Pub Date : 2001-09-01DOI: 10.1017/S146114570100253X
Robert C. Smith, Robert C. Smith, M. Infante, Abhay Singh, A. Khandat
Neurocognitive deficits are an enduring characteristic of schizophrenia, and remain prominent in patients whose positive symptoms have decreased after treatment with typical neuroleptics. Recent research has reported that olanzapine improves cognitive functioning in relapsing schizophrenia followed in an outpatient setting. Whether olanzapine will have an effect on improving cognitive function in chronic schizophrenics who have been hospitalized for long periods of time, and have shown a poor response to other conventional and atypical neuroleptics, has not been established. This study investigated cognitive function in chronic medication refractory schizophrenics who were treated with olanzapine or haloperidol in a double-blind study for 8 wk, and followed in an open olanzapine study for several additional months. Patients were evaluated with psychopathology rating scales and a battery of neuropsychological tests at baseline, end of double-blind and end of open-label phases of the study. At the end of the double-blind phase there were no significant differences between olanzapine and haloperidol, except for a trend for improvement on the Wisconsin Card Sort Test on olanzapine, which was significant at traditional but not corrected significance levels. After an additional 3 months of treatment with olanzapine doses of 20-40 mg/d, our statistical analysis showed significant improvement on overall neuropsychological test performance and specific cognitive tasks assessing verbal memory. However, these open-label results are difficult to interpret definitively because of the lack of a comparison drug group and the olanzapine dose escalation over time. Neurocognitive changes were not correlated with changes in psychopathology as assessed by PANSS or SANS scores.
{"title":"The effects of olanzapine on neurocognitive functioning in medication-refractory schizophrenia.","authors":"Robert C. Smith, Robert C. Smith, M. Infante, Abhay Singh, A. Khandat","doi":"10.1017/S146114570100253X","DOIUrl":"https://doi.org/10.1017/S146114570100253X","url":null,"abstract":"Neurocognitive deficits are an enduring characteristic of schizophrenia, and remain prominent in patients whose positive symptoms have decreased after treatment with typical neuroleptics. Recent research has reported that olanzapine improves cognitive functioning in relapsing schizophrenia followed in an outpatient setting. Whether olanzapine will have an effect on improving cognitive function in chronic schizophrenics who have been hospitalized for long periods of time, and have shown a poor response to other conventional and atypical neuroleptics, has not been established. This study investigated cognitive function in chronic medication refractory schizophrenics who were treated with olanzapine or haloperidol in a double-blind study for 8 wk, and followed in an open olanzapine study for several additional months. Patients were evaluated with psychopathology rating scales and a battery of neuropsychological tests at baseline, end of double-blind and end of open-label phases of the study. At the end of the double-blind phase there were no significant differences between olanzapine and haloperidol, except for a trend for improvement on the Wisconsin Card Sort Test on olanzapine, which was significant at traditional but not corrected significance levels. After an additional 3 months of treatment with olanzapine doses of 20-40 mg/d, our statistical analysis showed significant improvement on overall neuropsychological test performance and specific cognitive tasks assessing verbal memory. However, these open-label results are difficult to interpret definitively because of the lack of a comparison drug group and the olanzapine dose escalation over time. Neurocognitive changes were not correlated with changes in psychopathology as assessed by PANSS or SANS scores.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"11 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2001-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132207048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-09-01DOI: 10.1017/S1461145701002541
Kathryn A. Ellis, Pradeep J. Nathan
Experimental studies conducted primarily on non-human primates have begun to address the anatomical and neurochemical correlates of working memory. There is an associated growing body of experimental literature investigating whether modulating key neurotransmitters can facilitate working memory in humans. This paper reviews evidence that acute modulation of dopamine in particular, but also noradrenaline, acetylcholine and serotonin may influence working-memory performance in humans. Differences in neurochemical specificity with regard to stages of working memory, type of working memory (spatial or non-spatial) and cortical effects are also discussed. This evidence has contributed to neuropharmacological understanding of working memory in humans. The important therapeutic consequences of a better understanding of facilitation of working memory is discussed in reference to schizophrenia, Parkinson's disease and Alzheimer's disease.
{"title":"The pharmacology of human working memory.","authors":"Kathryn A. Ellis, Pradeep J. Nathan","doi":"10.1017/S1461145701002541","DOIUrl":"https://doi.org/10.1017/S1461145701002541","url":null,"abstract":"Experimental studies conducted primarily on non-human primates have begun to address the anatomical and neurochemical correlates of working memory. There is an associated growing body of experimental literature investigating whether modulating key neurotransmitters can facilitate working memory in humans. This paper reviews evidence that acute modulation of dopamine in particular, but also noradrenaline, acetylcholine and serotonin may influence working-memory performance in humans. Differences in neurochemical specificity with regard to stages of working memory, type of working memory (spatial or non-spatial) and cortical effects are also discussed. This evidence has contributed to neuropharmacological understanding of working memory in humans. The important therapeutic consequences of a better understanding of facilitation of working memory is discussed in reference to schizophrenia, Parkinson's disease and Alzheimer's disease.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"74 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2001-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122150069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-09-01DOI: 10.1017/S1461145701002486
P. R. Kritzinger, G. Jordaan
In view of reports in the literature that catatonia responds well to benzodiazepines, and the possible association between catatonia and seizure disorders, an open prospective study was conducted to explore the possibility that catatonia may be successfully treated with carbamazepine. Patients meeting DSM-IV criteria for catatonia were challenged with lorazepam IMI and their response assessed. Non-responders, partial responders and patients who had a recurrence of symptoms were put on a trial of carbamazepine and their response assessed. Nine patients were assessed at our unit. Six of the 9 had a complete, but transient response to lorazepam. All of the patients were given a trial of carbamazepine: 4 had a complete resolution of catatonic symptoms, 1 had a partial resolution and 4 patients did not show a significant improvement. Carbamazepine seems to be an effective treatment, both in the acute phase, and as maintenance in a subgroup of retarded catatonic patients.
{"title":"Catatonia: an open prospective series with carbamazepine.","authors":"P. R. Kritzinger, G. Jordaan","doi":"10.1017/S1461145701002486","DOIUrl":"https://doi.org/10.1017/S1461145701002486","url":null,"abstract":"In view of reports in the literature that catatonia responds well to benzodiazepines, and the possible association between catatonia and seizure disorders, an open prospective study was conducted to explore the possibility that catatonia may be successfully treated with carbamazepine. Patients meeting DSM-IV criteria for catatonia were challenged with lorazepam IMI and their response assessed. Non-responders, partial responders and patients who had a recurrence of symptoms were put on a trial of carbamazepine and their response assessed. Nine patients were assessed at our unit. Six of the 9 had a complete, but transient response to lorazepam. All of the patients were given a trial of carbamazepine: 4 had a complete resolution of catatonic symptoms, 1 had a partial resolution and 4 patients did not show a significant improvement. Carbamazepine seems to be an effective treatment, both in the acute phase, and as maintenance in a subgroup of retarded catatonic patients.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"20 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2001-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129302018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-09-01DOI: 10.1017/S1461145701002474
H. Matsunaga, N. Kiriike, T. Matsui, Y. Iwasaki, D. Stein
Taijin kyofusho (TKS) has been categorized as a "culture-bound" illness that is unique to the East, although an alternative view holds that some TKS patients are best conceptualized as having a form of social anxiety disorder (SAD). However, pharmacotherapeutic interventions for TKS have not yet been rigorously investigated. A review was undertaken of 48 TKS patients initially treated with serotonin reuptake inhibitors (SRIs) in an outpatient setting of a Japanese hospital. Psychiatric diagnoses were determined according to DSM-IV, and a set of TKS diagnostic criteria based on a modification of DSM-IV SAD criteria. In addition, response to SRIs (clomipramine and fluvoxamine) was evaluated retrospectively using the Clinical Global Impressions (CGI) scale. All 48 patients met SAD-based TKS diagnostic criteria. In the pretreatment assessment, DSM-IV Axis I diagnoses included SAD (38%), major depressive episode (27%), and delusional disorder somatic type (15%). Sixteen (48%) of 33 patients treated with clomipramine or fluvoxamine for at least 6 months were categorized as responders (CGI = 1 or 2). Compared to responders, non-responders were significantly less likely to have pretreatment major depression, and significantly more likely to have comorbid cluster A personality disorders and to have received augmentation with antipsychotic drugs. Although TKS may be a heterogeneous condition with various comorbidities, patients invariably fulfilled diagnostic criteria for TKS based on SAD criteria. SRIs may be effective for a substantial number of TKS patients. Prospective controlled trials are necessary to confirm these findings and to delineate the pharmacotherapeutic profile of TKS.
{"title":"Taijin kyofusho: a form of social anxiety disorder that responds to serotonin reuptake inhibitors?","authors":"H. Matsunaga, N. Kiriike, T. Matsui, Y. Iwasaki, D. Stein","doi":"10.1017/S1461145701002474","DOIUrl":"https://doi.org/10.1017/S1461145701002474","url":null,"abstract":"Taijin kyofusho (TKS) has been categorized as a \"culture-bound\" illness that is unique to the East, although an alternative view holds that some TKS patients are best conceptualized as having a form of social anxiety disorder (SAD). However, pharmacotherapeutic interventions for TKS have not yet been rigorously investigated. A review was undertaken of 48 TKS patients initially treated with serotonin reuptake inhibitors (SRIs) in an outpatient setting of a Japanese hospital. Psychiatric diagnoses were determined according to DSM-IV, and a set of TKS diagnostic criteria based on a modification of DSM-IV SAD criteria. In addition, response to SRIs (clomipramine and fluvoxamine) was evaluated retrospectively using the Clinical Global Impressions (CGI) scale. All 48 patients met SAD-based TKS diagnostic criteria. In the pretreatment assessment, DSM-IV Axis I diagnoses included SAD (38%), major depressive episode (27%), and delusional disorder somatic type (15%). Sixteen (48%) of 33 patients treated with clomipramine or fluvoxamine for at least 6 months were categorized as responders (CGI = 1 or 2). Compared to responders, non-responders were significantly less likely to have pretreatment major depression, and significantly more likely to have comorbid cluster A personality disorders and to have received augmentation with antipsychotic drugs. Although TKS may be a heterogeneous condition with various comorbidities, patients invariably fulfilled diagnostic criteria for TKS based on SAD criteria. SRIs may be effective for a substantial number of TKS patients. Prospective controlled trials are necessary to confirm these findings and to delineate the pharmacotherapeutic profile of TKS.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"7 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2001-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125801424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-09-01DOI: 10.1017/S1461145701002449
I. Massat, D. Souery, J. Del-Favero, L. Oruč, M. Jakovljevič, V. Folnegovic, R. Adolfsson, R. Kaneva, G. Papadimitriou, D. Dikeos, E. Jazin, V. Milanova, C. van Broeckhoven, J. Mendlewicz
Available data on gamma amino butyric acid (GABA) support the hypothesis that a dysfunction in the brain GABAergic system activity contributes to vulnerability to affective disorders (AD), including bipolar disorder (BPAD) and unipolar disorder (UPAD). The localization of the alpha3 subunit GABA receptor (GABRA3) gene in Xq28, a region of interest for BPAD suggests that GABRA3 may be a relevant candidate gene. In the present study, we tested the genetic contribution of the GABRA3 dinucleotide polymorphism in a European multicentre UPAD case-control sample [UPAD (n = 106), controls (n = 212)]. Our negative results suggest that GABRA3 does not confer susceptibility nor is it in linkage disequilibrium with another close gene involved in the genetic aetiology of UPAD.
{"title":"Lack of association between GABRA3 and unipolar affective disorder: a multicentre study.","authors":"I. Massat, D. Souery, J. Del-Favero, L. Oruč, M. Jakovljevič, V. Folnegovic, R. Adolfsson, R. Kaneva, G. Papadimitriou, D. Dikeos, E. Jazin, V. Milanova, C. van Broeckhoven, J. Mendlewicz","doi":"10.1017/S1461145701002449","DOIUrl":"https://doi.org/10.1017/S1461145701002449","url":null,"abstract":"Available data on gamma amino butyric acid (GABA) support the hypothesis that a dysfunction in the brain GABAergic system activity contributes to vulnerability to affective disorders (AD), including bipolar disorder (BPAD) and unipolar disorder (UPAD). The localization of the alpha3 subunit GABA receptor (GABRA3) gene in Xq28, a region of interest for BPAD suggests that GABRA3 may be a relevant candidate gene. In the present study, we tested the genetic contribution of the GABRA3 dinucleotide polymorphism in a European multicentre UPAD case-control sample [UPAD (n = 106), controls (n = 212)]. Our negative results suggest that GABRA3 does not confer susceptibility nor is it in linkage disequilibrium with another close gene involved in the genetic aetiology of UPAD.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"7 2 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2001-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125972945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-06-01DOI: 10.1017/S1461145701002413
Laurence L. Greenhill, James M. Perel, G. Rudolph, Bruce Feldman, Susan Curran, Joaquim Puig-Antich, Richard A. Gardner
Following a 0.9 mg/kg methylphenidate loading dose, serial plasma level determinations, self-scored mood ratings, and measures of motor persistence were gathered on eight previously unmedicated boys with attention deficit disorder with hyperactivity (ADHD) during a 9-h period. The measures were repeated using the same loading dose after 6 months of maintenance treatment with methylphenidate (1.3 mg/kg x d). Kinetic-dynamic modelling suggests inverse correlative relationships between motor performance errors and plasma levels. Pharmacokinetic parameters did not change between acute and maintenance drug treatment phases, and there was no evidence of long-term tolerance.
在给予0.9 mg/kg哌醋甲酯负荷剂量后，在9小时内收集了8名先前未服用药物的多动症(ADHD)男孩的连续血浆水平测定、自我评分情绪评分和运动持久性测量。在用哌甲酯(1.3 mg/kg x d)维持治疗6个月后，使用相同的负荷剂量重复测量。动力学模型显示运动表现误差与血浆水平呈负相关关系。药代动力学参数在急性和维持药物治疗阶段之间没有变化，并且没有证据表明长期耐受性。
{"title":"Correlations between motor persistence and plasma levels in methylphenidate-treated boys with ADHD.","authors":"Laurence L. Greenhill, James M. Perel, G. Rudolph, Bruce Feldman, Susan Curran, Joaquim Puig-Antich, Richard A. Gardner","doi":"10.1017/S1461145701002413","DOIUrl":"https://doi.org/10.1017/S1461145701002413","url":null,"abstract":"Following a 0.9 mg/kg methylphenidate loading dose, serial plasma level determinations, self-scored mood ratings, and measures of motor persistence were gathered on eight previously unmedicated boys with attention deficit disorder with hyperactivity (ADHD) during a 9-h period. The measures were repeated using the same loading dose after 6 months of maintenance treatment with methylphenidate (1.3 mg/kg x d). Kinetic-dynamic modelling suggests inverse correlative relationships between motor performance errors and plasma levels. Pharmacokinetic parameters did not change between acute and maintenance drug treatment phases, and there was no evidence of long-term tolerance.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"72 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2001-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127358653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-06-01DOI: 10.1017/S1461145701002358
B. Birmaher, Pedro Heydl
The objective was to review the literature on the biological correlates of major depressive disorder (MDD) in children and adolescents. A computerized search for articles published during the last 20 years was done and selected studies presented. To date, examination of growth hormone (GH), prolactin, and cortisol levels after pharmacological stimulation have shown abnormalities in the secretion of these hormones (e.g. blunted GH secretion after the administration of growth hormone releasing hormone). Identical results have been found in never-depressed children at high risk to develop MDD due to high family loading for MDD suggesting that alteration in certain hormonal systems may be trait markers for MDD. Other biological studies (e.g. the hypothalamic--pituitary axis, sleep electroencephalogram) have yielded more inconsistent results with subjects with melancholic symptoms, severe depressions, and older age showing some abnormalities similar to the ones reported in adults with MDD. Factors such age, sex, maturation, psychiatric family history and exposure to stress need to be considered since they also affect the same biological systems associated with the aetiology of MDD. Considerable biological research has been done in youth with MDD. Further research is needed to investigate whether these markers predict the development of new episodes of MDD, recurrences, and treatment response. Also, these and other studies using more sophisticated methods (e.g. functional MRI) aimed at elucidating the interrelationship between biological and other risk factors are needed.
{"title":"Biological studies in depressed children and adolescents.","authors":"B. Birmaher, Pedro Heydl","doi":"10.1017/S1461145701002358","DOIUrl":"https://doi.org/10.1017/S1461145701002358","url":null,"abstract":"The objective was to review the literature on the biological correlates of major depressive disorder (MDD) in children and adolescents. A computerized search for articles published during the last 20 years was done and selected studies presented. To date, examination of growth hormone (GH), prolactin, and cortisol levels after pharmacological stimulation have shown abnormalities in the secretion of these hormones (e.g. blunted GH secretion after the administration of growth hormone releasing hormone). Identical results have been found in never-depressed children at high risk to develop MDD due to high family loading for MDD suggesting that alteration in certain hormonal systems may be trait markers for MDD. Other biological studies (e.g. the hypothalamic--pituitary axis, sleep electroencephalogram) have yielded more inconsistent results with subjects with melancholic symptoms, severe depressions, and older age showing some abnormalities similar to the ones reported in adults with MDD. Factors such age, sex, maturation, psychiatric family history and exposure to stress need to be considered since they also affect the same biological systems associated with the aetiology of MDD. Considerable biological research has been done in youth with MDD. Further research is needed to investigate whether these markers predict the development of new episodes of MDD, recurrences, and treatment response. Also, these and other studies using more sophisticated methods (e.g. functional MRI) aimed at elucidating the interrelationship between biological and other risk factors are needed.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2001-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128034039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-06-01DOI: 10.1017/S1461145701002309
R. Lorenzo, Grazia Tondelli, Susanna Genedani
New atypical antipsychotics have opened a new era in the treatment of schizophrenia owing to their effectiveness both on positive, but especially negative, symptoms, without extrapyramidal side-effects (Tandon et al., 1999). The archetypal atypical antipsychotic is clozapine, whose main side-effect is agranulocytosis. Recently, other new atypical antipsychotics have been developed, such as olanzapine (Stephenson and Pilowsky, 1999), which do not produce any adverse haematological effects (Beasley et al., 1997). Clozapine and olanzapine share lower D2 and D3 receptor affinity in the basal ganglia and nigrostriatal system, and higher affinity to muscarinic (M) and histaminergic (H) receptors than haloperidol. Moreover, clozapine has higher affinity to adrenergic (α1 and α2) receptors, while olanzapine has higher affinity to D2, D3, D4 and serotonergic (5-HT-2A) receptors (ratio 5-HT-2A/D2 > 2) (Coward, 1992). The pharmacological profile can explain the efficacy of these drugs not only on the positive, but also especially on the negative symptoms, representing the originality of new antipsychotic treatment. The improvement of primary negative symptoms (Crow, 1980) and the absence of secondary symptoms (produced by extrapyramidal side-effects) result in an increased compliance (Marder, 1998) and improvement of cognitive functions (insight capacity, self-awareness, judgement) (Meyer-Lindenberg et al., 1997). The aim of our study was to evaluate the effectiveness of clozapine and olanzapine in the treatment of schizophrenic patients in our psychiatric department. This is constituted by hospital wards connected to community services (outpatient care, semi-residential and residential centres for rehabilitative social programmes).
{"title":"Effectiveness of clozapine and olanzapine: a comparison in severe, psychotically ill patients.","authors":"R. Lorenzo, Grazia Tondelli, Susanna Genedani","doi":"10.1017/S1461145701002309","DOIUrl":"https://doi.org/10.1017/S1461145701002309","url":null,"abstract":"New atypical antipsychotics have opened a new era in the treatment of schizophrenia owing to their effectiveness both on positive, but especially negative, symptoms, without extrapyramidal side-effects (Tandon et al., 1999). The archetypal atypical antipsychotic is clozapine, whose main side-effect is agranulocytosis. Recently, other new atypical antipsychotics have been developed, such as olanzapine (Stephenson and Pilowsky, 1999), which do not produce any adverse haematological effects (Beasley et al., 1997). Clozapine and olanzapine share lower D2 and D3 receptor affinity in the basal ganglia and nigrostriatal system, and higher affinity to muscarinic (M) and histaminergic (H) receptors than haloperidol. Moreover, clozapine has higher affinity to adrenergic (α1 and α2) receptors, while olanzapine has higher affinity to D2, D3, D4 and serotonergic (5-HT-2A) receptors (ratio 5-HT-2A/D2 > 2) (Coward, 1992). The pharmacological profile can explain the efficacy of these drugs not only on the positive, but also especially on the negative symptoms, representing the originality of new antipsychotic treatment. The improvement of primary negative symptoms (Crow, 1980) and the absence of secondary symptoms (produced by extrapyramidal side-effects) result in an increased compliance (Marder, 1998) and improvement of cognitive functions (insight capacity, self-awareness, judgement) (Meyer-Lindenberg et al., 1997).\u0000\u0000The aim of our study was to evaluate the effectiveness of clozapine and olanzapine in the treatment of schizophrenic patients in our psychiatric department. This is constituted by hospital wards connected to community services (outpatient care, semi-residential and residential centres for rehabilitative social programmes).","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"18 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2001-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134183312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-06-01DOI: 10.1017/S1461145701002322
Arif Khan, Shirin R F Khan, Robyn M. Leventhal, W. Brown
The assumption that depressed patients who are assigned to placebo in antidepressant clinical trials are exposed to substantial morbidity and mortality has not been based on research data. Because of worldwide concern about placebo use and the implications of our earlier findings of no increased suicide risk in placebo-treated patients, we conducted a replication study in a new patient sample. We assessed suicide risk and symptom reduction among placebo-treated patients participating in antidepressant clinical trials for two recently approved antidepressants, venlafaxine ER and citalopram, which were unavailable during our previous study. Among 23,201 participant patients, 32 committed suicide and 172 attempted suicide. Rates of suicide and attempted suicide did not differ significantly among the placebo- and drug-treated groups. Based on patient exposure years, annual rates of suicide and attempted suicide were 0.5 and 6.7% with placebo, 0.9% with active comparator (rates for attempted suicide are unavailable), and 0.6 and 6.3% with investigational antidepressants. Symptom reduction was 47.9% with investigational drugs (n = 1172), 47.5% with active comparators (n = 161), and 35.5% with placebo (n = 606). These data may inform discussions about the use of placebo in antidepressant clinical trials.
{"title":"Symptom reduction and suicide risk in patients treated with placebo in antidepressant clinical trials: a replication analysis of the Food and Drug Administration Database.","authors":"Arif Khan, Shirin R F Khan, Robyn M. Leventhal, W. Brown","doi":"10.1017/S1461145701002322","DOIUrl":"https://doi.org/10.1017/S1461145701002322","url":null,"abstract":"The assumption that depressed patients who are assigned to placebo in antidepressant clinical trials are exposed to substantial morbidity and mortality has not been based on research data. Because of worldwide concern about placebo use and the implications of our earlier findings of no increased suicide risk in placebo-treated patients, we conducted a replication study in a new patient sample. We assessed suicide risk and symptom reduction among placebo-treated patients participating in antidepressant clinical trials for two recently approved antidepressants, venlafaxine ER and citalopram, which were unavailable during our previous study. Among 23,201 participant patients, 32 committed suicide and 172 attempted suicide. Rates of suicide and attempted suicide did not differ significantly among the placebo- and drug-treated groups. Based on patient exposure years, annual rates of suicide and attempted suicide were 0.5 and 6.7% with placebo, 0.9% with active comparator (rates for attempted suicide are unavailable), and 0.6 and 6.3% with investigational antidepressants. Symptom reduction was 47.9% with investigational drugs (n = 1172), 47.5% with active comparators (n = 161), and 35.5% with placebo (n = 606). These data may inform discussions about the use of placebo in antidepressant clinical trials.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"23 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2001-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122643808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-06-01DOI: 10.1017/S1461145701002292
C. Stough, Jodi Clarke, J. Lloyd, P. Nathan
Ginkgo biloba extract (EGb) from the world's oldest living tree has been reputed to ameliorate cognitive decline in the elderly and slow cognitive deterioration in patients with dementia of the Alzheimer's type. EGb remains as one of the most popular plant extracts to alleviate symptoms associated with a range of cognitive disorders such as Alzheimer's disease, vascular dementia and age-related amnesic conditions. EGb is known to contain a range of chemically active components that have antagonistic effects on platelet-activating factor, free-radical scavenging activity and direct effects on the cholinergic neurotransmitter system. Recently there has been much speculation, that EGb may act as a 'smart drug' or nootropic agent in the healthy young to improve intelligence. We conducted a 30-d randomized, double-blind, placebo-controlled clinical trial in which 61 participants were administered a battery of validated neuropsychological tests before and after treatment. Statistical analysis indicated significant improvements in speed of information processing working memory and executive processing attributable to the EGb.
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