To describe the clinical and radiological findings of Cerebellar, hippocampal, and basal nuclei transient edema with restricted diffusion (CHANTER) syndrome in a female presenting with pulseless electrical activity after a potential opioid overdose.

CHANTER syndrome is a recently described complication of substance abuse, especially opioids, characterized by cytotoxic edema to bilateral hippocampi, basal ganglia and cerebellar cortices. Neuroradiology is distinct from anoxic brain injury as cerebral cortex, thalamus, and subcortical white matter are not involved.

64-year-old African American female with a past medical history of hypertension and depression (on prescribed diazepam), presented after a witnessed cardiac arrest at home with return of spontaneous circulation (ROSC) in the hospital. Pt was intubated on arrival and her initial CT head was unremarkable. Her pocket had multiple opioid pills and urine drug screen was also positive for opiates and benzodiazepines. MRI brain revealed areas of diffusion signal abnormality with corresponding T2 FLAIR hyperintensity in the bilateral cerebellar white matter, the bilateral basal ganglia, and bilateral hippocampi with some patchy involvement of the bilateral (left more than right) occipital lobes suggestive of CHANTER syndrome, as described in limited literature. The electroencephalogram revealed slow background activity but no seizures. A repeat MRI brain on day 8 showed diminished, but unresolved, diffusion restriction involving the supratentorial and infratentorial brain in a symmetric pattern relating to evolution of cytotoxic edema with corresponding improvement of her neurological status.

CHANTER syndrome’s prognosis depends on early identification and supportive treatment as patients can quickly progress to hydrocephalus. It may be difficult but imperative to differentiate CHANTER syndrome from anoxic brain injury. Further research is needed to identify optimal management strategies for this threatening neurotoxic phenomenon.