So how can you explain spasticity to patients and their significant others in a way that is easy to understand and scientifically valid?
Here is the story of spasticity. Spasticity happens because of a set of circumstances caught in an endless closed loop. The players in this story are the brain, the spinal cord and the spastic muscle (SM).
There is an injury to the brain. The brain can no longer control the SM. Muscle spindle sensitivity then develops because the flaccidity resulting from the lack of brain control causes overstretch of the SM.
The muscle spindle then sends a "Help, I'm being overstretched!" signal to the spinal cord. The spinal cord then sends the message to the brain. The brain would normally send down a mix of facilitory and inhibitory signals to stabilize the muscle. But the brain is not responding. So the spinal cord does.
The spinal cord says, "SM, do that thing you do!" The SM only does one thing: Flex. So flex it does. These messages go on and on during during most waking hours and for some who suffer from spasticicty, during all but the deepest of sleep. Eventually, the SM starts to lose sarcomeres (the contractile units in muscle) and the SM and other area muscles that are kept in a shortened position, lose length. The shortened muscle perceives everything as an overstretch and the alarm signals to the spinal cord proliferate. The process repeats itself in an endless cycle until contracture sets in.
Most therapeutic interventions therapists typically use are, at best, nominally effective against the symptoms of spasticity, and do little to address the underlying issues causing spasticity. Consider stretching. Stretching reduces spasticity, right? Stretching does retain soft tissue length and for that reason should be done often to spastic muscles. But research of the effectiveness of stretching in the reduction of spasticity, either through weight bearing, isotonic stretch without weight bearing as well as isokinetic stretching, is equivocal at best. Typically used modalities like cold and heat have a nebulous, short-term effect. There is strong evidence that splinting is ineffective in reduction of spasticity and contracture formation. Facilitory and handling techniques? Also no demonstrated effect.
Here is the story of spasticity. Spasticity happens because of a set of circumstances caught in an endless closed loop. The players in this story are the brain, the spinal cord and the spastic muscle (SM).
There is an injury to the brain. The brain can no longer control the SM. Muscle spindle sensitivity then develops because the flaccidity resulting from the lack of brain control causes overstretch of the SM.The muscle spindle then sends a "Help, I'm being overstretched!" signal to the spinal cord. The spinal cord then sends the message to the brain. The brain would normally send down a mix of facilitory and inhibitory signals to stabilize the muscle. But the brain is not responding. So the spinal cord does.
The spinal cord says, "SM, do that thing you do!" The SM only does one thing: Flex. So flex it does. These messages go on and on during during most waking hours and for some who suffer from spasticicty, during all but the deepest of sleep. Eventually, the SM starts to lose sarcomeres (the contractile units in muscle) and the SM and other area muscles that are kept in a shortened position, lose length. The shortened muscle perceives everything as an overstretch and the alarm signals to the spinal cord proliferate. The process repeats itself in an endless cycle until contracture sets in.
Most therapeutic interventions therapists typically use are, at best, nominally effective against the symptoms of spasticity, and do little to address the underlying issues causing spasticity. Consider stretching. Stretching reduces spasticity, right? Stretching does retain soft tissue length and for that reason should be done often to spastic muscles. But research of the effectiveness of stretching in the reduction of spasticity, either through weight bearing, isotonic stretch without weight bearing as well as isokinetic stretching, is equivocal at best. Typically used modalities like cold and heat have a nebulous, short-term effect. There is strong evidence that splinting is ineffective in reduction of spasticity and contracture formation. Facilitory and handling techniques? Also no demonstrated effect.
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