Freidkov V I, Bondarenko E S, Shiretorova D Ch
Zh Nevropatol Psikhiatr Im S S Korsakova. 1980;80(10):1453-8.
Owing to a high plasticity of the child's brain complete or partial compensation of a cerebral defect is possible. However an infection or a craniocerebral injury may interfere with the compensation of the premorbid defect of the nervous system: this was noted in 65% of children observed by the authors. Therefore, while specifying the syndromological structure of a disease one must take into account the time course of the premorbid defect. The compensation of that defect is hampered most often in children of the first year of the life. In these cases a loss of a part of acquired habits and appearance of earlier-age reflexes is noted. At the age of 2 to 5 years an aggravation of the atactic and hyperkinetic syndromes is observed, while at the age of over 5 years the negative time course of the premorbid defects is noted twice as rarer. Variants of the time course of the premorbid nervous disorders are specified. At the basis of reversible variants are disturbances on the part of hemodynamics and cerebrospinal fluid. This is confirmed by echo-EEG and REG findings. Persisting aggravation of the premorbid defect and appearance of new neurological symptoms are observed on development of hypoxic and metabolic disturbances. The nervous structures affected by perinatal hypoxia remain thenceforth to be especially sensitive to the effects of the latter. An analysis of the pathogenetic mechanisms of the premorbid defect decompensation may facilitate the realization of therapeutic and prophylactic measures.
由于儿童大脑具有高度可塑性,大脑缺陷有可能得到完全或部分代偿。然而,感染或颅脑损伤可能会干扰对病前神经系统缺陷的代偿:作者观察的儿童中有65%出现了这种情况。因此,在明确疾病的综合征结构时,必须考虑病前缺陷的病程。这种缺陷的代偿在一岁儿童中最常受到阻碍。在这些情况下,会出现部分已习得习惯的丧失和早期反射的出现。在2至5岁时,会观察到共济失调和多动综合征的加重,而在5岁以上时,病前缺陷的负面病程出现的频率则减少一半。明确了病前神经障碍病程的各种变体。可逆性变体的基础是血液动力学和脑脊液方面的紊乱。脑电地形图和脑血流图的结果证实了这一点。在出现缺氧和代谢紊乱时,会观察到病前缺陷持续加重并出现新的神经症状。受围产期缺氧影响的神经结构此后对其影响仍特别敏感。对病前缺陷失代偿的发病机制进行分析可能有助于实施治疗和预防措施。