Carpenter W T, Breier A, Buchanan R W, Kirkpatrick B, Shepard P, Weiner E
Maryland Psychiatric Research Center, Department of Psychiatry, University of Maryland, Baltimore, MD 21247, USA.
Neuropsychopharmacology. 2000 Oct;23(4):365-74. doi: 10.1016/S0893-133X(00)00115-9.
Hypodopaminergic and hyponoradrenergic pathophysiology may be a basis for primary and/or secondary negative symptoms in schizophrenia. The hypothesis that enhanced neurotransmission in these systems would be therapeutic for negative symptoms was tested by comparing mazindol and placebo in a double-blind, cross-over design trial. Outcome following mazindol supplementation was comparable to placebo supplementation (F(1,30) = 0.9; p = .57). Results for deficit and non-deficit schizophrenia subjects were similar, and were not affected by whether concurrent the antipsychotic drug treatment was clozapine, fluphenazine, or haloperidol. The efficacy hypothesis was not supported for either primary or secondary negative symptoms.
多巴胺能减退和去甲肾上腺素能减退的病理生理学可能是精神分裂症原发性和/或继发性阴性症状的基础。通过在双盲、交叉设计试验中比较马吲哚和安慰剂,对这些系统中神经传递增强对阴性症状具有治疗作用这一假说进行了检验。补充马吲哚后的结果与补充安慰剂相当(F(1,30) = 0.9;p = 0.57)。缺陷型和非缺陷型精神分裂症患者的结果相似,且不受同时使用的抗精神病药物是氯氮平、氟奋乃静还是氟哌啶醇的影响。原发性或继发性阴性症状的疗效假说均未得到支持。