Sensor-Rich Myofascial and Visceral Interfaces as Modulators of Afferent Signaling: A Biotensegrity-Based Mechanistic Hypothesis for Neurodevelopmental Conditions

Neurodevelopmental conditions are characterized by differences in sensory processing, motor control, and autonomic regulation. While substantial empirical research exists on individual components such as fascia as a sensory organ, interoceptive processing differences, and mechanotransduction, these findings have not yet been integrated into a coherent model focused on specific anatomical zones. This paper proposes that chronic mechanical restriction within sensor-rich anatomical zones — including the extraocular muscles, tensor tympani and stapedius, nasal musculature, tongue and floor of mouth, pharyngeal and laryngeal structures, suboccipital complex, visceral fascia and diaphragm, and pelvic floor and perineum — can distort afferent signaling through both neural and fluid-mediated pathways. Drawing on existing empirical literature on fascia as a sensory organ, interoception in autism, mechanotransduction, and biotensegrity, this paper outlines a mechanistic framework in which sustained constriction in these high-density sensory interfaces may contribute to the persistence of sensory and regulatory differences. The hypothesis identifies a set of anatomical targets and proposes that systematic investigation using objective tension measurement technologies represents a necessary and feasible next step.