Abstract
Segmental and unilateral hyperhidrosis are forms of sweating disorder. In some cases, these are accompanied by anhidrosis/hypohidrosis in other skin areas. The pathogenesis of these hyperhidrosis may be compensatory and is likely caused by underlying lesions in anhidrosis/hypohidrosis areas, but the precise mechanism remains unclear. Hyperhidrosis is often located horizontally contralateral same myelomere skin areas as the anhidrosis/hypohidrosis, whereas vertically ipsilateral adjacent to other rostral and caudal myelomere with anhidrosis/hypohidrosis. The similar efferent phase of the physiological “skin pressure-sweating reflex” might be associated with these mechanisms. This horizontal reflex is primarily due to inhibition of ipsilateral sweating by unilateral skin pressure, secondarily contralateral sweating increases. Microneurography indicates that this phenomenon occurs because unilateral skin pressure reduces the amplitude of ipsilateral sudomotor nerve activity and increases contralateral activity. Vertically, studies using the ventilated capsule method during heating, show that pressure on the bilateral skin of the back by supination decreases sweating on the upper body and increases sweating on the underbody. Central sudomotor sympathetic outflow (frequency of sweat expulsion) in response to body temperature is simultaneously hyperactivated, indicating that sweating is increased compensatorily to maintain a constant total sweating rate. In conclusion, segmental hyperhidrosis in segments other than those directly affected may be compensatory.
