(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.