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S.25.05 Smoking cessation treatment in patients with schizophrenia: outcomes, relapse vulnerability factors, and targeted interventions
S.26 Genes and schizophrenia disproportionately from antidepressant treatment. Odds of longterm abstinence were 2.3 times greater for MD Hx+ smokers treated with active medication and/or mood management therapy than for those treated with placebo and standard cessation therapy. MD Hx− smokers, in contrast, received significantly less of a cessation boost. References [1] Hitsman B, Borrelli B, McChargue DE, Spring B, Niaura R, 2003. History of depression and smoking cessation outcome: a meta-analysis. J Consult Clin Psychol 71: 657–663. [2] Hitsman B, Spring B, Borrelli B, McChargue D, Niaura R, 2004.Reply to Covey (Letter to the Editor). Nic Tob Res 6: 747–749. [3] Haas AL, Munoz RF, Humfleet GL, Reus, VI, Hall SM, 2004. Influences of mood, depression history, and treatment modality on outcomes in smoking cessation. J Consult Clin Psychol. 72: 563–570.
S.25.04 Preliminary results from a RCT of a smoking cessation intervention for smokers with a history of major depression G. Schippers1 ° , R. Van der Meer2 , M. Willemsen2 , P.H. Smit3 , P. Cuypers4 . 1 University of Amsterdam (AMC), Amsterdam Institute for Addiction Research, Amsterdam, The Netherlands; 2 Stivoro, The Hague, The Netherlands; 3 Trimbos Institute, Utrecht, The Netherlands; 4 Free University, Amsterdam, The Netherlands Smokers with a history of major depression who attempt to quit smoking have a higher risk of relapsing than smokers without a history of depression. This may be attributable to elevations in negative mood and depressive symptoms. These smokers may be able to quit more easily if they can better manage their mood. A new intervention was tested. This intervention consisted of proactive telephone counselling, including the delivering of a selfhelp mood management manual. The objective of the study is to evaluate the effectiveness of this intervention. Comparing condition will be proactive counselling without a mood management intervention. Data is gathered on the 485 smokers with a history of major depression who were randomly assigned to the mood management intervention (M M) or usual care (U C). The outcome measures are seven-day point prevalence, continuous abstinence, and depressive symptoms, at 6 and 12-months follow-up. In a randomized controlled trial of a smoking cessation intervention for smokers with a history of major depression, a new intervention was tested. S.25.05 Smoking cessation treatment in patients with schizophrenia: outcomes, relapse vulnerability factors, and targeted interventions T.P. George ° , J.C. Vessicchio, A.H. Weinberger, K.A. Sacco. Connecticut Mental Health Center, Department of PsychiatrySubstance Abuse Center room, New Haven, USA It is increasingly appreciated that amongst psychiatric cigarette smokers, those with schizophrenia have elevated rates of smoking compared to the general population, and great difficulty with smoking cessation. Convergent lines of evidence suggest that biological dysfunction associated with schizophrenia may predispose these patients to such high rates of co-morbid nicotine and tobacco addiction. Our research group has conducted a series of programmatic studies using a translational neuroscience approach to understanding the biology and treatment of nicotine addiction
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in patients with schizophrenia. First, the presentation will focus on endophenotypic deficits associated with schizophrenia such as neurocogntive deficits, which appear to be selectively modulated by nicotine and cigarette smoking, and which appear to be associated with cessation treatment failure. Second, a series of clinical treatment studies has sought to develop combined medication and behavioral treatments for co-morbid nicotine dependence in schizophrenia, and has utilized nicotine replacement, sustainedrelease bupropion, and group behavioral smoking counseling. We have found that with these combined treatments, overall cessation rates (biochemically-verified) can approach 35%, and suggest the safety and efficacy of bupropion in this subset of smokers. Furthermore, we have consistently demonstrated that treatment with atypical antipsychotics is associated with higher rates of cessation, independent of the type of cessation treatment. Identification of genetic factors which are linked with successful cessation is also discussed. Collectively, our data suggest that rationale treatment approaches based on our understanding of the pathophysiology of schizophrenia may lead to targeted and more efficacious treatments for nicotine addiction in this population of recalcitrant smokers. References [1] Sacco, K.A. et al., 2005. Effects of cigarette smoking on spatial working memory and attentional deficts in schizophrenia: Involvement of nicotinic receptor mechanims. Arch. Gen. Psychiatry. 62, 649–659. [2] Dolan, S.L. et al., 2004. Neuropsychological deficits are associated with smoking cessation treatment failure in patients with schizophrenia. Schizophrenia Res. 70, 263–275. [3] George, T.P. et al., 2000. Nicotine transdermal patch and atypical antipsychotic medications for smoking cessation in schizophrenia. Am. J. Psychiatry. 157, 1835–1842.
S.26 Genes and schizophrenia S.26.01 Neurotransmitter genes in causation and treatment response P. Gorwood ° , N. Hamdani, C. Dubertret, C. Boni. INSERM, U675, Paris, France Many candidate genes have been raised in schizophrenia, either in the vulnerability to the disorder, or in the specific type of response to antipsychotics observed in patients. Disentangling these two roles is not as straight forward as it seems, for example because some key receptors could be involved both in the disorder and in the type of response. Researching on the gene coding for the dopamine D3 receptor gene (DRD3) in schizophrenia may have a heuristic value, as this gene was associated on the one hand with schizophrenia, and on the other hand to induced dyskinesia. As neurological soft-signs are frequently found in excess in patients with schizophrenia, a partly common substratum is possible between these two phenotypes. Neurobiological research also suggests a significant role of the endocannabinoid system in schizophrenia (CNR1 as a susceptibility gene) and also in the efficacy/tolerance of antipsychotics (psychopharmacogenetics). Genetics could offer an opportunity to disentangle its involvement in the disease vulnerability versus a specific influence on antipsychotics’ effects. We thus assessed the possible role of a tag SNP (the 1359A/G polymorphism) of the CNR1 gene in schizophrenia and in therapeutic response to atypical antipsychotics. The G allele frequency was significantly higher among non-responsive versus responsive patients, with a
S.25.04 Preliminary results from a RCT of a smoking cessation intervention for smokers with a history of major depression G. Schippers1 ° , R. Van der Meer2 , M. Willemsen2 , P.H. Smit3 , P. Cuypers4 . 1 University of Amsterdam (AMC), Amsterdam Institute for Addiction Research, Amsterdam, The Netherlands; 2 Stivoro, The Hague, The Netherlands; 3 Trimbos Institute, Utrecht, The Netherlands; 4 Free University, Amsterdam, The Netherlands Smokers with a history of major depression who attempt to quit smoking have a higher risk of relapsing than smokers without a history of depression. This may be attributable to elevations in negative mood and depressive symptoms. These smokers may be able to quit more easily if they can better manage their mood. A new intervention was tested. This intervention consisted of proactive telephone counselling, including the delivering of a selfhelp mood management manual. The objective of the study is to evaluate the effectiveness of this intervention. Comparing condition will be proactive counselling without a mood management intervention. Data is gathered on the 485 smokers with a history of major depression who were randomly assigned to the mood management intervention (M M) or usual care (U C). The outcome measures are seven-day point prevalence, continuous abstinence, and depressive symptoms, at 6 and 12-months follow-up. In a randomized controlled trial of a smoking cessation intervention for smokers with a history of major depression, a new intervention was tested. S.25.05 Smoking cessation treatment in patients with schizophrenia: outcomes, relapse vulnerability factors, and targeted interventions T.P. George ° , J.C. Vessicchio, A.H. Weinberger, K.A. Sacco. Connecticut Mental Health Center, Department of PsychiatrySubstance Abuse Center room, New Haven, USA It is increasingly appreciated that amongst psychiatric cigarette smokers, those with schizophrenia have elevated rates of smoking compared to the general population, and great difficulty with smoking cessation. Convergent lines of evidence suggest that biological dysfunction associated with schizophrenia may predispose these patients to such high rates of co-morbid nicotine and tobacco addiction. Our research group has conducted a series of programmatic studies using a translational neuroscience approach to understanding the biology and treatment of nicotine addiction
S201
in patients with schizophrenia. First, the presentation will focus on endophenotypic deficits associated with schizophrenia such as neurocogntive deficits, which appear to be selectively modulated by nicotine and cigarette smoking, and which appear to be associated with cessation treatment failure. Second, a series of clinical treatment studies has sought to develop combined medication and behavioral treatments for co-morbid nicotine dependence in schizophrenia, and has utilized nicotine replacement, sustainedrelease bupropion, and group behavioral smoking counseling. We have found that with these combined treatments, overall cessation rates (biochemically-verified) can approach 35%, and suggest the safety and efficacy of bupropion in this subset of smokers. Furthermore, we have consistently demonstrated that treatment with atypical antipsychotics is associated with higher rates of cessation, independent of the type of cessation treatment. Identification of genetic factors which are linked with successful cessation is also discussed. Collectively, our data suggest that rationale treatment approaches based on our understanding of the pathophysiology of schizophrenia may lead to targeted and more efficacious treatments for nicotine addiction in this population of recalcitrant smokers. References [1] Sacco, K.A. et al., 2005. Effects of cigarette smoking on spatial working memory and attentional deficts in schizophrenia: Involvement of nicotinic receptor mechanims. Arch. Gen. Psychiatry. 62, 649–659. [2] Dolan, S.L. et al., 2004. Neuropsychological deficits are associated with smoking cessation treatment failure in patients with schizophrenia. Schizophrenia Res. 70, 263–275. [3] George, T.P. et al., 2000. Nicotine transdermal patch and atypical antipsychotic medications for smoking cessation in schizophrenia. Am. J. Psychiatry. 157, 1835–1842.
S.26 Genes and schizophrenia S.26.01 Neurotransmitter genes in causation and treatment response P. Gorwood ° , N. Hamdani, C. Dubertret, C. Boni. INSERM, U675, Paris, France Many candidate genes have been raised in schizophrenia, either in the vulnerability to the disorder, or in the specific type of response to antipsychotics observed in patients. Disentangling these two roles is not as straight forward as it seems, for example because some key receptors could be involved both in the disorder and in the type of response. Researching on the gene coding for the dopamine D3 receptor gene (DRD3) in schizophrenia may have a heuristic value, as this gene was associated on the one hand with schizophrenia, and on the other hand to induced dyskinesia. As neurological soft-signs are frequently found in excess in patients with schizophrenia, a partly common substratum is possible between these two phenotypes. Neurobiological research also suggests a significant role of the endocannabinoid system in schizophrenia (CNR1 as a susceptibility gene) and also in the efficacy/tolerance of antipsychotics (psychopharmacogenetics). Genetics could offer an opportunity to disentangle its involvement in the disease vulnerability versus a specific influence on antipsychotics’ effects. We thus assessed the possible role of a tag SNP (the 1359A/G polymorphism) of the CNR1 gene in schizophrenia and in therapeutic response to atypical antipsychotics. The G allele frequency was significantly higher among non-responsive versus responsive patients, with a