e., slower processing speed, response inhibition deficits and visuospatial memory impairments)

were associated both with brain volumetric changes in the OFC (Jenike et al. 1996; Grachev et al. 1998; Choi et al. 2004; Menzies et al. 2007) but also with changes in regions outside the orbitofrontal loop such as the parietal cortex, the cerebellum (Menzies et al. 2007) and the dorsolateral prefrontal GM (Christian et al. 2008). Taken Selleck SNS032 together, the reported evidence of neurobiological abnormalities in OCD suggests that the orbitofronto-striatal Inhibitors,research,lifescience,medical model may not be sufficient to fully explain the brain basis of the disorder (Piras et al. 2013a). From a neurobiological perspective, the “multiple-region pathogenesis” Inhibitors,research,lifescience,medical of OCD could be viewed as supportive of the notion that OCD emerges from disordered macro and

microstructure as well as function, of large scale neural systems (Menzies et al. 2008a). The concurrent observation of WM abnormalities in OCD patients may also suggest Inhibitors,research,lifescience,medical that the disorder could be hypothetically underpinned by disconnectivity of such neurocognitive networks (Menzies et al. 2008b; Garibotto et al. 2010; Piras et Inhibitors,research,lifescience,medical al. 2013b). Then again, from a cognitive point of view,

abnormalities across several brain regions and dysfunctionality at the system level could account for the reported incongruence between cognitive Inhibitors,research,lifescience,medical findings and the orbitofronto-striatal brain model of OCD. On the other hand, as heterogeneity in OCD neuroimaging originates from multiple differences across studies, first among many the clinical characteristics of the patient sample, it might be the case that the emerging picture of widespread structural brain changes in OCD is accounted for by the complex phenomenology GBA3 of the disorder. Thus, in studying the association between brain and cognitive dysfunction in OCD the indices of cerebral abnormalities (e.g., volume reduction or diffusivity increase) have been used separately in different studies. As a consequence, a coherent picture of the neural basis of cognitive deficits in OCD is still lacking. This study is aimed at filling this gap by analyzing brain macro and microstructural alterations and cognitive performances in a sample of OCD patients.