Reversible Inferior Colliculus Lesion in Metronidazole-Induced Encephalopathy

Abstract

Reversible inferior colliculus lesions could be considered as the characteristic for metronidazole-induced encephalopathy, next to the dentate nucleus involvement.

Sequential MR imaging (with diffusion-weighted imaging) changes in metronidazole-induced encephalopathy

“…They suggested axonal swelling with increased water content due to toxic injury or localized reversible ischemia due to vascular spasm as possible mechanism. A few subsequent case reports[234] have described symmetric lesions at additional sites as in colliculus, superior olive, and cochlear nuclei, indicating their reversibility. Other theories for signal changes including interstitial edema and ischemia as cause of signal intensity on diffusion-weighted imaging or cell damage to Purkinje cells due to binding of the drug to neuronal RNA, causing inhibition of protein synthesis, and axonal degeneration have also been postulated.…”

“…Other theories for signal changes including interstitial edema and ischemia as cause of signal intensity on diffusion-weighted imaging or cell damage to Purkinje cells due to binding of the drug to neuronal RNA, causing inhibition of protein synthesis, and axonal degeneration have also been postulated. [234]…”

Atypical Metronidazole-Induced Encephalopathy in Anaerobic Brain Abscess

“…Metronidazole attains 60-100% of plasma concentrations in most tissues, including the central nervous system13), so it is a drug of choice for the treatment of anaerobic brain abscess. The side effects include peripheral neuropathy, convulsive seizures, encephalopathy, ataxic gait, and dysarthria1,11,14-16). Among the side effects, MIE has been very rarely reported1,2,8,11,14-16).…”

“…The side effects include peripheral neuropathy, convulsive seizures, encephalopathy, ataxic gait, and dysarthria1,11,14-16). Among the side effects, MIE has been very rarely reported1,2,8,11,14-16). The mechanisms that underlie metronidazole's neuronal toxicity include the oxidation of catecholamine neurotransmitters (such as norepinephrine, dopamine, and related catecholamine derivatives) to form semiquinone radicals and nitro anion radicals, which reduce tissue oxygen and generate the superoxide radical and hydrogen peroxide in a reaction with 5-nitroimidazole derivatives, such as metronidazole15).…”

“…Typical findings include progressive clinical deterioration such as dysarthria, gait disturbance, sensory changes in the extremities, confusion, nausea, vomiting, and dysmetria with multiple signal changes in cerebellar dentate nuclei, corpus callosum, midbrain, and cerebral white matter1,2,8,11,12,14,16). The conditions tend to be reversed when drug use is stopped1,2,8,11,12,14,16). All the lesions associated with MIE have been reported as symmetric and this symmetric nature has been regarded as a key point of MIE.…”