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Published Online: 1 December 2011

Neurocognitive Response to Deep Brain Stimulation for Obsessive-Compulsive Disorder: A Case Report

To the Editor: When obsessive-compulsive disorder (OCD) symptoms are severe and refractory to both cognitive-behavioral therapy (CBT) and medication, deep brain stimulation (DBS) may be of value (1). Although OCD research has examined the effects of DBS on cognition (2), few studies have used translational computerized paradigms capable of fractionating dissociable aspects of cognition and their neural substrates. Neurocognitive assessments have the potential to help elucidate the underlying mechanisms of action of DBS in OCD and the optimal brain target.

Case Report

“Mr. T” is a 30-year-old man with a 5-year history of OCD with primary contamination obsessions and washing compulsions. He had stopped socializing, had dropped out of school, and was unemployed because of his OCD. Past adequate trials of all serotonin reuptake inhibitors, both as monotherapy and with multiple augmentation strategies, and 20 weeks of CBT using exposure response prevention provided only limited benefits.
After ethical review board approval, Mr. T underwent bilateral implantation of electrodes targeting the nucleus accumbens. At the time of surgery, his Yale-Brown Obsessive Compulsive Scale score was 32 while taking the following medications: clomipramine, 250 mg/day; ziprasidone, 120 mg/day; and clonazepam, 1 mg t.i.d. His medication dosages were unchanged before and after the cognitive testing.
We performed cognitive assessments at baseline (prestimulation) and again 8 months after DBS began. Tasks from the Cambridge Neuropsychological Test Automated Battery included the stop-signal test (assessing ability to suppress prepotent motor responses), the intradimensional/extradimensional set shift task (examining rule learning and behavioral flexibility), and the Cambridge Gamble Task (assessing decision making). The results of these assessments are summarized in Table 1.
TABLE 1. Cambridge Neuropsychological Test Automated Battery (CANTAB) Test Performance After Deep Brain Stimulation (DBS) Compared With Normative Dataa
 Meanz
Individual TestsBefore DBSAfter DBSBefore DBSAfter DBS
Stop-signal test reaction time (msec)211.58204.70–1.0–0.8
Stop-signal test median go reaction time (msec)449.00379.000.10.5
Intradimensional/extradimensional set shift task, pre-extradimensional errors6.007.000.2–0.1
Intradimensional/extradimensional set shift task, extradimensional errors1.002.000.80.6
Cambridge Gamble Task, overall proportion bet0.600.570.60.4
Cambridge Gamble Task, quality of decision making1.001.000.50.5
a
Normative data are taken from the Cambridge Cognition CANTAB database except for the stop-signal test, where data were unavailable and therefore were taken instead from Chamberlain et al. (3).
Before the DBS, Mr. T generally exhibited cognitive performance akin to healthy comparison subjects except for evidence of stop-signal reaction time impairment (z=1.0). His stop-signal reaction time performance changed little after DBS (posttreatment z=0.8); however, the DBS resulted in significant improvement in Mr. T's OCD symptoms, and his Yale-Brown Obsessive Compulsive Scale score decreased to 10. Mr. T returned to college and now has a social life and works part-time.

Discussion

This case indicates that DBS, targeting the nucleus accumbens, was associated with significant therapeutic benefits in treatment-refractory OCD in the absence of effects on response inhibition, set shifting, or decision making. The lack of effect of accumbens DBS on the stop-signal deficit accords with translational research indicating that accumbens damage (unlike cortical damage) has no effect on response inhibition on an equivalent animal task (4). While impaired response inhibition appears to be a trait marker for OCD, and was evident in Mr. T at baseline, DBS to the accumbens does not appear to ameliorate this problem. This case illustrates the value of DBS in patients with refractory OCD and the importance of including cognitive tests in such studies to identify meaningful predictors for successful DBS in OCD on an individual level.

Footnote

Accepted for publication in September 2011.

References

1.
Greenberg BD, Rauch SL, Haber SN: Invasive circuitry-based neurotherapeutics: stereotactic ablation and deep brain stimulation for OCD. Neuropsychopharmacology 2010; 35:317–336
2.
Denys D, Mantione M: Deep brain stimulation in obsessive-compulsive disorder. Prog Brain Res 2009; 175:419–427
3.
Chamberlain SR, Schreiber LRN, Odlaug BL, Grant JE: Association between tobacco smoking and cognitive functioning in young adults. Am J Addiction (in press)
4.
Eagle DM, Robbins TW: Lesions of the medial prefrontal cortex or nucleus accumbens core do not impair inhibitory control in rats performing a stop-signal reaction time task. Behav Brain Res 2003; 146:131–144

Information & Authors

Information

Published In

Go to American Journal of Psychiatry
Go to American Journal of Psychiatry
American Journal of Psychiatry
Pages: 1338 - 1339
PubMed: 22193674

History

Accepted: September 2011
Published online: 1 December 2011
Published in print: December 2011

Authors

Affiliations

Jon E. Grant, J.D., M.D.
Brian L. Odlaug, B.A.
Samuel R. Chamberlain, M.D., Ph.D.
Cambridge, United Kingdom

Funding Information

Dr. Grant has received research grants from Forest Pharmaceuticals, the National Center for Responsible Gaming, National Institute on Drug Abuse, NIMH, and Psyadon Pharmaceuticals. Mr. Odlaug reports no financial relationships with commercial interests. Dr. Chamberlain has consulted for Cambridge Cognition, P1Vital, and Shire Pharmaceuticals.

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