Abstract / Summary
The core mechanism of epilepsy is generally summarized as abnormal synchronized neuronal firing. Although antiseizure medications, surgery, vagus nerve stimulation, and the ketogenic diet continue to improve, some patients continue to have drug-resistant epilepsy and often also have forward head posture, neck pain, insomnia, anxiety, autonomic dysfunction, and brain fog. These comorbidities are difficult to attribute entirely to epilepsy itself or to medication side effects, suggesting an underrecognized downstream amplification mechanism. Within the framework of investing fascia–carotid sheath–six-system coupling, this paper proposes a testable hypothesis: in some patients with epilepsy, fibrosis of the investing fascia and mechanical coupling of the carotid sheath may act as downstream amplifying factors and contribute to a reduced seizure threshold through impaired venous return, decreased glymphatic and meningeal lymphatic clearance, autonomic imbalance, sleep disruption, and neuroinflammation. Investing fascia release, through mechanical unloading, may reduce abnormal mechanical input, improve clearance and autonomic function, and thereby reverse this amplification process and raise the seizure threshold. Currently, there is no direct clinical evidence for this hypothesis, and it cannot replace standard treatment. Another subgroup hypothesis is that in patients with epilepsy who have objective evidence of altered blood supply, investing fascia release may improve blood supply and raise the seizure threshold; in those without such evidence, the effect may be less apparent. This paper is a theoretical derivation based solely on published literature and proposes testable predictions and a validation framework.