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P023 A resting state fMRI study in patients with active Crohn’s disease

G. Thapaliya1, S. Eldeghaidy2, S. J. Radford1, S. Francis2, G. Moran*1

1The University of Nottingham, NIHR Nottingham Biomedical Research Centre, Nottingham University Hospitals NHS Trust and School of Medicine, Nottingham, UK, 2The University of Nottingham, Sir Peter Mansfield Imaging Centre, School of Physics and Astronomy, Nottingham, UK


Resting state functional magnetic resonance imaging (rsfMRI) measures spontaneous fluctuation in blood oxygen-level dependent (BOLD) signals in the brain at rest, generating neuroanatomically distinct functionally linked Resting State Networks (RSNs). Present RSN literature in CD is sparse, solely reporting in inactive disease and only focussed on specific RSNs. Here we use independent component analysis (ICA) to study changes across multiple RSNs in active CD.


29 active CD patients and 27 age-, BMI- and gender-matched healthy controls (HC) were recruited. Active disease was defined as CRP > 5 mg/dl, or faecal calprotectin (FCP) >250 μg/g or through ileocolonoscopy or MRE. A hospital anxiety and depression (HAD) score was used as a patient-reported outcome. RsfMRI datasets were acquired on a 3T Philips Achieva scanner, with data corrected for physiological noise and motion. ICA analysis was carried out using MELODIC (FSL software). A multi-session temporal concatenation was used to generate 30 independent component (IC) maps of RSNs. A dual regression analysis with variance normalisation was performed to identify differences in RSN between HCs and CD patients. Anatomical T1-weighted images were collected to determine structural (grey matter volume (GMV)/cortical thickness) differences in CD (CAT, SPM software).


CD participants had an age of (33 ± 14) years, Harvey–Bradshaw Index was (4 ± 1), CRP (9 ± 7) mg/dl and FCP (617 ± 554) µg/g. CD patients had significantly higher depression scores (CD: 3.0 ± 0.6, HC: 1.5 ± 0.5, p < 0.05). RSNs comprising the visual network, default mode network (DMN), salience network, dorsal attention network (DAN), frontal–parietal network (FPN), temporal and cerebellum networks were identified. Enhancement of activity and increased connectivity in DMN (posterior cingulate cortex (PCC)), the cerebellar network and thalamus, visual attention network, and FPN (postcentral cortex) was observed in CD. Atrophy (reduced GMV and cortical thickness (CT) in post-central gyrus and additional cortical thinning in right rostral middle-frontal cortex was seen in CD.

Figure 1. (A) RSNs (red = positive and blue = negative networks) areas of increased connectivity in CD>HC yellow in (i) DMN (posterior cingulate) and (ii) FPN (postcentral cortex). (B) Areas of atrophy in CD for (i) CT and (ii) GMV.


These data show abnormal increased connectivity in RSNs in CD patients in the DMN (PCC) and in FPN network (postcentral cortex which also showed associated atrophy). These changes may reflect neuroplasticity in response to chronic systemic inflammation and may relate to altered affective and cognitive self-referential processing.