Published online before print July 1, 2004, doi: 10.1161/01.STR.0000136388.80433.eb
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(Stroke. 2004;35:1787.)
© 2004 American Heart Association, Inc.
Letters to the Editor |
Spasticity After Stroke: Why Bother?
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
1. 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.
2. Cramer SC. Editorial comment–spasticity after stroke: what’s the catch? Stroke. 2004; 35: 139–140.
3. Twitchell TE. The restoration of motor function following hemiplegia in man. Brain. 1951; 74: 443–480.
4. Burke D. Spasticity as an adaptation to pyramidal tract injury. Adv Neurol. 1988; 47: 401–423.[Medline] [Order article via Infotrieve]
5. 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.
6. Landau WM. Clinical Neuromythology XIV. There you go again: the steadfast fad of fixing spasticity. Neurology. 1995; 45: 2295–2296.
7. Landau WM, Weaver RA, Hornbein TF. Fusimotor nerve function in man: differential nerve block studies in normal subjects and in spasticity and rigidity. Arch Neurol. 1960; 3: 10–23.[Medline] [Order article via Infotrieve]
8. Landau WM. Spasticity: the fable of a neurological demon and the emperor’s new therapy. Arch Neurol. 1974; 31: 217–219.
9. Sahrmann SA, Norton BJ. The relationship of voluntary movement to spasticity in the upper motor neuron syndrome. Ann Neurol. 1977; 2: 460–465.[CrossRef][Medline] [Order article via Infotrieve]
10. Landau WM. Clinical Neuromythology II. Parables of palsy pills and PT pedagogy: a spastic dialectic. Neurology. 1988; 38: 1496–1499.
11. Landau WM, Hunt CC. Dorsal rhizotomy, a treatment of unproven efficacy. J Child Neurol. 1990; 5: 174–178.[Medline] [Order article via Infotrieve]
12. McLaughlin JF, Bjornson KF, Astley SJ, Graubert C, Hays RM, Roberts TS, Price R, Temkin N. Selective dorsal rhizotomy: efficacy and safety in an investigator masked randomized clinical trial. Dev Med Child Neurol. 1998; 40: 220–232.[Medline] [Order article via Infotrieve]
13. Landau WM. Muscle tone: hypertonus, spasticity, rigidity. In: Elsevier’s Encyclopedia of Neuroscience, 3rd edition. 2001; 1–5.
Response
Department of Geriatric Medicine, Danderyd Hospital, Danderyd, Sweden, and Neurotec Department, Division of Physiotherapy, Karolinska Institute, Huddinge, Sweden
Department of Geriatric Medicine, Danderyd Hospital, Danderyd, Sweden
Neurotec Department, Division of Physiotherapy, Karolinska Institutet, Huddinge, Sweden
Stroke Unit, Division of Internal Medicine, Karolinska Institutet, Stockholm, Sweden
We thank Professor Landau for his appreciated comment on our article1 about spasticity after stroke. In the reported and commented study1 we found spasticity in only a minority of the hemiparetic patients assessed 3 months after acute stroke. The results from our population-based study provide an original clinical support of the theories proposed by Professor Landau in his comment of our article. Additional data, including the number of patients presenting with possible spasticity, ie, exaggerated reflexes as well as intrinsic changes of the muscles, according to the modified Ashworth scale,2 18 months after stroke, will soon be presented.
In the spiritual reflection on spasticity, Professor Landau points out the lack of scientific proof supporting the common interest in spasticity after stroke. Considering available scientific proof, both theoretical3 and clinical,1,4 the former assumption that hemiparesis depends on the lesion of the upper motor neuron with accompanying spasticity can no longer remain the basis for physiotherapy assessments or interventions in stroke rehabilitation. Physiotherapists "treating spasticity" most certainly do not treat any exaggerated reflexes but possibly the intrinsic changes of the muscles. As Professor Landau suggests: let us restrain the reflex temptation to treat this reflex.
References
1. 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.
2. Bohannon RW, Smith MB. Interrater reliability of a modified Ashworth scale of muscle spasticity. Phys Ther. 1987; 67: 206–207.
3. Sheean G. The pathophysiology of spasticity. Eur J Neurol. 2002; 9: 3–9.[CrossRef][Medline] [Order article via Infotrieve]
4. O’Dwyer NJ, Ada L, Neilson PD. Spasticity and muscle contracture following stroke. Brain. 1996; 119: 1737–1749.
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