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Neurophysiological basis of pain caused by trigger points
Commentary
Neurophysiological Basis of Pain Caused by Trigger Points David G. S i m o n s
his commentary responds to Mense's focus article. 1 It considers how the clinical features of myofascial pain, caused by trigger points (TrPs), relate to his observations. By their nature, the animal studies done under anesthesia can assess directly only tenderness. Mense assumes that his studies also apply to pain based on the reasonable premise that activity in nociceptive neurons elicits subjective pain. The expression referred pain is used here to describe pain what arises from one site and is felt at a distance. No distinction is made between pain that appears in discrete areas that are separate from the source and pain that extends continuously from the source because both patterns can be seen in the pain referred from one TrP. However, it is important to distinguish the continuous prolonged aching character of referred pain caused by TrPs from the sharp lighteninglike pain that arises from peripheral nerves and follows the course of the nerve.
T
CLINICAL CHARACTERISTICS COMPATIBLE WITH THE HYPOTHESIS Mense showed that new receptive fields commonly appear in separate locations from the original receptive field(s). Similarly, the appearance of multiple discrete pain locations, distant from the TrP source of the pain, is not unusual in myofascial pain patients. Figure 1 illustrates one of the most common myofascial pain syndromes that is caused by TrP1 of the upper trapezius muscle, s The pain pattern adjacent to the TrP is only occasionally described by the patient as including the location of the TrP. From the Department of Physical Medicine and Rehabilitation, University of California Irvine, Irvine, CA. Reprint requests: David G. Simons, MD, 9112 Mahalo Drive, Huntington Beach, CA 92646-7841.
APS Journal 3(1): 17-19, 1994
Animal studies 1 can be interpreted to reflect a twophase response. Injection of bradykinin into a receptive field in a muscle causes a relatively prompt (several seconds) response of the nociceptive dorsal horn cell. This may correspond to the local pain felt instantaneously as long as digital pressure is exerted on the TrP. Conversely, the appearance of new receptive fields takes 5 to more than 15 minutes to develop. This may correspond to the delay commonly observed following a muscle overload that initiates TrPs. The patient may not be aware of the referred pain for many minutes to hours following the initiating muscular overload. Later, when the TrP has become well established, it may take 5 or 10 seconds of pressure, applied to the TrP, before the patient becomes aware of the additional, distant, less clearly delineated referred component of pain, as compared to the pain felt instantaneously at the TrP site. s,5 A similar distinction was observed in experimentally induced pain of muscular origin. 4,7 The observation by Mense that, following bradykinin injection of hind limb muscles, all newly formed receptive fields were located in deep tissues and never in the skin, correlates well with the deep (not superficial) aching nature of pain arising from TrPs. Pain arising from TrPs may be very intense, but it is noted for its lack of precise borders. The pain tends to fade out around its periphery.
CLINICAL CHARACTERISTICS NOT ACCOUNTED FOR BY THE HYPOTHESIS One of the most remarkable (and clinically confusing) features of myofascial TrPs is the patient's initial awareness only of the location of the referred pain and not of its TrP source. The Mense hypothesis does not account for this feature, but his studies test primarily for evoked tenderness, not spontaneous pain. Interestingly, in patients, both the region of referred 17
18
COMMENTARY/Simons Ten percent of the 147 pain patterns described for the muscles t h r o u g h o u t the body occur only locally around the TrP. 2 These patterns could represent activation and enlargement of a previously present receptive field, or they could be the unmasking of a receptive field covering the region of the TrP. The latter could be considered analogous to the unmasking of a receptive field in the tibialis anterior muscle at the injection site in Figure 2 of Mense's focus article. It is not clear how one could distinguish between these two mechanisms clinically.
rP1
EXTENSION OF THE N E U R O A N A T O M I C A L MODEL Figure 2 presents an extension of the neuroanatomical model presented in Figure 3 of Mense's focus article. 1 There is no direct experimental evidence for
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Spinal Cord
Figure 1. Composite of referred pain patterns from trigger point (TrP) 1 in the upper trapezius muscle. From Travell and Simons.5 With permission.
pain and the TrP site are tender on examination, which fits the hypothesis. The fact that the region of referred pain is also a region of referred tenderness commonly misleads clinicians who are not aware of this characteristic of TrPs. Mense found that the great majority of newly formed receptive fields were located distal to the original ones, which would explain pain referred from a TrP in the proximal direction. However, analysis 2 of the 147 published referred pain patterns of TrPs t h r o u g h o u t the body s'6 showed that nearly half of them (48%) referred pain primarily in the distal direction and that only 5% referred pain primarily in the proximal direction. The direction pain referred by TrPs located in lower extremity muscle e was similar, 54% and 6%. This suggests that there are likely additional central mechanisms involved in the referral of pain from TrPs. One such mechanism could be the involvement of internuncial pathways, which would be very difficult to demonstrate experimentally.
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Trigger Point Figure 2. Extension of the neuroanatomical model presented in Figure 3 of Mense's focus article. 1 Although no direct experimental evidence substantiates this modification, it is compatible with the mechanisms described by Mense and helps to explain some trigger point characteristics not accounted for by his model. Neurons 1 and 2 correspond to neurons 1 and 2 in the Mense model. Neurons 1 and 4 are connected by solid lines to their respective receptive fields. These fields are the areas that would be identified as the source of nociception when neurons 1 and 4 are activated. Nociceptive input from the trigger point would activate neurOne 2 and could account for the initial localized pain in response to pressure applied to the trigger point. This activity is assumed to release substance P (SP) and calcitonin gene-related peptide (CGRP) in the dorsal horn that diffuses (stippling) to neurons 1 and 4. This increases the efficacy of latent connections (dashed lines) to these cells. Now, neurons 1 and 4 can be activated by nociceptive activity originating in the trigger point and would be perceived as referred pain.
COMMENTARY/Simons
this modification, because simultaneous monitoring of the appropriate dorsal horn cells would be prohibitively difficult. However, it is consistent with the principles demonstrated by Mense. It could help to account for the distinction between the immediate more localized pain, elicited by pressure on the TrP, and the more diffuse and usually less intense referred pain that may develop later, and also for the multiple component pain patterns generated by one TrP. Why the patient is initially aware of only the referred pain and is unaware of the TrP site still requires explanation. A possible mechanism would be if, in Figure 2, the connection between the TrP and neuron 2 is less effective than the connections with neurons 1 and 4. This is conceivable if the assumption is made that neuron 2 is tonically inhibited, which is true for many dorsal horn neurons with deep input.
References 1. Mense S: Referral of muscle pain: new aspects. APS J 3:1-9, 1994 2. Simons DG: Referred phenomena of myofascial trigger
3.
4.
5.
6.
19
points, pp. 341-357. In Vecchiet L, Albe-Fessard, Lindblom (eds): New trends in referred pain and hyperalgesia. Vol. 7. Pain research and clinical management. Elsevier, Amsterdam, 1993 Sola AE, Bonica JJ: Myofascial pain syndromes, pp. 352-367. In Bonica JJ, Loeser JD, Chapman CR, Fordyce WE (eds): The management of pain. 2nd ed. Lea and Febiger, Philadelphia, 1990 Steinbrocker O, Isenberg SA, Silver M, Neustadt D, Kuhn P, Schittone M: Observations on pain produced by injection of hypertonic saline into muscles and other supportive tissues. J Clin Invest 32:1045-1051, 1953 Travell JG, Simons DG: Myofascial pain and dysfunction: the trigger point manual. Vol. 1, p. 184. Williams & Wilkins, Baltimore, 1983 Travell JG, Simons DG: Myofascial pain and dysfunction: the trigger point manual. Vol. 2. Williams & Wilkins, Baltimore, 1992
7. Vecchiet L, Galletti R, Giamberardino MA, Dragani L, Marini F: Modifications of cutaneous, subcutaneous, and muscular sensory and pain thresholds after the induction of an experimental algogenic focus in the skeletal muscle. Clin J Pain 4:55-59, 1988
Neurophysiological Basis of Pain Caused by Trigger Points David G. S i m o n s
his commentary responds to Mense's focus article. 1 It considers how the clinical features of myofascial pain, caused by trigger points (TrPs), relate to his observations. By their nature, the animal studies done under anesthesia can assess directly only tenderness. Mense assumes that his studies also apply to pain based on the reasonable premise that activity in nociceptive neurons elicits subjective pain. The expression referred pain is used here to describe pain what arises from one site and is felt at a distance. No distinction is made between pain that appears in discrete areas that are separate from the source and pain that extends continuously from the source because both patterns can be seen in the pain referred from one TrP. However, it is important to distinguish the continuous prolonged aching character of referred pain caused by TrPs from the sharp lighteninglike pain that arises from peripheral nerves and follows the course of the nerve.
T
CLINICAL CHARACTERISTICS COMPATIBLE WITH THE HYPOTHESIS Mense showed that new receptive fields commonly appear in separate locations from the original receptive field(s). Similarly, the appearance of multiple discrete pain locations, distant from the TrP source of the pain, is not unusual in myofascial pain patients. Figure 1 illustrates one of the most common myofascial pain syndromes that is caused by TrP1 of the upper trapezius muscle, s The pain pattern adjacent to the TrP is only occasionally described by the patient as including the location of the TrP. From the Department of Physical Medicine and Rehabilitation, University of California Irvine, Irvine, CA. Reprint requests: David G. Simons, MD, 9112 Mahalo Drive, Huntington Beach, CA 92646-7841.
APS Journal 3(1): 17-19, 1994
Animal studies 1 can be interpreted to reflect a twophase response. Injection of bradykinin into a receptive field in a muscle causes a relatively prompt (several seconds) response of the nociceptive dorsal horn cell. This may correspond to the local pain felt instantaneously as long as digital pressure is exerted on the TrP. Conversely, the appearance of new receptive fields takes 5 to more than 15 minutes to develop. This may correspond to the delay commonly observed following a muscle overload that initiates TrPs. The patient may not be aware of the referred pain for many minutes to hours following the initiating muscular overload. Later, when the TrP has become well established, it may take 5 or 10 seconds of pressure, applied to the TrP, before the patient becomes aware of the additional, distant, less clearly delineated referred component of pain, as compared to the pain felt instantaneously at the TrP site. s,5 A similar distinction was observed in experimentally induced pain of muscular origin. 4,7 The observation by Mense that, following bradykinin injection of hind limb muscles, all newly formed receptive fields were located in deep tissues and never in the skin, correlates well with the deep (not superficial) aching nature of pain arising from TrPs. Pain arising from TrPs may be very intense, but it is noted for its lack of precise borders. The pain tends to fade out around its periphery.
CLINICAL CHARACTERISTICS NOT ACCOUNTED FOR BY THE HYPOTHESIS One of the most remarkable (and clinically confusing) features of myofascial TrPs is the patient's initial awareness only of the location of the referred pain and not of its TrP source. The Mense hypothesis does not account for this feature, but his studies test primarily for evoked tenderness, not spontaneous pain. Interestingly, in patients, both the region of referred 17
18
COMMENTARY/Simons Ten percent of the 147 pain patterns described for the muscles t h r o u g h o u t the body occur only locally around the TrP. 2 These patterns could represent activation and enlargement of a previously present receptive field, or they could be the unmasking of a receptive field covering the region of the TrP. The latter could be considered analogous to the unmasking of a receptive field in the tibialis anterior muscle at the injection site in Figure 2 of Mense's focus article. It is not clear how one could distinguish between these two mechanisms clinically.
rP1
EXTENSION OF THE N E U R O A N A T O M I C A L MODEL Figure 2 presents an extension of the neuroanatomical model presented in Figure 3 of Mense's focus article. 1 There is no direct experimental evidence for
:i ! ~ !
~ ~ . "':~...:'s't;:'.:" , ~.
Spinal Cord
Figure 1. Composite of referred pain patterns from trigger point (TrP) 1 in the upper trapezius muscle. From Travell and Simons.5 With permission.
pain and the TrP site are tender on examination, which fits the hypothesis. The fact that the region of referred pain is also a region of referred tenderness commonly misleads clinicians who are not aware of this characteristic of TrPs. Mense found that the great majority of newly formed receptive fields were located distal to the original ones, which would explain pain referred from a TrP in the proximal direction. However, analysis 2 of the 147 published referred pain patterns of TrPs t h r o u g h o u t the body s'6 showed that nearly half of them (48%) referred pain primarily in the distal direction and that only 5% referred pain primarily in the proximal direction. The direction pain referred by TrPs located in lower extremity muscle e was similar, 54% and 6%. This suggests that there are likely additional central mechanisms involved in the referral of pain from TrPs. One such mechanism could be the involvement of internuncial pathways, which would be very difficult to demonstrate experimentally.
~
~
Trigger Point Figure 2. Extension of the neuroanatomical model presented in Figure 3 of Mense's focus article. 1 Although no direct experimental evidence substantiates this modification, it is compatible with the mechanisms described by Mense and helps to explain some trigger point characteristics not accounted for by his model. Neurons 1 and 2 correspond to neurons 1 and 2 in the Mense model. Neurons 1 and 4 are connected by solid lines to their respective receptive fields. These fields are the areas that would be identified as the source of nociception when neurons 1 and 4 are activated. Nociceptive input from the trigger point would activate neurOne 2 and could account for the initial localized pain in response to pressure applied to the trigger point. This activity is assumed to release substance P (SP) and calcitonin gene-related peptide (CGRP) in the dorsal horn that diffuses (stippling) to neurons 1 and 4. This increases the efficacy of latent connections (dashed lines) to these cells. Now, neurons 1 and 4 can be activated by nociceptive activity originating in the trigger point and would be perceived as referred pain.
COMMENTARY/Simons
this modification, because simultaneous monitoring of the appropriate dorsal horn cells would be prohibitively difficult. However, it is consistent with the principles demonstrated by Mense. It could help to account for the distinction between the immediate more localized pain, elicited by pressure on the TrP, and the more diffuse and usually less intense referred pain that may develop later, and also for the multiple component pain patterns generated by one TrP. Why the patient is initially aware of only the referred pain and is unaware of the TrP site still requires explanation. A possible mechanism would be if, in Figure 2, the connection between the TrP and neuron 2 is less effective than the connections with neurons 1 and 4. This is conceivable if the assumption is made that neuron 2 is tonically inhibited, which is true for many dorsal horn neurons with deep input.
References 1. Mense S: Referral of muscle pain: new aspects. APS J 3:1-9, 1994 2. Simons DG: Referred phenomena of myofascial trigger
3.
4.
5.
6.
19
points, pp. 341-357. In Vecchiet L, Albe-Fessard, Lindblom (eds): New trends in referred pain and hyperalgesia. Vol. 7. Pain research and clinical management. Elsevier, Amsterdam, 1993 Sola AE, Bonica JJ: Myofascial pain syndromes, pp. 352-367. In Bonica JJ, Loeser JD, Chapman CR, Fordyce WE (eds): The management of pain. 2nd ed. Lea and Febiger, Philadelphia, 1990 Steinbrocker O, Isenberg SA, Silver M, Neustadt D, Kuhn P, Schittone M: Observations on pain produced by injection of hypertonic saline into muscles and other supportive tissues. J Clin Invest 32:1045-1051, 1953 Travell JG, Simons DG: Myofascial pain and dysfunction: the trigger point manual. Vol. 1, p. 184. Williams & Wilkins, Baltimore, 1983 Travell JG, Simons DG: Myofascial pain and dysfunction: the trigger point manual. Vol. 2. Williams & Wilkins, Baltimore, 1992
7. Vecchiet L, Galletti R, Giamberardino MA, Dragani L, Marini F: Modifications of cutaneous, subcutaneous, and muscular sensory and pain thresholds after the induction of an experimental algogenic focus in the skeletal muscle. Clin J Pain 4:55-59, 1988