Motor Control II Flashcards

1
Q

Describe a feedback and feedforward mechanism in controlling movement

A

A change in body position initiates rapid compensatory feedback message from the brainstem vestibular nuclei to spinal cord motor neurones to correct postural instability -> feedback

But, before movements begin, the brainstem reticular formation nuclei (which are controlled by the cortex) initiate feedforward anticipatory adjustments to stabilise posture -> feedforward

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2
Q

Describe the outcome of damage to descending motor pathways (UMN)

A

Cortical damage causes immediate flaccidity of contralateral muscle

  • Initial hypotonia – ‘spinal shock’ as spinal circuits are deprives of cortical input
  • Day later spinal circuits regain function – spared connection strengthens and new connections formed.
  • Bibinski sign – extension of toes to stimulus
  • Spasticity – increased muscle tone, hyperactive stretch reflex, clonus oscillatory muscle in response to stretch
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3
Q

What in the dorsal thalamus provides input into area 6 (prefrontal cortex)?

A

Vental lateral nucleus (VLo)

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4
Q

What does the VLo receive input from?

A

Basal ganglia

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5
Q

What does the basal ganglia receive input from?

A

The frontal, prefrontal and parietal cortex.

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6
Q

What is the loop of information?

A

From the cortex though the thalamus and basal ganglia, through the VLo and back up into the SMA in the cortex (area 6).

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7
Q

What are the major components of the basal ganglia?

A

Corpus striatum – include two principal nuclei, the caudate and the putamen.

  • They are input zone of the basal ganglia to receive input from all over the cortex
  • Corticostriatal pathway – multiple parallel pathway with different functions
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8
Q

What structure of the corpus striatum of the basal ganglia (caudate and putamen) makes these structures in input zone?

A

Medium spiny neurones in putamen and caudate nucleus receive excitatory (glutamatergic) cortical input on the dendrites.

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9
Q

What do the corpus stratum (caudate nucleus and putamen) communicate with the rest of the basal ganglia?

A

Cortical cell axons are inhibitory (GABAergic) and project to globus pallidus and to substantia nigra.

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10
Q

When do the putamen and caudate nucleus fire?

A

The putamen fires before limb/trunk movement and the caudate fires before eye movement. They are both predictive of movements.

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11
Q

In the motor loop, state which connection are inhibitory or excitatory

A
  1. Cortex to putamen – excitatory
  2. Putamen to globus pallidus – inhibitory
  3. Globus pallidus to VLo neurone – inhibitory
  4. VLo back to SMA – excitatory
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12
Q

Why does cortical activation of putamen boost cortical excitation?

A

At rest, globus pallidus neurones are spontaneously active and inhibit VLo.

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13
Q

Why is the motor loop a positive feedback loop?

A

So cortical excitation causes:

  1. Excites putamen which inhibits the inhibitory globus pallidus
  2. Inhibition of GP releases cell in VLo from inhibition, so activity in VLo boosts SMA activity (exciting UMN)
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14
Q

What are the two types of loops which cortical input connects to the basal ganglia?

A

Indirect and direct motor loops

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15
Q

Describe the direct loop from the cortex to the basil ganglia

A
  • Acts as a positive feedback loop
  • Enhances the initiation of movements by the SMA
  • GP neurones are spontaneously active at rest so they tonically inhibit (restrain) VL thalamus (VLo)
  • Inputs from the cortex release VLo inhibition –> excitation of SMA
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16
Q

Describe the indirect loop from the cortex to the basil ganglia

A

• Antagonises the direct route
1. Striatum (putamen, caudate) inhibits GPe (globus pallidus external) -> inhibits both GPi (GP internal) and STN (subthalamic nuclei)

  1. Excited STN excites GPi -> inhibits VLo
  2. But the cortex also excites STN; this excites GPI which inhibits the thalamus (VLo)
17
Q

What is the difference between the direct and indirect pathways?

A

Direct pathway selects specific motor actions (via caudate/putamen)
Indirect pathway suppresses competing/inappropriate action (via subthalmic nucleus)

18
Q

What causes Parkinson’s disease?

A

Degeneration of neurones in substantial migration (SN) and their dopaminergic (excitatory) inputs to the striatum

Dopamine can enhance cortical inputs through the ‘direct’ pathway and suppress inputs through ‘indirect’ pathway

The depletion of dopamine closes down activation of the focussed motor activities that funnel through thalamus to SMA, interfering with the direct and indirect pathway.

19
Q

What happens in Parkinson’s disease?

A

Slowness, difficult to make voluntary movements, increased muscle tone (rigidity), tremor of hand and jaw

20
Q

What happens in Huntington’s disease?

A

Hyperkinesia with dementia and personality disorders due to loss of basal ganglia

  • Hereditary
  • Characteristic chorea – spontaneous, uncontrolled, rapid flicks and major movements with no purpose
21
Q

What causes Hungtington’s disease?

A

Caused by profound loss of caudate, putamen and globus pallidus, so loss of the ongoing inhibitory effects of the ganglia

22
Q

What do lesions in the cerebellum cause?

A

Produce uncoordinated inaccurate movements -> ataxia

• Fail to touch nose with eye shut (similar to alcohol which depresses cerebellar circuits)

23
Q

What is the importance of the cerebellum?

A

Relays back to the cortex via ventrolateral thalamus and instructs on direction, timing and force of muscular contraction

Provide detailed sequence of timed contractions for skilled movements