11 showed that administering exogenous adenosine precipitated migraine. 10 observed elevated plasma levels of adenosine during migraine attacks whereas Brown et al. 9 Some studies have supported the purinergic hypothesis as an epiphenomenon rather than the factor triggering migraine. 8 This is the basis for the ‘purinergic’ hypothesis for migraine, a theory proposed in 1989 which suggests that purines trigger migraine attacks due to their powerful vasodilator effect. However, the analgesic action of caffeine is based on its powerful vasoconstrictor effect, which counteracts the vasodilator effect of purines. In this context, the hypothesis that caffeine has an analgesic effect and may be useful in acute management of headache may seem paradoxical. Caffeine induces a state of cortical hyperexcitability due to its inhibitory effect on adenosine receptors this process increases alertness and improves cognitive function. 7 In general terms, adenosine inhibits the release of excitatory neurotransmitters leading to decreased cortical excitability. A 1 receptors are the subtype of adenosine receptors with the widest distribution throughout the brain and spinal cord, and they also have the greatest affinity for caffeine ( Fig. 7 Four subtypes of adenosine receptors have been described to date: A 1, A 2A, A 2B, and A 3. It acts at the neuronal level thanks to the action of P1 receptors these receptors are also known as adenosine receptors and they are G protein-coupled. 6 Adenosine is a purine nucleotide released by adenosine triphosphate (ATP) from astrocytes. 6Ĭaffeine molecules, which are structurally similar to adenosine, bind to adenosine receptors in the cell surface without activating them, thereby acting as competitive inhibitors. 6 Caffeine has an oral bioavailability of almost 100% and a half-life ranging from 4 to 9 hours, depending on several factors: it is shorter in smokers and longer in women who are pregnant or taking oral contraceptives. It is synthesised from adenosine and metabolised by cytochrome P450 (CYP1A2) into different active metabolites: paraxanthine (84%), theobromine (12%), and theophylline (4%). 6 Caffeine, also known as trimethylxanthine, is a naturally occurring alkaloid in some plants. Caffeine: action mechanism and its association with the pathophysiology of headacheĬaffeine, a chemical compound found in coffee, was isolated in 1819 by German chemist Friedrich Ferdinand Runge this researcher coined the term ‘Kaffein’, which became ‘caffeine’ in English. 5 The purpose of our review article is to gain a better understanding of the physiological effects of caffeine and its association with headache, whether as a trigger factor for medication overuse headache or as a substance exacerbating primary headache. 4 The International Headache Society does not list caffeine among substances potentially causing analgesic-overuse headache but rather as a substance that may cause headache when regular consumption over 200 mg/day for more than 2 weeks is discontinued abruptly. Caffeine may also cause physical dependence which may manifest as withdrawal syndrome. In the long-term, however, excessive caffeine consumption may increase the risk of medication overuse headache and lead to chronification of some primary headaches. 3Īt high doses, caffeine has an antinoceptive effect and acts as an adjuvant to other analgesics. 2 Excessive caffeine consumption causes acute and long-term biological and physiological changes deriving in cognitive deficits, depression, fatigue, insomnia, cardiovascular problems, and headache, among others. In the USA, however, nearly 30% of the population consumes over 500 mg/day, and this tendency is most frequently seen among people aged 35 to 64. 1 Caffeine intake in healthy adults is not recommended to exceed 400-450 mg/day. In the USA, over 87% of the population consumes some amount of caffeine every day. Caffeine is the world's most widely consumed psychostimulant drug.
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