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

A

5 years

25
Q

how does L-DOPA work, and why not

A

boosts capacity of remaining dopaminergic neuron, but eventially not enough left

26
Q

give side effects of L-DOPA

A

increased motor response fluctuation and drug related dyskinesias (erratic movements)

27
Q

what does reduced dopaminergic input from substantia nigra to striatum cause for direct/indirect pathways (Parkinsons)

A

increased activity of indirect pathway
decreased activity of direct pathway

28
Q

Parkinsons- reduced dopamine input from substantia nigra to striatum causes less/more inhibition of GPi, and what does this cause?

A

less inhibition of GPi = increase inhibitory activites meaning less activity in VLo and less motor cortex activation (causing hypokinesis)

29
Q

what is a pallidotomy

A

removing GPi for parkinsons
this prevents VLo activity decreasing, causing less motor cortex activation

30
Q

how does DBS treat Parkinson

A

inhibit GPi hyperactivity

31
Q

what is commonness of huntingtons

A

3-7 per 100,000

32
Q

give symptoms for early Huntingtons

A

hyperkinesia (overactivity)
dyskinesia/chorea (involuntary jerking, twitches)= erratic, discoord movements

33
Q

give symptoms of late Huntingtons

A

akinesia, dystonia (muscle spasms)
dementia
personality disorder, psychosis

34
Q

what causes Huntingtons

A

autosomal dominant gene mutations

35
Q

in early huntingtons neuronal degeneration of indirect pathway, how does this cause hyperkinesis and chorea (including GPi, GPe and VLo)

A

initially in indirect pathway in striatum, reduced inputs to GPe so increased GPi inhibition, disinhibits VLo = inappropriate movement initiations

36
Q

in later huntingtons neuronal degeneration of direct pathway, how does this cause akinesis (including GPi, GPe and VLo)

A

in striatal direct pathway GPe degenerate so releases Gpi and overinhibits VLo

37
Q

compare occurance for PD, HD

A

PD idiopathic, sporadic, common and 10% inherited
HD rarely sporadic, rare, inherited

38
Q

compare gene mutations in PD, HD

A

PD multiple gene mutations with either low and common or high and rare penetrance
HD only HTT mutation

39
Q

explain how genetic mutations in HD, PD work

A

PD encodes proteins for protein degredation, mitochondiral function
HD, HTT protein unclear, perhaps in intracellular transport, protein aggregation

40
Q

explain how basal ganglia act as funnel

A

collects info from prefrontal and motor cortex, decides what info to act on

41
Q

connect cerebellum with motor learning

A

modulates upper motor neurons, no direct connections to spinal cord
needed for learning execution of planned, voluntary, multi-joint movements

42
Q

how does muscle memories form

A

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
Q

what does lesions to cerebellum cause

A

cerebellar ataxia- poorly integrated movement
dysynergia- lose ability to touch nose, coordinate multiple muscles and joints in sequence

44
Q
A