Session 5 The Motor System Flashcards
(17 cards)
What happens when LMN’s are activated?
Will cause muscle contraction
What are LMN’s controlled by?
controlled by UMN’s which descend through the cord or brainstem and synapse on LMNs
Where are LMN’s cell bodies found?
In the ventral horn and in cranial nerve motor nuclei
What are LMN’s typically activated by?
Incoming impulses from sensory neurones that communicate with muscle spindles (muscle stretch reflex), but can also be inhibited (inhibition of antagonist muscles such as hamstrings following patellar reflex activation)
When damaged, what are the signs seen in the muscles supplied by the damaged LMN?
- weakness - due to denervation
- areflexia - due to denervation
- wasting - due to loss of trophic support to the muscle from the LMN across the NMJ
- hypotonia - due to loss of muscle activation
- fasciculation - due to up-regulation of muscle nAChRs to try to compensate for denervation
- fibrillation - uncoordinated electrical activity (cant see)
Where are UMN’s found?
Primary motor cortex (precentral gyrus)
Where do UMN’s synapse onto LMN’s?
They synapse directly or indirectly in the ventral horn or cranial nerve motor nuclei
What is the net effect of UMN’s on LMN’s?
Inhibition
What structures fo axons of UMN’s descend through from the motor cortex?
- Corona Radiata
- Internal Capsule
- Cerebral peduncle in the midbrain
- Pons
- Medullary Pyramid
- Decussation of thee pyramids (in the caudal medulla)
- Lateral corticospinal tract (in the lateral funiculus of the cord)
- Ventral Horn
- Synapse (directly but usually indirectly via inhibitory interneurones) on LMN’s
What is the lateral corticospinal tract involved with?
Fine motor control in the limbs, primarily the distal extremities (but all of limb can be affected by a UMN lesion)
Where do UMN’s that supply facial structures leave thee pathway?
In the brainstem and form the corticonuclear (corticobulbar) tract which innervates LMN’’s in the cranial nerve motor nuclei
Why is the facial motor nucleus special?
It this split into tow halves
One half supplies the superior face (mostly occipitofrontalis) and one supplies the inferior face
Where does the part of the facial nucleus that supplies the upper half of the face receive UMN’s from?
Both hemispheres!
Where does the part of tee facial motor nucleus that supplies the lower half of the face receive UMN’s from?
Contralaterally!
Why do UMN lesions that involve the face, spare the forehead? (As opposed to true facial nerve palsies which affect all of the muscles of facial expression)
Upper half of facial nucleus - receives UMN input from both hemispheres
Lower half of facial nucleus - receives UMN input from contralateral hemispheres
What signs would be evident in the parts of the body supplied by the relevant UMNs?
Weakness - due to loss of direct excitatory inputs onto LMNs from UMNs
Hypertonic - due to loss of descending inhibition
Hyperreflexia - an over active reflex arc
Extensor Plantar reflexes - this is a reversion to the situation in a baby, due to loss of descending modulation of spinal reflexes
Clasp-knife rigidity
Atrophy
Describe the ‘spinal shock’ phenomenon
Occurs in the days immediately following a UMN lesion
Initially = flaccid paralysis with areflexia (like in LMN lesions) but then tone increases - becoming hypertonic and reflexes become exaggerated (hyperreflexia)
The mechanism is unclear but is related to neuroplasticity in the spinal cord
