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Clinical Neuroscience > Session 5: The Motor System > Flashcards

Session 5: The Motor System Flashcards

1
Q

What are the lower motor neurones? (LMNs)

A

The final common path and when they are activated a muscle contraction will ensue.

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2
Q

What are LMNs controlled by?

A

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

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3
Q

Where can the cell bodies of LMNs be found?

A

In the ventral horn (spinal nerve) or in the cranial nerve motor nuclei (cranial nerve) depending on which kind of nerve.

Examples of cranial nerve motor nuclei are; oculomotor nucles, trochlear nucleus, trigeminal motor nucleus.

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4
Q

How might you test the LMNs?

A

They participate in spinal reflexs and particularly in deep tendon reflexes.

So e.g. patellar tendon reflex can be tested in order to see if the lower motor neurones are intact.

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5
Q

Explain the interaction between lower motor neurones and a spinal reflex.

A

They are typically activated by incoming impulses from senosry neurones that communicate with muscle spindles.

However they can also be inhibited.

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6
Q

Give an example of an inhibition in spinal reflexes.

A

Inhibition of hamstrings which is a muscle antagonist to quadriceps in the patellar reflex activation.

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7
Q

What are primitive spinal reflexes?

A

Spinal reflexes that are found in babies.

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8
Q

Give examples of primitive spinal reflexes.

A

Upgoing plantars

Moro reflex

Palmar grasp

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9
Q

Why are primitive spinal reflexes not found in adults?

A

These reflexes will disappear as the baby grows due to the maturation of descending upper motor neurone pathways.

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10
Q

Signs of damage to LMNs.

A

Weakness

Areflexia

Muscle wasting

Hypotonia (loss of muscle tone)

Fasciculations/Clonus

Negative Babinski’s sign

Fibrillations

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11
Q

Why does damage to lower motor neurones cause muscle weakness?

A

Due to denervation

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12
Q

Why does damage to LMNs cause areflexia?

A

Due to denervation

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13
Q

Why does damage to LMNs cause muscle wasting?

A

Due to the loss of trophic support to the muscle from the LMN across the neuromuscular junction.

The LMNs supply trophic factors (growth factors) to the muscle. If this is lost then atrophy will ensue.

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14
Q

Why does damage to LMNs cause hypotonia?

A

Due to loss of muscle activation.

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15
Q

Why does damage to LMNs cause fasciculations?

A

Due to up-regulation of msucle nACh receptors to try to compensate for the denervation.

This causes spontaeous and brief contractions that looks like flickering.

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16
Q

Where are upper motor neurones found? (UMNs)

A

In the primary motor cortex (precentral gyrus)

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17
Q

How do the UMNs communicate with the LMNs?

A

They are synapse onto the LMNs directly or indirectly via interneurons in the ventral horn or cranial nerve motor nuclei.

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18
Q

Are neurones in the basal ganglia and cerebellum UMNs?

A

No

This means that damage here will not cause UMN syndromes.

19
Q

What is the net effect of UMNs on LMNs?

A

Inhibition

20
Q

Explain the route of the axon of a UMN.

A

Corono radiata -> internal capsule -> cerebral peduncle in the midbrain -> ventral pons -> medullary pyramids (where they decussate) -> lateral corticospinal tract (in lateral funiculus) -> ventral horn -> synapse (directly or indirectly by inhibitory interneurones).

21
Q

What is lateral corticospinal tract involved in?

A

Fine motor control in the limbs and primarily the distal extremities.

However all of limb can be affected by a UMN lesion.

22
Q

What do the corticospinal tracts supply?

A

The musculature of the body

23
Q

What do the corticobulbar tracts supply?

A

The musculature of the head and neck

24
Q

Explain the route of the upper motor neurones that supply facial structures.

A

They leave the pathway in the brainstem and form the corticobulbar tract.

This will innervate the LMNs in the cranial nerve motor nuclei.

25
Q

Why is the facial motor nucleus special?

A

Because it splits into two halves where one half supplies the superior face (occipitofrontalis) and the other half supplies the inferior face which is more or less the remaining muscles.

26
Q

What do the upper half of the face receive UMNs from?

A

Both hemispheres.

27
Q

Where does the lower half of the face receives UMNs from?

A

The contralateral UMN input

28
Q

What is the significance of superior face being supplied by both hemispheres and inferior face being supplied by contralateral UMN input?

A

This means that a UMN lesion involving the face will spare the forehead.

29
Q

What will a UMN lesion involving the face in the right hemisphere cause?

A

It will cause paralysis in the left lower quadrant of the face.

30
Q

How does a facial nerve palsy differ to a UMN lesion facial palsy?

A

A facial nerve palsy will involve all muscles of facial expression.

A UMN lesion facial palsy will only involve the contralateral lower part of the face sparing the forehead.

31
Q

Signs of UMN damage.

A

Muscle weakness

Hypertonia

Spasticity

Hyperreflexia

Clasp-Knife rigidity

Disuse atrophy (not denervation)

Extensor plantar reflexes also called positive Babinski’s sign

Acute flaccid paralysis

32
Q

Why is there weakness in UMN lesion?

A

Due to loss of direct excitatory inputs onto LMNs from UMNs.

33
Q

Why is there hypertonia in UMN lesion?

A

Due to loss of descending inhibition since the net effect of UMNs on LMNs is inhibition.

34
Q

Why is there hyperreflexia in UMN lesions?

A

Due to loss of descending inhibition leading to an overactive reflex arc.

35
Q

Why is there a positive Babinski’s sign?

A

Due to loss of descending modulation of spinal reflexes.

36
Q

Explain spinal shock.

A

A phenomenon that occurs in the days immediately following a UMN lesion.

There is initially flaccid paralysis with areflexia and will look like a LMN lesion.

However tone will then increase causing hypertonia and the reflexes will become exaggerated leading to hyperreflexia.

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

37
Q
A
38
Q

Are LMNs lesions found in CNS or PNS?

A

Could be either.

39
Q

Function of the ventral/anterior corticospinal tract.

A

Innervation of proximal postural muscles

40
Q

Where do axons going to the lateral corticospinal tract decussate?

A

They have decussated in the medulla pyramids

41
Q

Where do the anterior/ventral corticospinal tract decussate?

A

At the spinal level.

They do not decussate at the medullary pyramids and instead descend ipsilaterally.

42
Q

Shape of internal capsule in cross section.

A

V-shaped

43
Q

What does a LMN lesion of facial nerve cause?

A

Bell’s palsy

44
Q

Explain clasp knife rigidity.

A

A sign of upper motor neuron lesion and is due to golgi tendon reflex.

Clinical Neuroscience (22 decks)

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