Metronidazole induced encephalopathy
General description
Metronidazole is an antibiotic commonly used to treat anaerobic bacterial infections, liver abscesses, trichomoniasis, amoebic dysentery, pseudomembranous colitis, and to eradicate Helicobacter pylori. Initially developed as an antiprotozoal medication, it is now widely available in both oral and intravenous forms. Metronidazole is metabolized 30-60% by the liver, and in patients with impaired liver function, the drug's half-life is prolonged, increasing the risk of encephalopathy.
A key concern with metronidazole is its neurotoxicity, particularly when daily doses exceed 2g, which can lead to neurological symptoms such as peripheral neuropathy, cerebellar symptoms, and encephalopathy. These symptoms may include dysarthria, gait disturbances, limb muscle weakness, and altered consciousness, potentially progressing to coma. The drug readily crosses the blood-brain barrier, accumulating in the central nervous system and leading to side effects such as taste disturbances and limb sensory impairment.
In most cases, stopping metronidazole results in a full recovery from neurotoxic effects, underscoring the importance of dosage monitoring, especially in patients with liver dysfunction.
Radiographic features
MRI shows T2WI and FLAIR hyperintensity in the dentate nuclei in most cases, followed by the midbrain tectum, pons-medullary tegmentum, red nuclei, periaqueductal gray matter, and splenium of the corpus callosum. Typically, no contrast enhancement is observed.
T2WI and FLAIR hyperintensity
-
Dentate nucleus
-
BrainstemMidbrainRed nucleus
-
BrainstemMidbrainMidbrain tegmentumPeriaqueductal gray matter
-
BrainstemPonsPontine tegmentum
-
BrainstemMedullaMedulla tegmentum
-
Corpus callosumSplenium
Delete lesion
Do you really want to delete lesion T2WI and FLAIR hyperintensity?