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1. |
Tardive Syndromes and Other Drug‐Induced Movement Disorders |
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Clinical Neuropharmacology,
Volume 18,
Issue 3,
1995,
Page 197-214
Joseph Jankovic,
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ISSN:0362-5664
出版商:OVID
年代:1995
数据来源: OVID
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2. |
The Effects of Flumazenil in Neuropsychiatric Disorders |
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Clinical Neuropharmacology,
Volume 18,
Issue 3,
1995,
Page 215-232
Andrea Malizia,
David Nutt,
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摘要:
Flumazenil is a benzodiazepine receptor antagonist. It is currently used mainly in the anaesthetic and emergency rooms to reverse the effect of exogenous benzodiazepines. Its use in a variety of experimental animal models and in human neuropsychiatric disorders continues to generate a wealth of information on the possible role of the benzodiazepine-GABAAreceptor complex in their pathogenesis. In addition, labelled with carbon-11, flumazenil has proved to be one of the most successful positron emission tomography ligands stimulating research on the role of the benzodiazepine receptor in these disorders. This review focuses on the current state of play of flumazenil as a therapeutic or investigative agent in neuropsychiatry, citing also the relevant animal models.
ISSN:0362-5664
出版商:OVID
年代:1995
数据来源: OVID
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3. |
The Drug‐Drug Interaction Effects of Haloperidol on Plasma Carbamazepine Levels |
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Clinical Neuropharmacology,
Volume 18,
Issue 3,
1995,
Page 233-236
Kazuhiko Iwahashi,
Ryosuke Miyatake,
Hiroshi Suwaki,
Kiyoshi Hosokawa,
Yoshiyuki Ichikawa,
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摘要:
The metabolic interaction between carbamazepine (CBZ) and haloperidol (HP) was studied in Japanese schizophrenic patients treated with HP but not with CBZ and with both CBZ and HP. The serum CBZ concentrations in patients treated without HP were significantly decreased (p< 0.05), on average 40%, as compared to those in patients treated with both CBZ and HP, whereas the serum HP concentrations in patients treated with both HP and CBZ were significantly decreased (p< 0.05), as compared to those in patients treated with HP but not with CBZ. The effect of HP, which prevents the serum CBZ level from decreasing, was shown in this study.
ISSN:0362-5664
出版商:OVID
年代:1995
数据来源: OVID
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4. |
The Phencyclidine‐Glutamate Model of Schizophrenia |
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Clinical Neuropharmacology,
Volume 18,
Issue 3,
1995,
Page 237-249
Adam Halberstadt,
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摘要:
For the past 20 years, it has been widely assumed that schizophrenia results from chronic dopamine (DA) hyperactivity. However, large amounts of evidence exist that call into question this assumption. After examining the brains of schizophrenic patients, studies failed to find evidence of elevated levels of DA, alterations in DA-producing or degrading enzymes or both, or increased DA-receptor concentrations or affinity; thus, there are no direct observations linking psychosis to increases in DA activity. Therefore, it seems that mechanisms unrelated to altered dopaminergic functioning may be involved in the underlying pathology of schizophrenia. The anesthetic drug phencyclidine (PCP) is capable of inducing psychosis-like states through nondopaminergic mechanisms. PCP acts as a glutamate antagonist; glutamatergic abnormalities have been detected in the brains of schizophrenics. This evidence suggets that glutamate hypofunction may be involved in the pathology of psychosis. Additionally, a functional link exists between glutamate and DA neural systems. Based on these facts, as well as an extensive review of the literature, it is concluded that dysfunctional glutamatergic pathways are involved in psychotic pathology.
ISSN:0362-5664
出版商:OVID
年代:1995
数据来源: OVID
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5. |
L‐Deprenyl as an Adjunct to Low‐Dose Bromocriptine in Early Parkinson's DiseaseA Short‐Term, Double‐Blind, and Prospective Follow‐up Study |
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Clinical Neuropharmacology,
Volume 18,
Issue 3,
1995,
Page 250-257
S. Calzetti,
A. Negrotti,
A. Cassio,
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摘要:
The therapeutic efficacy of L-deprenyl (10 mg daily) as an adjunct to low-dose bromocriptine monotherapy (up to 25 mg daily) in patients with early Parkinson's disease (PD) was evaluated in a double-blind placebo-controlled short-term study (11 patients) and subsequently in a long-term prospective open follow-up (21 patients) until L-dopa was required, over a 4-year period. The combined regimen of bromocriptine plus L-deprenyl produced a mildly significant improvement, as shown by the majority of clinical rating scales used after 6 weeks of sustained treatment (as compared to bromocriptine alone and bromocriptine plus placebo). In the prospective long-term study, a stabilization of the clinical status was observed until 12 months of sustained treatment, whereas after that, a gradual worsening of the scores on all motor rating scales occurred. However, at 24 months, fewer than one third of the patients had required L-dopa, a proportion comparatively smaller than that reported in the literature with bromocriptine alone. This finding could be related to the persistence of initial symptomatic effect of L-deprenyl, but a slowing action on the course of the disease process exerted by the monoamine oxidase typeB (MAOB) inhibitor cannot be ruled out.
ISSN:0362-5664
出版商:OVID
年代:1995
数据来源: OVID
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6. |
Acute Administration of Levodopa‐Benserazide and Tolcapone, a COMT Inhibitor, in Parkinson's Disease |
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Clinical Neuropharmacology,
Volume 18,
Issue 3,
1995,
Page 258-265
P. Limousin,
P. Pollak,
J. Pfefen,
C. Tournier-Gervason,
R. Dubuis,
J. Perret,
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摘要:
Tolcapone, a catechol-O-methyltransferase inhibitor, can interfere with the metabolism of levodopa and dopamine and could prolong the motor effect induced by levodopa in parkinsonian patients. To test this hypothesis, we studied the motor effect induced by three acute administrations of a dose of levodopa-benserazide (Madopar) with either 200 mg or 400 mg of tolcapone or placebo, in a double-blind latin-square design. The duration of the on-phase could be compared in 10 parkinsonian patients suffering from square-shaped motor effect. In comparison to placebo, 200 mg and 400 mg of tolcapone significantly increased the mean duration of the on-phase by 61.7 min (±19.4 SEM) and by 72.2 min (±18.5), respectively. This clinical effect is suggested to be related mainly to the increase in levodopa area under the curve and half-life induced by tolcapone. The intensity in dyskinesias was increased by 400 mg of tolcapone. Tolcapone appears to be well tolerated and could be helpful as an adjuvant treatment to levodopa in parkinsonian patients with motor fluctuations.
ISSN:0362-5664
出版商:OVID
年代:1995
数据来源: OVID
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7. |
Tremorlytic Activity of BudipineA Quantitative Study with Long‐Term Tremor Recordings |
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Clinical Neuropharmacology,
Volume 18,
Issue 3,
1995,
Page 266-272
S. Spieker,
P. Löschmann,
C. Jentgens,
A. Boose,
T. Klockgether,
J. Dichgans,
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摘要:
The tremorlytic activity of the novel antiparkinson agent budipine was quantified in an open trial. Eleven patients with Parkinson's disease (PD) were treated with individual doses of budipine added to stable conventional antiparkinsonian medication. Tremor activity was measured using long-term electromyogram (EMG) recordings. Tremor intensity was reduced by 25%, tremor occurrence by 34%, and conventional “Unified Parkinson's Disease Rating Scale” (UPDRS) scores improved by 20% with this medication. There were two dropouts because of side effects. One dropout appeared not to be related to budipine. Apart from those, the drug was well tolerated by all patients. We conclude that budipine is an effective and well-tolerated tremorlytic drug and that the method of long-term EMG recording is suitable for tremor quantification in clinical studies.
ISSN:0362-5664
出版商:OVID
年代:1995
数据来源: OVID
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8. |
Trauma, Axonal Injury, and Amyotrophic Lateral SclerosisA Clinical Correlate of a Neuropharmacologic Model |
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Clinical Neuropharmacology,
Volume 18,
Issue 3,
1995,
Page 273-276
Jack Riggs,
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摘要:
Axonal injury induces cell death in selectively vulnerable motor neurons of immature animals. This extensively studied animal model of trauma-induced motor neuron death is being used to develop the theoretical basis for the therapeutic use of neurotrophic factors to “rescue” dying neurons in amyotrophic lateral sclerosis, Parkinson's disease, and Alzheimer's disease. Antecedent trauma has been implicated as a precipitating factor for amyotrophic lateral sclerosis in susceptible individuals. The animal model of traumainduced motor neuron death provides support for the concept that motor neurons in individuals susceptible to amyotrophic lateral sclerosis may be selectively vulnerable to trauma producing axonal injury. The case histories of six young adult men who developed amyotrophic lateral sclerosis after trauma with axonal injury are presented.
ISSN:0362-5664
出版商:OVID
年代:1995
数据来源: OVID
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9. |
Retroperitoneal Fibrosis in a Patient with Parkinson's Disease Treated with Pergolide |
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Clinical Neuropharmacology,
Volume 18,
Issue 3,
1995,
Page 277-279
Félix Jiménez-Jiménez,
Joaqín López-Alvarez,
Manuel Sánchez-Chapado,
Eduardo Montero,
Joaquín Miquel,
Adela Sierra,
Fernando Gutiérrez,
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PDF (137KB)
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ISSN:0362-5664
出版商:OVID
年代:1995
数据来源: OVID
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10. |
Vigabatrin and Multifocal Myoclonus in Adults with Partial Seizures |
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Clinical Neuropharmacology,
Volume 18,
Issue 3,
1995,
Page 280-280
M. Neufeld,
S. Vishnevska,
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摘要:
We report the appearance of multifocal myoclonus in two adult patients treated with vigabatrin as an add-on drug for complex partial seizures. The myoclonus subsided after dose reduction or discontinuation of the drug. There were no electroencephalogram correlates during the myoclonic jerks. This phenomenon may represent a apparently dose-related rare adverse drug event, similar to that seen occasionally with other anticonvulsants.
ISSN:0362-5664
出版商:OVID
年代:1995
数据来源: OVID
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