A Sympathetic Nervous System Theory of Migraine

TL;DR

This paper proposes a comprehensive theory that attributes migraine to dysregulated sympathetic nervous system activity, explaining its causes, symptoms, and treatments based on SNS sensitivity and neural mechanisms.

Contribution

It introduces a novel, complete theory of migraine involving SNS activity, baroreceptor hyperexcitability, and neural pathways, supported by extensive evidence.

Findings

Migraine involves chronically high SNS activity due to sensor sensitivity.

Migraine headache results from SNS desensitization or excess, leading to neural hyperexcitability.

The theory explains the mechanisms behind current migraine treatments.

Abstract

Migraine (MGR) ranks first among diseases in terms of years of lost healthy life in young adult and adult women. Currently, there is no theory of MGR. This paper presents a complete theory of migraine that explains its etiology, symptoms, pathology, and treatment. Migraine involves partially saturated (usually chronically high) sympathetic nervous system (SNS) activity, mainly due to higher sensitivity of the metabolic sensors that recruit it. MGR headache occurs when SNS activity is desensitized or excessive, resulting in hyperexcitability of baroreceptors, oxidative stress, and activation of pain pathways via TRPV1 channels and CGRP. The theory is supported by overwhelming evidence, and explains the properties of current MGR treatments.