Mon Y, Mizotani M
Department of Neurology, Kyoto Min-Iren Central Hospital.
Rinsho Shinkeigaku. 1992 Jul;32(7):718-21.
A case of hemihyperhidrosis and non-paralytic pontine exotropia due to brainstem infarction is reported. A 55-year-old hypertensive man developed right hemiparesis with slight dysarthria and nausea upon awaking. The right side of his face and right upper limb and trunk to the level of the Th8-9 territory showed hyperhidrosis, which disappeared in a week. Ocular motor examination revealed that during forward gaze with the left eye fixing, the right eye deviated outward. The patient was able to adduct the right eye to midposition with the right eye fixing. Rightward gaze elicited full abduction and right-beating nystagmus of the right eye, but the left eye did not adduct. When he attempted to gaze leftward, both eyes made the full excursion, but saccades were slow in that direction. Convergence was intact. Vertical gaze was full, and he did not show Horner's sign. This ocular sign, non-paralytic pontine exotropia, disappeared three days later. T2-weighted spin echo magnetic resonance imaging disclosed a small lesion with high intensity in the inner side of the left middle pons. This hyperhidrosis was thought to be caused by destruction of inhibitory fibers thermoregulating sweating. These findings suggest that at the level of the middle pons inhibitory fibers descend along the inner side of facilitatory fibers thermoregulating sweating, which are speculated to descend the dorso-lateral part of the pontine tegmentum. These findings also suggest that lesions of non-paralytic pontine exotropia may be located in the paramedian pontine reticular formation rostral to the abducens nucleus with ipsilateral medial longitudinal fasciculus lesion, but further investigation is necessary.
报告了一例因脑干梗死导致偏侧多汗症和非麻痹性脑桥外斜视的病例。一名55岁的高血压男性在醒来时出现右侧偏瘫,伴有轻微构音障碍和恶心。其右侧面部、右上肢体以及T8 - 9水平以上的躯干出现多汗症,一周后消失。眼动检查发现,当左眼注视前方时,右眼向外偏斜。当右眼注视时,患者能够将右眼内收至中间位置。向右注视时,右眼出现完全外展和右眼向右跳动性眼球震颤,但左眼不能内收。当他试图向左注视时,双眼能完全移动,但该方向的扫视缓慢。集合功能正常。垂直注视正常,且未出现霍纳氏征。这种眼征,即非麻痹性脑桥外斜视,三天后消失。T2加权自旋回波磁共振成像显示左中脑桥内侧有一个高强度小病灶。这种多汗症被认为是由调节出汗的抑制性纤维受损所致。这些发现表明,在脑桥中部水平,抑制性纤维沿着调节出汗的兴奋性纤维内侧下行,推测兴奋性纤维沿脑桥被盖背外侧部下行。这些发现还表明,非麻痹性脑桥外斜视的病灶可能位于展神经核嘴侧的脑桥旁正中网状结构,并伴有同侧内侧纵束损伤,但还需要进一步研究。