Session 5

Question 1

What are lower motor neurones?

Answer 1

• They are the ‘final common path’, and when activated will cause muscle contraction
• They are controlled by upper motor neurones, which descend through the cord or brainstem and synapse on LMNs
• Their cell bodies are found in the ventral horn and in cranial nerve motor nuclei (oculomotor nucleus, trochlear nucleus, trigeminal motor nucleus etc)
• They participate in spinal reflexes, particularly the deep tendon reflexes (highly clinically relevant)
• They are typically activated by incoming impulses from sensory neurones that communicate with muscle spindles (muscle stretch reflex), but can also be inhibited (best example is inhibition of antagonist muscles such as hamstrings following patellar reflex activation)

Question 2

Describe the spinal reflexes of babies

Answer 2

• ‘Primitive’ spinal reflexes exist in babies (such as up going plantars, Moro reflex and palmar grasp), but these reflexes disappear as a baby grows due to maturation of descending upper motor neurone pathways

Question 3

What can be seen when lower motor neurone are damaged?

Answer 3

• When damaged, the following signs can be seen in the muscles supplied by the damaged lower motor neurones:

o Weakness (due to denervation)

o Areflexia (due to denervation)

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

o Hypotonia (due to loss of muscle activation)

o Fasciculation (due to up-regulation of muscle nAChRs to try to compensate for denervation)

Question 4

What are upper motor neurones?

Answer 4

• They are found in the primary motor cortex (precentral gyrus)
• They synapse onto LMNs directly (or indirectly) in the ventral horn or cranial nerve motor nuclei . Hence, neurones in the basal ganglia and cerebellum are NOT upper motor neurones (damage to these structures does not cause an UMN syndrome, but something completely different)
• The net effect of UMNs on LMNs is inhibition – this explains most of the features of UMN lesions

Question 5

Describe the pathway of an upper motor neurone

Answer 5

• 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

Question 6

Which tract contains upper motor neurones involved in fine motor control in the limbs?

Answer 6

• The lateral corticospinal tract is involved with fine motor control in the limbs, primarily the distal extremities (but all of limb can be affected by a UMN lesion)

Question 7

How do upper motor neurones help innervate muscles in the face?

Answer 7

• UMNs that supply facial structures (i.e. structures innervated by cranial nerves not spinal nerves) 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)

Question 8

What signs are seen when upper motor neurones are damaged?

Answer 8

• When UMNs are damaged, the following signs are evident in the parts of the body supplied by the relevant UMNs

1. Weakness (due to loss of direct excitatory inputs onto LMNs from UMNs)
2. Hypertonia (due to loss of descending inhibition – remember that the net effect of UMNs on LMNs is inhibition)
3. Hyperreflexia (same as hypertonia – an overactive reflex arc)
4. Extensor plantar reflexes (this is a reversion to the situation in a baby, due to loss of descending modulation of spinal reflexes)

Question 9

What is spinal shock?

Answer 9

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