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Neuro III > Cerebellum and Basal Ganglia > Flashcards

Cerebellum and Basal Ganglia Flashcards

1
Q

What brain structure carries the major outputs from the cerebellum?

A

Superior cerebellar peduncle

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2
Q

What structures carry the major inputs to the cerebellum?

A

Middle and inferior cerebellar peduncles

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3
Q

What is the connectivity of the flocculo-nodular lobe (archicerebellum)

A

aka: vestibulocerebellum. inputs from vestibular organs, outputs to vestibular nucleus in the brainstem

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4
Q

What is the connectivity of the vermal and paravermal corticies (paleocerebellum)?

A

aka: spinocerebellum. inputs from spinal afferents. Outputs to motor control nuclei (eg: red nucleus)

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5
Q

What is the connectivity of the corticocerebellum (neocerebellum)?

A

Located on the lateral aspects of cerebellum, these regions are interconnected with the CEREBRAL corticies

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6
Q

The vermal zone extends outputs through which nucleus?

A

fastigial nucleus –> control of axial musculature, posture and balance, integration of head and eye movement

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7
Q

The paravermal zone extends outputs through which nuclei?

A

interposed nuclei –> fine-tuned movement of limbs

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8
Q

What is the functional role of the flocculo-nodular lobe?

A

axial control and vestibular reflex (balance and eye movement)

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9
Q

What is the functional role of the neocerebellum?

A

projections via dentate nucleus –> higher-level coordination of movement

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10
Q

What is the output connectivity of the medial (vermis and vestibulocerebellum) regions of the deep cerebellar nuclei?

A

Vermis –> fastigial nucleus –> bilateral vestibular nucleus and pontine reticular formation –> lateral vestibulospinal tract and pontine reticulospinal tract (equilibrium and posture)

Vestibulocerebellum –> vestibular nucleus of the BRAIN

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11
Q

What is the output connectivity of the lateral (paravermis and neocerebellum) regions of the cerebellar deep nuclei?

A

Paravermis –> interposed nuclei –> contralateral red nucleus –> motor output through rubrospinal tract (lateral descending system)

Neocerebellum –> dentate nucleus –> contralateral VL thalamus –> M1 and pre-motor cortex

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12
Q

Where in the cerebellum do vestibular inputs go?

A

flocculo-nodular lobe (vestibulocerebellum)

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13
Q

Where in the cerebellum do spinal inputs go?

A

vermal and paravermal portions

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14
Q

What is the primary afferent input in the neocerebellum?

A

There is none! Contralateral cortex crosses and synapses in pontine nuclei –> lateral cerebellum

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15
Q

From what side do deficits arise upon cerebellar damage?

A

ipsilateral! (sensory/descending cerebellar inputs are uncrossed; corticocerebellar tracts decussate, therefore right cerebellum = right side of body = left cortex)

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16
Q

How does a large cerebellar lesion present?

A

ipsilateral loss of coordination, with spared sensation and muscle strength

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17
Q

What is the mnemonic for symptoms of cerebellar lesions?

A 
HANDS Tremor!
Hypotonia
Ataxia (3D's: dysdiadochokinesia, decomposition of movement, dysmetria)
Nystagmus
Dysarthria
Stance and gait problems
Tremor
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18
Q

What is dysdiadochokinesia?

A

impairment of rapid, alternating movements

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19
Q

What is dysmetria?

A

inability to bring a limb to required/desired point in space (past-pointing)

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20
Q

Describe the cellular constituents of the uppermost layer of cerebellar cortex

A

parallel fibers, dendrites of Purkinje cells, Stellate cells, and basket cells

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21
Q

Describe the cellular constituents of the middle layer of cerebellar cortex

A

bodies of Purkinje cells

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22
Q

Describe the cellular constituents of the lowest layer of cerebellar cortex

A

Granule cells (processes extend superficially to become parallel fibers of top layer)

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23
Q

How does information flow through cerebellar cortex?

A

Climbing fibers and mossy fibers

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24
Q

What is the connectivity of climbing fibers?

A

Input from CONTRALATERAL inferior olivary nucleus. Output to Purkinje cells

25
Q

What is the connectivity of mossy fibers?

A

Receives all input not carried by climbing fibers (mostly vestibular afferents and pontine nuclear cells). Output: granule cells –> parallel fibers –> purkinje cell excitation

26
Q

What are the only cells in cerebellar cortex that do NOT make inhibitory connections with target neurons?

A

granule cells

27
Q

What is the function of basket and stellate cells?

A

inhibition of Purkinje cells –> disinhibition of deep cerebellar neurons –> increased firing rate of deep cerebellar neurons

28
Q

What is the function of golgi cells?

A

feedback inhibition of granule cells

29
Q

Describe the climbing fiber activity when presented with intense, novel motor movement

A

climbing fibers activate purkinje cells –> numerous complex spikes in Purkinje activity

30
Q

Describe the climbing fiber activity as the movement is learned

A

complex spikes from purkinje cells stop; replaced by simple spikes from mossy fibers, which fire at lower frequency

31
Q

What structure senses discrepancies between planned and actual motor performance?

A

inferior olive

32
Q

What is the significance of long term depression in the cerebellum

A

Occurs after climbing fiber activation when learning a new motor movement. Leads to decreased sensitivity to mossy fiber input (lower frequency of simple stroke)

33
Q

Describe the cascade leading to LTD

A

Climbing fiber activation –> VSCC activation on Purkinje fibers –> Ca influx –> LTD

34
Q

How are parallel fibers involved in motor learning?

A

Release glutamate –> AMPA binding (depolarization of Purkinje cells); metabotropic receptor binding (PKC activation)

35
Q

Nearly all non-traumatic, metabolic disruption of motor control involves:

A

basal ganglia dysfunction

36
Q

80% of the brain’s dopamine levels reside in:

A

the basal ganglia

37
Q

what is the result of a unilateral basal ganglia deficit?

A

contralateral functional deficit

38
Q

What is the major input source for basal ganglia

A

cerebral cortex

39
Q

What is the major output source of the basal ganglia?

A

globus pallidus

40
Q

From the globus pallidus, where does information about motor function travel?

A

VA and VL of the thalamus

41
Q

From globus pallidus, where does cognitive and associational travel through?

A

DM thalamus

42
Q

Are the basal ganglia inhibitory or excitatory?

A

Inhibitory

43
Q

What are characteristic features of Parkinson’s disease?

A

Increased tone (simultaneous activation of flexors/extensors), bradykinesia, resting tremor

44
Q

What is the probable cause of Parkinson’s disease?

A

Loss of dopamine neurons in substantia nigra –> reduced disinhibition on thalamus (bradykinesia), tremor

45
Q

What is the treatment of Parkinson’s disease?

A

levodopa –> maximal dopamine output of remaining dopaminergic neurons –> diminuation of symptoms

Carbidopa blocks degradation of levodopa

46
Q

What is hemiballismus?

A

Unilateral flailing movements of arms/legs

47
Q

How would stroke in the subthalamic nucleus cause hemiballismus?

A

Stroke in PCA –> unilateral subthalamic nucleus damage –> reduced inhibitory outflow of globus pallidus –> disinhibited thalamus –> hemiballismus

48
Q

What is the indication for use of deep brain stimulation in patients with Parkinson’s disease?

A

patients who still benefit from meds, but have debilitating on/off episodes

49
Q

What is the mechanism of action of DBS in Parkinson’s disease?

A

DBS –> hyperpolarization of subthalamic nucleus or globus pallidus interna –> regained inhibition of globus pallidus –> disinhibition of thalamus –> attenuated bradykinesia, decreased tone

50
Q

What is the genetic cause of Huntington’s disease?

A

autosomal dominant mutation of chromosome 4 –> increased CAG repeats

51
Q

What is the average age of onset of Huntington’s disease?

A

Age 30-50

52
Q

What would be considered early onset Huntington’s disease?

A

Before age 20

53
Q

What basal ganglia areas are involved in Huntington’s disease

A

Striatum. Contains cholinergic and GABAergic neurons. Glutamate exicitotoxicity leads to cell death. Loss of striatal action on globus pallidus externa (indirect pathway) leads to Huntington’s chorea

54
Q

Relationship between globus pallidus and subthalamic nucleus

A

Subthalamic nucleus: inhibitory input from GP; excitatory output to GP

55
Q

Dopamine effect on striatum

A

excitation. Decrease DA –> decreased inhibition of GP –> increased inhibition of thalamus –> parkinson’s symptoms

56
Q

Describe the indirect pathway of movement

A

motor cortex –> glutamate release to striatum –> GABA to globus pallidus externa –> disinhibition of subthalamic nucleus –> glutamate to globus pallidus interna –> GABA to thalamus –> inhibition of thalamic excitation to motor cortex –> decreased muscle movement

57
Q

What is the result of indirect pathway dysfunction?

A

dyskinesias (eg: tardive dyskinesia, Huntington’s disease)

58
Q

Describe the direct pathway of movement

A

motor cortex –> glutamate to striatum –> GABA to globus pallidus interna and substantia nigra pars reticulata –> disinhibition of thalamus –> glutamate to motor cortex –> increased movement

59
Q

What is the result of dysfunction of direct pathway of movement?

A

decreased movement (eg: parkinson’s)

Neuro III (17 decks)

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