Monday, November 24, 2014

BRAINS! (get used to it)


     
     Out of all the organs in the human body we know the least about the brain. Every other organ in the body and we know to the cellular, if not the molecular level.


But the brain... You've heard the clich├ęs, I'm sure; given the interdependence of neurons, the human brain is the most complex structure in the known galaxy, including the galaxy itself. The estimate of planets in the galaxy is upwards of 1 trillion. The most conservative estimate of the number of synaptic connections in the human brain is 1000 trillion!

"But," you may think, "I can't even figure out which socks match my shoes." That maybe true, but remember: while you're trying to figure that out, your brain is keeping every one of the trillions of cells in your body in relative harmony.

 We need to start looking at the brain. Yes, its squishy, yes its bloody, yes it is huge and pulsates in aliens from Mars. But we need to get over this "Its too weird!" posture, or we, its owner, can't really understand the darned thing.

Here's a place to start... Below is a video of the surgery for a subdural hematoma. This type of stroke is the least common (about 7%), but the most deadly.

Warning: this video is graphic. Frankly, I had a hard time sitting through it.I would suggest watching just one portion – a few seconds, from 1:32 to 1:39. This is the good part, where the surgeon rids the brain of this sort of cap of blood that has accumulated between the skull and the brain. If this sort of surgery is not done, the brain will continue to compress, furthering damage.

Enjoy!


Tuesday, November 4, 2014

Resistance Training After Stroke

Got a good question the other day about resistance training the other day. Please see the Q&A, below...
Q
     I am a 43 year old stroke survivor(2010).  I walk ok(not too pretty), can do light manual work, and can't run.  My left affected side is considerqbly weaker than my dominnant, nonaffected right side.
    I want to return to higher impact activities one day, but I just don't think I have the physical strength to do so.
  I have read several articles by Sroke survivors who benefitted greatly from barbell-base systematic weight training as a  means to advance recovery.  
    One writer mentioned (book) as a good place to begin.  It emphasizes combination weight exercises that employ multiple muscle groups and run through a full range of motion.
    Do you have any opinions or clinical experiences on the subject  of Strength Training following Stroke or could direct me towards some materials to get started?
A
     I did a quick review of the literature (example) and found that there's a general consensus that resistance training is a good thing post stroke. A really good thing. But there seems to be no consensus on what type of resistance training it should be. 
    Keep in mind: Resistance training can injure. There are a ton of questions before you begin, like...
  1. How stable is your "bad" shoulder?
  2. Will you have the strength and coordination to hold whatever (barbell, band, etc) and not drop it?
  3. Do you have sensation enough to know if you are injuring the limb?
    One concern that therapists mistakenly have is that if you use muscles that have spasticity you will increase the spasticity. This is wrongheaded, and not true. So don't worry about using spastic muscles to help move you.
    I have seen people who've had a stroke run again. They're almost always young (younger than 60). I would think that as long as you are okay with "a new normal" the sky is the limit.
   
The hard part, of course, is putting the work in.
Previous article I wrote about this subject.

Tuesday, October 14, 2014

Stroke Statistics zzzzz

15 million people suffer stroke worldwide each year.

In the USA...
  • 10% of survivors recover completely or almost completely recover.
  • 25% recover with minor impairments
  • 40% experience moderate to severe impairments that require special care
  • 10% require care in a nursing home or other long-term facility
  • 15% die shortly after the stroke
  • Approximately 14% of stroke survivors experience a second stroke in the first year following a stroke.
If we concentrate on the people who may need help with recovery we'd include survivors with
  • minor impairments to... 
  • those requiring care in a nursing facility 
This includes everything from occupational therapy to AFOs. Therefore...

11.25 million people per year worldwide will require these services and equipment. 

Thursday, October 9, 2014

AFO after stroke: Once its on there, its on there for life.

(Warning: ENDING THE USE OF AN AFO CAN LEAD TO FALLS AND INJURIES. 

Never discontinue the use of an orthotic without first consulting the appropriate health care provider. Then call your doctor. Then have your doc talk to any other providers as needed. Then discuss it some more. Thank you.)


For years I've been pointing out how what clinicians focus on can hurt recovery. Clinicians focus on having the patient be safe and functional (able to do everyday tasks). Clinicians have the "safe and functional" mantra running through their heads constantly. There are two other things that influence what clinicians will to use to help survivors recover:   
 1. What managed care will pay for
 2. What therapists know about stroke recovery

This leaves a very small group of available options. These options may or may not lend themselves to promoting the highest level of recovery. Recovery, yes. But not necessarily the highest level of potential recovery.

I think the best example of this is the AFO. 


Before I get too technical, let me ask you a hypothetical.... Let's say you're a survivor. Your ankle is not moving well after stroke. But you know that recovery is unpredictable. 



Here's my question: During the time in which your ankle is trying to come back, would you put it in a cast?


Probs not. If you casted it and the ankle tried to come back it wouldn't be able to. It would be stuck in one position by the cast. This is where clinicians lose the plot (as the English say). They see this ankle issue as an ankle issue. But its not an ankle issue! Its a brain issue. And what's the first rule of the brain? What's the one rule that everybody knows about the brain? 

Use it or lose it.



Now this is only a slight exaggeration of what happens when stroke survivors are put into an AFO.

Generally, AFOs are prescribed by clinicians waaaay to early. The brain has not revealed what it's capable of doing during the first few months after stroke. This phase, known as the subacute phase, typically last from 3 to 6 months. Clinicians will often prescribe the AFO in the first, second or third month after stroke.


And even before that... sometimes within the first 2-3 weeks after stroke, there is an effort to somehow bind the ankle in such a way that it is not required to move.



These all essentially lock the joint, disengaging the ankle muscles from what they've been using to lift the foot at the ankle since that survivor was born.


So why do clinicians do it? 

Simple; They don't focus on what the brain needs. They're more... peripheral in their perspective. They're about muscles and bones and tendons and ligaments and things they can see. You you can't see neurons, can't see the brain, can't see the brain "reawaken" after stroke, and you can't see cortical plasticity. The mind, for many clinicians, is out of sight out of mind.

And who do they listen to? Orthotists. And what do orthotists make? AFOs. So will the orthotist say to a clinician suggesting an AFO, "Naw, AFOs lead to learned nonuse." Probs not.

It's not the clinicians mean to do you harm. They want you to be safe and functional. They want you to be where you want to be: home. So there is a trade-off: Put you in an AFO and get you home and safe early, or wait and see what develops. Here's one thing that managed care won't pay for: Waiting to see what develops. 

Its the instant gratification thing. Put an AFO on and survivors walk better instantly! But they also promote muscle atrophy, lock the joint (which joints hate because they like to move) and lead to learned nonuse.

AND AFOs discourage walking.

"Hey mom, dad didn't put his ankle thingy on!"
"OK, lets just take the wheelchair!"
(Wanna know how hard? This hard!    

Oh, and one more thing... once the AFO is on there, its on  for life. Why? Because an AFO will atrophy both the neurology and the muscles involved in walking. Further, it will so change your "gait kinematics" that NOT wearing will become a risk. 

BTW: I'm not saying AFOs are never appropriate. Its just that they are not appropriate too early and they're not appropriate for everyone.

Monday, September 15, 2014

Exercising the Brain after Stroke

What drives stroke recovery? This question is both complicated and profoundly simple. It’s complicated because recovery involves rewiring the brain, and the brain is...complicated. It’s simple because the brain rewires in response to very simple instructions. In fact, these instructions have been known to athletes, musicians and other skilled workers for thousands of years. 
In the rehab clinic, exercises are called "thera ex (short for therapeutic exercise).
Therapists usually want to know which are the best thera ex for helping stroke survivors recover.       Beyond exercising, the other big option used in clinics are collectively called handling techniques. Handling techniques are just like they sound, the therapist moves you. Handling techniques, if you believe the research, don't much help. (If they did, I'd pay someone to "handle me" into being a better skier!). Exercise, for its part, is great! Exercise makes the muscles that need strengthening, stronger. The problem is, exercise is only mildly effective at changing the brain-- and stroke is a brain injury. Let me put it this way: a muscle can be strong, but useless because it does not know what to do. "Muscle memory" does not exist. The brain controls while muscles can only do two things: contract and relax. It's the brain stupid. 
Consider the one stroke recovery option that has consistently done really well in research, constraint induced therapy (CIT). In CIT, there are no specific exercises. Movement is required, however. The movements required during CIT very little resemble thera ex because focus is on repetitive practice, not muscle strengthening. And there are no handling techniques. In fact, CIT is decidedly and pointedly hands-off. It is cause of some curiosity among researchers why this hands-off philosophy is so difficult for therapists to accept. The only way of driving cortical change towards recovery is through volitional efforts by the stroke survivor. These efforts are actively encouraged no matter how ugly, synergistic or uncoordinated they are. Edward Taub, the person who developed CIT is a psychologist. As he was developing CIT in animal models, handling techniques and exrcises may have been the furthest thing from his mind. The closest, certainly, was operant conditioning which does appear to change the brain. Stroke is a brain injury, not a problem specific to muscle weakness. The term “neuromuscular re-education” is used a lot in PT and OT. In fact, you can bill for it. But the term is a misnomer. If it was an honest term it would be "motor-cortical reduction", or "movement reeducation." Relearning how to move after stroke has little to do with the muscles and everything to do with the brain. Stroke recovery involves brain reeducation. Different focus, different organ, different paradigm, different rules, different outcome measures. 

Friday, September 5, 2014

Stop the &%$%^ cap!

Addendum 9.18.14: 
As of today 220 members of the 435 congressmen have signed on as co-sponsors of the House bill to repeal the therapy caps. --Thank you Rebecca Dutton!

Let's say you've had a stroke. Not much of a stretch, huh? Now imagine a federal algorithm that determines the amount of therapy you'll get before you even have a stroke. Can't be done you say? Every stroke is different and so would need a different amount of therapy. 

You'd think the amount of therapy you'd get would be based on what the clinicians sitting in front of you think you need. But yeah, no. That's not the way its done. 


And what really confuses me is why the Federal guidelines are not in concert with what the research says! 

So, if you're with me on this, click the red image above and let 'er rip. 

PS, the congressman who had a stroke, how much therapy did he get given the insurance provided congress? "...nearly a year of intense, grueling physical and occupational therapy." 

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.

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