Pathogenesis of headaches

Pathogenesis of headaches

Pathogenesis of tension headache. The pathophysiological changes observed in patients with migraine may also exist in patients with tension headache. In general, tension headache has quality characteristics similar to migraine, differing only in lower intensity.

For this reason, many headache specialists consider migraine and tension headache as a single condition, suggesting that migraine is a more severe form of headache with a gross adjustment disorder, and tension headache is a moderate headache and does not have a significant effect on working capacity.

The similarities in the pathophysiology of migraine and tension headaches determine the similar tactics of their drug and non-drug correction. For example, triptans used in migraine (including sumatriptan and rizatriptan®) have been shown to be effective in treating headaches of non-migraine etiology and tension headaches.

Pathogenesis of drug-induced headache

The analgesic effect of acetylsalicylic acid and acetaminophen® can in part be explained by the suppression of the functional activity of the cortical 5-HT2 receptors.

If intermittent use of analgesics can alleviate headache, then continuous, daily use of these drugs contributes to an increase in the activity of postsynaptic serotonin 5-HT2 receptors, which stimulates pain receptors and explains the increase in headaches during prolonged and uncontrolled administration of analgesics or other drugs that increase serotonin activity (for example, triptans).

After rejection of regular medication, the activity of serotonin receptors slowly normalizes, usually within 3 months. This is supported by the fact that patients with drug-induced headache after the abolition of analgesics require several months for their headaches to return to their original (before the formation of abuse) level.