Such an integrated hypothesis involves local myofascial tissues, the central nervous system (CNS), and biomechanical factors.Ī biopsy of local myofascial tissue in the vicinity of TrPs revealed that the tissues contained “contraction knots,” described as “large, rounded, darkly staining muscle fibers and a statistically significant increase in the average diameter of muscle fibers.” 9 Electromyographic (EMG) studies of TrPs have indicated spontaneous electrical activity (SEA) in TrPs, while adjacent muscle tissues are electrically silent.
#Travell and simons criteria manual#
The 1999 edition of Travell and Simons' Myofascial Pain and Dysfunction: The Trigger Point Manual 5 proposes an “integrated hypothesis” regarding the etiology of TrPs.
Most of the material in this article was mistakenly deleted from the final version of the Foundations chapter.
8 This article serves as a companion piece to Kuchera and McPartland's chapter in Foundations, describing a new working hypothesis regarding the etiology of TrPs and the way in which this new hypothesis changes our treatment of these points.
#Travell and simons criteria full#
A full account that describes the diagnosis and treatment of Travell TrPs is provided by Kuchera and McPartland in Foundations for Osteopathic Medicine. Myofascial trigger points can be inactivated by a variety of approaches, including osteopathic manipulative treatment (OMT), massage therapy, ultrasound therapy, “spray and stretch,” as well as needling (acupuncture or injection). 7 (TART is a mnemonic for the four criteria of somatic dysfunction: tissue texture abnormality, asymmetry, restriction of motion, and tenderness. 7 An interrater-reliability study of this counterstrain system demonstrated that clinicians agreed 73% of the time (κ = 0.45) the palpation of patients' TrPs proved more reliable than the standard osteopathic TART examination. 6 The reliability of diagnosing TrPs is similar to the reliability of diagnosing tender points in the counterstrain system developed by Lawrence H. Palpation is a reliable diagnostic criterion for locating TrPs in patients. Trigger point of the left rectus capitis posterior major (marked by an X) and its referred pain pattern (stippling). The purpose of this article is to review these new concepts and describe new resulting approaches to the treatment of TrPs. Scientists are now proposing and reporting the results of new approaches using capsaicin, a vanilloid-receptor agonist, and ACh antagonists (eg, dimethisoquin hydrochloride, botulinum toxin, quinidine, linalool). As an example, Travell and Simons abandoned the application of ischemic compression to TrPs instead the authors adopted several techniques associated with osteopathic medicine (ie, muscle-energy, myofascial, counterstrain high-velocity, low-amplitude). This working hypothesis regarding the etiology of TrPs has changed the approach to treating TrPs. This article expands the proposed etiology to include presynaptic, synaptic, and postsynaptic mechanisms of abnormal depolarization (ie, excessive release of acetycholine, defects of acetylcholinesterase, and upregulation of nicotinic ACh-receptor activity, respectively). New research results suggest that TrPs are evoked by the abnormal depolarization of motor end plates. The proposed etiology of Travell trigger points (TrPs) has undergone a fundamental revision in recent years.