Introduction

Focal hand dystonia (FHD) is characterized by dystonic hand contractions that are often aggravated by purposeful actions and may be specific to a particular task. For example, a patient may have dystonia when using the hand for writing but not for other tasks such as eating or typing. The term “occupational dystonia” is used when dystonia affecting performance of the job arises in individuals with a particular occupation, usually an occupation requiring repetitive and excessive fine motor activity. The occupations particularly prone to have focal task-specific dystonia are listed in Table 10.1. Most of these hand dystonias fall under the rubric of primary focal dystonias.

This chapter discusses writer’s cramp and musician’s dystonia (cramp) in detail, the two most common occupational dystonias, followed by a discussion of other focal occupational dystonias.

Pathogenesis

The exact cause of FHD is not yet elucidated. A consistent physiological finding is excessive activation of antagonists and overflow and prolongation of muscle activation. Both of these are thought to reflect deficiency of inhibition at multiple levels of the motor system circuitry (Hallett, 2000, 2006a,b). Dopamine dysfunction has also been implicated. Although FHD is a movement disorder, somatosensory dysfunction is also present, including distorted sensory maps of the affected hand (Bara-Jimenez et al., 1998) and impaired sensory discrimination (Sanger et al., 2001). Structural MRI analyses have shown increased gray matter volume in the basal ganglia of musicians (Granert et al., 2011) and writers (Garraux et al., 2004) with FHD. Functional MRI has shown impaired activation of the primary sensorimotor and supplementary motor cortex during voluntary muscle relaxation and contraction (Oga et al., 2002). A genetic factor in the development of hand dystonia is possible, as up to 20% of patients with writer’s cramp have family members with dystonia.