An Jae Young, Park Sung Kyung, Han Si Ryung, Song In Uk
Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Intern Med. 2010;49(6):615-8. doi: 10.2169/internalmedicine.49.3069. Epub 2010 Mar 15.
Central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM) are osmotic demyelination syndrome. A 45-year-old man with a history of alcoholism visited the ER with dysarthria and dysphagia for 2 days. These symptoms occurred 3 days after he had stopped drinking alcohol. The neurological symptoms progressed to anarthria, pseudobulbar palsy and gait disturbance. During admission, the electrolyte studies were within the normal range. Diffusion-weighted images revealed high signal intensities in the pons, thalamus and basal ganglia. Apparent diffusion coefficient image showed low signal intensities in the pontine lesion, but isosignal intensities in the extrapontine lesion. The symptoms gradually improved after 1 month with only conservative treatment. The 1 month-follow-up MRI showed significant reduction of the previous extrapontine lesions. These findings suggest that cytotoxic edema is central to the pathogenesis of CPM, but vasogenic edema plays an important role in the pathogenesis of EPM occurring during alcohol withdrawal.
中央桥脑髓鞘溶解症(CPM)和脑桥外髓鞘溶解症(EPM)是渗透性脱髓鞘综合征。一名有酗酒史的45岁男性因构音障碍和吞咽困难2天就诊于急诊室。这些症状在他戒酒3天后出现。神经症状进展为失音、假性球麻痹和步态障碍。入院期间,电解质检查在正常范围内。弥散加权成像显示脑桥、丘脑和基底节区高信号强度。表观扩散系数图像显示脑桥病变处低信号强度,但脑桥外病变处等信号强度。仅经过保守治疗,1个月后症状逐渐改善。1个月后的随访磁共振成像显示先前脑桥外病变明显减轻。这些发现表明,细胞毒性水肿是CPM发病机制的核心,但血管源性水肿在戒酒期间发生的EPM发病机制中起重要作用。