DELAYED DECLINE: A CASE OF DELAYED POST-HYPOXIC LEUKOENCEPHALOPATHY

ABSTRACT

CASE A 44 year old female with history of depression and recent suicide attempt presents with one week of cognitive and functional decline. One month prior to presentation, patient attempted suicide with opioids requiring intubation for respiratory depression and stroke sequelae. She was discharged from this stay after 12 days having returned to mental and functional baseline. Two weeks later, she demonstrated decreased focus and concentration, progressing to decreased mobility and akinesis, eventually presenting to our hospital. Admission metabolic and toxic workup was negative. CT head redemonstrated findings of previously known stroke. MRI demonstrated new increased T2 Flair of the parietal lobes and the cerebral white matter. LP was without evidence of infection or inflammation. Encephalitis panel and autoimmune workup were negative. Neurology consult suggested delayed post-hypoxic leukoencephalopathy as a possible diagnosis, given clinical course of improvement and subsequent decline, along with akinetic mutism and deep cortical white matter flair abnormalities. After failed trial of lorazepam, she was started on amantadine and her cognitive and functional status improved slowly. IMPACT/DISCUSSION: Delayed post-hypoxic leukoencephalopathy (DPHL) is a rare syndrome characterized by biphasic time course with initial recovery and subsequent cognitive and functional decline. DPHL can follow any event of prolonged cerebral hypoxia most frequently CO poisoning. It can occur with more common causes of hypoxia including overdose, cardiac arrest, and seizures;recent case reports have reported DPHL following severe covid infection. The clinical course involves a hypoxic event followed by a return to functional baseline typically lasting 7-21 days, after which progressive physical and mental decline occur. Signs include neuropsychiatric symptoms like amnesia and disorientation, as well as parkinsonism or akinetic mutism (1). The mechanism of DPHL is unclear. One possible mechanisms involves diffuse demyelination. The half life of myelin basic proteins is approximately 20 days, the length of the lucid interval. Hypoxia may abruptly halt the myelination process but symptoms may not emerge until a critical threshold of loss was achieved. Evaluation of DPHL involves considering other causes of encephalopathy, such as infection, substance use, stroke, catatonia, and toxins. In the absence of other causes, diagnosis of DPHL is based on characteristic time course following hypoxic event, symptoms, and MRI findings of diffuse T2 hyperintensity of cerebral white matter are pathognomonic (1). Treatment of DPHL is generally supportive. Limited evidence suggests amantadine may be of benefit. CONCLUSION: Physicians should consider DPHL in patients who have experienced cerebral hypoxia and present with the characteristic time course and imaging findings.