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I've read with interest the recent 5-page JNNP editorial directive by Thompson et al. for “Management of Spasticity.” This paper is not only remarkable for its authoritative vigour; the authors frankly confess, “There is no agreed evidence-based model available for the management of spasticity…A key component of management is the education of all involved.”
But their educational argument is unfor...
But their educational argument is unfortunately afflicted with imprecise definitions, lack of clinical data base, and consequent conceptual perversion. “Stretch reflexes in healthy subjects are complex.…Spasticity is seen after an upper motor neuron (UMN) lesion, the relative importance of descending pathways remains unclear….Lack of descending control over spinal cord interneuronal circuits results in a decrease in the effectiveness of spinal inhibitory circuits such as those mediating reciprocal, presynaptic, and recurrent inhibition….The paucity of inhibitory spinal cord control means that this activity could, once triggered, continue relatively unabated…. Spasms or sudden involuntary, often painful, movements are often included under the umbrella term of spasticity. However, physiologically these appear to be an independent entity….Spasticity and spasms are, however, only two of the symptoms of the UMN syndrome. Other symptoms such as muscle weakness, decreased postural responses, and reduced dexterity all have an impact on an individual’s function. These features may be independent of each other, but it is often difficult to assess the relative contribution each has to reduction in function.” (The editorial’s Reference , “Pathophysiology of spasticity,” is a misprinted citation to next century volume 238 of JNNP.) Not cited is James Lance’s non-complex, now classical definition, “Spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the UMN syndrome.”
This confusion is more than an issue of academic semantics; the product is their all-inclusive causal indictment: “Spasticity can cause discomfort and stiffness, while spasms can be annoying and painful and may interfere with function. Physical activities such as walking, transferring, picking up objects, washing, dressing, and sexual activity can all be affected. Likewise the ongoing presence of spasticity and spasms can have an emotional impact on, for example, mood, self image, and motivation. Poorly managed spasticity can also be responsible for muscle shortening and the development of tendon and soft tissue contractures, which together with spasms can lead to compromised safety in lying and sitting.” Secondary indictments from contractures include “difficulties with personal hygiene or dressing, positioning, and at times the inability to sit, which may lead to restricted community mobility and social isolation…development of pressure sores…in children...failure of normal muscle growth…torsion of long bones…joint instability and degeneration.” Thus they attribute all of the disabilities of upper motor neuron impairment (UMNI) to spasticity.
Joint and muscle contracture are the consequence of every variety of chronically restricted joint excursion, whether due to muscular dystrophy, arthritis, local pain, trauma, or orthopaedic fixation. Blaming the reflexes rather than the primary disuse hallmark of UMNI is justified neither by Occam’s razor nor the practical facts.
“Symptom” is the subjective verbalization by the patient of what isn’t functioning properly. The negative symptom language of a patient with UMNI includes words like “weak, clumsy, numb, paralyzed, stiff, tired.” Among these concepts, either patient or physician may play verbal games like attributing “weakness” to “stiffness,” or the reverse; empirical evidence of such relationships does not exist. Nor is there evidence that subjective “stiffness” in task performance is a valid measure of “spasticity.” “Spasticity” is a technical doctor word, not a patient’s symptom complaint. It specifies a complex observation by the physician, inferred to be the result of brain/spinal cord dysfunction or lesion, not a cause. The central concept is increased reactivity, not steady state. Spastic muscles at rest are flaccid. The negative symptoms of UMNI, disturbed voluntary (Jackson’s term) coordination, dexterity, and maintenance of force are attributed to functional or structural disconnection of the spinal final common path from finely tuned integrated brain control. Cerebral cortex Brodmann area 4 (M-1), its corticomotoneuronal projection fibres, and the much broader hemispheral source of the pyramidal tract are only the major central output components. The essential working machinery includes thalamus, basal ganglia, cerebellum, and brain stem. A variety of physiological approaches have consistently failed to show that spasticity phenomena contribute significantly to the negative symptoms of UMNI.
Recent study of a large series of hemiplegic strokes showed that “Spasticity was present in only 19% three months after stroke. Severe disabilities were seen in almost the same number of non-spastic as spastic patients. These findings indicate that the focus on spasticity in stroke rehabilitation is out of step with its clinical importance.” I know of no evidence that the Ashworth scale of spasticity has reliable correlation with the functional performance that patients seek to restore. A much needed recent review of oral antispastic drugs found that none improved motor function significantly, with the exception of some flexor spasm relief by baclofen.
The claim that local injection of botulinum toxin is efficacious is specious. Regarding lifelong spinal infusion of baclofen for the most seriously afflicted patients, I share reservations about the perpetual technical tie-up, economic cost, risk of infection, and arachnoiditis. Since sphincter function is already seriously impaired in most such patients, I concur that the alternative concept of intrathecal phenol deserves more careful study.
The authors’ recommendation of individualized “seamless and multidisciplinary” long-term management of UMNI in order to sustain maximal patient autonomy is not controversial. The critical lack of any controlled, much less Cochrane standard data base for both medications and procedures is apparent. Our patients’ management merits more than a model map.
1. Thompson AJ, Jarett L, Lackley L, Marsden J, Stevenson VL. Editorial: Clinical management of spasticity. J Neurol Neurosurg Psychiatry 2005; 76:459-463.
2. Landau WM. Muscle tone: hypertonus, spasticity, rigidity. Elsevier’s Encyclopedia of Neuroscience, Third Edition: 1-5, 2001.
3. Sommerfeld DK, Eek EU-B, Svensson A-K, Holmqvist LW, von Arbin MH. Spasticity after stroke. Its occurrence and association with motor impairments and activity limitations. Stroke 2004; 35:134-140. Landau WM. Letter to the editor: Spasticity after stroke: Why bother? Stroke 2005; 35:1787-1788.
4. Montané E, Vallano A, Laporte JR. Oral antispastic drugs in nonprogressive neurologic diseases. a systematic review: Neurology 2004; 63:1357-1363. Landau WM. Letter to the editor. Neurology 2005; 64:1989-90.
5. Landau WM. Letter to the editor: Botulinum toxin for spasticity after stroke. New Engl J Med 2003; 348-258.