doi: 10.3174/ajnr.A0655
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American Journal of Neuroradiology 28:1652-1658, October 2007
© 2007 American Society of Neuroradiology
BRAIN
MR Imaging of Metronidazole-Induced Encephalopathy: Lesion Distribution and Diffusion-Weighted Imaging Findings
a Department of Radiology and Institute of Radiation Medicine, Seoul National University College of Medicine, Seoul, Korea
b Department of Radiology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
c Department of Radiology, Research Institute of Radiologic Science, Yonsei University College of Medicine, Seoul, Korea
d Department of Radiology, Seoul Metropolitan Boramae Hospital, Seoul, Korea
Please address correspondence to Dong Gyu Na, MD, Department of Radiology and Institute of Radiation Medicine, 28 Yongon-dong, Chongno-gu, Seoul, 110-744, Korea; e-mail: dgna{at}radiol.snu.ac.kr
BACKGROUND AND PURPOSE: MR imaging features of metronidazole-induced encephalopathy (MIE) have not been fully established. This study was undertaken to determine the topographic distributions and diffusion-weighted imaging (DWI) findings of MIE.
MATERIALS AND METHODS: We retrospectively evaluated the initial MR images (n = 7), including DWI (n = 5), and follow-up MR images (n = 4) after drug discontinuation in 7 patents with clinically diagnosed MIE. The topographic distributions of lesions were evaluated on MR images, and DWI signal intensities and apparent diffusion coefficient (ADC) values of the lesions were assessed.
RESULTS: MR images demonstrated bilateral symmetric T2 hyperintense lesions in the cerebellar dentate nucleus (n = 7), midbrain (n = 7), dorsal pons (n = 6), medulla (n = 4), corpus callosum (n = 4), and cerebral white matter (n = 1). Brain stem lesions involved the following: tectum (n = 5), tegmentum (n = 4), red nucleus (n = 3) of the midbrain, vestibular nucleus (n = 6), and a focal tegmental lesion involving the superior olivary nucleus (n = 6) and abducens nucleus (n = 4) of the pons and vestibular nucleus (n = 4) and inferior olivary nucleus (n = 1) of the medulla. DWI (n = 5) showed isointensity or hyperintensity of lesions, and the decreased ADC value was found only in the corpus callosum lesions (n = 2). All detected lesions were completely reversible at follow-up except for the single corpus callosum lesion with an initial low ADC value.
CONCLUSION: Brain lesions were typically located at the cerebellar dentate nucleus, midbrain, dorsal pons, medulla, and splenium of the corpus callosum. According to DWI, most of the lesions in MIE probably corresponded to areas of vasogenic edema, whereas only some of them, located in the corpus callosum, corresponded to cytotoxic edema.
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