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1. |
Passing of the Baton |
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Clinical Neuropharmacology,
Volume 26,
Issue 6,
2003,
Page 285-285
Christopher Goetz,
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ISSN:0362-5664
出版商:OVID
年代:2003
数据来源: OVID
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2. |
Adverse Reactions to Mirtazapine are Unlikely to be Serotonin Toxicity |
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Clinical Neuropharmacology,
Volume 26,
Issue 6,
2003,
Page 287-288
Geoffrey Isbister,
Ian Whyte,
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ISSN:0362-5664
出版商:OVID
年代:2003
数据来源: OVID
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3. |
Mirtazapine: Unable to Induce Serotonin Toxicity? |
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Clinical Neuropharmacology,
Volume 26,
Issue 6,
2003,
Page 288-289
Peter Gillman,
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ISSN:0362-5664
出版商:OVID
年代:2003
数据来源: OVID
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4. |
Adverse Reactions to Mirtazapine are Unlikely to be Serotonin ToxicityandMirtazapine: Unable to Induce Serotonin Toxicity?—Response |
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Clinical Neuropharmacology,
Volume 26,
Issue 6,
2003,
Page 289-290
Eroboghene Ubogu,
Bashar Katirji,
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PDF (189KB)
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ISSN:0362-5664
出版商:OVID
年代:2003
数据来源: OVID
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5. |
Possible Relationship Between Testosterone and Comorbid Major Depressive Episode in Male Patients With Schizophrenia Treated With Typical Antipsychotic Medications |
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Clinical Neuropharmacology,
Volume 26,
Issue 6,
2003,
Page 291-293
Yasuhiro Kaneda,
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摘要:
In this cross-sectional study, the author tested the hypothesis that serum testosterone levels were associated with depressive illness in chronic male schizophrenia patients. The subjects were 49 male inpatients meeting DSM-IV criteria for schizophrenia treated with typical antipsychotic medications. The author found that the schizophrenia patients with major depressive episodes (MDE) had been taking significantly higher dosages of antipsychotic medications than those without an MDE. Also, there was a trend for the serum testosterone concentration to be lower in schizophrenia patients with an MDE. It is suggested that we should be aware of testosterone levels when we find depression in chronic male schizophrenia patients, especially those treated with high-dose typical antipsychotic medications.
ISSN:0362-5664
出版商:OVID
年代:2003
数据来源: OVID
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6. |
Low Doses of Topiramate are Effective in Essential Tremor: A Report of Three Cases |
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Clinical Neuropharmacology,
Volume 26,
Issue 6,
2003,
Page 294-296
Emilia Gatto,
M. Claudia Roca,
Gabriela Raina,
Federico Micheli,
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摘要:
We here report on 3 patients with essential tremor, otherwise unresponsive to pharmacological treatment, who greatly benefited from low doses of topiramate (50 mg/d). No side effects were observed and improvement was sustained during a mean of 7 months (range 3–12 months) follow up. Our results suggest that topiramate titration should be performed gradually, so as not to neglect cases responsive to low doses.
ISSN:0362-5664
出版商:OVID
年代:2003
数据来源: OVID
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7. |
Adjunctive Quetiapine Decreases Symptoms of Tardive Dyskinesia in a Patient Taking Risperidone |
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Clinical Neuropharmacology,
Volume 26,
Issue 6,
2003,
Page 297-298
Matthew Nelson,
Rhonda Reynolds,
Deanna Kelly,
Robert Conley,
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摘要:
Tardive dyskinesia is a potentially permanent and disfiguring side effect associated with the use of conventional, or first generation, antipsychotics. Quetiapine is a second generation antipsychotic with transient dopamine receptor occupancy, a property shared with clozapine. Quetiapine was administered to a patient who had persistent choreoathetoid movements that developed during treatment with conventional antipsychotics and remained unimproved during longterm treatment with risperidone. During 10 weeks of monotherapy with quetiapine, his Abnormal Involuntary Movement Scale score fell from 11 to 3. He was subsequently switched back to risperidone and his movements returned. The addition of quetiapine to his risperidone regimen once again resulted in a decrease of his tardive dyskinesia symptoms. The mechanism by which quetiapine improved tardive dyskinesia symptoms in this patient is not known, but differential treatment effects between the novel antipsychotics may exist. Controlled trials of quetiapine in the treatment of tardive dyskinesia should be pursued.
ISSN:0362-5664
出版商:OVID
年代:2003
数据来源: OVID
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8. |
Noradrenergic Drugs for Levodopa-Induced Dyskinesia |
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Clinical Neuropharmacology,
Volume 26,
Issue 6,
2003,
Page 299-305
Carlo Colosimo,
Alessandra Craus,
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摘要:
Dyskinesia frequently mars the long-term therapeutic response to levodopa (LD) in Parkinson's disease (PD). New treatment strategies for levodopa-induced dyskinesia (LID) currently being investigated include some that target the nondopaminergic pathways. Indeed, LID in parkinsonism can be modulated by drugs acting on different neurotransmitters including glutamate, &ggr;-aminobutyric acid, noradrenaline, acetylcholine, serotonin, adenosine, and cholecystokinin. In many cases, the possibility of using specific compounds to counteract LID was raised by the previously shown efficacy of such compounds in the treatment of other types of dyskinesia. More data are now available on drugs that act on the noradrenergic system. Two studies have recently shown how the &agr;-2 adrenoreceptor antagonist idazoxan can significantly reduce LID in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned primate model of parkinsonism and in patients with advanced PD. The experimental paper, which studied the antagonistic action of idazoxan on dyskinesia induced by both LD and apomorphine in marmosets with MPTP-induced parkinsonism, showed that the pharmacologic mechanisms underlying LID and apomorphine-induced dyskinesia in PD are probably distinct. LD, although not apomorphine-induced, dyskinesia was found to be influenced by adrenoreceptor antagonists. Indeed, the action of &agr;-2 adrenoreceptor antagonists may involve the blockade of the action of noradrenaline synthesized from LD. The hypothesis is that because dopamine agonists are not metabolized to noradrenaline, &agr;-2 adrenoreceptor antagonists do not reduce dyskinesia produced by such agents. This finding is particularly relevant in planning clinical studies in which LD or dopamine agonist challenges are used to assess the potential antidyskinetic properties of new drugs. The clinical study assessed the effects of idazoxan on LID in 18 patients with advanced PD: An improvement in LID, without the reappearance of parkinsonian symptoms, was observed. The practical outcome of this research is that, although the mechanisms underlying the manifestations and the priming process for dyskinesia have yet to be fully elucidated, a nondopaminergic approach to therapy may provide an effective way of preventing, or at least limiting, the expression of involuntary movements in PD.
ISSN:0362-5664
出版商:OVID
年代:2003
数据来源: OVID
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9. |
Neutropenia as a Complication of High-Dose Intravenous Immunoglobulin Therapy in Adult Patients With Neuroimmunologic Disorders |
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Clinical Neuropharmacology,
Volume 26,
Issue 6,
2003,
Page 306-311
Masayuki Matsuda,
Waki Hosoda,
Yoshiki Sekijima,
Kenichi Hoshi,
Takao Hashimoto,
Susumu Itoh,
Shu-ichi Ikeda,
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摘要:
To investigate clinical aspects of the neutropenia induced by high-dose intravenous immunoglobulin therapy (IVIG) we performed serial hematology, including differentiation of white blood cells (WBC), before and after 22 instances of IVIG in 16 patients with neuroimmunologic disorders. WBC and neutrophils showed a significant decrease with a nadir 2 days after IVIG, but returned to previous values by 14 days with no treatment except in 2 cases. No patient showed any infectious complication. Both WBC and neutrophils were significantly decreased in cases without corticosteroid therapy but not in those with medication. In nine instances (4 with and 5 without corticosteroid treatment), CD11b and CD16 on neutrophils were investigated using flow cytometry. In 3 of 5 instances without corticosteroid treatment the expression of CD11b was decreased after IVIG, while no change was detected in CD16. There was no difference in either CD11b or CD16 between before and after IVIG in instances with corticosteroid therapy. Neutropenia commonly and transiently develops just after IVIG, and can be prevented by corticosteroid pretreatment. Circulating neutrophils might bind to the vascular wall mainly with the involvement of CD11b and migrate into a storage pool, resulting in an apparent neutropenia after IVIG.
ISSN:0362-5664
出版商:OVID
年代:2003
数据来源: OVID
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10. |
Prevalence and Characteristics of Subjective Akathisia, Objective Akathisia, and Mixed Akathisia in Chronic Schizophrenic Subjects |
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Clinical Neuropharmacology,
Volume 26,
Issue 6,
2003,
Page 312-316
Jong-Hoon Kim,
Hee-Jung Byun,
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摘要:
Akathisia is a complex syndrome that is characterized by subjective inner restlessness and objective motor manifestations, and it can be classified into several subtypes. The purpose of this study was to examine the prevalence of subjective akathisia, objective akathisia, and mixed akathisia, and to evaluate their relationships with other drug-induced movement disorders, in chronic schizophrenic subjects treated with antipsychotics. One hundred and forty-two in-patients were assessed for akathisia, drug-induced parkinsonism, and tardive dyskinesia. The subtypes of akathisia were specified according to the Barnes Akathisia Rating Scale. Drug-induced parkinsonism and tardive dyskinesia were assessed using the Simpson-Angus Scale and the Abnormal Involuntary Movement Scale, respectively. The prevalence of subjective, objective, and mixed akathisia was 11.3%, 6.3%, and 16.9%, respectively. Regarding concurrence rates of akathisia subtypes and other extrapyramidal syndromes, the comorbidity rates of mixed akathisia with parkinsonism and tardive dyskinesia were higher. In conclusion, the present study presented the prevalence of subjective, objective, and mixed akathisia among hospitalized schizophrenic subjects. Mixed akathisia showed an association with parkinsonism and tardive dyskinesia, suggesting a common vulnerability involved in these drug-induced movement disorders. Further studies are required to elucidate more detailed clinical characteristics of each subtype of akathisia.
ISSN:0362-5664
出版商:OVID
年代:2003
数据来源: OVID
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