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1. |
Clinical Pharmacology of Monoamine Oxidase Inhibitors |
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Clinical Neuropharmacology,
Volume 9,
Issue 3,
1986,
Page 207-234
Keith McDaniel,
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ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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2. |
Neuropharmacology ofS-Adenosyl Methionine |
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Clinical Neuropharmacology,
Volume 9,
Issue 3,
1986,
Page 235-243
M. Carney,
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PDF (508KB)
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ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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3. |
Ergotamine Tartrate DependencyFeatures and Possible Mechanisms |
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Clinical Neuropharmacology,
Volume 9,
Issue 3,
1986,
Page 244-256
Joel Saper,
J. Jones,
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摘要:
Summary:Based on our clinical experience and the data reviewed and presented in this report, we propose that a state of physical dependency to ergotamine tartrate exists. This dependency state is characterized by the irresistible and dependable use of ergotamine tartrate and is contingent upon a self-sustaining, rhythmic headache/medication cycle that reflects the dependency. The headache and accompaniments (withdrawal headache?) represent the primary withdrawal symptoms. The presence of this state appears to render patients refractory to other forms of preventative therapy, which can be effective only when ergotamine is discontinued and the cycle broken. If the condition is left untreated, it is likely though by no means certain that the more traditional aspects of ergotism will evolve, although variable susceptibility and tolerance to ergotamine tartrate have been demonstrated. The mechanism of this disorder remains uncertain but might be related to the influence of ergotamine tartrate on the limbic-hypothalamic-pituitary-adrenal axis and other aminergic centers (locus ceruleus), areas considered by some as the central loci for the pathogenesis and associated symptoms of migraine.
ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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4. |
GABA‐Agonist Therapy for Alzheimer's Disease |
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Clinical Neuropharmacology,
Volume 9,
Issue 3,
1986,
Page 257-263
Erich Mohr,
Giuseppe Bruno,
Norman Foster,
Marjorie Gillespie,
Christiane Cox,
Theodore Hare,
Carol Tamminga,
Paul Fedio,
Thomas Chase,
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摘要:
Summary:Evidence suggesting a reduction of cerebral γ-aminobutyric acid (GABA) neurons in Alzheimer's disease has been reported. To evaluate the possible contribution of GABA system dysfunction to the intellectual decline associated with this disorder, a controlled therapeutic trial of a potent and specific GABA agonist, THIP [4,5,6,7-tetrahydroisoxazolo(5,4,-c)pyridin-3-ol], was undertaken. Six Alzheimer patients with mild to moderately severe dementia and low spinal-fluid GABA levels received THIP at maximum individually tolerated dosage. No significant change in cognitive function could be discerned, despite attainment of dose levels that produced centrally mediated adverse effects similar to those of other GABA agonists. The results support the views that pharmacologie attempts to stimulate central GABA-mediated synaptic function may not confer therapeutic benefit to patients with Alzheimer's disease and that a GABA system deficit may not serve as a critical determinant of the dementia that characterizes this disorder.
ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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5. |
A Neuropathic Substrate for Stimulant Drug Effects in Hyperactive Children |
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Clinical Neuropharmacology,
Volume 9,
Issue 3,
1986,
Page 264-281
Randall Evans,
C. Gualtieri,
Robert Hicks,
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摘要:
Summary:Behavioral, physiological, and cognitive data are presented from a sample of 55 hyperactive children undergoing methylphenidate treatment. Consistent with previous research, considerable variability exists on these measures in this clinical population with little evidence for a consistent profile on any of these dimensions. A theoretical discussion is offered reflecting these findings with reference to a proposed pathophysiologic basis for the disorder. The proposed model postulates a particular emphasis on the functional responsibilities of the frontal-striatal system. A neural substrate for the abnormal oscillations that characterize hyperactive children, the correction of which is germane to therapeutic stimulant effects, is presented in terms of the regulatory functions of the frontal lobe.
ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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6. |
Differential Alterations in Striatal Acetylcholine Function in Rats During 12 Months' Continuous Administration of Haloperidol, Sulpiride, or Clozapine |
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Clinical Neuropharmacology,
Volume 9,
Issue 3,
1986,
Page 282-292
N. Rupniak,
R. Briggs,
M. Petersen,
S. Mann,
C. Reavill,
P. Jenner,
C. Marsden,
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摘要:
Summary:Rats were treated continuously for 12 months with therapeutically equivalent doses of either haloperidol (1.4–1.6 mg/kg/day), sulpiride (102–109 mg/kg/day), or clozapine (24–27 mg/kg/day). After treatment for 3 and 12 months with haloperidol or clozapine but not sulpiride, striatal acetylcholine levels were increased. Striatal choline acetyltransferase activity was not altered by any drug treatment.Vmaxfor striatal acetylcholinesterase activity during the course of 12 months' treatment with haloperidol or clozapine, but not with sulpiride, tended to increase;Kmwas not altered by any drug treatment.Bmaxfor specific striatal [3H]quinuclidinyl benzilate binding was not altered by haloperidol or sulpiride treatment but was transiently elevated after 6 months of clozapine treatment, thereafter returning to control levels.Kdwas not altered by any drug treatment. These findings indicate that alterations in striatal acetylcholine content caused by chronic treatment with some but not all neuroleptics are due to changes in cholinergic neuronal activity rather than neurotransmitter synthesis or destruction. The effects of haloperidol but not those of clozapine may be related to the emergence of functional striatal dopamine receptor supersensitivity. Since haloperidol (which is associated with a high prevalence of tardive dyskinesias) but not clozapine (which is not) had similar effects on striatal cholinergic function, the latter may not be related to the emergence of tardive dyskinesias during chronic therapy.
ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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7. |
Dystonia in Untreated Parkinsonism |
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Clinical Neuropharmacology,
Volume 9,
Issue 3,
1986,
Page 293-297
Peter LeWitt,
Richard Burns,
Richard Newman,
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摘要:
Summary:While parkinsonism and dystonia generally are distinct clinical syndromes, both may be prominent features even prior to the use of antiparkinsonian medications. In 10 patients with typical parkinsonism, coincident dystonic features included neck, upper extremity, oromandibular, unilateral upper-lower extremity, and unilateral foot dystonia. Six patients were first affected before the age of 45. For some, dystonia preceded parkinsonism (for ½ to 20 years). Limb symptoms tended to be unilateral; in seven patients, parkinsonism also was limited to that side. While levodopa was adequate for improvement of parkinsonism, dystonic symptoms benefited from the combination of levodopa with a dopaminergic ergot. The dystonic features (which also can result from parkinsonian therapy) often add pain and disability to the deficits in parkinsonism. The coexistence of dystonia may constitute a distinctive syndrome of parkinsonism and points to possible etiologic mechanisms shared by these two extrapyramidal disorders.
ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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8. |
Dystonia‐Parkinson SyndromeDifferential Effects of Levodopa and Dopamine Agonists |
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Clinical Neuropharmacology,
Volume 9,
Issue 3,
1986,
Page 298-302
Harold Klawans,
Nina Paleologos,
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摘要:
Summary:Eleven patients who presented with predystonic syndrome later developed pure dystonic syndromes and later developed parkinsonism. This suggests that dystonic syndromes can be the precursor to a mixed syndrome including both dystonia and parkinsonism. While the parkinsonian features in such patients respond to either levodopa or direct-acting agonists, levodopa often exacerbates the underlying dystonia. Direct acting agonists appear to be less liable to do this.
ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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9. |
Macronodular Adrenal Hyperplasia with Hypothalamic‐Pituitary-Adrenal Suppression by Ultra‐High-Dose DexamethasoneRegression Following Hypophysectomy |
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Clinical Neuropharmacology,
Volume 9,
Issue 3,
1986,
Page 303-308
Hamilton Fish,
Douglas Sobel,
Carol Miegel,
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摘要:
Summary:Cushing's syndrome associated with macronodular adrenal hyperplasia (MAH) may present with high-dose dexamethasone (dex) nonsuppressible hypercortisolemia. This has been interpreted as suggesting a primary adrenal disorder, leading to recommendations for curative adrenalectomy in these cases. The present case of MAH demonstrates high urinary and serum cortisol levels, sufficiently suppressed only by ultra-high-dose (32 mg/day × 2 day) dex, with parallel reduction of plasma adrenocorticotrophin noted as well. Subsequent clinical cure by transsphenoidal hypophysectomy and identification of a pituitary adenoma confirmed the secondary nature of adrenal cortical hypersecretion. The conceptual evolution of macronodules and altered feedback dynamics of the hypothalamo-pituitary-adrenal axis in MAH are briefly discussed.
ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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10. |
Neurotoxins in Clinical Practice |
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Clinical Neuropharmacology,
Volume 9,
Issue 3,
1986,
Page 309-309
Christopher Goetz,
Robert Feldman,
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PDF (74KB)
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ISSN:0362-5664
出版商:OVID
年代:1986
数据来源: OVID
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