Godlevsky Leonid S, van Luijtelaar G, Shandra A A, Coenen A M L
Department of Biophysics, Informatics and Medical Devices, Medical University, Odessa, Ukraine.
Med Hypotheses. 2002 Mar;58(3):237-43. doi: 10.1054/mehy.2001.1499.
Examples from experimental epilepsy in animals are used to illustrate the view that a crucial role of the transfer of mechanisms from compensatory into pathogenic (e.g. lethal ones in the course of a disease), is played by the power of pathologic stimuli. In the genesis of epilepsy it is suggested that a critical increase of endogenous factors may underlie the conversion of the absence form of epilepsy into a generalized self-supporting form. The ability to precipitate endogenous self-augmenting mechanisms of diseases may have increased in the course of evolution. The lethal result of a serious pathogenic process leads to the suggestion that organisms cope with the disease by dying. This prevents spreading of the putative infectious disease within the population. This mechanism of disease aggravation could play a role in the survival of the species and in further evolutionary progress. This may explain why certain species may have survived in evolution and supports the theory of synthetic evolution.
动物实验性癫痫的例子被用来说明这样一种观点，即从代偿性机制转变为致病性机制（例如疾病过程中的致死性机制）的关键作用是由病理刺激的强度发挥的。在癫痫的发生过程中，有人提出内源性因素的临界增加可能是癫痫失神形式转变为全身性自我维持形式的基础。在进化过程中，引发疾病内源性自我增强机制的能力可能有所增加。严重致病过程的致死结果表明，生物体通过死亡来应对疾病。这可防止假定的传染病在种群内传播。这种疾病加重机制可能在物种生存和进一步进化进程中发挥作用。这或许可以解释为什么某些物种在进化中得以幸存，并支持了综合进化理论。
