A CONTROLLED STUDY OF THE ANTIPSYCHOTIC AND SEDATIVE EFFECTS OF NEUROLEPTIC DRUGS AND AMPHETAMINE IN CHRONIC SCHIZOPHRENICS: A clinical and experimental‐psychological study

Antipsychotic drugs for patients with schizophrenia and predominant or prominent negative symptoms: a systematic review and meta-analysis

“…The PRISMA flowchart is shown in eFigure 1. Of the 15 excluded studies, four studies may be noteworthy, because they somehow described their patients as having mainly negative symptoms in the "Introduction" or "Discussion" [51][52][53][54]. However, as negative symptoms were not defined by inclusion/exclusion criteria, these studies were excluded (see eAppendix 3).…”

Effects of amphetamine on local cerebral metabolism in normal and schizophrenic subjects as determined by positron emission tomography

“…Effects in normal subjects are dose related and include activation and changes in mood (Angrist 1983) and at high doses, induction of schizophreniform symptoms (Connell 1958;Griffith et al 1968;Angrist and Gershon 1970). In schizophrenics, reported clinical effects include exacerbation of psychotic symptoms (Janowsky et al 1973;Angrist et al 1980), transient decrease in psychoses , and improvement in negative symptoms (Guttman and Sargant 1937;Davidoff and Reifenstein 1938;Cesarec et al 1974;Angrist et al 1982). This variability in schizophrenics' responses may be related to state (Angrist and van Kammen 1984).…”

The Dopamine Hypothesis: An Overview of Studies With Schizophrenic Patients

“…Finally, Kornetsky (1976; table 2) found that multiple oral doses of d-amphetamine did not affect the psychotic symptomatology of 25 chronically hospitalized schizophrenics. Cesarec, Eberhard, and Nordgren (1974) similarly failed to find any worsening psychosis in nine chronic schizophrenics during a 14-day regimen of oral amphetamine. It seems that a particular population of chronic schizophrenics, possibly prevalent in chronic-care institutions, may be unresponsive to the psychotogenic effect of DA agonists.…”

“…For example, Inanaga et al (1975) reported that /-DOPA increased motivation, active contact, and activity while having little effect on hallucinations and delusions. Cesarec, Eberhard, and Nordgren (1974) found an improved initiative and interest in the surroundings when 15-to 20-mg daily oral doses of amphetamine were added to the neuroleptic regimen. Segal and Janowsky (1978) observed that those patients who improved following a methylphenidate infusion were often chronically deteriorated, chronically hospitalized schizophrenics.…”

“…A nondopaminergic etiology might also explain the absence of psychosis-exacerbation after DA agonist (Kornetsky 1976;Segal and Janowsky 1978) and MAOI (Brenner and Shopsin 1980) administration to chronically hospitalized schizophrenics. In fact, the predominant response to DA agonists in a significant proportion of chronic schizophrenics appears to be an improvement in negative symptoms (Cesarec, Eberhard, and Nordgren 1974;Buchanan et al 1975;Gerlach and Luhdorf 1975;Inanaga et al 1975;Ogura, Kishimoto, and Nakao 1976). Foreshadowing Crow's formulation, Segal and Janowsky (1978) suggested that the dichotomous (improvement vs. worsening) responses to DA agonists may reflect at least two different types of schizophrenia.…”