Abstract
Recent approaches have suggested that deep brain stimulation (DBS) for obsessive-compulsive disorder relies on distributed networks rather than local brain modulation. However, there is insufficient data on how DBS affects brain metabolism both locally and globally. We enrolled three patients with treatment-refractory obsessive-compulsive disorder with ongoing DBS of the bilateral ventral capsule/ventral striatum. Patients underwent resting-state 18F-fluorodeoxyglucose and positron emission tomography in both stimulation ON and OFF conditions. All subjects showed relative hypometabolism in prefronto-basal ganglia-thalamic networks compared to a healthy control cohort when stimulation was switched OFF. Switching the stimulation ON resulted in differential changes in brain metabolism. Locally, volumes of activated tissue at stimulation sites (n = 6) showed a significant increase in metabolism during DBS ON compared to DBS OFF (Mean difference 4.5% ± SD 2.8; p = 0.012). Globally, differential changes were observed across patients encompassing prefrontal increase in metabolism in ON vs. OFF condition. Bearing in mind limitations of the small sample size, we conclude that DBS of the ventral capsule/ventral striatum for obsessive-compulsive disorder increases brain metabolism locally. Across distributed global networks, DBS appears to exert differential effects, possibly depending on localization of stimulation sites and response to the intervention.
Highlights
Obsessive-compulsive disorder (OCD) is among the most common psychiatric disorders with a lifetime prevalence of 2–3 % [1]
To assess changes in glucose metabolism induced by ongoing VC/VS-deep brain stimulation (DBS), we calculated differential contrasts between DBS ON and OFF conditions
DBS for Parkinson’s disease (PD) is clinically more established than DBS for OCD which is only performed in a small subset of severely affected, treatment-resistant patients, which limits potential study participants
Summary
Obsessive-compulsive disorder (OCD) is among the most common psychiatric disorders with a lifetime prevalence of 2–3 % [1]. Characterized by the presence of unwanted and aversive thoughts (obsessions) and consequent repetitive neutralizing actions (compulsions), it is a chronic, often severely disabling disorder. Beyond an ongoing debate on which target may be best to treat OCD, recent approaches have suggested that clinical effects may be driven by broader network changes rather than focal brain modulation [3]. This notion is supported by reports of network modulations in DBS for other disorders such as Parkinson’s disease (PD) or Alzheimer’s disease [4,5]. There is insufficient data on how DBS for OCD affects brain functioning and metabolism both locally as well as in in broader global networks
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