Trigger Point Injections
Myofascial pain syndrome (MPS) as defined by Travell and Simons is characterized by trigger points (TrP), limited ROM of the affected muscle(s), and neurologic symptoms (autonomic, proprioceptive) (Simons DG, Travell JG, Postgrad Med 73:66–108, 1983). The
- PDF / 1,562,167 Bytes
- 11 Pages / 595.28 x 790.87 pts Page_size
- 71 Downloads / 173 Views
Trigger Point Injections Stephen Nickl and Lauren M. Terranova
Myofascial pain syndrome (MPS) as defined by Travell and Simons is characterized by trigger points (TrP), limited ROM of the affected muscle(s), and neurologic symptoms (autonomic, proprioceptive) [1, 2]. The diagnosis of MPS is based on the presence of 1 or more trigger points. Trigger points (TrP) can be latent or active [1]. Latent TrP are associated with stiffness and restricted ROM but no pain unless palpated. Active TrP produce a referred pain pattern specific to that muscle spontaneously and when the TrP is palpated. The physical findings for diagnosis of a myofascial trigger point are (1) palpation of a tender nodule in a taut band, (2) a referred pain pattern specific for the muscle, (3) a local twitch response (LTR) with snapping palpation or triggering with needle, and (4) restricted ROM [2].
Pathophysiology of Trigger Points The pathophysiology behind the TrP is becoming clearer. Shah summarizes the current concept well stating that active TrP “are a source of ongoing peripheral nociception that may induce central sensitization.” [3] In 1999, Simons presented the “integrated hypothesis” which involves (1) problems with biomechanics, (2) development of trigger points, and (3) sensitization of the spinal cord [4]. It states that trigger points are initiated by biomechanical factors, resulting in local muscle injury in the form of trigger points. These tender taut bands are associated with increased motor end plate activity and focal hypertonicity [5, 6]. This process leads to increased energy demand from the taut band producing “a local energy crisis.” This energy crisis leads to ischemia and the release of noxious substances. It was not until Shah in 2005, using a microdialysis needle, revealed that substance
S. Nickl, DO (*) • L.M. Terranova, MD, DO Department of Rehabilitation Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA e-mail: [email protected]; [email protected]
P, calcitonin gene-related peptide (CGRP), bradykinin, 5-hydroxytryptophan (5-HT), norepinephrine, TNF-alpha, and interleukin-1beta were elevated in the active TrP of patients with MPS confirming Simons’ “Integrated hypothesis.” [7–9] Additionally, CGRP is specifically associated with increased end plate activity which supports studies conducted by Hubbard and Simons using electromyography [5, 6]. The sustained nociceptive activity caused by the trigger point leads to sensitization of the dorsal horn. This results in allodynia and hyperalgesia, the hallmarks of central sensitization [10, 11]. Wide dynamic range (WDR) neurons in the dorsal horn become sensitized which may explain the referred pain patterns, autonomic symptoms, and activation of the limbic system [11–13]. Woolf suggests that injury to any body part can lead to central sensitization [11]. The treatment should focus on treating the trigger point and turning off the nociceptive input. Many physicians feel that if the sources of the biomechanical maladaptations (i.e., spinal sten
Data Loading...
