Migraine is a common, chronic, incapacitating, multifactorial disorder, mainly neurovascular, characterized by recurrent and severe episodes of pulsatile headache with systemic or neurological symptoms.

Symptoms include headache, nausea or vomiting, painful avoidance of light and sound, and aggravated by regular physical activity or its avoidance.
The symptoms of migraine have many consequences in daily life and social activities, psychological aspects, loss of working hours, etc.
These vary among individuals, and different symptoms may occur during different attacks. Migraine attacks can also differ in duration and frequency, generally lasting from 4 to 72 hours.

Most migraine attacks start at puberty and affect people between 35 and 45 years old. The prevalence is higher in women (5-25%) than in men (2-10%). The incidence of migraine attacks tends to reach its peak among adolescents and the elderly, older than 60 years (I. E. Morillo et al., R.B. Lipton et al.).
The Global Burden of Disease 2015 study classifies migraine as the fourth cause of years lived with disability in women and the eighth leading cause of men due to its clinical manifestations (pain of moderate to severe intensity, nausea/vomiting, sensitivity to light and sound).
The World Health Association has classified headache as a major health disorder and has rated migraine amongst the top 20 most disabling lifetime conditions.

An extensive bibliography states that migraine occurs as a consequence of the activation or irritation of the trigeminal nerve fibers, under the called “neurogenic inflammation” process.

Some neuropeptides are released (sensory calcitonin gene-related peptide -CGRP-and substance P) and may take part in neurogenic inflammation (plasma protein extravasation and vasodilatation) of the intracranial vasculature and peripheral and central sensitization of the trigeminal system.

The trigeminal nerve is the nerve that transmits the sensitivity of the head and has three branches (ophthalmic, maxillary and mandibular). The fibers that come from the first branch surround the blood vessels located in the meninges.

The meninges are made up of several layers of tissue that line the brain, and they are the structures that “hurt”. The brain itself does not hurt, only its covers.
Inflammation of the meninges occurs during a migraine attack as a consequence of the release of inflammatory substances by the trigeminal. This noninfectious inflammation or “meningitis” is responsible for causing the pulsatile pain or feeling the heartbeat.

In addition, this inflammation means that, when we move our heads, the pain will worsen or increase and, therefore, that we will be more relieved if we go to bed or do not move.
Despite all the advances in the field of migraine, there are still many gaps about the triggers and all the mechanisms that can intervene, but it is assumed that the pain of migraine is due to a malfunction of the pain system, which causes the occurrence -for causes that are unknown for now- a stimulation of the trigeminal terminals at the level of the meninges. This produces a release of substances that promote inflammation and, in turn, not only irritate the nerve endings themselves but also sends this information back to the central level to finally have the perception of pain.

The main triggers are genetic inheritance, stress, alterations in hormone levels (serotonin levels, especially in women), seasonal changes, trigeminal nerve sensitization, oxidative stress, mitochondrial dysfunction and inflammation.

According to the American Migraine Foundation (AMF), the main triggers of migraine are:

– Stress
– Changes in sleep schedule or irregular sleep
– Hormones
– Caffeine and alcohol
– Diet
– Dehydration
– Light
– Smells
– Excessive use of medication

The most common forms of migraine are divided into two main categories, migraine with aura (MA) and migraine without aura (MO). MO is the most common type of migraine, and approximately 80% of patients with migraine have this type. MA is characterized mainly by the presence of focal neurological symptoms, such as blurred vision, vertigo or hallucination, and these symptoms usually precede or accompany headache attacks.

The neurovascular theory of the pathogenesis of migraine attacks is the most widely accepted. The stimulation of the trigeminal nerve occurs through neuronal and chemical pathways, through serotonin, histamine and prostaglandins. Migraine-inducing factors can act directly on these chemical mediators or through the mediators of the nervous system.

Serotonin may contribute to pain in migraine by generating inflammation and sensitization of sensory nerves (Lambert GA).

Las formas más comunes de migraña se dividen en dos categorías principales, la migraña con aura (MA) y la migraña sin aura (MO). La MO es el tipo más común de migraña, y aproximadamente el 80% de los pacientes con migraña tienen este tipo. La MA se caracteriza principalmente por la presencia de síntomas neurológicos focales, como visión borrosa, vértigo o alucinación, y estos síntomas generalmente preceden o acompañan a los ataques de dolor de cabeza.

La teoría neurovascular de la patogénesis de ataques de migraña es la más ampliamente aceptada. La estimulación del nervio trigémino se produce a través de vías neuronales y químicas, a través de la serotonina, la histamina y las prostaglandinas. Los factores inductores de migraña pueden actuar directamente sobre estos mediadores químicos o a través de los mediadores del sistema nervioso.

La serotonina podría contribuir al dolor en la migraña mediante la generación de inflamación y sensibilización de los nervios sensoriales (Lambert GA).