Session 5 - motor system Flashcards
where are upper motor neurone cell bodies found?
in the primary motor cortex in the pre central gyrus (medial)
where are lower motor neurone cell bodies found?
in the brain stem (all 3 portions) and the ventral horn of the spinal cord
Where do LMN axons span?
they span across the CNS and the PNS
describe the patella reflex
- tapping patellar ligament stretches the quadriceps fibres → detected by muscle fibres
- the spindle fibres detect stretch, so the sensory neurone is activated and synapses on the lower motor neurone in L3
- the sensory neurone activates the L3 LMN causing contraction of the quadriceps
- the sensory neurone also branches off and synapses with an inhibitory interneurone at L5 causing the hamstring to relax
where is the primary motor cortex found?
in the pre central gyrus
what are the LMN lesion signs?
- weakness
- Hypo/arreflexia - diminished/absence of reflexes
- Hypotonia - due to loss of muscle activation
- Atrophy - due to loss of growth factor (LMN supplies tropic factors to muscle) and electrical activity form motor neurone. Atrophy of interossi
- Fasciculations - uncoordinated involuntary contraction. Common in the tongue. The muscle fibres up regulate AcH to compensate but they become very sensitive to small amount of AcH in the interstitial fluid for example
Give an example of low muscle tone
Babies have low muscle tone meaning the can’t stay upright, their necks can’t stay up - have to support them
what is the function of UMNs?
- they excite LMNs by direct synapses or they inhibit LMNs by projecting onto inhibitory interneurones
- their net effect is inhibit, so a lesion of UMNs leads to hyperactivity of muscles
what are some UMN lesion signs?
- weakness - excitatory inputs form brain to LMN is blocked therefore weakness
- Hyperreflexia - LMN more easily activate/loss of descending inhibition (overactive reflex arc)
- Hypertonia - muscle tone increases because activity increases
- Disuse atrophy - not overt atrophy but eg in a stroke you wouldn’t use your limb so it leads to disuse atrophy
What UMN lesion signs does spasticity refer to?
hyperreflexia and hypertonia
what is lead pipe rigidity?
- seen in Parkinson’s disease
- constant resistance on range of movement
what is clasp knife rigidity and what is this caused by?
- UMN damage
- when you pull on the limb, it offers resistance and then suddenly gives way
- cause - Golgi tendon organs
why is hyperactivity seeing UMN lesions?
- there’s still constant input from muscle spindles so the monosynaptic reflex arc is still active, but the descending pathways from the UMN that usually inhibit the LMN are inhibited → increased activity of muscles → UMN signs
what is spinal shock?
- seen in the acute phase of UMN lesions
- initially there’s flaccid paralysis with areflexia
- but then after a few weeks, tone increases (becoming hypertonia) and reflexes become exaggerated (hyperreflexia)
- related to neuroplasticity in the spinal cord and LMN shutting down following UMN lesion
what is the Golgi tendon reflex?
- proprioceptive sensory receptor organ that senses changes in muscle tension and is activated in high tension to protect the bone and muscles
- inhibits the lower motor neurone in a reflect to protect bone and muscle and excites the antagonising muscle
- it prevents muscles from contracting too strongly and causing damage to themselves or their tendons
- when golgi tendon organs which are located in the tendons of muscles detect tension they send signals to the spinal cord which in turnsends inhibitory signals to the motor neurones that innervate the muscle → which in turn causes it to relax.
what is the internal capsule?
a bidirectional white matter pathway that connects the cerebral hemisphere with the rest of the CNS
What is the internal capsule continuous with superiority and inferiority?
- superiorly - corona radiata
- Inferiorly - cerebral peduncle
What does the internal capsule contain?
Mainly contains descending axons of upper motor neurones but also has ascending axons of 3rd order sensory neurones
What are the 3 divisions of the internal capsule and what do each of them contain?
- anterior limb - contains axons connecting the motor cortex with the cerebellum
- genu - the bend Contains axons of the upper motor neurones supplying the face
- Posterior limb - contains axons of upper motor neurones supplying upper limb, trunk and lower (from anterior to posterior). They also contains third order sensory neurones connecting the thalamus to the post central gyrus
What type of stroke is the internal capsule important in?
lacunar stroke
What is the internal capsule supplied by?
lenticulostriate arteries (branches of MCA)
what is a peduncle?
white matter connecting a hemisphere
what does the lateral corticospinal tract supply?
distal muscles
what is the pathway of the UMNs from the motor cortex to the LMNs for spinal nerves?
- axons run within the corona radiata
- then though the internal capsule - white matter pathway/space between the Lentiform nucleus and the thalamus
- then they go through the cerebral peduncle in the midbrain
- pons
- medullary pyramids in the medulla
- decussation of the pyramids
- travel down the lateral corticospinal tract (in the lateral funiculus of the spinal cord)
- descend to ventral horn (of the required spinal level)
- synapse (directly or indirectly via inhibitory interneurones) on LMNs
how do UMNs travel when they’re travelling to cranial nerves? (facial nerve as example)
- facial motor nuclei is split into 2 halves, supplying the upper (mainly occipitofrontalis) and lower half of the face (rest of muscles)
- the part of the of the facial motor nucleus that supplies the upper half of the face receives UMNs from both hemispheres - so UMNs supplying the upper face project contralaterally and ipsilaterally
- UMNs supplying the lower face project contralaterally only
how many axons decussate at the pyramids and what do the remaining axons do?
- 85% decussate
- the remaining 15% remain ipsilateral and descend in the ventral funicular at the ventral corticospinal tract
- the remaining axons decussate at the level of the target LMN
if there was a stroke affecting the left upper motor in the facial area of the homunculus, what would be the motor loss to the muscles of facial expression and why?
- there would be loss of contralateral supply to the right lower half of the face - due to decussation
- there will be forehead/upper half of face sparing because of contralateral and ipsilateral nerve supply to the upper half of the face - so despite the contralateral/ipsilateral side being damage, the other side will compensate (I hope this makes sense lol)
what is the difference between an UMN lesion and LMN lesion?
- UMN lesion eg stroke - the forehead will be spared
- LMN lesion eg bell’s palsy - this is a lesion of the actual facial nerve so all of the muscles of facial expression will be affects
in the lateral corticospinal tract, what is the topography of the trunk, arms and legs?
arm most medially, then trunk, then leg most laterally
what is the nucleus ambiguus?
- the nucleus in the medulla containing LMNs that distribute through the vagus nerve
- controls swallowing and protection of the airway
- it has bilateral innervation
