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Year 2 NSB > Motor Learning and neurological Syndromes > Flashcards

Motor Learning and neurological Syndromes Flashcards

1
Q

What is the Brodmann area for the primary motor cortex?

1 - 1, 2 and 3
2 - 4
3 - 17
4 - 41 and 42

A

2 - 4

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2
Q

What is the Brodmann area for the premotor area also known as the supplementary motor area?

1 - 1, 2 and 3
2 - 4
3 - 6
4 - 41 and 42

A

3 - 6

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3
Q

What is the Brodmann area for the posterior parietal cortex?

1 - 1, 2 and 3
2 - 4
3 - 17
4 - 5 and 7

A

4 - 5 and 7

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4
Q

What is the function of the pre-motor area (broadmann area 6), also known as the supplementary motor area?

1 - activating muscles
2 - cognitive thought
3 - planning and organising movements
4 - modulating co-ordination

A

3 - planning and organising movements

- located anteriorly to motor cortex, precede the action of the motor cortex

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5
Q

What is a homunculus used to represent in the brain?

A
  • represents regions of the body in relation to the brain
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6
Q

When looking at the homunculus which is used to represent regions of the body in relation to the brain, what are the sizes of the cortex associated with the brain relative to?

A
  • function of the body part
  • hands have a large area as they require more fine motor skills
  • shoulders have a smaller area
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7
Q

What is a parasaggital meningioma?

  • para = either side of
  • sagittal = midline plane
A
  • meningioma = tumour in CNS formed in the meninges along the sides of the sagittal plane (not in brain parenchyme though)
  • not inside the brain, but puts pressure on the brain
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8
Q

A parasaggital meningioma is a tumour in CNS formed in the meninges along the side of the sagittal plane. It is not directly inside the parenchyme brain tissue, but can put pressure on the brain tissue. Why is identifying exactly which part of the homunculus (region of cortex in the brain) is affected in this type of tumour?

A
  • it can identify what part of the body will be affected

- also following symptoms can help identify where the meningioma is

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9
Q

What is spastic paraparesis (greek for half stricken)?

  • para = half
  • paresis = weakness
  • spastic = spasms
A
  • gradual weakness with muscle spasms (spastic weakness) in the legs
  • can be hereditary or caused by parasaggital meningioma
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10
Q

What are some common signs of upper motor neuron disorders?

A
  • weakness
  • spasticity
  • brisk reflexes (exaggerated reflex response)
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11
Q

The Babinski sign is a test to assess upper motor neuron disorders which involves scratching the underneath of the patients foot. What is a normal and abnormal response?

1 - normal = flexion of toes, abnormal = extension of toes
2 - normal = extension of toes, abnormal = flexion of toes

A

1 - normal = flexion of toes, abnormal = extension of toes

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12
Q

Why can a stroke or other damage to the brain cause spasticity?

A
  • neurons in the brain controlling muscle contraction are damaged and do not tell the muscle to stop contracting
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13
Q

In upper motor neuron disorders patients can have brisk reflex form a tendon test, why is this?

A
  • there is no upper motor neurons that regulate the reflex
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14
Q

What are some of the common signs of lower motor neuron disorder?

A
  • weakness
  • wasting of muscles
  • fasciculations (involuntary muscle contraction/relaxation)
  • reduction in muscle tone
  • reduced reflexes
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15
Q

There are 2 main types of upper motor neurons, the corticospinal and corticobulbar tract. Where does the corticospinal start?

1 - somatosensory cortex
2 - pre motor cortex
3 - motor cortex
4 - cerebellum

A

3 - motor cortex

  • cortico = cortical/cortex and spinal = spine
  • voluntary movement
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16
Q

There are 2 main types of upper motor neurons, the corticospinal and corticobulbar tract. Where does the corticobulbar start and end?

1 - somatosensory cortex
2 - pre motor cortex
3 - motor cortex
4 - bulb of brain stem

A

4 - bulb of brain stem

  • cortico = cortical/cortex and bulbar = bulb of the brain stem
  • starts in cortex and goes to the spinal cord
  • voluntary movement
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17
Q

There are 2 main types of upper motor neurons, the corticospinal and corticobulbar tract. The corticospinal starts starts in cortex and goes to the spinal cord. Do neurons of the corticospinal tract decussate in the medulla or in the spinal cord?

A
  • in the medulla at the pyramids

- 80% decussate and 20% do not decussate

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18
Q

There are 2 main types of upper motor neurons, the corticospinal and corticobulbar tract. The corticospinal starts starts in cortex and goes to the spinal cord. The neurons of the corticospinal tract decussate in the medulla, specifically the pyramids and synapse where in the spinal cord?

A
  • 80% that decussate = travel in lateral fascicules and then synapse in ventral horn
  • 20% that do not decussate = travel in anterior fascicules and then synapse in ventral horn
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19
Q

There are 2 main types of upper motor neurons, the corticospinal and corticobulbar tract. The corticobulbar starts in cortex and goes to the bulb of the brain stem and synapses with specific cranial nerve (CN) nuclei, what are the 4 CN nuclei located in the pons and medulla involved in motor function?

A

1 - CN V (5) trigeminal (mastication)
2 - CN VII (7) facial nerve (facial expression)
3 - nuclear ambiguous (group of large motor neurons) innervating CN IX (9) glossopharyngeal nerve, CN X (vagus nerve) and CN XI (11) accessory nerve
4 - CN XII (12) hypoglossal

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20
Q

Where do the lower motor neurons receive their input from?

A
  • upper motor neurons
  • corticospinal tract = anterior grey horn (also called ventral horn)
  • corticobulbar tract = cranial nerve nuclei
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21
Q

Fasciculations are spontaneous muscle twitch that is involuntary muscle contraction and relaxation. Do fasciculation’s occur in upper or motor neuron lesions?

A
  • only occur in lower motor lesion
  • no innervation from UMN means there is increased receptor concentration on muscles to compensate for lack of innervation
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22
Q

Fasciculations, are spontaneous muscle twitches that are involuntary muscle contraction and relaxations. They only occur in lower motor lesions (LML). Lesions affecting LMN result in a decrease in neurotransmitter release into the synaptic cleft. This causes the synaptic cleft to desensitise, meaning any small amounts of an excitable neurotransmitter will cause hypersensitivity and an up-regulation of muscarinic (M1, M3 or M5) receptors on the muscle cell membrane. What is this neurotransmitter called?

1 - acetylcholine
2 - glutamate
3 - dopamine
4 - serotonin

A

1 - acetylcholine

- results to all of the above is a fasciculation

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23
Q

Fasciculations, are spontaneous muscle twitches that are involuntary muscle contraction and relaxations. They only occur in lower motor lesions (LML). LML decrease levels of ACh released into the synaptic space, causing desensitisation and an up-regulation of ACh receptors on the muscle cell membrane. With lots of ACh receptors what can happen to them in relation to depolarisation?

1 - hypo-sensitive and no depolarisation
2 - hypersensitive and depolarisation
3 - hypo-sensitive and depolarisation
4 - hypersensitive and no depolarisation

A

2 - hypersensitive and depolarisation

  • muscle cell depolarises, Na+ flows in and K+ flows out and muscle contraction occurs
  • BUT muscle contraction is pathological
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24
Q

In upper motor lesions patients can present with an increase in muscle tone, why is this?

A
  • corticospinal tract innervates the ventral horn of the spinal cord for voluntary movement
  • reticulospinal tract is involved in fine tuning motor movements
  • reticulospinal tract receives innervation from corticospinal, spinocerebellar, spinothalamic and dorsal column ascending tracts which provide input to tweak the movement
  • if reticulospinal tract is impaired the inhibition and fine tuning is impaired, essentially meaning there is no safety switch
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25
Q

In upper motor lesions (UML) patients can present with an increase in reflex, why is this?

A
  • alpha neurons = muscle fibres (extrafusal)
  • gamma neurons = muscle spindles (intrafusal)
  • in UML patients have increased alpha and gamma activity
  • reticulospinal tract is involved in fine tuning motor movements
  • no inhibition from reticulospinal tract causes increased muscle tone and reflex
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26
Q

A combination of increased muscle tone and muscle spindle reflex in upper motor neuron disorders is called what?

1 - spasticity
2 - dysdiadochokinesia
3 - ataxia
4 - coordination

A

1 - spasticity

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27
Q

There are 2 neurons that are involved in innervating muscles, called - alpha and gamma neurons. What do each of these neurons do?

A
  • alpha neurons = innervate muscle fibres (extrafusal) (contraction/relaxation)
  • gamma neurons = muscle spindles (eintrafusal) (involved in reflex)
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28
Q

In lower motor lesions (LML) patients can present with a decrease in muscle reflex and tone, why is this?

A
  • alpha neuron firing is decreased = decreased muscle tone

- gamme neuron firing is decreased = decreased muscle reflex

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29
Q

When we think about the hierarchy of control of movement, there are 3 main stages, what are they?

1 - practice, tactics and execution level
2 - information gathering, tactics and execution level
3 - strategy, practice and execution level
4 - strategy, tactics and execution level

A

4 - strategy, tactics and execution level

30
Q

When we think about the hierarchy of control of movement, there are 3 main stages, strategy, tactics and execution level. What is stage 1 the strategy level?

A
  • goal of the movement, for example i want o shoot a basketball hoop
  • basal ganglia and areas of the neocortex (part of the cerebral cortex, linked with higher cognitive functioning)
31
Q

When we think about the hierarchy of control of movement, there are 3 main stages, strategy, tactics and execution level. What is stage 2 the tactics level?

A
  • how the body puts into action sequences to provide muscle coordination through muscle contraction
  • associated with motor cortex and cerebellum
  • how to actually shoot the shot in basketball
32
Q

When we think about the hierarchy of control of movement, there are 3 main stages, strategy, tactics and execution level. What is stage 3 the execution level?

A
  • activation of motor neuron/interneuron pools to generate movement and corrections
  • involves the brainstem and spinal cord
33
Q

The posterior parietal cortex is really important for motor functions, why is this?

A
  • somatosensory cortex is based here
  • this provides sensory information to help guide and coordinate the movement
  • provides sensory information
34
Q

The posterior parietal cortex is really important for motor functions, as the somatosensory cortex is based here which provides visual and sensory information. What are 2 key tracts a few key features of the parietal lobe that contribute?

A
  • spinothalamic tract (provides info to the brain about pain, temperature, itch, and general or light touch sensations)
  • spinocerebellar tract (unconcious proprioception)
  • does this via the thalamus
35
Q

Once the somatosensory cortex has received sensory information, where will this information then be transported to in the brain?

1 - cerebellum
2 - pre-motor cortex
3 - motor cortex
4 - brain stem

A

2 - pre-motor cortex

  • pre motor area (just before primary motor cortex)
  • info is processed here before movement is initiated
36
Q

If the parietal cortex is damaged due to a stroke for example, what can this lead to?

A
  • neglect in function, specifically mental imagery
  • patients can perceive an image
  • BUT patients are unable to direct and sustain attention to a person, location, object, or event
37
Q

The pre-motor area of the brain is brodmanns area 6 and sits in-front of the primary motor cortex. This can be further subdivided into the lateral premotor cortex (LPC) and medial supplementary motor area (MSMA). What is the main function of both of these areas?

A
  • LPC = important in movements requiring visual guidance

- MSMA = important in coordinating complex voluntary movement

38
Q

What is apraxia (greek for without action)?

1 - patient posses no desire or ability to move, but are unable to move
2 - patient possess the desire and ability to move, but are unable to move
3 - patient possess the desire and ability to move, but are unable to move
4 - patient possess no desire to move, but moves anyway

A

3 - patient possess the desire and ability to move, but are unable to move
- a neurological disorder affecting specific skilled movements and gestures

39
Q

Apraxia, a neurological disorder where patients posses desire and physical ability to perform skilled movement, BUT patients are unable to execute or carry out skilled movements and gestures. This can be subdivided into Ideational and Ideomotor apraxia. What is the different between Ideational and Ideomotor apraxia?

A
  • ideational apraxia = unable to put together higher sequences to perform action eg “Show me how to brush your hair”
  • ideomotor apraxia = unable to use tool, eg show me how to use these scissors
40
Q

Apraxia is a neurological disorder where patients posses desire and physical ability to perform skilled movement, BUT patients are unable to execute or carry out skilled movements and gestures. This can be subdivided into Ideational (inability to put together higher sequences to perform action eg “Show me how to brush your hair”) and ideomotor apraxia (inability to use tool, eg show me how to use these scissors? What region of the brain would have to be damaged or have a lesion to cause apraxia?

1 - cerebellum
2 - pre-motor cortex
3 - motor cortex
4 - brain stem

A

2 - pre-motor cortex

- the processing of the thoughts to do the actions

41
Q

Motor control of movement is modulated by the extra-pyramidal system. What 3 key subcortical structures are important for this to function correctly?

1 - basal ganglia, thalamus, cerebellum
2 - brain stem, thalamus, cerebellum
3 - basal ganglia, brain stem, cerebellum
4 - basal ganglia, hippocampus , cerebellum

A

1 - basal ganglia, thalamus, cerebellum

42
Q

The basal ganglia/nuclei are a group of subcortical nuclei, of varied origin, located deep within the brain. What are the parts of the basal nuclei? Use the names below to label the image:

  • Striatum: caudate nucleus, putamen, nucleus accumbens
  • Globus pallidus: External (or lateral) and Internal (or medial)
  • Subthalamic nucleus
  • Substantia nigra - basal ganglia, thalamus, cerebellum
A 
1 - subthalamic nucleus
2 - nucleus accumbens
3 - substantia nigra
4 - caudate nucleus
5 - putamen
6 - globus pallidus lateral (external)
7 - globus pallidus medial (internal)
43
Q

The basal ganglia do not cause movement themselves, but they are involved in controlling which muscle groups are activated and motor learning. How do they do this?

A
  • cerebral motor cortex innervates the basal ganglia
  • basal ganglia innervate the thalamus
  • thalamus innervates the cerebral motor cortex
  • direct and indirect pathways tweak movements
44
Q

Although the basal ganglia doesn’t directly cause movement, it is able to modulate movement through receiving innervation from the motor cortex, which then feeds into the thalamus and back into the motor cortex. To do this there are 2 motor loops involved, the direct and indirect pathways. What do each of these pathways tell the body to do, in relation to movement?

A
  • direct = promotes activity

- indirect = inhibits activity

45
Q

Although the basal ganglia doesn’t directly cause movement, it is able to modulate movement through receiving innervation from the motor cortex, which then feeds into the thalamus and back into the motor cortex. To do this there are 2 motor loops involved, the direct and indirect pathways. The direct pathway promotes activity, but what is the basic flow of neurons in this pathway?

A
  • motor cortex innervates the striatum (caudate nucleus and putamen)
  • striatum innervate globus pallidus internal (but with GABA)
  • globus pallidus internal releases low amounts of GABA (or reduces) at the thalamus
  • thalamus is not inhibited and innervates the motor cortex
46
Q

In the direct pathway involving the basal ganglia the motor cortex innervates the striatum, composed of the putamen and caudate nucleus. What type of fibre provides this innervation and what neurotransmitter is released?

A
  • glutaminergic fibres
  • release the neurotransmitter glutamate
  • stimulates neurons on the striatum
47
Q

In the direct pathway involving the basal ganglia the motor cortex innervates the striatum, composed of the putamen and caudate nucleus. Glutaminergic fibre provides this innervation releasing the neurotransmitter glutamate that promotes the activity and innervation of the striatum. Which neuron is then releases at the globus pallidus internus?

1 - GABA
2 - glutamate
3 - dopamine
4 - serotonin

A

1 - GABA

  • neurotransmitter GABA is released
  • inhibits the activity of the globus pallidus internal/medial
48
Q

In the direct pathway involving the basal ganglia the motor cortex innervates the striatum, composed of the putamen and caudate nucleus. Glutaminergic fibre provides this innervation releasing the neurotransmitter glutamate that promotes the activity and innervation of the striatum. The neurotransmitter GABA is released and inhibits the activity of the globus pallidus internal/medial. What does this then do to the synapse with the thalamus?

1 - releases glutamate that can then stimulate the thalamus
2 - releases lots of GABA which then inhibit the thalamus
3 - release less GABA so no inhibition of the thalamus
4 - release low levels of glutamate so only small activation of the thalamus

A

3 - release less GABA so no inhibition of the thalamus

- thalamus is able to send movement activity to motor cortex

49
Q

Although the basal ganglia doesn’t directly cause movement, it is able to modulate movement through receiving innervation from the motor cortex, which then feeds into the thalamus and back into the motor cortex. To do this there are 2 motor loops involved, the direct and indirect pathways. The indirect pathway promotes inhibition (reduces/fine tunes motor activity), but what is the basic flow of neurons in this pathway?

A
  • motor cortex innervates the striatum (caudate nucleus and putamen)
  • striatum innervate globus pallidus lateral (GPL)
  • GPL innervates the subthalamic nuclei
  • the subthalamic nuclei innervates the globus pallidus medial (GPM)
  • the GPM innervates the thalamus
  • thalamus innervates the motor cortex
50
Q

In the indirect pathway involving the basal ganglia the motor cortex innervates the striatum, composed of the putamen and caudate nucleus. What type of fibre provides this innervation and what neurotransmitter is released?

1 - releases glutamate that can then stimulate the striatum
2 - releases lots of GABA which then inhibit the striatum
3 - release less GABA so no inhibition of the striatum
4 - release low levels of glutamate so only small activation of the striatum

A

1 - releases glutamate that can then stimulate the striatum

51
Q

In the indirect pathway involving the basal ganglia the motor cortex innervates the striatum, composed of the putamen and caudate nucleus. Glutaminergic fibre provides this innervation releasing the neurotransmitter glutamate that promotes the activity and innervation of the striatum. What then happens at the synapse at the globus pallidus external (GPE)?

1 - releases glutamate that can then stimulate the GPE
2 - releases lots of GABA which then inhibit the GPE
3 - release less GABA so no inhibition of the GPE
4 - release low levels of glutamate so only small activation of the GPE

A

2 - releases lots of GABA which then inhibit the GPE

52
Q

In the indirect pathway involving the basal ganglia the motor cortex innervates the striatum, composed of the putamen and caudate nucleus. Glutaminergic fibre provides this innervation releasing the neurotransmitter glutamate that promotes the activity and innervation of the striatum. The neurotransmitter GABA is released and inhibits the activity of the globus pallidus lateral/external. What does this then do to the synapse with the subthalamic nuclei?

1 - releases glutamate that can then stimulate the subthalamic nuclei
2 - releases lots of GABA which then inhibit the subthalamic nuclei
3 - release less GABA so no or little inhibition of the subthalamic nuclei
4 - release low levels of glutamate so only small activation of the subthalamic nuclei

A

3 - release less GABA so no or little inhibition of the subthalamic nuclei
- SN can then send excitatory glutamate to GPI

53
Q

In the indirect pathway involving the basal ganglia the motor cortex innervates the striatum, composed of the putamen and caudate nucleus. Glutaminergic fibre provides this innervation releasing the neurotransmitter glutamate that promotes the activity and innervation of the striatum. The neurotransmitter GABA is released and inhibits the activity of the globus pallidus lateral/external. The globus pallidus external inhibits the synapse with the subthalamic nuclei (SN) through the release of GABA, which then causes what?

1 - SN can release high glutamate and activate the globus pallidus medius (GPM)
2 - lots of GABA released from the SN which then inhibit the GPM
3 - less GABA so no or little inhibition of the subthalamic nuclei
4 - low levels of glutamate so only small activation of the subthalamic nuclei

A

1 - SN can release high glutamate and activate the globus pallidus medius (GPM)

  • GPM is stimulated and can release high levels of GABA
  • high levels of GABA will then inhibit/reduce activity of the thalamus
54
Q

In the indirect pathway involving the basal ganglia the motor cortex innervates the striatum, composed of the putamen and caudate nucleus. Glutaminergic fibre provides this innervation releasing the neurotransmitter glutamate that promotes the activity and innervation of the striatum. The neurotransmitter GABA is released and inhibits the activity of the globus pallidus lateral/external. The globus pallidus external inhibits the synapse with the subthalamic nuclei through the release of GABA, which then causes the synapse from the subthalamic nuclei to the globus pallidus medial (GPM) to be stimulated with glutamate. Increased activity to the GPM increases the release of GABA, which then causes what to the thalamus?

A
  • thalamus is then inhibited/reduced firing to the motor cortex
55
Q

How does the substantia nigra (SN) affect the direct pathway?

1 - SN releases dopamine to bind with D1 receptors that accentuate the direct pathway
2 - SN releases dopamine to bind with D1 receptors that inhibits the direct pathway
3 - SN releases dopamine to bind with D2 receptors that accentuate the direct pathway
4 - SN releases dopamine to bind with D2 receptors that inhibits the direct pathway

A

1 - SN releases dopamine to bind with D1 receptors that accentuate the direct pathway

  • SN innervates striatum (caudate nucleus and putamen) through release of dopamine
  • dopamine binds to D1 receptors triggering stimulation
  • glutamate and dopamine increase inhibition or the globus pallidus medial/internal (GPM) by release of GABA
  • GPM is unable to inhibit thalamus and increases thalamus innervation to cortex
56
Q

What does the substantia nigra do to the direct pathway?

A
  • increase motor activity

- amplify the direct pathway and increase muscle activity

57
Q

What disease can damage to the direct pathway with and without the enhanced activity of the substantia nigra (SN) cause?

A
  • Parkinsons disease
  • reduce the initial activity in normal direct pathway
  • reduce the activity of the SN in direct pathway
  • essentially patients struggle to initiate motor activity and maintain motor activity
58
Q

How does the substantia nigra affect the indirect pathway?

1 - SN releases dopamine to bind with D1 receptors that accentuate the direct pathway
2 - SN releases dopamine to bind with D1 receptors that inhibits the direct pathway
3 - SN releases dopamine to bind with D2 receptors that accentuate the indirect pathway
4 - SN releases dopamine to bind with D2 receptors that inhibits the direct pathway

A

3 - SN releases dopamine to bind with D2 receptors that accentuate the indirect pathway

  • substantia nigra innervates striatum (caudate nucleus and putamen) and releases dopamine
  • dopamine binds to D2 receptors (inhibitory), inhibiting the striatum stimulation
  • reduces inhibition of the globus pallidus external (GPE) due to lower levels of GABA
  • GPE has less inhibition so it can increase action potentials on the subthalamic nucleus
  • increased GABA released at subthalmic nucleus meaning less inhibition of the subthalamic nucleus (SN)
  • SN then sends large amounts of glutamate to the GPM
  • GPM is stimulated and releases large amounts of GABA at synapse with the thalamus
  • thalamus has decreased innervation to cortex
59
Q

What does the substantia nigra do to the indirect pathway?

A
  • normal indirect inhibits thalamus

- with substantia nigra there is increased inhibition of the thalamus, meaning less movement

60
Q

Huntingtons disease is classed as a hyperkinetic movement disease. Although the exact mechanism is not fully understood, what is the most likely mechanism?

1 - increased activity of the direct pathway
2 - increased activity of the indirect pathway
3 - reduced activity of the direct pathway
4 - reduced activity of the indirect pathway

A

4 - reduced activity of the indirect pathway

- leads to involuntary movements

61
Q

How is the brainstem connected to the cerebellum?

A
  • 3 peduncles

- anterior, middle and superior

62
Q

The brainstem is connected to the cerebellum by 3 peduncles; anterior, middle and superior. Which peduncles provide afferent and efferent nerve fibres?

A
  • Inferior = mainly afferent
  • Middle = mainly afferent
  • Superior = mainly efferent
63
Q

The cerebellum has 3 lobes, which are related to their function, label them using the terms here:

  • Anterior
  • Posterior
  • Flocculonodular
A

1 - Anterior lobe
2 - Posterior lobe
3 - Flocculonodular lobe

64
Q

What separates the 2 hemisphere of the cerebellum?

1 - falx cerebri
2 - tentorium cerebelli
3 - falx cerebelli
4 - vermis

A

4 - vermis

65
Q

What is the outer grey matter of the cerebellum called?

A
  • cerebellar cortex
66
Q

Within the cerebellum there is the deep cerebellum nuclie, composed of 4 nuclei. Remembering the nemonic, from external to medial:

  • Dont = Dentate nuclei
  • Eat = Emboliform nuclei
  • Greasy = Globose nuclei
  • Food = Fastigial nuclei

Using the names above, label the image:

A

1 - Fastigial nuclei
2 - Globose nuclei
3 - Emboliform nuclei
4 - Dentate nuclei

67
Q

Are all afferents that enter the cerebellum excitatory?

A
  • yes
  • can enter cerebellum cortex
  • can enter cerebellum nuclei
68
Q

The efferents neurons that leave the cerebellum can go one of 2 places, what are they?

1 - motor cortex and basal ganglia
2 - motor cortex and spinal cord
3 - spinal cord and brainstem
4 spinal cord and motor cortex

A

3 - spinal cord and brainstem

69
Q

The cerebral cortex generally sends signal down to the spinal cord to initiate a muscle action. However, the cerebral cortex can also send afferent neurons to the cerebellum. What is the pathway for these afferent neurons to enter the cerebellum?

A
  • cerebral cortex to pons of the brain stem
  • leave the pons and enter the cerebellum
  • crucial for fine tuning motor movements and motor learning
70
Q

The cerebral cortex generally sends signal down to the spinal cord to initiate a muscle action. However, the cerebral cortex can also send afferent neurons to the cerebellum. The cerebral cortex sends afferent neurons to the pons of the brain stem, which then leave the pons and enter the cerebellum. What then happens?

A
  • afferent neurons activate purkinje fibres
  • purkinje fibres send inhibitory signals to dentate nucleus in deep cerebellum nuclei
  • the inhibitory information will travel back to the cerebral cortex to fine tune movement and learn from mistakes

Year 2 NSB (53 decks)

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