Member Comments are provided by individuals and reflect their personal opinions only. Under NO circumstances should you act on any advice or opinion posted in this forum. ALWAYS check with your personal physician before taking any action regarding your health! MedHelp International and our partners, sponsors and affiliates have no obligation to monitor any comments posted on this site, or the content and/or accuracy of such exchanges. MedHelp International does not endorse the views of any user.
Stroke Community
This patient support community is for discussions relating to stroke, rehabilitation, ability to eat/swallow, alertness, bowel/bladder control, depression, motor skills, nutrition, orthotics/braces, pain, prevention, senses, and spasticity.
Spasticity After Stroke: Why Bother?
by oc1dean, May 05, 2008 12:53PM
Here is a letter to the editor of Stroke magazine. I talked to my doctor on this subject and he believes in treating spasticity if the patient has problems with it. You might want to ask your doctor what s/he believes about treating spasticity.
Here is the letter.
Stroke. 2004;35:1787.)
© 2004 American Heart Association, Inc
Spasticity After Stroke: Why Bother?
William M. Landau, MD
Department of Neurology, School of Medicine, Washington University in Saint Louis, Saint Louis, Missouri
To the Editor:
Perseveration of behavior is a significant clinical symptom among intentional disorders of organic brain disease, attributed by some authors especially to prefrontal brain impairment. However, the perseverative preoccupation of professional neurologists and therapists with the purpose of overpowering the spasticity ogre seems to be an endemic, intractably-taught delusion that afflicts both academic scholars and clinicians.1,2
In 1951, Thomas Twitchell published a 37-page analysis of the clinical course of recovery of 121 acute hemiplegic stroke patients in the Boston City Hospital.3 Early on they were examined daily, and 25 were carefully followed for weeks or months until they reached a stable status of recovery or disability. Twitchell described in great detail both the usual and exceptional patterns of functional recovery, along with the associated patterns of reflex phenomena. Following transient flaccidity associated with acute paralysis, resistance to passive stretch evolved during the first several days.
Twitchell concluded, "The great disability which results when recovery is halted in the phase of heightened proprioceptive activity has prompted many earlier investigations. Walshe (1919) clarified the previously confused views as to the nature of spasticity, and showed its identity with the type of exaggeration of postural reflexes seen in decerebrate rigidity. The analysis of Sherrington and his collaborators subsequently identified the stretch reflex as the fundamental reaction of such disorder. It has often been assumed that if spasticity could be abolished, willed movement could be more effectively performed. The present study indicates that the first movements to appear following hemiplegia are themselves facilitated stretch reflexes. The problem at that stage is not so much to abolish the spastic reaction, as to harness its diffuse hyperactivity." Burke’s extensive neurophysiological analysis points out that spasticity may be a functionally useful adaptation to pyramidal tract injury.4 The only substantive clinical performance accomplishment of baclofen is partial diminution of phasic flexor spasms.5 Tizanidine does no better.6
Like the nociceptive extensor plantar reflex of Babinski and tendon jerk proprioceptive hyperreflexia, spasticity is also a release phenomenon. There are no data or rationale to suggest that severing the extensor hallucis longus tendon may improve recovery from stroke. Similarly, regarding spasticity, I have yet to find any adequately controlled demonstration that the steadfast fad of fixing this phantom facilitates functional recovery from hemiplegia; there is much evidence to the contrary.4–13 The integrated forebrain and hindbrain organizations that accomplish fine adaptive coordination, as in handwriting, piano playing, walking down steps, or ballet dancing, are orders of magnitude beyond the simplistic spinal reflex concept of competitive force between agonist and antagonist about a single joint.
I do applaud the rediscovery by Sommerfeld et al that the "focus on spasticity in stroke rehabilitation is out of step with its clinical importance." I hope, too, that the editorial reviewer, Dr Kramer, may cease to search for "additional studies needed to refine guidelines for treating spasticity after stroke." George Leigh Mallory’s personal rationale for climbing to the peak of Everest was "because it is there." Mallory failed. "Because it is there" constitutes neither scientific nor ethical rationale for the reflex temptation to treat this reflex.
References
Sommerfeld DK, Eek EU, Svensson AK, Holmqvist LW, von Arbin MH. Spasticity after stroke: its occurrence and association with motor impairments and activity limitations. Stroke. 2004; 35: 134–139.[Abstract/Free Full Text]
Cramer SC. Editorial comment–spasticity after stroke: what’s the catch? Stroke. 2004; 35: 139–140.[Free Full Text]
Twitchell TE. The restoration of motor function following hemiplegia in man. Brain. 1951; 74: 443–480.[Free Full Text]
Burke D. Spasticity as an adaptation to pyramidal tract injury. Adv Neurol. 1988; 47: 401–423.[Medline] [Order article via Infotrieve]
Landau WM. Spasticity: What is it? What is it not? In: Feldman RG, Young RR, Koella WP, eds. Spasticity: Disordered Motor Control. Chicago, Ill: Yearbook Medical Publishers; 1980; 17–24.
Here is the letter.
Stroke. 2004;35:1787.)
© 2004 American Heart Association, Inc
Spasticity After Stroke: Why Bother?
William M. Landau, MD
Department of Neurology, School of Medicine, Washington University in Saint Louis, Saint Louis, Missouri
To the Editor:
Perseveration of behavior is a significant clinical symptom among intentional disorders of organic brain disease, attributed by some authors especially to prefrontal brain impairment. However, the perseverative preoccupation of professional neurologists and therapists with the purpose of overpowering the spasticity ogre seems to be an endemic, intractably-taught delusion that afflicts both academic scholars and clinicians.1,2
In 1951, Thomas Twitchell published a 37-page analysis of the clinical course of recovery of 121 acute hemiplegic stroke patients in the Boston City Hospital.3 Early on they were examined daily, and 25 were carefully followed for weeks or months until they reached a stable status of recovery or disability. Twitchell described in great detail both the usual and exceptional patterns of functional recovery, along with the associated patterns of reflex phenomena. Following transient flaccidity associated with acute paralysis, resistance to passive stretch evolved during the first several days.
Twitchell concluded, "The great disability which results when recovery is halted in the phase of heightened proprioceptive activity has prompted many earlier investigations. Walshe (1919) clarified the previously confused views as to the nature of spasticity, and showed its identity with the type of exaggeration of postural reflexes seen in decerebrate rigidity. The analysis of Sherrington and his collaborators subsequently identified the stretch reflex as the fundamental reaction of such disorder. It has often been assumed that if spasticity could be abolished, willed movement could be more effectively performed. The present study indicates that the first movements to appear following hemiplegia are themselves facilitated stretch reflexes. The problem at that stage is not so much to abolish the spastic reaction, as to harness its diffuse hyperactivity." Burke’s extensive neurophysiological analysis points out that spasticity may be a functionally useful adaptation to pyramidal tract injury.4 The only substantive clinical performance accomplishment of baclofen is partial diminution of phasic flexor spasms.5 Tizanidine does no better.6
Like the nociceptive extensor plantar reflex of Babinski and tendon jerk proprioceptive hyperreflexia, spasticity is also a release phenomenon. There are no data or rationale to suggest that severing the extensor hallucis longus tendon may improve recovery from stroke. Similarly, regarding spasticity, I have yet to find any adequately controlled demonstration that the steadfast fad of fixing this phantom facilitates functional recovery from hemiplegia; there is much evidence to the contrary.4–13 The integrated forebrain and hindbrain organizations that accomplish fine adaptive coordination, as in handwriting, piano playing, walking down steps, or ballet dancing, are orders of magnitude beyond the simplistic spinal reflex concept of competitive force between agonist and antagonist about a single joint.
I do applaud the rediscovery by Sommerfeld et al that the "focus on spasticity in stroke rehabilitation is out of step with its clinical importance." I hope, too, that the editorial reviewer, Dr Kramer, may cease to search for "additional studies needed to refine guidelines for treating spasticity after stroke." George Leigh Mallory’s personal rationale for climbing to the peak of Everest was "because it is there." Mallory failed. "Because it is there" constitutes neither scientific nor ethical rationale for the reflex temptation to treat this reflex.
References
Sommerfeld DK, Eek EU, Svensson AK, Holmqvist LW, von Arbin MH. Spasticity after stroke: its occurrence and association with motor impairments and activity limitations. Stroke. 2004; 35: 134–139.[Abstract/Free Full Text]
Cramer SC. Editorial comment–spasticity after stroke: what’s the catch? Stroke. 2004; 35: 139–140.[Free Full Text]
Twitchell TE. The restoration of motor function following hemiplegia in man. Brain. 1951; 74: 443–480.[Free Full Text]
Burke D. Spasticity as an adaptation to pyramidal tract injury. Adv Neurol. 1988; 47: 401–423.[Medline] [Order article via Infotrieve]
Landau WM. Spasticity: What is it? What is it not? In: Feldman RG, Young RR, Koella WP, eds. Spasticity: Disordered Motor Control. Chicago, Ill: Yearbook Medical Publishers; 1980; 17–24.
Member Comments (1)
by Karen611, Jun 02, 2008 04:29PM
To: William M. Landau, M.D.
You seem to downplay the importance to the patient of muscle spasticity. My father, who had a hemoraghic stroke a year ago, has truly suffered this year with spasticity in his right arm. He says that it often feels like a rubber band is being twisted tighter and tighter and he cannot control small motor functioning of his right arm and hand because of the spasticity. He sometimes feels that it would help to have a tendon cut to release the constant tightening. It is painful and the severity of the spasticity, from day to day, determines whether he is having a good day or a bad day. I think he would tell you that more research would benefit many sufferers of this condition. It may not be life threatening but it does affect daily living.
Post Comment
