Although the findings from volumetric imaging studies of OCD have been fairly inconsistent, with reports of either increases or decreases (Szeszko et al. 1999) in brain regions thought to be implicated in the pathophysiology of the disorder, our result is

consonant with previous investigations that also failed to detect any macrostructural difference between groups of OCD patients and HC subjects (Jenike et al. 1996; Inhibitors,research,lifescience,medical O’sullivan et al. 1997; Rosenberg et al. 1997; Bartha et al. 1998; Riffkin et al. 2005). We already discussed the sources of discrepancy in volumetric studies of OCD, however, it is also possible that abnormalities at the microstructural level, as investigated using DTI, could Inhibitors,research,lifescience,medical play a role in the neuropathology of the disorder (Szeszko et al. 2005). Indeed, we did find microstructural diffusivity

changes in our OCD patients, with increased MD in several cortical regions (left dorsal ACC, insula, thalamus and parahippocampal gyrus, right frontal Inhibitors,research,lifescience,medical operculum and temporal lobe, left parietal lobe) and reduction in FA values (a putative measure of fibre density, axonal diameter and myelination) in two WM tracts (the left SLF and the body of CC). As both diffusion indices are used to interrogate pathological changes in cerebral tissue and probe the integrity of WM fibre tracts (Basser and Jones 2002), we can assume that altered architecture in specific cortical areas and WM tracts may be responsible for OCD pathophysiology. Provided that there are no previous DTI studies examining brain cortical MD in OCD Inhibitors,research,lifescience,medical patients, our results selleck chemicals cannot be compared with other investigations, although volumetric neuroimaging studies may supply some Inhibitors,research,lifescience,medical insight into the role of the aforementioned areas in OCD pathogenesis. Actually, compelling evidence suggests that abnormalities in orbitofrontal, cingulate, thalamic, and temporolimbic regions play

a central role in the pathophysiology of OCD (Piras et al. 2013a). The pattern of brain alterations in OCD patients is characterized by reduced volume in the cingulate gyrus, and increased volume in the putamen, striatum, thalamus, and temporolimbic regions, suggesting that volume reduction in the cortical source of not the orbitofronto-striatal loop, and relative expansion of tissue at the deep GM nuclei and limbic level, may have a primary role in OCD (Pujol et al. 2004; Piras et al. 2013a). Also the insular cortex, a region directly linked to the ventral part of the striatum and probably functionally related to the frontostriatal system, has been implicated in the pathogenesis of OCD by VBM studies showing either increased GM volume in the right and left insula (Valente et al. 2005) or volume reduction in the same regions (Pujol et al. 2004; Yoo et al. 2008).