Migraine is a complex neurological event involving a cascade of changes across multiple brain regions. This sequence transforms the brain from a normal state to one of heightened sensitivity and pain, followed by recovery. Understanding this process requires observing the electrical and chemical disturbances within the brain’s regulatory centers that define the entire attack.
The Brain’s Early Warning System
The earliest signs of an impending attack, known as the prodrome, often begin hours to days before any head pain starts. This initial phase involves the activation of regulatory centers like the hypothalamus and the brainstem.
The hypothalamus, which controls homeostasis, is implicated in symptoms such as fatigue, excessive yawning, and food cravings. This suggests the attack is initiated by a central system losing control over internal processes, often linked to mood changes like irritability. Activity in the brainstem, which manages many automatic functions, can contribute to other early symptoms like neck stiffness and nausea. These non-pain symptoms are the brain signaling that an attack has been initiated, sometimes up to 48 hours in advance.
The Electrical Wave Phenomenon
Following the early regulatory changes, some migraine sufferers experience the aura, a temporary period of sensory or visual disturbance. This phenomenon is the result of Cortical Spreading Depression (CSD), a slow-moving wave of intense electrical activity across the brain’s surface.
This electrical surge is immediately followed by a period of profound inactivity or “depression,” which causes the temporary loss of normal function. If the wave travels across the visual cortex, it produces visual aura symptoms like flashing lights or zigzag lines. CSD involves the redistribution of ions, such as potassium, and the release of excitatory neurotransmitters like glutamate, initiating the electrical cascade. The sensory effects of the aura typically last for minutes and resolve as the wave of electrical depression passes.
The Source of Pain Activation
The throbbing head pain that defines the migraine is triggered by the activation of the trigeminovascular system, a network of nerves and blood vessels surrounding the brain. Central brain activity activates the trigeminal nerve, a major sensory pathway. This activation leads to the release of neuropeptides, most notably Calcitonin Gene-Related Peptide (CGRP), a potent vasodilator and driver of migraine pain.
When CGRP is released, it causes blood vessels in the meninges—the protective layers around the brain—to dilate. This release also results in neuroinflammation, which sensitizes the trigeminal nerve endings. The combination of dilation and inflammation makes the nerve endings hypersensitive to the mechanical pulse of blood flow, perceived as the characteristic throbbing pain. This process lowers the pain threshold, causing typically non-painful stimuli to be perceived as painful.
Pain signals are transmitted from the sensitized meningeal nerves through the trigeminal ganglion and into the brainstem. From the brainstem, these signals are relayed to other brain areas, including the thalamus, which processes sensory input. This leads to the full experience of debilitating head pain, often accompanied by sensitivity to light and sound.
The Recovery and Lingering Effects
After the pain subsides, the final stage, known as the postdrome, begins as the brain gradually returns to its pre-migraine state. This recovery phase can last for hours or even a couple of days. Functional imaging shows that changes in blood flow and neural activity persist during this time, particularly in the brainstem and other regions involved in the attack.
Symptoms often include fatigue, difficulty concentrating, and cognitive fogginess. The brain is still regulating the neurotransmitter and inflammation levels that were disturbed during the pain phase. The lingering effects reflect the temporary exhaustion of the central nervous system following the major neurological event.