In every
case, and many more, short-term "instant gratification" often
gets in the way of a more complete recovery.
Why and
how?
The irony
of stroke is that deficits to lifting the foot, swallowing, balance,
etc. are exactly what needs to be embraced to promote recovery. So instead
of throwing an external aid at the problem, sometimes its best
to challenge the challenge.
If you want
to speak French better, do you get an app?
If you want
to learn how to work on your car do you hire a better mechanic?
If you want
to be better at driving directions do you get a GPS?
In stroke, sometimes it is better to use the aid, no doubt. But choose your acquiescence wisely.
I've said before and I'll say it again, "brain training" games -- like those developed by lumosity -- have very little proven
efficacy. Do they change the brain? Yes. But so does just about everything else. Let me explain... there was a story that we used to tell in the lab and it went like this...
"If I throw you a set of keys, and you catch it, there will be neuroplastic change.
If I throw you a set of keys, and you try catch it drop it, there will be neuroplastic change.
If I throw you a set of keys, and you just watch the keys hit the floor, there will be neuroplastic change."
So do "brain traing " games change your brain? Yes. The change your brain to be better at the games. If the end result you want is to be better at the games, have at it, and become better at those games. But are the skills that you gain from these games generalizable to anything else in your life? Not that we know of.
Here is a recent article that says... well, let's put it this way... if you work for luminosity, you'll hate it...
Again, the key word here is "generalizable." Here's another article that makes the same point: "The authors conclude that memory training programs appear to produce short-term, specific training effects that do not generalize."
An article called "Emerging Treatments for Motor Rehabilitation After Stroke." They include: 1. mirror therapy 2. motor imagery or mental practice 3. constraint-induced movement therapy 4. noninvasive brain stimulation 5. selective serotonin reuptake inhibitor medications
A coupla itzy problems: These treatment options have been around for at least a decade and at least one has little proven efficacy.
Let's
get the 5th one out of the way; these meds (SSRIs) are things like
prozak and paxil and they usually treat depression. They've been used
forever to treat depression in survivors. Do they help depression, yeah.
Do they help you recover, no. SSRI's effectiveness-- if you take JAMA's
word for it: meh. BTW, Mild to moderate depression is probably better treated with exercise. (A review here from Harvard.) And exercise is what survivors ought to be doing anyway, so its a two-fer!
The
2nd and 3rd I've been involved in published clinical trials and have
written about in my book, blog entries and magazine articles. In fact,
our group, led by our fearless leader Stephen J. Page,
was the first to do a modification of constraint induced therapy, and
the first to look at motor imagery post stroke. And this goes back to
the late 90s. "Emerging Treatments." Yeah. No. I've written about
it extensively in every edition of my book as well as magazine articles, journal articles and every talk I've ever done.
Mirror therapy has been around for stroke, again, since the late 90s. I've written about it in this blog, in my book and in every talk.
Noninvasive
brain stimulation is nonspecific but they're talking about Transcranial
Magnetic Stimulation (TMS), which has been around for quite some time.
Our group has done
a lot of work with the "next gen" of this called Navigated
Transcranial Magnetic Stimulation -- basically its more accurate. But
there is no research that shows that sapping the "stroked" brain with
TMS does anything--yet. Promising, maybe, but not much there...yet.
So
we have 3 "emerging" treatment option that have been around for more
than a decade, one option that probs does not work and one that we're
not sure what it does or how to use it.
Stroke survivors and caregivers are often frustrated with stroke recovery research. Why are the simple questions not even asked, they wonder. Typical questions are:
1. Why are there no "head to head" comparisons between interventions. For instance, why don't they compare electrical stimulation to the Saeboflex?
2. Why don't they combine interventions the way a therapist would do therapy? For instance, why aren't there studies that look at electrical stimulation and the Saebo flex?
3. Why aren't simple questions answered, like, "What is the most effective treatment option given my level of arm movement?"
These are the sort of questions that confuse people that are not in research. I hate to be an apologist for research and researchers, but let me offer some insight...
Head to head comparisons are never done, in any pathology, for any intervention, initially. For instance you probably didn't see a lot of comparisons between different cholesterol drugs, initially. One company makes a cholesterol drug, they put a lot of research into it, and then they put it on the market. A second company does the same thing. But both those companies will make money off of those drugs, so the cost of the studies are justified. If there's a comparison study done, nobody's can make any money. In fact, one of the two drugs is gonna look really bad, and sell even less. So who's going to fund a study like that?
Now you may find studies that compare different cholesterol drugs. Cholesterol drugs have been around since the early 1970s. Rehabilitation research into stroke really started in the mid-to-late 90s. It wasn't that people weren't doing research before then, it was just that the outcome measures were really poor. Let's put it this way, to test how well somebody was moving-- prior to the mid-1990s-- we used a fancy protractor, and a VCR. Now we use kinematics labs. Prior to the early 1990s we had no way to image the brain, and now we have MRI, functional MRI, transcranial magnetic stimulation, and on and on.
Again, not to be an apologist for researchers, but there are other issues as well. For instance, when should you do the studies? Should you do them when the stroke survivor is acute, or during the subacute phase, or the chronic phase? Or should you do all three? It takes some time to explain, but recovery is very different during those three phases. And here's another problem: recruitment. It is very difficult to recruit stroke survivors during the acute and subacute phases. It has to do with the fact that, first of all, you can't get in the way of "standard of care." That is, it is unethical for research to get in the way of what a stroke survivor would typically get. Also, what that standard of care is doing is considered a "confound" in research. A confound is something that the researchers have no control over. In this case the confound would be the therapist, and the therapy that the therapist is offering. Each therapist is different, and each therapy or combination of therapies is different. The researcher can do nothing about those variables (confounds).
Also, for acute studies, it's incredibly difficult to recruit. "Hi Mr. Smith, my name is Pete, I'm from research down the hall. You had a stroke two days ago. Would you like to get involved in a clinical trial? Is now a good time are you, or are you busy?" You see the problem.
The reason they don't combine interventions is because we haven't even figured out if the interventions by themselves work. Within one intervention, let's say electrical stimulation for example, we don't even know what the proper dosage should be. Is it a half an hour three times a day? Is it 15 minutes five times a day? Does it depend on how well the stroke survivor moves to begin with? What about their spasticity-- how does that affect things? So research tends to focus on a very tight question. Let's get that tight question answered first, then we can be pretty safe to start as the second, third, fourth... 15th question.
What works best for what stroke survivor in what situation is impossible to determine at this point. The algorithm for this stuff is incredibly complicated because the stroke can hit any part of the brain, people can have different sequelae (symptoms other stroke), and different comorbidities (illnesses outside the stroke). Further, they can be of different motivational levels, different ages, and on and on.
But that doesn't help you. You don't have time. If you're reading this blog is because you need answers now. The good news is, if you're willing to educate yourself a little bit, your guess is as good as ours.
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 clichés, 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.
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...
How stable is your "bad" shoulder?
Will you have the strength and coordination to hold whatever (barbell, band, etc) and not drop it?
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.
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 whatclinicians 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 (casting example) is only a slight exaggeration of what happens when stroke survivors are put into an AFO.
Generally, AFOs are prescribed by clinicians waaaay too 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. 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 that 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 safe and 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 may 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 it is to put on an AFO with one hand? 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. Further reading: Here.
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.
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."
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.
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.
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.
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. Andmovement 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.
