Sunday, November 29, 2015

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, 


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.  

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. 

Saturday, November 14, 2015

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 itHere'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.

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