Migraine is "a common episodic neurological disorder with complex pathophysiology that
manifests as recurrent attacks of typically throbbing and unilateral, often severe
headache with certain associated features such as nausea, phonophobia, and photophobia".
Worldwide, estimated prevalence was 13.8% to 15%. Quality of life of a migraine patient
is extremely low and migraine badly hampers one's physical, emotional, and social
efficiency and disrupt familial, social and professional relationships. Diagnosis is
solely clinical depending on characteristics of headache and associated symptoms.
Neuroimaging can be done only when exclusion of another cause of headache is needed.
Exact etiology and pathophysiology of migraine is unknown and multifactorial. There are
several hypotheses of migraine pain generation. Local dilatation of intracranial and
extracerebral vessels activate trigeminal nerve surrounding cerebral and meningeal
vasculature. Migraine pain starts from the activation of trigeminovascular system.
Afferent fibers innervating cerebral and meningeal vessels project to central nervous
system and releases vasoactive peptides and inflammatory mediators. Some important
mediators like Calcitonin gene related peptide (CGRP), NO, Substance P play role in
inflammation and vasodilatation. Then sensitization and discharge of thalamic neuron and
subsequent projection to sensory cortical neurons occurs. Thus, pain perception is
received in migraine.
In studies, elevated levels of C reactive protein (CRP) and Transforming growth factor β
(TGF-β) provides evidence of neuroinflammation. In migraine, impairment of cerebral
mitochondrial energy metabolism and oxidative stress occurs. As a result, abnormalities
in cerebral vasculature results in Cortical Spreading Depression (CSD).
Niacin, which is known as nicotinic acid or Vitamin B3 is the precursor of Nicotinamide
Adenine Dinucleotide (NAD) or Nicotinamide Adenine Dinucleotide Phosphate (NADP). From
dietary tryptophan, through kynurenine pathway, NAD is produced, and rest 1% tryptophan
is catabolized to form serotonin (5- hydroxytryptamine/ 5-HT). Migraine is a serotonin
deficient condition. It has been estimated that, dietary intake of Niacin is low in
migraine patients.
Niacin supplementation provides enough NAD to inhibit Kynurenine pathway and accelerate
production of 5-HT from tryptophan. Serotonin acting on 5-HT1 receptor, causes
vasoconstriction. It may activate nerve endings in cerebral microcirculation and
sensitize them to vasodilatory kinins. Serotonin also inhibits synthesis, release of NO,
glutamate, Calcitonin gene-related peptide (CGRP). As a result, inhibition of afferent
pain transmission and prevention of neuroinflammation occurs. Niacin also reduces
inflammation evidenced by decrease level of pro inflammatory cytokines like IL-6, IL-1β,
TNF α, high-sensitivity C-reactive protein (hs-CRP). Increasing level of Niacin also
improves brain energy deficiency, and has potent antioxidant properties, which may be
helpful in migraine prevention. However, more prospective investigations are necessary to
validate niacin's preventive effect on migraine.