In 1999, Nuttin et. al from Belgium showed that Deep Brain Stimulation (DBS) can also be applied for the treatment of OCD. They chose the anterior limb of internal capsule as the target. They reported results of 26 patients operated at four different centers around the world. Over a period of time they realized that patients who had more ventrally and posteriorly implanted electrodes had better outcomes. So they moved the target to VC/VS and later on nucleus accumbens and bed nucleus of stria terminals. One of the hypotheses for this is that in the posterior area the cortico-striatal-thalamo-cortical tract fibers are more condensed and the target can serve as node. The surgical procedure is very safe and similar to that offered for movement disorders.
Recently a meta-analysis of all the DBS studies for OCD was performed. The aim of this study was to measure the response to DBS in severe treatment resistant OCD patients using the meta-analysis. The data available from 116 subjects produced a global percentage of Y-BOCS score reduction of 45.1% and a global percentage of responders of 60.0%. Better response to DBS was associated with an older age at the time of OCD onset and with the presence of sexual or religious obsessions and compulsions. These results confirm that DBS appears to have an efficacy comparable to that reported for capsulotomy or cingulotomy, ablative techniques after which 64% and 56% of patients respectively are rated as significantly improved.
Nevertheless, severe adverse effects seem to be less frequent with DBS than with lesional neurosurgery. Three cases of intracranial hemorrhages were reported, representing 2.6% of the total number of patients. Five subjects presented an infection of the scalp, chest or abdominal wound, but they were controlled with antibiotic therapy and just one patient suffered a tonic-clonic seizure. Interestingly, no persistent frontal syndrome, cognitive impairment or personality changes have been described for OCD patients treated with DBS. Nevertheless, almost all studies describe these stimulation-related adverse effects as mild, transient and reversible after the adjustment of the stimulation parameters.
Most patients report a significant improvement in at least some aspects of their quality of life. Interestingly, this improvement was not directly correlated with the reduction of symptom severity and was reported even by non-responding patients. Also, QOL keeps on improving years after the initiation of DBS, and even when there was no further reduction of OCD severity was evident, suggesting than factors other than OCD intensity such as anxiety release, reward processing and motivation or affective status, influence QOL. The effects of DBS on abnormal neural connectivity in the CSTC circuit involved in the mechanism of OCD, might explain why stimulation of different brain regions, achieves similar percentages of improvement finally.
Stimulation of STN has been reported to decrease mPFC and OFC metabolism as well as ACC activity, while stimulation of the ALIC has similarly been associated with decreased OFC, subgenual ACC and right DLPFC metabolism. Interestingly, though stimulation of STN did not significantly modify comorbid depressive and anxiety symptoms but a significant and early improvement was observed in anxiety and mood levels, preceding any change in OCD severity, is commonly reported in patients receiving stimulation in the striatal areas. Future studies should address the local and distant effects responsible for mutual as well as distinct mechanisms of action of DBS depending on specific targets in order to personalize the choice of the optimal implantation area according to the individual presentation of the illness.
Our own observation about DBS in two patients of OCD, have been very encouraging. Both patients had more than 60% improvement in their YBOCS scores with significant improvement in the quality of life.