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Ishibashi et al1 reported the excellent efficacy of mexiletine for the treatment of segmental hyperhidrosis in two patients (who had syringomyelia and cavernous haemangioma of the spinal cord, respectively). They presented the decrement in the patients' sweat rate by oral administration of mexiletine.1
Previously we performed a clinical study focusing on sweating and identified 10 patients with segmental hyperhidrosis among 30 patients with syringomyelia. We followed up the patients with hyperhidrosis for 1–10 (mean 5.0) years. The amount of sweating did not change in any of them during the follow up period,2 although we did not perform a quantitative analysis. Consequently, we speculated that hyperhidrosis persists for at least a year. It is possible that the course of signs in the cases reported by Ishibashi et al were modified by the growth or activity of spinal cord lesions. We consider it imperative that these authors describe any spinal cord lesions and how they may have shifted. However, although they did not mention the duration and time courses of the improvement in their patients, we suppose that the duration of the follow up for each patient would not have exceeded several months, judging from how the authors described their experience. In addition, even though they did not test the effects of mexiletine on control subjects or on other parts of the body in the same patients, we can be assured that the improvement in hyperhidrosis was due to the oral administration of mexiletine, on the assumption that the spinal cord tumour could not have changed in such a short time. We consider that it would be informative for clinicians if Ishibashi et al were to disclose the drug dosage and the time course of its effects and to describe the features of the spinal cord lesions.
We are grateful Sudo et al, as they allow us to clarify a point of our study that was not discussed in the paper recently published in this Journal.1 They asked about the possibility of natural remission and the non-specific effect of mexiletine on sweating.
We administered 200 mg/day mexiletine or 400 mg/day carbamazepine to our patients. Both patients noticed their hyperhidrosis was relieved within two days after administration. Although we did not perform a quantitative analysis several months after treatment, the clinical improvement of hyperhidrosis persisted. In addition, the magnetic resonance images of spinal cord lesions (syringomyelia and cavernous haemangioma) in both patients were followed up for two years. During the follow up period, the spinal cord lesions did not change their size, position, and intensity on magnetic resonance imaging. Therefore, the natural course of the spinal cord lesions could not explain the improvement of hyperhidrosis during the treatment and quantitative analysis in our patients.
The sweat rate of the area of observed hyperhidrosis was decreased without a change of the absolute sweat rate on the healthy side after oral administration of mexiletine. We calculated the ratio of the sweat rate on the affected side to that on the healthy side—the ratio was 2.13 before treatment and decreased to 0.97 on day 7 after the treatment. We therefore consider that the mexiletine had an excellent effect only on the area with hyperhidrosis. Although we did not test the effects of mexiletine on control subjects, we think that the result on a healthy area of each patient was an appropriate internal controls for the evaluation of the drug's effect on hyperhidrosis.
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