Cortical and basal ganglia diffusion restriction following benzodiazepine overdose: An unusual MRI pattern of evolving hypoxic–ischemic encephalopathy

Hypoxic-ischemic encephalopathy (HIE) is a severe neurological consequence of global cerebral hypoxia. Drug intoxication may cause profound central nervous system depression and severe hypoxemia, potentially resulting in hypoxic-ischemic brain injury. We report an unusual MRI pattern of evolving HIE in the setting of benzodiazepine intoxication and severe hypoxemia. A 29-year-old man with a history of substance abuse was admitted with profound impairment of consciousness following reported diazepam and haloperidol ingestion. His Glasgow Coma Scale score was 5/15 and oxygen saturation was 70% on room air, requiring immediate intubation and mechanical ventilation. Toxicological screening identified diazepam, while quantitative serum concentration was unavailable. Initial CT showed mild diffuse cerebral edema and minimal subarachnoid hemorrhage. On day 10, follow-up CT and MRI demonstrated diffuse, symmetrical cortical and bilateral basal ganglia abnormalities involving the caudate nuclei, putamina, and globi pallidi. These regions showed DWI hyperintensity with corresponding low ADC signal, together with T2/FLAIR hyperintensity and subtle cortical and basal ganglia enhancement. The findings were consistent with evolving hypoxic-ischemic brain injury in the subacute phase. The patient subsequently recovered consciousness, with a documented GCS score of 15/15. This case highlights an uncommon pattern of diffuse cortical and bilateral basal ganglia involvement in the setting of benzodiazepine intoxication and severe hypoxemia. The imaging pattern is not specific to benzodiazepine toxicity and should be interpreted in conjunction with the clinical context, toxicological findings, and timing of MRI.