2.5 Principles of Cerebellar Disease Flashcards

1
Q

Explain cerebellar anatomy.

A

a part of the brain that modulates the RATE, RANGE, and FORCE of movement via modulation of signals reaching UMN

  • small: comprises 10% of the brain’s volume, but contains over 50% of its neurons
  • located in caudal cranial fossa
  • separated from forebrain by the osseous tentorium
  • 1 midline vermis: divided into 9 lobules
  • 2 cerebellar hemispheres (one on either side of the vermis)
  • primary fissure separates rostral and caudal lobe
  • surface is folded into FOLIA
  • peduncles connect cerebellum to brainstem and act as a conduit for afferent/efferent fibers
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2
Q

What is the difference between white and gray matter in the cerebellum?

A

cerebellar white matter forms the center of the cerebellum

  • white lamina extends into each folia, forming the arbor vitae, or the “tree of life”
  • the cerebellar MEDULLA is the ‘trunk’ of this tree

cerebellar grey matter is the outermost layer of the cerebellum, and is also called the CORTEX

the cerebellar cortex is made up of three layers:
1. molecular layer (outtermost)
2. purkinje cell layer: all efferent signals leave via the purkinje layer!
3. granule cell layer

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3
Q

What are the three functional zones of the cerebellum?

A
  1. pontocerebellum: cerebellar hemispheres and mid-vermis
  2. spinocerebellum: vermis and paraflocculus
  3. vestibulocerebellum: flocculonodular lobe
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4
Q

What do the functional zones of the cerebellum control?

A
  1. pontocerebellum: fine, skilled movement
  2. spinocerebellum: limb movement and gait
  3. vestibulocerebellum: balance and posture
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5
Q

What are the most common signs of cerebellar dysfunction?

A
  1. cerebellar ataxia
  2. wide based stance
  3. hypertonia (spasticity)
  4. decerebellate posture
  5. intention tremor
  6. abnormal menace response
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6
Q

What are the three forms of ataxia?

A

(1) PROPRIOCEPTIVE

  • disruption of proprioceptive information reaching the brain for processing and perception
  • animal is effectively less aware/unaware of its feet and limb position
  • results in an inconsistent stride length and inconsistent foot placement
  • most commonly seen with spinal cord diseases (often also paretic as a lesion that disrupts ascending proprioceptive information also disrupts descending motor information)

(2) VESTIBULAR

  • loss of equilibrium leads to head tilt, leaning/falling to the side, turning in tight circles
  • typically a very lateralized ataxia
  • “drunken” appearance to movement/gait

(3) CEREBELLAR

  • inability to regulate rate, range and force of movement, aka DYSMETRIA
  • most commonly, HYPERMETRIA is seen: increased rate, range, and force
  • animals make jerky, sudden, excessive movements that have a burst-like quality
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7
Q

What is hypertonia?

A

increased muscle tone
- often seen in animals with cerebellar disease due to loss of inhibition of UMNs and loss of inhibition of muscle spindles
- excessive extensor tone

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8
Q

What is decerebellate posture?

A

due to a lesion in the rostral lobe of the cerebellum

  • forelimbs locked in extension
  • hindlimbs locked in flexion under body
  • opisthotonos
  • CONSCIOUS mental status

note: different from decerebrate and schiff-sherrington posture

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9
Q

What is an intention tremor?

A
  • arises due to failure to coordinate activity of agonist and antagonist muscles acting around a joint
  • the muscles effectively fight each other causing the joint to oscillate
  • classically a fine head and neck tremor
  • becomes increasingly apparent during goal-orientated movement (e.g., reaching for food or a toy)
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10
Q

Is paresis a feature of cerebellar disease?

A

paresis (muscle weakness: partial paralysis) is NOT a feature of cerebellar disease

  • remember that the cerebellum does not activate LMNs, it purely regulates the UMNs, modulating their stimulation of the LMNs
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11
Q

Why is the menace response abnormal in some cases of cerebellar disease?

A
  • the menace response pathway synapses in the cerebellar cortex
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12
Q

What some common conditions affecting the cerebellum?

A

cerebellar cortical degeneration:

  • postnatal neurodegeneration
  • largely affects cerebellar cortex
  • symmetrical, progressive cerebellar ataxia
  • recognized in various breeds including Gordon setters and Old English sheepdog
  • no treatment available

ischemic infarct:

  • infarction of the right or left rostral cerebellar artery (RCA)
  • peracute onset of lateralized cerebellar signs
  • MRI reveals a characteristic, well-demarcated hyperintensity in the vascular territory of RCA
  • 50% of dogs will have an underlying disease (e.g., chronic renal disease, hypertension, endocrine disease)
  • often improve with conservative treatment, and addressing the underlying cause (where identified)

neospora caninum:

  • intracellular protozoan parasite
  • in adult dogs, it can cause a severe diffuse cerebellitis with secondary cerebellar atrophy, myositis
  • DIAGNOSIS: serology to detect antibodies to Neospora, MRI, CSF analysis
  • TREATMENT: Clindamycin or Trimethoprim sulphonamides (3-4 week course)
  • clinical signs usually improve with treatment
  • permanent neurological deficits possible, and relapses may occur
  • MRI(?) shows bright white layer surrounding cerebellum: it has atrophied and CSF has filled the space
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