神经性肺水肿(NPE)发生于各种急性中枢神经系统(CNS)损伤(通常是致命性的)之后,而病人原来并无肺、心疾病。用实验方法损坏动物CNS不同部位可产生NPE,也有许多CNS疾患伴发NPE的报导。但其发病原理尚不清楚。 CNS损伤后可很快发生肺水肿。在头部创伤或向第四脑室注射纤维素当即致死的动物常显示全肺的肺水肿。人体也有同样的情况,有人在8例头部创伤当即死亡的病人全都见到肺水肺。在单纯头部枪弹穿通伤即刻致死的士兵也常有肺水肿。这种起病形式提示NPE是由损伤的大脑迅速发放神经冲动的结果。与丘脑下部病损的关系各种CNS损伤都与NPE有关,因此它的发生 Neuropathic pulmonary edema (NPE) occurs after a variety of acute central nervous system (CNS) lesions, usually fatal, without previous pulmonary and heart disease. Experimental methods to damage different parts of the animal CNS produce NPE, there are many reports of CNS disorders associated with NPE. But its pathogenesis is not clear. Pulmonary edema can occur very quickly after CNS injury. Animals that are immediately fatal to head trauma or intracelluar injection of cellulose often show pulmonary edema throughout the lungs. The same is true in the human body, with some seeing pulmonary scrubbing in all eight patients who died immediately after a head injury. Soldiers who die immediately after a simple head-gunshot wound often have pulmonary edema. This form of onset suggests that NPE is the result of nerve impulses released rapidly by the injured brain. Relationship with lesion in the inferior thalamus Various CNS lesions are associated with NPE and therefore its occurrence