Writer's cramp is characterised by a muscular spasm in the hand of the writing arm, and is often provoked during specific tasks such as writing. Because of its highly task specific nature, some neurologists believed that writer's cramp was of psychogenic origin. However, recent electrophysiological and neuroimaging studies unanimously confirmed basal ganglia dysfunction in patients with writer's cramp. As a consequence, writer's cramp is currently regarded as a form of focal dystonia with neurophysiological pathogenetic mechanisms.1

On the other hand, in the classic psychiatric literature, clinicians sporadically pointed out obsessive-compulsive personalities in patients with writer's cramp. Bindman and Tibbetts described 10 patients with writer's cramp, nine of whom had obsessional personalities.2 These findings have never been confirmed using reliable psychometric measures. However, because of the above mentioned evidence of basal ganglia pathophysiology in writer's cramp, together with the growing evidence of basal ganglia involvement in obsessive-compulsive disorder, it is of great interest to elucidate the relation between writer's cramp and obsessive-compulsive symptoms.

In the present study, we evaluated obsessive-compulsive symptoms in patients with writer's cramp. Obsessive-compulsive symptoms may simply be a psychological reaction to the writing impairment. To rule out this possibility, patients with writing impairment due to peripheral nerve lesions were included as a second group of control subjects, in addition to normal healthy control subjects.

Twelve consecutive patients with writer's cramp who visited the dystonia outpatient clinic of the Department of Neurology at Kyoto University from May 1998 to December 1998, were evaluated with the Yale-Brown obsessive-compulsive scale (Y-BOCS). All patients had been treated with muscle afferent block for more than 3 months.3 As a consequence, their writing disabilities were moderately improved. All of them could write their names in four to six Chinese characters at the time of assessment. A disease control group consisted of seven patients with carpal tunnel syndrome, three with cervical spondylotic radiculopathy, one with chronic inflammatory demyelinating polyneuropathy, and one with myasthenia gravis. All these patients showed disabilities in finger movements due to peripheral nerve lesions of an upper limb, and were recruited from the outpatient clinic of the Department of Neurology at Kyoto University. A healthy control group, age and sex matched to the writer's cramp group, consisted of office clerks or secretaries of Kyoto University and Shiga University. None of the subjects had received antidepressive or neuroleptic medication for at least 6 months before the study. None of the subjects had a history of any psychiatric diseases.

For these three groups, obsessive-compulsive symptoms were evaluated by trained psychiatrists, based on the semistructured interviews assessing Y-BOCS. The scores of the writer's cramp group and two control groups on Y-BOCS were compared using a two tailed Kruskall-Wallis test for non-parametric data. p Values lower than 0.05 were considered to be significant. When the result was significant, the analysis was repeated with each pair of groups, and the p values were multiplied by three to correct for multiple comparisons (two tailed Mann-Whitney tests). Informed consent was obtained from all the participants after the procedure of the study had been fully explained.

The 12 patients with writer's cramp, 12 patients in the disease control group, and 12 normal controls did not differ in age or sex ratio (table 1). Mean Y-BOCS scores were 5.8 (SD 5.5, range 0–18) for the writer's cramp group, 1.0 (SD 1.4, range 0–4) for the disease control group, and 1.0 (SD 1.0, range=0–2) for the normal control group, respectively. There was a significant effect of diagnosis on the total scores of Y-BOCS (Kruskal-Wallis test, χ²=5.99, p=0.012), with significant differences between the writer's cramp group and disease control group (p=0.030, corrected for three comparisons) or normal control group (p=0.036) but not between the disease control group and the normal control group (p>0.99). The compulsive symptoms of the writer's cramp group were mainly related to cleaning and ordering.

The result of our study showed that patients with writer's cramp had higher obsessive-compulsive symptoms than the disease control group or normal control group. Although according to the classic literature the patients with writer's cramp often have obsessive personality features,2 the present study is the first to confirm the clinical finding using objective psychometric measures.

The disease control group consisted of patients with peripheral nerve lesions, who had discomfort in writing comparable with the patients with writer's cramp in this study, who were treated with muscle afferent block.3 Thus the current result does not support the idea that physical distress and social disability due to writing impairment is the main cause of the obsessive-compulsive features of patients with writer's cramp, but supports the notion that writer's cramp and obsessive-compulsive symptoms would develop due to common pathophysiological mechanisms. However, it should be noted that our patients with writer's cramp had been under the treatment for more than 3 months and the duration of disease was relatively short. In most cases of writer's cramp without treatment, it is known that writing disability is extremely severe, causing a significant effect on their lifestyle. The present result does not deny the possibility that the condition could cause abnormal psychopathology in writer's cramp.

Recent studies reported abnormal metabolic activity in basal ganglia together with frontal and anterior cingulate areas in patients with obsessive-compulsive disorder. These data suggest basal ganglia dysfunction as a neural basis of obsessive-compulsive symptoms (for a review, see Saxena et al 4). Therefore, we suspect that basal ganglia dysfunction is the common neural basis of writer's cramp and obsessive-compulsive symptoms. In other forms of focal dystonia such as spasmodic torticollis and blepharospasm, high obsessive-compulsive symptoms were reported.5 Thus, the basal ganglia hypothesis of obsessive-compulsive symptoms may be applied to focal dystonia in general. As obsessive-compulsive symptoms of the patients in this study were not severe enough for the diagnosis of obsessive-compulsive disorder, and due to the small sample size, these findings should be interpreted with caution. Larger studies are necessary in clarifying the pathophysiology of writer's cramp and associated obsessive-compulsive symptoms.