B S Kim1, Y I Kim, K S Lee. 1. Department of Neurology, Catholic University Medical College, Seoul, Korea.
Abstract
BACKGROUND: Excessive sweating from cerebral infarction has been reported rarely in the available stroke literature, and its pathophysiological mechanisms and clinical significance have remained obscure. In addition, there have been no reports that medullary infarction results in only contralateral hemihyperhidrosis without ipsilateral Horner's syndrome. In the hope of increasing recognition of this phenomenon, we describe five patients with hyperhidrosis, including two patients with medullary infarction, and discuss the clinicoanatomic correlations. CASE DESCRIPTIONS: Contralateral hyperhidrosis occurred in two patients with large strokes involving both superficial cortical and deep subcortical structures of the middle cerebral artery territory and in two patients with medullary infarctions. Bilateral hyperhidrosis of the face was noted in one patient with basilar artery thrombosis and bilateral cerebellar and pontine infarctions. The hyperhidrosis typically involved the face and arm and was transient, lasting from 2 days to 2 months. No associated Horner's syndrome, hypothalamic dysfunction, or other autonomic dysfunction was observed. CONCLUSIONS: The phenomenon of hyperhidrosis might be attributed to a lesion of a putative sympathoinhibitory pathway that controls sweating. This pathway might originate in the cortex, possibly in the operculum, and make terminal connections with the contralateral thoracic spinal cord. Our observations suggest that the fibers of this putative pathway may be very close to the corticospinal tract.
BACKGROUND: Excessive sweating from cerebral infarction has been reported rarely in the available stroke literature, and its pathophysiological mechanisms and clinical significance have remained obscure. In addition, there have been no reports that medullary infarction results in only contralateral hemihyperhidrosis without ipsilateral Horner's syndrome. In the hope of increasing recognition of this phenomenon, we describe five patients with hyperhidrosis, including two patients with medullary infarction, and discuss the clinicoanatomic correlations. CASE DESCRIPTIONS: Contralateral hyperhidrosis occurred in two patients with large strokes involving both superficial cortical and deep subcortical structures of the middle cerebral artery territory and in two patients with medullary infarctions. Bilateral hyperhidrosis of the face was noted in one patient with basilar artery thrombosis and bilateral cerebellar and pontine infarctions. The hyperhidrosis typically involved the face and arm and was transient, lasting from 2 days to 2 months. No associated Horner's syndrome, hypothalamic dysfunction, or other autonomic dysfunction was observed. CONCLUSIONS: The phenomenon of hyperhidrosis might be attributed to a lesion of a putative sympathoinhibitory pathway that controls sweating. This pathway might originate in the cortex, possibly in the operculum, and make terminal connections with the contralateral thoracic spinal cord. Our observations suggest that the fibers of this putative pathway may be very close to the corticospinal tract.