Spasticity is my subject for ranting on. None of my doctors were able to explain it or how to recover from it.
When I finally got access to a computer and started researching it I came accross this letter
to the editor of Stroke magazine from William M. Landau.
http://stroke.ahajournals.org/cgi/content/full/35/8/1787
Spasticity After Stroke: Why Bother?
(Stroke. 2004;35:1787.)
© 2004 American Heart Association, Inc.
This alone was very depressing
Then I found another research study that came to the same conclusion.
Found an interesting site Movement Disorder Virtual University that has lots of detail on
spasticity. Here is the link http://www.mdvu.org/library/disease/spasticity/spa_mpath.asp
If you follow it down quite a few levels you can find this
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Subject: Incidence and Consequences of Spasticity After Stroke
Date: 2/20/2004
Spasticity affects less than one quarter of stroke victims, according to this study.
Muscle overactivity and its consequences were assessed in 95 patients both immediately after
and three months a first-time stroke. Seventy-seven (81%) were initially hemiparetic, of whom
20 had spasticity. Among these 20 patients, 14 had hyperreflexia. Within these patients, 3 had
clonus, and 3 had muscle stiffness. Modified Ashworth score was grade 1 in 10 patients, grade
1+ in 7, and grade 2 in 3. None had grades of 3 or 4. At three months, 64 patients (67%) were
hemiparetic, and 18 spastic, reflecting 5 whose tone normalized and 3 who became spastic in the
interim. The correlation between muscle tone and a range of motor and activity scores was low
for most measures at both time points, except for active movements initially, and rapid
movement scores and 9-Hole Peg Test scores at three months.
The authors conclude, “spasticity seems to contribute to motor impairments and activity
limitations and may be a severe problem for some patients after stroke,” but, given the
relatively low numbers of patients with spasticity, they note, “Our findings support the
opinion…that the focus on spasticity in stroke rehabilitation is out of step with its clinical importance.
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Basically since only 25% of stroke survivors have it and most seem to be able to do ADL's,
clinical research seems unlikely. So we are on our own unless we can somehow change that mindset.
Would these researchers have the same comments if they had to recover from spasticity?
Another one from William M. Landau
Landau, W.M., Clinical Neuromythology XIV: There you go again: The steadfast fad of fixing spasticity. Neurology 45:2295-2296, 1995
He even wrote a book about some of it
Clinical Neuromythology and Other Arguments and Essays, Pertinent and Impertinent by William M. Landau
I haven't read the book because I can't find it in a library and I don't want to put any money in his pocket by buying the book.
But there was some hope when I found an article by Peter Levine
For Recovery, Stretch Those Sarcomeres
http://physical-therapy.advanceweb.com/Editorial/Search/AViewer.aspx?
AN=PT_08apr21_ptp48.html&AD=04-21-2008
www.advanceweb.com
By Pete Levine, BA, PTA
Here are some selected paragraphs on this
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Spasticity after brain injury keeps muscle in a shortened position long enough to loose
sarcomeres. Brain injury kills the part of the brain responsible for contraction and relaxation
of particular muscles. This lack of executive control over muscles leads to a feed-forward
"dance" between the spinal cord and muscles.
Here's how it works. Muscles, ever sensitive to the possibility of being overstretched, send a
never-ending barrage of "help!" signals to the spinal cord. The spinal cord responds by sending back "contract!" messages to all the affected muscles. Only some of the affected muscles are shortened.
For instance, the elbow flexors may have the same relative amount of spasticity as the elbow extensors. But in that battle, as in many of the spastic battles after brain injury, the flexors "win." The "winner" loses by being left in a shortened position 24 hours a day, seven
days a week, 365 days a year. The result is a loss in number of sarcomeres and a pathological
shortening of muscles.
It comes as some surprise to most therapists, but there is very little scientific evidence that
stretching muscle reduces spasticity. In the very short-term, there is a small reduction in spasticity. But spasticity is not reduced in any lasting way by stretching, because spasticity
is not caused by muscles. Spasticity is caused by brain injury. Brain injury causes the brain to cede muscular control to spinal reflexes. Increasing the number of sarcomeres will not
reduce spasticity. If it did, every case of spasticity would be eliminated by a regimented stretching program.
Stretching does have an important role to play, however. The basis of all recovery from brain
injury has to do with neuroplastically rewiring the brain. You can rewire the brain until the cows come home, but once contracture has set in, there is no possibility of improving active range of motion. Stretching provides a flexible template on which neuroplastically driven motor recovery can take place.
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I posted a question asking if spasticity research is still being done to
National Institute of Neurological Disorders and Stroke
National Institutes of Health
but have not heard a reply yet.
I am extremely interested in this subject since if I was truly completely paralyzed I could recover much faster using neuroplasticity if I don't have to stop my spasticity first. It truly is an oxymoron that I am not paralyzed enough to 'easily recover'.
If anyone has more/better information please post it here. Or just rant like I needed to do.
Hope this is useful to someone
Dean