Patel Shomeet V, Parish David C, Patel Rajendrakumar M, Grimsley Edwin W
Department of Internal Medicine, Mercer University School of Medicine, Macon, GA 31201, USA.
Am J Med Sci. 2007 Dec;334(6):490-2. doi: 10.1097/MAJ.0b013e318068b224.
We report a case of a 20-year-old African-American female, hospitalized and treated for hyperemesis gravidarum and hypokalemia with a normal serum sodium level. Two to 3 days into her hospitalization, she developed urinary incontinence, weakness, and pain in her lower extremities. An MRI brain scan showed central pontine signal alteration, leading to a diagnosis of CPM. A 4-month follow-up MRI brain scan showed complete resolution of the central pontine signal, with symptomatic improvement manifested by resolution of urinary incontinence and increased strength. Our case describes CPM occurring secondary to hypokalemia, with resolution of characteristic MRI findings at follow-up. Sole hypokalemia-induced CPM is very rare. What makes our patient even more unique is the complete resolution of the central pontine lesion on follow-up MRI. The cause of this cannot be completely explained and warrants further study.
我们报告一例20岁非裔美国女性病例，该患者因妊娠剧吐和低钾血症入院治疗，血清钠水平正常。住院2至3天后，她出现尿失禁、下肢无力和疼痛。脑部磁共振成像（MRI）扫描显示脑桥中央信号改变，从而诊断为渗透性脱髓鞘综合征（CPM）。4个月后的脑部MRI复查显示脑桥中央信号完全消失，尿失禁症状缓解、肌力增强，症状有所改善。我们的病例描述了低钾血症继发的CPM，随访时特征性MRI表现消失。单纯由低钾血症引起的CPM非常罕见。更让我们的患者独特的是，随访MRI显示脑桥中央病变完全消失。其原因尚不能完全解释，值得进一步研究。
