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Migraines Explained: How Stress and Nervous System Overload Trigger Attacks
Migraines represent a complex disorder rooted in nervous system imbalance rather than just a simple vascular problem.
Modern research shows that migraines arise from instability across multiple regulatory systems, including the trigeminal-vascular pathway, neuroinflammatory signaling, autonomic regulation, and mitochondrial energy capacity (Goadsby et al., 2017 PubMed; Edvinsson, 2018 PubMed).
Viewing migraine as a state of nervous system overload, rather than a single localized malfunction, helps explain the wide range of symptoms and why regulation-focused approaches often reduce sensitivity, attack frequency, and overall instability. Let’s dive into what these regulation-focused approaches look like.
- Published on Dec 12th, 2025
If you’ve ever had a migraine or know someone who has, you understand it is far more than just a bad headache. Now, with thanks to incredible modern research, we have seen a reframe of migraines through the lens of nervous system regulation rather than outdated vascular theories. This shift offers a clearer understanding of what is actually happening. Let’s explore this further.
For a long time, the leading idea was that migraines were caused by blood vessels in the brain spasming opening and closing. That model is now considered incomplete. Today, migraine is understood as a disorder of nervous system imbalance rather than one isolated malfunctioning part. The entire system becomes unstable. Let’s dive into how this occurs.
A helpful analogy is to imagine the nervous system as a complex and sensitive power grid. A migraine is not one wire breaking or a single fuse blowing. It resembles a citywide brownout in which the demand on the system becomes greater than what it can handle, and the whole network struggles to stay stable.
The Brain's Pain Switch:
Unpacking the Mechanism
What Is Happening Inside the Brain
At the center of a migraine attack is the trigeminal-vascular system. This large network of nerves manages both sensation in the face and head and the regulation of blood flow. It functions like a central circuit board.
When a migraine is triggered, this system becomes overloaded and initiates a cascade of events. One of the most important molecules involved is CGRP (calcitonin gene-related peptide). When trigeminal nerves are activated, they release CGRP, which is a strong vasodilator that widens blood vessels and produces inflammation, which in turn is what is amplifying pain signals (Edvinsson, 2019 PubMed). This is why many of the newest migraine medications target CGRP pathways.
Repeated activation of this pathway can lead to central sensitization, a state in which the brain becomes more efficient at producing pain. During this phase, light, sound, or even light physical contact can feel intensely painful because the brain’s alarm system becomes stuck in an “on” position (Burstein et al., 2010 PubMed).
The Core Regulators:
Systems Behind the Scenes
The Systems That Normally Maintain Stability
Zooming out, several major systems help keep the nervous system’s “power grid” stable.
- The autonomic nervous system (ANS)
The ANS manages blood flow in the brain. Under chronic stress, the sympathetic fight-or-flight branch dominates. This creates instability as blood vessels constrict and dilate unpredictably, contributing to the classic throbbing pain of migraine. - Neuroinflammation
Stress, gut disturbances, and other triggers activate immune cells such as mast cells in the brain. These cells release inflammatory chemicals that further sensitize the trigeminal system, lowering the threshold for a migraine attack. - Mitochondrial energy production
The brain requires large amounts of energy. When mitochondrial energy output cannot meet demand, neurons become unstable and hyperexcitable. This energy deficit is believed to trigger cortical (the body’s stress hormone) which then spreads depression, like a slow wave of altered electrical activity associated with migraine aura (Pietrobon & Moskowitz, 2012 PubMed).
Stressors on The System:
Lowering the Threshold
What Are The Other Additional Factors That Cause Stress On The System
Several other stressors can add load to an already strained system. Scientific research is still developing in some of these areas, but evidence continues to grow.
Hormonal shifts, particularly changes in estrogen, alter vascular and neural stability which add to the stress on the nervous system. There is also gut–brain signalling which allows gastrointestinal inflammation to influence inflammatory activity within the brain. Another factor to consider is chronic neck tension from posture or prolonged screen exposure continuously feeds irritative input into brainstem pain-processing centers. And finally, the emotional stress activates limbic circuits, which in turn is what reduces the brain’s capacity to modulate pain.
Together, these inputs increase the system’s overall vulnerability.
How to Restore Balance:
Suppression to Regulation
How To Restore Balance To The System
Understanding these mechanisms offers a new path forward. Instead of only trying to suppress pain when it appears, the broader strategy is to restore balance to the entire system.
Across all the mechanisms, vascular changes, neuroinflammation, energy deficits, and hormonal variability, the common thread is a loss of regulation. The system loses flexibility, becomes rigid, and reacts strongly to internal and external stressors. It’s almost like the system is stuck in that ‘fight-or-flight’ mode, and is in constant stress.
The goal becomes building a more resilient system from the ground up. This includes supporting cellular energy, improving autonomic stability, reducing inflammatory load, and strengthening the system’s ability to adapt. When this happens, both the frequency and intensity of migraines often decrease.
Migraine is not a random series of unpredictable attacks. It is an output from a system under significant strain. When that system is supported and rebalanced, stability often increases and migraine patterns shift toward improvement.
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What causes the intense pain during a migraine?
Migraine pain originates from activation of the trigeminal-vascular system. Once triggered, these nerves release CGRP, which widens blood vessels and increases inflammation, intensifying pain signaling (Edvinsson, 2018 PubMed).
Why do lights, sounds, or touch feel unbearable during an attack?
Repeated trigeminal activation can lead to central sensitization, where the brain’s pain-processing centers become more reactive. During this state, normal sensory input becomes painful (Burstein et al., 2010 PubMed).
How does stress affect migraine severity?
Chronic sympathetic activation destabilizes blood-flow regulation and increases neuroinflammatory signaling, both of which lower the threshold for a migraine to begin.
Can the gut influence migraine?
Yes. Disturbances in the gut–brain axis can activate immune pathways that create additional neuroinflammation, increasing sensitivity in pain circuits.
What is the connection between hormones and migraine?
Shifts in estrogen influence vascular stability and pain-processing networks, contributing to predictable migraine patterns around hormonal transitions.
What role do mitochondria play in migraine?
The brain requires high energy output. When mitochondrial energy production is insufficient, neurons become hyperexcitable and more vulnerable to cortical spreading depression, which is associated with mood and aura.
Is migraine a permanent, unchangeable condition?
Evidence shows migraine is an output of a system under strain rather than a fixed structural disorder. When energy, inflammation, autonomic balance, and regulatory capacity improve, frequency and intensity often decrease.
References
- Burstein R, Noseda R, Borsook D.
Migraine: multiple processes, complex pathophysiology.
Nature Reviews Neuroscience. 2015.
PubMed: https://pubmed.ncbi.nlm.nih.gov/20055767 - Edvinsson L.
The CGRP Pathway in Migraine as a Viable Target for Therapies.
Headache. 2018.
PubMed: https://pubmed.ncbi.nlm.nih.gov/29561371 - Goadsby PJ, Holland PR, Martins-Oliveira M, Hoffmann J, Schankin C, Akerman S.
Pathophysiology of Migraine: A Disorder of Sensory Processing.
Physiological Reviews. 2017. https://pubmed.ncbi.nlm.nih.gov/28179394/ - Levy D.
Migraine pain, meningeal inflammation, and mast cells.
Current Pain and Headache Reports. 2012.
PubMed: https://pubmed.ncbi.nlm.nih.gov/22553081 - Noseda R, Burstein R.
Migraine pathophysiology: anatomy of the trigeminovascular pathway and associated neurological symptoms.
Headache. 2013. https://pmc.ncbi.nlm.nih.gov/articles/PMC3858400/ - Olesen J, Burstein R, Ashina M, Tfelt-Hansen P.
Origin of pain in migraine: imaging and electrophysiological studies. Pubmed: https://pubmed.ncbi.nlm.nih.gov/19539239/ - Pietrobon D, Moskowitz MA.
Pathophysiology of Migraine.
Annual Review of Physiology. 2014.
PubMed: https://pubmed.ncbi.nlm.nih.gov/24365315
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