Tuesday, August 26, 2014

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

       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.

Friday, August 22, 2014

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 swurvivors 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 diagnostics. This allows researches to test new treatments ever more accurately. We can now see, with functional magnetic resonance imaging (fMRI), 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 algorithmic data analysis and a three dimensional view of patient progress become startlingly 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 PT who perseverates that he has “fifteen years of neurological experience.” I recently asked him what therapeutic interventions he used for reduction of spasticity. He listed 5 or 6 treatments that “…reduce spasticity in my patients.” His answer was remarkable for two reasons. First, few of the interventions were effective, using peer-reviewed literature as metric. Second, he was not trained in measurement of spasticity, so even if something did work there’d be no way to measure success, or report that success in his notes.

“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 neuroplastcicty 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 was glad for the question because it was something I’d done quite a bit of research on. 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. 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 subsequently 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.

Sunday, August 17, 2014

A blog entry about football-induced brain injury.

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

Friday, July 25, 2014

Flaccid or spastic; what strategy works best?

Here's a recently email question I got....

Hi there,

I recently read your article about spasticity located here

The article seems to focus on therapies and treatments for patients who still have some motor control over muscles -- i.e. the brain is still in the loop.  Would the same treatments apply to a patient with little or no muscle control over muscles. i.e. muscles remain mostly flaccid post stroke.  Or is there little in the way of physical therapy that can be applied in this situation?

Specific patient is currently being treated with ativan and tizanidine, with the resulting effect that their ability to remain active is significantly deteriorated due to drowsiness.

(Name withheld)

Muscles hate to be overstretched, so if the brain is not online (as is often true after stroke) the muscles rely on the spinal cord to take over the job of protecting the muscles from being overstretched. But the spinal cord is a dumb brain. It can only tell muscles to tighten. The bottom line is: once the spinal cord takes over you end up with tight spastic muscles.

There is emerging research that suggests that if you can reestablish brain control over spastic muscles, the spinal cord will get it out of the way, and spasticity will decline.

So, as you can see the question, above, is a bit confusing because the writer asks, "Will the same treatments apply… in muscles that remained mostly flaccid post stroke?"

When the muscle is flaccid, there is no brain control over the muscle. If that's the case early in recovery (the first few weeks) you may find that the survivor becomes spastic or regains voluntary movement through the arc of recovery. But if the survivor is flaccid for more than a few weeks, the only thing that may have potential is electrical stimulation.  

(Note: because tizanidine -trade name Zanaflex- in particular is used specifically for spasticity, the person you are talking about is spastic. In that case they would have voluntary control into flexion - i.e. if you passively stretch the fingers to "open" the hand, they can squeeze your hand. If this is true, then I'd follow this strategy. It is a common misconception that everyone who is spastic has no control over their muscles. If they can squeeze, have them squeeze over and over and over and over... Tough to do when "their ability to remain active is significantly deteriorated due to drowsiness.")

If you want to see all this blog's entries on spasticity click here.

Friday, July 11, 2014

Pot Decreases Spasticity.

If you want to reduce spastcicity, move to Colorado. Pot (or the active ingredients in pot) can potentially reduce spasticity. This includes every pathology in which spasticity is a sequelae, like...

  • stroke
  • multiple sclerosis
  • spinal cord injury 
  • dystonia (see reference section)

  • But wait there's more! It turns out that pot make have a beneifit for much of what ails survivors from arterial disease to seizures (10% of survivors experience a seizures). So why has your MD not talked to you about Mary Jane as a possible treatment for, well, anything? Simple. It is  the burning weed with its roots in hell duh!

    And its dangerous. Very Very Dangerous.

    Monday, June 30, 2014

    Vision Problems After Stroke

    Two great resources if you have vision problems caused by stroke. 

    Both of these are presented by the University College London. Both are free!

    The first one is for a disorder called Hemianopic Alexia (HA). 

    HA is difficulty tracking along a line of text to find the next word in a sentence. If you have this problem, click on the image, below.

    The same organization has options for hemianopia (loss of vision to one side) and spatial neglect (loss of attention to items on one side).  You can find training for those here.

    Sunday, June 22, 2014

    You Done Yet?

    I'm always pretty confused about when recovery ends. I haven't had a stroke, so I only know what I've heard. For some people recovery ends when therapy ends. In fact it's pretty common that once therapy ends survivors actually decline to various degrees. But some people seem to trudge onward. I hear this a lot; "I've been at it for three years, and I'm still making progress. It's a long road – but it's worth it."

    Some survivors believe that recovery ends when they're able to do so much with their life that you're too busy living to continue working on recovery.

    But just like an athlete trying to get better, a little means a lot. This is the thing that clinicians often don't know. Clinicians think that the world is binary – that you're either functional or nonfunctional. That is you're either able to do the task (i.e. walking, dressing, etc.), or you're not. I've always thought it should be more nuanced than that; little bits of movement are important irrespective of the function. It probably comes from my involvement in research. In research you measure little bits of "better" movement.

    What good is "better" movement? What does it get you?
    Better movement means …

    less spasticity
    better blood flow (when muscles contract there is "venous return" of blood back towards the heart)
    better cardiovascular health (the more you move, the stronger your heart gets) 
    You get the idea. More movement generally means more health. And health is measurable. It's measurable in terms of... 
    •a reduced heart rate
    •less chance of falling
    •the ability to fight infection better etc. etc.
    So call it what you will. Recovery. 

    Sunday, June 15, 2014

    Recovery is done in three phases.

    Recovery from stroke is done in three phases.

    1. The acute phase (~day 1 to day 7 [note all time periods are highly variable]). This is usually done in the hospital. In terms of recovery your main responsibility is to keep yourself healthy. Therapists will typically focus on helping you do what you can do. This is a time for convalescence.
    2. The subacute phase (~day 7 to 3 months). This is usually done with some help from therapists. You will experience the most recovery during this phase. This is the time that rehabilitation should "put the pedal to the metal." This is where the hard work begins. During the subacute phase the brain is "primed" to recover. Make the most of this phase because it is a window of opportunity to reach the highest level of recovery.Squander it and squander the highest level of potential recovery.
    3. The chronic phase (~3 months to the end of life). Typically the survivor has very little contact with rehabilitation professionals during the chronic phase. This is the time to implement a "do-it-yourself" plan for recovery. Recovery comes at fits and starts and is much more difficult than during the subacute phase. Still, important gains can be made during this phase. Up to very recently it was thought that no recovery could be made during the chronic phase. We now know, however, because of the brain's amazing ability to rewire itself, essential progress can be made during the chronic phase.

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