1005 - Managing Catatonia in Anti-NMDAR Encephalitis Rehabilitation

Thursday, February 19, 2026

5:00 PM - 6:30 PM AST

Presenting Author(s)

RE

Rosalie Ellis, DO

Resident
MossRehab
Philadelphia, Pennsylvania, United States

Co-Author(s)

CB

Chase Bauer, DO

resident
Jefferson Moss Magee
Philadelphia, Pennsylvania, United States
MS

Miriam Segal, MD

Program Director
Jefferson Moss Magee Rehabilitation Hospital
Elkins Park, Pennsylvania, United States

Submitter(s)

RE

Rosalie Ellis, DO

MossRehab
Philadelphia, Pennsylvania, United States

Case Diagnosis: Anti-NMDAR Encephalitis

Case Description: A 24-year-old female with no significant past medical history developed new onset auditory and visual hallucinations and dystonia. Soon after acute hospital admission, she developed seizure-like activity and became obtunded requiring intubation. A lumbar puncture confirmed a diagnosis of anti-NMDAR encephalitis. Following a negative malignancy work up, and treatment with plasmapheresis, rituximab, and tocilizumab, the patient was transferred to an acute inpatient rehabilitation hospital. Her rehabilitation was limited due to catatonia, which slowly improved with benzodiazepines. She was also trialed on adjunctive treatments, with significant cognitive improvement noted on amantadine. Memantine was not as effective, nor was methylphenidate. Recovery was delayed due to rebounding of catatonia after missed medication doses during a facility transfer, and again after too rapidly tapering benzodiazepines. After two months of acute inpatient rehabilitation, the patient was discharged home.

Discussions: Anti-NMDAR encephalitis, the most common cause of nonviral encephalitis, is an autoimmune mediated disease. Left untreated, it can progress from simple memory impairments to movement abnormalities, autonomic dysregulation, seizure, and even death with mortality rates as high as 4%. Treatment should be tailored to manage the clinical presentation, which included catatonia in this patient. Benzodiazepines are a cornerstone of catatonia treatment, due to their rapid onset and ability to target the underlying GABAeric dysfunction. Amantadine and memantine are other treatments for catatonia that are aimed at improving cognitive function. Methylphenidate, while being able to improve arousal and cognition in the general population and other acquired brain injuries, has not been shown to improve symptoms associated with catatonia.

Conclusions: Anti-NMDAR encephalitis can be complicated with catatonia, limiting rehabilitation potential. Treatment with benzodiazepines and other medications are effective, so long as they are routinely given with a slow taper.