Migraine is among the most common neurological disorders, affecting roughly 14 to 15% of the world’s population and around three times more women than men, and it is a leading cause of disability in women under 50. Yet it is still widely described as a bad headache. The research picture is quite different: migraine is understood as a disorder of brain excitability, in which a wave of electrical change and a shift in sensory processing produce pain as one symptom among several.

What Is Cortical Spreading Depression?

Cortical spreading depression is a slow, self-propagating wave of depolarization that spreads across the cerebral cortex. Neurons in its path fire intensely and then fall briefly silent as the wave passes, moving across the surface of the brain at a few millimetres per minute.

This is the process associated with migraine aura. When the wave crosses the visual cortex, the result is the slowly expanding shimmering arc or blind spot that many people describe — a scintillating scotoma. The speed of the visual disturbance matches the speed of the wave, which is one reason the link is well established.

Animal research indicates the wave does more than produce visual symptoms: cortical spreading depression causes intracranial neurogenic inflammation around meningeal blood vessels, including plasma protein extravasation and release of pro-inflammatory peptides. That inflammatory response is a key step between the electrical event and the pain.

If Only Some People Get Aura, What About Everyone Else?

About one in three people with migraine experience visual aura before an attack. The remaining two thirds have migraine without aura — but that does not necessarily mean no cortical wave occurs.

A wave crossing a silent region of cortex would produce no noticeable symptom. The current understanding frames migraine broadly as a disorder of brain excitability characterized by dysregulation of excitatory-inhibitory balance, with vulnerability to cortical spreading depression as one feature. Aura is the visible version of a process that may be more widespread.

This matters practically: the absence of aura does not make an attack less neurological or less real. It simply means the process did not pass through territory that announces itself.

Why Do Light and Sound Become Unbearable?

Because the filter changes, not the sensor. Your eyes and ears are working normally during a migraine. What has shifted is how aggressively the brain suppresses ordinary sensory input before it reaches awareness.

A healthy nervous system continuously discards most incoming signal — ambient noise, background light, the feeling of clothing. During a migraine that gating loosens, and stimuli that are normally filtered out arrive at full strength. Ordinary daylight becomes genuinely painful.

This is the same mechanism, in an acute form, that explains persistent sensory sensitivity in other conditions. Our article on why some people feel everything more intensely covers how sensory filtering works when it is chronically altered rather than temporarily disrupted.

Does a Migraine Start Before the Pain?

Usually, yes — often by hours. The prodrome phase can begin well before any head pain and produces symptoms that rarely get connected to migraine: yawning, food cravings, mood shifts, neck stiffness, unusual fatigue, difficulty concentrating, increased thirst.

These are not warning signs of a coming attack in the way a storm cloud precedes rain. They are the attack, in its early phase. The brain has already changed state.

Recognizing personal prodrome symptoms is genuinely useful, because interventions are generally more effective earlier in the process. Many people discover, on paying attention, that they have a consistent and identifiable early pattern they had simply never tracked.

There is a postdrome too — the washed-out, foggy day afterwards that many describe as a migraine hangover. Counting only the pain hours substantially understates how long an attack actually occupies.

Why Is Stress Such a Reliable Trigger?

Because migraine is fundamentally about excitability thresholds, and stress lowers them. A brain running a sustained stress response has less margin before a triggering event tips it into an attack — the same amplification that sustains chronic pain.

The commonly reported let-down pattern — attacks arriving on the first day off rather than during the difficult week — fits this. The abrupt physiological shift as sustained arousal drops appears to be its own destabilizing event.

Sleep works the same way, in both directions. Too little sleep and too much both feature in trigger lists, which points to the same underlying principle: what destabilizes a migraine-prone brain is change in routine rather than any particular amount. This is one of the few areas where consistency itself is protective.

None of this makes migraine a stress disorder. It is a neurological condition with a genetic component. But because the threshold is modifiable, the regulation of the nervous system is one of the few levers genuinely available.

What Can Actually Be Done?

Medical management comes first, and this article is not a substitute for it. Effective acute and preventive treatments exist, and anyone with frequent or worsening attacks should be evaluated by a physician — particularly if the pattern changes, which always warrants prompt assessment.

Alongside that, the threshold itself is worth addressing. Consistent sleep and wake times, regular meals and a stable routine all support the stability that a migraine-prone brain benefits from. These are unexciting and genuinely effective.

Where nervous system regulation is part of the picture, LENS neurofeedback therapy aims to support more stable brainwave patterns. It is not a migraine cure and should not be presented as one; the rationale is that a better-regulated nervous system tends to have more margin. Brain mapping can show what your baseline regulation looks like between attacks, and what to expect covers how a first visit works.