Pathogenesis (developmental mechanisms) of migraine
Head structures that are sensitive to pain include skin, bones, paranasal sinuses, blood vessels, and muscles. The parenchyma of the brain is insensitive to pain. Secondary headaches occur during stretching, inflammation and damage to the bones of the skull or increased intracranial pressure, which affect pain-sensitive structures.
It is believed that the appearance of primary headaches is associated with the activation of neurons conducting pain impulses in the brain. The overwhelming majority of types of primary headaches develop due to an imbalance or activity of neurotransmitters. The most studied for primary headaches are disorders in the serotonergic system.
Traditionally, migraine has been considered as a vascular headache. It is now established that migraine is the primary neurogenic disease in which vascular disorders are the result of changes in the activity of the nervous system. The pathogenesis of migraine is based on three phases:
• increased excitability of brain stem neurons;
• spreading cortical depression, manifested by aura;
• activation of the trigemo-vascular system, manifested by symptoms of a migraine attack.
Increased excitability of the brain stem in migraine. Immediately before the development of aura and headache in migraine, stem brain structures are activated. Hereditary dysfunction of calcium channels and other genetic defects can contribute to such increased excitability of neurons. It is believed that the activation of brain stem structures before the onset of a migraine attack may increase the sensitivity of migraine patients to a variety of potential triggers.
Spreading cortical depression with migraine. The first pervasive cortical depression has been described by Leo. Despite the name, the spreading cortical depression is a slowly progressive wave of excitation of neurons in the cerebral cortex, followed by a decrease in cortical activity. The speed of its spread (about 2-6 mm / min) corresponds to the development of a progressive scotoma during a migraine attack, described by Lashley. In this regard, most researchers consider the migraine aura as a consequence of pervasive cortical depression.
Following a wave of pervasive cortical depression, there is a wave of hypoperfusion of the brain. The primacy of the neurogenic mechanisms in migraine is confirmed by the development of pervasive cortical depression apart from the blood supply to the brain. Activation of the trigeminal system in migraine.
The activation of the trigeminal nerve system is the central component of the neurogenic-vascular theory of migraine, proposed by Moskowitz (Moskowitz). During a migraine attack, algogenic substances activate the end of the trigeminal nerve – the main source of pain sensitivity. Through the trigeminal nerve, impulses reach other structures providing a whole complex of various migraine symptoms. Trigeminal activation can also cause an increase in skin sensitivity to the action of irritants, causing allodynia.