The PSS ultrastructure suggests that a local episodic inflammatory response can be an imprtant component in pathogenesis of the syndrome. In particular, the presence of  mononuclear infiltrate and the accumulation of extracellular fluid with increased intercellular spaces support this idea. Measurements of acute-phase proteins (SAA), Th1/Th2 cytokines and a better characterization of inflammatory cells in the ocular liquids could be very useful. In addition, the mononuclear infiltrate suggests a chronic/autoimmune response. A crucial question with a difficult answer is: what is the trigger of the recurrent local inflammation? This question is frequently posed in many different human pathologies such as coronary vasospam (with/witout infarction), vasospasm/vasodilation in migraine, etc. A possible answer is that an activation of the HIF/NFkB axis occurs, due to a local transient ischaemic hypoxia.  The very low incidence of PSS and the absence of an animal model are formidable obstacles in clarifying the problem.