Abstract

Since the publication of Insel’s commentary Towards a Neuroanatomy of Obsessive-Compulsive Disorder ( 1 Insel T.R. Towards a neuroanatomy of obsessive compulsive disorder. Arch Gen Psychiatry. 1992; 49: 739-744 Crossref PubMed Scopus (412) Google Scholar ) 20 years ago, the finding of increased regional metabolic activity in orbitofrontal cortex and caudate in obsessive-compulsive disorder (OCD) patients versus controls, in both resting and symptomatic states, has been one of the most replicable findings in psychiatric imaging. Using resting positron emission tomography, Schwartz et al. ( 2 Schwartz J.M. Stoessel P.W. Baxter L.R. Martin K.M. Phelps M.E. Systematic changes in cerebral glucose metabolic rate after successful behavior modification treatment of obsessive compulsive disorder. Arch Gen Psychiatry. 1996; 53: 109-113 Crossref PubMed Scopus (546) Google Scholar ) were the first to report on a functional connectivity measure that led to the speculation that the orbital striatal thalamic loop was overly synchronized in OCD and that successful behavioral or pharmacologic treatment led to the desynchronization of the network. Since that initial study, advances in Bayesian dynamic causal modeling have allowed us to gain an understanding of how slow resting state rhythms are synchronized across brain regions and has led to a new era in exploring functional connectivity in psychiatric disease ( 3 Fox M.D. Raichle M.E. Spontaneous fluctuations in brain activity observed with functional magnetic resonance imaging. Nat Neurosci Rev. 2007; 8: 700-711 Crossref PubMed Scopus (4769) Google Scholar ). Functional connectivity studies have brought home the importance of complex network connections as well as the significance of synchrony versus desynchrony between structures as a potential target for therapeutic intervention. In 2009 Harrison et al. ( 4 Harrison B.J. Soriano-Mas C. Pujol J. Ortiz H. Lopez-Sola M. Hernandez-Ribas R. et al. Altered corticostriatal functional connectivity in obsessive compulsive disorder. Arch Gen Psychiatry. 2009; 66: 1189-1200 Crossref PubMed Scopus (419) Google Scholar ) were the first of several groups to report on resting-state functional connectivity in OCD. Their major findings confirmed previous positron emission tomography and functional magnetic resonance imaging data that pointed to abnormalities in orbital striatal function in OCD and whose magnitude was correlated with OCD severity. In the current issue, Harrison et al. ( 4 Harrison B.J. Soriano-Mas C. Pujol J. Ortiz H. Lopez-Sola M. Hernandez-Ribas R. et al. Altered corticostriatal functional connectivity in obsessive compulsive disorder. Arch Gen Psychiatry. 2009; 66: 1189-1200 Crossref PubMed Scopus (419) Google Scholar ) have replicated their initial findings with a much larger sample of 74 patients and controls and report on the similarities and differences in functional connectivity ( 5 Harrison BJ, Pujol J, Cardoner N, Deus J, Alonso P, López-Solà M, et al. (2013): Brain corticostriatal systems and the major clinical symptom dimensions of obsessive-compulsive disorder. Biol Psychiatry 73:321–328. Google Scholar ) that are correlated with OCD symptom dimensions measured by the Dimensional Yale Brown Obsessive Compulsive Scale (DYBOCS) ( 6 Mataix-Cols D. Rosario-Campos M.S. Leckman J.F. A multidimensional model of obsessive compulsive disorder. Am J Psychiatry. 2005; 162: 228-238 Crossref PubMed Scopus (728) Google Scholar ). The findings validate a host of other clinical, imaging, and genetic findings that demonstrate both the overlap and unique features of symptom dimensions in OCD. These data support OCD’s phenotypic and etiologic heterogeneity. Brain Corticostriatal Systems and the Major Clinical Symptom Dimensions of Obsessive-Compulsive DisorderBiological PsychiatryVol. 73Issue 4PreviewFunctional neuroimaging studies have provided consistent support for the idea that obsessive-compulsive disorder (OCD) is associated with disturbances of brain corticostriatal systems. However, in general, these studies have not sought to account for the disorder’s prominent clinical heterogeneity. Full-Text PDF

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call