PART 2 - SPASTICITY ( BRADDOM 5TH EDITION )
EDITED BY ME
1 DORSAL RST IS INHIBITORY
2 MEDIAL RST AND VST IS FACILITATORY
PATHOLOGICAL / ABNORMAL CONDITIONS ( IN SUMMARY ) - CAUSALGIA
1 increased afferent inputs to spinal motor neurons IN IMMOBILISATION - increased gain of stretch reflex ( V IMP )
2 altered intraneuronal reflex circuits
3 changes in intrinsic properties of spinal motor neurons - disruption of descending inputs as in SCI ( complete SCI ) or incomplete disruption ( stroke , TBI , MS , incomplete SCI ) - PLASTIC REARRANGEMENT
IN HUMANS RST EXCITABILITY CAN BE TESTED BY ACOUSTIC STARTLE REFLEX - a brainstem mediated reflex via reticulospinal tracts
VV IMP - RETICULOSPINAL PATHWAY
1 have bilateral projections - as it involves divergent projections ( sole cause of development of flexor synergies in upper limb and extensor synergies in lower limb in patients with stroke *** )
2 there is hyperexcitability in spastic stages only - eg recruitment of both dorsiflexors and plantarflexors during normal breathing at rest
CLASSIFICATION OF SPASTICITY
I -
A ) TONIC - also kn as static components of muscle stretch reflexes
B ) PHASIC - or dynamic
II -
A ) EXTRINSIC -
1 - are involuntary muscle spasms that occurs in response to percieved noxious stimuli originating from sources that are extrinsic to the muscle
2 - example - flexor withdrawal spasms ( commonly seen in SCI ) - are triggered by afferent input from the skin , subcutaneous , muscle and joints ( flexor reflex afferents ) - so , as there is disruption of descending inhibitition after SCI - EVEN IT OCCURS IN NORMAL STIMULUS AS WELL ( VV IMP )
B ) INTRINSIC -
1 describes symptoms such as - tendon hyperreflexia and clonus
2 tendon hyperreflexia is caused by exaggeration of phasic component of stretch reflex secondary to reduced presynaptic I a inhibition
3 clonus is defined as involuntary rhythmic muscular contraction that results in distal joint oscillations - most often occurs at ankle( v imp )
A ) clonus is caused by recurrent activation of stretch reflex - example - mutual and alternating activation of ( vv imp ) plantarflexors and dorsiflexor stretch reflexes
PATHOPHYSIOLOGY OF INCOMPLETE AND COMPLETE SCI
1 in incomplete SCI - both the CST and dorsal RST are often damaged in dorsolateral cord
A ) damage to dorsal RST leads to release phenomenon ( viva voce - what is release phenomenon ?? ) producing flexor spasms and hyperreflexia
B ) in complete SCI , situation is different - both excitatory and inhibitory supraspinal descending inputs to spinal cord is absent and thus stretch reflex and flexor afferents are completely disinhibited - results in predominant flexion features
C ) there is downregulation of KCC 2 ( pottasium chloride cotransporter ) - reduces the strength of post synaptic inhibition
BRUNNSTORM STAGING - AN ORDERLY PATTERN BUT EVOLUTION CAN BE ARRESTED
Stage 1 - flaccidity
Stage 2 - appearance of synergies and some spasticity
Stage 3 - marked spasticity
Stage 4 - out of synergies , less spasticity
Stage 5 - selective control of movement
Stage 6 - coordinated movement
SPASTICITY REFLECTS A PHENOMENON OF ABNORMAL PLASTICITY
PERIPHERAL CONTRIBUTION TO SPASTICITY
1 Secondary to changes in mechanical properties of muscle ( alteration in tendon compliance , physiologic changes in muscle fibers )
2 when a paralysed muscle is held in a shortened position - it loses sarcomeres ( vv imp ) to adjust its length so that optimal force can be produced
RESULT
1 muscle fibers in spastic position are twice as stiff than in non spastic position
2 Contracture formation