S6 - The Motor System Flashcards

1
Q

if the Lower motor neurons (LMN) are damaged what signs are seen?

A

Weakness (due to denervation)

Areflexia (due to denervation)

Wasting/Atrophy (due to loss of trophic support to the muscle from the LMN across the neuromuscular junction)

Hypotonia (due to loss of muscle activation)

Fasciculation (due to up-regulation of muscle nAChRs to try to compensate fordenervation)

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2
Q

if the Upper motor neurons (UMN) are damaged what signs are seen?

A

Weakness (due to loss of direct excitatory inputs onto LMNs from UMNs)

Hypertonia (due to loss of descending inhibition – remember that the net effect ofvUMNs on LMNs is inhibition)

Hyperreflexia (same as hypertonia – an overactive reflex arc)

Extensor plantar reflexes (this is a reversion to the situation in a baby, due to loss of descending modulation of spinal reflexes)

Spinal Shock (acute flacid paralysis)

clasp Knife rigidity

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3
Q

what is spinal shock ?

A

Spinal shock is a phenomenon that occurs in the days immediately following a UMN Lesion.

Initially there is flaccid paralysis with areflexia (like in LMN lesions) but then tone increases (becoming hypertonia) and reflexes become exaggerated (hyperreflexia).

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4
Q

where are LMN cell bodies found?

A

Their cell bodies are found in the ventral horn, brainstem

and in cranial nerve motor nuclei (oculomotor nucleus, trochlear nucleus, trigeminal motor nucleus etc)

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5
Q

LMN, when activated cause muscle contraction. They are controlled by UMN, which sends mostly inhibitory signals to prevent constant muscular contraction.

A

this can be said like:

net inhibtion of LMN’s by UMN’s via Inhibitory Interneurons

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6
Q

what and where do motor neurons run through the spinal cord, and what is the clinical relevance

A

they descend in the lateral corticospinal tract, which lies between the dorsal and ventral horns.

they are affected commonly in strokes

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7
Q

UMN: cell body location

A

located in the primary motor cortex

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8
Q

where are UMN and LMN located ?

A

UMN are entirely in the CNS

LMN’s are split between the CNS and PNS - so can be affected by either location.
BUT
a LMN cell body or axon destruction cause the same sings

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9
Q

explain out loud the coordination of LMN for the patellar reflex

A

check this against your drawing in 6,7

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10
Q

outline and explain the pathway from motor cortex to LMN of a UMN

A

Their axons descend from the motor cortex through the following structures:

  1. Corona radiata
  2. Internal capsule
  3. Cerebral peduncle in the midbrain
  4. Pons
  5. Medullary pyramids
  6. Decussation of the pyramids (in the caudal medulla)
  7. Lateral corticospinal tract (in the lateral funiculus of the cord)
  8. Ventral horn
  9. Synapse (directly but usual indirectly via inhibitory interneurones) on LMNs
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11
Q

what are the roles of the Lateral corticospinal tract and the ventral corticospinal tract

A

distal muscle - fine control

proximal postural muscles

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12
Q

how do UMN innervate cranial nerves ?

explain the case of Facial nerve and check vs your drawing in 6,7 (drawing may help)

A

UMNs that supply facial structures leave the pathway in the brainstem and form the corticobulbar (aka the
corticonuclear) tract, which innervates LMNs in the cranial nerve motor nuclei

  1. The facial motor nucleus is a special case of a cranial nerve motor nucleus, in that it
    is split into two halves – one supplies the superior face (mostly occipitofrontalis) and one the inferior face (most of the remaining muscles)
  2. The part of the facial motor nucleus that supplies the upper half of the face receives UMNs from both hemispheres, whereas the part that supplies the lower face only receives a contralateral UMN input
  3. Hence UMN lesions involving the face will spare the forehead (as opposed to true facial nerve palsies which affect all of the muscles of facial expression)
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