MR Imaging of Metronidazole-Induced Encephalopathy: Lesion Distribution and Diffusion-Weighted Imaging Findings

E Kim,D.G Na,J.H Kim,K.R Son,K.H Chang,E.Y Kim

doi:10.3174/ajnr.a0655

Abstract

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. 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. 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. 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.

Highlights

AND PURPOSE: MR imaging features of metronidazole-induced encephalopathy (MIE) have not been fully established
Brain lesions were typically located at the cerebellar dentate nucleus, midbrain, dorsal pons, medulla, and splenium of the corpus callosum
According to diffusion-weighted imaging (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

Summary

Methods

We retrospectively evaluated the initial MR images (n ϭ 7), including DWI (n ϭ 5), and follow-up MR images (n ϭ 4) after drug discontinuation in 7 patents with clinically diagnosed MIE. Patients This study included 7 patients in whom the final clinical diagnosis was MIE, during a period of 4 years. Final clinical diagnoses of MIE were determined on the basis of probable adverse drug reactions to conventional categories of adverse drug reactions.[17] All patients had been administered metronidazole therapy for several weeks before their neurologic signs and symptoms were developed. When MIE was clinically suspected, metronidazole medication was stopped in all patients. Medical records were reviewed to assess clinical parameters, such as total metronidazole dose, duration of administration, duration of symptom onset after administration, neurologic symptoms and signs, and duration of recovery after discontinuation

Results

Discussion

Conclusion