Motor System Flashcards
What is a motor unit?
An alpha motor-neurone and the group of muscle fibres it innervates
What happens to a motor unit with ageing?
They get larger = lower precisional control
Atrophy in muscle that has lost innervation = build up of CT = stiffness
How is motor unit force controlled?
Vary frequency of activation = summation of force
Vary amounts of motor units = fibre:unit – lower ratio means more precision
Vary in the type of motor uni present/activated = S, FR, FF
Outline the patella reflex arc (knee jerk, deep tendon reflex)
Strike patella lig = quad muscle spindle stretched = afferent L3 spinal N activated = to ventral horn = synapses with lower motor neurone = activated = contraction of muscle to resume original position
Hamstring – reciprocal inhibition = stops the reflex being antagonised: another branch coming off the sensory neurone from quads – descends down the cord segments – synapses on inhibitory interneurone with L5 = inhibit LMN supplying hamstrings
What is a lower motor neurone (LMN)?
Cell body in ventral horn of spinal cord or cranial nerve motor nuclei
Leave CNS as axons to innervate skeletal muscle
Activate = muscle twitch
Discuss lower motor neurone (LMN) lesions
Damaged by CNS lesion or PNS lesion
Signs map the distribution of the affected peripheral N
Signs = muscle weakness, muscle wasting, loss of tone, decreased/absent reflexes, fasciculation
Causes = trauma, peripheral neuropathy, diabetic neuropathy, motor neurone disease
What are the key signs of LMN damage?
Weakness – interrupted pathway
Areflexia – interrupted pathway
Muscle wasting – loss of LMN trophic factors
Hypotonia – loss of low level contraction maintaining tone
Fasciculation – uncoordinated muscle contractions
What are the key signs of UMN damage?
Late (days-weeks) =
Hypertonia – lost the net effect of UMN on LMN = inhibitory
Hyper-reflexia - lost the net effect of UMN on LMN = inhibitory
Extensor plantar reflex
Acute =
Weakness – interrupted pathway
Spinal shock – hypotonia, areflexia
What is an upper motor neurone (UMN)?
Cell body in the primary motor cortex in the precentral gyrus
Remain within the CNS
Not found in the basal ganglia or cerebellum
Control LMNs = excitatory or inhibitory
Discuss upper motor neurone lesions
Can only be damaged by CNS lesions
Cardinal feature = hyperactivity of LMNs due to inhibitory loss
What are motor nuclei?
Instead of ventral horn ascending up into the brain – there is a number of distinct motor nuclei containing a number of cell bodies of motor neurones which run through cranial nerves
E.g. Oculomotor nuclei – contain cell bodies of LMNs whose axons travel through the oculomotor N
Superior continuation of the grey mater in the ventral horn
How do UMNs effect LMNs?
UMN synapse directly with LMN = excitatory
UMN synapse on inhibitory interneurones that then synapse on LMN = inhibitory
The NET effect of UMNs on LMNs is inhibitory
Outline the pathway of motor axons through the brain and lateral corticospinal tract
UMN has cell bodies in the motor cortex
UMN send axon through white matter of hemisphere = corona radiata
Axon descends between thalamus and lentiform nucleus, condensed = internal capsule (most common site for strokes)
Axon continues to descend – enters midbrain – runs through cerebral peduncle (connects brainstem to cerebral hemispheres)
Axon runs through the medullary pyramids and crosses in medulla = lateral corticospinal tract
Axons descend down the lateral funiculis of the cord
Synapse a LMN – goes to its final destination
Not all of the axons decussate at the medullary pyramids = 20% remain ipsilateral
Where is the lateral corticospinal tract located?
Lateral funiculis of the cord
How are axons arranged in the corticospinal tract?
Upper limb axons = medial
Trunk axons = intermediate
Lower limb axons = lateral
