Blood levels of neuroleptics: state of the art

Simpson, G M; Yadalam, K

doi:10.1097/00004714-198510000-00013

Cited by 4 publications

(5 citation statements)

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“…Perhaps more difficult than identifying a good response to neuroleptic treatment is identifying resistance to such treatment. Apparent nonresponse can result from both an inadequate dose and, in some instances, from too high a dose (Volavka and Cooper 1977; Simpson and Yadalam 1985). Neuroleptic toxicity or side effects can be misidentified as nonresponse (Bishop et al 1965; van Putten and Marder 1986).…”

Section: Identification Of Neuroleptic Responsivenessmentioning

confidence: 99%

Response to Neuroleptic Drugs as a Device for Classifying Schizophrenia

Brown

Herz

1989

Schizophrenia Bulletin

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Although schizophrenic patients are routinely treated with neuroleptic medication, the diversity in response to such treatment is noteworthy; some patients are exquisitely responsive to neuroleptic treatment, while others are clearly resistant. The authors examine the hypothesis that neuroleptic-responsive and neuroleptic-resistant patients have different illnesses by considering the following issues: the reliability of the distinction between neuroleptic responsiveness and resistance; the consistency in neuroleptic responsiveness over time; the association between neuroleptic responsiveness and other clinical features; and the neuroleptics' therapeutic action. On the basis of the data available and on theoretical and historical grounds, the distinction between neuroleptic-responsive and neuroleptic-resistant patients warrants application in both clinical and research settings.

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Section: Identification Of Neuroleptic Responsivenessmentioning

confidence: 99%

Response to Neuroleptic Drugs as a Device for Classifying Schizophrenia

Brown

Herz

1989

Schizophrenia Bulletin

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“…There was also considerable variability in clinical control, with a median value of 12 for the sum of the SANS items (range, [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] (20,27,28). There were no significant associations between the age or sex of the patient or the duration of fluphenazine decanoate therapy and the dosage or steady-state plasma concentration of fluphenazine.…”

Section: Resultsmentioning

confidence: 99%

“…Consequently, the determination of plasma levels of the antipsychotics is becoming more common in clinical practice as a potential means of assessing and improving patient compliance, reducing adverse effects, and improving antipsychotic effects. It has been suggested that plasma-level monitoring should be performed at least once a year during the maintenance treatment of chronic psychotic disorders (14), to shorten the duration of patients' disability and hospital stay, lessen the relapse rate and reduce the incidence of adverse effects (8,14,16). Several studies have examined the relationship between plasma concentrations of fluphenazine and clinical response, and a therapeutic range of approximately 0.2-2 ng/ml has been proposed (12)(13)(14)(15)(16)(17)(18)(19)(20).…”

Section: Introductionmentioning

confidence: 99%

Monitoring plasma levels of fluphenazine during chronic therapy with fluphenazine decanoate

et al. 1995

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This study was conducted to examine the interpatient variability in steady-state plasma concentrations of fluphenazine by repeat depot intramuscular administration, and to determine the relationship between these concentrations and clinical state. Steady-state pre-dose concentrations of fluphenazine in plasma were measured using a sensitive and specific gas chromatography/mass spectrometry (GC/MS) assay in 24 patients with schizophrenia who were receiving continuous treatment with depot intramuscular fluphenazine decanoate. Clinical response was measured using the Andreasen Scale for positive and negative symptoms. Steady-state plasma concentrations of fluphenazine ranged from undetectable (< 0.1 ng/ml) to 27.9 ng/ml, with a median of 0.5 ng/ml. No significant associations were found between plasma concentration and dosage, or age and sex of the patient. Steady-state plasma concentrations in patients taking anticholinergic agents were significantly higher than in patients not receiving such drugs (P < 0.05 by Mann-Whitney U-test). Poorer control, expressed as the sum of the negative symptom scores or the sum of the positive and negative symptom scores, was related to higher log transformed plasma concentration of fluphenazine and higher fluphenazine decanoate dosage. The log transformed plasma concentrations of fluphenazine and the fluphenazine decanoate dosages were weakly related. Patients receiving another antipsychotic drug in addition to fluphenazine decanoate tended to have poorer clinical control and higher dosages of fluphenazine decanoate. These results indicate the useful role that plasma level monitoring can fulfil in identifying patients who are therapy-resistant despite high plasma levels.

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“…These are the first experiments to explore chronic effects of psychoactive drugs on brain temperature in mammals. The facts that clinically relevant drug doses were used in these studies, and that therapeutic plasma neuroleptic (Tang et al 1984;Simpson and Yadalam 1985;Sramek et al 1987) and antidepressant drug levels were associated with temperature changes suggest that similar effects may occur in humans; however, there is reason to be cautious in this interpretation. A full range of doses was not used in these studies.…”

Section: Clinical Relevancementioning

confidence: 97%

Antidepressant Drug-Induced Hypothalamic Cooling in Syrian Hamsters

Duncan¹,

Johnson²,

Wehr³

1995

Neuropsychopharmacol

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Antidepressant drugs have been reported to alter the circadian pattern of body temperature, but specific effects on the amplitude or on average body temperature are not consistent, and there have been no specific studies to examine chronic drug effects on brain temperature. To address these issues, hypothalamic temperature (Thy) was monitored telemetrically in hamsters treated with three antidepressant drugs: the monoamine oxidase inhibitor (MAOI), clorgyline; the 5HT reuptake inhibitor, fluoxetine; and the alkali metal, lithium. For comparison, hamsters were also treated with two neuroleptic drugs, chlorpromazine and haloperidol. Each of the three antidepressant drugs, but neither of the neuroleptic drugs, produced a chronic decrease in diurnal (rest-phase) hypothalamic temperature. The Thy-decreasing effect of clorgyline was not prevented by pinealectomy, and Thy decreased more than peritoneal temperature (Tp), thus reducing the temperature difference between the hypothalamus and the peritoneal cavity. Less general effects of the antidepressants were also observed. Clorgyline and fluoxetine, but not lithium, delayed the 24-hour rhythm of Thy. Clorgyline and lithium, but not fluoxetine decreased the average 24-hour Thy. The neuroleptics chlorpromazine and haloperidol decreased the amplitude of the 24-hour Thy rhythm. The fact that chronic antidepressant drugs, but not neuroleptic drugs, decrease Thy is consistent with their different neurotransmitter effects and clinical applications, and raises the possibility that their antidepressant property might be related to their capacity to decrease Thy during sleep.

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Blood levels of neuroleptics: state of the art

Cited by 4 publications

References 0 publications

Response to Neuroleptic Drugs as a Device for Classifying Schizophrenia

Response to Neuroleptic Drugs as a Device for Classifying Schizophrenia

Monitoring plasma levels of fluphenazine during chronic therapy with fluphenazine decanoate

Antidepressant Drug-Induced Hypothalamic Cooling in Syrian Hamsters

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