Senanayake N, Karalliedde L
N Engl J Med. 1987 Mar 26;316(13):761-3. doi: 10.1056/NEJM198703263161301.
Acute neurotoxic effects during the cholinergic phase of organophosphorus insecticide poisoning and delayed neurotoxic effects appearing two to three weeks later are well recognized. We observed 10 patients who had paralysis of proximal limb muscles, neck flexors, motor cranial nerves, and respiratory muscles 24 to 96 hours after poisoning, after a well-defined cholinergic phase. The compounds involved were fenthion, monocrotophos, dimethoate, and methamidophos. Four patients urgently required ventilatory support. The paralytic symptoms lasted up to 18 days. A delayed polyneuropathy later developed in one patient. Three patients died. Electromyographic studies showed fade on tetanic stimulation, absence of fade on low-frequency stimulation, and absence of post-tetanic facilitation, suggestive of a postsynaptic defect. This neuromuscular junctional defect may have been the predominant cause of the paralytic symptoms, with neural and central components contributing to various degrees. Our patients appeared to have a distinct clinical entity (a so-called intermediate syndrome) that developed after the acute cholinergic crisis and before the expected onset of the delayed neuropathy.
有机磷杀虫剂中毒胆碱能期的急性神经毒性作用以及两到三周后出现的迟发性神经毒性作用已广为人知。我们观察了10例患者，在明确的胆碱能期过后，于中毒后24至96小时出现近端肢体肌肉、颈部屈肌、运动性颅神经及呼吸肌麻痹。涉及的化合物有倍硫磷、久效磷、乐果和甲胺磷。4例患者急需通气支持。麻痹症状持续长达18天。1例患者后来出现迟发性多发性神经病。3例患者死亡。肌电图研究显示强直刺激时波幅递减、低频刺激时波幅无递减以及强直后易化消失，提示为突触后缺陷。这种神经肌肉接头缺陷可能是麻痹症状的主要原因，神经和中枢成分也有不同程度的作用。我们的患者似乎有一种独特的临床病症（所谓的中间综合征），发生在急性胆碱能危象之后、预期迟发性神经病发作之前。
