There is evidence that pain symptoms or limitations of movement can be attributed to muscle spasm: Zhu and colleagues recently concluded that “the close correlation among evoked potentials, paraspinal muscle spasm and clinical symptoms suggest that the measurement of muscle activity may be more important to low back pain than is commonly accepted.”1
My study was not based on a subjective diagnosis of pain and range of motion. As noted in my article, I measured pain using an authenticated visual analogue scale and I used a standard clinical examination to determine range of motion.2 I did not measure “tenderness.”
Involuntary muscle spasm (dystonia) has been extensively studied by neurologists and neurophysiologists. It has been treated with some success with anticholinergics and other therapeutics, particularly botulin toxoid.3,4,5,6
On a purely practical and clinical level, muscle spasm remains an important cause of patient suffering. Alleviating that suffering, by non-narcotic means if possible, is the bottom line. Perry Rush and I are in agreement that this case series must be put through the rigours of a randomized controlled trial before benztropine becomes the standard of care, as I suggested in my article.2