Kim B S, Kim Y I, Lee K S
Department of Neurology, Catholic University Medical College, Seoul, Korea.
Stroke. 1995 May;26(5):896-9. doi: 10.1161/01.str.26.5.896.
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.
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.
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.
在现有的卒中文献中，关于脑梗死导致多汗的报道很少，其病理生理机制和临床意义仍不明确。此外，尚无髓质梗死仅导致对侧偏身多汗而无同侧霍纳综合征的报道。为提高对这一现象的认识，我们描述了5例多汗患者，其中包括2例髓质梗死患者，并讨论临床与解剖的相关性。
2例累及大脑中动脉区域浅表皮质和深部皮质下结构的大面积卒中患者以及2例髓质梗死患者出现对侧多汗。1例基底动脉血栓形成伴双侧小脑和脑桥梗死的患者出现面部双侧多汗。多汗通常累及面部和手臂，且为一过性，持续2天至2个月。未观察到相关的霍纳综合征、下丘脑功能障碍或其他自主神经功能障碍。
多汗现象可能归因于控制出汗的假定交感抑制通路受损。该通路可能起源于皮质，可能在岛盖，并与对侧胸段脊髓形成终末连接。我们的观察结果表明，这条假定通路的纤维可能与皮质脊髓束非常接近。
