Teaching Hospital Kandy, Sri Lanka
Dr. S.M.RathnasiriBandarais waiting to complete his PhD in 2017 at faculty of medicine ,University of Peradeniya in Sri Lanka on the topic of paranasal nitric oxide and migraine and working as second in charge in youth friendly clinic at teaching hospital Kandy,Sri Lanka .He has published 2 papers on hypoxic nitric oxide theory( SHNOT) for migraine and psychiatric disorders in a reputed journal. thatwas related to a new hypothesis connected to pranasal sinus nitric oxide and neuropsychiatric disorders.He also has served as the president of human protection foundation in Sri Lanka since 2005
Migraine is a debilitating illness that has no exact bio molecule to explain its pathology. After reviewing the neurophysiological and biochemical basis of the research findings of nitric oxide and migraine, I present to the best of my knowledge the first para sinus nitric oxide mediated neurobiophysiological hypothesis for migraine of sinorhinogenic origin. The diffused paranasal sinus nitric oxide in the nasal mucosa could be the primary molecule that initiates migraine and is termed Sinus Hypoxic Nitric Oxide Theory. This hypothesis regards repetitive or intermittent activation of the trigeminal sensory nerve and blood vessels in the nasal mucosa. Production of paranasal sinus nitric oxide is mainly induced by hypoxia due to several independent factors and the diffusion of paranasal sinus nitric oxide depends on the vulnerable surface area in the nasal cavity. Apart from the known trigeminal nociceptive impulse in the migraine, two main peripheral trigeminal nerve activating mechanisms may induce migraine. First the nerve endings of the nasal mucosa which are directly stimulated by diffused paranasal sinus nitric oxide are indirectly stimulated by vasoactive substances released by antidromic activation of the nerve, parasympathetic efferent of the nerve and sterile neurogenic inflammation. Secondly, the perivascular nerve of nasal mucosal and the meningial blood vessels are directly stimulated by either diffused paranasalsinus nitric oxide or by shear stress mediation. The nerve impulses of the trigeminal sensory nerve, projected at trigeminal nucleus caudalis to the central nerve system and low plasma magnesium due to theconsequence of shear stress gives rise to the symptoms of migraine. Moreover sinorhinogenic impulses may mediate to disruption of inhibitory sensitization modulated of sensory input and cause sensory hiperexcitability. In addition neuronal stimulation proposed by some migraine hypotheses could also give rise to migraine headache when the sinorhinogenic vulnerable factors induce the migraine pathophysiology. Indeed this article explains a new pathophysiological initiation between sinorhinogenic nitric oxide effects and migraine and provides an initial step for the obscured or neglected etiologically important neuro vascular impulse generating pathway. The patients who are clinically suspected of having headaches should receive comprehensive sinorhinological examination and evaluation based on the sinus hypoxic nitric oxide theory. A standard surgical and medical management of migraine that links with the sinus hypoxic nitric oxide theory may restore the hypoxic state or reduce or remove the paranasalsinus nitric oxide diffusing surface. It warrants clinical testing.