
    • ipsilateral cerebellar hemisphere (lateral & flocculonodular lobes) & vermis
  • Other clues for diagnosis: vascular risk factors
    • HTN, smoking, diabetes, high cholesterol
26
Q

How can you differentiate between chronic and acute alcohol intoxication affecting the cerebellum?

A

One of the most common causes of ataxia

  • Acute symptoms:
    • inability to walk with frequent falls
    • no ‘checking’ of loss of balance
    • slurred speech
    • caused by cerebellar neuronal dysfunction
  • Chronic symptoms:
    • ataxia with walking/maintaining balance
    • difficulty with finger dexterity
    • caused by Purkinje cell destruction & subsequent atrophy of vermis
  • Signs:
    • difficulty walking/tandem gait, dysarthria, dysmetria of limbs, nystagmus
  • Localization:
    • cerebellar vermis
27
Q

What would you expect to see with an essential tremor? How is it localized?

A

Most common movement disorder

  • Usually symmetric, bilateral, postural or action tremor that is persistent & visible:
    • no other cause found
    • usually **autosomal dominant **
    • involves arms/hands, voice, head
    • chronic neurodegenerative disorder
    • gradual loss of Purkinje cells
  • Signs:
    • dysmetria, ataxic gait, head titubation
  • Localization:
    • cerebellar hemispheres & vermis
28
Q

Cerebellar ataxia:

A
  • Group of autosomal dominant ataxic disorders
    • degeneration of afferent & efferent cerebellar pathways
    • destruction of Purkinje cells
  • CAG triplet repeat expansion at different genetic loci
  • Slowly progressive ataxia of limbs/trunk, scanning speech, slowed saccades
  • Profound cerebellar atrophy
  • Higher morbidity & mortality than essential tremor
  • Localization:
    • entire cerebellum
29
Q

Astrocytoma:

A

Most common childhood primary brain tumor

  • low grade tumor composed of astrocytes
  • Localization:
    • tumor usually grows in cerebellar hemisphere
  • Slowly progressive ipsilateral:
    • limb/truncal ataxia, scanning speech, nystagmus due to tumor compressing on adjacent cerebellar parenchyma
  • Signs of increased intracranial pressure
    • ​morning headaches, blurred vision, may culminate in nausea/vomiting, difficulty concentrating in school
  • ↑ICP occurs because of any lesion that takes up space in a closed calvarium
30
Q

What is multiple sclerosis?

A
  • autoimmune/inflammatory disorder affecting CNS white matter
    • Predilection for young (25-40’s), white females
    • Each lesion is referred to as a ‘plaque’
31
Q

Which regions of white matter are attacked in a multiple sclerosis patient?

A

Regions of CNS that are attacked:

  • **Optic nerves **⇒ causes sudden (over 1 day or so) vision loss
    • usually cloudy, hazy, blurry that improves over weeks
    • no double vision
  • Cerebral white matter regions
    • all tracts descending/ascending to cortex
  • Cerebellar white matter
    • especially the middle cerebellar peduncle
  • Medial longitudinal fasciculus
    • mediates eye movements
    • lesion causes internuclear ophthalmoplegia
  • **Spinal cord **⇒ complete or incomplete spinal cord lesion in transverse section affecting ascending/descending tracts
    • called a transverse myelitis

Med Neuro Block 3 (14 decks)

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