Hypodopaminergic and hyponoradrenergic pathophysiology may be a basis for p
rimary and/or secondary negative symptoms in schizophrenia. The hypothesis
that enhanced neurotransmission in these systems would be therapeutic for n
egative symptoms was tested by comparing mazindol and placebo in a double-b
lind, cross-over design trial. Outcome following mazindol supplementation w
as comparable to placebo supplementation (F(1,30) = 0.9; p = .57). Results
for deficit and non-deficit schizophrenia subjects were similar, and were n
ot affected by whether concurrent the antipsychotic drug treatment was cloz
apine, fluphenazine, or haloperidol. The efficacy hypothesis was not suppor
ted for either primary or secondary negative symptoms. (C) 2000 American Co
llege of Neuropsychopharmacology. Published by Elsevier Science Inc.