Lamprecht F
J Neural Transm. 1977;40(2):159-70. doi: 10.1007/BF01250566.
This paper reviews some of the evidence in the literature that suggests neurochemical processes by which the regulation of seizure threshold and the onset of schizophrenic-like symptoms are interrelated. For those patients who experience the alternation of seizures and acute psychoses the following working hypothesis is presented: The central dopaminergic synapse is described as a malfunctioning regulatory circuit. Insufficient feedback inhibition or lifting of the setpoint leads to an increased number of occupied receptors. This might cause schizophrenic-like symptoms. Insufficient release of feedback control or lowering of the setpoint leads to a decreased number of occupied receptors. This might increase seizure susceptibility. The neurochemical arguments in support of this hypothesis will be discussed in detail. The localization of the dopaminergic synapses involved in the development of schizophrenic-like symptoms is subject to speculation. The meso-limbic dopaminergic system has to be taken into consideration.
本文回顾了文献中的一些证据，这些证据表明调节癫痫阈值和精神分裂症样症状发作的神经化学过程是相互关联的。对于那些经历癫痫发作和急性精神病交替发作的患者，提出了以下工作假设：中枢多巴胺能突触被描述为一个功能失调的调节回路。反馈抑制不足或设定点升高会导致被占据受体数量增加。这可能会导致精神分裂症样症状。反馈控制释放不足或设定点降低会导致被占据受体数量减少。这可能会增加癫痫易感性。支持这一假设的神经化学论据将详细讨论。参与精神分裂症样症状发展的多巴胺能突触的定位尚待推测。中脑边缘多巴胺能系统必须予以考虑。
