A functional neuroimaging investigation of deep brain stimulation in patients with obsessive–compulsive disorder

Rauch, Scott L.; Dougherty, Darin D.; Malone, Donald A.; Rezai, Ali R.; Friehs, Gerhard; Fischman, Alan J.; Alpert, Nathaniel M.; Haber, Suzanne N.; Stypulkowski, Paul H.; Rise, Mark T.; Rasmussen, Steven A.; Greenberg, Benjamin D.

doi:10.3171/jns.2006.104.4.558

Cited by 237 publications

(140 citation statements)

References 37 publications

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“…These latter regions have been described to be hypermetabolic in depressed states. In patients with obsessive-compulsive disorder, selective monopolar stimulation of essentially the same targetFalbeit with a larger single electrode contactFproduced acute metabolic effects after 10-20 min that are generally consistent with those found in our study after 1 week of stimulation, supporting the hypothesis that cortical-thalamic-striatal-cortical circuitry can be modulated by DBS at this target site (Rauch et al, 2006). The group of Mayberg et al (2005) has demonstrated that improvement of depressive symptomatology in response to different treatment modalities including DBS to it is invariably associated with a metabolic decrease in Brodmann area 25 (Cg25).…”

Section: Discussionsupporting

confidence: 88%

Deep Brain Stimulation to Reward Circuitry Alleviates Anhedonia in Refractory Major Depression

Schläepfer

Cohen

Frick

et al. 2007

Neuropsychopharmacol

898

561

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Deep brain stimulation (DBS) to different sites allows interfering with dysfunctional network function implicated in major depression.Because a prominent clinical feature of depression is anhedoniaFthe inability to experience pleasure from previously pleasurable activitiesFand because there is clear evidence of dysfunctions of the reward system in depression, DBS to the nucleus accumbens might offer a new possibility to target depressive symptomatology in otherwise treatment-resistant depression. Three patients suffering from extremely resistant forms of depression, who did not respond to pharmacotherapy, psychotherapy, and electroconvulsive therapy, were implanted with bilateral DBS electrodes in the nucleus accumbens. Stimulation parameters were modified in a double-blind manner, and clinical ratings were assessed at each modification. Additionally, brain metabolism was assessed 1 week before and 1 week after stimulation onset. Clinical ratings improved in all three patients when the stimulator was on, and worsened in all three patients when the stimulator was turned off. Effects were observable immediately, and no side effects occurred in any of the patients. Using FDG-PET, significant changes in brain metabolism as a function of the stimulation in fronto-striatal networks were observed. No unwanted effects of DBS other than those directly related to the surgical procedure (eg pain at sites of implantation) were observed. Dysfunctions of the reward systemFin which the nucleus accumbens is a key structureFare implicated in the neurobiology of major depression and might be responsible for impaired reward processing, as evidenced by the symptom of anhedonia. These preliminary findings suggest that DBS to the nucleus accumbens might be a hypothesis-guided approach for refractory major depression. Neuropsychopharmacology (2008) 33, 368-377; doi:10.1038/sj.npp.1301408; published online 11 April 2007 Keywords: deep brain stimulation; major depression; anhedonia; nucleus accumbens; brain stimulation; Cg25 INTRODUCTIONTraditional methods of alleviating depression largely stem from serendipitous observations of antidepressant effects of substances such as iproniazid (originally developed as a treatment for tuberculosis) or imipramine (originally developed as a treatment for schizophrenia). In particular, increasing levels of monoamine neurotransmitters in the synaptic cleft are associated with improvements of depressive symptoms. This insight led to a more targeted drug discovery process, resulting in drugs with fewer side effects, such as SSRIs. These medication treatments, in conjunction with certain methods of psychotherapy and electroconvulsive therapy, are effective at alleviating depressive symptomatology in most patients (Andrews and Nemeroff, 1994;Mann, 2005). However, these treatments do not work for all patients. A sizable minority of patients does not respond. Indeed, twelve percent of patients suffering from major depression have a poor outcome even after 5 years of treatment (Keller et al, 1992). Patien...

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Section: Discussionsupporting

confidence: 88%

Deep Brain Stimulation to Reward Circuitry Alleviates Anhedonia in Refractory Major Depression

Schläepfer

Cohen

Frick

et al. 2007

Neuropsychopharmacol

898

561

View full text Add to dashboard Cite

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“…An initial study using O15-PET imaging in patients from this series found that acute high-frequency DBS increased perfusion of orbitofrontal cortex, anterior cingulate cortex, striatum, pallidum, and thalamus compared to control conditions. Acute DBS at the VC/VS target thus was associated with activation of circuitry implicated in OCD (Rauch et al, 2006). Another potential use of imaging is response prediction.…”

Section: Limitationsmentioning

confidence: 99%

Three-Year Outcomes in Deep Brain Stimulation for Highly Resistant Obsessive–Compulsive Disorder

Greenberg

Malone

Friehs

et al. 2006

Neuropsychopharmacol

716

436

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Deep brain stimulation (DBS) of the anterior limb of the internal capsule has been shown to be beneficial in the short term for obsessive-compulsive disorder (OCD) patients who exhaust conventional therapies. Nuttin et al, who published the first DBS for OCD series, found promising results using a capsule target immediately rostral to the anterior commissure extending into adjacent ventral capsule/ventral striatum (VC/VS). Published long-term outcome data are limited to four patients. In this collaborative study, 10 adult OCD patients meeting stringent criteria for severity and treatment resistance had quadripolar stimulating leads implanted bilaterally in the VC/VS. DBS was activated openly 3 weeks later. Eight patients have been followed for at least 36 months. Group Yale-Brown Obsessive Compulsive Scale (YBOCS) scores decreased from 34.670.6 (mean7SEM) at baseline (severe) to 22.372.1 (moderate) at 36 months (po0.001). Four of eight patients had a X35% decrease in YBOCS severity at 36 months; in two patients, scores declined between 25 and 35%. Global Assessment of Functioning scores improved from 36.671.5 at baseline to 53.872.5 at 36 months (po0.001). Depression and anxiety also improved, as did self-care, independent living, and work, school, and social functioning. Surgical adverse effects included an asymptomatic hemorrhage, a single seizure, and a superficial infection. Psychiatric adverse effects included transient hypomanic symptoms, and worsened depression and OCD when DBS was interrupted by stimulator battery depletion. This open study found promising long-term effects of DBS in highly treatment-resistant OCD.

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“…Imaging studies of patients with OCD have revealed dysfunctional activity in the orbitofrontal and anterior cingulate cortex, the striatum and the thalamus. Hyperactivity in the orbitofrontal cortex correlates with the severity of OCD; it increases when OCD symptoms are present and decreases with successful medical or surgical treatment [93,94]. OCD has been called folie du doute, referring to pathological doubt.…”

Section: Obsessive-compulsive Disordermentioning

confidence: 99%

Deep brain stimulation in Parkinson disease—what went wrong?

Krack

Hariz

2010

Nat Rev Neurol

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A functional neuroimaging investigation of deep brain stimulation in patients with obsessive–compulsive disorder

Cited by 237 publications

References 37 publications

Deep Brain Stimulation to Reward Circuitry Alleviates Anhedonia in Refractory Major Depression

Deep Brain Stimulation to Reward Circuitry Alleviates Anhedonia in Refractory Major Depression

Three-Year Outcomes in Deep Brain Stimulation for Highly Resistant Obsessive–Compulsive Disorder

Deep brain stimulation in Parkinson disease—what went wrong?

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