Basal Ganglia, Cerebellum & Diseases of Motor System Flashcards

1
Q

Describe the basal ganglia

A

no direct input/projections with SC

Input via cerebral cortex
Outputs via thalamic nuclei

encodes start/stop/direction/amplitude/expression of movement

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2
Q

Describe the 4 subcortical nuclei of the basal ganglia

A

Striatum: caudate nucleus/putamen/nucleus accumbens (main input for BG)

Globes pallidus: internal (output nuclei sends GABA to thalamus) and external segment

Substantia nigra: pars reticulata (inhibitory output) and pars compacta (dopaminergic cells to striatum)

Subthalamic nucleus: BG connectivity, pacemaker defines sync/timing of BG outputs

BG: large grey matter masses control thalamus activity

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3
Q

Describe basal ganglia circuitry

A

complex wiring ensures well integrated input from different brain regions, ensures output is regulated

thalamus activity managed via balance of excitatory/inhibitory (tonic) pathways

direct pathway facilitates movement
indirect pathway inhibits movement

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4
Q

Describe the direct pathway

A

releases thalamus from tonic inhibition - voluntary movement
(inhibition of inhibitory GPi neurons)

+ve feedback loop

striatal neurons (D1 dopamine) receive input from dopaminergic neurons from SubNigra enhancing excitation

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5
Q

Describe the indirect pathway

A

increases tonic inhibition of thalamus - suppress movement
(inhibition of inhibitory GPe neurons)

-ve feedback loop

striatal neurons (D2 dopamine) input from SubNigra counters excitatory input, weaker pathway

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6
Q

What are the basal ganglia loops?

A

Motor: skeletomotor/oculomotor loops
Cognitive (prefrontal): higher cortical functions
Limbic: emotion

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7
Q

Describe the cerebellum

A

posterior fossa (10% of brain, 75% of brain neurons); evaluates difference between intended movement/actual motor response subconsciously

maintains balance/coordinates voluntary movements/motor learning/cognition

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8
Q

What are some cerebllar damage effects?

A

Reduced muscle tone
Impaired balance/motor learning
Disrupted spatial accuracy
Disrupted temporal coordination
Impaired cognition

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9
Q

Describe the cerebellum anatomy

A

2 symmetrical cerebellar hemispheres with parallel convolutions (folia) each with 3 lobes separated by fissures

thin outer grey matter, internal white matter

3 grey matter masses (dentate/interposed/fastigal nuclei)

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10
Q

Describe the cerebellar peduncles

A

Superior: somatosensory info to ant. lobe, afferent visual/auditory fibres to post. lobe, efferent from dentate to cerebral motor cortex

Middle: afferent carry voluntary movement info from motor cortex pons to post. lobe
no efferent

Inferior: afferent carry sensory info from vestibular nuclei in brainstem/muscle proprioreceptors via medulla to flocculonodular lobe
efferent carry info back and from vermis to inferior olivary nucleus

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11
Q

Describe the 3 functional regions of the cerebellum

A

Flocculondular lobe: vestibulocerebellum afferent input to lateral vestibular nuclei (balance/eye movement control)

Vermis (mid regions - spine cerebellum): vermis receives sensory input to fastigal nucleus (gaze/posture), mid region receives somatosensory input from limbs to interposed nucleus (limb coordination)

Cerebrocerebellum: input from cerebral cortex via dentate nucleus to PF, M, PM cortices (mental performance of complex motor actions/distal limb coordination)

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12
Q

Describe the microscopic layers of the cerebellum

A

Molecular layer: granule axons form parallel fibres, purkinje cells orient dendritic fields perpendicular to parallel fibres

Purkinje layer: receive input from climbing/parallel fibres, send GABA to deep nuclei (dentate) - inhibitory output

Granule layer: mossy fibres (main input) terminate here, contact granule cells/golgi neurons regulate cerebellar glomeruli (200 granule cells for each mossy fibres)

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13
Q

Describe 2 input sources for the cerebellum

A

Mossy fibres (SC/brainstem nuclei): excitatory connections to granule cell dendrites - parallel fibres - purkinje cell action potential

Climbing fibres (inferior olivary nucleus): around purkinje neurons; depolarises them/complex spike

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14
Q

Explain long-term depression

A

Climbing fibres reduce parallel fibre input to purkinje creating depression in synapses between them via calcium influx

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15
Q

Explain myasthenia gravis

A

signal transmission failure at neuromuscular junction
autoimmune cause, congenital cause, inherited
reduced ACh receptors/muscle activation

abnormal muscle fatigue, remission, relapse

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16
Q

Explain Guillain-Barré Syndrome

A

autoimmune disorder with rapid onset of muscle weakness where immune system damages peripheral nervous system (myelin sheaths of lower motor neuron axons)

treated with plasmapheresis/iv administration of immunoglobulins reducing antibodies effecr

17
Q

Describe features of lower/upper moptom neuron disease

A

Lower: muscle weakness/atrophy, decreased muscle tone/tendon reflexes, muscle twitch/fasciculations

Upper: muscle weakness (little atrophy/paralysis), increased tendon reflexes/muscle tone
Babinski reflex

18
Q

Which tests distinguish neurogenic/myopathic diseases?

A

Clinic observations: distribution of muscle weakness, muscle pain/twitch

Blood/urine for soluble enzyme (myoglobin)
Electromyography
Nerve conduction studies
Muscle biopsy
DNA studies

19
Q

What are some symptoms of cerebellar disorders?

A

Cerebellar hypotonia
Dysmetria
Ataxia
Dysdiadochokinesia
Scanning speech
Nystagmus
Intention tremor

20
Q

Describe Parkinson’s

A

hypokinetic disorder (dementia)

resting tremor, akinesia, stiffness, slow movement (bradykinesia)
Unstable posture/walking/balance

substantia nigra death:
less dopaminergic input, under active direct/overactive indirect pathway
increased GPi output suppressed thalamus/movement (treated with L-dopa)

21
Q

Explain ballistic (hyperkinetic basal ganglia disorder)

A

damage to STN reduces GPi excitation/thalamus inhibition
excessive motor cortex activation
Dyskinesia (ballistic)
treat with DA receptor antagonists

22
Q

Explain Huntington’s disease

A

inherited autosomal dominant disorder
striatal death (mainly indirect pathway(

Reduced GPe inhibition
Increased STN inhibition
GPi under activated
Thalamus under inhibited

Motor cortex over activated
Dyskinesia (chorea)
Treat with DA receptor antagonists