Movement Flashcards

1
Q

Define a “motor unit” (1)

A

An alpha motor neuron and the muscle fibres it innervates.

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2
Q

Explain how motor neurons use a rate code to signal the amount of force to be exerted by a muscle (6)

A

An increase in the rate of action potentials fired by the motor neuron causes an increase in the amount of force that the motor unit generates. When the motor neuron fires a single action potential, the muscle twitches slightly, and then relaxes back to its resting state. If the motor neuron fires after the muscle has returned to baseline, then the magnitude of the next muscle twitch will be the same as the first twitch. However, if the rate of firing of the motor neuron increases, such that a second action potential occurs before the muscle has relaxed back to baseline, then the second action potential produces a greater amount of force than the first (i.e., the strength of the muscle contraction summates). With increasing firing rates, the summation grows stronger, up to a limit, and when successive action potentials no longer produce a summation of muscle contraction (because the muscle is at its maximum state of contraction), the muscle is in a state called tetanus.

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3
Q

With the aid of an annotated diagram showing the relevant pathways, explain how Mr Davies’s brain controls movement of his right arm (5)

A

Diagram indicating:

  • UMN in motor cortex, anterior to central sulcus projecting axon through internal capsule, brain stem, decussating in pyramids of the medulla to synapse in cervical level of spinal cord on LMN in ventral horn of spinal cord
  • The UMN releases glutamate which stimulates the LMN to release acetylcholine onto the target muscle at the neuromuscular junction
  • Acetylcholine acts on nicotinic receptors in the postsynaptic membrane to depolarize the muscle membrane, opening voltage-gated sodium channels, producing an action potential in the muscle membrane which leads to muscle contraction.
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4
Q

Use a diagram(s) to show the arrangement of the neurones (and their neurotransmitters) involved in the efferent pathway for locomotion, including the site of the lesion (5½)

A

Diagrams showing:

  • Cell body of UMN in motor cortex, terminal in spinal cord (1)
  • Cell body of LMN in ventral horn of spinal cord terminal on target muscle fibre (1)
  • Compression of descending fibres of UMN (1)
  • UMN uses glutamate as a neurotransmitter (1) - UMN = site of lesion (½)
  • LMN uses acetylcholine as a neurotransmitter (1)
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5
Q

Describe the role & function of the basal nuclei in movement & describe how movement will be affected by a SN tumour (10)

A

The basal ganglia has no direct access to local circuitry neurons in the spinal cord, it controls movement by regulating the activity of upper motor neurons. Abnormalities in the basal ganglia results in a wide spectrum of movement disorders (e.g. Parkinson’s disease, Huntington’s disease) (1)

Direct pathway: Glutamatergic input from the cortex to the striatum stimulates the medium spiny neurons of the striatum to secrete GABA which in turn inhibits the globus pallidus internal segment so that less GABA is secreted & less inhibition (disinhibition) of the thalamus results in more glutamate being released to stimulate the cortex to initiate muscle contraction (4)

Indirect pathway: Glutamatergic input from the cortex to the medium spiny neurons in the striatum stimulate the secretion of GABA which in turn inhibits the globus pallidus external segment resulting in less inhibition (decreased GABA secretion) of the subthalamic nucleus (disinhibition) resulting in the stimulation of globus pallidus internal segment by glutamate to secrete GABA and inhibition of the thalamus. By inhibiting the thalamus glutamate is not secreted to stimulate the cortex and no movement is initiated (4)

A SN tumour will result in decreased dopaminergic transmission to stimulate the striatum. Dopamine acts to stimulate the direct pathway via D1 receptors and acts to inhibit the indirect pathway via D2 receptor signalling (1)

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6
Q

Hyperactivity may result from a disturbance in the dopamine neurotransmitter system in the brain. Explain how dopamine acts to initiate movement (5)

A

Dopamine acts on D1 receptors in the striatum to stimulate the direct pathway, i.e. glutamate neurons projecting from cortex to striatum to inferior globus pallidus, or substantia nigra pars reticulate, to thalamus and back to cortex, to provide positive feedback to the cortex. At the same time dopamine acts on D2 receptors to inhibit the indirect pathway, cortex - striatum - external GP-STN - internal GP/SNr – thalamus – cortex, which is inhibitory thereby disinhibiting neurons in the thalamus to give positive feedback to the cortex to select and initiate appropriate movement.)

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7
Q

Use a diagram (2) to illustrate the different parts of the cerebellum and the nuclei that are involved in planning complex movements (1), control axial muscles (1), control distal muscles of the limbs (1)

A

Diagram showing four main subdivisions (1)

  • The cerebrocerebellum & dentate nuclei - planning complex movements (1)
  • The vermis & fastigial nucleus control axial muscles (1)
  • Intermediate hemisphere & interposed nuclei control the distal muscles of limbs (1)
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8
Q

Briefly discuss the role of the cerebellum in terms of its neural input and output related to movement (3)

A

The cerebellum influences movement by adjusting the operation of the motor centers in the cortex and brainstem to match the actual movement (monitored via proprioceptive feedback) more closely with the planned movement (1). The cerebellum is able to do this by receiving neural input from the cortex, brain stem, and spinal cord (1) [afferent fibers, mainly Mossy fibers, synapse with granule cells, Purkinje dendrites and other cerebellar neurons in the molecular layer. Efferent cerebellar cortex fibers are the Purkinje cell axons that form white matter tracts below the granular layer and synapse with the deep nuclei.] and returning neural output from the deep cerebellar nuclei to the premotor and motor cortex via brainstem relays (thalamus, RN, VN) and hence indirectly to the spinal cord (1).

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9
Q

Describe the mechanism by which the cerebellum is able to correct for motor signal errors and how synaptic plasticity within the cerebellum circuitry contributes to motor learning (6)

A

The mossy fibre inputs to the cerebellum convey the sensory information used to evaluate the overall sensory context of the movement (1)

The error signal is believed to be conveyed by the climbing fibre inputs (1)

Climbing fibres are known to be especially active when an unexpected event occurs, e.g. when a greater load than expected is placed on a muscle (1)

The large divergence of input from the mossy fibres to the granule cells to the parallel fibres is believed to create complex representations of the entire sensory context and the desired motor output (1)

When the desired output is not achieved, the climbing fibres signal this error and trigger a calcium spike in the Purkinje cell (1)

The influx of calcium changes the synaptic connection strengths (plasticity) between parallel fibres and Purkinje cells, such that the next time the same behavioural context occurs, the motor output will be modified to more closely approximate the desired output (1)

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10
Q

Explain why damage to the cerebellum causes past-pointing (1)

A

Damage to the intermediate hemisphere causes past-pointing due to poor control of antagonist muscles at end of movement

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11
Q

Name the part of the nervous system that, if damaged, would give rise to impairment of fine motor skills with poor hand eye coordination (1) & Name one other possible consequence of damage to this structure (1)

A

Intermediate hemisphere of the cerebellum  Impaired planning of movement, impaired learning of motor skills, difficulty maintaining balance.

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