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1. |
Calcium Channel Antagonists and the Treatment of Migraine |
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Clinical Neuropharmacology,
Volume 9,
Issue 4,
1986,
Page 311-328
David Greenberg,
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ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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2. |
Antidepressants and Convulsive SeizuresClinical, Electroencephalographic, and Pharmacological Aspects |
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Clinical Neuropharmacology,
Volume 9,
Issue 4,
1986,
Page 329-360
J. Edwards,
S. Long,
E. Sedgwick,
H. Wheal,
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PDF (1745KB)
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ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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3. |
Treatment of Muscular Dystrophies and Inflammatory Myopathies |
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Clinical Neuropharmacology,
Volume 9,
Issue 4,
1986,
Page 361-372
William Kingston,
Richard Moxley,
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PDF (749KB)
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ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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4. |
Buspirone, Parkinson's Disease, and the Locus Ceruleus |
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Clinical Neuropharmacology,
Volume 9,
Issue 4,
1986,
Page 373-378
Carol Ludwig,
Daniel Weinberger,
Giuseppe Bruno,
Marjorie Gillespie,
Koenrad Bakker,
Peter LeWitt,
Thomas Chase,
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摘要:
Summary:Buspirone is a novel anxiolytic whose pharmacological profile differs from that of the benzodiazepines and includes dopaminergic agonist effects. Because of these properties, buspirone's usefulness in the management of idiopathic Parkinson's disease was evaluated in a controlled study of 16 outpatients with stage I–IV disease. At doses of 10 to 60 mg/day, no significant group or individual effects could be discerned on standardized disability, dyskinesia, anxiety, or depression scales. At high dose levels (100 mg/day) however, there was a significant worsening of disability ratings and a decrease in dyskinesia scores; anxiety ratings were also significantly increased. The results indicate that buspirone is well tolerated by parkinsonian patients at conventional antianxiety doses of 10 to 40 mg. Clinical effects of high dose treatment, on the other hand, resemble those associated with a reduction in central dopamine mediated synaptic function. Since buspirone reportedly produces dose-dependent stimulation of norepinephrine containing neurons in the locus ceruleus and behavioral symptoms of such activation were observed, these clinical observations support the concept that central noradrenergic stimulation can adversely affect parksinsonian symptoms.
ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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5. |
Affective Illness andS-Adenosyl MethionineA Preliminary Report |
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Clinical Neuropharmacology,
Volume 9,
Issue 4,
1986,
Page 379-385
M. Carney,
James Edeh,
Teodoro Bottiglieri,
E. Reynolds,
B. Toone,
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PDF (339KB)
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摘要:
Summary:S-Adenosyl methionine may well have an antidepressant action beyond a placebo effect but this is virtually confined to endogenous depression. This should be subjected to further study. Our own double-blind placebo-controlled study is still incomplete. The indications are that SAM specifically affects folate, dopamine, and serotonin metabolism as well as activating and switching brain mechanisms. This suggests exciting prospects for further investigations. SAM is a nontoxic physiological metabolite virtually free of side effects.
ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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6. |
Serum Haloperidol Levels of Schizophrenics Receiving Treatment for Tuberculosis |
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Clinical Neuropharmacology,
Volume 9,
Issue 4,
1986,
Page 386-386
Masatoshi Takeda,
Keiji Nishinuma,
Shozo Yamashita,
Takeyuki Matsubayashi,
Shiro Tanino,
Tsuyoshi Nishimura,
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PDF (532KB)
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摘要:
Summary:Serum haloperidol levels were studied in schizophrenic patients with and without antituberculosis therapy, and the effect of these agents on serum haloperidol level was evaluated. Rifampicin caused significant suppression of serum haloperidol levels in all cases studied (n = 7). The serum haloperidol clearance rate was accelerated in patients taking rifampicin, with a shortened half-life (4.9 h) compared with the control group (9.4 h). Among 18 schizophrenic patients receiving isoniazid, three showed significantly elevated serum haloperidol levels. It is possible that isoniazid can elevate haloperidol levels in some patients depending upon some unknown factors. The elevation of serum haloperidol level was thought to be due to prolonged clearance of haloperidol secondary to isoniazid interaction with hepatic enzymes involved in drug metabolism. These observations suggest that haloperidol doses in schizophrenic patients receiving rifampicin or isoniazid must be carefully monitored.
ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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