Nov 20, 2018

Flaccid or spastic; what strategy works best?

Here's a recently email question I got....

Hi there,

I recently read your article about spasticity located here

The article seems to focus on therapies and treatments for patients who still have some motor control over muscles -- i.e. the brain is still in the loop.  Would the same treatments apply to a patient with little or no muscle control over muscles. i.e. muscles remain mostly flaccid post stroke.  Or is there little in the way of physical therapy that can be applied in this situation?

Specific patient is currently being treated with ativan and tizanidine, with the resulting effect that their ability to remain active is significantly deteriorated due to drowsiness.

Thanks,
(Name withheld)


Muscles hate to be overstretched, so if the brain is not online (as is often true after stroke) the muscles rely on the spinal cord to take over the job of protecting the muscles from being overstretched. But the spinal cord is a dumb brain. It can only tell muscles to tighten. The bottom line is: once the spinal cord takes over you end up with tight spastic muscles.

There is emerging research that suggests that if you can reestablish brain control over spastic muscles, the spinal cord will get it out of the way, and spasticity will decline.

So, as you can see the question, above, is a bit confusing because the writer asks, "Will the same treatments apply… in muscles that remained mostly flaccid post stroke?"

When the muscle is flaccid, there is no brain control over the muscle. If that's the case early in recovery (the first few weeks) you may find that the survivor becomes spastic or regains voluntary movement through the arc of recovery. But if the survivor is flaccid for more than a few weeks, the only thing that may have potential is electrical stimulation.  

(Note: because tizanidine -trade name Zanaflex- in particular is used specifically for spasticity, the person you are talking about is spastic. In that case they would have voluntary control into flexion - i.e. if you passively stretch the fingers to "open" the hand, they can squeeze your hand. If this is true, then I'd follow this strategy. It is a common misconception that everyone who is spastic has no control over their muscles. If they can squeeze, have them squeeze over and over and over and over... Tough to do when "their ability to remain active is significantly deteriorated due to drowsiness.")

If you want to see all this blog's entries on spasticity click here.

Nov 19, 2018

Recovery is done in three phases.

Recovery from stroke is done in three phases.

ACUTE    SUBACUTE    CHRONIC
1. The acute phase (~day 1 to day 7 [note all time periods are highly variable]). This is usually done in the hospital. In terms of recovery your main responsibility is to keep yourself healthy. Therapists will typically focus on helping you do what you can do. This is a time for convalescence.
2. The subacute phase (~day 7 to 3 months). This is usually done with some help from therapists. You will experience the most recovery during this phase. This is the time that rehabilitation should "put the pedal to the metal." This is where the hard work begins. During the subacute phase the brain is "primed" to recover. Make the most of this phase because it is a window of opportunity to reach the highest level of recovery.Squander it and squander the highest level of potential recovery.
3. The chronic phase (~3 months to the end of life). Typically the survivor has very little contact with rehabilitation professionals during the chronic phase. This is the time to implement a "do-it-yourself" plan for recovery. Recovery comes at fits and starts and is much more difficult than during the subacute phase. Still, important gains can be made during this phase. Up to very recently it was thought that no recovery could be made during the chronic phase. We now know, however, because of the brain's amazing ability to rewire itself, essential progress can be made during the chronic phase.

Nov 12, 2018

A blog entry about football-induced brain injury.

There is a problem when it comes to the issue of football and brain injury....

Nov 6, 2018

Spasticity After Stroke III: Options for Treatment

      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.

Nov 5, 2018

Spasticity I: The "Magic" "Cure" for Spasticity Reduction?



       

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.