Neurologic Complications in Patients with Inflammatory Bowel Disease: Increasing Relevance in the Era of Biologics

Extraintestinal manifestations of inflammatory bowel disease (IBD) can involve almost every organ system. Neurologic complications are not infrequent in patients with IBD, but are poorly recognized and underreported. Pathophysiologically, these may represent immune-mediated phenomenon, nonimmunologic complications due to micronutrient deficiencies, thromboembolism, or be medication-induced. Peripheral neuropathy is the most common neurologic complication of IBD and may be immune-mediated, or caused by therapy with anti-tumor necrosis factor-alpha (TNF-alpha) therapy or metronidazole. Multiple sclerosis occurs with a greater frequency in patients with IBD. Anti-TNF-alpha therapy can cause neurologic disease characterized by central demyelination that mimics multiple sclerosis. Hence, patients with a history of demyelinating diseases or with symptoms of polyneuropathy should be carefully evaluated before initiation of anti-TNF-alpha therapy. Natalizumab has been associated with fatal progressive multifocal leukoencephalopathy due to reactivation of JC virus, and occurs with greater frequency in patients with previous JC virus infection. Stroke secondary to venous or arterial thromboembolism can be seen in patients with active Crohn's disease. It is important for gastroenterologists to be aware of the neurologic complications in patients with IBD. Neurologic symptoms in these patients should be promptly evaluated. (Inflamm Bowel Dis 2013; 19: 864-872)