Long-term Pimozide Pretreatment Differentially Affects Behavioral Responses to Dextroamphetamine in Schizophrenia

Kammen, Daniël P. van; Docherty, John P.; Marder, Stephen R.; Rayner, Judith; Bunney, William E.

doi:10.1001/archpsyc.1982.04290030017003

Cited by 29 publications

(2 citation statements)

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“…Lower CSF DBH in acutely psychotic drug-free patients was associated with a better clinical response to antipsychotic treatment and better pre-morbid functioning (measured by the Phillips scale) (Sternberg et al 1982a(Sternberg et al , 1983. This seems inconsistent with the report that CSF dopamine-/?-hydroxylase (DBH) was decreased in patients with large ventricle brain ratios (VBRs) (van Kammen et al 1983), since brain atrophy has in some cases been associated with poor treatment response (Weinberger et al 1980;Nasrallah et al 1983;Schulz et al 1983;Andreasen et al 1990) and poor pre-morbid functioning (Cannon-Spoor et al 1982).…”

Section: Csf Dopamine /Miydroxylase (Dbh)mentioning

confidence: 85%

The biochemical basis of relapse and drug response in schizophrenia: review and hypothesis

Kammen

1991

Psychol. Med.

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SYNOPSISThis review of the literature suggests that antipsychotic drug response is determined by dopamine (DA) turnover and norepinephrine (NE) activity prior to treatment. The data suggest that NE modulates the DA system. Drug-free psychotic patients with relatively increased DA and NE activity, including release, are more likely to be treatment responsive, while patients who show evidence of enhanced DA and NE activity during treatment with antipsychotic drugs are likely to relapse soon after neuroleptic withdrawal. Basal release of DA and NE is decreased and associated with residual positive and negative symptoms. Improvement during neuroleptic treatment is associated with decreases in DA and NE phasic or stimulus induced release. The variable response to antipsychotic drugs is most likely to be a result of dysregulated DA and NE release, i.e. under state-dependent control, rather than evidence of a heterogeneous aetiology. Because catecholamines regulate gain, signal-to-noise ratio and gating in the brain, this model allows for environmental factors to interact with biochemical state and drug treatment. The author proposes that impaired homeostasis of NE and DA in schizophrenia causes instability in NE and DA neuronal firing and release, presumably related to mechanisms down-stream from the receptors, such as G proteins. This instability of catecholamine release may explain the observed variability in clinical states and drug response in schizophrenia.

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Section: Csf Dopamine /Miydroxylase (Dbh)mentioning

confidence: 85%

The biochemical basis of relapse and drug response in schizophrenia: review and hypothesis

Kammen

1991

Psychol. Med.

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“…Consequently, they should lose the ability to buffer a dopamimetic challenge. In agreement with this hypothesis are data indicating that those schizophrenic patients whose symptoms increase following administration of amphetamine are those who are more psychotic at baseline [Cahil et al, 1977;van Kammen et al, 1982avan Kammen et al, , 1982b To further test this hypothesis, schizophrenics were given a fixed dose of Sinemet, as displayed in Table 3, for a 7-day period, and the effects of this challenge were recorded with the Brief Psychiatric Rating Scale (BPRS) [Keefe et al, 19851. Figure 2 demonstrates the relationship between the effects of L-dopa on symptom severity and the length of time that patients were able to remain neuroleptic free and in remission.…”

Section: Implications Of a Dysregulation Hypothesismentioning

confidence: 98%

Dopaminergic dysregulation in schizophrenia: A target for new drugs

Davis¹,

Fiori²,

Davis³

et al. 1986

Drug Development Research

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The dopamine hypothesis postulates that at least some schizophrenic symptoms are a reflection of central nervous system hyperdopaminergia. The evidence for this model is briefly reviewed and its shortcomings highlighted. The dysregulation hypothesis of schizophrenia should be a useful reformulation. Rather than conceptualizing a static hyperdopaminergic state, schizophrenia might be better understood as a reflection of a relative failure of dopaminergic regulation. Evidence for such dysregulation is examined and possible mechanisms are presented. Avenues of future drug research are proposed.

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