The Motor System Flashcards

1
Q

Where are the cell bodies of the upper motor neurones found?

A

In the primary motor cortex

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2
Q

Where are the cell bodies of the lower motor neurones found?

A

In the ventral horn of the spinal cord and brain stem

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3
Q

What are the basic units of the motor system (descending tracts)?

A

Upper motor neurones project onto lower motor neurones which project onto muscles

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4
Q

Where will you not find upper motor neurones (within the CNS)?

A

In the cerebellum or the basal ganglia

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5
Q

Where are upper motor neurones vulnerable to damage?

A

Vulnerable within the CNS only

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6
Q

What is the main motor tract of interest?

A

Lateral Corticospinal Tract

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7
Q

What do upwards extensions of the vertebral horns create?

A

Create cranial nerve motor nuclei

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8
Q

Explain the principles of the patellar reflex arc

A
  • Activation of receptors in the quadracepts travels to spinal cord via the dorsal root ganglion
  • Sensory neurones synapse onto Motor neurones in the ventral horn at L3 to activate contraction of the quads
  • At the same time… the sensory neurones project down to L5 to activate an inhibitory inter neurone that switches off the hamstrings
  • Causes knee jerk reflex
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9
Q

What are the cardinal signs of lower motor neurone damage?

A
  • Hypotonia (little muscle tone)
  • Areflexia (loss of relex arc)
  • Atrophy (of the myotomes supplied)
  • Weakness (if only 1 segment involved- most muscles recieve input from 2 spinal nerves)
  • Fasciculation (flickering contractions under the skin)
  • Fibrillation (uncoordinated contraction of individual muscle fibres)
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10
Q

Why does damage to lower motor neurones cause atrophy?

A

Lower motor neurones supply action potentials and growth factors (trophic factors)

These growth factors are lost if the neurone is transected → atrophy

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11
Q

What type of input are the majority of projections onto lower motor neurones?

A

The majority of inputs to LMN are from inhibitory interneurones

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12
Q

What is the name given the the tracts in which UMN from the face and neck terminate in the brainstem?

A

Corticonuclear / Corticobulbar

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13
Q

Describe the route of neurones in the motor pathway

A
  • Primary motor neurones begin in the primary motor centre of the cortex
  • Multiple motor fibres descend as the corona radiata
  • Motor fibres then converge into the internal capsule (dense white matter)
  • Upper motor neurones continue to descend in the cerebral peduncle of the midbrain and then through the anterior/ventral pons
  • At the level of the medullary pyramids upper motor neurones can take 2 paths
    • 85% decussate and form the lateral corticospinal tract
    • 15% descend ipsilaterally as the anterior/ ventral corticospinal tracts and the decussate at the level of the lower motor neurone of interest
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14
Q

Explain the organisation of upper motor neurones supplying the muscles of the face

A
  • Muscles of facial expression are supplied by the facial nerve (CN VII)
  • The facial nerve motor nuclei is split into an upper and lower half
    • superior 1/2 supplies upper facial musculature
    • inferior 1/2 supplies inferior facial musculature
  • The UMN supplying the superior 1/2 of the face supplies the superior motor nuclei contralateral AND ipsilateral
  • The UMN supplying the inferior 1/2 of the face supplies the inferior motor nuclei contralaterally only
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15
Q

Explain why a stroke is forehead sparing in relation to facial muscle weakness

A

The upper half to the face i.e. forehead, recieves input from both the left and right side due to the contralateral and ipsilateral supply of upper motor neurones to the upper facial nerve nuclei

Therefore damage to one side of the brain in stroke will lose input to the lower half of the face but the upper half is supplied by the unaffected side

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16
Q

How do you distinguish between stroke and Bell’s Palsy?

A

Stroke is forehead sparing

Bell’s palsy all muscles on one half of the face are lost as lesion is in the facial nerve itself

17
Q

What are the signs of upper motor neurone damage?

A
  • Hypertonia (spasticity)
  • Hyper-reflexia
  • Clasp-Knife Rigidity
  • Weakness (develops due to disuse, not denervation)
18
Q

What is clasp knife rigidity?

Explain the pathophysiology for this

A

Initially there is great resistance to pulling a limb that suddenly gives way if pressure continue to be applied

As you pull the limb you activate golgi tendons that activate inhibitory neurones acting on LMN, but golgi tendons have high thresholds so only activate once a high stimulus has been reached

19
Q

What is spinal shock/ acute flacid paralysis?

A

In acute phase UMN lesions can present as acute flaccid paralysis → eventually this will develop into hypertonia over time

20
Q

Identify 1-3 of the internal capsule

A

1= Genu

2= Posterior limb

3= Anterior limb

21
Q

What are the different components of the lenitform nucleus?

A

Putamen (lateral) and Globus pallidus (medial)

22
Q

Where does the upper body map to in the lateral corticospinal tract?

A

The upper body maps medially (opposite to somatosensory)

23
Q

What components make up the striatum?

A

The Caudate + Putamen