L10: Motor Control- The Cerebellum Flashcards

(83 cards)

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
What cell is the only output from the deep cerebellar nuclei
Purkinje fibres
26
What type of output does purkinje fibres have
Inhibitory output
27
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
The inhibition from the purkinje fibres modulate the level of excitation
28
Overall what is the output of the cerebellum
Inhibitory
29
What does the deep cerebellar nuclei do
Compare the 2 inputs from the mossy and climbing cells and after processing an inhibitor signal is sent
30
Where does the deep cerebellar nuclei send the information to
Brain stem and thalamus
31
What is the comparison of the deep cerebellar nuclei of
Intended movement Actual movement Via mossy and climbing fibres
32
Summarise the 4 roles of the cerebellum
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
33
What does the basal ganglia integrate
Sensory and moto info
34
What type of movement does the basal ganglia initiate
Voluntary movement
35
What is the basal ganglia composed of
Subcortical nuclie
36
Where does the sensory and motor info to the basal ganglia come from
Cortex
37
When the basal ganglia has intergrated the info where does it send info to
Pre-motor Cortex via thalamus
38
In normal resting situation what is the outflow of the basal ganglia
Inhibitory to the cortex
39
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
Excitatory flow
40
What does the excitatory outflow from the pre-frontal cortex do to the basal ganglia
Switch it off
41
What does switching off basal ganglia do to the thalamus
Switch it on as it is no longer inhibited by the basal ganglia = disinhibition
42
What type of signal is sent to the supplementary motor cortex
Excitatory so it initiates a movement
43
What are the structures in the basal ganglia
Caudate nucleus, putamen, nucleus accumbens = striatum Subthalamic nuclues globus pallidus: internal and external Substantia niagra: reticulata and pars compacta
44
Where does input from the cortex go to in the basal ganglia
Striatum
45
Where is output from the basal ganglia from
Globus pallidus: internal | Substantia nigra: reticulata
46
Where does the output of the internal segment of globus pallidus and reticulata of substantia nigra go to
Thalamus
47
What is the signal of output of the basal ganglia to the thalamus at rest
Inhibitory
48
What are the 2 pathways within the basal ganglia called
Direct pathway | Indirect pathway
49
What does the direct pathway involve
Signal from the striatum directly to the substantia nigra reticulata and globus pallidus internal
50
What is the indirect pathway
Signal from the striatum indirectly to the globus pallidus external a and subthalamic nucleus
51
When the cortex signal to the striatum what happens as a result of the direct pathway
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
What does the substantia nigra pas compact release
Dopamine
53
What receptors does dopamine act on
D1 receptors on the striatum
54
When dopamine binds to D1 receptors in the striatum, what happens to the striatum
Increases inhibition down the direct pathway to cause the activation of the thalamus and SNR and GPI are inhibited
55
What is the overall outcome of the indirect pathway in the basal ganglia
Suppress movement
56
How does the indirect pathway inhibit movement
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
When dopamine is released by the substantia nigra pars compacta what receptors does the dopamine act on to become involved in the indirect pathway
D2 receptors
58
What affect does the binding of dopamine to D2 receptors have on the striatum
Striatum becomes inhibited
59
If the striatum becomes inhibited by dopamine what affect does this have on the globus pallidus external
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
Regardless of the pathway being direct or indirect what does dopamine do
Cause the initiation of movement
61
If there is an imbalance in direct and indirect pathway what does this result in
Motor dysfunction
62
What are the 2 broad categories of disorders
Hypokinetic | Hyperkinetic
63
What does hypokinetic disorders mean
Less movement disorders
64
Give an example of less movement disorders
Parkinson’s disease
65
What does hyperkinetic disorders mean
Too much movement disorders
66
Name examples of hyperkinetic disorders
Huntington’s disease Hemiballism Tardive dyskinesia
67
What are the 3 main symptoms of Parkinson’s disease
Tremor Bradykinesia Rigidity
68
What are the causes of Parkinson’s disease
Loss of nitro-strait also dopaminergic pathway
69
What is the treatment for Parkinson’s disease
L-dopa Dopamine agonist Drugs that prevent dopamine breakdown e.g monoamine oxidase b inhibitors
70
What are the 3 symptoms of Huntington’s disease
Excessive movement Uncontrollable rapid motor patterns Dementia or psychiatric disturbance
71
What is the cause of Huntington’s disease
Autosomal dominant disorder
72
What is the primary pathology of Huntington’s disease
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
What are the 3 treatments for symptomatic relief for Huntington’s disease
Tetrabenazine Chlorpromazine Baclofen
74
What does tetrabenazine do
Decreases dopamine release by inhibiting VMAT
75
What is chlorpromazine
Dopamine antagonist
76
What is baclofen
GABA- b agonist which decreases spinal reflexes that are increased in Huntington’s disease
77
What is the symptom of hemiballismus
Violent flailing movement to limbs
78
What is the cause of hemiballismus
Damage to STN
79
What is the effect of tardive dyskinesia
Uncontrolled movement of face and trunk muscles
80
What is the cause of tardive dyskinesia
Long term exposure to antipsychotic drugs (dopamine receptor antagonist)
81
What dysfunction can occur if there is damage to the spinocerebellum
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
What dysfunction can occur if there is damage to the vestibulo-cerebellum
Ataxia Slow saccades (slow movement of the eye to left to right ) Nystagmus (vibration of the eye)
83
What dysfunction can occur if there is damage to the cerebro-cerebellum
Ataxia (unsteady gait) Dysmetria(intention tremor) Dysarthria (articular speech due to poor oropharngeal control)