Muscle pain: mechanisms and clinical significance

Abstract

Introduction: Muscle pain is common, but the understanding of its causes is still patchy. This article addresses the mechanisms of some important types of muscle pain.

Methods: Selective literature review, predominantly of data derived from neuroanatomical and electrophysiological experiments on anesthetized rats.

Results: Muscle pain is evoked by specialized nerve endings (nociceptors). Important stimuli for muscle pain are adenosintriphosphate (ATP) and a low tissue pH. Excitation of muscle nociceptors leads to hyperexcitability of spinal sensory neurones (central sensitization). Low frequency activity in muscle nociceptors is sufficient to induce central sensitization.

Discussion: Central sensitization leads to increased excitation in the spinal cord and to referral of muscle pain. The motoneurones of a painful muscle are centrally inhibited. Muscular spasm is mostly secondary to a painful lesion in another muscle or joint. The pain of fibromyalgia is assumed to relate to a dysfunction of central nociceptive processing. Psychosocial factors also contribute to pain.

Keywords: fibromyalgia; muscle pain; muscle spasm; myofascial trigger point; nociceptor; sensitization.

Figure 1

The activation of a single muscle nociceptor by adenosine triphosphate (ATP). a) The impulse-firing activity of single nociceptors was recorded from sciatic nerve filaments in anesthetized rats. The gastrocnemius-soleus (GS) muscle was dissected free, the receptive nerve ending was localized within it with mechanical stimuli, and the excitatory substance was injected in the vicinity of the nerve ending. b) The nociceptive ending was found in the medial head of the gastrocnemius muscle (MG; black spot). The injection of the solvent Tyrode (control substance) had no effect, but the injection of a 7.6 mM solution of ATP induced activity lasting for minutes (modified after [5]). RF, receptive field.

Figure 2

The mechanism of generation of referred muscle pain. Normally, the L4 and L5 segments are the main area in which the GS nerve exerts its effects in the rat (GS, gastrocnemius-soleus muscle), characterized by effective synapses (grey triangles) that reliably excite the postsynaptic neurons. Local pain arising in these segments is felt at the site of the lesion (black arrows). In animals with an inflamed GS muscle, the area of influence of the GS nerve was found to have expanded into the L3 segment, which contains only ineffective synapses (open triangles) of GS afferent fibers. These synapses do not normally induce any action potentials in the L3 neurons. In the presence of a lesion in the muscle, the muscle afferents in the L4 and L5 segments secrete substances (e.g., SP = substance P, black dots) that diffuse to the L3 segment and convert the ineffective synapses there into effective ones. Thus, it was newly possible for impulses from GS nociceptors (open arrows) to excite the L3 neurons, ultimately giving rise to referred pain that was felt in the distribution of the fibular nerve (lateral calf and foot).

Figure 3

Pain referral from a myofascial trigger point (MTrP) in the soleus muscle to the sacroiliac (SI) joint. As shown in figure 2, referral of pain to the SI joint can be explained as follows: first, nociceptors in the trigger point induce local pain. The nociceptive impulses arising from the trigger point are then carried over spinal cord neurons belonging to the segments L5–S1, which are the normal relay stations for impulses from the soleus muscle. As excitation spreads in the spinal cord (in this case, mainly in the caudal direction), the normally ineffective connections between the soleus muscle and the neurons of the S2–S4 segments become effective. Impulses from the trigger point nociceptors can now activate neurons in S2–S4 that otherwise provide sensory innervation to the SI joint. The individual therefore feels pain referred to the SI joint.