Migraine is now considered to be neurovascular, and not just vascular, arising from a disorder of brain sensory processing.6

Many symptoms will originate from the hypothalamus, particularly the premonitory symptoms. Migraine also involves activation and sensitisation of the neurons in the trigeminal nerves. These control cerebral blood vessels (the trigeminovascular pathways), the brainstem and the diencephalon, which connects the midbrain to the forebrain and contains structures including the hypothalamus and pineal gland.

Among the identified processes associated with migraine are a slower metabolism of pain processing nociceptive areas in the brain, a link between trigeminal system activation and increased photosensitivity or photophobia, and different responsiveness to external stimuli in the brain’s cerebral cortex.

Migraine aura possibly relates to a slow wave of depolarisation spreading across the brain cortex (cortical spreading depression or CSD), which may also be linked to the pain.6,16

The autonomic nervous system (ANS) is also involved, but effects on the autonomic reflexes in the cranium and the cardiovascular system, such as blood vessel constriction or dilation, can change with age. Serotonin 5-HT1D receptors occur on neurons innervating lachrymal glands and the trigeminal ganglion, allowing them to modulate activation of trigeminal pain pathways and autonomic symptoms.6,17