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Re: Reply to Landau

In our review, we concluded that the efficacy of oral antispastic treatment of nonprogressive neurological diseases is poor or even nil. As Landau points out, spasticity is not the cause of the disease, but the result. However, as mentioned in the discussion, an effective antispastic treatment would be worth when the activities of daily living are severely impaired.

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Re: Oral antispastic drugs in nonprogressive neurologic diseases: A systematic review

Secondary conflict of interest embarrasses the valuable review of anti-spastic drugs by Montané et al. [1] Their reference for treatment rationale is the non-peer reviewed drug house pamphlet, “Role of tizanidine in the treatment of spasticity.” [2] They state, “[Spasticity] can severely impair normal daily functions such as walking, eating, and dressing, and contributes to patient disability. The therapeutic objective is to reduce the excessive muscle tone in the affected limbs, with the aim of increasing patient’s functional capacity and reducing discomfort….Treatment should be considered when patient’s functionality is affected or when pain causes discomfort.” Spasticity is branded with all of the symptomatic disabilities of the upper motor neuron syndrome.

Vocabulary is the central issue of controversy. Descriptive words most often used by afflicted patients are weak, clumsy, awkward, numb, stiff, off-balance, tired, and paralyzed. The professional lingo is more complicated. Gowers’ coherent concept of upper motor segment includes the cerebrospinal structures that control the lower segment, the anterior horn cells, which Sherrington later labeled the final common path. [3] The upper motor neuron syndrome then came to mean impairment of those activities that Jackson specified as the most voluntary and least automatic movements. Negative symptoms due to disconnection from forebrain neurons comprise impairment of purposeful fine coordinated and maximal controlled force behaviors. Positive symptoms are the stereotyped hyperactive reflexes organized at the disjoined spinal and brain stem levels, especially the stretch reflexes. [4]

For a century, careless use of the terms spastic and spasticity in the professional literature provided only inconsistent confusion. [5] In 1980, with consensus support at an international meeting, James Lance drafted an invaluable working definition of spasticity: “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 upper motor neuron syndrome.” [6] Spasticity is a pathological result, not a cause. By analogy, the pathological precordial murmur doesn’t cause the leaky valve or congestive heart failure.

Among only 12 of 325 articles that were deemed worthy of review, Montané et al. emphasize the lack of efficacy in real-life useful movement performance. No evidence yet relates any attributes of spasticity like the Ashworth scale, clonus, tendon reflexes, and muscle tone to impaired or improved functional autonomy. If these outcome measures are deleted from the reviewers’ tables, still leaving flexor spasms and “adverse events,” practical therapeutic prowess for most spastic patients nears nil.

References:

1. Montané E, Vallano A, and Laporte JR. Oral antispastic drugs in nonprogressive neurologic diseases: a systematic review. Neurology 2004; 63:1357-1363.

2. Landau WM. Clinical Neuromythology XIV: There you go again: The steadfast fad of fixing spasticity. Neurology 1995; 45:2295-2296.

3. Phillips CG and Landau WM. Clinical Neuromythology VIII: Upper and lower motor neuron: The little old synecdoche that works. Neurology 1990; 40:884-886.

4. Landau WM. Muscle Tone: Hypertonus, spasticity, rigidity. Elsevier’s Encyclopedia of Neuroscienc. 2001; Third Edition: 1-5.

5. Landau WM. Spasticity: The fable of a neurological demon and the emperor's new therapy. Arch Neurol 1974; 31:217¬-219.