Don't believe the hype -OR- Have you been lowballed? -OR- Clinician fulfilled prophecy

Bottom line: 
What the therapist predicted: Very little
What the survivor achieved: A lot

Let me tell you about a stroke survivor I worked with a year or so ago. I'll call him "Sam."

I was working in a skilled nursing facility. The physical therapist (PT) did Sam's evaluation.  The PT then told me Sam would be added to my caseload. 

I read the PT evaluation and it was pretty shocking. One thing stuck out: The "long-term goals" were one thing: "bed mobility." 

There it was. The best that Sam was expected to do was to be able to roll around in his bed. He wouldn't be able to stand. And walking was beyond belief.

The day Sam was to have his first treatment I went to the nurses station to read his chart before I met him. Nursing facilities often have a cluster of patients in wheelchairs right around the nurses station. It's where all the action is.

As I began to read Sam's chart I asked one of the nurses to point Sam out to me. She pointed to a gent in a wheelchair. "That couldn't be him"- I thought. If he could not get around the bed, how did nurses get him in a wheelchair?  The nurse: "That's him. He came in yesterday." 

This was the guy who's long-term goals were "bed mobility."
That day he took his first step. Two weeks later he was lapping the facility several times, without an AFO, and beginning to walk outside. Yes, we were both a "hot mess" by the end of treatments, but it was fun. Sam would get called out by staff "Amazing! Keep going Sam! Lookin' good!" In fact, some of the folks with dementia thought it was some sort of conga line so by the end of our walk we'd have a parade! 

P.S: There may be several reasons for the physical therapist lowballing expectations. Maybe Sam was exhausted by the experience of being transferred from hospital to skilled nursing. Maybe his meds had changed. Maybe he was admitted so late that by the time the therapist got there he was asleep and the therapist had to wake him and he was very tired. 

Or maybe: 

Some clinicians are so concerned with deficits that they miss potential.

Splinting after stroke? Why?

The research into splinting stroke survivors is clear: It does not work. Let’s have a look. 

Forget individual studies… they don’t count for much. Rather, let’s look at the meta-analyses (or “metas”). Metas are studies of all the studies available and will quickly tell you if something works. Or at least its the best tool we have to come as close as possible to "the truth." 

The granddaddy of all metas, the Cochrane review, has looked at splinting after stroke. The review states, 

"A total of 787 participants were included in the analyses.  The mean difference of splinting on joint mobility was 0°."

Ouch.

...

After stroke there are a number of reasons that you’re supposed to splint the wrist/hand/fingers. Here is the logic:

The survivor tends to posture with the wrist and fingers flexed (bent at the wrist and the fingers in a fist). Why do survivor’s posture like that? It has to do with the brain injury. Because the brain is no longer in full control, the stronger of the two muscle groups takes over. Imagine you have a ping pong paddle in your hand… what movement do you think is stronger: The wrist extended (like the follow through in a ping pong backhand), or the wrist forward (like the follow through in a ping pong forehand)? It’s actually the forehand/ flexion posture. OK, that’s why the wrist flexes (down, towards the forearm). What about the fingers? Same thing… the moment of the fingers to close the fingers (fist) is stronger than the movement to open the hand.

But why does this natural posture in survivors suggest to therapists that the hand and wrist be splinted? In some ways, it has to do with the same philosophy that scientific medicine has about treating everything. If she has a fever, try to cool the her down. If she can’t sleep, give her sleeping meds. If she’s nauseous, give her a pill to reduce the nausea.  Of course, there is the opposite view. For instance we know that the immune system works better when the body is feverish, so maybe we should let the fever run its course. If someone can’t sleep, maybe there is a reason and the person should exercise. If there is nausea, maybe what the body is trying to rid itself of… should uh... be expelled.  

Let’s get back to splinting of the wrist/hand… What does the joint want to do? Flex. So the scientific perspective would be: do the opposite-- extend. What keeps joints in an extended position? Splints. So when therapists splint, they’re taking the scientific medical perspective. But as shown by the Cochrane meta, above, the science disagrees. 

One last thing; I’m sure I will hear it from the pro-splinting lobby. Please save your time if you have anecdotal “splinting worked great for me” “evidence.” Unless you are willing to collect data using high reliability/validity outcome measures and have that data accepted as a result of the peer reviewed process, it is not evidence. On the other hand, you may just be an outlier and splinting did work on you. I'd suggest, however, if you do think it worked on you, you establish that it did in fact, work. What and how did you measure? Was your measurement accurate? Was your test valid and reliable? These are the things we sweat in research. In fact, I'd suggest that if you are measuring the two things splints purport to effect, range of motion and spasticity (i.e. goniometery and the modified Ashworth), that you have a partner given that both of these tests have to be done by someone other than the tested. 

How Instant Gratification Can Hurt Recovery

(Note: The following is a fleshing out of a previous blog entry)
Instant gratification can hurt stroke recovery. Here’s how…

Let’s say you want to retain soft tissue length in finger and wrist flexors. What do you do? How about a static splint?

It makes sense; you hold the soft tissue in a lengthened position and the soft tissue won’t shorten, right? There’s only one problem: The evidence suggests static hand/ wrist splinting does not improve movement, function, reduction of spasticity, nor does it retain soft tissue length. So what does splinting do? It provides instant gratification. The therapist can claim they’ve done something and the stroke survivor believes something is being done.

Here are some other options that play the same trick… 

• Stretching to reduce spasticity
• Handling techniques
• Tapping a tendon to get a muscle to fire

All of the above are good and bad

• The good: Instant gratification
• The bad: no evidence of long term efficacy.

Then again, what’s the harm? If a therapist wants to progress the leg during gait by tapping the quads, why is that bad? It’s not bad, but it may be… unhelpful, confusing to the survivor and a waste of therapy resources. Using the same the same example, tapping the quads to progress the leg here’s how it may be unhelpful:

A survivor with footdrop is in the parallel bars (II bars to the rehab nerds). The therapist taps the quads, progressing the tibia at the knee. The tapping puts a quick stretch which the golgi tendon organ perceives as potentially damaging to the quad which, through spinal reflexes, contracts to protect itself, progressing the tibia. The survivor is able to take a step.

OK, we have the instant gratification done. Now, what about the next step? Another tap? What happens when the survivor wants to take a step on their own? They felt their own muscles contracting when the therapist tapped them, but can the survivor do the same thing to himself? That’s confusing. And what is the carryover of the tendon tapping? Is there any physiological advantage the next day, the next hour, the next step? 

Most of the rehab and neuroscience research suggests having the survivor struggle to get their leg to through swing, by hook or by crook, utilizing whatever they have. This sort of “productive struggle” is what drives neuroplasticity post-stroke. If there’s one thing we know about brain plasticity its this: it won’t happen if it’s easy. Tapping makes it easy, but there is no long term benefit. Further, it is confusing to the patient. "Wow, I did that!"- they may think. If you elicit one of your spinal reflexes, yes, it is your muscles doing the movement. But it is not voluntary movement. The only way to get that movement again is to elicit the reflex again.

The same is true with stretching to reduce contractures and/or spasticity. Does stretch have a short term effect? Sure. Might that effect have some clinical usefulness? Sure. Will the impact of a single stretching session or even long term program of stretching reduce spasticity? Again, there is neither supporting research nor long term efficacy.

And handling techniques like NDT? Instant gratification, yes because you can get a survivor who can’t move to move and move without “pathological movement patterns” because, basically, the clinician is moving the survivor. But there is a bit of skepticism among researchers. Here is the Wikipedia take on it.  Here's my take on NDT. 

My suggestion is for clinicians to ask, “What will be the effect after the next associated reaction (laughing, sneezing, getting up from a chair), later the same day, later in the week, 6 months later, and so on?”

And survivors should be asking the same question.

Saebo: Faster than ever!

"My son" loves the show "The Flash" and lo and behold, he (Mr. Flash) was wearing a Saeboflex in tonight's episode! 

The 2 minute survivor exam that tells you a ton

I've been involved in a lot of trials that have involved brain scanning. (example)

But I've never been a big fan of using brain scans to try to predict the deficit. In school we were taught to look at the artery that was blocked. The artery that was blocked leading to the brain or in the brain was supposed to give you some indication about what deficits were.

I would suggest this is where neurology and physiatry on one hand-- and neuroscience on the other-- kind of disagree. The neurologist and phsyiatrist say that this info (brain scan and/or artery blocked) helps determine the deficit, and even the chance of recovery.

But neuroscientists would suggest that, because the brain wiring is "random access" (that any part of the brain may be wired to any other part of the brain), looking at a brain scan maybe grossly predictive, but really tells you not much at all.

In all my seminars I suggest that the thing to do is to examine the patient in a very limited way.

Here's suggestions that will give you global insight into the potential for recovery:

1. Can they move their hand? First, let's define "hand movement." I would suggest that hand movement is any movement from the wrist to fingers, in any direction. The easiest movement for most survivors is closing (fist) the hand. The problem is that many strokes survivors think that they can't close their hand. If they think they can't, do this: 

• Bend (technically: Flex) the wrist. This will allow you to open the fingers. 
• Put the elbow in more than 90° of extension (more straight than a "shake hands" position) 
• With your fingers inside the palm ask the survivor to try to touch their chin. 
• This will force the flexor synergy into play, and if they are able, the fingers will flex and you'll feel the pressure on your fingers. Voilà: they have hand movement! From that you can determine potential for recovery of the hand. (Hint: there is potential).

2. Brush both forearms lightly with your fingertips. Ask the survivor if they feel the same, and if not, how they feel different. If they do feel different, this suggests that sensation has been hit. Try to get them to give you a percentage ("My bad arm feels about 25% of my my good arm feels"). There is a general association between tactile (brushing your fingertips) and proprioception (feeling where that limb is in space). And proprioception has huge implications for recovery.

3. Vision: Can they follow the tip of a pen with their head held straight in front of them all the way towards their affected side? If they tend not to follow things on the affected side, this suggests a hemi field cut and possibly "unilateral neglect" – an inability to attend to the affected side.

4. Speech: can they speak; do they understand what's being said?

5. Are they walking, how well, how fast are they walking?

There-- now you have global insight into that stroke survivor. Isn't that more important than knowing that an occlusion of the inferolateral arterial group infarcted the posterolateral thalamus?

The Wrong Question

"What is the single most important thing you should know about stroke rehab treatments?"

That's easy: You're asking the wrong question.

If you are talking about rehabilitation treatments you are talking clinical stuff. You are talking about a clinician-- usually a therapist-- in a clinical setting. And both clinician and clinic are great but they are not enough during two time periods:

1.  Every day

2. Once you're discharged from therapy.

Let's consider why clinical stuff "every day" is not enough. How much therapy might you get? An hour-- two-- three? Recovery is a full time job during the first few months after stroke and it is the first few months after stroke that you're still seeing therapists. So even when therapists are there, there almost always not there enough.

OK, now lets take "Once your discharged from therapy." Discharged from therapy is in and of itself the very definition of not enough therapy, because you've been discharged. Discharged like a bullet from a gun, off you go! So once you are discharged you are definitely not getting enough clinical stuff.

So maybe the question ("What is the single most important thing you should know about stroke rehab treatments?") is wrong. What if instead the question was "What is the single most important thing you should know about stroke recovery options?"

Isn't that freeing? You are no longer under the rules of managed care because managed care does not care if you try, on your own, to take on your recovery using whatever options you can find. You can spend as much time as you want. And even if recovery options are an adjunct to rehabilitation treatments, they expand the opportunities for recovery.

So, "What is the single most important thing you should know about stroke recovery options?"

Sweat equity. That's it. The more you put in, the more you make your brain uncomfortable and force it to change. The more repetitions, the more challenge, the more focus— the more recovery.

Oh dear blog, how I have neglected thee!

Oh dear blog, how I have neglected thee!

But I have a good excuse. In fact I have many. But let me just give you the two big hits:

1. As usual, I'm on the road a lot, doing talks on stroke recovery. If you a are a survivor, please note that my talks are available at a discounted rate. Jus' sayin'. Love to see you there. We'd probably use you as a guinea pig, so be forewarned.

2. At the beginning of last summer I was offered work as a consultant for a lab at Ohio State. It's a long story, but this lab is the latest iteration of the lab that I've worked for— or with— for the last 15 years.

And in all those 15 years, I've been involved in all kinds of cool stroke recovery studies. I've been involved in studies of constraint induced therapy. I've been involved in studies of mental practice (imagery), electrical stimulation machines, as well of the song whole host of other gizmos. I was lucky enough to also be involved in a transcranial magnetic stimulation (TMS) study. Boy! That was a cool study! Basically we were able to touch stroke survivor's brains, without having to go through the messy business of opening up part of the skull.

I could write much more than this blog entry can hold about TMS. But I'd like to tell you a little bit about the latest study I've been involved in. It's the coolest!

A pharmaceutical company run by neuroscientists, called Dart Neuroscience, thinks it may have come up with a pill to help stroke survivors recover.

This pill is thought to help the brain produce BDNF (brain derived neurotrophic factor). BDNF is called by some

neuroscientists "miracle grow for the brain." It is produced by the brain for the brain during times in which the brain needs to learn.
For instance, BDNF comes out right after birth. And you can imagine why – the infants brain is trying to figure out what that smell is, who that face belongs to, how to use their hand, and on and on. So the brain needs help, so it produces BDNF to make all that stuff easier to learn.BDNF is also produced by the brain after brain injury – including stroke.

This is one of the reasons that the stroke survivor's brains are said to be in in "infantile state" — because, like an infant's brain, the stroke survivors brain is awash in BDNF.

But if there was a pill that produced BDNF in survivors it would help in two ways:

1. Typically BDNF is only available in the brain for about a three month period after the stroke. If a pill would produce even more BDNF it would open a larger window of opportunity for recovery.

2. Some stroke survivors just don't produce BDNF— at all— after their stroke. This medication would help those people. A lot.

To get a study like this off the ground involves a pretty monumental effort by dozens of people. I am one of those people.

So, dear blog, I apologize! 

But I'm back!

ANGER: It helps recovery!

Quick funny stroke survivor story. This comes from an OT who told it at one of my stroke recovery seminars.

"I had this guy, he was a right hemi and totally expressively aphasic but could understand everything. I kept telling him that he had to move his right arm. "You gotta move it or it wont get better.' 

He got so frustrated with me he would just keep giving me the finger. "It wont get better unless you use it!' Finger. 'How are you going to get it back if you don't use it?' Finger.

So finally I said, "Tell you what: You can give me the finger all you want, but you got to do it with your right hand."

So, apparently he goes home and spends all night trying to get that finger up and sure enough... the next day he walks in to the gym and gives me the finger with the right hand! And I was like, "THAT'S GREAT! Now we have something to work with!'

And everyone looked at us like we were crazy."

Shortened Achilles? Here's an option.

There are 3 reasons drop-foot happens:

1. Stroke is a brain injury. The brain injury no longer provides enough "brain power" to  activate the muscle that lift the foot (tibialis anterior).

2. Survivors often have spasticity of the calf muscles. The job of the calf is to cause a "toe down" posture at the ankle. A spastic calf muscle is one that contracts too much, forcing the "toe down" position.

3. Because of both #1 and 2, above, there is often a contracture (permanent shortening) of the calf muscle and the Achilles tendon.

There are a number of aids and shots and exercises and so on to help drop-foot, but I'd like to focus on one option. Its called Percutaneous Achilles Tendon Lengthening.

Quick hits:

• It is a surgery, often done outpatient and under a local. 
• Healing takes 6-8 weeks
• GRAPHIC video here 
• Its permanent
• Its effect is (after healing) immediate

Do doctors know?

Medical doctors. MDs. They can be your best friend. If you’ve had a stroke they spent a lot 

Sherrington: 
A great MD/Scientist

that advanced stroke recovery

of their decade-plus of schooling training to save your life and save as much of your brain as they possibly could. When some MDs show up at the Pearly Gates, St. Peter is going to provide velveteen pathways to the VIP room.

BUT.

Let’s be clear about this, your doctor is probably not a scientist. Very few are. The ones that are usually work at major academic institutions. Think Johns Hopkins.

A few quick points here…

1. Without a doubt, a rare few MDs do great, great scientific work that promotes medicine. 

2. Almost all medical science is developed by neuroscientists, biologists, chemists, etc. Scientists develop treatments (from x-ray

Taub: 
A great
psychologist who
advanced stroke recovery.

to antibiotics) and MDs make it illegal for anyone beyond themselves to prescribe them. Sometimes they make great gatekeepers, but they often screw it up. 

In fact, assuming your MD is even committed to the science may be a bit of folly. "Only a fraction of what physicians do is based on solid evidence from Grade-A randomized, controlled trials; the rest is based instead on weak or no evidence and on subjective judgment. When scientific consensus exists on which clinical practices work effectively, physicians only sporadically follow that evidence correctly." (Scientific American)

Most MDs don’t do science, don’t do clinical trials and are not qualified as scientists. Many MDs are not qualified to interpret the science they need to do their jobs, especially if they are not specialized in the area in question. Asking a GP about leading-edge rheumatoid arthritis treatment is like asking a soccer player about basketball’s triangle offence; they may know, but they probs don’t. Even asking, say, a neurologist about, say, migraine is a mistake. How many pathologies do neurologists treat? Countless, that’s how many. Will they be an expert on migraine? Maybe.

So what does this mean to you, dear survivor? It means you have to do your own research, and find your own experts.

There is a bit of good news…if you are willing to work a bit. If you go to PubMed and ask it your questions (i.e.: aphasia stroke recovery) articles by scientists who are experts will bubble up and from there it’s just a hop-skip and jump to their email address. Ask the scientists on the bleeding edge your question. (Hint; be clear, specific and respectful for the best results.) Hack through the pseudo-scientific gobbledygook of medicine (haven’t you exhausted that already anyway?) and get to the extraordinary.

Off you go… 

C'mon baby...

Here is a flowchart used to guide recovery of walking after stroke...

Click image to make larger

Boy, that's complicated! 

How do we learn how to walk in the first place- as infants? Does it involve "treatments" that span from "Task Specific Training" to orthotics?

Stroke recovery is hurt by complexity. When rehab options become too complicated the stroke survivor is separated from their own recovery because they don't know what to do. 

Forget survivors for the moment... At some point stroke recovery can become so complicated that even clinicians don't understand it. Or they don't understand the technology in the complicated system because they never interface with that complicated technology. 

Have a look at the algorithm above. I would argue the whole thing is not only way too complicated, it's also incorrect.

I would like to rewrite the entire algorithm like this...

Click image to make larger

Post-stroke ambulation most benefits from task specific training. Translation: Walking more improves walking.

Socializing, Play and Moving Helps Drive Recovery

Part of your recovery may depend on how much fun your having while you recover.

Enriched environments (EE) are what we all want. It's why we send our kids to good schools, why we seek out new experiences and why we travel.  It turns out that enriched environments are very good for the brain. One of the main enrichments of environment that humans have is social interaction.

What do enriched environments have to do with stroke recovery? A ton.

What hurts social interaction? A stroke.

It turns out that there's pretty good evidence that stroke survivors engaged in enriched environments recover more. More than what, you may ask. Survivors involved in environments rich in social interaction, physical activity, and interesting experiences recover more than survivors who are not in enriched environment.

There is one caveat… Most of this research has been done on animals. The reason was done in animals is that it would be impossible to do the same sort of research and humans. Imagine a human study like this would go…

You would have to groups:

The control group: survivors would be involved in a highly social environment in which there were a lot of games played, a lot of conversations and a lot of physical activity.

The experimental group: survivors would be put in a cell where they were fed well, but did not engage any other humans in anyway.

A study like that on humans would be considered… What's the word? Unethical. That's the word: Unethical.

How do you find rats that have had a stroke? You give them one. Researchers surgically cause a stroke in the rats. (video here) 

They then separated the rats into an experimental 

and control group. 

(Note: the idea of enriching environments is beginning to be tested in human survivors. It is made ethical by letting one group do what they normally would do while the experimental group got an increase in physical, cognitive, and social activity.)

What does the research show about the effect of enriched environments on stroke recovery? The rat stroke survivors in the enriched environments had better proprioception (sense of movement) than the rats that were left to themselves. 

Also...

• EE plays an important role in the recovery of damaged neural function
• Housing rats in an enriched environment can enhance functional outcome after focal brain ischemia
• Significant improvements in sensorimotor function

Recovery depends on neuroplasticity? Yeah...not entirely.

There's this notion among many clinicians and survivors that recovery is all about neuroplasticity. It's the thesis of my book, the focus of the work of me and fellow lab rats (colleagues), as well as much of our stuff in journal articles. But it's not 100% true. A lot of recovery comes from stuff other than neuroplasticity.

Healing First, Neuroplasticity Later

To explain this, let's nail down two things:
1. What neuroplasticity is
2. When neuroplasticity is important

What is neuroplasticity, and where does it happen?
Neuroplasticity–the simplest definition: Changing the structure and/or function of neurons in the brain. Actually, this is not entirely true. Neuroplasticity can happen anywhere in the nervous system. Even peripheral nerves can change in terms of structure and function. This is why, when it comes to stroke, researchers often talk about "cortical plasticity." They are being very specific about where the plasticity is happening: in the cortex of the brain. 

The cortex is where all the "learning" neurons are. The cortex is where all the neuroplastic action is.

The definition of neuroplasticity as a relates to stroke is this: Changing the structure and or function of neurons in the cortex of the brain.

When is neuroplasticity important?
The first thing to do is figure out when neuroplasticity is not that important. The cortex of the brain is constantly rewiring in all of us–all of the time. But it is only robust enough to make a difference in a stroke survivor once they are chronic. The chronic phase is generally defined as "after the first three months after stroke." But probably a better way to define it is: the point after the plateau. So once a survivor has plateaued from then to the end of their life they are considered chronic.

During the chronic phase neuroplasticity is vitally important to recovery. It is only through forging new pathways a chronic stroke survivor learn to move better. "Forging new pathways" is neuroplasticity.

This will tell you where to focus on all phases of recovery.

So neuroplasticity is vital to recovery during the chronic phase. And make no mistake: for most very successful stroke survivors recovery done during the chronic phase is represents a huge part of their recovery.

However, most recovery, for most survivors happens during the subacute phase (from 7 days to 3 months, average). But during the subacute phase neuroplasticity is not the predominant driver of recovery.

So what is the primary driver during the subacute phase?

To put it simply, recovery during the subacute phase has to do with healing (more technically "reengaging the penumbra").

The penumbra is the portion of the brain that surrounds the area that was killed by the stroke. NOT using the whole penumbra is the essence of learned nonuse.

So, to review:

SUBACUTE PHASE (~7 DAY TO ~3 MONTHS): Most recovery during this phase is what would be called "spontaneous recovery" or "natural recovery." CHRONIC PHASE ~3 MONTHS UNTIL THE END OF LIFE) Recovery comes from the hard work of the survivor driving their own brain towards recovery neuroplastically.