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basal ganglia Flashcards

1
Q

what structures are involved in the neural control of movement?

A

brainstem and spinal cord
descending pathways
cerebellum
basal ganglia

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2
Q

what is the function of the cerebellum?

A

sensory motor coordination of ongoing movement

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3
Q

what is the function of the motor cortex?

A

planning, initiating and directing voluntary movement

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4
Q

what is the function of the brainstem centres?

A

basic movements and postural control

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5
Q

what are the basal ganglia?

A

caudate
putamen
globus pallidus

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6
Q

what are the parts of the caudate?

A

globular head
tapering body
down curving tail

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7
Q

where are the basal ganglia found?

A

cerebral cortex

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8
Q

where is the caudate found?

A

from the frontal cortex to the temporal cortex

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9
Q

what is the putamen attached to?

A

caudate head

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10
Q

what are the parts of the globus pallidus?

A

internal and external segments

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11
Q

what does the internal segment of the globus pallidus do?

A

sends output to the thalamus

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12
Q

what does the external segment of the globus pallidus do?

A

relays info between the other basal ganglia nuclei and GPi

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13
Q

what is the corpus striatum?

A

caudate

putamen

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14
Q

what is the lentiform nucleus?

A

caudate

globus pallidus

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15
Q

what is the internal capsule and what does it do?

A

white matter structure (myelinated fibres) – separates lentiform nucleus from caudate and thalamus

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16
Q

what are the functions of the basal ganglia?

A
  1. Movement – initiation, maintenance, inhibiting antagonistic movements and switching (stopping/starting movement)
  2. Processing info – emotion, motivation and cognition
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17
Q

what is the blood supply to the caudate?

A

middle cerebral

anterior cerebral

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18
Q

what is the blood supply to the putamen?

A

middle cerebral

anterior cerebral

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19
Q

what is the blood supply to the globus pallidus?

A

middle cerebral

anterior choroidal

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20
Q

what is the blood supply to the internal capsule?

A

middle cerebral
anterior cerebral
anterior choroidal

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21
Q

what gives input into the basal ganglia?

A

cerebral cortex

substantia nigra pars compacta

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22
Q

what is the corticostriatal pathway?

A

pathway from cerebral cortex to the basal ganglia

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23
Q

what is the nigrostriatal pathway?

A

pathway from the substantia nigra pars compacta

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24
Q

what is the main neuron type in the corpus striatum?

A

medium spiny neurons

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25
Q

what gives input into the corpus striatum and what type of input is it?

A
  1. Cortical neurons (glutamatergic)
  2. Substantia nigra pars compacta neurons (dopaminergic)
  3. Local circuit neurons in corpus striatum (GABAergic inhibitory input)
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26
Q

where do medium spiny neurons converge?

A

on GP and SNPR

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27
Q

what is the corpus striatum output zone?

A

globus pallidus and substantia nigra pars reticulata

28
Q

what are the projections from the output zone to?

A
  • subthalamic nucleus
  • VA/VL thalamic nuclear complex
  • superior colliculus
29
Q

where are the subthalamic nuclei?

A

under the thalamus

30
Q

what is the input into the subthalamic nuclei?

A

cerebral cortex and GPe

31
Q

what is the output from the subthalamic nuclei?

A

GPi and SNPR

32
Q

what is the input into the VA/VL thalamic nuclear complex?

A

GPi

33
Q

where does the VA/VL complex project to?

A

motor areas of the cerebral cortex

34
Q

what is the function of the superior colliculus?

A

controls eye movements

35
Q

what is disinhibition?

A

inhibition of inhibition

excitation by double inhibition

36
Q

what is the effect of the GP on the VA/VL complex at rest?

A

tonically inhibits it

37
Q

what is the function of the direct pathway?

A

allows basal ganglia to initiate movement

38
Q

what neurons do the corpus striatum and the GP mainly contain?

A

contain mainly inhibitory GABAergic neurons

39
Q

explain the direct pathway

A
  • Activation of corpus striatum causes inhibition of GPi
  • GPi is tonically inhibiting the VA/VL complex of the thalamus
  • So, inhibition of GPi stops inhibition of the VA/VL thalamus complex
  • Motor cortex can be activated  initiation of movement
40
Q

what is the function of the indirect pathway?

A

• Antagonises direct pathway – stops movement initiation and terminates movements

41
Q

describe how the indirect pathway occurs

A

• A subset of nuclei in the corpus striatum receive inhibitory SNPC (D2)
• Striatum then inhibits the GPe via inhibitory GABA neurons
o GPe tonically inhibits the subthalamic nucleus
• Activated subthalamic nucleus activates the GPi
• GPi continues to inhibit VA/VL complex  cant transmit to the frontal cortex

42
Q

what part of the globus pallidus feeds into the subthalamic nucleus?

A

external segment

43
Q

during repetitive movements, are the direct and indirect pathways active or inactive?

A 
direct = inactive
indirect = active
44
Q

when is the direct pathway active?

A

when you want to change your motor program

45
Q

what receptors are expressed by the corpus striatum?

A

D1 or D2 dopamine receptors

46
Q

which pathway uses D1 receptor-expressing neurons?

A

direct

47
Q

which is stimulated by dopamine and what effect does it have - D1 or D2?

A

D1

activates motor programme change

48
Q

which is inhibited by dopamine and what effect does it have - D1 or D2?

A

D2

blocks motor programme change

49
Q

which pathway uses D2 receptor expressing neurons?

A

indirect

50
Q

what type of movement disorder is parkinsons?

A

hypokinetic

51
Q

what is parkinson’s disease characterised by?

A

o Resting tremor
o Slowness of movement (bradykinesia)
o Muscular rigidity
o Minimal facial expressions

52
Q

what causes parkinsons?

A

Caused by loss of dopaminergic neurons in SNPC which project to and innervate the corpus striatum

53
Q

what % of dopamine neurons have to degenerate before clinical symptoms show?

A

80%

54
Q

what change occurs to the parkinsons pathways?

A

Shift to indirect pathway – inhibition of the thalamus  decreased excitation of frontal cortex  decrease in movement

55
Q

how do you treat early parkinson’s with cardinal symptoms but no medication related complications?

A

Levodopa
Dopamine agonists
MAO-B inhibitors

56
Q

how do you treat PD with motor and non-motor complications, medication side-effects and unrelieved symptoms?

A

COMT inhibitors
Apomorphine
Amantadine

57
Q

what type of movement disorder is huntington’s?

A

hyperkinetic movement disorder

58
Q

how is huntington’s inherited?

A

autosomal dominant

59
Q

which gene is affected in huntington’s?

A

huntingtin gene

60
Q

what is huntington’s characterised by?

A

o Mood alterations (e.g. depression)
o Personality alterations (e.g. irritability, impulsive or eccentric behaviour)
o Defects in memory and attention
o Involuntary movements (hallmark of the disease)

61
Q

what is the hallmark of huntington’s?

A

involuntary movements

62
Q

what causes the defects in motor function of huntington’s?

A

due to the loss of GABAergic neurons in the corpus striatum, which project to and innervate the globus pallidus

63
Q

which pathway is the balance shifted to in huntington’s?

A

direct pathway

64
Q

what is chorea?

A

rapid, involuntary, jerky-type movements

65
Q

what is athetosis?

A

slow, involuntary, smooth, writhing-type

66
Q

what is ballismus?

A

rapid, involuntary, wild flinging-type movements

b2 (5 decks)

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