“…This is likely to involve a combination of excessive release of vasoconstrictive mediators, exaggerated vasoconstrictive response, and reduced vasodilatory response [1,9]. Endothelin-1 and calcitonin generelated peptide are key influencers of these systems, the former responsible for vasoconstriction and the latter released from sensory afferents and resulting in vasodilatation [2,4,9]. Activation of alpha2 adrenoreceptors, structural abnormalities of large and small vessels, and disordered coagulation, including increased platelet aggregation and blood viscosity, have also been implicated [4,9].…”