Lecture 9: Motor Control, Basal Nuclei, and Cerebellum Flashcards

1
Q

function/purpose of thalamus

A

relay center for all functions of nervous system

functional integration

consists of multiple nuclei and projects to different cerebral corex

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2
Q

Where does the anterior thalmic nuclei project to

A

limbic lobe

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3
Q

where does the VA nucleus project to

A

SMA and other parts of frontal lobe

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4
Q

where does the VL nucleus get info from

A

substantia nigra input

oral part = PM, mainly from basal nuclei

caudal part = M1, mainly from cerebellum

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5
Q

function of centromedian nucleus

A

gate keeper of thalamus

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6
Q

where does the dorsal medial nucleus project to

A

limbic system

emotion

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7
Q

purpose of common projectsions with other thalamic nuclei

A

modulating functions

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8
Q

parts of the basal nuclei that develop from telencephalon

A

caudate
nucleus accumbens
putamen
globus pallidus
- external/lateral segment
- internal/medial segment

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9
Q

part of basal nuclei that develops from diencephalon

A

subthalamic nucleus

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10
Q

part of basal nuclei that develops from mesencephalon/midbrain

A

substantia nigra
- pars compacta (posterior)
- pars reticulata (anterior)

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11
Q

general functions fo the basal nuclei

A

psychomotor functions
- aka extrapyramidal motor system: name is misleading but still under use; not directly in motor functions

  • modulating motor loops for planning, coordinaiton, and execution (i.e. body movement loop and oculomotor loop)

cognition

emotion

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12
Q

the basal nuclei recieves afferent info from what structures

A

cerebral cortex - whole cortices/all functions

thalamus- parafascicualr nucleus (medial centromedian nucleus)

pars compacts of substantia nigra: not strictly an afferent

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13
Q

main visceral pain pathway from the thalamus to basal nuclei

A

archispinal tract

functions not fully defined

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14
Q

Type of info sent to thalamus from pars compacta of substantia nagar

A

Efferent and afferent

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15
Q

what portions of the basal nuclei send efferent signals and where do they send signals to

A

internal segment of globus pallidus and pars reticulata of substantia nigra

signals to VL/VA nuclei = body motor function

signals to superior colliculus = eye movement functions

**spatiotemporal innervation = basic pattern for neural circuit function

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16
Q

from where do medium spiny neurons recieve afferent info

A

pyramidal cells send orders from cerebral cortex

neurons from parafascicular nucleus

substantia nigra pars compacta: modulate the direct and indirect paths

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16
Q

what/where are medium spiny neurons

A

gate keepers of basal nuclei system

mainly in striatum of basal nuclei

type of interneuron

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17
Q

where do medium spiny neurons send efferent info to

A

GPi: direct/indirect

Pars reticulata pathways (SNpr)

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18
Q

describe the direct pathway of the basal nuclei

A

cerebral cortex projects to striatum via glutamate

striatum projects to globus pallidus internal via GABA

GPi projects to VA/VL thalamic nuclei via GABA

VA/VL projects back to cerebral cortex via glutamate

Total function = phasic activation of cortex; initiating and increasing activities

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19
Q

describe the indirect pathway of the basal nuclei

A

cerebral cortex projects to striatum via glutamate

striatum projects to globus pallidus external segment via GABA

GPe projects to subthalamic nucleus via GABA

subthalamic nucleus projects to internal segment via glutamate

internal segment projects to VA/VL thalamic nuclei via GABA

VA/VL projects back to the cortex via glutamate

total function = tonically inhibition of cerebral cortex; ending/inhibiting activities

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20
Q

describe how direct and indirect pathways work in a sort of parallel processing

A

multiple acon terminals with temporal and spatial regulation

direct path = activating WANTED programs
-convergence projection: multiple medium spiny neurons vs single neuron in GPi

indirect path = inhibiting UNWANTED programs
-divergence projection: single medium spiny neuron vs multiple neurons in GPi

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21
Q

what type of neurons are found in substantia nigra pars compacta (SNpc)

A

dopaminergic neurons

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22
Q

what is the nigrostriatal pathway; describe it

A

Substantia Niagara pars compacta projects to the striatum

activates direct path = initiating/increasing activities
- medium spiny neurons with D1 receptors for dopamine

inhibites indirect path = ending decreasing activities
- medium spiny neurons with D2 receptors for dopamine

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23
Q

what is the hyper direct pathway

A

cerebral cortex directly activates subthalamic nucleus

24
Q

what is the super direct pathway

A

parafascicular nucleus directly activate subthalamic nucleus

provides major sub thalamic excitatory input

25
Q

what is the GPe-GPi pathway

A

branch from indirect pathway

neutralize inhibition by GPe

26
Q

total function of enhancement pathways

A

enhanced general inhibition of cerebral cortex

inhibition by GPi is TONIC

inhibiton from left lateral prefrontal cortex is essential for functional execution

27
Q

describe the pathophysiology of parkinsons

A

death of dopaminergic neurons in SNpc

decreased excitatory effects on direct path

increased inhibitory effects on indirect path

total effect = difficult to initiate wanted activities with extra unwanted activities

28
Q

describe what hyperkinetic vs hypokinetic S&S of parkinsons may look like

A

hypokinetic = decreased direct path activation
- wanted programs are decreased/inhibitied
- Akinesia = rigidity/bradykinesia

hyperkinetic = decreased indirect pathway inhibition
- unwanted programs are increased/activated
-dyskinesia = unique resting tremor (pin rolling), tardive dyskinesia

29
Q

ways to clincally manage parkinsons

A

PT
MD treatment = L-dopa, crossing BBB

surgical:
- pallidotomy/VL or VA removal- unexpectedly effective
- deep brain stimulation- subthalamic electrode placement

combination of treatment = more effective wanted motor functions

30
Q

describe what occurs with deep brain stimulation

A

placement location to modulate indirect pathways = late stage of disorders

GPi/subthalamic nucleus/parafascicular nucleus are targeted

bilateral placement

effective with unknown mechanisms: contradictory to the function of those nuclei

31
Q

How much of Huntington’s disease is genetically related

A

100%

mutation of huntingtin gene

autosomal dominant chromosome 4

32
Q

when do you start to see symptoms for Huntington’s? Major presentation? S&S?

A

around 30-50

chorea is the major presentation: indirect path lost at GPe

lost inhibition = personality changes, cognition, and emotion

33
Q

survival after huntingtons disease

A

10-20 years after diagnosis

34
Q

what happens in the brain with huntingtons

A

general atrophy of the brain

basal nuclei atrophy

caudate is the most prominent loss

35
Q

what is Hemiballismus

A

unilateral subthalamic nucleus is impaired = loss if indirect pathway

increased contralateral unwanted motor programs = lateralization

36
Q

describe the projection of the basal nuclei system in relation to oculomotor control

A

frontal eye field projects to caudate and causes glutamate release

caudate projects to substantia nigra, pars reticulata (SNpr) and causes GABA release

SNpr projects to superior colliculus and causes GABA release

total effect = disinhibit tonic inhibition of SNpr on superior colliculus nuclei for eye movement

37
Q

how active is the basal nuclei system in EARLY learning phase

A

increased activity

most active in decision making = turning point

38
Q

how active is the basal nuclei system in LATE learning phase

A

decreased basal nuclei activities

only active during initiating and ending activities

learned programs are stored as an “APP” (MEMORY)

39
Q

afferent pathway of cerebellum

A

goes to both nuclei and cerebellar cortex

40
Q

fibers involved with cerebellar afferent signals

A

climbing = to sagittal plane purkinje dendritic tree in molecular layer

mossy = to granular layer then parallel fibers in coronal plane to purkinje dendritic tree

multilayer = to all 3 cortical layers with different neurotransmitters

41
Q

what fibers send efferent signals from cerebellum

A

purkinje cells via GABA

42
Q

where do purkinje cells send efferent info from cerebellum

A

to cerebellar nuclei (fastigial, interposed, and dentate)

vestibular nuclei (lateral nucleus- functionally separate from fastigial)

43
Q

important afferent pathways form cerebral cortex

A

cerebral cortex to contralateral cerebellum

spinal cord to spinocerebellum via ips inferior cerebellar peduncle

vestibular to vestibulocerebellum vis ips inferior cerebellar peduncle

44
Q

what regions/relays are involved in the afferent pathway of cerebral cortex to contralateral cerebellum

A

pons relay through pontine nuclei and basilar pons

red nucleus to inferior olivary nucleus then to cerebellar cortex via climbing fibers

45
Q

ascending portion of efferent components in the superior cerebellar peduncle

A

VL for M1

46
Q

horizontal communication involved in efferent components of superior cerebellar peduncle

A

red nucleus to rubrospinal tract AND inferior olivary nucleus

tectal nucleus to tectospinal tract

superior colliculus for oculomotor functions

47
Q

what are the purposes of the spinocerebellum in motor control

A

spinocerebellum to ipislateral superior colliculus = for oculomotor control at superior cerebellar peduncle

spinocerebellum goes through superior colliculus to RF at the inferior cerebellar peduncle
- from there pons and medulla reticulospinal tract control posture and proximal extremity muscle control

48
Q

purpose of vestibulocerebellum in motor control

A

inferior cerebellar peduncle sends signal to vestibular nuclei

lateral vestibulospinal tract = ipsilateral VSR and proximal extremity control

medial vestibulospinal tract = ipsilayeral VCR for head position/eye movement control

49
Q

describe the feedback control system involved in coordination

A

slow movements = posture control

new skill learning = trial and errord

50
Q

describe the feedforward control system involved in coordination

A

used with learned skills

fast movements; saccades of eyes

51
Q

mechanism of intention tremor of a normal subject

A

antagosists slightly lag

similar forces

braking agonists correctly

52
Q

mechanism of intention tremor in patients with cerebrocerebellar function impaired

A

antagonists lag obviously

stronger forces involved

agonists need to contract again followed by antagonists

intention tremor is induced

53
Q

describe prism learning in pts with and without cerebellar injury

A

without = dart throwing affected at beginning with prism glasses but pt adapts fast;
- trend of learning wiht prism on
- pt can revert after removing glasses

with injury = no adaptation; perform motion learned in the past
- no trend of learning with prism

54
Q

what happens if there is damage to inferior olivary nucleus/cerebellar nuclei

A

difficulty learning motor skills

mainly through encoding but not much consolidation/retrieval

55
Q

what is retrograde tracing

A

involves looking at the reciprocal projections between the basal nuclei and cerebellum circuits

56
Q

what happened when rabies viral vector was injected into striatum

A

projected to thalamus and traced to dentate nucleus

57
Q

what happened when rabies viral vector was injected into cerebellar cortex

A

projected to pontine nucleus

traced to subthalamic nucleus

different systems but be coordinated