Original Article

Neuropsychopharmacology (2006) 31, 644–650. doi:10.1038/sj.npp.1300851; published online 10 August 2005

Clinical Research

Cue-Induced Brain Activity Changes and Relapse in Cocaine-Dependent Patients

Thomas R Kosten1, Barbara Ellen Scanley2, Karen A Tucker1, Alison Oliveto1,3, Chekema Prince4, Rajita Sinha2, Marc N Potenza2, Pawel Skudlarski5 and Bruce E Wexler2

  1. 1Department of Psychiatry, Yale University School of Medicine, VA Connecticut Healthcare System, West Haven, CT, USA
  2. 2Department of Psychiatry, Yale University School of Medicine, Connecticut Mental Health Center, New Haven, CT, USA
  3. 3Department of Psychiatry, University of Arkansas for Medical Sciences, Little Rock, AR, USA
  4. 4Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA
  5. 5Department of Radiology, Yale University School of Medicine, New Haven, CT, USA

Correspondence: Dr TR Kosten, Department of Psychiatry, Yale University School of Medicine, 151D – Bldg 35, VA Connecticut Healthcare System, 950 Campbell Avenue, West Haven, CT 06516, USA. Tel: 203 932 5711 ext 7438; Fax: 203 937 4915; E-mail: thomas.kosten@yale.edu

Received 13 September 2004; Revised 3 June 2005; Accepted 7 June 2005; Published online 10 August 2005.



This study used functional magnetic resonance imaging (fMRI) to examine the association between brain activation during exposure to cocaine-related cues and relapse to drug use in cocaine-dependent (CD) patients. We imaged 17 CD subjects during a 2-week in-patient stay. The subjects then entered a 10-week outpatient placebo-controlled, double-blind randomized clinical trial where urine toxicologies were assessed three times weekly to calculate the treatment effectiveness score (TES). Worse TES correlated with BOLD activation in the left precentral, superior temporal, and posterior cingulate cortices (PCC), and right middle temporal and lingual cortices (R>0.65; P<0.005). The left PCC activation also distinguished eight nonrelapsers (TES above mean and completed treatment) from nine relapsers. Cocaine-free urines were significantly greater in the nonrelapsers (92%) than in the relapsers (66%), who also remained in treatment for an average of only 3.2 weeks. Self-reports of craving during fMRI did not differ between nonrelapsers and relapsers and did not correlate with TES. Relapse to cocaine abuse was associated with increased activation in the sensory association cortex, the motor cortex, and PCC while viewing images of cocaine-related cues. These results suggest that relapse to cocaine abuse is associated with increased brain activation to cocaine cues in sensory, motor, and cognitive-emotional processing areas. This physiological activation was a better predictor of relapse than subjective reports of craving, and may be a useful target for treatment development.


cocaine, fMRI, posterior cingulate cortex, treatment outcome, drug cues, sertraline

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