The Cervicogenic Hyperarousal Hypothesis of Insomnia: Investing Fascia–Carotid Sheath–Six-System Coupling Drives Central Hyperarousal and a Positive Feedback Loop

Abstract This paper proposes a testable hypothesis, not a proven mechanism. Traditional mechanistic models of chronic insomnia center on hyperarousal and involve hypothalamic–pituitary–adrenal (HPA) axis hyperactivity, locus coeruleus–norepinephrine (LC-NE) system overactivation, insufficient gamma-aminobutyric acid (GABA)ergic inhibition, orexin system abnormalities, glymphatic clearance impairment, and neuroinflammation (Perlis et al., 2022); however, these mechanisms mainly explain how insomnia is maintained and amplified and still lack a unified upstream trigger-layer explanation. Building on the “investing layer of the deep cervical fascia (investing fascia)–carotid sheath–six-system coupling” framework, this paper proposes the “cervicogenic hyperarousal hypothesis of insomnia.” This hypothesis posits that chronic forward head posture, long-term stress, aging, and chronic low-grade inflammation jointly drive investing fascia fibrosis; after the loss of elastic buffering, abnormal shear stress generated by subtle head and neck movements is transmitted through the three layers of the deep cervical fascia to the carotid sheath; elevated pressure within the carotid sheath, as an inferred intermediate variable, simultaneously affects six systems—arterial, venous, lymphatic, glymphatic, sympathetic, and vagal; abnormalities in these six systems drive hyperarousal through the nucleus tractus solitarius–locus coeruleus–norepinephrine (NTS-LC-NE) pathway, the HPA axis, the GABA/glutamate system, and neuroinflammatory networks; and the six systems amplify one another through positive feedback loops, forming a closed loop of “mechanical abnormality → six-system dysfunction → hyperarousal/insomnia → anxiety/fatigue → postural deterioration → worsening mechanical abnormality.” This hypothesis applies only to the cervicogenic insomnia subtype characterized by forward head posture, neck pain, elevated deep cervical fascia shear wave elastography (SWE) values, autonomic dysfunction, brain fog, or fatigue; it does not apply to primary insomnia without cervicogenic mechanical abnormalities and does not replace cognitive behavioral therapy for insomnia (CBT-I) or pharmacotherapy.