Formation Lawrence H. Jones

Chapter 13.

Strain and Counterstrain

Randall S. Kusunose

13

Strain and CounterstrainRANDALL s. KUSUNOSE

action IS

ORIGIN

an indirect technique because itsaway from the restricted barrier.

Observing a skilled strain and counterstrainpractitioner you are immediately impressedwith how gentle and nontraumatic this tech­nique is for the patient and the operator. Howquickly they are able to assess the musculo-skeletal system for the areas of dysfunction Jones was motivated to experiment with theand the involvement of the patient in assisting concept of positional release in part from histo guide the operator to the final treatment frustration with the rationale of his time forposition. the osteopathic lesion (which has since

This innovative system for the treaonent changed names to somatic dysfunction). Heof somatic dysfunction was developed by was schooled to believe that somehow jointsLawrence Jones, DO, FAAO. He defines became locked or subluxed and the only waystrain and counterstrain as a "passive posi- to treat them was to burst them loose via hightional procedure that places the body in a velocity thrust techniques. His results wereposition of greatest comfort, thereby relieving generally good, but occasionally a case wouldpain by reduction and arrest of inappropriate enter his office that resisted all of his ma-proprioceptor activity that maintains somatic nipulative skills, until Jones states, "onlydysfunction." srubbornness kept me from admitting I was

From the definition it is clear that the stumped." He recounts that he was treatingstrain and counterstrain concept is not di- just such a case when he discovered positionalrected toward tissue injury or tissue damage release.2•3

but aberrant neuromuscular reflexes within A young man with psoasitis (stooped pos-that tissue. Specifically, the primary proprio- rure, unable to come completely erect withcepcive nerve endings are singled out as severe pain across the low lumbar area) hadreporting false information to the central ner- been treated by Jones using high velocityvous system and maintaining somatic dysfunc- techniques for 6 weeks with no reliefof symp-tion.' The operator will affect this system by toms. He had been treated previously by twopassively positioning the patient's dysfunc- chiropractors for 2- 1;2 months with similartional segment toward comfort or ease and results. He complained of pain in bed and anaway from pain, bind, and restricted barriers. inability to find a comfortable position thatThe position results in ma:cimal shortening of he could stay in for any longer than 15 min-the involved muscle and its proprioceptors utes. SO,]ones devoted one treatment sessionand evenrual reduction of neuromuscular fir- to finding a reasonably comfortable positioning to tonic levels. Strain and counterstrain is for the patient to sleep in. After 20 minutes

323

324

of experimentation, a position of amazingcomfort was found. Jones relates that: "Hewas nearly rolled into a ball with the pelvisrotated about 45 degrees and laterally flexedabout 30 degrees." This was the first positiveresponse the patient had had after 4 monthsof treatment, so Jones propped him in theposition and went off to treat another patient.When he returned, he helped the patient up­right and was astonished to find he couldstand completely erect in total comfort. Ex­amination revealed fuJI and near pain-freerange of motion. All Jones had done was putthe patient in a position of comfort and theresults were dramatic after his best efforts hadrepeatedly failed.

This was the inspiration that started Jones'experimenting with positional release and ap­plying it to all somatic dysfunctions. Dnringthis developmental period he observed thatthe return to neutral done very slowly wasimportant to the outcome of the positionalrelease. If the patient was moved too quickJy,especially in the first 15 degrees of motion,the benefit from the positioning was lost.Also, after initially supporting the patient inthe position of release for 20 minutes, he wassystematically able to reduce the period to 90seconds. Anyrlling less than 90 seconds andhis results were inconsistent; but more than90 seconds did not appear to increase thebenefit to the patient.

The second feature to strain and coun­terstrain was the discovery of palpable myo­fascial tender points and their correlation tospecific somatic dysfunction. Jones describestender points as "small zones of tense, tender,edematous muscle and fascial tissue about acentimeter in diameter." These points, foundby moderate palpatory pressure, are directlyrelated to somatic dysfunction and with suchconsistency that they became his diagnostictool. Tender points are four times more ten­der than normal tissue. Palpation with lessthan sufficient pressure to cause pain in nor­mal tissue will elicit a sharp local pain char­acteristic of a strain and counterstrain tenderpoint. Most of the tender points are foundoverlying the muscle involved in the dysfunc-

RATIONAL MANUAL THERAPIES

tion. Tender points found in the paravertebralmusculature or over spinous processes are es­pecially valuable for diagnosing segmentaldysfunction in the vertebral column.

RESEARCH DATA

Prior studies have shown the efficacy of pal­pation on pressure-sensitive points in accu­rately diagnosing spinal dysfunction.4-6Quantitative studies done by Denslow andassociates? showed how spinal dysfunctioncould be objectively confirmed with gaugedpressure on the spinous processes and mea­surement of the motor reflex threshold.

Denslow' observed that when he pushedon a dysfunctional vertebral segment on eitherside of the spinous process or in the para­vertebral area he would elicit local pain anda muscular contraction in the erector spinaegroup. From this clinical observation he de­signed a study to measure the amount of pres­sure it would take to elicit an initial muscleresponse from these points, which was calledmotor reflex threshold. Pressure was appliedto the spinous processes by a self-designedpressure meter, and electromyographic elec­trodes were placed in the paravertebralmusculature. The exact amount of pressurenecessary to elicit a muscle response was mea­sured. What he found was that at levels wherehe had made a palpatory diagnosis ofvertebraldysfunction he was consistently able to cor­relate a lower motor reflex threshold. It tookless pressure to elicit pain and a correspondingmuscle contraction. Nondysfunctional seg­ments responded with little or no pain andmuscle contractions at the highest pressuresettings.

Denslow correlated a second characteristicof joint dysfunction with a lower motor reflexthreshold, this being differences in tissue tex­ture. At sites of low threshold he describespalpable changes in tissue texture as "doughyand boggy." He used these terms to describethe tense, edematous feel of the tissue. Tissuetexture changes and reflex muscle contractionwith palpatory pressure were so consistent

CHAPTER 13 , STRAIN AND COUNTERSTRAN

that he was able to predict low mOtor thresh­old levels with 95% accuracy.

Another observation of Denslow's, usingelectromyograms, was that muscle completelyat fest was characterized by an absence ofaction potentials. At low threshold segments,despite the apparent relaxation of the subject,he found "rest activity," action potentialsfrom the paravertebral musculature even atrest. l-Ie states, "It was often necessary toposition and reposition the shoulder girdle,upper extremity, head and at times the lowerextremities in order to eliminate rest activity."

Denslow concluded that "low thresholdsegments are apparently hyper-excitable notonly to pressure stimuli applied to the corre­sponding spinous process but also to impulsesfrom proprioceptors associated with position­ing."

The phenomenon of the elimination ofEMG "rest activity" may be associated withstrain and counterstrain. Denslow's studytested the thoracic levels 4, 6, 8, and 10. Thestrain and counterstrain treatments for poste­rior thoracic dysfunction at those segmentswould include passive positioning of theshoulder girdle, upper extremity, head, andlower extremities to find the position of re­lease.

TENDER POINTS

Tender POi11ts are not only found over spi­nous processes or paravertebral muscularure.Figure 13.1 shows the magnitude of the num­ber of diagnostic tender points that Jones hasmapped out over the entire body. This illu­stration represents just a small portion of theclose to 200 tender points that Jones has cor­related with specific dysfunction. Tenderpoints in the posterior torso over spinousprocesses or paravertebral mllsculanrre areclosely associated with the area and level ofposterior pain complaint. Tender points inthe anterior torso and pelvis are also closelyassociated with an area and level of posteriorpain. Patients usually have no awareness ofthese anterior tender points until they areprobed. Many osteopathic clinicians believe

325

the discovery of anterior tender points, theirrelated dysfunctions, and their correlation toposterior pain to be one of Jones's most sig­nificant contributions to the trea011ent ofmusculoskeletal dysfunction. Jones feels that50 percent of the dysfunction that producesthe patient's posterior pain is represented onthe anterior aspect of the body. Failure toconsider these dysfunctions may lead to dis­appointing results.

An added characteristic of tender pointsbesides their value as a diagnostic tool is theiruse as a monitoring point. By monitoring thetender point for changes in tissue tension andthe patient's feedback of either increasing ordecreasing sensitivity, the operator is guidedto a position of maximum palpatory relaxationbeneath the monitoring finger. Marked andprompt decrease in subjective tenderness en­sues. Jones calls this the "mobile point." Itis the point of ma.x.imum ease or relaxationwhere movement in any direction will in­crease tissue tension beneath the monitoringfinger. The mobile point signifies the idealposition for release.

Jones2 explains the use of tender points inthis way. "A physician skilled in palpationtechniques will perceive tenseness and/oredema as well as tenderness, although the ten­derness (often a few times greater than thatof normal tissue) is for the beginner the mostvaluable diagnostic sign. He maintains his pal­pating finger over the tender point to monitorexpected changes in tenderness. With theother hand he positions the patient into aposrure of comfort and relaxation. He mayproceed successfully just by questioning thepatient as he probes intermittently while mov­ing toward the position. If he is correct, thepatient can report diminishing tenderness inthe tender area. By intermittent deep palpa­tion he monitors the tender point, seeking theideal position at which there is at least twothirds reduction in tenderness." Finding theposition of release in this way, holding thisposition for 90 seconds and returning to neu­tral very slowly are the major components ofa strain and counterstrain technique.

A common question is the relationship of

326 RATIONAl MANUAl THERAPIES

Figure 13.1. Location of tender points. With permission, Jones LH. Strain and counterstrain.Newark, OH: American Academy of Osteopathy, 1981.

strain and counterstrain tender points toTravell's trigger points, Acupuncture points,Chapman reflex points, Shiatsu points, etc.There is, of course, a great deal of overlap inpoint locations and the palpatory feel of thetissue. However, there are two major differ­ences. First, strain/counterstrain tender pointstend to be more segmental in origin. Pointsalong the vertebral column designate segmen­tal dysfunction at the corresponding vertebrallevel. The other philosophies8 identify pointsas related to full body systems and are moreholistic in nature. Second, Jones feels strainand counterstrain tender points are a sensorymanifestation of a neuromuscular or muscu­loskeletal dysfunction. The points are used to

make the diagnosis and to monitor the effec­tiveness of the treaOllent technique. Treat­ment is not directed at the tender point butat the dysfunction that produces the tenderpoint. If the treatment is effective the tenderpoint diminishes in tenderness, tissue tension,and edema. In the other philosophies thetreatment is directed toward the painful point,by injection, needling, deep pressure, electri­cal stimulation, and vapocoolants.

RATIONALE

The rationale for strain and counterstrain isbased on a neurologic model first proposedby Dr. Irvin Korr in 19756 .9 His hypothesis

CHAPTER T3 , STRAIN AND COUNTERSTRAIN

incriminated the muscle spindle or primaryproprioceptive nerve endings as the basis forjoint dysfunction. His concept is derivedfrom: a) the consensus on the importance ofdecreased joint mobility or decreased jointrange of motion for determining somatic dys­function, and b) on the muscle's function asa "brake" to retard or resist joint motion.Korr explains, "While usually thinking ofmuscles as the motors of the body, producingmotion by their contraction, it is importantto remember that the same contractile forcesare also utilized to oppose motion. By theapplication ofcontrolled counteracting forces,contracting muscle absorbs momentum (forexample, of a swinging limb) and regulates,resists, retards and arrests motion." He ex­panded on his observation of "ease" and"bind," the behavior of a dysfunctional jointto move freely and painlessly in certain planesof motion and the painful resistance to motionin the opposite direction. Korr reasoned thatimpairment of joint motion in distinct planeswas produced by a unilateral active con­traction of muscles pulling the joint in a cer­tain direction. Contraction of these musclesaround the joint would resist (bind) motionin directions that would tend to lengthen orstretch the muscles and surrender (ease) tomotion in directions that would shorten orapproximate the muscles.

327

Karr's premise is that high gamma dis­charge exaggerates afferent firing from themuscle spindle producing a reflex musclespasm which fixates the joint in a certain di­rection and resists any attempts to rerurn toneutral. At this point a review of the strucrureand function of the muscle spindle!!,!2 is inorder to establish a common understanding(Fig. 13.2).

MUSCLE SPINDLE

Muscle spindles are highly specialized sensoryreceptors which are scattered throughout theextrafusal fibers of muscle. Muscle spindledensity will vary with function. Phasic muscleshave more muscle spindles than postural mus­cles due to the precision of control required.Each spindle is fluid-filled and contained in aconnective tissue sheath about 3-5 mm long,enclosing 5-12 thin specialized muscle fibersknown as intrafusal fibers. They lie in parallelto the extrafusal fibers and are attached tothem at each end. There are two types ofintrafusal fibers: larger fibers with centrallylocated nuclei aggregated into a bag-likepouch called a nuclear bag fiber, and smallerfibers containing only a single row of nucleiin their central portion called a nuclear chainfiber. These fibers can be thought of as havingthree regions, a central or equatorial portionwhere the nuclei are concentrated, and the

Nuclear bag fiber=-+""-+-':::'--nr-

Nuclear chain fiber

Trail ending

Figure 13.2. Muscle spindle, With permission, Ganong WF. Review of medical physiology. 9th ed.Los Altos, CA: Lange Medical Publications, 1979.

328

two polar ends which contain the contractilematerial. In the equatorial portion lie the pri­mary afferent nerve endings also ""lied theannulospiral endings which coil around thenuclear regions. Secondary or flower sprayafferent nerve endings terminate on eitherside of the primary endings closer to the con­tractile polar ends.

Innervating the intrafusal fibers aregamma motor neurons whose cells originatein the ventral horn, pass through the ventralroot, and terminate on the contractile polarends. In contrast to the alpha motor neuronsinnervating the extrafusal fibers, these neu­rons' are small and their axons thin.

The muscle spindle is sensitive to lengthchanges. When the extrafusal fibers arestretched the muscle spindle is stretched,causing the annulospiral and flower spraynerve endings to fire. These fibers end mono­synaptically directly at the motor neurons ofthe muscle containing the excited spindles.The excitatory effect produces a reflex con­traction of the extrafusal muscle fibers, resist­ing the stretch. This is the familiar stretchreflex.

The frequency of firing of the annulospiral

Afferentfiber

Extensor

+

RATIONAl MANUAL THERAPIES

and flower spray nerve endings is in directproportion to the change in length. The an­nulospiral nerve ending has the additionalcharacteristic that its frequency of firing is inproportion to changes in the rate of stretch­ing. Therefore, the annulospiral nerve endingmeasures length plus velocity of the stretchand the flower spray nen'e ending measuresonly length. Though the effect of these nerveendings is excitatory on the motor neuron ofthe involved agonist muscle, accessory im­pulses are transmitted to adjacent interneu­rons which form an inhibitory pathway to themotor neurons of the antagonist muscle. Thisis ""lied reciprocal inhibition (see Fig. 13.3).

Gamma efferent stimulation of the intra­fusal fibers will also stimulate afferent spindlefiring. Impulses transmitted through thegamma efferent neurons will evoke contrac­tion of the polar ends of the intrafusal fibers.Contraction of the polar ends stretches thenuclear portion stimulating the annulospiraland flower spray nerve endings to fire. Theresponse is equal to that produced by stretch­ing the extrafusal fibers. By controlling thecontraction of the intrafusal fibers throughgamma stimulation the central nervous system

Inhibitoryinterneuron

Figure 13.3. Stretch reflex and reciprocal inhibition, Astrand P-O, Rodahl K.Textbook of work physiology. New York: McGraw-Hili, 1970.

CHAPTER 13 , STRAIN AND COUNTERSTRAIN 329

SpindleTendon Extrafusal fiber

.. /' .......Sensory./ nerve

Discharge ratein sensory nerve

..'".,'"

,

""'"•I",•

Resting muscle

Increased gammaefferent discharge

Muscle stretched

Muscle contracted

Increased gamma efferentdischarge - muscle stretched

Figure 13.4. Effect of various conditions on musclespindle discharge. Adapted from Ganong WF. Reviewof medical physiology. 9th ed Los Altos, CA: LangeMedical Publications, 1979.

range of motion. ]ones2 states, "It is wellknown that for each painful joint there is aspecific direction of position that greatly ag­gravates the pain and stiffuess. Movement of

MUSCLE SPINDLE ANDSOMATIC DYSFUNCTION

Discussion of the role of the muscle spindlein somatic dysfunction would be best initiatedwith a definition of somatic dysfunction. Thecurrent, accepted definition is: impaired oraltered function of the related components ofthe somatic (body framework) system, skele­tal, arthroidial, and myofascial structures; andrelated vascular, lymphatic and neural ele­ments. It is widely accepted that somatic dys­function involves alterations in systems otherthan the musculoskeletal. Sympathic involve­ment in somatic dysfunction is well docu­mented but poorly understood and not withinthe scope of relevance for this topic. Thesomatic dysfunctions considered here are pri­marily produced during mechanical trauma.

The components of somatic dysfunctionimportant to a strain and counterstrain diag­nosis would be: first, tissue texture changesdescribed as tense, ropey, and boggy. This ismost commonly represented as muscle hyper­tonicity and tissue edema involving a muscleor muscles investing a particular joint; second,specific tender points which, when palpated,elicit exquisite local pain. Each point indicatesa specific somatic dysfunction; and third, im­pairment in the amplitude and quality of joint

is able to set and reset muscle length, muscletonc, and muscle spindles' sensitivity tostretch. This mechanism provides for a stateof preparedness for the muscle to respond toslight changes in length. Thus the higher thegamma stimulation the greater the spindlesensitivity to stretch. Stretch of the musclewith high gamma stimulation produces amorc intense spindle discharge and thereforea stronger reflex muscle contraction (see Fig.13.4).

Approximation of the muscle by activecontraction or passive shortening will de­crease spindle discharge proportionately, andwith maximal shortening may even silence it.With high gamma stimulation the musclemust shorten even more to approach the sameproportionate reduction in spindle discharge.

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the joint in this direction results in immediatereflex and voluntary muscle resistance, to thepoint of rigidity. The converse is also true;for each painful joint there is a specific direc­tion of position that greatly relieves pain andmuscle tension. Movement of the joint in thisdirection results in immediate and progressivereflex and voluntary muscle relaxation, to thepoint of complete relaxation and comfort."

Muscle spindle involvement in somaticdysfunction will be described using an illustra­tion (see Fig. 13.5). This is a sequence of ageneric joint. It has a Muscle A and a MuscleB. Below is represented the firing frequencyof the annulospiral nerve endings. Plate 1 de­picts a joint in neutral. Muscles A and Barein balance and the annulospiral firing frequen­cies are equal, indicating a tonic rest conditionof the muscles. Plate 2 depicts a joint in"strain." Muscle A is severely overstretchedand Muscle B is maximally shortened. Theannulospiral firing frequency is increased be­cause of the stretch on Muscle A and its spin­dle. The firing frequency ofMuscle B is prac­tically nil. Shortening of the muscle slacks thespindle and reduces afferent firing and thestretch on Muscle A reciprocally inhibitsMuscle B. Now, if the body reacts to thisstrain position in a slow and deliberate man­ner to rerurIl to the neutral position then the

RATIONAL MANUAl THERAPIES

stretched Muscle A is eased back to restinglength with no pain and afferent firing returnsto tonic levels. vVhat occurred was an over­stretching and nothing more. But if the bodyreacts to this strain position with a quick,sudden, or forceful movement, a panic reac­tion, to restore the joint to neutral then Mus­cle B and its spindle are quickly stretched.

Now, since the responsibility of the spin­dle in Muscle B is to detect the rapid rate ofchange of ti,e extrafusal fiber lengths and thefrequency of firing of the annulospiral nerveending is in direct proportion to that rate ofchange, the spindle in Muscle B begins toreport a stretch to the eNS even before themuscle reaches its normal resting length. Thisresults in a sharp reflex muscle spasm, not inMuscle A, the overstretched muscle, but inMuscle B, the hypershortened muscle. Plate3 depicts a joint in dysfunction. Muscle B inspasm fixates the joint in a certain directionand resists any attempts to lengthen and re­turn the joint to neutral. The annulospiralfiring frequency of Muscle B is immenselyincreased, reporting to the eNS a continuingmessage of strain which maintains the musclein spasm. Korr6 explains, "Under the influ­ence of gravitational forces, antagonists andpostural retlexes, which would be tending to

stretch the muscle back toward resting length,

I n ill

A B

WllllillWI I I

Wil1illJ

llll.lJ.I.UllllFigure: 13.5. Somatic dysfunction at a joint.

CHAPTER 13 , STRAJN AND COUNTERSTRAIN

the spindle would be continually dischargingand through the CNS ordering the muscle toresist. The more the stretch, the much morethe resistance."

It comes to mind that if Muscle B isspasmcd and its attachments approximatedthis would shorten and slack the spindle, re­duce the afferent discharge to the CNS, andrelieve the spasm. Korr postulates that in theposition of strain (with Muscle B maximallyshortened and its afferent firing practicallynil) the C S, receiving no information fromMuscle B, would greatly increase gamma neu­ron discharge to the intrafusal fibers ,mtil thespindle resumes reporting. This is what os­teopaths refer to as "high gamma gain." With"high gamma gain" you increase spindle sen­sitivity to stretch. Now, with a panic reactionstretch to the hypershortened Muscle B theresultant spasm is of such an intensity that thebody is unable to reduce it on its own. Korr6states, "The higher the gamma activity be­cause of its influence on the excitatory spindledischarge, the more forceful the muscle con­traction and the greater its resistance to beinglengthened. During high gamma activity thespindle may, in effect, be calling for a con­traction when the muscle is already shorterthan its resting length."

Therefore, somatic dysfunction occurs notbecause of strain, but because of the body'sreaction to strain. If the reaction is slow anddeliberate somatic dysfunction is avoided. Ifthe reaction is panic-like, the velocity ofmovement sets off the reflex muscle spasmproducing dysfunction.

Patient accounts of their mechanism ofinjUlY bear this out. The person who is bend­ing forward or squatting and experiences anexcessive strain forward will react with astrong backward movement toward neutralThe patient will describe pain not in the strainposition but with the return to neutral. Theperson involved in a minor motor vehicle ac­cident is rear-ended at a speed which wouldnot appear to cause tissue injury, but theperson's cervical spine in maximal flexion un­derwent a quick extension. The complaint of

331

posterior cervical pam IS aggravated withextension movement, and muscle guardingwould be noted. Flexion movement is pain­free and relaxing. Examination reveals numer­ous anterior cervical tender points and relatedanterior cervical joint dysfunction.

PURPOSE OF STRAINAND COUNTERSTRAIN

What strain and counterstrain attempts to ac­complish with its position of comfort is torelax the muscle spasm by reducing aberrantafferent flow from the muscle spindle. Thisis accomplished by mimicking the originalstrain position or applying a "counterstrain."By passively mimicking the original strain po­sition the operator moves the joint in a direc­tion of ease and maximally shortens the in­volved muscle. Holding for 90 seconds allowsthe spindle to slow down its afferent firingfrequency. Returning to neutral in a slow anddeliberate manner avoids reexciting the pre­viously spasmed muscle. Korr6 explains, "Theshortened spindle nevertheless continues tofire, despite the slackening of the main mus­cle, and the CNS is gradually enabled to turndown the gamma discharge, and, in turn, en­ables the muscle to return to 'easy neutral' atits resting length. In effect, the physician hasled the patient through a repetition of thelesioning process with, however, two essentialdifferences: first, it is done in slow motionwith gentle muscular forces, and second, therehas been no 'surprise' for the CNS; the spin­dle has continued to report throughout."

CASE STUDY

Most of the knowledge about the nature ofsomatic dysfunction and what strain andcounterstrain accomplishes with its positionof comfort is based on patient accounts oftheir mechanisms of injury, their response to

positional treatment, and the observations ofskilled practitioners. Neurophysiologic stud­ies in this area are woefully limited. There­fore, the presentation of a case study seems

332

an appropriate way to lend support and givethe reader insight into the rationale.

This case, Jones's favorite, involves amiddle-aged man who had a habit of fallingasleep supine on the sofa. While asleep hisright ann would occasionally fall off the edgeand hang in marked extension at the elbow.For years, his wife, noticing her husband nap­ping in this position, would slowly and gentlyreplace the arm across his chest without awak­ening him (a slow return to neutral). And foryears the man would awaken from his napwith no complaint of discomfort. One day,while his wife was out, he was awakenedabruptly by the ring of a telephone near hishead, while his elbow was in marked exten­sion. He was so startJe~ that he violentlyjerked his right elbow into flexion. He im­mediately began to feel pain in the right bicepespecially with movement into flexion. A di­agnosis of bicep strain was made for his con­dition on the basis of painful elbow flexion,even though palpation revealed no clinical ev­idence of strained or injured tissue. By thetime he saw Jones he had been disabled for 2years with pain and progressive weakness ofthe biceps. Examination of the biceps failedto reveal any information as to the nature ofthe problem. However, palpation of the distaltriceps uncovered exquisitely sharp tenderpoints (evidence of triceps dysfunction). Thetriceps had been maximally shortened thensuddenly lengthened with a panic response.

Treatment consisted of positioning theelbow in hyperextension so that the tricepswas maximally shortened (mimicking theoriginal strain position), holding the positionfor 90 seconds while monitoring the tenderpoints, and slowly returning to the neutralposition. After three treatments full and pain­free function was restored.

This case demonstrates: first, how import­ant the slow return from a strain position isin avoiding joint dysfunction; second, that thepalpable evidence of dysfunction is frequentlyfound on t1,e opposite side of pain in theantagonist of the overstretched muscle; andthird, how treannent techniques mimic theoriginal strain position. The apparent weak-

RATIONAl MANUAL THERAPIES

ness in the biceps was attributed to disuse andreciprocal inhibition due to the continuouscontraction of the triceps.

STRAIN AND COUNTERSTRAININ THE MANUAL MEDICINEARMAMENTARIUM

Strain and counterstrain can be used as a soletreaonent modality or as an adjunct to othermanual medicine techniques. Its therapeuticuses range from the very acute to the chronicpatient.

Its value with the acute patient is un­matched because it is so gentle and nontrau­matico The operator is guided by what feelsgood to the patient, and often dramaticchanges are made in subjective pain, muscleguarding, and edema.

The gentleness of strain and countersrrainmakes it safe and effective for treating somaticdysfunction on fragile patients (i.e., elderly,osteoporotic, fractures, pregnancy) and in­fants.

Srrain and countersrrain is valuable withchronic patients for two reasons, first, a scanfor tender points provides a quick assessmentof the problem areas of the body and allowsthe operator to delineate the areas of dysfunc­tion contributing to the pain complaint, andsecond, the treannent will reduce the aberrantflow of afferent impulse in the involved mus­cles which have maintained the joint inchronic dysfunction.

The approach with strain and Counter­strain is to passively put a slight strain into adysfunctional joint. Patients ,vith severelylimited range of Illotion (adhesive capsulitis,cervical spondylosis) find strain and coun­terstrain helpful to reduce secondary muscleguarding. Positions of comfort are easilyfound, but within the available range whichwill be in lesser degrees of motion than pa­tients with full range of motion. Measurablegains in range and quality of motion can bemade.

Pain associated with hypermobility canalso be treated. The approach is still to put astrain upon the joint; therefore hypermobile

CHAPTER 13 , STRAJN AND COUNTERSTRAIN

patients are usually treated in greater degreesof motion than patients with normal range.

Strain and countersrrain can make a sig­nificant contribution when integrated withother manual medicine techniques. Used inconjunction with articular techniques (i.e.,joint mobilization, high velocity manipula­tion) which restore position and motion, itwill normalize the imbalance of muscle ten­sion affecting the joint so that recurrence ofdysfunction is decreased.

Strain and counterstrain and muscle en­ergy can be combined with effective results9 ,IO

Isometric muscle energy's inhibitory effect oncontracted muscle by increasing Golgi tendonorgan discharge or through reciprocal inhibi­tion call enhance strain and counterstrain'sinhibitory effect on the same muscle. Muscleenergy can also be valuable to strengthen theantagonist muscle (weakened by reciprocal in­hibition) to bring the joint back to posturalbalance.

Strain and counterstrain can be usedbefore myofascial release techniques. Byclearing corresponding tender points, coun­terstrain can assist in reducing neurophysio­logic barriers, allowing myofascial release tobreak down biomechanical barriers withgreater ease.

CONCLUSION

Strain and counterstrain is an indirect manip­ulative technique of extreme gentleness forthe treatment of somatic dysfunctions. It isbased on a neurologic model that proposes,for some, a new concept for the productionof somatic dysfunction. The hypothesis is ab­errant afferent Aow from the muscle spindleproduces a reAex muscle spasm that fixates ajoint in a certain direction and resists anyattempts to reUlTn the joint to neutral. Diag­nosis is made by the presence of a specifictender point that overlies the muscle. Usingthe tender point as a monitor the operator isguided into a position of comfort that reducesaberrant afferent Aow and returns the muscleto "easy neutral." I-Iolding the position ofcomfort for 90 seconds and returning toneutral slowly following the positional release

333

are t\vo very important aspects of this pro­cedure.

Though research data are limited in thisarea to suppOrt the model, the observationsof practitioners, recounting the immediatechanges in palpable pain, tissue tension, andease of movement following positional re­lease, point to a neural basis.

Recognition must be given to LawrenceJones for decades of arduous experimentationon patients and his own body to develop strainand counterstrain. His book, Strain and Coun­t<1;t1'/lill,1 has mapped out hundreds of themost common tender points and positions fortreatment. To the beginner, the treaOnentsappear straightforward and easily mastered,but development of the palpatOlY skills re­quired to find the optimal position of releasetakes practice and perseverance. A completestudy of the book and the teachings of Law­renee]ones are highly recommended.

REFERENCES

I. KOTT 1M. Proprioceptors and somatic dysfunction.J Am Osteopath Assoc 197;; 74,638-50.

2. Jones LJ-I. Strain and counterstTain. Newark, 01-1:American Academy of Osteop:nhy, 1981.

3. Jones U-1. Spontancous relcase by positioning. D.O.1964; 4,109-16.

4. Greenman PE. Principlcs of manual mcdicine. Bal­timore: Williams & Wilkins, 1989.

5. Korr LM. The segmentalncrvous system as mediatorand organiz.er ofdisease processes. The physiologiCOlIbasis of osteopathic medicine. The Postgraduate In­stitute of Osteopathic Medicine and Surgery, 1970.

6. Korr lM. The neural basis of the osteopathic Icsion.The collected papers of Irvin M. Korr. Newark, OH:AmeriCOln Academy of Osteopathy, 1979.

7. DenslowJS, Korr 1A1, Krems AD. Quantitative stud­ies of chronic facilitation in human motOtnCufonpools. The collected papers of Irvin 1\11. Korr. New­ark, OH: Amcrican Acadcmy of Osteopathy, 1979.

8. Travell JG. Simons OJ. Myofascial pain and dys­function: the trigger point manual. Baltimore: Wil­liams & vVilkins, 1983.

9. Korr L\'l. The facilitated segment: a factor in injuryto the bod)' framework. The collected papers of LrvinAI. Korr. I ewark, OH: American Academy of Os­teopathy. 1979.

10. Chaitow L. Soft-tissue manipulation. Rochester,Vf: Healing Arts Press, 1980.

11. Ganong WF. Review of mcdical physiology. 9th cd.Los Altos, CA Lange Medical Publications, 1979.

12. O'Conncll AL, Gardner EB. Understanding the sci­entific basis of human movement. Baltimorc:\Nil­Iiams & Wilkins, 1972.