5.1.2 Upper Motor Neurones Flashcards

1
Q

Where do you find UMNs?

A

Primary motor cortex (pre-central gyrus)

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2
Q

Where do UMNs syanpse?

A

Syanpse directly onto LMNs in the ventral horn or cranial nerve motor nuclei

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3
Q

What type of neurones are in the basal ganglia and cerebellum?

A

Not upper motor neurones- damage to these structures does not cause an UMN syndrome

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4
Q

What is the net of UMNs on LMNs?

A

Inhibiton, only causes excitation when stimulus large enough to overcome inhibition

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5
Q

Outline the pathway in which UMNs descend from the motor cortex

A
  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) Only 85%
  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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6
Q

Where do UMNs decussate?

A

85% decussate in the medullary pyramids forming the lateral corticospinal tract

15% decussate at the level of their target LMNs forming the ventral corticospinal tract

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7
Q

What is the lateral corticospinal tract involved in?

A

Fine motor control in the limbs
Primarily distal extremities (all of limb can be affected by a UMN lesion)

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8
Q

What is the route of UMNs supplying facial structures?

A

Leave the pathway in the brainstem and form the corticobulbar tract which innervates LMNs in the cranial nerve motor nuclei

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9
Q

What is significant about the facial motor nucleus?

A

Split into two halves, one half supplies the upper half of the face and the other supplies the lower half of the face

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10
Q

How do the superior and inferior nucleus innervations differ?

A

Superior has both contralateral and ipsilateral innervation

Inferior only has contralateral control

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11
Q

Why are UMN lesions involving the face forehead sparing?

A

Forehead is an upper face structure, when the contralateral supply is knocked out the lower half of the face no longer has any nerve supply but the upper half also has the ipsilateral innervation, thus still recieves impulses

In stroke you may have forehead sparing

True facial nerve palsy you will not have any sparing as the entire facial nerve nucleus is affected

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12
Q

What are some signs of UMN lesions?

A

Weakness- due to loss of excitatory inputs onto LMNs from UMNs

Hypertonia- loss of descending inhibition (also called spasticity, flexers are stronger than extensors)

Hyperreflexia- overactive reflex arc, no inhibition

Extensor plantar reflexes- reversion to situation in baby, loss of descending modulation of spinal reflexes

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13
Q

What is spinal shock syndrome?

A

Occurs days immediately following a UMN lesion

Initially flaccid paralysis with areflexia shadowing a LMN lesion

Tone then increases becoming hypertonia and reflexes become exaggerated hyperreflexia

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14
Q

What signs are present in both UMN and LMN lesions simultaneously?

A

LMN lesion signs as these are needed to transmit the UMN signs

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15
Q

What is the golgi-tendon reflex?

A

Golgi bodies sit in tendons and detect sudden high increases in bone and muscle tension

Causes stimulation of antagonist to inhibit muscle action

e.g. suddenly carrying heavy box, triceps innervated to antagonise action and drop the box to prevent damage

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16
Q

Why does a stroke affecting the lateral motor cortex compromise swallowing?

A

Lateral side is pharynx, larynx etc.

Results in denervation of cranial nerve nuclei which distribute lower motor neurones in the vagus nerve

Difficulty swallowing

17
Q

What midbrain structure is important for motor control

A

Red nucleus