Department of Neurosurgery, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo, Japan.
Neurol Sci. 2011 Feb;32(1):165-8. doi: 10.1007/s10072-010-0417-z. Epub 2010 Oct 22.
Reversible posterior leukoencephalopathy syndrome (RPLS) is theoretically associated with hypertensive encephalopathy because the most patients demonstrate abrupt increasing of blood pressure (BP). A 59-year-old woman, who had undergone cholecystectomy 4 days before, complained of a headache and rapidly progressing visual disturbance. Her BP was postoperatively controlled at around 150/80, but her BP was 89/46 when she noticed her symptoms. Magnetic resonance imaging showed vasogenic edema in bilateral occipital and right parietal lobes, and intracranial magnetic resonance angiography revealed bilateral diffuse peripheral vasoconstriction. After discontinuing ropivacaine administration via epidural catheter, her BP rose to 114/62 and her symptoms completely disappeared within a few days. Except for hypotension, the clinical course and the radiological evidences in our case were consistent with RPLE. This case supports another hypothesis of RPLS mechanism that arterial endothelial injury by toxic drug effect results in transudation of fluid from blood vessels causing vasogenic brain edema.
可逆性后部白质脑病综合征（RPLS）理论上与高血压脑病有关，因为大多数患者表现为血压突然升高（BP）。一名 59 岁女性，在 4 天前行胆囊切除术，主诉头痛和视力迅速恶化。她的术后血压控制在 150/80mmHg 左右，但当她注意到症状时，血压为 89/46mmHg。磁共振成像显示双侧枕叶和右顶叶血管源性水肿，颅内磁共振血管造影显示双侧弥漫性周围血管收缩。停止经硬膜外导管给予罗哌卡因后，她的血压升至 114/62mmHg，数天内症状完全消失。除了低血压外，我们的病例的临床过程和影像学证据与 RPLE 一致。该病例支持 RPLS 机制的另一种假说，即毒性药物作用导致动脉内皮损伤，导致血管内液体渗出，引起血管源性脑水肿。
