L10: Motor Control- The Cerebellum Flashcards

1
Q

Where is the cerebellum located

A

Close to the brainstem

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2
Q

What is the cerebellum involved in

A

Control of motor tone
Sensorimotor coordination
Motor learning e.g playing an instrument

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3
Q

What are the 3 anatomical components of the cerebellum

A

Spino-cerebellum
Vestibulo-cerebellum
Cerebro-ponto-cerebellum

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4
Q

Which region is Spino-cerebellum located within the cerebellum

A

Medial region

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5
Q

Which region is the vestibulo cerebellum located within the cerebellum

A

Caudal region

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6
Q

Which region is the cerebro-cerebellum located

A

Lateral hemispheres

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7
Q

What input does the spino-cerebellum receive

A

Receive sensory input from spinal cord

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8
Q

What is the output of the spino-cerebellum from

A

Reticular formation

Red nucleus

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9
Q

What pathways does the spine-cerebellum involve

A

Medial and lateral descending pathways

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10
Q

From the reticular formation and red nucleus where does the info go

A

Motor cortex

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11
Q

From the motor cortex what is the output

A

Control over axial musculature (medial pathway)

And posture

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12
Q

What does the vestibulo-cerebellum receive input from

A

Vestibular nucleus (ventromedial pathway)

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13
Q

What is the output of the vestibulo-cerebellum to

A

Vestibular nucleus (ventromedial pathway)

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14
Q

What does the output of vestibulo-cerebellum control

A

Posture and balance and eye movement

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15
Q

What is the input of the cerebral-cerebellum from

A

Primary motor cortex

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16
Q

What is the output of the cerebro-cerebellum to

A

Primary motor cortex

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17
Q

Therefore what is the cerebral-cerebellum involved in

A

Intra cerebral motor loop

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18
Q

What is the parallel fibres in the cerebellum derived from

A

Granule cells

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19
Q

What are mossy fibres

A

Fibres that carry sensory into into cerebellum that interact with granule cells and then parallel cell fibres and then purkinje fibres

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20
Q

What is the the role of climbing fibres

A

Sensory input directly to purkinje fibres

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21
Q

Where does purkinje fibres send signal to

A

Deep cerebellar nuclei

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22
Q

What other cells in the cerebellum can directly interact with the deep cerebellar nucleus

A

Mossy fibres

Climbing fibres

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23
Q

What effect does climbing fibres have on the purkinje fibres

A

Excitatory influence

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24
Q

What effect does mossy fibres have on purkinje fibres

A

Indirect excitatory influence via parallel fibres of granule cells

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25
Q

What cell is the only output from the deep cerebellar nuclei

A

Purkinje fibres

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26
Q

What type of output does purkinje fibres have

A

Inhibitory output

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27
Q

If the mossy fibres and climbing fibres that give an excitatory input to the deep cerebellar nuclei, what does the inhibitory input from the purkinje fibres do

A

The inhibition from the purkinje fibres modulate the level of excitation

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28
Q

Overall what is the output of the cerebellum

A

Inhibitory

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29
Q

What does the deep cerebellar nuclei do

A

Compare the 2 inputs from the mossy and climbing cells and after processing an inhibitor signal is sent

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30
Q

Where does the deep cerebellar nuclei send the information to

A

Brain stem and thalamus

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31
Q

What is the comparison of the deep cerebellar nuclei of

A

Intended movement
Actual movement
Via mossy and climbing fibres

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32
Q

Summarise the 4 roles of the cerebellum

A

1) regulate posture by adjusting the descending motor pathways
2) acts as a compactor of actual movement and intended movement
3) acts as time to result in smooth muscle performance
4) involved in motor memory

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33
Q

What does the basal ganglia integrate

A

Sensory and moto info

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34
Q

What type of movement does the basal ganglia initiate

A

Voluntary movement

35
Q

What is the basal ganglia composed of

A

Subcortical nuclie

36
Q

Where does the sensory and motor info to the basal ganglia come from

A

Cortex

37
Q

When the basal ganglia has intergrated the info where does it send info to

A

Pre-motor Cortex via thalamus

38
Q

In normal resting situation what is the outflow of the basal ganglia

A

Inhibitory to the cortex

39
Q

When the pre-frontal cortex is switched on i.e when the body wants to move (voluntary movement) what type of signal is sent to the basal ganglia from the cortex

A

Excitatory flow

40
Q

What does the excitatory outflow from the pre-frontal cortex do to the basal ganglia

A

Switch it off

41
Q

What does switching off basal ganglia do to the thalamus

A

Switch it on as it is no longer inhibited by the basal ganglia = disinhibition

42
Q

What type of signal is sent to the supplementary motor cortex

A

Excitatory so it initiates a movement

43
Q

What are the structures in the basal ganglia

A

Caudate nucleus, putamen, nucleus accumbens = striatum
Subthalamic nuclues
globus pallidus: internal and external
Substantia niagra: reticulata and pars compacta

44
Q

Where does input from the cortex go to in the basal ganglia

A

Striatum

45
Q

Where is output from the basal ganglia from

A

Globus pallidus: internal

Substantia nigra: reticulata

46
Q

Where does the output of the internal segment of globus pallidus and reticulata of substantia nigra go to

A

Thalamus

47
Q

What is the signal of output of the basal ganglia to the thalamus at rest

A

Inhibitory

48
Q

What are the 2 pathways within the basal ganglia called

A

Direct pathway

Indirect pathway

49
Q

What does the direct pathway involve

A

Signal from the striatum directly to the substantia nigra reticulata and globus pallidus internal

50
Q

What is the indirect pathway

A

Signal from the striatum indirectly to the globus pallidus external a and subthalamic nucleus

51
Q

When the cortex signal to the striatum what happens as a result of the direct pathway

A

1) Promoting movement as the stratium sends an inhibitory signal to the substantia nigra reticulata and globus pallidus internal to inhibit it
2) inhibitory signal is no longer sent to the thalamus so it becomes activated = disinhibition

52
Q

What does the substantia nigra pas compact release

A

Dopamine

53
Q

What receptors does dopamine act on

A

D1 receptors on the striatum

54
Q

When dopamine binds to D1 receptors in the striatum, what happens to the striatum

A

Increases inhibition down the direct pathway to cause the activation of the thalamus and SNR and GPI are inhibited

55
Q

What is the overall outcome of the indirect pathway in the basal ganglia

A

Suppress movement

56
Q

How does the indirect pathway inhibit movement

A

1) the striatum sends an inhibitory signal to the globus pallidus external
2) globus pallidus external becomes inhibited and therefore can no longer inhibit the subthalamic nucleus which usually drives the SNR and GPI
3) subthalamic nucleus is also further excited by the cortex which sends an excitatory signal to the SNR/GPI that inhibits the thalamus

57
Q

When dopamine is released by the substantia nigra pars compacta what receptors does the dopamine act on to become involved in the indirect pathway

A

D2 receptors

58
Q

What affect does the binding of dopamine to D2 receptors have on the striatum

A

Striatum becomes inhibited

59
Q

If the striatum becomes inhibited by dopamine what affect does this have on the globus pallidus external

A

1) GPE is no longer inhibited
2) GPE sends inhibitory signals to the subthalamic nucleus
3) subthlamic nuclues reduces in the excititory signal to SNR/GPI so outflow of SNRI/GPI is reduced
4) thalamus becomes activated
5) movement is initiated

60
Q

Regardless of the pathway being direct or indirect what does dopamine do

A

Cause the initiation of movement

61
Q

If there is an imbalance in direct and indirect pathway what does this result in

A

Motor dysfunction

62
Q

What are the 2 broad categories of disorders

A

Hypokinetic

Hyperkinetic

63
Q

What does hypokinetic disorders mean

A

Less movement disorders

64
Q

Give an example of less movement disorders

A

Parkinson’s disease

65
Q

What does hyperkinetic disorders mean

A

Too much movement disorders

66
Q

Name examples of hyperkinetic disorders

A

Huntington’s disease
Hemiballism
Tardive dyskinesia

67
Q

What are the 3 main symptoms of Parkinson’s disease

A

Tremor
Bradykinesia
Rigidity

68
Q

What are the causes of Parkinson’s disease

A

Loss of nitro-strait also dopaminergic pathway

69
Q

What is the treatment for Parkinson’s disease

A

L-dopa
Dopamine agonist
Drugs that prevent dopamine breakdown e.g monoamine oxidase b inhibitors

70
Q

What are the 3 symptoms of Huntington’s disease

A

Excessive movement
Uncontrollable rapid motor patterns
Dementia or psychiatric disturbance

71
Q

What is the cause of Huntington’s disease

A

Autosomal dominant disorder

72
Q

What is the primary pathology of Huntington’s disease

A

1) Loss of striata output in indirect pathway
2) GPE is inhibited less and sends inhibitory signals to STN
3) STN decreases input to SNR and GPI
4) output to thalamus decreases
5) this causes involuntary movement

73
Q

What are the 3 treatments for symptomatic relief for Huntington’s disease

A

Tetrabenazine
Chlorpromazine
Baclofen

74
Q

What does tetrabenazine do

A

Decreases dopamine release by inhibiting VMAT

75
Q

What is chlorpromazine

A

Dopamine antagonist

76
Q

What is baclofen

A

GABA- b agonist which decreases spinal reflexes that are increased in Huntington’s disease

77
Q

What is the symptom of hemiballismus

A

Violent flailing movement to limbs

78
Q

What is the cause of hemiballismus

A

Damage to STN

79
Q

What is the effect of tardive dyskinesia

A

Uncontrolled movement of face and trunk muscles

80
Q

What is the cause of tardive dyskinesia

A

Long term exposure to antipsychotic drugs (dopamine receptor antagonist)

81
Q

What dysfunction can occur if there is damage to the spinocerebellum

A

Ataxia (unsteady gait)
Dysmetria (inaccurate termination of movement) and intention tremor
Dysdiadochokinesia (inability to perform rapid alternating movements)- get patient to tap their foot quickly or flip hands
Hypotonia (decreased muscle tone)

82
Q

What dysfunction can occur if there is damage to the vestibulo-cerebellum

A

Ataxia
Slow saccades (slow movement of the eye to left to right )
Nystagmus (vibration of the eye)

83
Q

What dysfunction can occur if there is damage to the cerebro-cerebellum

A

Ataxia (unsteady gait)
Dysmetria(intention tremor)
Dysarthria (articular speech due to poor oropharngeal control)