Abstract / Summary
Abstract Sequelae of tuberculous meningoencephalitis (TBM) involve multisystem damage, including meningeal fibrosis, hydrocephalus, vasculitis, cranial nerve damage, hypothalamic–pituitary–adrenal (HPA) axis injury, spinal cord and nerve root involvement, and persistent neuroinflammation. After entering the stable phase, some patients still experience head pressure, fatigue, brain fog, insomnia, mood disorders, autonomic symptoms, ocular symptoms, and blood glucose fluctuations, which cannot be fully explained by structural damage. This article proposes a minimal testable version of the “Cervicogenic Mechanical–Six-System Coupling–Amplification Hypothesis in the Rehabilitation Phase of TBM Sequelae”: during TBM rehabilitation, secondary cervicogenic mechanical factors (forward head posture, cervical compensation, and deep cervical fascia thickening) may, through mechanical coupling in the carotid sheath region, preferentially affect venous return, meningeal lymphatic drainage, and glymphatic clearance, and subsequently induce autonomic and neuroimmune changes, forming a positive feedback loop of “central injury → cervical compensation → fascial remodeling → clearance impairment → persistent symptoms.” Cervicogenic mechanical factors are positioned as downstream amplifying or maintaining factors, rather than as the initiating cause of TBM sequelae or an independent “second hit.” Mechanical interventions such as investing fascia release are proposed only as an investigational adjunctive hypothesis and cannot replace standard treatment. This article proposes core predictions, falsification criteria, and a three-stage validation framework, and emphasizes that the evidence base is extremely immature and requires rigorous validation.