The Magic Cure for Spasticity Reduction

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Vol. 18 • Issue 11 • Page 47

“Why do I have spasticity? What can I do to get rid of spasticity? When will it go away?”

People who have any number of pathologies can suffer from spasticity. Spinal cord injury, multiple sclerosis, amyotrophic lateral sclerosis (Lou Gehrig’s disease) and other pathologies have spasticity as a sequela. This column will discuss spasticity as it relates to acquired brain injury which includes traumatic brain injury, cerebral palsy and stroke.

Most clinicians provide patients with overly simplified, incomplete and often inaccurate information about what spasticity is, its etiology and its cure. Therapists generally believe that patients don’t want detailed explanations. But patients need to understand their spasticity. Why? Having patients understand their spasticity is essential because spasticity will only reduce if executive control over the spastic muscles, by the brain, is restored. And executive control over muscles will only happen with repeated firing of the muscle in question, and repeated firing will only happen if the patient wants it to happen.

The Explanation

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.

Options for Treatment

But what can therapists do that is evidence-based? Repetitive, task-specific massed practice, if done properly, has the ability to rewire the brain to restore voluntary control over muscles. As executive muscular control emerges, spasticity dissipates. There are quite a few therapist-initiated treatment options that will vector this sort of practice, from EMG based electrical stimulation to modified constraint induced therapy. Focus research on therapies that have proven neuroplastic effect and you’re half way there.

What else works? BOTOX® (botulinum toxin type A) can be injected directly into the spastic muscles to provide months of spasticity relief. Intrathecal baclofen (ITB) therapy delivers spasticity medication to the intrathecal space (fluid flows around the spinal cord) corresponding to the spinal level of the spastic muscles. Oral medication, dorsal root rhizotomy, orthopedic surgeries and other treatments do reduce spasticity. And if you think that these medical interventions have nothing to do with therapists, think again. Physiatrists and neurologists believe that spasticity that limits function is one of the triggers for appointments for these experts in spasticity reduction. Who better than therapists to gently guide patients to these doctors for spasticity treatment?

A word of caution here: Once directed to a doctor who specializes in spasticity interventions, patients sometimes forget what to say and end up saying something vague like, “I want to move better.” Prior to sending patients with spasticity to these doctors, tell them in clear and concise terms exactly what muscles you want the doctor to work on. If the patient has trouble with dorsiflexion because of spastic triceps surae, having the doctor BOTOX® the finger flexors is not going to help.

The Holy Grail for spasticity reduction is a melding of doctor-prescribed medical interventions and therapist-delivered neuroplastic treatment options. The proper mix of these interventions is emerging as research goes forward. Guiding patients back to neurology and physiatry and accepting neuroplasticity as the substrate for authentic spasticity reduction are good first steps.

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About Author

Pete Levine, BA, PTA

Peter G. Levine is co-director of the Neuromotor Recovery and Rehabilitation Laboratory (rehablab.org) and the author of Stronger After Stroke (Demos Health, 2008). He also conducts seminars teaching research-based, neuroplasticity-producing stroke recovery strategies. E-mail him at StrongerAfterStroke@yahoo.com.

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