Abstract
Theories regarding the molecular pathophysiology of myofascial trigger points (MFTrPs) have undergone fundamental revisions in recent years. New research suggests that MFTrPs are evoked by the abnormal depolarization of motor end plates. The motor endplate transduces electrical potential into muscle contraction. This review article expands the proposed etiology to include presynaptic, synaptic, and postsynaptic mechanisms, such as excessive release of acetycholine (ACh), defects of acetylcholinesterase, and upregulation of nicotinic ACh receptors, respectively. Dysfunctional motor endplates and sustained muscular contraction give rise to a localized "ATP energy crisis" associated with sensory and autonomic reflex arcs that is sustained by central sensitization. This working hypothesis has given rise to several new approaches in the treatment of MFTrPs.