Session 5: The Motor System

Question 1

What are the lower motor neurones? (LMNs)

Answer 1

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

Question 2

What are LMNs controlled by?

Answer 2

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

Question 3

Where can the cell bodies of LMNs be found?

Answer 3

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.

Question 4

How might you test the LMNs?

Answer 4

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.

Question 5

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

Answer 5

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

However they can also be inhibited.

Question 6

Give an example of an inhibition in spinal reflexes.

Answer 6

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

Question 7

What are primitive spinal reflexes?

Answer 7

Spinal reflexes that are found in babies.

Question 8

Give examples of primitive spinal reflexes.

Answer 8

Upgoing plantars

Moro reflex

Palmar grasp

Question 9

Why are primitive spinal reflexes not found in adults?

Answer 9

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

Question 10

Signs of damage to LMNs.

Answer 10

Weakness

Areflexia

Muscle wasting

Hypotonia (loss of muscle tone)

Fasciculations/Clonus

Negative Babinski’s sign

Fibrillations

Question 11

Why does damage to lower motor neurones cause muscle weakness?

Answer 11

Due to denervation

Question 12

Why does damage to LMNs cause areflexia?

Answer 12

Due to denervation

Question 13

Why does damage to LMNs cause muscle wasting?

Answer 13

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.

Question 14

Why does damage to LMNs cause hypotonia?

Answer 14

Due to loss of muscle activation.

Question 15

Why does damage to LMNs cause fasciculations?

Answer 15

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.

Question 16

Where are upper motor neurones found? (UMNs)

Answer 16

In the primary motor cortex (precentral gyrus)

Question 17

How do the UMNs communicate with the LMNs?

Answer 17

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

Question 18

Are neurones in the basal ganglia and cerebellum UMNs?

Answer 18

No

This means that damage here will not cause UMN syndromes.

Question 19

What is the net effect of UMNs on LMNs?

Answer 19

Inhibition

Question 20

Explain the route of the axon of a UMN.

Answer 20

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).

Question 21

What is lateral corticospinal tract involved in?

Answer 21

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

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

Question 22

What do the corticospinal tracts supply?

Answer 22

The musculature of the body

Question 23

What do the corticobulbar tracts supply?

Answer 23

The musculature of the head and neck

Question 24

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

Answer 24

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

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

Question 25

Why is the facial motor nucleus special?

Answer 25

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.

Question 26

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

Answer 26

**Both** hemispheres.

Question 27

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

Answer 27

The **contralateral** UMN input

Question 28

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

Answer 28

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

Question 29

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

Answer 29

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

Question 30

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

Answer 30

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.

Question 31

Signs of UMN damage.

Answer 31

Muscle weakness Hypertonia Spasticity Hyperreflexia Clasp-Knife rigidity Disuse atrophy (not denervation) Extensor plantar reflexes also called positive Babinski's sign **Acute** flaccid paralysis

Question 32

Why is there weakness in UMN lesion?

Answer 32

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

Question 33

Why is there hypertonia in UMN lesion?

Answer 33

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

Question 34

Why is there hyperreflexia in UMN lesions?

Answer 34

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

Question 35

Why is there a positive Babinski's sign?

Answer 35

Due to loss of descending modulation of spinal reflexes.

Question 36

Explain spinal shock.

Answer 36

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.

Question 37

Answer 37

Question 38

Are LMNs lesions found in CNS or PNS?

Answer 38

Could be either.

Question 39

Function of the ventral/anterior corticospinal tract.

Answer 39

Innervation of proximal postural muscles

Question 40

Where do axons going to the lateral corticospinal tract decussate?

Answer 40

They have decussated in the medulla pyramids

Question 41

Where do the anterior/ventral corticospinal tract decussate?

Answer 41

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

Question 42

Shape of internal capsule in cross section.

Answer 42

V-shaped

Question 43

What does a LMN lesion of facial nerve cause?

Answer 43

Bell's palsy

Question 44

Explain clasp knife rigidity.

Answer 44

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