S5) The Motor System Flashcards
What is a lower motor neurone?
A lower motor neuron (LMN) is a multipolar neuron which connects the upper motor neurone (UMN) to the skeletal muscle it innervates
Where is a lower motor neurone found?
A lower motor neurone is located in either the ventral horn of the spinal cord or the cranial nerve nuclei of the brainstem
What do lower motor neurones do?
LMNs participate in spinal reflexes, particularly the deep tendon reflexes
What are primitive spinal reflexes and when are they seen?
Primitive spinal reflexes are reflexes which exist in babies but disappear as a baby grows due to maturation of descending upper motor neurone pathways
LMNs can be activated and inhibited.
Describe how they are activated
LMNs are activated by incoming impulses from sensory neurones that communicate with muscle spindles (muscle stretch reflex)
Describe the role of the interneuron in the reflex arc at the knee
- Inhibitory interneuron inhibits the contraction of the flexor hamstring muscles
- Stimulatory interneuron stimulates the contraction of the extensor muscles
What are the five principle features of LMN damage?
- Fasciculations
- Muscle atrophy
- Hyporeflexia/ areflexia
- Hypotonia/ atonia
- Flaccid muscle weakness or paralysis
Explain the pathophysiology of the fasciculations seen in LMN damage
Fasciculations caused by uncoordinated muscle contractions due to up-regulation of muscle nAChRs to try to compensate for damaged motor neurones (denervation)
Explain the pathophysiology of the muscle atrophy seen in LMN damage
Muscle atrophy is caused by the loss of neurotrophic growth factors from the α-motor neuron to the muscle membrane (across neuromuscular junction)
Explain the pathophysiology of the hyporeflexia seen in LMN damage
Hyporeflexia/areflexia caused by disruption of the efferent portion of the reflex arc leading to decreased/absent reflexes
Explain the pathophysiology of the hypotonia seen in LMN damage
Hypotonia / atonia caused by loss of muscle activation due to loss of α-motor neurons
Explain the pathophysiology of the muscle weakness seen in LMN damage
Flaccid muscle weakness due to α-motor neuron damage, muscles receive a weakened/absent signal to contract
What is an upper motor neurone?
An upper motor neuron is a neuron whose cell body originates in the cerebral cortex or brainstem and terminates within the brainstem or spinal cord
Where is an upper motor neurone found?
An upper motor neuron originates either in the primary motor cortex (pre-central gyrus) / in the brain stem (CNS)
Where in the CNS are upper motor neurones absent?
- Basal ganglia
- Cerebellum
Hence, damage to these structures does not cause an UMN syndrome
What effect do UMNs have on LMNs?
The net effect of UMNs on LMNs is inhibitory (inhibition > stimulation)
Describe the 8 structures which the descending axons of UMNs pass through
⇒ Corona radiata
⇒ Internal capsule
⇒ Cerebral peduncle in the midbrain
⇒ Pons
⇒ Medullary pyramids
⇒ Decussation of the pyramids (in the caudal medulla)
⇒ Ventral horn
⇒ Synapse (directly/via inhibitory interneurones) on LMNs
What is the role of the lateral corticospinal tract?
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)
Describe the anatomical course of UMNs that innervate facial structures (i.e. structures innervated by cranial nerves not spinal nerves)
UMNs that supply facial structures leave the pathway in the brainstem and form the corticobulbar tract (aka corticonuclear tract) which innervates LMNs in the cranial nerve motor nuclei
Explain how the facial motor nucleus differs from a usual cranial nerve motor nucleus
The facial motor nucleus is split into two halves – one supplies the superior face (mostly occipitofrontalis) and one the inferior face (most of the remaining muscles)
Explain how the facial motor nucleus functions
- The part of the facial motor nucleus that supplies the upper half of the face receives UMNs from both hemispheres
- The part of the facial motor nucleus that supplies the lower face only receives a contralateral UMN input
Explain how UMN lesions differ from true facial nerve palsies
- UMN lesions involving the face will spare the forehead
- True facial nerve palsies will affect all of the muscles of facial expression
What are the four principle features of UMN damage?
When UMNs are damaged, the following signs are evident in the parts of the body supplied by the relevant UMNs:
- Weakness
- Hypertonia
- Hyperreflexia
- Extensor plantar reflexes
Explain the pathophysiology of the weakness seen in UMN damage
Weakness due to loss of direct excitatory inputs onto LMNs from UMNs
Explain the pathophysiology of the hypertonia seen in UMN damage
Hypertonia due to loss of descending inhibition (net effect of UMNs on LMNs is inhibition)
Explain the pathophysiology of the hyperreflexia seen in UMN damage
Hyperreflexia due to loss of descending inhibition (an overactive reflex arc)
Explain the pathophysiology of the extensor plantar reflexes seen in UMN damage
Extensor plantar reflexes due to the loss of the descending modulation of spinal reflexes (reversion to the situation in a baby)
What is spinal shock?
- Spinal shock is a phenomenon that occurs in the days immediately following a UMN lesion
- Initially there is flaccid paralysis with areflexia, following by hypertonia and thereafter hyperreflexia
A motor homunculus represents a map of brain areas dedicated to motor processing for different parts of the body. Sensory and/or motor loss can spread due to homunculus.
Describe the layout of the motor homunculus
A sensory homunculus represents a map of brain areas dedicated to sensory processing for different parts of the body. Sensory and/or motor loss can spread due to homunculus.
Describe the layout of the sensory homunculus
