For many years, the use of botulinum toxin in the management of dystonia and associated conditions, has been recognized as not only having a beneficial effect on muscle tone and activity, but also to be associated with significant and prolonged pain relief. It is difficult to understand how this effect could be mediated solely on the basis of the toxin's well-known property of chemodenervation of motor end plates. A second mode of action is demonstrated, in which effects on the muscle spindle play a prominent role, and which may enhance analgesia. A hypothesis is presented that a toxin degradation product may provide pain relief by mechanisms yet to be elucidated.