motor system, muscle tone, and UMN/LMN part 2

rigidity

velocity independent increase to passive motion
associated disorders: severe brainstem lesions, basal ganglia disorders
mechanism: increased activation of LMNs

gamma motor loop

gamma MN innervates intrafusal muscle fibers in muscle spindle, spindle has Ia afferents that can cause alpha MN to fire (DTR)
stimulation of muscle spindle → Ia afferents fire → alpha MN fires

decerebrate rigidity

aka gamma rigidity
lesion between sup and inf colliculi interrupts bilat CS, corticoreticular, and rubrospinal
VST and somatosensory input is spared, reticulospinal spared but lose drive to lat RST which causes increased excitability of gamma MN due to loss of inhibition
posture: extension of all 4 limbs

decerebellate rigidity

aka alpha rigidity
same lesion as decerebrate plus lesion of anterior cerebellum which increases excitability of vestibular nuclei d/t loss of purkinje cells
posture: same as decerebrate but even more rigidity, cutting dorsal root does not abolish rigidity so vestibulospinal tracts directly affect alpha MN

decorticate rigidity

lesion above superior colliculi, rubrospinal now intact so UE has some flexion tone
posture: LE ext, UE flex
can progress to decerebrate which is a bad sign meaning lesion has extended

paresis

partial loss of voluntary contraction, occurs in UMN lesions as a consequence of inadequate facilitation of LMNs
common after stroke, spastic CP, TBI, incomplete SCI

paralysis

complete loss of voluntary contraction, occurs in muscles innervated by LMNs below the level of a complete spinal cord lesion
muscles can still move spontaneously/reflexively but no volitional mvmt

disorder of LMNs

trauma, infection, degenerative or vascular disorders, tumors
affected muscles undergo loss of reflexes, atrophy, flaccid paralysis, fibrillations

fibrillations

single muscle fibers spontaneously fire off, cannot palpate/sense

fasciculations

spontaneous contractions of single motor unit, can palpate/sense

UMN syndrome

can cause paresis or paralysis, loss of fractionation of movement, abnormal reflexes, velocity-dependent hypertonia

loss of fractionation of movement

fractionation is ability to activate individual muscles independently of other muscles, fine motor control
interfere with fine movements such as hand dexterity in UE or dorsiflexing in LE

abnormal cutaneous reflexes

babinski’s sign: ext of great toe accompanied by fanning of other toes

cocontraction

simultaneous contraction of antagonist muscles, stabilizes joints to allow for precise movements and standing on unstable surfaces
if it remains too long can become problematic