Myofascial Genesis Of

Myofascial Genesis of Unpleasant Thoughts and Emotions: Its Neural Basis

Dr. John C. Lowe Reprinted from: Digest of Chiropractic Economics, 31(5):78-81, 1989.

It is common for patients who are laden with chronic, intense myofascial constrictions to report severe mental agitation, fretting, insomnia, and other unpleasant thoughts and emotions. It is also common to hear these patients exclaim how profoundly relieved they are of their unpleasant thoughts and emotions after therapy relieves their constrictions and associated trigger points.

In the typical chiropractic office, both the doctor's and the patient's attention are usually on physical pain, and it's easy for the doctor to overlook the relation of the physical pain to the patient's emotional suffering. Even when a patient makes it clear that his emotions are being adversely affected by his physical pain, the doctor may be hesitant to deal with the patient's disturbed emotions. The doctor may feel, for example, that lengthy counseling may be needed and that this is incompatible with the time constraints of a chiropractic practice.

Unless the doctor has had special training in psychotherapy, it is probably best that he leave that form of treatment to clinicians who specialize in it. Giving encouragement, emotional support and practical advice is possibly the limit of what the typical doctor can reasonably provide in the way of psychological care. Fortunately, though, a great deal of patients' unpleasant thoughts and emotions are based on the state of their myofascial tissues; and the appropriate therapy is not psychotherapy but treatment the D.C. can deliver rapidly and effectively during the usual office visit.

In this paper, I briefly review the neuroanatomical relationship of constricted myofascia to unpleasant thoughts and emotions. Understanding how these relate can encourage the D.C. to more often use his clinical skills to alleviate patients' emotional suffering by relaxing their myofascial constrictions. If a patient's emotional condition is of myofascial origin, the quickest, most effective, and most reliable way to give him thoroughgoing relief is through treatment directed to his myofascia.[1]

Myofascial Receptors Pain motivates most patients with myofascial constrictions and trigger points to seek clinical care. Receptors that give rise to the perception of pain are housed in the myofascia, and sustained myofascial constrictions and their trigger points tend to activate these receptors. Presumably, the adequate stimulus for the pain is an event in the myofascia that threatens or causes tissue damage.[2] Constrictions may cause tissue damage by compressing the arteries, veins and lymphatics that course through the constricted myofascia.

Myofascial tissue apparently contains few mechanoreceptors or thermoreceptors. It is, however, richly supplied with type A delta (Group III) and type C (Group IV) receptors. In man, type A delta fibers in skin" mediate sharp, stinging or pricking (epicritic) pain, and type C fibers in skin mediate poorly localized, dull, burning-aching (protopathic) pain.[3] In myofascial tissues, however, both type A delta and type C fibers give rise to delayed dull, agonizing pain felt to be deep and arising from a broad region of the myofascia.[4] Type C nociceptors respond to a wide variety of noxious stimuli: direct mechanical pressure, 5 per cent NaCl, weak acids, temperatures above 41 degrees centigrade or below 25 degrees centigrade, ischemia, and possibly serotonin. This type C response can be long-sustained.[5]

More than half the sensory fibers from myofascia are either type A delta or type C. It is significant that these fibers are highly responsive not only to mechanical and thermal stimuli, but also to chemical stimuli in their local environment. It has been hypothesized that high concentrations of certain chemicals in circumscribed areas of muscle and its fascia hypersensitize receptors and give rise to the trigger point phenomenon.[6]

A large percentage of the A delta fibers are metaboceptors; that is, they respond to chemical changes caused by muscular activity, such as increases in phosphate, lactate, and hydrogen ion concentrations.[7] The type C nociceptors have been shown to respond to bradykinin, serotonin, histamine, and potassium chloride.[8] It has also been shown that prostaglandin E2 and serotonin heighten the responsiveness of muscle receptors to bradykinin.[9] There is significant variation, however, in the responsiveness of types of muscle receptors to noxious chemical and mechanical stimuli. In general, type A delta and type C fibers are similar in their responsiveness to noxious chemical stimuli, although type A delta fibers have a lower threshold to potentially harmful mechanical stimuli.[10]

Intraneuronal stimulation of single afferent fibers in man produced responses in both type A delta and type C fibers.[11] Distinct sensations of dull pain and tension were perceived as coming from muscle. Neither sharp pain nor itch were perceived. Stimulation of less than half of the afferent fibers provoked pain felt in other areas of the body in addition to the pain felt in the myofascia itself. This referred pain phenomenon was not produced by stimulation of skin fibers.[12]

Spinal Cord Circuits and Pathways Sensory signs from the myofascia that give rise to dull, poorly localized pain are transmitted through the older paleospinothalamic pathway. This "pathway provokes the powerful unpleasant affective and aversive responses of avoidance and activity. It accounts for much of the suffering associated with pain."[13] In this pathway, the primary sensory fibers conduct impulses from pain receptors in the myofascia to the posterior horn of the cord. There, the fibers synapses with secondary fibers that transmit impulses to the opposite side of the cord and ascend in the anterolateral tract to the thalamus.

The posterior grey horn of the spinal cord, through its complex circuitry, rearranges and modulates incoming sensory signals before sending them on to higher levels. Numerous mechanisms determine which incoming signals are sustained, which are potentiated, and which are nullified.

One mechanism is the complex interconnection of intrinsic fibers in the tract of Lissauer (situated at the outer tip of the posterior horn). As the rootlets of the sensory fibers penetrate the posterolateral aspect of the cord, most of the type A delta and type C fibers form a lateral group.

These small fibers either bifurcate or bend and then travel through one or two segments before they send collaterals to the substantia gelatinosa, located more centrally inside the posterior horn. The relatively short intrinsic fibers of the tract of Lissauer make up about 25 per cent of the tract. [14] They interconnect as many as five or six spinal segments.

This makes it possible for sensory signals from one segment to influence signals from other segments. And this intersegmental interaction appears to modulate to some degree the A delta and C sensory signals from the myofascia. Melzack's explanation of the Gate Theory has helped us to understand in part how sensation is modulated within these structures of the spine cord.[15] [16] Another important mechanism for altering incoming pain signals is a system of descending spinal pathways that strongly inhibit pain at the spinal level. This system is referred to as the serotonergic and noradrenergic spinal pathways.[17][18]

Subcortical Mechanism It is at the subcortical level, in the brain stem and thalamus, that the sensory signals from constricted myofascia spark the neural mechanisms that give rise to aversive cognitive activity. As the pain pathways pass through the brain stem, some of their fibers terminate in its reticular activating area. As the pathways reach the thalamus, they separate into two separate pathways: the pricking pain pathway and the burning-aching pain pathway.

The pricking pain pathway terminates in the thalamus close to the tactile sensation fibers. There, it makes synaptic connection with fibers that transmit impulses to other parts of the thalamus and to the cortex. The close proximity of the pain and tactile fibers may account for the well-localized quality of pricking pain from cutaneous type A delta fibers.

Dull pain fibers, on the other hand, terminate in the reticular activating formations of both the brain stem and the thalamus. The reticular activiating system then conducts excitatory signals to all parts of the brain. The signals are transmitted from the thalamus to all areas of the cerebral cortex. They are also transmitted laterally into the basal regions around the thalamus, such as the hypothalamus and limbic system. These regions bring about emotional responses to noxious stimulation.

Guyton has pointed out that pain impulses, along with proprioceptive impulses, are the more potent stimuli in provoking arousal through the reticular system.[19] He has also clearly stated the effect of burning-aching pain signals: "The burning and aching pain fibers, because they do excite the reticular activating system, have a very potent effect for activating essentially the entire nervous system, that is, to arouse one from sleep, to create a state of excitement, to create a sense of urgency, and to promote defense and aversion reactions designed to rid the person or animal of the painful stimulus. The signals that are transmitted through the burning pain pathway can be localized only to very gross areas of the body. Therefore, these signals are designed almost entirely for the single purpose of calling one's attention to injurious processes in the body. They create suffering that is sometimes intolerable."[20] Korr has also pointed out that when noxious centripetal impulses are excessive, they "produce . . . important psychological changes with potentially serious and extensive changes in motor and visceral activity."[21]

Apparently even small isolated myofascial constrictions can give rise to great misery. Guyton writes of burning-aching pain signals, ". . . even weak pain signals can summate over a period of time by a process of temporal summation to create an unbearable feeling even though the same pain for short periods of time may be relatively mild."[22] Kimmel has pointed out[23] that spinal fixations also may give rise to centripedal stimuli that are subliminal but cumulative. Haldeman's[24] concurring viewpoint is that noxious signals from spinal joints are probably capable of stimulating the reticular activating system and providing generalized activation of the central nervous system.

Psychological Effects Haldeman has written that insomnia is a well-documented emotional effect of somatic stimulation. [25][26] Jacobson found in many clinical observations and physiological studies [27,28,29,30,31,32,33,34,35] that disturbed thoughts and emotions are accompanied by electrically measurable heightened muscle tension. He also found that relaxing the tightened muscles relieved the unpleasant thoughts and emotions, even though the subjects had no knowledge of what the experimenters expected to occur. As a result of his studies, Jacobson wrote: "There has been abundant evidence in these as well as in many other of our clinical studies that with the relaxation of such muscular acts, the entire process of thinking practically ceases for brief intervals." He also wrote: "It is true that maintaining general relaxation succeeds in markedly reducing, perhaps to zero, disturbed mental states."[36]

Jacobson demonstrated that heightened muscle tension (the basis of myofascial constrictions and trigger points) gives rise to unpleasant thoughts and emotions. He also demonstrated and stated that anxiety and muscle relaxation are physiologically incompatible.[37][38] Wolpe, considered the father of behavior modification, reiterated this incompatibility and reported that it was the basis of his effective clinical procedure called systematic desensitization.[39]

During this procedure, relaxation is systematically used to eliminate unpleasant thoughts and emotions that occur as conditioned responses to various stimuli. The efficacy of this extensively investigated procedure is additional clinical and experimental confirmation of Jacobson's conclusion that anxiety and general muscle relaxation can not occur simultaneously.

Conclusions Sustained myofascial constrictions are likely to activate type C and type A delta sensory nerve fibers. The action potentials of these fibers travel through spinal cord pathways to the brain stem and thalamic reticular activating formations. From the thalamic reticular formation, signals are relayed throughout the brain and induce generalized physiological arousal. This arousal gives rise to behaviors whose aim is to remove the aversive stimulus.

The physiological arousal and behavioral activation are accompanied by unpleasant cognitions and emotions. As would be predicted from our understanding of the relevant neuroanatomy, when the myofascial constrictions and their trigger points are relieved, the unpleasant thoughts and emotions subside.

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