To describe variable CNS presentations related to TNF inhibiters exposure. 

TNF-α, a cytokine binds to TNF receptors 1 and 2 (TNFR1, TNFR2). TNFR1 triggers inflammation via its death domain, while TNFR2 maintains immune tolerance, aiding remyelination and oligodendrocyte regeneration. Inhibiting TNF can upset T cell balance, allowing autoreactive T cells to evade surveillance, potentially triggering autoimmune nervous system disorders via humoral immunity stimulation.

 43 years old woman with Crohn’s disease, been receiving adalimumab for 4 months prior to admission, admitted for acute onset encephalopathy, rapid behavior change and abnormal dystonic movements.

Extensive diagnostic workup with brain imaging, EEG, CSF analysis, autoantibody screening, were unremarkable. normal CT chest and abdomen and pelvis . Given high clinical suspicion of adalimumab induced limbic encephalitis, she was started on 5 days of IV steroid followed by 5 sessions of plasma exchange with remarkable response. At 4 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.

61 YO woman with rheumatoid arthritis on Adalimumab since 2017. Admitted for vertigo and tinnitus. Brain MRI showed multiple T2 hyperintensities in subcortical white matter with one area of right parietal lobe enhancement, normal CTA head and neck. Adalimumab switched to Tofacitinib. No residual symptoms, stable brain MRI lesions 3 years, no cord enhancement MRI spine

37yo women with psoriatic arthritis admitted for new onset focal to bilateral GTC seizure one month following adalimumab initiation. Brain MRI demonstrated PRES. Discontinuation of adalimumab and blood pressure management led to resolution of symptoms with normal MRI findings 3m after discharge.