Stretching reduces spasticity. Yeah, no.

OK class, here's your quiz:

1. Stretching decreases spasticity T/F

2. Stretching increases the length of spastic muscles T/F

3. Stretching reduces the chance of contracture (muscle stuck at a shortened length) T/F

4. Stretch helps make joints more mobile T/F

First of all, why stretching is good: 

Stretch is good for joints. Every time we move, joints are "lubricated." That is, joints require movement in order for the fluid in the joint (synovial fluid) to be properly distributed. Stroke survivors, because they are typically weak on one side, don't get the joints on the "bad" side to move enough. How much is enough? Look at it this way, on the "good" side your joints, all of them, will be moved through their entire arc of movement (called range of motion) dozens if not hundreds of times per day. How many times are your "bad" side joints moved? Because they have trouble moving, it is wise to move them either with the "good" side doing the work, or a caregiver doing the work. This is called passive ranging.

But while stretching may be good for joints, the affect of stretch on muscles and other soft tissue (ligaments, blood vessels, fat, etc.) is, so far as the science says, negligible. So the answer to your quiz is F, F, F, and F.

I know this is hard to believe. And it is counter to what some therapists think. But it is confusing. There is an immediate effect of stretch on spasticity, everyone knows that. But this is one of the many reasons stroke is so devious; what is true now may not be true 5 minutes from now.

This is a frustration for many clinicians. You observe something is true (i.e. spasticity wanes with stretch) only to find that with the next big movement by the survivor, spasticity comes right back.

Further reading from this blog on spasticity here and here. 
                            

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.

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.

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

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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.

Spasticity II: The Explanation

          So how can you explain spasticity to patients and their significant others in a way that is easy to understand and scientifically valid?
     Here is the story of spasticity. Spasticity happens because of a set of circumstances caught in an endless closed loop. The players in this story are the brain, the spinal cord and the spastic muscle (SM).
         There is an injury to the brain. The brain can no longer control the SM. Muscle spindle sensitivity then develops because the flaccidity resulting from the lack of brain control causes overstretch of the SM.
      The muscle spindle then sends a "Help, I'm being overstretched!" signal to the spinal cord. The spinal cord then sends the message to the brain. The brain would normally send down a mix of facilitory and inhibitory signals to stabilize the muscle. But the brain is not responding. So the spinal cord does.
       The spinal cord says, "SM, do that thing you do!" The SM only does one thing: Flex. So flex it does. These messages go on and on during during most waking hours and for some who suffer from spasticicty, during all but the deepest of sleep. Eventually, the SM starts to lose sarcomeres (the contractile units in muscle) and the SM and other area muscles that are kept in a shortened position, lose length. The shortened muscle perceives everything as an overstretch and the alarm signals to the spinal cord proliferate. The process repeats itself in an endless cycle until contracture sets in.
     Most therapeutic interventions therapists typically use are, at best, nominally effective against the symptoms of spasticity, and do little to address the underlying issues causing spasticity. Consider stretching. Stretching reduces spasticity, right? Stretching does retain soft tissue length and for that reason should be done often to spastic muscles. But research of the effectiveness of stretching in the reduction of spasticity, either through weight bearing, isotonic stretch without weight bearing as well as isokinetic stretching, is equivocal at best. Typically used modalities like cold and heat have a nebulous, short-term effect. There is strong evidence that splinting is ineffective in reduction of spasticity and contracture formation. Facilitory and handling techniques? Also no demonstrated effect.

The problem with Botox

When it comes to spasticity reduction, Botox is the 600 pound gorilla. It is the Oracle. If Oz was the world of spasticity, Botox would be its Wizard. Allergan, the company that makes Botox dictates the conversation. Why? Cold hard cash. Allergan made significantly more than $1 billion in the third quarter of 2012 alone.
 
Keep in mind that Allergan makes other drugs besides Botox. And spasticity isnt the main reason Botox makes 'em money.  The main reason Botox makes money is because of its wrinkle reduction qualities. Bottom line: they have plenty of cash. And they use that cash to influence opinion. This is inevitable, but also unfortunate. The influence that can be bought chips away at a discussion of other possibilities.

What are the other possibilities?

Phenol blocks. In the book "Spasticity: Diagnosis and Management" phenol blocks are called: a "Dying Art" That Merits Revival.
 

Why does it merit revival? Phenol blocks do pretty much the same thing as Botox for spasticity. But it costs less. Much, much less. This is something you should discuss with your doctor. It may be true that Botox is the best option. But it may save you some money to ask about phenol blocks. How much money is saved?

For muscles in the arm/hand, this is one estimate...
Botox: $1014.84
Phenol: $7.85

Another thing about Botox. For a long time the suggestion by Allergan was that Botox should be administered, and that's it. Botox provided a "vacation" from spasticity. They are in the business of selling drugs, not in the business of reduction of spasticity in any sort of permanent way. Remember, Botox does not cure spasticity. Phenol blocks are the same. All Botox and phenol blocks do is provide a window of opportunity to to regain executive (brain) control over spastic muscles. A classic example is of somebody that cannot open their hand. Spasticity in the muscles to close the hand is so strong that they can't open the hand. Botox or a phenol block is used to weaken the muscles that close the hand. This "unmasks" the movement that was always there: Hand opening. Now the hand can open because it's not fighting the spastic muscles that are trying to close the hand. But instead of treating this as a vacation, the person works hard to get the brain re-involved in all the muscles. (Allergan has changed its tune about this with prompting by me and others. They now say: administer Botox and then get therapy.)

During the "vacation" block provide hard work can help permanently reduce spasticity. 

Otherwise, it's just a vacation.