Spasticity, Motor Recovery, and Neural Plasticity after Stroke as originally seen in Frontiers in Neurology
Before we go anywhere, let’s define spasticity: “Clinically, poststroke spasticity is easily recognized as a phenomenon of velocity-dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex.”
Tangent: I would like to point out that there was a rather long discussion between the platform and several people on the floor at IVStep about the definition of “spasticity.” As you can see, an integral part of this definition is the increased reflexes. (Meaning that when you whack person’s knee with the little rubber hammer, their foot nearly kicks you off the stool, amongst other reflexes.) However, you can have increased muscle tone (this feels like the muscles are hard as rocks and won’t move easily) without the hypereflexia. Currently, the two scenarios are given the same term — “spasticity”– in many circles; however, experts are now advocating for calling the hypereflexive pattern “spasticity” and the hypertonia-only pattern “reversible hypertonia.” Since I don’t know where my colleagues always fall in the spectrum of what definitions they use, I just describe what I see clinically when discussing these symptoms. All that to say, I would advise being aware of what words you are using and why in discussion of these topics. That definition above comes straight from the article, so you know what we’re talking about here.
The first bit of the article addressed how we measure and describe spasticity. I personally use the Modified Ashworth Scale to quantify the hypertonia, then test the deep tendon reflexes with my little rubber hammer and place the reaction on the 0-4 scale. To describe the effects of spasticity on motor recovery, the Brunnstrom Stages of Motor Recovery are useful. I use this to educate patients on their prognosis too, although I use the simplified 3 stage version for them: flaccid (no muscle tone, no movement), spastic (high muscle tone, high reflexes which contribute to poor coordination/abnormal movement of the effected parts) and recovered (more or less normal). With this I can explain that spasticity is normal (everyone is always relived when they hear that what they are experiencing is normal in stroke recovery), but that it obviously isn’t “normal” for human movement, making it a problem we need to work on in therapy. Spasticity and motor recovery go down different pathways in the brain, so while we may use the spasticity at some points as a part of a compensatory strategy (say hypertonic quads keep a knee from buckling in stance), we eventually must break it up in order to achieve normalized movement. Not everyone will achieve full recovery from spasticity. These different recovery levels in chronic stroke survivors may indicate slightly different pathophysiologies in the pathways.
To understand the pathophysiology (what parts are damaged), first you have to understand how a reflex is supposed to work under normal circumstances (physiology). The reflex has 2 parts that makes it go: 1) a feed forward system in the spinal cord (this part isn’t under control of the brain) which controls turning the reflex on and 2) a part of the brain that turns the reflex off or at least controls the reaction. Next time you get your knee whacked by the little rubber hammer, you think really hard about making that foot not move. Some people have enough control that they can totally turn it off, where others can just make it a lot less of a reaction. That’s your brain part at work. If that part gets damaged in a stroke, you only have the part that turns the reflex on… so it keeps getting turned on all the time. This is how hypereflexia and hypertonia create spasticity.
Treating spasticity is very difficult, but not impossible. This needs a combination of medical and therapeutic treatment to have a chance at success. Medically, there are several medicines they use to decrease spasticity. These could include: baclofen, tizanidine hydrochloride, benzodiazepines, or dantrolene sodium. One of the main side effects of these medicines is that it makes you weaker all over. The medicines aren’t going to only work on the spastic muscles, they work on the whole body, since you put it in your whole body. I don’t see these on my patients’ medicine lists very often at my level of therapy care. I work with people in the first few weeks after their stroke, so getting stronger in EVERY muscle is a major goal. I believe the physicians prefer to add these later on once a person is generally strong again, if the spasticity is still a problem. Another medical treatment option is botulism toxin or phenol injections. Yes, the same horrible growth they warn you away from in canned food and also the same stuff they inject to make pouty lips (Botox). It is a nerve toxin. They inject it at the muscles that are spastic, so that specific muscle relaxes. This is temporary lasting up to several weeks. There is also the option of having a baclofen pump installed into your spinal cord, putting a block on that continually turning on part of the reflex system since the brain can’t do it. This requires surgery and isn’t necessarily permanent either as the pump needs to be refilled with medicine periodically. But this is a very serious step and shouldn’t be considered lightly. (Caveat: I am no medical doctor and have no idea which if any of those medical treatments might be right for you or your patient. Speak with your physician or pharmacist if you have medicine questions; they’re the experts on that!)
Therapeutically, the old stand-by treatment is LOTS of stretching of that spastic muscle. At some point, stretching braces may be involved. This is generally not comfortable and not for the feint of heart. A newer treatment that isn’t yet approved by the US FDA is transcranial e-stim. Another pathophysiology lesson: When a stroke happens, the parts of the brain that weren’t damaged by the stroke try to take over the job of the parts that were damaged. Which is very nice of your brain, helping out like that, but the old saying that we only use half our brain is totally false. Those other parts are usually used for something else, so they may not be very easily re-programmed to take over what the damaged parts were doing. They are using the transcranial e-stim to temporarily turn off the part of the brain that is trying to take over for the damaged part. Or they may try to stimulate the damaged part to turn back on quicker and get back to work. With either method, the point is to give the damaged part a chance to come back on line and reprogram itself to do what it’s supposed to do, whether that’s controlling an arm or leg or making your throat muscles work so you can swallow food or your face muscles smile. Other treatment strategies that are currently in use are intensive therapies such as constraint-induced movement therapy, robotic therapies and body weight supported treadmill training. The point of all these therapies is forcing the damaged parts to work, work hard and work for long periods of time. In constraint-induced movement therapy, you tie up an arm that works fine, so you’re forced to use the one that doesn’t work so well on daily tasks, like brushing your teeth, cooking, etc… but ideally you would do this for around 3 hours a day. I’ve seen robots that are attached to legs and pump them up and down while the person is walked by the robot on a treadmill. And again, the more time spent—I mean hours—the better. Then there’s body weight supported treadmill training, which is similar to the robot idea, except you are floated above a treadmill in a harness. With less weight on your legs, they move easier and sometimes therapists help your legs move as you walk the treadmill… again, for an hour to hour and a half preferably. These intensive therapies are best used in conjunction with a medical treatment that will decrease the spasticity. The intensive therapies are designed to re-program your brain to move normally again. It’s a lot harder to get reprogrammed if you’re fighting the old, spastic program all the time during treatment. Another fairly new (or at least new to me) treatment is auditory stimulation through rhythmic cuing and music therapy. I honestly have no idea what that entails, and the article didn’t go into much detail either beyond how is works physiologically, which was rather neat if you have a bit to read into the article.
Well, I’m not sure how much of a “summary” this post was, since it’s fairly long, but I do think it’s a fair distillation of a heady topic that gave me a headache reading about. Which is why I’m posting it today and didn’t on Saturday as planned; it took too long!