Focal hand dystonia--a disorder of neuroplasticity?

Abstract

The term dystonia collectively refers to a heterogeneous group of movement disorders characterized by sustained involuntary muscle contractions that result from co‐contracting antagonistic muscles and overflow into extraneous muscles (Hallett, 1998). Like other types of focal dystonias, writer’s cramp develops in the absence of known structural changes in the nervous system and it often requires extensive repetition of movements to emerge. The pathophysiology of dystonia has been shown to comprise abnormalities in both motor and somatosensory systems. Neuronal representations are believed to be shaped by prior experience through physiological processes commonly referred to as neuroplasticity. Numerous studies have revealed that neuronal representations may be altered in focal hand dystonia. One such alteration is a severe degradation of finger representations in the somatosensory cortex which are normally highly somatotopically organized (Bara‐Jimenez et al ., 1998; Elbert et al ., 1998). In an animal model of focal hand dystonia, somatosensory dedifferentiation resulted from manipulations involving excessive repetitive associative stimulation of skin regions on different digits not normally stimulated conjointly (Byl et al ., 1996). Although considerable disagreement exists as to whether such abnormalities of somatosensory processing alone are sufficient to induce a dystonic phenotype, two other questions are raised by these observations. First, do the abnormal movements in dystonia themselves lead to somatosensory dis‐organization and …