TNF blockers have revolutionized the management of immune-mediated inflammatory diseases. Despite their relatively safe profile, an increasing number of reported neurological adverse events suggest a role for TNF inhibitors in the induction of central and peripheral nervous system demyelination.
We report a 21 year-old Qatari gentleman who was on adalimumab for HLA-B27 negative peripheral spondyloarthritis. After being maintained on adalimumab for 2 years, he presented acutely with headache, urinary incontinence and bilateral lower limb numbness that progressed to mid-trunk over 2 days. The neurological examination revealed dysesthesias of lower extremities and trunk up to T4 dermatomes with brisk tendon reflexes. His muscle power and cranial nerves examination were normal. 
A diagnosis of multiple sclerosis has been suggested by the typical findings of classical multiple hyper-intense enhancing lesions (figure 1). Our patient has no family history for such diagnosis. 
Discontinuation of Adalimumab resulted in complete resolution of the neurological symptoms within a month. However, he then developed abdominal pain with loose bloody motions for which Ilio-colonoscopy and biopsy confirmed the diagnosis of Crohn´s disease. We think that his GI symptoms were unmasked by the discontinuation of his Adalimumab. Interestingly we found that he has a strong family history of inflammatory bowel disease. 
This case illustrates the importance of being vigilant for neurological side effects of anti-TNFa blockers with early discontinuation of the TNF-a blockers and urgent MRI scan. Long term follow up is mandated in such cases to trace relapse rate and clinical outcome.

Adalimumab-induced multiple sclerosis in a patient with IBD-related arthritis