Autoimmune Limbic Encephalitis in the Setting of TNF-Inhibitor Use for Crohn’s Disease
Zainab Al Obaidi1, Toluwanimi Shaanu2, Ahmad Al-Awwad3, Nidhiben Anadani4
1University of Oklahoma Health Sciences Center, 2The Capitol, 3University of Oklahoma, 4University Of Oklahoma Health Science Center
Objective:
To describe a case of seronegative autoimmune limbic encephalitis secondary to adalimumab treatment, and to highlight the importance of initiating treatment early.
Background:
Autoimmune encephalitis secondary to Adalimumab exposure is fairly rare and very few cases have been reported in the medical literature.
Design/Methods:
Case report and review of literature.
Results:
43 years old woman with Crohn’s disease, been receiving adalimumab for 4 months prior to admission, admitted for acute onset encephalopathy and delirium including rapid behavior change, confusion, abnormal dystonic movements, catatonia, and visual hallucinations. Notably, there was no preceding infection, vaccination, fever, or headache.
Extensive diagnostic workup, including brain imaging, cerebrospinal fluid analysis, autoantibody screening, and viral panels, all were unremarkable. Given high clinical suspicion of limbic encephalitis possibly due to adalimumab, she was started on five days of intravenous steroid followed by 5 sessions of plasma exchange therapy with excellent response. After 19 days of hospitalization, she was discharged home with a steroid tapering regimen. At four-weeks follow-up appointment, she reported a return to her baseline condition, with a score of 28/30 on the Montreal Cognitive Assessment test and no neurological deficits on examination.
Conclusions:
Seronegative limbic encephalitis, particularly in the context of TNF inhibitor use, represents a challenging diagnostic scenario, due to limited case reports and difficulties in detecting autoantibodies, especially in the early phases of the disease. Nevertheless, this case highlights the crucial significance of maintaining a vigilant stance toward autoimmune encephalitis, even in the absence of detectable autoantibodies. Timely diagnosis and the immediate initiation of immunotherapy hold the potential to arrest the underlying immunological processes, thereby preventing irreversible brain damage.