Neurologic manifestations in inflammatory bowel diseases: current knowledge and novel insights

• Published in: Journal of Crohn's and colitis Vol. 4; no. 2; pp. 115 - 124
• Main Authors: Zois, Christos D, Katsanos, Konstantinos H, Kosmidou, Maria, Tsianos, Epameinondas V
• Format: Journal Article
• Language: English
• Published: England 01.06.2010
• Subjects: Anti-Inflammatory Agents - adverse effects; Central Nervous System Diseases - etiology; Cerebrovascular Disorders - etiology; Colitis, Ulcerative - drug therapy; Colitis, Ulcerative - physiopathology; Cranial Nerve Diseases - etiology; Crohn Disease - drug therapy; Crohn Disease - physiopathology; Gastrointestinal Agents - adverse effects; Humans; Inflammatory Bowel Diseases - drug therapy; Inflammatory Bowel Diseases - physiopathology; Muscular Diseases - etiology; Nervous System Diseases - etiology; Peripheral Nervous System Diseases - etiology; Thromboembolism - etiology
• ISSN: 1873-9946; 1876-4479
• DOI: 10.1016/j.crohns.2009.10.005

Crohn's disease (CD) and ulcerative colitis (UC), widely known as inflammatory bowel diseases (IBD), are thought to result from an inappropriate activation of the mucosal immune system driven by intestinal bacterial flora. Although the extraintestinal manifestations of IBD are well documented, the association of IBD with neurologic and neuromuscular involvement is rare and often controversial, with sporadic and conflicting data on its prevalence and spectrum. In addition, a serious number of the latter manifestations may become life-threatening, playing a very important role in disease morbidity. To define the pattern of neurologic involvement in IBD, the most important manifestations in these patients have been reviewed, exploring also their clinical significance. There is evidence that UC and CD can manifest both in the PNS and CNS. Thrombotic complications are common in IBD patients, but cerebral vascular involvement is rare. Neurologic manifestations in IBD patients are more common than previously estimated and may follow a different pattern of involvement in CD and UC. Small numbers of patients currently preclude a better characterization of the clinical spectrum and a better understanding of pathogenesis.