BMS11004 WEEK 11 - THURSDAY Flashcards

basal ganglia, cerebellum, Parkinsons, Huntingtons, genes

1
Q

give location of motor cortex

A

telencephalon

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2
Q

location of basal ganglia, and its subcomponents

A

forebrain
cuadate, putamen, globus pallidus, subthalamic nucleus

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3
Q

give location of lateral nucleus of thalamus

A

diencephalon

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4
Q

give location for substantia nigra

A

midbrain

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5
Q

give key components in initiation of movement

A

motor cortex (telencephalon)
basal ganglia (forebrain)
ventral lateral nucleus of thalamus (diencephalon)
substantia nigra (midbrain)

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6
Q

what is motor loop

A

motor cortex connecting to basal ganglia, feedbacks to premotor area via ventrolateral complex of thalamus (VLo) = indirect and direct pathway

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7
Q

what does VLo stand fo

A

ventrolateral complex of Thalamus

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8
Q

detail direct pathway for basal ganglia and motor loop in movement initiation

A

doesnt initiate cortical input, globus pallidus inhibits VLo
inputs from cortex converge on striatum, which inhibits GPi activity and releases VLo to active area 6 which then initiates movement

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9
Q

why is the direct pathway of basal ganglia for movement initiation set up as convergence of cortical input on striatum? what does this allow

A

integrating cortical input to trigger response allows rapidity of response, with “engine running” and inhibition of inhibition releasing “brake”

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10
Q

give an overview of role of indirect pathway of basal ganglia for initiating movement

A

module direct pathway, involves substantia nigra which acts via striatum to maintain balance between inhibiting/activating VLo
and GP external segment

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11
Q

detail indirect pathway for basal ganglia initiating movement

A

SN excitatory input stimulates VLo (by activating GPi inhibition via direct, and GPe inhibiting GPi in indirect which stops it inhibiting VLo)
GPe is inhibited by caudate putamen = VLo inhibitied
SN inhibition decreases GPe inhibition from caudate putamen
this allows GPi inhibition, so activates VLo
so SN balances VLo activation

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12
Q

in the whole GPi, GPe, VLo pathway, where does substantia nigra get info from

A

decision-making, emotive centres involved in risk/reward judgements

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13
Q

what does degeneration in GPi, GPe, VLo circuit cause

A

Parkinsons’/Huntington’s

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14
Q

what does GPe inhibition from caudate putamen cause

A

VLo inhibition

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15
Q

what does VLo activation from SN result from

A

direct= inhibit GPi
indirect= GPe inhibit GPi, which stops it inhibiting VLo

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16
Q

when GPi is inhibited, what does this allo

A

activates VLo

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17
Q

outline incidence of Pakinsons (family, sporadic)

A

10-15% genetic mutation
sporadic for 85-90%

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18
Q

define hypokinesia

A

paucity/insufficiency of movement

19
Q

define bradykinesia

A

very slow movements

20
Q

define akinesia

A

no movement

21
Q

give symptoms of Parkinsons

A

hypok/brady/akinesia
ridigity, resting tremor (4-5Hz)
shuffling gait, bad balance, flexed posture
mask-like expression
mood disorder
lost smell sense

22
Q

where are dopaminergic neurons lost in Parkinsons

A

Substantia Nigra

23
Q

what is degeneration of dopaminergic neurons marked by?

A

presence of Lewy bodies- intracellular protein aggregate

24
Q

how long does L-DOPA work as a treatment

25
how does L-DOPA work, and why not
boosts capacity of remaining dopaminergic neuron, but eventially not enough left
26
give side effects of L-DOPA
increased motor response fluctuation and drug related dyskinesias (erratic movements)
27
what does reduced dopaminergic input from substantia nigra to striatum cause for direct/indirect pathways (Parkinsons)
increased activity of indirect pathway decreased activity of direct pathway
28
Parkinsons- reduced dopamine input from substantia nigra to striatum causes less/more inhibition of GPi, and what does this cause?
less inhibition of GPi = increase inhibitory activites meaning less activity in VLo and less motor cortex activation (causing hypokinesis)
29
what is a pallidotomy
removing GPi for parkinsons this prevents VLo activity decreasing, causing less motor cortex activation
30
how does DBS treat Parkinson
inhibit GPi hyperactivity
31
what is commonness of huntingtons
3-7 per 100,000
32
give symptoms for early Huntingtons
hyperkinesia (overactivity) dyskinesia/chorea (involuntary jerking, twitches)= erratic, discoord movements
33
give symptoms of late Huntingtons
akinesia, dystonia (muscle spasms) dementia personality disorder, psychosis
34
what causes Huntingtons
autosomal dominant gene mutations
35
in early huntingtons neuronal degeneration of indirect pathway, how does this cause hyperkinesis and chorea (including GPi, GPe and VLo)
initially in indirect pathway in striatum, reduced inputs to GPe so increased GPi inhibition, disinhibits VLo = inappropriate movement initiations
36
in later huntingtons neuronal degeneration of direct pathway, how does this cause akinesis (including GPi, GPe and VLo)
in striatal direct pathway GPe degenerate so releases Gpi and overinhibits VLo
37
compare occurance for PD, HD
PD idiopathic, sporadic, common and 10% inherited HD rarely sporadic, rare, inherited
38
compare gene mutations in PD, HD
PD multiple gene mutations with either low and common or high and rare penetrance HD only HTT mutation
39
explain how genetic mutations in HD, PD work
PD encodes proteins for protein degredation, mitochondiral function HD, HTT protein unclear, perhaps in intracellular transport, protein aggregation
40
explain how basal ganglia act as funnel
collects info from prefrontal and motor cortex, decides what info to act on
41
connect cerebellum with motor learning
modulates upper motor neurons, no direct connections to spinal cord needed for learning execution of planned, voluntary, multi-joint movements
42
how does muscle memories form
strengthen existing neural pathways cerebellum form loop with motor cortex using spinal cord, vestibular system project back to motor cortex via thalamus and detects, corrects differences between intended/actual movements
43
what does lesions to cerebellum cause
cerebellar ataxia- poorly integrated movement dysynergia- lose ability to touch nose, coordinate multiple muscles and joints in sequence
44