Nociceptive Considerations in Treating with Counterstrain

• Nociceptive considerations in treating with counterstrain

MARK BAILEY, PhD LORANE DICK, DO

The proprioceptive mechanis- nism by which counterstrain techniques ame- tic model of somatic dysfunction proposed liorate somatic dysfunction has not been ex- by Korr is accepted as the neurophysiolo- plained conclusively. (Somatic dysfunction is gic basis of counterstrain by the developer defined3 as "Impaired or altered function of re- of that manipulative technique. We sug- lated components of the somatic [body frame- gest that the physician should also take work] system: skeletal, arthrodial, and myofas- into account the physical damage, if any, cial structures, and related vascular, lym- that the original trauma produced. We pro- phatic, and neural elements." Korr o has de- pose that with tissue injury, nociceptive scribed a proprioceptive mechanism of somatic reflexes could produce patterns of motion dysfunction that Jones2 accepts as underlying restriction opposite that predicted by a counterstrain. This explanation is compatible solely proprioceptive model. A nociceptive with personal clinical impressions of changes component is suggested as an explanation observed during counterstrain treatment. for the origin and maintenance of somatic However, it seems unlikely that propriocep- dysfunction and its response to the coun- tive reflexes represent the sole element in- terstrain technique. In actuality, both pro- volved in how counterstrain works, a position prioceptive and nociceptive responses with which Korr agrees (conversation, May may occur in dysfunctional states. Other 1989). Advances in physiologic knowledge of physiologic responses also may be in- the proprioceptive functions have not changed volved. These views are consistent with Korrs concepts. These advances, in fact, have clinical experience. clarified the theoretical basis for somatic dys- (Key words: Counterstrain, osteo- function and explanations for response to ma- pathic manipulative treatment, nocicep- nipulative treatments. In this paper, we (1) sug- tive reflexes, somatic dysfunction.) gest an updated theoretical basis for somatic dysfunction involving nociceptive stimuli, and Counterstrain is a passive, positional-re- (2) examine the responses to counterstrain treat- lease manipulative technique, developed by ment. Our proposed theoretical role of nocicep- Lawrence Jones. 1,2 Counterstrain techniques tive mechanisms in initiating or maintaining place somatic systemic elements into the posi- somatic dysfunction (or both) and proposed ba- tion of greatest perceived ease, or comfort, by sis for effects of counterstrain treatment ex- passively approximating the attached surfaces tend the concepts related to proprioceptive func- of those elements. Osteopathic physicians have tions. demonstrated time and again that counterstrain is a clinically valid and useful entity. Basic reflexes However, the theoretical physiologic mecha- First, let us apply Korrs proprioceptive model to a simple hinge-type joint, the elbow. To fa- Dr Bailey, currently a senior student at the College of cilitate the discussion, let us concern ourselves Osteopathic Medicine of the Pacific, Pomona, Calif, will with only two antagonistic muscles that act be starting a neurology residency at the University of Alabama at Birmingham. Dr Dick, past chairman of the across the elbow joint: the lateral head of the Department of Osteopathic Principles and Practice, Col- triceps brachii muscle, an extensor of the fore- lege of Osteopathic Medicine of the Pacific, is currently arm, and the brachialis muscle, a forearm in private practice in San Dimas, Calif. Reprint requests to Mark Bailey, PhD, 2128 South- flexor (Figure 1). Now let us assume that while wood Rd, Jackson, MS 39211. the elbow is semiflexed, a weight is placed in (continued on page 337)

334 • JAOA • Vol 92 • No 3 • March 1992 Brief report • Bailey and Dick the hand. To lift the load, the brachialis mus- of the central nervous system, that is, from cle shortens (contracts), and the triceps mus- the brain rather than the spinal cord. 2 Col- cle is concurrently stretched. Both brachialis lectively, the muscle spindles provide proprio- and triceps muscles contain specialized encap- ceptive information, and the reflexes they me- sulated receptors called muscle spindles 6 that diate are called proprioceptive reflexes. are responsive to stretch. When the muscle is stretched, the spindles are activated. The in- Proprioceptive reflexes and somatic nervated muscle is reflexively induced to con- dysfunction tract, and the contraction is accompanied by What does this elementary neurophysiology the reciprocal inhibition of its functional an- have to do with somatic dysfunction and, more tagonists. 7 This simple reflex arc is the famil- specifically, its treatment by counterstrain? To iar myotactic or stretch reflex. When the mus- answer this question, let us return to our pre- cle shortens, the spindles are "unloaded" and, vious example in which a weight was placed as a result, their responses are quieted or even on the semiflexed upper extremity (Figure 2A). silenced.8 Thus, in our example, the spindles Furthermore, assume that the weight is ap- in the triceps muscle increase their response plied suddenly. The upper extremity is rates as the muscle is stretched. Similarly, the abruptly "loaded," and the forearm is forced spindles in the brachialis muscle decrease immediately toward extension. The brachialis their rate of firing momentarily as the muscle muscle is suddenly stretched (the strain part shortens. of Jones original strain/counterstrain), and the In simple terms, we have now defined the triceps muscle is shortened (Figure 2B). primary muscle-spindle afferent response. Mus- Subsequent reflexive reactions establish cle spindles, however, are complex receptors, and maintain the somatic dysfunction. Propri- and the primary afferent response is only one oceptive reflexes come into play (Figure 2C), constituent of an entire informational spec- and the brachialis muscle is contracted, such trum. In addition to primary spindle informa- contraction applying physiologic "brakes" to tion, there is another component provided by the runaway movement of the forearm. Accord- their gamma-efferents. 9 The functioning of the ing to Korrs4,6 explanation, this sudden shorten- gamma-efferent system and its interactions ing and concurrent silencing of the spindles with the spindle primaries is both subtle and in the triceps muscle (Figure 2E) causes both complex. For the purpose of this discussion, the gamma "gain" in the triceps muscle to be it is sufficient to state that the gamma-effer- reflexively turned up, and the muscle itself to ents augment and fine-tune the activity of the be reflexively contracted (the counterstrain of primary afferent system. 19 In our example, the strain/counterstrain) (Figure 2F). The central primary afferent spindle response of the brachi- nervous system regains its all-important spin- alis muscle is quieted, so that the central nerv- dle information but at the expense of a short- ous system is provided with little information ened triceps muscle. This muscle now reports regarding the degree of brachialis stretch. to the central nervous system that it is being The gamma efferent system subserving the stretched, even before it attains its neutral brachialis muscle would "turn up" the sensi- length. On recovery from the sudden exten- tivity of its primary afferents and restore some sion movement, flexion is resisted by a triceps level of spindle activity and information in- muscle that is now tonically shortened by its flow to the central nervous system. The pri- inappropriately high gamma gain. mary spindle afferent stretch reflex functions Clinical findings associated with this exam- largely at a segmental level." This means that ple include the forearms moving easily into the specific segment of the spinal cord respon- extension (the direction of ease), but resistance sible for the innervation of the muscle is also to movement into flexion (the direction of bind) responsible for its myotactic reflexes. In con- and pain. Thus, normal symmetry of motion trast to the primary afferents, the gamma sys- about the elbow joint is disrupted. There are tem is controlled from suprasegmental levels tender points, or painful foci, located on the

Brief report • Bailey and Dick JAOA • Vol 92 • No 3 • March 1992 • 337 posterior aspect of the upper arm/forearm, with from the influence of the primary afferent spin- associated changes in tissue texture. Jones2 dle stimuli, the inappropriately exaggerated pointed out that the pathologic alteration in gamma gain can be reset by the central nerv- this type of somatic dysfunction involves tis- ous system. The forearm would be held by the sues with an essentially atraumatic history; physician in this position for a short time (typi- for example, the only external events to which cally, about 1 minute). Accompanying the nerv- the triceps muscle (the counterstrained ele- ous system–mediated release are palpable tis- ment) was exposed was that it was suddenly sue texture changes and a resolution of the allowed to shorten. Only the brachialis mus- tender points. The upper extremity is then cle (the strained element) was suddenly slowly returned to a more neutral semiflexed stretched. position. All movements of the forearm must The proprioceptive model of somatic dysfunc- be accomplished by the physician without ac- tion as applied to our example may be sum- tive assistance from the patient. 13 On reexami- marized as follows: The forearm is suddenly nation, a pain-free, symmetric range of fore- moved from the resting position (Figure 2A) arm motion is expected. into extension; the brachialis muscle is stretched (loaded) and its spindles increase Painful comparisons their firing rate (Figure 2B and 2E), that is, Now that we have reviewed the mechanisms the brachialis muscle is strained. The triceps that are proposed by Korr4,5 to underlie so- muscle is shortened (unloaded) and its spin- matic dysfunction and discussed their appli- dles decrease their firing rate (Figure 2B and cation to counterstrain, let us add another di- 2E). mension to our previous example. Assume now Bereft of triceps spindle information, the cen- that the weight is applied to the forearm with tral nervous system turns up the gain of the sufficient intensity and abruptness to injure triceps gamma system; the triceps muscle, re- the brachialis muscle and to cause pain. Ex- flexively contracts (counterstrain), and in- cept for this addition, all other conditions are creases its rate of spindle firing (Figure 2C and identical: same weight, same forearm. Will the 2F). The triceps muscle now reports a "neu- predicted results, such as ease of motion and tral" position even though the forearm is posi- localization of pain, be the same? To fully an- tioned toward extension. swer these questions, we must first consider The brachialis muscle responds to being the outcomes of activating pain-mediated (no- stretched by reflexively contracting; because ciceptive) reflexes. the triceps muscle is now shortened; flexion Nociceptive reflexes are powerful and capa- is limited and the somatic dysfunction is es- ble of overriding voluntary behavior. 14 Even tablished. Such dysfunction is maintained by by conscious design, it is nearly impossible to the continued increased gamma gain in the abrogate nociceptive reflexes. When we step triceps muscle so that the forearms neutral on a sharp object, it is exceedingly difficult to position is reset toward extension; normal sym- avoid withdrawal of the foot and possibly stum- metry of forearm motion is compromised. bling, even if circumstances, such as carrying a dozen eggs at the time, forbid. Counterstrain treatment Flexor withdrawal is a multisegmental, no- Counterstrain treatment of the just described ciceptive reflex that moves the affected body dysfunction would be accomplished by pas- region away from a noxious stimulus. In our sively placing the forearm into a position of example, the noxious stimulus is insult to the extension, thereby approximating the ends of brachialis muscle and its associated tissues, the tonically contracted triceps muscle. This resulting in either frank tears or less severe procedure recreates the direction of the origi- stress, both of which result in the initiation nal injury. With the tension removed from the of nociceptive responses. The nociceptive re- counterstrained muscle (triceps), its spindles flex then takes the form of contraction of the are unloaded and slow their firing. Released brachialis muscle, drawing the forearm into

338 • JAOA • Vol 92 • No 3 • March 1992 Brief report • Bailey and Dick fibers oriented in random directions, so that normal joint motion is even more restricted.18 The following summarizes the nociceptive component of somatic dysfunction as applied to our example: The forearm is moved into extension with sufficient force to cause some degree of trauma to the brachialis muscle or its surrounding tissues (or both). Pain receptors are activated both directly by the tissue damage and by subsequently released tissue factors. The brachialis muscle is reflexively induced to contract, so that the forearm is pulled Figure 1. Lateral head of triceps brachii muscle and into flexion. As long as the noxious stimulus brachialis muscle with bony attachments on upper ex- is present, the brachialis muscle will continue tremity. to contract. Symmetry of motion is disrupted. It is possible that both proprioceptive and flexion, 15 guarding and protecting the injured nociceptive reflexes function in synergistic fash- extremity. ion. Recall that in the original example of pro- Note that application of the same weight ap- prioceptive reflex functioning, the direction of plied across the same joint produces physical restricted motion was toward flexion, because findings opposite to those described in the pro- of a tonically contracted triceps muscle. Also prioceptive model. The damaged brachialis mus- recall that there were painful tender points cle is held in a state of contraction. Ease of associated with the posterior aspect of the arm/ motion is now toward flexion, not extension forearm. Given this scenario, it is consistent as before. The anterior aspect of the extrem- with a nociceptive model that the triceps mus- ity is tender and painful. What happened to cle, which is anatomically associated with the the proprioceptive reflexes that acted in our area of painful stimulation, tends to contract.17 first example? We propose that the proprio- Local tissue conditions such as ischemia, cir- ceptive reflexes are still present and probably culatory stasis, and edema associated with the functional, but are being masked by the more somatic dysfunction18 maintain nociceptive potent nociceptive reflex. It is possible that the nociceptive reflex represents a predominately acute phase of the injury, whereas the proprioceptive mechanism functions in more chronic aspects. This could certainly be the case if the damage to the brachialis muscle were mini- mal and the noxious stimuli were resolved quickly. In that circumstance, we expect the proprioceptive reflex to be unmasked on resolution of the noxious input. However, given 1111111111111111111111E1 1 1 111111111111111 Brachialis the more potent nature of the nociceptive re- I I 11111111 Triceps flex, if the damage to the brachialis muscle t t t were severe, we expect tonic brachialis con- D E F traction to be both the acute and the chronic effect, restricting the range of motion about the elbow joint for a potentially extended pe- Figure 2. Position of upper extremity (A,B,C) and the riod. If the somatic dysfunction is not resolved, primary muscle spindle activities (D,E,F) of brachialis and triceps muscles during a sudden extension of fore- there is evidence that the connective tissues arm. A and D, resting conditions. B and E, immediate in the upper extremity will reorganize. Fibro- effects of sudden extension movement. C and F, proprio- cytes will undergo proliferation, but with their ceptive reflexive response.

Brief report • Bailey and Dick JAOA • Vol 92 • No 3 • March 1992 • 339 stimulation, and further aggravate the dysfunc- phenomenon of human injury. Both proprio- tional state. Similarly, in the second example ceptive and nociceptive mechanisms find ex- in which the injured brachialis muscle is the pression in our whiplash example. Local tis- source of the noxious stimulus, the painful mus- sue injury can play a role in both the genesis cle contracts, so that the forearm tends to be and the maintenance of somatic manifesta- drawn into flexion. tions.19 The intimate association of the cervi- The previous example of the injured brachi- cal portions of the sympathetic chains and gan- alis muscle provides a simple example of pro- glia with the affected anterior tissues should prioceptive or nociceptive mechanisms (or be considered. Similarly, the affected posterior both) creating and maintaining a pathologic tissues are associated with the suboccipital and functional state. Let us now examine a more occipital nerves and the vertebral artery. It complex physical insult. Whiplash is a rela- seems likely that these important structures tively common injury characterized by sudden will bring their own influences into the clini- hyperextension of the cervical spine. It is clear cal presentation. Which effects predominate is that the consequences of such an injury would largely dictated by the individual circum- be profound and widespread. However, for the stances of the injury and the individual pa- purposes of our discussion let us focus our atten- tient. tion on two functional groups that act as agon- Further complicating the whiplash exam- ist/antagonist pairs in the cervical spine. The ple is the fact that whiplash is usually not anterior group (flexors) includes the scalene, solely a hyperextension injury. More com- suprahyoid, infrahyoid, and prevertebral mus- monly, the cervical spine is thrown violently cles. The posterior group (extensors) consists first into hyperextension and then, with almost predominantly of the erector muscles of the equal force, into extreme flexion. In effect, each spine, but includes the transversospinal, suboc- forward/backward movement of the head cre- cipital, splenius, and trapezius muscles. ates its own "layer" of somatic dysfunction. On physical examination of the whiplash pa- The question of which tissues were "strained" tient, clinical findings may include edema, ten- and which were "counterstrained" becomes derness, and increased muscle tension in the moot, as most of the tissues in the cervical re- anterior tissues. The posterior tissues typically gion receive varying degrees of damage from have multiple cervical tender points, increased such an event. muscle tension, and ease of motion toward ex- To treat whiplash with counterstrain tech- tension. In the initial impact, the patients cer- nique, the physician must decide which com- vical spine is thrown violently into sudden hy- ponent is treated first. This decision is usu- perextension. The tissues of the cervical flexor ally made by determining the direction of great- region are rapidly stretched, while those of the est ease of passive cervical motion, as well as cervical extensor region are suddenly short- assessing the quantity and quality of tender ened. Proprioceptive mechanisms are activated points in the associated tissues. The head in the extensor muscles so as to result in their would be positioned in such a way as to allow reflexive contraction. The findings in the an- those most painful regions to relax, effectively terior cervical region, which indicate tissue treating at least the most acute and noxious damage, are more easily attributed to nocicep- "layer" of the whiplash injury. Subsequent tive mechanisms. The direct traumatization of treatments would be necessary to address the these tissues during the initial impact initi- other "layers." ates local tissue inflammatory responses (ac- If we assume that at least some of the pa- companied by initiation of nociceptive stim- thologic alteration has a nociceptive compo- uli) and sets the stage for muscular guarding. nent, how would we expect counterstrain treat- Clinically, the result is a patient with a stiff, ment to help? Empirically, we find that so- painful neck. matic dysfunction resulting from painful tis- This example exposes the difficulties of im- sue damage responds quite well to counter- posing simplistic explanations for the complex strain treatment. Possibly counterstrain treat-

340 • JAOA • Vol 92 • No 3 • March 1992 Brief report • Bailey and Dick ment resolves underlying proprioceptive ele- pressed in simplistic form, are consistent with ments of the somatic dysfunction and allows clinical experience. more effective healing of the tissue damage component. Counterstrain techniques appear Acknowledgment to restore physiologic motion by affecting the Appreciation is expressed to Tim Schultz, DO; John origins of somatic dysfunction, allowing patholo- Jones III, DO; Richard Sugarman, PhD; Irvin M. gically perpetuated reflexes to normalize and Korr, PhD; and Lawrence Jones, DO, FAAO, for the symptom complex to resolve. Clinically, their editorial comments and suggestions during the counterstrain treatment is appropriate for both preparation of this manuscript. the simple and the complex patient presentation, irrespective of the physiologic model being applied. References 1.Jones LH: Spontaneous release by positioning. The DO Comment 1964;4:109-116. 2. Jones LH: Strain and Counterstrain. Newark, Ohio, Ameri- Probably very few dysfunctional states result can Academy of Osteopathy, 1981. from either a purely proprioceptive, or nocicep- 3. Glossary of osteopathic terminology. In American Osteopathic tive response. Both are likely to occur simul- Association: 1991 Yearbook and Directory of Osteopathic Physi- cians, ed 82. Chicago, Ill, American Osteopathic Association, taneously. Additional factors such as auto- 1991. nomic responses, other reflexive activities, 4. Korr IM: Proprioceptors and somatic dysfunction. JAOA joint receptor responses, or emotional states 1975;74:638-650. must also be accounted for. What predomi- 5. Korr IM: The neural basis of the osteopathic lesion. JAOA 1947;48:191-198. nates is largely a matter of degree, determined 6. Matthews PBC: Muscle spindles and their motor control. by conditions both external and intrinsic to the Physiol Rev 1964;44:219-288. injured tissues. 7. Matthews PBC: Muscle spindles: Their messages and their The symptomatic patient represents the ac- fusimotor supply, in Brooks VB (ed): Handbook of Physiology, Section 1: The Nervous System, vol 2, Motor Control. Bethesda, cumulated total of an intricate variety of physi- Md, American Physiological Society, 1981, pp 189-228. ologic responses. Our understanding of such 8. Hunt CC, Kuffier SW: Stretch receptor discharges during mus- complexity begins at the level of the simplis- cle contraction. J Physiol 1951;113:298-315. tic neurophysiologic analysis proposed here. It 9. Crowe A, Matthews PBC: The effects of stimulation of static and dynamic fusimotor fibers on the response to stretching of the must progress with the incorporation of such primary endings of muscle spindles. J Physiol 1964;174:109-131. concepts into the awareness that our patients 10.Vallbo AB: Discharge patterns in human muscle spindle are more than a complex collection of reflexes. afferents during isometric voluntary contractions. Acta Physiol Scand 1970;80:552-566. Human beings represent a gestalt, that is, 11.Lloyd DPC: Conduction and synaptic transmission of the more than the sum of the parts, and as such reflex response to stretch in spinal cats. J Neurophysiol cannot be fully comprehended by reductionis- 1943;6:317-326. tic analysis. Realizing this, we are returned 12.Feldman AG, Orlovsky GN: The influence of different de- scending systems on the tonic stretch reflex in the cat. Exp Neu - to a primary osteopathic tenet that rational rol 1972;37:481-494. therapy is based on an understanding of body 13.Schwartz HR: The use of counterstrain in an acutely ill in- unity, self-regulatory mechanisms, and the in- hospital population. JAOA 1986;86:433-442. terrelatedness of structure and function. 14.Perl ER: Crossed reflex effects evoked by activity in myeli- nated afferent fibers of muscle. J Neurophysiol 1958;21:101-112. 15.Eccles RM, Lundberg A: Synaptic actions in motoneurons Conclusions by afferents which may evoke the flexion reflex. Arch Ital Biol A nociceptive component-stimuli, reflexes, re- 1959;97:199-221. actions, and responses-is proposed as a theo- 16.Hettinga DL: Normal joint structures and their reaction to injury: I. J Orthop Sports Phys Ther retical explanation for the initiation and main- 1979;1:16-22. 17.Hagbarth KE: Excitatory and inhibitory skin areas for flexor tenance of somatic dysfunction and its re- and extensor motoneurons. Acta Physiol Scand 1952;26(suppl sponse to counterstrain manipulative treat- 94)a:58. ment. This component and others that may be 18.Awal EA: Interstitial myofibrosis: Hypothesis of the mechanism Arch Phys Med 1973;54:440-453. present have characteristics similar to those 19.Van Buskirk RL: Nociceptive reflexes and the somatic dys- of the proprioceptive component. The ideas, ex- function: A model. JAOA 1990;90:792-809.

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