Metronidazole-induced cytotoxic edema of corpus callosum: a case report

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LETTER TO THE EDITOR

Metronidazole‑induced cytotoxic edema of corpus callosum: a case report C. Ulukan1   · E. Ekizoglu1 · N. Yesilot1 · O. Coban1 Received: 23 May 2019 / Accepted: 30 January 2020 © Belgian Neurological Society 2020

Introduction Involvement of the corpus callosum secondary to various conditions leading to cytotoxic edema has been defined as “Cytotoxic lesions of the corpus callosum (CLOCCs)”. These lesions are mostly associated with encephalitis, chronic alcoholism, malignancy, trauma, subarachnoid hemorrhage, metabolic disorders, antiepileptic drug toxicity or withdrawal, infection and various other causes [1]. This distinctive clinicoradiological entity usually presents with altered consciousness and seizures but presentation with callosal disconnection syndrome has not been described. Clinical outcome is reported to be favorable in most patients with complete recovery, unless there is a severe underlying disorder. Although the pathophysiologic mechanism is not completely understood, release of cytokines is considered as the initiator of the cascade producing the cytotoxic lesions. Corpus callosum, particularly the splenium, is the typical brain region vulnerable to this cytokinopathy [1]. We present a metronidazole-induced CLOCCs case with poor prognosis, manifesting an extensive callosal lesion extending into the extracallosal (more lateral) white matter fibers.

Case report Fifty-seven-year-old male presented with severe vomiting, acute speech disturbance and ataxia. He had a generalized tonic–clonic seizure evolving to status epilepticus shortly after admission. Glasgow Coma Scale score was 7 and noninvasive mechanical ventilation was started. One week after discharge from the intensive care unit, he became disorientated and uncooperative. He had nonfluent speech, he could * C. Ulukan [email protected] 1



Department of Neurology, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey

only follow a few simple commands and repeat some single words. Despite lack of evident motor weakness, he was unable to sit without support. The patient was recently diagnosed with rectal adenocarcinoma, underwent colorectal surgery and lost hearing in the right ear following the operation 2 weeks before the acute neurological presentation. He was on metronidazole 1000 mg/day, a total dose of 60 g over 2 months, for diarrhea attacks following colorectal surgery. Contrast-enhanced brain MR imaging (MRI) performed to investigate acute hearing loss was unremarkable. Blood count and serum biochemistry results were normal. Brain MRI revealed a lesion involving the whole splenium of the corpus callosum and the adjacent deep cerebral white matter on the left hemisphere. The lesion was slightly hyperintense on FLAIR sequences with a prominent diffusion restriction and low signal on the ADC map, suggesting cytotoxic edema (Fig. 1a, b). Of note, the dentate nuclei had hyperintense signal abnormalities bilaterally (Fig. 1c). Cerebrospinal fluid (CSF) was acellular (without any malignant cells); prote