Migraine is a complex neurological condition characterized by episodes of moderate to intense, throbbing pain, typically on one side of the head. It is frequently accompanied by symptoms such as nausea, vomiting, and extreme sensitivity to light (photophobia) and sound (phonophobia). Understanding migraine requires separating the underlying biological cause—the internal mechanism in the brain—from the various triggers—the factors that initiate that mechanism. This distinction is fundamental to managing a disorder that affects millions globally.
The Underlying Neurovascular Mechanism
The primary cause of a migraine attack is a neurological event involving the trigeminovascular system, a network of nerves and blood vessels surrounding the brain. The process begins with the activation of the trigeminal nerve, which is responsible for sensation in the face and head. This activation leads to the release of neurochemicals from the nerve endings in the meninges, the protective layers covering the brain.
The most studied of these neurochemicals is Calcitonin Gene-Related Peptide (CGRP), a neuropeptide that plays a major role in pain transmission and vasodilation. When CGRP is released, it binds to receptors on blood vessels, causing them to widen (vasodilation). This CGRP release and subsequent inflammation sensitizes the trigeminal nerve endings, which send intense pain signals back to the brainstem and upper spinal cord.
This constant signaling leads to central sensitization, where the pain pathways in the brain become highly reactive to mild stimuli. The result is the characteristic throbbing pain, often exacerbated by routine physical activity. This underlying biological cascade of neurogenic inflammation and hypersensitivity is the direct cause of the pain.
Environmental and Lifestyle Triggers
External factors often serve as the trigger that initiates an attack. One of the most commonly reported triggers is stress, which involves a hormonal response that can lower the migraine threshold. The period immediately following a high-stress event, due to the subsequent drop in stress hormones, is frequently when a migraine is initiated.
Disruptions to the sleep cycle are also powerful triggers, as both deprivation and over-sleeping can induce an attack. Maintaining a consistent sleep schedule helps regulate the brain’s chemical balance; sudden changes, like sleeping late on weekends, can destabilize this rhythm. Sensory overstimulation is another trigger, causing the brain to become overwhelmed by external input.
Bright or flickering lights (photophobia) and loud, repetitive sounds (phonophobia) can provoke a migraine by activating sensitive neural pathways. Strong odors (osmophobia), such as those from perfumes, cleaning products, or smoke, also act as triggers for some individuals. Shifts in weather, particularly sharp drops in barometric pressure, are frequent triggers due to the body’s internal pressure sensors reacting to the atmospheric change.
Dietary and Chemical Triggers
Substances consumed through food and drink act as direct chemical triggers by interacting with the body’s vascular and nervous systems. Certain compounds naturally found in foods can initiate the neurovascular cascade. Tyramine, an amino acid that occurs naturally as proteins break down, is a common culprit.
Foods that are aged, fermented, or cured often contain high levels of tyramine, including aged cheeses, cured meats, and pickled items. Nitrates and nitrites, chemical preservatives used in processed meats, can trigger migraines by causing blood vessel dilation.
Certain food additives also pose a risk, most notably the artificial sweetener aspartame and the flavor enhancer Monosodium Glutamate, or MSG. These chemicals are thought to overstimulate nerve cells, contributing to the onset of an attack. Alcohol, especially red wine, is a frequent trigger, likely due to a combination of compounds like histamine, tyramine, and the dehydrating effects of ethanol. Caffeine exhibits a dual relationship with migraines, as both withdrawal from regular consumption and excessive intake can precipitate an episode.
Hormonal and Medication-Related Factors
Internal chemical changes, particularly involving hormones, are a major class of migraine triggers, especially for women. Estrogen fluctuations are strongly implicated in the timing and severity of many attacks. The sharp decline in estrogen levels just before menstruation is the most common hormonal trigger, leading to menstrual migraines.
This sudden drop in estrogen is thought to increase pain sensitivity and destabilize the brain’s pain regulation systems. Fluctuations during other life stages, such as pregnancy, perimenopause, or when starting or stopping hormonal birth control, can also alter a woman’s migraine pattern. The incidence dramatically increases for females after menarche, underscoring the role of sex hormones.
Medication Overuse Headache
Another distinct cause of chronic migraine is Medication Overuse Headache (MOH), formerly known as rebound headache. This condition develops when acute migraine medications are taken too frequently, leading the body to adapt to the constant presence of the drug. The overuse of triptans, opioids, or combination analgesics can paradoxically increase headache frequency. As the medication wears off, it triggers a withdrawal-like headache, creating a vicious cycle of dependency and escalating chronic pain.