PATHOPHYSIOLOGIC STUDIES OF Ill GULF WAR VETERANS & CONTROLS

待检验的假设如下：海湾战争综合征是由于在战争中暴露于有机磷化合物导致脑干损伤。 脑干调节过程的功能障碍导致中枢性睡眠呼吸暂停，其通过外周或中枢化学反射敏化产生交感神经过度活跃，导致神经源性高血压的形式。 或者，脑干损伤区域中受损的小胶质细胞可能过度产生白细胞介素-6，这反过来又刺激皮质醇、去甲肾上腺素和交感神经系统活性的过度产生，正如最近在CVA患者中发现的那样。 从药理学上中断脑干功能障碍的代谢后果可能会大大缓解海湾战争综合征的许多症状。

The hypotheses to be tested are as follows: The Gulf War syndrome is due to exposure to combinations of organophosphates in the war that caused brainstem injury. Malfunction of the brainstem regulatory processes are causing central sleep apnea, which is producing sympathetic nerve hyperactivity through peripheral or central chemoreflex sensitization, resulting in a form of neurogenic hypertension. Alternatively, it is possible that injured microglia in the area of brainstem injury are overproducing interleukin-6, which in turn is stimulating overproduction of cortisol, norepinephrine and sympathetic nervous system activity, as has recently been found in patients after CVA's. Pharmacologically interrupting the metabolic consequences of the brainstem dysfunction may provide substantial relief from many of the symptoms of Gulf War syndrome.