S5 The motor system Flashcards
describe the motor system in summary
Upper motor neurones cell body found in primary motor cortex (UMN)
synapses on a lower motor neurone whose axons connect UMNS to various skeletal muscle targets
LMN cell bodies reside in the ventral horn of the spinal cord and also in brainstem nuclei
CNS lesion can damage UMN, CNS or PNS lesion can damage a LMN
describe LMNs
grey matter in SC continues up into brainstem
Controlled by UMN
when activated by sensory neurones, they cause muscle contraction/deep tendon reflexes
do primitive spinal reflexes exist in babies ?
yes but these disappear with age due to the maturation of descending UMN pathways
where are distinct motor nuclei containing cell bodies carried up ?
e.g in midbrain, oculumotor nuclei contains cell bodies of LMN, whose axon travels through the oculomotor nerve to reach eye muscles
in Pons we have trigeminal motor nucleus
pontomedullary junction we have abducens nerve nuclei, axons travel through this to reach lateral rectus muscle
NB motor neurones are superior continuations of SC
How do LMN contribute to spinal reflexes
hitting patellar ligament activates muscle spindle
impulse passes through spinal nerve, into the ventral horn, where it synapses onto LMN activating it, causing a muscle twitch - quad contraction
reciprocal inhibition - when we switch on the reflex arc we inhibit hamstring contraction - branch off spindle at L3 which synapses on an inhibitory interneuron on the L5 segment, this inhibits the LMN which would normally supply the hams (L3/L4 mediates contraction in the quads, L5 contracts Hams)
these reflexes are to maintain posture
what are signs of LMN damage to cell body or axon
weakness due to interruption of info from neurone to muscles
areflexia - absent tendon reflexes from denervation; damage to axon causes an incomplete reflex arc
muscle wasting - denervation shall interrupt the source of trophic factors from LMN across NMJ
fasciculation -uncoordinated muscle contractions from up-regulation of nAChrs
hypotonia - decreased muscle tone (causes floppy limbs) as AP movement from LMN to a muscle has been interrupted so no muscle activation
describe UMNS
found in Primary motor cortex
2 major effects on LMN- excite LMN and communicates with LMN through inhibitory interneurons inhibiting LMN
the net effect of UMN on LMN is inhibition
UMN lesion will cause hyperactivity in LMN
how do UMN reach LMN
axon descends to a region between thalamus and lentiform nucleus called the internal capsule, this is a common site for strokes, radiation fibres become condensed (corona radiata)
axons enter midbrain and run through the
cerebral peduncle
axon decussates in medulla and runs through medullary pyramids
after crossover known as lateral corticospinal tract
descent to lower cord and synapse on LMN which shall go to lower limb
NB not all axons cross, some remain ipsilateral
what is the function of lateral corticospinal tract
dexterous movement in distal extremeties
where do UMNS supplying the face form
leave the pathway forming the corticobulbar tract which innervates LMNs in the cranial nerve nuclei
describe Facial motor nuclei
facial motor nuclei - regions of grey matter containing UMN cell bodies which supply facial muscles
split into two halves - supply muscles of lower and upper face
these nuclei go on to form facial nerve
FMN supplies upper face receives bilateral UMN innervation from both hemispheres
FMN supplies lower half of the face receive contralateral UMN
Hence UMN lesion shall spare the forehead due to bilateral innervation(only true facial nerve palsies affect whole face)
what are some UMN damage signs ?
weakness - loss of excitatory inputs onto LMNS from UMNS
Hypertonia - increased muscle tone, rigid limbs, as there is less descending inhibition of UMN on LMN so the increased activity of LMN
Hyperreflexia - enhanced reflexes, due to less descending inhibition so the increased activity of LMN
Extensor plantar reflex - an extension of the big toe
- apart from weakness, last 3 are all late signs, occur in days to weeks after a UMN lesion
Spinal shock: occurs after UMN lesion - mimics LMN then UMN lesions - areflexia - hyperreflexia so LMN stop functioning then go into overdrive
