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585-6

Spasticity

TermDefinition
spasticity Velocity dependent increase in stretch reflexes with increased excitability of tendon jerk reflexes Increased tone at rest
common etiologies CP Stroke MS TBI SCI All of the above have spasticity as a common symptom
lateral corticospinal tract (LCT) 1. Starts at cortex 2. Decussates at medulla 3. Goes down spinal cord & synapses 4. Motor neuron goes to muscle
stroke vs. MS on LCT Damage to motor cortex & internal capsule vs. Demyelination leading to multiple lesions throughout NS
CP vs. TBI/ SCI on LCT Due to perinatal stroke. Damage to internal capsule. vs. Lesions in variety of regions, may impact LCT
pathophysiology of spasticity 1. Increase in stretch reflex excitability 2. Reappearance of developmental reflexes 3. Increase in co-contraction during voluntary movements (clonus, decreased reciprocal inhibition, clasp-knife response) 4. Abnormal distant co-contraction
How does LCT lesion lead to hyper-reflexivity? 1. Loss of descending control of reflexes 2. Increase reflex arc excitability 3. Long term adaptations 4. Rearrangement of spinal circuitry
descending control of reflexes Via inhibition Voluntary movements require CST, at the same time we are suppressing reflexes
increase reflex arc excitability Stretch reflex Decrease presynaptic inhibition with GABA We cut off the presynaptic inhibition & reciprocal Ia inhibition (inhibit the inhibitors)
long term adaptations Prolonged increase in reflex activity strengthens those synapses Sustained activity in muscles will change muscles from fast twitch to slow twitch Increase in a-y co-contraction
a-y co contraction If only extrafusal fibers contract, the muscle spindle won't contract. Normally intrafusal & extrafusal contract together which keeps muscle spindle tight Continual hyperactivity will make muscle spindle more sensitive to changes in length
rearrangement of spinal circuitry Due to prolonged activity we increase the number of synapses Resting membrane potential is closer to threshold Loss of inhibitory inputs and closer to threshold will result in easier firing of AP
consequences of spasticity on motor control 1. Leads to disordered motor control 2. Contractures
leads to disordered motor control Unable to predict motor output- can't predict what the response to the command will be Results in no motor learning because response is never consistent. Poor cerebellum is all over the place
contractures Result of chronic muscle shortening due to stretch reflex Connective tissue becomes shorter & lose elasticity of tendons Will decrease ROM & strength (less room to produce a contraction)
management of spasticity 1. Restore inhibitory balance 2. Suppress "abnormal" reflexes 3. Passive stretching to increase ROM 4. Muscle relaxants 5. Motor training 6. Orthotics
restoring inhibitory balance Gold standard Use baclofen (GABA agonist) If we add GABA back in, we have more inhibitory state of the spinal cord & lower muscle excitability
suppress abnormal reflex Use Bobath/ NDT Use certain stretching activities which will suppress stretch reflex on affected limb Presynaptic inhibition of heteronymous muscles Similar mechanism to Baclofen, but more natural
passive stretching Increase ROM Helps decrease contractures Allows greater voluntary control Possible tendon lengthening surgeries (helps with ROM)
muscle relaxants Can be systemic & local. Prevents communication between NS & muscle to decrease contractility Last resort- surgical (cut ventral roots to eliminate motorneurons, cut dorsal to reduce Ia afferent feedback [eliminates any other sensory feedback])
motor training Promote normal descending control tried to invoke adaptations Can be coupled with decreased sensory feedback (baclofen), apply fundamentals of synaptic plasticity
orthotics Promote function & voluntary actions Ties into increase ROM & motor training but may have compensation as a result People will end up doing more activities if they can do it with orthotics
Created by: craftycats_
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