Trigger Points and Central Modulation—A New Hypothesis

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Objective: A new hypothesis is proposed to explain the pathogenesis, symptomatology, and treatment of the trigger points [TrPs], which define the myofascial pain syndrome [MPS].Hypothesis: TrPs are formed due to sustained α-motoneuron plateau depolarization, which is maintained by one of two different central nervous system [CNS] mechanisms. “Antecedent” TrPs are formed in withdrawal reflex agonist muscles due to central sensitization of the C fiber nociceptive withdrawal reflex [NWR], visceromotor reflex [VMR], or nociceptive jaw-opening reflex [NJOR]. “Consequent” TrPs result in withdrawal reflex antagonist muscles due to compensatory reticulospinal or reticulo-trigeminal motor facilitation. Afferent nociceptive signals arise from both latent and active TrPs. However, latent TrPs are not spontaneously painful, because of complete inhibition of nociceptive transmission at the spinal cord or trigeminal nucleus [SC/TN] levels. Marked SC/TN sensitization [especially with a reduced antinociceptive functional reserve] may overwhelm the brainstem antinociceptive mechanism, going beyond the MPS into the generalized allodynia of the fibromyalgia syndrome [FMS]. The principal brainstem nuclei involved in TrP sensory and motor modulation have other diverse homeostatic roles; therefore TrP-induced brainstem dysfunction may contribute to the pathogenesis of a variety of sensory, motor, and autonomic disorders. Treatment involves noxious stimulus-induced transient inhibition of the CNS mechanisms that sustain TrPs. This allows stretching of the contractured muscle fibers to resolve the TrP local energy crisis, and to reverse muscle nociceptor and CNS sensitization.Conclusion: This hypothesis proposes that TrPs result in the muscles due to sustained α-motoneuron plateau depolarization. Descending inhibition normally ensures that most TrPs remain latent, but FMS may result if this inhibitory mechanism is overwhelmed.