P483 Fatigue and brain morphology in active and remitted Crohn’s Disease

Abstract

Abstract Background Extraintestinal symptoms like fatigue and psychosocial impairments are highly prevalent in IBD, especially during active phases of the disease. They not only significantly impair patients’ quality of life, but can also alter the disease course. Disturbances of brain-gut-interactions may contribute to these symptoms. The aim of this study was to examine associations between brain structure, inflammatory biomarkers and symptoms of fatigue, depression and anxiety in persons with Crohn’s Disease (CD) in different disease states. Methods We prospectively enrolled n=109 participants (n=67 persons with CD, n=42 healthy controls). All participants underwent cranial magnetic resonance imaging at 3Tesla, provided stool samples for analysis of faecal calprotectin and completed questionnaires to assess symptoms of fatigue, depression and anxiety. We analysed differences in grey matter volume (GMV) between patients and controls and associations between regional GMV alterations, neuropsychiatric symptoms and faecal calprotectin. Results Symptoms of fatigue, depression and anxiety were increased in patients with CD compared to controls, with the highest scores in active CD (Table 1). Patients exhibited regionally reduced GMV in cortical and subcortical sensorimotor regions, occipitotemporal and medial frontal areas. GMV in some of these regions showed a significant negative association with fatigue, but not with depression or anxiety (Fig. 1a). Subgroup analyses revealed symptom-GMV-associations for fatigue in remitted (Fig. 1b), but not in active CD (Fig. 1c), while fatigue was positively associated with fCal in active (Fig. 1c), but not remitted disease (Fig. 1b). Conclusion Our findings support disturbances of brain-gut-interactions in the development extraintestinal symptoms in CD, which may be particularly relevant for fatigue during remitted disease. Reduced GMV in the precentral gyrus and other sensorimotor areas could reflect key contributions to fatigue pathophysiology in CD. A sensorimotor model of fatigue in CD could also pave the way for novel treatment approaches, such as targeted noninvasive brain stimulation. Moreover, differences in gut-brain-disturbances between active and remitted disease with regard to fatigue may indicate the need for differential therapeutic approaches dependent on the disease state.