Spasticity I: The "Magic" "Cure" for Spasticity Reduction?

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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.

Spasticity II: 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.

Spasticity After Stroke III: Options for Treatment

      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.

Dangerous Phrases

In the Seinfeld episode "The Kiss Hello" George Costanza describes his physical therapist as “… so mentally gifted that we mustn't disturb the delicate genius.” This could describe many of us involved in neurorehabilitation. We assume that we’re making the treatment choices for stroke survivors because we have a lot of experience. A lot of experience is a good thing, right?

Not necessarily.

“It works in my patients”

Neurorehabilitation research is now in a “golden age” with an exponential rise in quality of measuring recovery. This allows researches to test new treatments ever more accurately. For example, with functional magnetic resonance imaging (fMRI) we can see the work of the brain as it attempts to control movement. Triangulate changes in fMRI with computer-driven kinematic data capture, movement outcome measures, and data analysis and a three dimensional view of recovery becomes clear. But like the proverbial tree falling in a forest, are therapists listening? 

“It works in my patients” represents observation as justification of treatment. Researchers call observations “anecdotal data.” Anecdotal data does not carry enough scientific weight to justify therapeutic interventions as best practice. Researchers do not consider observations robust enough to be published in journal articles, and journal articles provide the foundation for evidenced-based practice.

Example: I know a therapist who keeps telling me that he has “fifteen years of neurological experience.” "What do you do to treat spasticity in stroke survivors," I asked him. He listed 5 or 6 treatments that “…reduce spasticity in my patients.” His answer was remarkable for two reasons. First, few of his "treatments" were effective (if we are to believe the scientific journals). Second, he was not trained in measurement of spasticity. So even if something did work there’d be no way to measure success.

“I’ve seen research that said…"
It is rare to find a therapist who reads rehabilitation research. Therapists often rely on textbooks and lectures from school, research filtered through magazines or seminars. There is nothing inherently wrong with these sources of information, but the process does promote a scatter-shot perception of available therapies and can lead to a patchwork of treatment strategies, which may or may not be considered “best practice.”

College and university professors often tend to teach what they know and they know what they were taught and what they've used clinically. This provides an echo chamber in which present teachings are based on old, often refuted, research. Proof of this is available through a quick Internet perusal of course descriptions and syllabi for PT/A and OT/A programs. The most didactic and clinical neurorehabilitative teachings on the secondary education level involve treatment techniques that are 50 years old and that remain largely unproven. Textbooks cannot possibly keep pace with the enormous amount of research that unfolds, daily. Our best hope remains the development of the doctor of physical therapy (DPT). DPT’s tend have an inherent appreciation for peer review research and, just as important, they have the skills to access that research. For their part, practicing therapists and assistants hold some responsibility to pull the best that rehabilitation research has into their practice. Entropy often exists because therapists are more comfortable with the known that is ineffective than something new and effective, but that has to be learned. Example: I finished a talk on neuroplasticity in stroke and a PT came up to me and said, “That stuff on neuroplasticity was really interesting. The only problem is that if the stroke survivor has loss of sensation and proprioception then there’s no way to get them to move in any sort of functional way.”

I discussed with the therapist how a critical mass of studies has shown that relatively normal and functional movement can be relearned without sensation and proprioception. And movement can improve sensation and proprioception. The therapist was correctly referencing research but was referencing research that was over 60 years old and had been successfully and completely refuted in a large amount of animal and human studies. Therapists often know research. But now more than ever research has become such a fast moving beast that, don’t blink, what was “true” may no longer be.

“I use a mix of therapies”
Many therapists are successful, and many renowned, for a particular therapy mix. And it may be true that their mix that they’ve developed provides superior outcomes. But there are two inherent problems with using therapies not subjected to standardized testing:
1. There is no way to know if the therapy actually works. Anecdotally (see “it works in my patients,” above) it may work but since there has been no clinical research there is no way to establish efficacy.
2.    Since a “mix” of therapies is inherently complicated to define in terms of dosage and individualized treatments for individual patients, actual definitions of the therapy are difficult to pin down and so, impossible to duplicate and test.

Example: I spoke to an OTA program recently and showed some data that a particular therapy technique was not effective in chronic stroke survivors. While I was speaking I noticed that a few of the students were hiding their faces. “What?” I asked. They whispered, “Our program director loves that therapy, she’s certified in it and says it’s the best.” After I finished speaking the program director came to the podium and I said, “I’m sorry. I didn't mean to insult—.“ She cut me off. “It’s OK, I use a mix of therapies,” she said.

I didn't have ANY data on her mix.

A blog entry about football-induced brain injury.

There is a problem when it comes to the issue of football and brain injury....

The people that know about football know nothing about the brain, and the people who know about the brain know nothing about football.

I know a little bit about both. Here's my 2¢:

I played football all through high school from freshman to senior. During my sophomore year, I never left the field. Kickoff, kickoff return, punt, punt return, every play on offense, every play on defense. I played pretty much every position on the field from nose tackle to linebacker and defensive back to quarterback to receiver.

https://www.hopkinsmedicine.org/

Frontotemporal Dementia (FTD)

Frontotemporal dementia (FTD) is a form of progressive dementia in which mental ability is gradually lost over time. The disease typically begins with two broad groups of symptoms: (1) progressive changes in behavior, or (2) progressive problems with language. The changes in behavior can involve either impulsivity and social inappropriateness or extreme listlessness and disinterest in things. The changes in language are usually slowly progressive, including difficulty with naming, reading and writing. Most patients develop the disease in middle age.

The term FTD actually refers to a group of syndromes that include: Pick’s disease, Frontotemporal Lobar Degeneration, Semantic Dementia and Primary Progressive Aphasia. Some patients with FTD also develop a form of motor neuron disease known as ALS. The symptoms of FTD are associated with degeneration of the frontal and temporal lobes of the brain. The pathological changes in the brain that cause this form of dementia vary; sometimes abnormal formations in the brain called Pick Bodies are seen, but sometimes there is only evidence of nerve cell loss and degeneration of the supporting tissues of the brain.

Are you interested in having your kids play football? Are you wondering if the years you played may have left a residual effect on your brain? Here are a few things that you should know: Other sports have head injuries. A lot of the popular press points this out. They say "Well, you hit your head in soccer when you head the ball." "When you play hockey you can get checked, that can cause a head injury." Of course they're both true. You could potentially have a head injury in almost any sport. Absolutely. No question. You could hit your head a few times a game.

What most folks don't realize is that in football you hit your head on almost every play. You are either blocking someone, trying to run over someone or falling. When you fall in football it is not a controlled fall. There's a variety of forces -usually other peoples bodies-- that impact the trajectory of your fall. All control is gone. Also, a lot of the time your hands are full, usually with somebody else's jersey.

As you fall your head hits the ground. It may hit many other things on the way to the ground, but it will almost always hit at the ground. When your head hits the ground the skull stops, but the brain keeps going. In fact, during any hit to the head in football, the brain keeps going...

And because the brain keeps going players cannot be protected by any kind of helmet. This is because, once again, the head will stop, the skull will stop, but because the brain is in fluid (cerebrospinal fluid) the brain will keep going. And you might think, who cares? So it keeps going but the skull is really smooth and so it hits a smooth area and it kind of sloshes around a little bit. So what? The impact wouldn't be significant enough to damage the brain. This is where a pretty intimate knowledge about the anatomy of the skull is important. People think of the skull they think of a really smooth surface. In fact, only the top half of the skull is smooth.

The bottom half is so convoluted and has pieces that are so sharp, that if you pressed your hand into it with a few pounds of force, you would  open the skin. So as the brain continues to move forward it is scraped against these many sharp edges that stick up into the bottom of the brain. And because there is a head hit in every play (okay not every play, you may be a decoy and not have to hit anybody. But for most positions almost play the head will get hit. I played QB for a year. I took the worst hits that year) the brain will be scraping every time. There is no good data on what this does to the brain. Everybody is focused on concussions, but because this ("scraping") is done over and over and over to the brain, it may actually be more damaging in the long term.

So how many hits do high school player take to the head?

A high school football player may take anywhere from 200 to 1,800 hits to the head during the course of a single season. 

Is your game more important than the organ that most makes us human?