Predictors of treatment response to fluvoxamine in obsessive–compulsive disorder: An fMRI study

Abstract

Recent neuroimaging studies suggest that the pathophysiology of obsessive-compulsive disorder (OCD) may involve more widely distributed large-scale brain systems, including the parietal, occipital, and cerebellar areas, rather than the conventional orbitofronto-striatal model. We hypothesized that not only orbitofrontal cortex and caudate nucleus activities but also posterior brain regions might be associated with subsequent treatment response to serotonin reuptake inhibitors in OCD. The participants were 17 patients with OCD. Each patient was required to undergo fluvoxamine pharmacotherapy for 12 weeks. Before treatment, fMRI images of the subjects were obtained in the context of a symptom-provocation paradigm. The percentage changes in total Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) scores, from pre- to post-treatment, served as the index of treatment response. Statistical Parametric Mapping was used to identify brain loci where pre-treatment brain activation significantly correlated with the subsequent treatment response. Fifteen of 17 patients completed the 12-week treatment. During the symptom provocation task, patients showed brain activation in the left superior temporal gyrus (STG), left precuneus, left frontal cortices, right cerebellum, and right frontal cortices. We found that pre-treatment activation in the right cerebellum (Z-score=5.10, x,y,z=22,-84,-18) and the left STG (Z-score=4.95, x,y,z=-62,-22,0) was positively correlated with the improvement in the Y-BOCS score. Our results suggest that pre-treatment activation in the right cerebellum and in the left STG predict subsequent reduction in OCD symptom severity. There is every possibility that fMRI can be used as a tool to predict treatment response.

Differences in Metabolic Network Modulation Between Capsulotomy and Deep-Brain Stimulation for Refractory Obsessive-Compulsive Disorder

“…Furthermore, we found reduced metabolism in the posterior cingulate cortex, the superior frontal cortex, the supplementary motor cortex, and the inferior parietal cortex, again in agreement with previous findings (11,22,23). In particular, Saxena et al showed an elevated frontal metabolism at baseline in patients with comorbid OCD and major depressive disorder (MD) (22).…”

“…This finding is at odds with previous work on OCD in which the precuneus was hypermetabolic after symptom provocation tests (20,23,33), and a trend toward a positive correlation between baseline metabolism and symptom severity has been shown (34). The precuneus is part of the default network (21).…”

“…Previous studies reported involvement of the cerebellum in OCD symptomatology (23,30,32). Zuo et al (12) showed a postoperative decrease in the cerebellar tonsil, inferior to the pyramis.…”

“…A negative correlation was also found between postoperative HAM-D changes and preoperative metabolism in the superior temporal cortex. Previous studies already suggested that the superior temporal cortex has a role in OCD with comorbid MD (29), as well as in OCD (23) or MD alone (24).…”

Stress response in postpartum women with and without obsessive–compulsive symptoms: an fMRI study

“…It has also been linked to OCD pathophysiology, with patients with OCD having higher regional cerebral blood flow at rest and during presentation of neutral and symptom-related stimuli 50 and increased BOLD signal in response to symptom provocation. [51][52][53] Rotge and colleagues 53 suggested that the left STG activation was related to the anxiety manifestations rather than an engagement of the neural circuitry underlying OCDrelated symptoms. It is thought that cerebral hyperactivity seen in patients with OCD might mediate the formation of improper error detection and contribute to uncontrollable OCD symptoms, such as excessive doubt and compulsive checking.…”