Augmentation of behavior therapy with D-cycloserine for obsessive-compulsive disorder

被引:245
作者
Wilhelm, Sabine
Buhlmann, Ulrike
Tolin, David F.
Meunier, Suzanne A.
Pearlson, Godfrey D.
Reese, Hannah E.
Cannistraro, Paul
Jenike, Michael A.
Rauch, Scott L.
机构
[1] Massachusetts Gen Hosp, Obsess Compuls Disorders Clin, Dept Psychiat, Boston, MA 02114 USA
[2] Massachusetts Gen Hosp, McLean Hosp, Boston, MA USA
[3] Harvard Univ, Sch Med, Boston, MA USA
[4] Inst Living, Hartford, CT USA
关键词
ANTAGONIST MK-801 BLOCKS; PLACEBO-CONTROLLED TRIAL; LONG-TERM POTENTIATION; EXPOSURE THERAPY; CONDITIONED FEAR; CLINICAL IMPLICATIONS; RESPONSE PREVENTION; EXTINCTION; AMYGDALA; SCHIZOPHRENIA;
D O I
10.1176/appi.ajp.2007.07050776
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
Objective: This study examined whether D-cycloserine, a partial agonist at the N-methyl-D-aspartate (NMDA) glutamatergic receptor, enhances the efficacy of behavior therapy for obsessive-compulsive disorder (OCD). Method: A randomized, double-blind, placebo-controlled trial investigating D-cycloserine versus placebo augmentation of behavior therapy was conducted in 23 OCD patients. Patients first underwent a diagnostic interview and pretreatment evaluation, followed by a psychoeducational/ treatment planning session. Then they received 10 behavior therapy sessions. Treatment sessions were conducted twice per week. One hour before each of the behavior therapy sessions, the participants received either D-cycloserine, 100 mg, or a placebo. Results: Relative to the placebo group, the D-cycloserine group's OCD symptoms were significantly more improved at mid-treatment, and the D-cycloserine group's depressive symptoms were significantly more improved at posttreatment. Conclusions: These data provide support for the use of D-cycloserine as an augmentation of behavior therapy for OCD and extend findings in animals and other human disorders suggesting that behavior therapy acts by way of longterm potentiation of glutamatergic pathways and that the effects of behavior therapy are potentiated by an NMDA agonist.
引用
收藏
页码:335 / 341
页数:7
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