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N. P. V. Nair - One of the best experts on this subject based on the ideXlab platform.
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levomepromazine versus chlorpromazine in treatment resistant Schizophrenia a double blind randomized trial
Journal of Psychiatry & Neuroscience, 2006Co-Authors: J. X. Thavundayil, Lawrence Annable, Ng Ying Kin Nm, N. P. V. Nair, A Gabriel, G. SchwartzAbstract:Objective We compared the effect of levomepromazine (LMP) with chlorpromazine (CPZ) in Treatment-Resistant Schizophrenia (TRS).
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Levomepromazine receptor binding profile in human brain—implications for treatment—resistant Schizophrenia
Acta Psychiatrica Scandinavica, 1993Co-Authors: N. P. V. Nair, D. Cecyre, Rémi QuirionAbstract:: The receptor binding profile of levomepromazine (LMP) in human brain was compared with that of clozapine (CLOZ) and chlorpromazine (CPZ). LMP showed significantly greater binding affinity for both alpha-1 and serotonin-2 binding sites than either CLOZ or CPZ, and significantly greater binding to alpha-2 sites than CPZ. A potent pharmacological effect at these receptor sites may explain the beneficial effect of LMP on psychotic symptoms and akathisia in Treatment-Resistant Schizophrenia recently described in 2 open studies. LMP requires further appraisal as a potentially useful neuroleptic in the management of Treatment-Resistant Schizophrenia.
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levomepromazine receptor binding profile in human brain implications for treatment resistant Schizophrenia
Acta Psychiatrica Scandinavica, 1993Co-Authors: N. P. V. Nair, D. Cecyre, Rémi QuirionAbstract:: The receptor binding profile of levomepromazine (LMP) in human brain was compared with that of clozapine (CLOZ) and chlorpromazine (CPZ). LMP showed significantly greater binding affinity for both alpha-1 and serotonin-2 binding sites than either CLOZ or CPZ, and significantly greater binding to alpha-2 sites than CPZ. A potent pharmacological effect at these receptor sites may explain the beneficial effect of LMP on psychotic symptoms and akathisia in Treatment-Resistant Schizophrenia recently described in 2 open studies. LMP requires further appraisal as a potentially useful neuroleptic in the management of Treatment-Resistant Schizophrenia.
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is levomepromazine a useful drug in treatment resistant Schizophrenia
Acta Psychiatrica Scandinavica, 1992Co-Authors: N. P. V. NairAbstract:: Levomepromazine (LMP) unexpectedly improved 16 of 23 chronic Treatment-Resistant schizophrenic patients who were hospitalized in most cases for at least 2 years and who manifested positive symptoms, irritability and, in many cases, restlessness, hostility, uncooperativeness, poor concentration and aggressive behavior. Improvement led to discharge in 7 (6 to a foster home), placement on a waiting list for a foster home in 4 and improved behavior and autonomy in 5 patients. Five subjects developed seizures and 1 agranulocytosis. Whether improvement with LMP is caused by unique antischizophrenic properties or by diminished liability to induce side effects such as akathisia, a formal controlled study of LMP in Treatment-Resistant Schizophrenia is merited.
Rémi Quirion - One of the best experts on this subject based on the ideXlab platform.
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Levomepromazine receptor binding profile in human brain—implications for treatment—resistant Schizophrenia
Acta Psychiatrica Scandinavica, 1993Co-Authors: N. P. V. Nair, D. Cecyre, Rémi QuirionAbstract:: The receptor binding profile of levomepromazine (LMP) in human brain was compared with that of clozapine (CLOZ) and chlorpromazine (CPZ). LMP showed significantly greater binding affinity for both alpha-1 and serotonin-2 binding sites than either CLOZ or CPZ, and significantly greater binding to alpha-2 sites than CPZ. A potent pharmacological effect at these receptor sites may explain the beneficial effect of LMP on psychotic symptoms and akathisia in Treatment-Resistant Schizophrenia recently described in 2 open studies. LMP requires further appraisal as a potentially useful neuroleptic in the management of Treatment-Resistant Schizophrenia.
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levomepromazine receptor binding profile in human brain implications for treatment resistant Schizophrenia
Acta Psychiatrica Scandinavica, 1993Co-Authors: N. P. V. Nair, D. Cecyre, Rémi QuirionAbstract:: The receptor binding profile of levomepromazine (LMP) in human brain was compared with that of clozapine (CLOZ) and chlorpromazine (CPZ). LMP showed significantly greater binding affinity for both alpha-1 and serotonin-2 binding sites than either CLOZ or CPZ, and significantly greater binding to alpha-2 sites than CPZ. A potent pharmacological effect at these receptor sites may explain the beneficial effect of LMP on psychotic symptoms and akathisia in Treatment-Resistant Schizophrenia recently described in 2 open studies. LMP requires further appraisal as a potentially useful neuroleptic in the management of Treatment-Resistant Schizophrenia.
Masaomi Iyo - One of the best experts on this subject based on the ideXlab platform.
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Recent discussions on dopamine supersensitivity psychosis: Eight points to consider when diagnosing Treatment-Resistant Schizophrenia
Current Neuropharmacology, 2021Co-Authors: Nobuhisa Kanahara, Hiroshi Kimura, Yasunori Oda, Fumiaki Ito, Masaomi IyoAbstract:: Dopamine supersensitivity psychosis is a clinical concept characterized by an unstable psychotic state and tardive dyskinesia in Schizophrenia patients at the chronic stage. This state is thought to be induced by a compensatory upregulation of dopamine D2 receptors, which is provoked by long-term and/or high-dose medications. Recent clinical data suggest that patients who responded well to medication but later exhibit dopamine supersensitivity develop tolerance to antipsychotics’ effects and eventually transit to Treatment-Resistant Schizophrenia, indicating that dopamine supersensitivity could be an etiology contributing to Treatment-Resistant Schizophrenia. However, any clinicians and researchers consider dopamine supersensitivity psychosis a minor phenomenon during the clinical course and do not make much of it. This opinion is often based on numerous clinical data which indicating that dopamine supersensitivity psychosis is a relatively rare event. This review examines the data dealing with dopamine supersensitivity with the five themes of frequency, severity, withdrawal studies, switching to aripiprazole, and tardive dyskinesia. These themes’ effects on discussions of the clinical meaning of dopamine supersensitivity psychosis are then reviewed. The present review will help clinicians to speculate as to the background of severe psychopathology in a given patient; to make diagnoses of Treatment-Resistant Schizophrenia and dopamine supersensitivity psychosis; and to plan antipsychotic medication regimens with the goal of achieving better long-term prognosis.
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Efficacy and Safety of Yokukansan in Treatment-Resistant Schizophrenia: A Randomized, Multicenter, Double-Blind, Placebo-Controlled Trial
Evidence-based complementary and alternative medicine : eCAM, 2015Co-Authors: Tsuyoshi Miyaoka, Rei Wake, Sadayuki Hashioka, Motohide Furuya, Jun Horiguchi, Masaya Thoyama, Kenta Murotani, Norio Mori, Yoshio Minabe, Masaomi IyoAbstract:Objectives. We aimed at evaluating both the efficacy and safety of TJ-54 (Yokukansan) in patients with Treatment-Resistant Schizophrenia. This randomized, multicenter, double-blind, placebo-controlled study was conducted. Methods. One hundred and twenty antipsychotic-treated inpatients were included. Patients were randomized to adjuvant treatment with TJ-54 or placebo. During a 4-week follow-up, psychopathology was assessed using the Positive and Negative Syndrome Scale (PANSS). Results. TJ-54 showed a tendency of being superior to placebo in reduction total, positive, and general PANSS scores in Treatment-Resistant Schizophrenia, but the difference was not statistically significant in both per-protocol set (PPS) and intention-to-treat (ITT). However, in PPS analysis, compared to the placebo group, the TJ-54 group showed statistically significant improvements in the individual PANSS subscale scores for lack of spontaneity and flow of conversation (TJ-54: −0.23 ± 0.08; placebo: −0.03 ± 0.08, P < 0.018), tension (TJ-54: −0.42 ± 0.09; placebo: −0.18 ± 0.09, P < 0.045), and poor impulse control (TJ-54: −0.39 ± 0.10; placebo: −0.07 ± 0.10, P < 0.037). Conclusions. The results of the present study indicate that TJ-54 showed a tendency of being superior to placebo in reduction PANSS scores in Treatment-Resistant Schizophrenia, but the difference was not statistically significant. However, compared to the placebo group, TJ-54 group showed statistically significant improvements in the individual PANSS subscale scores.
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Efficacy and Safety of Yokukansan in Treatment-Resistant Schizophrenia: A Randomized, Multicenter, Double-Blind, Placebo-Controlled Trial
Hindawi Limited, 2015Co-Authors: Tsuyoshi Miyaoka, Rei Wake, Sadayuki Hashioka, Motohide Furuya, Jun Horiguchi, Masaya Thoyama, Kenta Murotani, Norio Mori, Yoshio Minabe, Masaomi IyoAbstract:Objectives. We aimed at evaluating both the efficacy and safety of TJ-54 (Yokukansan) in patients with Treatment-Resistant Schizophrenia. This randomized, multicenter, double-blind, placebo-controlled study was conducted. Methods. One hundred and twenty antipsychotic-treated inpatients were included. Patients were randomized to adjuvant treatment with TJ-54 or placebo. During a 4-week follow-up, psychopathology was assessed using the Positive and Negative Syndrome Scale (PANSS). Results. TJ-54 showed a tendency of being superior to placebo in reduction total, positive, and general PANSS scores in Treatment-Resistant Schizophrenia, but the difference was not statistically significant in both per-protocol set (PPS) and intention-to-treat (ITT). However, in PPS analysis, compared to the placebo group, the TJ-54 group showed statistically significant improvements in the individual PANSS subscale scores for lack of spontaneity and flow of conversation (TJ-54: −0.23±0.08; placebo: −0.03±0.08, P
Robert R. Conley - One of the best experts on this subject based on the ideXlab platform.
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Novel factor-based symptom scores in treatment resistant Schizophrenia: implications for clinical trials.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2002Co-Authors: Robert P. Mcmahon, Deanna L. Kelly, Julie Kreyenbuhl, Brian Kirkpatrick, Raymond C. Love, Robert R. ConleyAbstract:To study the factor structure of symptoms in patients with treatment resistant Schizophrenia and whether it is altered by treatment, we analyzed ratings on the Brief Psychiatric Rating Scale (BPRS) from two independent groups of patients with treatment resistant Schizophrenia. With confirmatory factor analysis of pre-clozapine BPRS scores in 1074 patients in an administrative data base, the Clozapine Authorization and Monitoring Program (CAMP), we assessed the fit of published factor models and developed a better-fitting model. Model fit was validated in an independent group of 197 research unit participants. Stability of model fit six months post-clozapine was assessed in 834 CAMP patients. A new 4-factor model (negative symptoms, reality distortion, disorganization, and anxiety/depression) had better fit in both data sets than two commonly used factor models, and also fit better post-clozapine. We recommend these four factor scores as clinical trial outcomes in patients with treatment resistant Schizophrenia.
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Olanzapine Compared With Chlorpromazine in Treatment-Resistant Schizophrenia
The American journal of psychiatry, 1998Co-Authors: Robert R. Conley, Raymond C. Love, Carol A. Tamminga, John J. Bartko, Charles M. Richardson, Michael Peszke, Jami S. Lingle, Judith Hegerty, Cathy Gounaris, Sandra ZarembaAbstract:OBJECTIVE: The purpose of this study was to compare the efficacy of olanzapine with that of chlorpromazine plus benztropine in patients with Treatment-Resistant Schizophrenia. METHOD: One hundred three previously Treatment-Resistant patients with Schizophrenia diagnosed according to the DSM-III-R criteria were given a prospective 6-week trial of 10–40 mg/day of haloperidol. Eighty-four of them failed to respond to that trial and agreed to be randomly assigned to an 8-week fixed-dose trial of either 25 mg/day of olanzapine alone or 1200 mg/day of chlorpromazine plus 4 mg/day of benztropine mesylate. RESULTS: Fifty-nine (70%) of the 84 subjects completed the trial. The primary outcome measures were Brief Psychiatric Rating Scale total score and positive symptom score, Scale for the Assessment of Negative Symptoms global score, and Clinical Global Impression score. An analysis of variance for the subjects who completed the study showed no difference in efficacy between the two drugs. Seven percent of the ola...
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Evaluation of Treatment-Resistant Schizophrenia
Schizophrenia bulletin, 1997Co-Authors: Robert R. Conley, Robert W. BuchananAbstract:A systematic approach to the evaluation and characterization of treatment resistance in Schizophrenia has become increasingly important since the introduction of clozapine, risperidone, and olanzapine. The need for accurate evaluation will increase with the introduction of the next generation of antipsychotic medications. People with Schizophrenia may manifest a poor response to therapy secondary to intolerance of medication, poor compliance, or inappropriate dosing, as well as true resistance of their illness to antipsychotic drug therapy. Clinicians facing the decision of when to change from one antipsychotic to another must clearly understand the appropriate length of a trial and what target symptoms respond to antipsychotics in order to maximize the response in patients with Treatment-Resistant Schizophrenia.
Tsuyoshi Miyaoka - One of the best experts on this subject based on the ideXlab platform.
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Remission of Psychosis in Treatment-Resistant Schizophrenia following Bone Marrow Transplantation: A Case Report.
Frontiers in psychiatry, 2017Co-Authors: Tsuyoshi Miyaoka, Rei Wake, Sadayuki Hashioka, Maiko Hayashida, Arata Oh-nishi, Ilhamuddin Abdul Azis, Muneto Izuhara, Keiko Tsuchie, Tomoko Araki, Ryosuke ArauchiAbstract:The authors present the case of a 24-year-old male with Treatment-Resistant Schizophrenia, with predominant severe delusion and hallucination, who received bone marrow transplantation (BMT) for acute myeloid leukemia (AML). After BMT, he showed a remarkable reduction in psychotic symptoms without administration of neuroleptics. He also showed drastic improvement in social functioning. Follow-up evaluations two and four years after BMT showed persistent significant improvement of the psychotic state and social functioning. Recent findings show that the major underlying pathogenic mechanism of Schizophrenia is immune dysregulation. Thus, conceptually, BMT, a cellular therapy, that facilitates the counteractive processes of balancing inflammation by immune regulation, could produce beneficial clinical effects in patients with Treatment-Resistant Schizophrenia. Further studies are required to define the true benefits of BMT for the possible curative treatment of Schizophrenia.
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Efficacy and Safety of Yokukansan in Treatment-Resistant Schizophrenia: A Randomized, Multicenter, Double-Blind, Placebo-Controlled Trial
Evidence-based complementary and alternative medicine : eCAM, 2015Co-Authors: Tsuyoshi Miyaoka, Rei Wake, Sadayuki Hashioka, Motohide Furuya, Jun Horiguchi, Masaya Thoyama, Kenta Murotani, Norio Mori, Yoshio Minabe, Masaomi IyoAbstract:Objectives. We aimed at evaluating both the efficacy and safety of TJ-54 (Yokukansan) in patients with Treatment-Resistant Schizophrenia. This randomized, multicenter, double-blind, placebo-controlled study was conducted. Methods. One hundred and twenty antipsychotic-treated inpatients were included. Patients were randomized to adjuvant treatment with TJ-54 or placebo. During a 4-week follow-up, psychopathology was assessed using the Positive and Negative Syndrome Scale (PANSS). Results. TJ-54 showed a tendency of being superior to placebo in reduction total, positive, and general PANSS scores in Treatment-Resistant Schizophrenia, but the difference was not statistically significant in both per-protocol set (PPS) and intention-to-treat (ITT). However, in PPS analysis, compared to the placebo group, the TJ-54 group showed statistically significant improvements in the individual PANSS subscale scores for lack of spontaneity and flow of conversation (TJ-54: −0.23 ± 0.08; placebo: −0.03 ± 0.08, P < 0.018), tension (TJ-54: −0.42 ± 0.09; placebo: −0.18 ± 0.09, P < 0.045), and poor impulse control (TJ-54: −0.39 ± 0.10; placebo: −0.07 ± 0.10, P < 0.037). Conclusions. The results of the present study indicate that TJ-54 showed a tendency of being superior to placebo in reduction PANSS scores in Treatment-Resistant Schizophrenia, but the difference was not statistically significant. However, compared to the placebo group, TJ-54 group showed statistically significant improvements in the individual PANSS subscale scores.
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Efficacy and Safety of Yokukansan in Treatment-Resistant Schizophrenia: A Randomized, Multicenter, Double-Blind, Placebo-Controlled Trial
Hindawi Limited, 2015Co-Authors: Tsuyoshi Miyaoka, Rei Wake, Sadayuki Hashioka, Motohide Furuya, Jun Horiguchi, Masaya Thoyama, Kenta Murotani, Norio Mori, Yoshio Minabe, Masaomi IyoAbstract:Objectives. We aimed at evaluating both the efficacy and safety of TJ-54 (Yokukansan) in patients with Treatment-Resistant Schizophrenia. This randomized, multicenter, double-blind, placebo-controlled study was conducted. Methods. One hundred and twenty antipsychotic-treated inpatients were included. Patients were randomized to adjuvant treatment with TJ-54 or placebo. During a 4-week follow-up, psychopathology was assessed using the Positive and Negative Syndrome Scale (PANSS). Results. TJ-54 showed a tendency of being superior to placebo in reduction total, positive, and general PANSS scores in Treatment-Resistant Schizophrenia, but the difference was not statistically significant in both per-protocol set (PPS) and intention-to-treat (ITT). However, in PPS analysis, compared to the placebo group, the TJ-54 group showed statistically significant improvements in the individual PANSS subscale scores for lack of spontaneity and flow of conversation (TJ-54: −0.23±0.08; placebo: −0.03±0.08, P
