Terasaki Tadashi, Hashimoto Yoichiro, Miyashita Fumio, Kozaki Yanosuke, Naganuma Masaki, Uchino Makoto, Mabe Hiroyo
Department of Neurology and Strokology, Kumamoto City Hospital.
Rinsho Shinkeigaku. 2002 Feb;42(2):145-8.
A 21 year-old female college student with a history of Turner syndrome at age 9, and 6-year growth hormone replacement therapy noticed weakness of right extremities when she got up on March 26, 2001. On admission, she showed right hemiparesis (4+/5) and hypesthesia on the right of body. The hemiparesis progressed (3-/5) in spite of antithrombotic therapy. Brain MRI revealed a high intensity lesion with a diameter of 1.5 cm in the posterior limb of the left internal capsule and putamen on DWI and T2WI. MR angiography and TC-CFI revealed no stenosis in her left middle cerebral artery, but > 50% stenosis in the horizontal portion (M1) of her right middle cerebral artery. Branch lesions were presumed to exist in the left M1. Non-atherosclerotic angiopathy, coagulopathy, and other conventional risk factors of brain infarction were not found. Pathogenesis of Turner syndrome might have played a role in the development of brain infarction in this patient.
一名21岁的女大学生，9岁时被诊断为特纳综合征，接受了6年的生长激素替代治疗。2001年3月26日起床时，她发现右肢无力。入院时，她表现为右侧偏瘫（4+/5），身体右侧感觉减退。尽管进行了抗血栓治疗，偏瘫仍有进展（3-/5）。脑部MRI显示，在弥散加权成像（DWI）和T2加权成像（T2WI）上，左侧内囊后肢和壳核有一个直径1.5厘米的高强度病变。磁共振血管造影（MRA）和经颅彩色多普勒血流成像（TC-CFI）显示，她的左侧大脑中动脉无狭窄，但右侧大脑中动脉水平段（M1）狭窄超过50%。推测左侧M1存在分支病变。未发现非动脉粥样硬化性血管病、凝血障碍和其他脑梗死的传统危险因素。特纳综合征的发病机制可能在该患者脑梗死的发生中起了作用。
