Motor System Flashcards

1
Q

What controls LMNs?

A

Upper motor neurones which descend through the cord or brainstem and synapse on LMNs.

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2
Q

Where are the cell bodies of LMNs found?

A

Ventral horn and in cranial nerve motor nuclei (e.g. oculomotor nucleus, trochlear nucleus, trigeminal motor nucleus..)

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3
Q

What happens to LMNs when they receive impulses from sensory neurones?

A

They are typically activated.

BUT, can be inhibited e.g. hamstrings are inhibited following the patellar reflex (as otherwise the knee wouldn’t move as the antagonise the quads).

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4
Q

Give examples of some of the primitive reflexes that occur in babies.

A

Up going plantars
Moro reflex (arms our when feel like falling)
Palmar grasp

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5
Q

Why do the primitive motor reflexes disappear as we become toddlers?

A

Because of the maturation of descending upper motor neurone pathways.

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6
Q

What signs are seen in a muscle supplied by a damaged lower motor neurone.

A

Weakness (due to denervation)

Areflexia (due to denervation)

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

Hypotonia (due to loss of muscle activation)

Fasiculations (due to up-regulation of muscle nAChTs to try and compensate for denervation)

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7
Q

Where are UMNs found?

A

Found in the primary motor cortex (pre-central gyrus)

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8
Q

What is the net effect of UMNs on LMNs?

A

Inhibition - this explains most of the features of UMN lesions

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9
Q

List the structures the UMNs travel through as they descend from the motor cortex

A

Corona radiata
Internal capsule
Cerebral peduncle in the midbrain
Pons
Medullary pyramids
Decussation of the pyramids (in the caudal medulla)
Lateral corticospinal tract (in lateral funiculus of the cord)
Ventral horn
Synapse (directly or (usually) indirectly via inhibitory interneurones) on LMNs

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10
Q

What is the lateral corticospinal tract involved in?

A

Fine motor control in the limbs, primary the distal extremities.

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11
Q

What is the corticobulbar / corticonuclear tract involved in?

A

UMNs that supply facial structures (structures innervated by cranial rather than spinal nerve) leave the brainstem and form the tracts which innervate LMNs in the cranial motor nuclei

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12
Q

Why is the facial motor nucleus special?

A

Because it is split into two halves.

One supplies the superior face (mostly occipitofrontalis) and one supplies the inferior face (most of the remaining muscles).

The part of the facial nucleus that supplies the upper half of the face receives UMNs from both hemispheres whereas the part that supplies the lower face onto receives a contralateral UMN input.

Hence, UMN lesions involving the face will spare the forehead (as opposed to true facial nerve palsies which affect all muscles of facial expression).

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13
Q

What are the signs of a damaged UMN?

A

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

Hypertonia (due to loss of descending inhibition)

Hyperreflexia (overactive reflex arc)

Extensor plantar reflexes (due to loss of descending modulation of spinal reflexes)

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14
Q

What is spinal shock?

A

A phenomenon that occurs immediately following a UMN lesion.

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

The mechanism of this is unclear, but is related to neuroplasticity in the spinal cord.

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