A model of somatic dysfunction is developed in which restriction in mobility and autonomic, visceral, and immunologic changes are produced by pain-related sensory neurons and their reflexes. Nociceptors are known to produce muscular guarding reactions, as well as autonomic activation, when musculoskeletal or visceral tissue is stressed or damaged. This guarding causes abnormal musculoskeletal position and range of motion. Local inflammatory responses and autonomic reflexes further reinforce nociceptor activity, maintaining restriction. Nociceptive autonomic reflexes also evoke changes in visceral and immunologic function. Finally, maintenance of muscles, joints, and related tissues in an abnormal guarding position causes changes in the connective tissues, solidifying the abnormal position. Stretching these tissues into a normal range of motion will restimulate the nociceptor, reflexly reinforcing the somatic dysfunction. This model has evolved from Korr's neurologic model but emphasizes the nociceptor and its reflexes as a source of the connective tissue, circulatory, visceral, and immunologic changes seen in the somatic dysfunction.

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