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P.3.e.006 Nicotine effects on attention in schizophrenia: a simultaneous EEG-fMRI study
P.3.e. Psychotic disorders and antipsychotics − Others (clinical) In summary, program results show modest yet significant improvements in several metabolic health parameters in this atrisk population. This naturalistic program evaluation has several limitations: diagnostic heterogeneity and the uncontrolled nature of psychotropic medications received by each participant. It is however also a strength of this program evaluation conducted in “real world conditions”.
P.3.e.005 Effects of galantamine on cognitive deficits in schizophrenia patients H. Kim1 ° , K.J. Lee1 . 1 Inje University Ilsan Paik Hospital, Dept.of Psychiatry, Goyang, South-Korea Objectives: People with schizophrenia are characterized by a broad range of emotional, ideational, and cognitive impairments. A large body of evidence ascribes cognitive dysfunctions to a combination of neurochemical and neuropathological changes. Although dopamine has been regarded as the key neurotransmitter involved in the pathogenesis of symptoms of schizophrenia, several studies have established that the cholinergic neurotransmitter system, involving both nicotinic and muscarinic receptors, is important for the neuromodulation of cognitive processes in schizophrenia[1]. Most authors agree that cholinergic projections to the cortex and basal forebrain play an important role in compromised cognitive constructs in schizophrenia[2]. Therefore, drugs act on cholinergic pathways may improve cognitive dysfunctions in schizophrenia. The possible existence of cholinergic deficits in schizophrenia provides the rationale for examining the efficacy of cholinesterase inhibitor adjunctive therapy for the treatment of cognitive dysfunctions in patients with schizophreia. There is preliminary evidence that galantamine can improve cognitive functions and negative symptoms in schizophrenia. The primary purpose of this study was to evaluate the efficacy of galantamine in schizophrenia for the treatment of cognitive impairments Methods: 22 subjects with schizophrenia (according to DSM-IV) were included in this study. The patients had been medicated on atypical antipsychotics and stablized in their psychotic symptoms. The starting dose of galantamine was 8 mg daily, with the daily dose increasing at 2-week intervals to 16 mg. The patients was assessed with computerized neurocognitive function tests of digit span, continuous performance test, finger tapping test. The cognitive battery included measures of working memory, attention, vigilance, psychomotor speed. Mini-mental Status Examination (MMSE) and Scale for the Assessment of Negative Symptoms (SANS) were evaluated at baseline and at 8 week of galantamine treatment. Results: The average age of the 22 schizophrenia subjects was 42.5+/-3.5 years. 13 patients were male and 9 patients were female. There was no significant difference in mean digit span score 4.2+/−0.9 (forward), 3.2+/−0.8 (backward) at baseline and 4.4+/−1.0 (forward), 3.3+/−0.9 (backward) after 8 weeks of galantamine therapy (p > 0.05). Also there was no significant diffences in the mean finger tapping test score 33.2+/−8.3 (right), 30.4+/−7.9 (left) at baseline and 34.3+/−9.0 (right), 31.3+/−8.2 (left) after 8 weeks (p > 0.05). The MMSE score was 22.3+/−3.4 at baseline and 23.0+/−3.7 after 8 weeks (p > 0.05). There were no significant differences in working memory, motor speed and total scores of MMSE at baseline and after 8 weeks. There were significant improvements in continuous performance test of computerized neurocognitive
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function test including correct responses 127.4±3.5 (baseline) to 132.5±2.7 (after 8 weeks), omission errors 8.7±3.7 at baseline to 5.2±3.1 after 8 weeks, and reaction time 0.59±0.09 at baseline to 0.47±0.04 after 8 weeks. Conclusions: These results suggest that galantamine may have some effects on cognivie defect in patients with schizophrenia especially for aspects of selective attention. Positive allosteric modulatory properties may have contributed to the observed improvement in negative symptoms in schizophrenic patients. References [1] Schubert MH, Young KA, Hicks PB. Galantamine improves cognition in schizophrenic patients stabilized on risperidone. Biol psychiatry 2006; 60(6): 530–533. [2] Sharma T, Reed C, Aasen I, Kumari V. Cognitive effects of adjuvant 24-week rivastigmine treatment to antipsychotics in schizophrenia: a randomized, placebo-controlled, double-blind investigation. Schizophr Res 2006; 85(1−3): 73−83.
P.3.e.006 Nicotine effects on attention in schizophrenia: a simultaneous EEG-fMRI study A. Mobascher1 ° , T. Warbrick2 , J. Brinkmeyer3 , F. Musso3 , T. Stoecker2 , N.J. Shah2 , S. Vossel2 , G. Winterer4 . 1 University of Mainz, Department of Psychiatry, Mainz, Germany; 2 Research Center Juelich, Institute of Neurosciences and Medicine, Juelich, Germany; 3 University of Duesseldorf, Department of Psychiatry, Duesseldorf, Germany; 4 University of Cologne, Cologne Center for Genomics, Cologne, Germany Background: Schizophrenia is associated with cognitive deficits and alterations in task-induced brain activity in several cognitive domains such as attention and working memory. Nicotine dependence is more frequent in schizophrenic patients than in the general population [1]. According to the “self-medication hypothesis” patients with schizophrenia consume nicotine to counteract schizophrenia-associated cognitive deficits. However there is sparse literature on the effects of nicotine on task-induced brain activation in patients suffering from schizophrenia. It was the purpose of the present study to investigate the acute effects of nicotine on the attention network as revealed by EEG (electroencephalography) P300-informed fMRI (functional magnetic resonance imaging) in schizophrenic smokers compared to healthy smoking control subjects. Methods: We performed a randomized, double-blind, placebocontrolled cross-over nicotine (1 mg nasal spray) challenge with simultaneous EEG-fMRI recording. We investigated 16 smoking patients suffering from schizophrenia and 19 smoking controls (Fagerstr¨om test for nicotine dependence/FTND score >4) during a visual choice reaction time task similar to an oddball task. EEG data were analyzed using the software BrainVision Analyzer 2 (Brain Products, Germany); fMRI data were analyzed using the software package FSL (FMRIB’s Software Library, www.fmrib.ox.ac.uk/fsl). In addition to “conventional” fMRI analysis of task-related brain activity, single trial peak amplitudes of the EEG P300 event-related potential were included as regressors in the general linear model (GLM) analysis of the fMRI data [2]. Results: Only when applying the EEG P300-informed fMRI BOLD model in schizophrenic smokers we found higher clustercorrected brain activation (Z>2.3; p < 0.05) in the nicotine condition compared to placebo (nicotine > placebo). Activated regions comprised a fronto-parietal network that has been implicated in attention such as prefrontal areas and the anterior cingulate cortex.
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P.3.e. Psychotic disorders and antipsychotics − Others (clinical)
In contrast no significant nicotine effects compared to placebo on the fMRI BOLD (blood oxygen-level dependent) signal were observed in schizophrenic smokers in the conventional fMRI analysis (no EEG considered). In smoking controls neither model (P300informed or conventional) revealed significant nicotine effects. Conclusions: To our knowledge this is the first study addressing the effects of nicotine on task-induced brain activity in schizophrenic smokers that applied a simultaneous EEG-fMRI approach. Our data suggest that EEG-informed fMRI may be suited to study drug effects on cognitive processes. These effects may be subtle − like in the case of nicotine − and may not be captured when solely averaged task-induced fMRI BOLD activation without additional single trial information is considered. The sensitivity of EEG single trial amplitude-informed fMRI may be higher compared to conventional analyses of the fMRI BOLD signal. Moreover the EEG-informed analysis can emphasize certain aspects of taskinduced brain activity such as neuronal sub-processes that are reflected by P300 amplitude. In view of the relationship between P300 amplitude, cognitive performance and schizophrenia our data suggest that positive effects of nicotine on cognition (as measured by a nicotine-induced increase in the P300 amplitudeinformed fMRI BOLD signal) may be pronounced in patients with schizophrenia. This interpretation would be consistent with the self-medication hypothesis. References [1] Mobascher, A.; Winterer, G., 2008 The Molecular and Cellular Neurobiology of Nicotine Abuse in Schizophrenia. Pharmacopsychiatry 41 (Suppl. 1) S51–S59. [2] Warbrick, T.; Mobascher, A.; Brinkmeyer, J.; Musso, F.; Richter, N.; Stoecker, T.; Fink, G.R.; Shah, N.J.; Winterer, G., 2009 Single-trial P3 amplitude and latency informed event-related fMRI models yield different BOLD response patterns to a target detection task. NeuroImage 47, 1532–1544.
P.3.e.007 Use of valproate for aggressive behaviour in forensic inpatients with schizophrenia A. Popescu1 , M.D. Mosescu1 , M. Bragau1 ° , A.G. Andries1 . 1 Psychiatry Hospital Sapoca, Acute Department, Buzau, Romania Background: Aggression encompasses physical acts against others, oneself (self-mutilation, suicidal gestures or acts), or objects, as well as verbal assaults. Although most patients with schizophrenia are not aggressive, epidemiologic evidence shows an increased risk for violence in this group when compared with the general population [1]. There are many possible causes for aggressive behavior: hallucinations, delusions, poor impulse control, personality characteristics, unstable home or hospital situation. The patients may become aggressive for different reasons at different times. Aggressive behavior in patients with schizophrenia still remains a challenge, especially in forensic unity. Medications are frequently used in the management of aggression and longterm treatment is directed to reduce the frequency and intensity of episodes [2]. Additional adjunctive medications may be necessary when standard therapeutic approaches are ineffective. Mood stabilizers, used initially in bipolar disorders, are currently used also for schizophrenia as adjunctive treatment to antipsychotics and, especially valproate, for aggressive behavior [3]. There are a few small studies about using valproate for aggressive behavior on forensic patients with schizophrenia. Objective: To analyze the efficacy of valproate as adjunctive therapy to antipsychotics on forensic inpatients with schizophrenia for aggressive behavior.
Methods: The study was observational and has been achieved in forensic unit of Psychiatry and Safety Measures Sapoca, Buzau, Romania between May and September 2010. The design of the study was approved by Ethical Board of the hospital. 23 male inpatients were included in this study. Patients met DSM-IV-R criteria for schizophrenia and mean age was 41.78 years (SD = 7.98). Before start the study, all patients received antipsychotics more than 6 months and their aggressive behavior not improved (clinical evaluation). Data were collected from files. Treating psychiatrist started with valproate as adjunctive to antipsychotic treatment (mean dose 1373.91 mg/day, SD = 541.22). All patients were assessed at baseline and at the end of 8 weeks treatment period. The outcome measures was PANSS (Positive and Negative Syndrome Scale)-total score and CGI-severity (psychopathology) and PANSS-excited component (aggressive behavior). Results: All scores were improved: PANSS-T mean 94.30 (SD = 10.45) at baseline and 75.17 (SD = 12.97) endpoint (reduction with 21%), PANSS-EC mean 19.57 (SD = 2.51) at baseline and 14.04 (SD = 3.26) endpoint (reduction with 28.3%) and CGI-S mean 5.07 (SD = 0.73) at baseline and 3.87 (SD = 0.81) endpoint (reduction with 23%). Valproate was correlated with a greater decrease of aggressive behavior (PANSS-EC) compared with psychopathology (PANSS total and CGI-severity). There was no significant correlation between dose of valproate and violence offense index. Conclusions: We suggest that valproate as an adjunctive to antipsychotics therapy improved aggressive behavior on forensic inpatients with schizophrenia. The mechanism of action of valproate to aggression is unclear. Because most of the reported trials used valproate as adjunctive treatment, some of the effects possible depend on pharmacodynamic and pharmacokinetic interactions with antipsychotics. Further study is needed to support these results and to clarify the more precise role of valproate in aggressive behavior. Medication and nonpharmacologic measures should be instituted for reduce aggressive behavior. References [1] Swanson, J. W., 1994, Mental disorder, substance abuse, and community violence: an epidemiological approach. In Violence and Mental Disorder: Developments in Risk Assessment (eds J. Monahan & H. J. Steadman); pp. 101–136. Chicago, IL: University of Chicago Press. [2] Muscari M.E: What is the best pharmacotherapy for violent or aggressive behavior? In Medscape Psychiatry&Mental Health 2006 (http:// medscape.com). [3] Citrome L, Casey DE, Daniel DG, et al: Adjunctive divalproex and hostility among patients with schizophrenia receiving olanzapine or risperidone. Psychiatr Serv 2004; 55: 290–294.
P.3.e.008 Treatment adherence in schizophrenia using risperidone long-acting injectable: as early as possible, as long as possible A. Viala1 ° , V. Boulicot1 , A. Merlot1 , D. Pinede1 , M.N. Vacheron1 . 1 Centre Hospitalier Sainte-Anne, Secteur 13, Paris Cedex 14, France Introduction: Relapses and rehospitalisations, but also cognitive symptoms, social, familial and professional desinsertion, worsen the prognosis of patients with schizophrenia. Treatment with longacting antipsychotics, which encourage adherence, can avoid the risk of interruption of treatment, which is the main cause of relapse and rehospitalisation. This type of treatment, used as early
P.3.e.005 Effects of galantamine on cognitive deficits in schizophrenia patients H. Kim1 ° , K.J. Lee1 . 1 Inje University Ilsan Paik Hospital, Dept.of Psychiatry, Goyang, South-Korea Objectives: People with schizophrenia are characterized by a broad range of emotional, ideational, and cognitive impairments. A large body of evidence ascribes cognitive dysfunctions to a combination of neurochemical and neuropathological changes. Although dopamine has been regarded as the key neurotransmitter involved in the pathogenesis of symptoms of schizophrenia, several studies have established that the cholinergic neurotransmitter system, involving both nicotinic and muscarinic receptors, is important for the neuromodulation of cognitive processes in schizophrenia[1]. Most authors agree that cholinergic projections to the cortex and basal forebrain play an important role in compromised cognitive constructs in schizophrenia[2]. Therefore, drugs act on cholinergic pathways may improve cognitive dysfunctions in schizophrenia. The possible existence of cholinergic deficits in schizophrenia provides the rationale for examining the efficacy of cholinesterase inhibitor adjunctive therapy for the treatment of cognitive dysfunctions in patients with schizophreia. There is preliminary evidence that galantamine can improve cognitive functions and negative symptoms in schizophrenia. The primary purpose of this study was to evaluate the efficacy of galantamine in schizophrenia for the treatment of cognitive impairments Methods: 22 subjects with schizophrenia (according to DSM-IV) were included in this study. The patients had been medicated on atypical antipsychotics and stablized in their psychotic symptoms. The starting dose of galantamine was 8 mg daily, with the daily dose increasing at 2-week intervals to 16 mg. The patients was assessed with computerized neurocognitive function tests of digit span, continuous performance test, finger tapping test. The cognitive battery included measures of working memory, attention, vigilance, psychomotor speed. Mini-mental Status Examination (MMSE) and Scale for the Assessment of Negative Symptoms (SANS) were evaluated at baseline and at 8 week of galantamine treatment. Results: The average age of the 22 schizophrenia subjects was 42.5+/-3.5 years. 13 patients were male and 9 patients were female. There was no significant difference in mean digit span score 4.2+/−0.9 (forward), 3.2+/−0.8 (backward) at baseline and 4.4+/−1.0 (forward), 3.3+/−0.9 (backward) after 8 weeks of galantamine therapy (p > 0.05). Also there was no significant diffences in the mean finger tapping test score 33.2+/−8.3 (right), 30.4+/−7.9 (left) at baseline and 34.3+/−9.0 (right), 31.3+/−8.2 (left) after 8 weeks (p > 0.05). The MMSE score was 22.3+/−3.4 at baseline and 23.0+/−3.7 after 8 weeks (p > 0.05). There were no significant differences in working memory, motor speed and total scores of MMSE at baseline and after 8 weeks. There were significant improvements in continuous performance test of computerized neurocognitive
S515
function test including correct responses 127.4±3.5 (baseline) to 132.5±2.7 (after 8 weeks), omission errors 8.7±3.7 at baseline to 5.2±3.1 after 8 weeks, and reaction time 0.59±0.09 at baseline to 0.47±0.04 after 8 weeks. Conclusions: These results suggest that galantamine may have some effects on cognivie defect in patients with schizophrenia especially for aspects of selective attention. Positive allosteric modulatory properties may have contributed to the observed improvement in negative symptoms in schizophrenic patients. References [1] Schubert MH, Young KA, Hicks PB. Galantamine improves cognition in schizophrenic patients stabilized on risperidone. Biol psychiatry 2006; 60(6): 530–533. [2] Sharma T, Reed C, Aasen I, Kumari V. Cognitive effects of adjuvant 24-week rivastigmine treatment to antipsychotics in schizophrenia: a randomized, placebo-controlled, double-blind investigation. Schizophr Res 2006; 85(1−3): 73−83.
P.3.e.006 Nicotine effects on attention in schizophrenia: a simultaneous EEG-fMRI study A. Mobascher1 ° , T. Warbrick2 , J. Brinkmeyer3 , F. Musso3 , T. Stoecker2 , N.J. Shah2 , S. Vossel2 , G. Winterer4 . 1 University of Mainz, Department of Psychiatry, Mainz, Germany; 2 Research Center Juelich, Institute of Neurosciences and Medicine, Juelich, Germany; 3 University of Duesseldorf, Department of Psychiatry, Duesseldorf, Germany; 4 University of Cologne, Cologne Center for Genomics, Cologne, Germany Background: Schizophrenia is associated with cognitive deficits and alterations in task-induced brain activity in several cognitive domains such as attention and working memory. Nicotine dependence is more frequent in schizophrenic patients than in the general population [1]. According to the “self-medication hypothesis” patients with schizophrenia consume nicotine to counteract schizophrenia-associated cognitive deficits. However there is sparse literature on the effects of nicotine on task-induced brain activation in patients suffering from schizophrenia. It was the purpose of the present study to investigate the acute effects of nicotine on the attention network as revealed by EEG (electroencephalography) P300-informed fMRI (functional magnetic resonance imaging) in schizophrenic smokers compared to healthy smoking control subjects. Methods: We performed a randomized, double-blind, placebocontrolled cross-over nicotine (1 mg nasal spray) challenge with simultaneous EEG-fMRI recording. We investigated 16 smoking patients suffering from schizophrenia and 19 smoking controls (Fagerstr¨om test for nicotine dependence/FTND score >4) during a visual choice reaction time task similar to an oddball task. EEG data were analyzed using the software BrainVision Analyzer 2 (Brain Products, Germany); fMRI data were analyzed using the software package FSL (FMRIB’s Software Library, www.fmrib.ox.ac.uk/fsl). In addition to “conventional” fMRI analysis of task-related brain activity, single trial peak amplitudes of the EEG P300 event-related potential were included as regressors in the general linear model (GLM) analysis of the fMRI data [2]. Results: Only when applying the EEG P300-informed fMRI BOLD model in schizophrenic smokers we found higher clustercorrected brain activation (Z>2.3; p < 0.05) in the nicotine condition compared to placebo (nicotine > placebo). Activated regions comprised a fronto-parietal network that has been implicated in attention such as prefrontal areas and the anterior cingulate cortex.
S516
P.3.e. Psychotic disorders and antipsychotics − Others (clinical)
In contrast no significant nicotine effects compared to placebo on the fMRI BOLD (blood oxygen-level dependent) signal were observed in schizophrenic smokers in the conventional fMRI analysis (no EEG considered). In smoking controls neither model (P300informed or conventional) revealed significant nicotine effects. Conclusions: To our knowledge this is the first study addressing the effects of nicotine on task-induced brain activity in schizophrenic smokers that applied a simultaneous EEG-fMRI approach. Our data suggest that EEG-informed fMRI may be suited to study drug effects on cognitive processes. These effects may be subtle − like in the case of nicotine − and may not be captured when solely averaged task-induced fMRI BOLD activation without additional single trial information is considered. The sensitivity of EEG single trial amplitude-informed fMRI may be higher compared to conventional analyses of the fMRI BOLD signal. Moreover the EEG-informed analysis can emphasize certain aspects of taskinduced brain activity such as neuronal sub-processes that are reflected by P300 amplitude. In view of the relationship between P300 amplitude, cognitive performance and schizophrenia our data suggest that positive effects of nicotine on cognition (as measured by a nicotine-induced increase in the P300 amplitudeinformed fMRI BOLD signal) may be pronounced in patients with schizophrenia. This interpretation would be consistent with the self-medication hypothesis. References [1] Mobascher, A.; Winterer, G., 2008 The Molecular and Cellular Neurobiology of Nicotine Abuse in Schizophrenia. Pharmacopsychiatry 41 (Suppl. 1) S51–S59. [2] Warbrick, T.; Mobascher, A.; Brinkmeyer, J.; Musso, F.; Richter, N.; Stoecker, T.; Fink, G.R.; Shah, N.J.; Winterer, G., 2009 Single-trial P3 amplitude and latency informed event-related fMRI models yield different BOLD response patterns to a target detection task. NeuroImage 47, 1532–1544.
P.3.e.007 Use of valproate for aggressive behaviour in forensic inpatients with schizophrenia A. Popescu1 , M.D. Mosescu1 , M. Bragau1 ° , A.G. Andries1 . 1 Psychiatry Hospital Sapoca, Acute Department, Buzau, Romania Background: Aggression encompasses physical acts against others, oneself (self-mutilation, suicidal gestures or acts), or objects, as well as verbal assaults. Although most patients with schizophrenia are not aggressive, epidemiologic evidence shows an increased risk for violence in this group when compared with the general population [1]. There are many possible causes for aggressive behavior: hallucinations, delusions, poor impulse control, personality characteristics, unstable home or hospital situation. The patients may become aggressive for different reasons at different times. Aggressive behavior in patients with schizophrenia still remains a challenge, especially in forensic unity. Medications are frequently used in the management of aggression and longterm treatment is directed to reduce the frequency and intensity of episodes [2]. Additional adjunctive medications may be necessary when standard therapeutic approaches are ineffective. Mood stabilizers, used initially in bipolar disorders, are currently used also for schizophrenia as adjunctive treatment to antipsychotics and, especially valproate, for aggressive behavior [3]. There are a few small studies about using valproate for aggressive behavior on forensic patients with schizophrenia. Objective: To analyze the efficacy of valproate as adjunctive therapy to antipsychotics on forensic inpatients with schizophrenia for aggressive behavior.
Methods: The study was observational and has been achieved in forensic unit of Psychiatry and Safety Measures Sapoca, Buzau, Romania between May and September 2010. The design of the study was approved by Ethical Board of the hospital. 23 male inpatients were included in this study. Patients met DSM-IV-R criteria for schizophrenia and mean age was 41.78 years (SD = 7.98). Before start the study, all patients received antipsychotics more than 6 months and their aggressive behavior not improved (clinical evaluation). Data were collected from files. Treating psychiatrist started with valproate as adjunctive to antipsychotic treatment (mean dose 1373.91 mg/day, SD = 541.22). All patients were assessed at baseline and at the end of 8 weeks treatment period. The outcome measures was PANSS (Positive and Negative Syndrome Scale)-total score and CGI-severity (psychopathology) and PANSS-excited component (aggressive behavior). Results: All scores were improved: PANSS-T mean 94.30 (SD = 10.45) at baseline and 75.17 (SD = 12.97) endpoint (reduction with 21%), PANSS-EC mean 19.57 (SD = 2.51) at baseline and 14.04 (SD = 3.26) endpoint (reduction with 28.3%) and CGI-S mean 5.07 (SD = 0.73) at baseline and 3.87 (SD = 0.81) endpoint (reduction with 23%). Valproate was correlated with a greater decrease of aggressive behavior (PANSS-EC) compared with psychopathology (PANSS total and CGI-severity). There was no significant correlation between dose of valproate and violence offense index. Conclusions: We suggest that valproate as an adjunctive to antipsychotics therapy improved aggressive behavior on forensic inpatients with schizophrenia. The mechanism of action of valproate to aggression is unclear. Because most of the reported trials used valproate as adjunctive treatment, some of the effects possible depend on pharmacodynamic and pharmacokinetic interactions with antipsychotics. Further study is needed to support these results and to clarify the more precise role of valproate in aggressive behavior. Medication and nonpharmacologic measures should be instituted for reduce aggressive behavior. References [1] Swanson, J. W., 1994, Mental disorder, substance abuse, and community violence: an epidemiological approach. In Violence and Mental Disorder: Developments in Risk Assessment (eds J. Monahan & H. J. Steadman); pp. 101–136. Chicago, IL: University of Chicago Press. [2] Muscari M.E: What is the best pharmacotherapy for violent or aggressive behavior? In Medscape Psychiatry&Mental Health 2006 (http:// medscape.com). [3] Citrome L, Casey DE, Daniel DG, et al: Adjunctive divalproex and hostility among patients with schizophrenia receiving olanzapine or risperidone. Psychiatr Serv 2004; 55: 290–294.
P.3.e.008 Treatment adherence in schizophrenia using risperidone long-acting injectable: as early as possible, as long as possible A. Viala1 ° , V. Boulicot1 , A. Merlot1 , D. Pinede1 , M.N. Vacheron1 . 1 Centre Hospitalier Sainte-Anne, Secteur 13, Paris Cedex 14, France Introduction: Relapses and rehospitalisations, but also cognitive symptoms, social, familial and professional desinsertion, worsen the prognosis of patients with schizophrenia. Treatment with longacting antipsychotics, which encourage adherence, can avoid the risk of interruption of treatment, which is the main cause of relapse and rehospitalisation. This type of treatment, used as early