Stephenson J B
Br Med J. 1978 Sep 9;2(6139):726-8. doi: 10.1136/bmj.2.6139.726.
The duration of cardiac asystole induced by ocular compression was measured in 100 consecutive children referred for electroencephalographic examination after one or more febrile convulsions (FC). The children were classified into three groups-namely, those with anoxic FCs, those with epileptic FCs, and "others"-according to the appearances of the FC and the electroencephalogram (EEG). In 14 children the description of the FC suggested non-epileptic anoxic cerebral seizures such as are seen after prolonged syncope or breath-holding. In 35 children the FCs were assumed to be epileptic in mechanism on the basis of unilateral (hemiclonic) twitching, known cerebral disease, a family history of epilepsy, or spikes on the EEG. In the 51 "others" the FCs could not be classified. Definitely abnormal asystole (four seconds or over) was induced by ocular compression in half the anoxic group, in 16% of the "others," but in none of the epileptic group. The differences between the degree of asystole induced in each of the three groups was highly significant (P=0.005).These results support the hypothesis that vagal-mediated cerebral ischaemic anoxia is implicated in the genesis of FCs that resemble anoxic seizures and in a substantial number of those without an obvious epileptic mechanism. The significance, genetics, management, and prognosis of FCs must now be re-examined in this light.
对100名因一次或多次热性惊厥(FC)而接受脑电图检查的连续儿童,测量了眼压迫诱发的心搏停止持续时间。根据热性惊厥的表现和脑电图(EEG),将这些儿童分为三组,即缺氧性热性惊厥组、癫痫性热性惊厥组和“其他”组。在14名儿童中,热性惊厥的描述提示为非癫痫性缺氧性脑惊厥,如长时间晕厥或屏气后所见。在35名儿童中,基于单侧(半侧阵挛性)抽搐、已知的脑部疾病、癫痫家族史或脑电图上的棘波,热性惊厥在机制上被认为是癫痫性的。在51名“其他”组儿童中,热性惊厥无法分类。眼压迫在缺氧组半数儿童中诱发了明确异常的心搏停止(4秒或更长),在“其他”组的16%中诱发了这种情况,但癫痫组中无一例出现。三组中每组诱发的心搏停止程度差异具有高度显著性(P = 0.005)。这些结果支持这样的假说,即迷走神经介导的脑缺血缺氧与类似于缺氧性惊厥的热性惊厥的发生以及大量无明显癫痫机制的热性惊厥的发生有关。现在必须据此重新审视热性惊厥的意义、遗传学、管理和预后。