Interaction of Low-Dose Amphetamine Use with Schizophrenia in Outpatients: Three Case Reports

West, Albert

doi:10.1176/ajp.131.3.321

Cited by 19 publications

(8 citation statements)

References 9 publications

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“…The administration of ¿-dopa and dopa mine-related drugs to our patients gave results which differ substantially from those reported to occur in actively ill schizophrenics by Davis et al (1972), Davis and Janowsky (1973), Angrist et al (1973), Angrist and Gershon (1974) , Janowsky et al (1974), Janowsky and Davis (1976), West (1974), andGershon et al (1975) . In fact, we observed neither worsening of pre-existing symptoms, nor appearance of new ones, in particular the psychomotor excite ment, hallucinations, delusion and hostility previously reported in the literature.…”

Section: Discussioncontrasting

confidence: 76%

“…According to some investigators, an excess of dopamine in the brain or in specific brain areas might ex plain part of the symptomatology, the response to neuroleptic drugs, which are mainly antidopaminergics, and the similarity to amphe tamine psychosis, which is dopamine-dependent (Ellinwood, 1972;Klawans et al, 1972;Randrup et al, 1972;Griffith et al, \912\Snyder et al, 1970;Angrist et al, 1973;Angrist and Gershon, 1974;West, 1974;Gershon et al, 1975) . The excess of dopamine could be due either to increased production, increased sensitivity of the dopamine receptors, or to a decrease in the dopamine antagonists (Keyth et al, 1976).…”

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confidence: 99%

“…In order to test the theory of dopamine excess in schizo phrenia, several groups of investigators have administered a variety of dopamine-related or dopamine-stimulating drugs, such as ¿-dopa, methylphenidate, tricyclic antidepressants, MAOI, apomorphine, D-and ¿-amphetamine in high doses to actively ill schizophrenics (Davis et al, 1972;Davis and Janowsky, 1973;Angrist et al, 1973;Angrist and Gershon, 1974;Janowsky et al, 1974;Janowsky and Davis, 1976;West, 1974;Gershon et al, 1975). They always observed a worsening of the pre-existing symptoms or tire development of new psychotic symptoms, characterized by global deterioration, dose-dependent increase in con ceptual disorganization, hallucinations, delu sion, bizarre behaviour, emotional lability and agitation.…”

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confidence: 99%

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Catecholaminergic Drugs in Chronic Schizophrenia

et al. 1979

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The effect of dopaminergic-related and stimulatory drugs have been studied in chronic hebephrenic schizophrenics untreated with neuroleptic drugs. 6 patients received therapy of 2 g L-dopa + 200 mg carbodopa per day orally for 30 days, then placebo for 30 days. Following that 3 of the same patients received therapy of 2 g L-dopa + 200 mg carbodopa + 300 mg imipramine orally for 30 days, then placebo for 30 days. Following that the same 3 patients recieved 1 mg apomorphine s.c. for 15 days, then placebo for 15 days, then 1 mg apomorphine s.c. + 2 g L-dopa + 200 mg carbodopa per os daily for 15 days, then placebo for 15 days. The patients were examined psychologically by the Wittenborn Rating Scale, the Weigl Object-Sorting Test, and tests for verbal learning and verbal association, before and after each therapeutic trial. Levels of FSH, LH, testosterone and GH were assayed radioimmunologically before, in the middle of and after each course of therapy. 2 patients showed improvement in the affective-behavioural symptomatology during therapy, while the other 4, who had a more severe degree of mental deterioration and destruction, were unchanged. FSH and LH levels, very low under basal conditions, did not change under therapy. Testosterone was very low before therapy and increased in only 1 subject. Normal basal GH levels increased during therapy in some of the patients, but not constantly. The results obtained are discussed in relation to the catecholamine hypotheses of schizophrenia.

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confidence: 76%

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Catecholaminergic Drugs in Chronic Schizophrenia

et al. 1979

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“…Their use is strongly advised against in most psychiatric and pharmacological text-books. Exacerbations of schizophrenic symptomatology induced by sympathomimetics in diet pills and even respiratory congestants have been observed (19,20). Intravenous injections of methylphenidate have been commented on as a diagnostic aid because of the ability of the drug to provoke latent schizophrenic symptomatology (17).…”

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confidence: 99%

Differential response to amphetamine in schizophrenia

Cesarec

Nyman

1985

Acta Psychiatr Scand

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Amphetamine added to maintenance therapy with neuroleptic drugs was accompanied by relief of complaints in 32 of 48 chronic schizophrenic patients with a long-standing incapacity for work. In 22 cases this relief was followed by increased work efficiency. These gains were lost at experimental withdrawal of amphetamine. The response to amphetamine varied with type of schizophrenic symptomatology. All current regressive symptoms meant worsening in spite of concomitant neuroleptic treatment, in accordance with the dopamine hypothesis. Non-regressive subjects displaying florid symptoms, however, benefited. Worsening, in a few cases, occurred only in the absence of neuroleptics. A few subjects with negative symptoms only, seemed totally unresponsive. These findings point at variations in sensitivity to dopaminergic stimulation in schizophrenic subjects. Worsening and improvement with amphetamine were each clearly connected with type of symptomatology only when current psychotic or florid non-regressive symptoms were exhibited. In cases with negative symptoms only, the type of response could not be reliably based on clinical data. Studies of autonomic functioning and attention were therefore performed in a sub-sample. Skin conductance level, reactivity and habituation rate were found to be lower in positive responders before amphetamine. After amphetamine there were no such differences. Attention tests showed no initial differences between groups but the performance of positive responders improved with amphetamine.

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“…Amphetamines and related compounds can exacerbate the symptoms o f schizophrenia (Janowsky et al, 1973a;West, 1974) while producing in non schizophrenics a psychosis that is frequently misdiagnosed as schizophrenia {Connell, 1958) and which, like schizophrenia, responds to neuroleptics (Angrist et al, 1974). As mentioned, the amphetamine psychosis has been proposed as a model o f schizophrenia (K ety, 1959).…”

Section: Amphetamine and Related Compoundsmentioning

confidence: 99%

The Dopamine Hypothesis of Schizophrenia A Critical Analysis

Luchins¹

1975

Neuropsychobiology

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The evidence linking dopamine and schizophrenia is reviewed. Surveyed are studies on dopamine metabolites in schizophrenia, the effects of dopamine agonists, antagonists and depletors on schizophrenia and the action of present treatments of schizophrenia on dopamine. As well, the interrelationship of dopaminergic, cholinergic and gabanergic pathways is examined. It is concluded that the relationship between dopaminergic mechanisms and schizophrenia is nonspecific. The dopamine hypothesis is shown to reflect an attitude towards schizophrenia that emphasizes acute, florid symptoms. It is suggested that research directed towards studying dopaminergic mechanisms in specific psychopathological symptoms, not syndromes, might prove fruitful.

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Interaction of Low-Dose Amphetamine Use with Schizophrenia in Outpatients: Three Case Reports

Cited by 19 publications

References 9 publications

Catecholaminergic Drugs in Chronic Schizophrenia

Catecholaminergic Drugs in Chronic Schizophrenia

Differential response to amphetamine in schizophrenia

The Dopamine Hypothesis of Schizophrenia A Critical Analysis

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