TBI
Gabrielle N. Avancena, MD
Resident Physician
NYU Grossman School of Medicine
Long Island City, New York, United States
Jing Lin, MD
Attending Physician
NYU Grossman School of Medicine
New York, New York, United States
Cherie Chen, DO
Resident Physician
NYU Grossman School of Medicine
New York, New York, United States
Gabrielle N. Avancena, MD
NYU Grossman School of Medicine
Long Island City, New York, United States
Delayed Toxic/hypoxic leukoencephalopathy
Case Description: A 43-year-old male was initially admitted into acute care after being found unresponsive in Colombia after a suspected unintentional zolpidem overdose. Patient was treated for aspiration pneumonia, but never returned to his neurocognitive baseline. MRI revealed extensive confluent areas of periventricular T2/FLAIR intensity consistent with delayed hypoxic/toxic leukoencephalopathy. Patient then developed catatonic symptoms, including mutism, Gegenhalten, and motor restlessness, which failed to improve with lorazepam trial but improved with amantadine. Sinemet was later added, given potential underlying Parkinsonian symptoms. On discharge from acute rehab, the patient showed significant gains in verbal and motor initiation, command following, and spontaneous movements, progressing from maximal assistance for functional mobility to contact guard/supervision assistance for ADLs and iADLs.
Discussions: Diffuse posthypoxic/toxic leukoencephalopathy (DPHL) is a rare demyelinating condition that can manifest with a myriad of neuropsychiatric symptoms days to weeks after an apparent recovery from a prolonged period of global cerebral hypoxia. It can manifest with a constellation of symptoms, including impaired cognition, emotional lability, poor motor control, decreased responsiveness, and catatonia. Lorazepam is generally the first-line treatment for catatonic symptoms. In patients who do not respond to benzodiazepine trials, it is important to consider trials of dopaminergic agents like Amantadine and Sinemet. Results in functional improvement may suggest catatonia with underlying Parkinsonism and akinetic mutism as a result of the brain injury.
Conclusions: Catatonia as a presentation of DPHL can often be misinterpreted. Given the nature of brain injury, the patient’s clinical presentation may be complicated by Parkinsonism, which oftentimes can be difficult to distinguish given the substantial clinical overlap. Both can present with motor inactivity, rigidity, and decreased responsiveness. Dopaminergic agents should be considered if a patient does not respond to a trial of benzodiazepine to improve verbal planning, attention, and functional mobility.
