Timsit-Berthier M
Rev Electroencephalogr Neurophysiol Clin. 1981 Nov;11(2):236-44. doi: 10.1016/s0370-4475(81)80058-5.
After a review of the literature stressing the biological factors underlying CNV genesis, the author sets up a tentative biological model of CNV, based on the neurophysiological and neurochemical findings of Skinner and Yingling (1977) and Marczynski (1978). In terms of balance between excitatory and inhibitory processes this model encompasses different CNV abnormalities in amplitude or duration frequently observed in mental pathology. The interest of such a model lies in the physiopathologic and therapeutic hypotheses it may lead to. In this respect, CNVs of prolonged duration, which would reflect a catecholaminergic hyperactivity, could constitute an indication for treatment by neuroleptics and/or benzodiazepines. CNVs with a weak amplitude would rather invite one to prescribe antidepressant drugs.
在回顾了强调CNV发生的生物学因素的文献后,作者基于Skinner和Yingling(1977年)以及Marczynski(1978年)的神经生理学和神经化学研究结果,建立了一个关于CNV的初步生物学模型。就兴奋和抑制过程之间的平衡而言,该模型涵盖了在精神病理学中经常观察到的不同幅度或持续时间的CNV异常。这种模型的意义在于它可能引发的病理生理学和治疗假设。在这方面,持续时间延长的CNV反映了儿茶酚胺能亢进,可能成为使用抗精神病药物和/或苯二氮䓬类药物治疗的指征。幅度较弱的CNV则更倾向于使用抗抑郁药物。