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Neuro > Cerebellum B&B > Flashcards

Cerebellum B&B Flashcards

1
Q

describe the anatomical parts of the cerebellum

A

middle = vermis (“worm”)

2 lateral hemispheres

anterior lobe + posterior lobe + flocculonodular lobe (inferior)

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2
Q

what are the cerebellar peduncles?

A

peduncles = in/out pathways

  1. inferior cerebellar peduncle = INPUT
  2. middle cerebellar peduncle = INPUT
  3. superior cerebellar peduncle = OUTPUT
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3
Q

what is carried by the inferior cerebellar peduncle?

A

major pathway INTO the cerebellum from the SPINE, carrying ipsilateral proprioception information

from, for ex - spinocerebellar tract, cuneocerebellar tract, olivocerebellar tract, vestibulocerebellar tract

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4
Q

which cerebellar peduncle does this describe:

major pathway INTO the cerebellum from the spine, carrying ipsilateral proprioception information

A

inferior cerebellar peduncle

from, for ex - spinocerebellar tract, cuneocerebellar tract, olivocerebellar tract, vestibulocerebellar tract

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5
Q

what is carried by the middle cerebellar peduncle?

A

carries CONTRALATERAL pontocerebellar tract fibers INTO the cerebellum

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6
Q

which cerebellar peduncle carries contralateral pontocerebellar tract fibers into the cerebellum?

A

middle cerebellar peduncle

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7
Q

climbing vs mossy fibers

A

2 types of axons which ENTER the cerebellum

climbing fibers: arise from inferior olivary nucleus

mossy fibers: all other cerebellar inputs (lots of branches = mossy)

both synapse on Purkinje cells and deep nuclei of cerebellum

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8
Q

what is carried by the superior cerebellar peduncle?

A

major OUTPUT of cerebellum, carrying axons from deep cerebellar nuclei (from which ALL cerebellar outputs originate)

carry fibers to red nucleus and thalamus, which help modulate movement

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9
Q

which cerebellar peduncle does this describe: major OUTPUT of cerebellum, carrying axons from deep cerebellar nuclei to red nucleus and thalamus

A

superior cerebellar peduncle: major OUTPUT of cerebellum, carrying axons from deep cerebellar nuclei (from which ALL cerebellar outputs originate)

carry fibers to red nucleus and thalamus, which help modulate movement

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10
Q

what is the function of the Purkinje cells of the cerebellum?

A

cerebellar neurons which receive many inputs and project to the deep nuclei with INHIBITORY GABA to modify movements

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11
Q

what is the respective function of the 4 deep nuclei of the cerebellum?

A

send axon projections OUT of the cerebellum

  1. dentate nucleus (most lateral) - to contralateral ventral anterior and ventral lateral nuclei of thalamus

2,3. interposed nuclei (globose + emboliform) - to contralateral red nucleus

  1. fastigial (most medial) - to vestibular nuclei and reticular formation
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12
Q

to where do each of the deep nuclei of the cerebellum send their axons?
1. dentate nucleus
2/3. interposed nuclei (globose + emboliform)
4. fastigial

A
  1. dentate nucleus (most lateral) - to contralateral ventral anterior and ventral lateral nuclei of thalamus
    2/3. interposed nuclei (globose + emboliform) - to contralateral red nucleus
  2. fastigial (most medial) - to vestibular nuclei and reticular formation
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13
Q

are symptoms of lesions to the cerebellum ipsilateral or contralateral? explain.

A

IPSILATERAL (left lesion = left symptoms)

some cerebellar fibers influence contralateral cortex, but efferent motor fibers cross over at decussation, so double crossover = ipsilateral effect

also proprioception is ipsilateral already

so basically everything is ipsilateral !

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14
Q

how do lateral vs midline lesions of the cerebellum differ?

A

lateral lesions: damage cerebellar hemispheres + dentate nucleus (most lateral deep nuclei), affect EXTREMITIES (direction, force, speed, amplitude of movement)

midline lesions: damage vermis, emboliform nucleus, globus nucleus, fastigial nucleus, floculonodular lobe, affect TRUNK/MIDLINE

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15
Q

how do lateral lesions of the cerebellum present? (3)

A

lateral lesions: damage cerebellar hemispheres + dentate nucleus (most lateral deep nuclei), affect EXTREMITIES (direction, force, speed, amplitude of movement)

—> dysmetria (failed finger to nose)
—> intention tremor
—> fall towards affected side

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16
Q

how do midline lesions of the cerebellum present? (2)

A

midline lesions: damage vermis, emboliform nucleus, globus nucleus, fastigial nucleus, floculonodular lobe, affect TRUNK/MIDLINE

—> truncal ataxia (can’t stand/ sit straight, due to damage to vermis)
—> nystagmus, vertigo (due to damage to flocculonodular lobe, which connects to vestibular nuclei)

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17
Q

what kind of gait will patients with any kind of lesion to the cerebellum have?

A

“wide-based” gait due to cerebellar ataxia and loss of balance

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18
Q

what is the Romberg Test used for?

A

tests for sensory ataxia - by making patient stand with their eyes closed, there is loss of compensation through vision

losing balance = positive test for sensory ataxia

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19
Q

how will patients with cerebellar ataxia do with the Romberg test?

A

patients with cerebellar ataxia will be off balance WITH OR WITHOUT their eyes closed because vision is not enough to compensate !!

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20
Q

hypotonia + scanning speech + dyssyngergia = what kind of lesion?

A

cerebellar symptoms

[dyssynergia = loss of coordinated movement]

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21
Q

name 3 ways in which dyssynergia can manifest (loss of coordinated movement)

A
  1. dysmetria: under or over-shoot intended position of hand (finger to nose)
  2. intention tremor: can’t get hand to target [contrast with resting tremor of Parkinson’s]
  3. dysdiadochokinesia: can’t make rapid changes of motion (flipping hand over and over)
22
Q

resting tremor =
intention tremor =

A

resting tremor = Parkinson’s, damage to basal ganglia (can’t inhibit movement)

intention tremor = cerebellar syndrome (can’t coordinate fine movement)

23
Q

what type of nystagmus will occur in patients with lesion to the cerebellum?

A

up/down beat aka vertical nystagmus

can also see gaze-evoked nystagmus (movement of eyes in gazing in one direction or another)

24
Q

what is the blood supply to the cerebellum? aka, where would strokes occur? (3)

A
  1. superior cerebellar artery (SCA)
  2. anterior inferior cerebellar artery (AICA)
  3. posterior inferior cerebellar artery (PICA)
25
Q

ataxia telangiectasia (AT) and Friedreich’s Ataxia are both examples of what kind of disease, affecting which part of the brain?

A

autosomal recessive hereditary ataxias affecting motor coordination of the cerebellum

26
Q

how does ataxia telangiectasia present? (4) what is the hereditary pattern?

A

autosomal recessive hereditary ataxia affecting the cerebellum

  1. cerebellar atrophy (1st year of life)
  2. telangiectasias (dilation of capillary vessels on skin of ears, nose, face, neck)
  3. sinus/respiratory infections (severe immunodeficiency)
  4. high risk of cancer!! (defective ATM gene for dsDNA NHEJ repair)
27
Q

Pt presents to their GP with a sinus infection. PMH includes progressive ataxia that began ~1 year old, with use of a wheelchair by age 10. PE reveals capillary dilations under the skin of the face and neck. What is the long-term prognosis of this patient?

A

ataxia telangiectasia: autosomal recessive hereditary ataxia affecting cerebellum

high risk of cancer!! over time

cause is defective ATM gene (ch. 11) needed to repair dsDNA breaks (NHEJ) —> DNA hypersensitivity to ionizing radiation

28
Q

what is the cause of ataxia telangiectasia?

A

autosomal recessive hereditary ataxia affecting the cerebellum, caused by defective ATM gene (ch. 11) needed for dsDNA repair break via non-homologous end joining (NHEJ)

  1. cerebellar atrophy (1st year of life)
  2. telangiectasias (dilation of capillary vessels on skin of ears, nose, face, neck)
  3. sinus/respiratory infections (severe immunodeficiency)
  4. high risk of cancer!! (DNA hypersensitivity to ionizing radiation)
29
Q

what 2 abnormal lab findings are present in patients with ataxia telangiectasia (AT)?

A

[due to defective ATM gene (ch. 11) for NHEJ]

  1. increased AFP (alpha-fetoprotein)
  2. dysgammaglobulinemia - usually low or absent IgA
30
Q

what is the cause of Friedreich’s Ataxia? what is the hereditary pattern?

A

autosomal recessive hereditary ataxia affecting the cerebellum

mutation in frataxin gene (ch. 9) encoding mitochondrial protein (frataxin) —> trinucleotide repeat (GAA) leads to decreased protein levels

abnormal frataxin —> mitochondrial dysfunction, normally present in high levels in brain/heart/pancreas

31
Q

what is the trinucleotide repeat of Friedreich’s Ataxia?

A

GAA

autosomal recessive hereditary ataxia affecting the cerebellum

mutation in frataxin gene (ch. 9) encoding mitochondrial protein (frataxin) —> trinucleotide repeat (GAA) leads to decreased protein levels

abnormal frataxin —> mitochondrial dysfunction, normally present in high levels in brain/heart/pancreas

32
Q

which spinal cord tracts degenerate in Friedreich’s Ataxia? (3)

A

AR trinucleotide repeat (GAA) causing decreased production of mitochondrial frataxin protein

  1. spinocerebellar tract —> ataxia, dysarthria
  2. dorsal columns —> loss of position/ vibration
  3. corticospinal tract —> UMN weakness in lower extremities
33
Q

what are the extra-CNS features of Friedreich’s Ataxia? (4)

A

AR trinucleotide repeat (GAA) causing decreased production of mitochondrial frataxin protein, which is normally in high levels in brain/heart/pancreas

  1. hypertrophic cardiomyopathy
  2. diabetes (via beta cell dysfunction)
  3. kyphoscoliosis
  4. pes cavus (high arch foot abnormality)
34
Q

what are 3 types of tumors that can involve the cerebellum?

A
  1. pilocytic astrocytoma
  2. medulloblastoma
  3. ependymoma
35
Q

what are the respective functions of the cerebrocerebellum, spinocerebellum, and vestibulocerebellum?

A
  1. Lateral hemispheres (cerebrocerebellum): Motor planning/learning + cognitive functions
  2. Vermis and intermediate parts (spinocerebellum): The coordination of ongoing voluntary movement
  3. Flocculonodular lobe (vestibulocerebellum): Maintenance of balance and posture (eye movement)
36
Q

which 2 tracts send input to the cerebellum via the inferior cerebellar peduncle? what do they each carry specifically?

A
  1. dorsal spinocerebellar tract: leg proprioceptors originating in nucleus dorsalis of Clark found in C8-L3 (ipsilateral)
  2. cuneocerebellar tract: arm proprioceptors originating in external cuneate nucleus found in medulla (ipsilateral)
37
Q

what input do climbing fibers provide to the cerebellum via the inferior cerebellar peduncle?

A

input from red nucleus, cortex, brainstem, spinal cord via inferior olivary nucleus

38
Q

what are the cellular layers of the cerebellum?

A
  1. molecular (outermost): stellate cells + basket cells
  2. Purkinje cells
  3. granular layer (innermost): granule cells + Golgi cells
39
Q

what are the 5 types of cells found in the cerebellum, what NT do they use, and which type is the only kind to provide outflow from the cerebellar cortex?

A
  1. Golgi cells - GABA
  2. Stellate cells - GABA
  3. Basket cells - GABA
  4. granule cells - glutamate (only excitatory cells, project onto Purkinje cells via parallel fibers)
  5. Purkinje cells - GABA, only output

[cerebellar input is excitatory, but output is inhibitory!]

40
Q

function of climbing vs mossy fibers

A

both excitatory (glutamate)

mossy fibers synapse on granule cells (which then synapse on Purkinje cells with glutamate), arriving from spinocerebellar + pontocerebellar + vestibulocerebellar nuclei

climbing fibers (olivocerebellar fibers) synapse directly on Purkinje cells, arriving from inferior olivary nucleus (via inferior cerebellar peduncle) - important for motor learning

41
Q

contrast function of vermis vs lateral cerebellar hemispheres vs flocculonodular lobe

A
  1. Vermis: smoothing ongoing motor movement, Input mostly arriving from spinal cord (originated from muscle spindles and Golgi tendon organs)
  2. Lateral hemispheres: motor planning/learning/coordination, Input mostly arriving from inferior olivary nucleus and indirectly from cerebral cortex via pontine nuclei
  3. Flocculonodular lobe: balance and eye movements, Input mostly arriving from CN VIII (vestibular part)
42
Q

what symptoms present with cerebellar lesion? (hint: mnemonic)

A

DANISH:
Dysdiadochokinesis, Dysmetria
Ataxia
Nystagmus
Intention tremor
Scanning speech
Hypotonia

43
Q

which anti-epileptic can cause bilateral cerebellar dysfunction?

A

carbamazepine

44
Q

____ gene deletions and duplications are associated with cerebral vermis hypoplasia, mega cisterna magna, and Dandy-Walker malformation

A

FOXC1

45
Q

congenital failure of cerebellar vermis to develop + agenesis of corpus callosum presenting with massively dilated 4th ventricle and reduced cerebellum, often accompanied by hydrocephalus

A

Dandy-Walker malformation

46
Q

Dandy-Walker malformation

A

congenital failure of cerebellar vermis to develop + agenesis of corpus callosum presenting with massively dilated 4th ventricle and reduced cerebellum, often accompanied by hydrocephalus

47
Q

Chiari I malformation

A

Congenital downward displacement of cerebellar tonsils and the medulla through the foramen magnum.

This lesion is mostly asymptomatic but frequent association with syringomyelia

48
Q

Chiari II malformation

A

Congenital downward displacement of cerebellar vermis, tonsils and medulla through the foramen magnum.

Obstruction of cerebrospinal fluid flow commonly results in obstructive hydrocephalus. May manifest as papilledema and projectile vomiting (due to area postrema in lateral wall of 4th ventricle)

Often also associated with lumbar meningomyelocele (meninges and neural tissue (eg, cauda equina) herniate through bony defect)

49
Q

where does the most common benign CNS tumor in children most commonly arise?

A

pilocytic astrocytoma: most commonly in cerebellum, GFAP positive

well-differentiated/benign tumor of astrocytes, imaging shows cystic lesion with mural nodule, biopsy shows Rosenthal fibers (thick, cork-screw processes of astrocytes)

commonly associated with activated mutation in BRAF, favorable prognosis

50
Q

from where is the most common malignant CNS tumor in children derived?

A

medulloblastoma: derived from granular cells of cerebellum (neuroectoderm origin)

histology shows small/round blue cells + Homer-Wright rosettes (also seen in neuroblastoma)

grows rapidly, spreads via CSF, poor prognosis

51
Q

Cerebellar hemisphere lesions produce symptoms [ipsilateral/contralateral] to the lesion.

Unilateral cerebellar lesion will cause patient to fall [towards/away from] the lesion side

A

Cerebellar hemisphere lesions produce symptoms ipsilateral to the lesion.

Unilateral cerebellar lesion will cause patient to fall towards the lesion side

52
Q

compare presentations of: anterior cerebellar lobe syndrome vs posterior vermis syndrome vs flocculonodular (vestibulocerebellar) lobe syndrome

A

anterior lobe syndrome: general ataxia + gait ataxia (legs > arms affected) + broad-based, staggering gait

posterior vermis syndrome: truncal ataxia (severe hypotonia) + dysmetria

flocculonodular lobe syndrome: truncal ataxia + nystagmus

Neuro (50 decks)

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