Loh Yince, Watson William D, Verma Ajay, Krapiva Pavel
Department of Neurology, Walter Reed Army Medical Center, 6900 Georgia Ave NW, Washington, DC 20307, USA.
J Neuroimaging. 2005 Oct;15(4):373-5. doi: 10.1177/1051228405279037.
Acute Wernicke's encephalopathy (WE) is caused by profound vitamin B1 (thiamine) deficiency and commonly presents with the classic clinical triad of mental confusion, ataxia, and ophthalmoplegia. This characteristic presentation results from the propensity of acute thiamine deficiency to preferentially injure specific brain regions: the dorsomedial thalamus, periaqueductal gray, and mamillary bodies. In these regions, abnormal magnetic resonance signaling on conventional sequences has been well described; however, diffusion restriction has only recently been reported. The authors demonstrate diffusion-weighted imaging (DWI) abnormalities of the splenium of the corpus callosum in a patient with acute WE, which has not been reported previously, and suggest a potential pathological mechanism. With the recent addition of DWI, MRI is becoming more sensitive to the changes in acute WE. Furthermore, the use of apparent diffusion coefficient mapping to evaluate the extent of likely underlying cytotoxic injury may help determine long-term response to vitamin therapy and, thus, disability.
急性韦尼克脑病（WE）由严重的维生素B1（硫胺素）缺乏引起，通常表现为精神错乱、共济失调和眼肌麻痹这一经典临床三联征。这种特征性表现源于急性硫胺素缺乏倾向于优先损伤特定脑区：丘脑背内侧核、导水管周围灰质和乳头体。在这些区域，传统序列上的异常磁共振信号已得到充分描述；然而，扩散受限直到最近才被报道。作者展示了1例急性WE患者胼胝体压部的扩散加权成像（DWI）异常，这在之前未曾报道过，并提出了一种潜在的病理机制。随着最近DWI的加入，MRI对急性WE的变化变得更加敏感。此外，使用表观扩散系数图来评估可能存在的潜在细胞毒性损伤程度，可能有助于确定对维生素治疗的长期反应，进而确定残疾情况。
