© Associated Press.

For rock musicians, an episode of cramp may well result in the sounding of the wrong note, but it is unlikely to result in headlines across the world in quite the same way as some of the other 'occupational' hazards of being a rock star. Musician's cramp is nonetheless a serious problem for those afflicted and is part of a wider class of disorders known as task-specific focal dystonias, which are characterized by involuntary movements and abnormal and often painful postures. Dystonia is often refractory to pharmacological intervention and the underlying mechanisms are unclear at present.

Monkey studies indicate that sensory cortical representations might be disrupted in focal dystonias. However, it is uncertain whether these changes are the cause or the result of the motor abnormalities observed in dystonia. Given the plasticity of these systems, abnormal postures might be expected to lead to changes in sensory systems over time, but it is less clear how motor changes could be triggered by sensory modification. Sanger and Merzenich have addressed this problem by devising a computational model to explain how modifications to sensory representations could lead to abnormal motor behaviour with the characteristics of focal dystonia.

The key to their model is the idea that dystonia might result from an unstable sensorimotor control loop. This loop involves the motor cortex and the sensory systems that provide sensory feedback to the sensory cortex and eventually to motor centres. Sanger and Merzenich's model suggests that increased gain in this loop might lead to dystonia. Because gain is determined, in part, by the size of the sensory cortex devoted to a particular movement, behaviours that lead to abnormal increases in sensory cortical representations are predicted to lead to dystonia. Simulations showed that several different mechanisms that increased gain via plasticity within the sensory cortical representation led to sustained and uncontrolled motor activity in the sensorimotor loop. Although the clinical relevance of this model remains to be tested, the demonstration that changes in sensory representation could provide a mechanism for the aetiology of dystonia represents an intriguing development. Indeed, re-tuning the sensory representation of patients with dystonia might even be a possible treatment strategy.