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Background Delayed hypoxic leukoencephalopathy (DHL) is a rare demyelinating syndrome characterized by acute neurological deterioration following an initial recovery from a hypoxic insult. Presentation can vary but usually includes cognitive decline, akinetic mutism or parkinsonism. Gradual recovery occurs but neurological deficits usually persist.Case A 52-year-old man with schizoaffective disorder and a history of polysubstance misuse was found unresponsive with pinpoint pupils and vomitus, having last been seen well two days prior. He was hypoxic but normotensive. Urine drug screening was positive for amphetamines, benzodiazepines, methadone, and opiates. A diagnosis was made of acute respiratory failure with multiorgan dysfunction secondary to polypharmacy overdose. He was intubated and managed in the Intensive Care Unit. He was extubated 5 days later and was alert, orientated and mobile. He was transferred to the mental health unit as he remained thought disordered. Two weeks later, there was deterioration in his cognitive function, coupled with the development of akinetic mutism, severe rigidity and tremor. Serum and CSF infectious, metabolic, autoimmune and paraneoplastic panels were unremarkable, and EEG was normal. MRI brain demonstrated diffuse subcortical white matter hyperintensities on T2 based sequences, consistent with DHL. The patient was transferred back to the medical ward for supportive care and later inpatient rehabilitation. Over four months, he showed gradual neurological improvement and was discharged home with NDIS support.Conclusion This case highlights the biphasic nature of DHL and the importance of recognizing delayed neurological deterioration after hypoxic injury. Early identification, supportive care, and rehabilitation can facilitate functional recovery.