UMN lesions paralyze
movements
-single possible movements
peripheral lesions paralyze
muscles
-so by destroying the nerve to the muscle the movements it does also deletes
hallmarks of UMN damage
clinical signs of UMN lesions
hallmarks of LMN damage
hallmarks of peripheral damage
distinguish from LMN by sensory involvement and fibrillations
facial lesions
corticobulbar inputs bilaterally to upper half and contralat to lower
-UMN lesion contralat quarter lower face
-LMN lesion entire contralat half
extensor flexor imbalance
arms xs flexor tone + legs xs extensor tone = altered gait
UMN lesion
clonus
rapid, rhythmic contractions elicited by stretch of muscle
-over active stretch reflexes OR loss of inhibition from cortex = inc gamma neurons
clasped knife phenomenon
inc resistance to passive stretch of elbow extensors as moved into flexion > sudden collapse of resistance = easy flexion
hypertonicity/spasticity
inc resistance of flexors as extending esp with rapid attempts at passive movement
-from corticospinal tract disease
spinal muscular atrophy
SMN1 dysfunction = motor neuron death of LMNs
-weakness in upper legs, arms, trunk
myasthenia gravis
autoimmune so antibodies target acetylcholine receptors at NMJ
-weakness, rapid fatigue inc with exercise
-maybe respiratory failure, swallowing, breathing problems
ALS
both LMN and UMN so
-weakness, twitching, atrophy + stiffness, cramping
phases of spinal shock