Is there any point to vasovagal syncope?

The above considerations do not provide a definite answer regarding the putative meaning of VVS. We add to the confusion by suggesting two new hypotheses (the last two), even if there are perhaps already too many theories for the number of facts. The animal reflexes provide only fragmentary bases for the human reflex, and explain almost none of its clinical richness. The critical link between the animal precursor and human syncope is unknown. We do feel that VVS in its current form cannot be considered beneficial. Even if it is based on a beneficial principle, its expression suggests a response that has gone out of control. Are there ways to prove or disprove any of these hypotheses? Perhaps there are; at present we know the pathway of the reflex from the brainstem nuclei to the effector mechanisms. Hardly anything is known about the afferent pathway, however. It seems unlikely that standing and fear have completely identical afferent pathways. The organ giving off signals that set the reflex in motion needs to be identified. If central hypovolemia is involved in VVS evoked by standing, it may be possible to find out whether receptors in, for instance, abdominal underfilled veins or arteries are involved. If this succeeds, people with clear fear-induced VVS can be investigated to see if this mechanism operates in them as well. Once these paths are better known, perhaps we can identify the origin or origins of this oddest of reflexes.