The

PainB y E r i k D a l t o n

Part Two

GameGameGamePainGame

98 M A S S A G E & B O DY WO R K • A U G U S T / S E P T E M B E R 2 0 0 6

A U G U S T / S E P T E M B E R 2 0 0 6 • M A S S A G E & B O DY WO R K 99

Clients suffering fromchronic pain are con-fronted with a unique

disorder—a personal experi-ence unlike other physicalproblems such as a broken legor an infection. Everyoneknows that a broken leg can beconfirmed by X-ray. An infec-tion is detected using simpletests measuring white bloodcell count. Regrettably, there isno universally reliable test tomeasure pain levels, causingmany common musculoskeletalcomplaints to be mis-assessed,improperly treated, or simplyignored and ambiguously tossedinto classifications such asacute, subacute, recurrent, andchronic. Since multiple strainpatterns commonly overlap in chronic injury cases(particularly shoulder injuries), standardized assess-ment results often prove unreliable from therapist totherapist (see Figure 1). Frustration and anxiety buildwhen clients return week after week complaining ofthe same pain. To remedy the problem, many pain-management therapists have learned to begin sessionsby creating length/tension/postural balance before“chasing the pain.”

Acute pain serves the evolu-tionary function of warning fortissue damage, but chronic paindoes little except to annoy andsometimes immobilize our ailingpopulation. Of the estimatedfifty million sufferers in theUnited States, more than halfreceive no medical relief andmany may never be given a diag-nosis. Part two of the “PainGame” opens with a brief histo-ry of popular pain theories andfollows with recent findings andtreatment options for correctingpain-ridden clients seen daily inthe manual therapy workplace. The goal is to shednew light on a much-researched, but sometimes mis-understood phenomenon.

The Specificity Theory of Pain

René Descartes of the “I think, therefore I am”fame, introduced one of the original pain theories

in 1664. His practical model proposed a simplified sys-tem detailing how pain messages were transmitted

directly from pain receptorsin the skin to a pain center inthe brain. He compared it to abell-ringing mechanism in achurch tower pulled by a ropeat the tower’s lower chambersso the bell rings throughoutthe landscape. Descartesbelieved there is a one-to-onerelationship between tissueinjury and the amount ofpain a person experiences.Think about it. If you stickyour finger with a needle, youwould experience minimalpain; whereas, if you cut yourhand with a knife, muchmore pain would be felt.Thus, the specificity theoryproposes that the intensity ofpain is directly related to the

amount of tissue injury. The specificity theory wasmodified throughout the nineteenth and early twenti-eth centuries, but the basic assumptions remained thesame.

Descartes’ specificity theory has generally proven tobe accurate for acute pain, but falls short when appliedto many types of chronic pain. Regrettably, variationson the specificity theory are still taught (or at least

emphasized) in many medicalschools, and a majority ofdoctors still ascribe to it inpractice. The theory assumesthat if surgery or medicationcan eliminate the allegedcause of the pain, then thepain will disappear. In chron-ic pain cases, particularly ofmusculoskeletal origin, this isoften not true. If a doctorcontinues to apply the speci-ficity theory to a chronic painproblem, the patient may beat risk for surgeries, medica-tions, and procedures thatmay not work as the search

for the source of the pain presses forward. Ultimately,the validity of the patient’s pain complaints will bechallenged if reasons cannot be found and the treat-ments do not work. This can often lead to the familiar“it’s all in your head” diagnosis.

One of many findings that has led to the downfall ofthe specificity theory was that of phantom limb pain.Often, patients who have undergone limb amputationcontinue to report sensations that seem to emanate

Figure 1. Gerber’s Lift-off Test for possiblesubscapularis injury. Since multiple strain pat-terns typically exist in chronic injuries (partic-ularly shoulder injuries), it makes sense toestablish length/tension/postural balancebefore chasing the pain. Courtesy of Erik Dalton.

Acute pain serves theevolutionary functionof warning for tissue

damage, but chronic paindoes little except to annoyand sometimes immobilize

our ailing population.

100 M A S S A G E & B O DY WO R K • A U G U S T / S E P T E M B E R 2 0 0 6

from the missing limb. Some reportthat the limb feels as if it is still therewhile others actually feel pain in thearea of the missing body part. Ofcourse, these sensations cannot becoming from the limb since it hasbeen removed from the person’s body.The specificity theory cannot accountfor these findings since there is noongoing tissue injury in the amputat-ed limb.

The specificity theory also cannotexplain how hypnosis can be used foranesthesia during surgery. Certainpeople under hypnosis can withstandhigh levels of pain that would normal-ly cause them to cry out. Surgery hasbeen done on almost every part of thebody using only hypnosis for anesthe-sia. Obviously, significant tissue dam-age is occurring during the surgerybut the patient under hypnosis isexperiencing no pain. This findingdealt the specificity theory a signifi-cant blow.

A New Approach Needed

Ronald Melzack and Patrick Wall’spopular neurological discovery intro-

duced in the mid-sixties has been instru-mental in helping understand the inti-mate relationship between nociceptionand mechanoreception as discussed in part one of thisseries. Two unlikely researchers—one a psychologist, theother a physicist—conceptualized a pain conductionmodel that has generally been embraced throughout themedical and manual therapy communities, even thoughthe exact underlying neurobiological mechanism detailinghow the gate theory works is still in question.

Melzack and Wall’s gate control theory1 suggestedthat when body tissues are damaged, messages carry-ing information about the injury travel toward thebrain along two separate sets of nerve fibers. The larg-er (mechanoreceptive) fibers transport messages aboutsensations other than pain (joint movement, heat,touch, etc.), and the smaller (nociceptive) fibers carrythe pain signals. The messages that travel along thelarger fibers tend to arrive at the spinal cord before themessages traveling along smaller fibers. Therefore, aslong as the large-diameter channels are adequatelyfilled with normal non-painful sensations, the smallerpain-generating messengers are crowded out, unable toget through to the brain (see Figure 2). Problems arisewhen normal mechanoreceptive input is disrupted,allowing increased nociceptive transmission.

According to Melzack, “Pain messages flowing alongperipheral nerves to the spinal cord on their way to

the brain encounter ‘nerve gates’ that can inhibit(close) or facilitate (open) the incoming nerve impuls-es.”2 However, if pain signals are allowed to reach thebrain, a number of different things can happen.Certain parts of the brain stem can inhibit or mufflethe incoming messages by the production of endor-phins, a naturally occurring morphine-like substance(see Figure 3, page 102). Stress, excitement, and vigor-ous exercise are among the things that stimulate theproduction of endorphins. This is why athletes maynot notice the pain of a fairly serious injury until thebig game is over. Additionally, this explains why regu-lar aerobic exercise can be an excellent method to helpcontrol chronic pain.

Testing the Gating Mechanism

Once the gate control theory had been accepted, itwas possible to explain all sorts of natural phe-

nomena that up until then had been a mystery. Itbecomes clear, for example, that when we rub a sorespot we are increasing the number of non-pain mes-sages traveling toward the spinal cord and brain. If youbang an elbow against a door, you automatically reachto rub the spot knowing (subconsciously) the pressureof rubbing decreases the amount of pain experienced.

Figure 2. Pain from an injured index finger (left) is fast-tracked to thebrain ungated. However, when the large-diameter fibers are needle pricked(right), pain signals are gated. Finger pressure also downgrades cutaneouspain. Adapted from Bill Allen with permission.

p a i n g a m e

�

102 M A S S A G E & B O DY WO R K • A U G U S T / S E P T E M B E R 2 0 0 6

Try the following experiment to test your pain-gat-ing ability:

� Apply a clothespin to one arm. Initially the pres-sure will produce pain that may be quite intenseas the skin and surface muscles are compressed.Peripheral nerve fibers detect this pressure andtransmit a pain signal to the spinal cord and on tothe brain. At first, it is the nociceptive fast painsignals that get through, and the intensity of thepain experience is fairly proportional to theamount of pressure applied. Everyone could agreethis is acute pain.

� The slower pain signals are not far behind, howev-er, and a dull ache may soon be noticed. After ashort while, most people will notice a reduction inthe pain coming from the pinched tissue as thespinal nerve gates close. This downgrading occursas the brain begins to view the pain signals asnon-harmful, i.e., the pressure may be painful ini-tially but is not incapacitating. As time goes on,the brain gives the pain message less priority andawareness decreases greatly.

� The brain knows the clothespin is not causing anyinjury. Therefore, the thalamus and cerebral cor-tex gradually begin turning down the volume tothe point where it is barely noticeable after aboutthirty minutes. Although skin and muscle com-pression is still occurring, it is now perceived as amild discomfort, if noticed at all.

Explaining the basics of this theory to clients canhelp establish the credibility of hands-on, pain-man-agement interventions. It will also actively demon-strate that changing the way one mentally perceivespain can actually change (decrease) the experience ofpain on a physiological level. A groundbreaking new

study underway at Stanford University’sNeuroimaging and Pain Lab3 reinforces this assump-tion that people can indeed alter the way they experi-ence pain. Using cutting-edge technology, leadresearcher Sean Mackey, PhD, allows subjects to visu-ally observe their own brain activity while exposed topainful stimuli. The intent is to see if subjects are ableto consciously reorganize brain pathways to controltheir pain. A futuristic real-time imaging device allowsparticipants to assess how well they are able toincrease and decrease pain by watching the activationof cerebral areas involved in chronic pain. This newestform of M.R.I. called functional magnetic resonanceimaging (f.M.R.I.), used in combination with sophisti-cated state-of-the-art software, allows chronic pain suf-ferers to mentally take movies of their cerebral activityand redirect the pain messages to non-painful corticalareas. Mackey’s biofeedback-type experiment maysoon help chronic pain sufferers learn to abolish painby controlling their brains.

Gating in Action

Many clients presenting with muscle/joint paincould be actively experiencing the gating process.

Prolonged sitting while holding a telephone with oneshoulder can jam (and lock) cervical and thoracic facetjoints closed on the ipsilateral side or open on theoverstretched side creating alterations in normalmechanoreceptive cerebral input (see Figure 4). As thelarger fibers begin to break down, the small unmyeli-nated free nerve endings (nociceptors) are able tosneak through and fast track noxious signals to the

brain, warning of possible tissue damage from themotion-restricted joints. Mechanical deformation andaccompanying inflammation ignite nociceptive activity(due to strain) in the following spine-related tissues:transversospinalis muscles; overstretched spinal liga-ments and joint capsules; and compressed facet jointcartilages and intervertebral discs.

Figure 4. Facet joints (right) lock closed during pro-longed right cervical sidebending. Note the reflex spasmin the intertransversarii muscle. Adapted from Tom Bowmanwith permission.

Figure 3. Pain gating does not necessarily occur at thesite of injury.The brain stem can inhibit or muffle low-priority, incoming pain messages (bum knee) by theproduction of endorphins. Adapted by Bill Allen with permission.

p a i n g a m e

Continuous neural bombard-ment eventually triggers stubbornreflexes that amplify muscu-loskeletal tone (protective muscleguarding), distort posture (func-tional scoliosis), and up-regulatesympathetic nervous system activ-ity (anxiety). Regrettably, thebrain has the ability to relearnthese aberrant patterns as normal.Neuroscientists label this condi-tion—where distorted posturesremain in the body long after theoriginal stimulus has beenremoved—as spinal learning,reflex entrainment, and neuro-plasticity. Although therapistscommonly encounter these chron-ically crooked bodies, we oftensettle for immediate symptomalleviation rather that digging forthe root of the problem. As thegreat Czech researcher VladimirJanda, MD, once said: “The neu-romusculoskeletal system mustbe assessed and treated as awhole, with muscle dysfunctionconsidered in relation to the

functional status of the whole motor system, includingarticular and nerve structures. Any change in the stat-ics or dynamics of the distal trunk and lower extremi-ties will, in some way, be mirrored in the function ofthe upper complex, and vice-versa.”4 Despite the vari-ety of pain-management approaches available intoday’s ever-expanding bodywork field, the therapeuticgoal should remain the same: Restoration of maximalpain-free movement within postural balance.

Flexion-Addiction

One of the most frustrating and elusive conditionsencountered by all somatic therapists today is

lumbo-pelvic pain due to our population’s growingflexion-addiction. Prolonged sitting and sleeping inflexed positions promotes length-tension imbalancesoften resulting in tight/short hip flexors and neurologi-cally weakened hip extensors. Davis’ Law reminds usthat when contractile tissues are placed in a slackenedposition for extended periods of time, the muscle’stonus is taken up. As prolonged flexed sitting andsleeping shortens the iliopsoas and rectus femoris mus-cles, lumbar lordosis increases, excessive weight istransferred to the posterior facet joints, spinal liga-ments are strained, and ultimately intervertebral discsbegin to degrade. This massive group of average

American workers and couch potatoesare labeled by myoskeletal therapists asflexaholics. All somatic practitioners(massage, Pilates, yoga, personal train-ers, etc.) must join forces to reverse oursociety’s destructive trend toward flex-ion-addiction.

Developing successful hands-on, flex-ion-addiction corrections typicallybegins by balancing tonic and phasicmuscle groups using practical posturalassessment models such as Janda’sfamous upper and lower crossed syn-dromes (see Figure 5). Once balanceand symmetry has been established inthe sagittal plane, therapists oftennotice a reduction in side-to-side (scoli-otic) torsional patterns, but not always.Leg length discrepancies, cranial andsacral base unleveling, and genetic ortraumatically-induced structural disor-ders often produce stubborn asymmet-rical compensations at key crossoverjunctions (atlantooccipital, cervicotho-racic, thoracolumbar, and lumbosacral)(see Figure 6).

If the compensatory scoliotic adapta-tions are functional (fixable) and notstructural (fixed), therapists shouldincorporate specific gating maneuversto help release the reflexogenic musclespasm resulting from loss of joint-play.

Figure 6. Foot hyperpronationshortens the leg, causing painfulpostural compensations detailed in highlighted areas. Courtesy of ErikDalton.

Figure 5.V. Janda’s upper and lower crossed syndromes.MediClip, Lippincott,Williams & Wilkins, 2005 with permission.

A U G U S T / S E P T E M B E R 2 0 0 6 • M A S S A G E & B O DY WO R K 103

104 M A S S A G E & B O DY WO R K • A U G U S T / S E P T E M B E R 2 0 0 6

The key is to develop a gating maneuver that safely co-activates and normalizes function in all four types ofjoint, ligament, and paravertebral muscle mechanore-ceptors. As normal mechanoreceptive flow to the cordand brain returns, pain is gated, muscle guardingdiminishes, posture improves, and clients revel in theirnew-found flexibility and pain-free bodies. But how isthis accomplished?

Traditional relaxation massage of a peripheral painsite temporarily calms cutaneous skin and fascialreceptors, reducing local superficial pain (see Figure7). But to alleviate deep-seated, joint-complex pain, theclient must be actively involved. For example, as thetherapist holds specific directional sustained pressureto motion-restricted joint capsules, spinal ligaments,and deep transversospinalis muscles in the upper tho-racic lamina groove, the client is asked to engage therestricted area by adding movement. Enhancers suchas chin tucking, arm rotations, head sidebending, orpelvic tilting are but a few examples, but be creative(see Figure 8). Adding any variety of movement pat-terns through a restricted joint complex stimulatesarticular receptors, reflexogenically releases protectivemuscle guarding, and helps mobilize stuck vertebralsegments (see Figure 9, page 106). Deep-tissue mas-sage techniques are supercharged when nociception is

gated and normal flow returns to cutaneous and articular receptors. As scientists like to say, “Down-regulate pain-perception circuitry and up-regulatepain-modulating circuitry.”

Designed to Experience Joint Pain?

Since there is less nociceptive innervation of themuscular system than other joint-related tissues,

today’s manual therapist must begin thinking outsidethe traditional muscle-pain, tender-point, fibromyalgiabox to include soft-tissue techniques for breakingreflexogenic pain/spasm/pain cycles caused by the lossof joint-play. Recall that all the body’s synovial joints(spine included) must have at least one-eighth inch ofmovement not controlled by muscle contraction.5 Thefacets are said to be idling. This built-in cartilage pro-tective mechanism serves as an instrumental neurolog-ic key for abolishing abnormal reflexes that perpetuatemuscle guarding, leading to destructive pain/spasm/pain cycles.

Compared with nociceptors, significantly fewermechanoreceptive afferents leave joints. The predomi-nant receptor is the nociceptor—especially in contextthat more than 90 percent of joint innervation is noci-ceptive. These theories were originally determined byanimal studies,6 then subsequently confirmed in stud-ies with human spinal joint capsules.7 This heavy con-centration of nociceptive fibers in joints suggests

Figure 7.The therapist’s fingertips search andrelease painful fascial adhesions on each side of theclient’s dowager’s hump by stimulating cutaneousreceptors. Courtesy of Erik Dalton.

Figure 8.The therapist holds sustained cephalad pressureto motion-restricted joint capsules, spinal ligaments, andlamina groove muscles as the client slowly chin tucks. If abony knot pushes back during head flexion, the ipsilateralfacet joint is not opening and the associated rib may beexternally rotated. Courtesy of Erik Dalton.

p a i n g a m e

�

106 M A S S A G E & B O DY WO R K • A U G U S T / S E P T E M B E R 2 0 0 6

humans are basically built to experience joint painwhen considering how many people suffer joint-relat-ed neck and back pain during their lifetime. Thevicious decompensation cycle must be stopped beforethe onset of more serious degenerative conditions suchas osteoarthritis, dowager’s humps, spondylolisthesis,and radiculopathies.

Myoskeletal Approach

To achieve a noticeable reduction of increasedexcitability in the neuronal pool, the pain-generat-

ing stimulus must be interrupted until the memoryburned into the nerve cells has been completely forgot-ten. For many chronic pain cases, a serial-type, deep-tissue therapy works best where clients are seen twiceweekly until hyperexcited receptors feeding the centralnervous system are quieted. This will eventually inhib-it the chemical activation of pain at the site of itsperipheral stimulation.

Therapists should expect positive clinical results toimprove with each myoskeletal alignment session dueto increased mechanoreceptive activation and less jointcomplex nociception. But successful management ofchronic pain depends on much more than intellectualknowledge. It must be teamed with keen observationskills, patience, compassion, and a constant reminderthat the healer is ultimately within each client.

Therapists serve only as helpful facilitators in theongoing journey toward optimum health and shouldgratefully utilize the body’s innate self-regulatory sys-tem to help guide the therapeutic process.

Summary

The myoskeletal joint receptor concept attempts tooverride the idea that pain is primarily a conse-

quence of conditions such as pinched nerves that couldultimately be freed by removing bony obstructions.Although spinal nerves travel through small interverte-bral foraminal openings, rarely does a bone-on-nervedysfunction occur. Significant facet hypertrophy, disccollapse, or intraneural edema must accompany the ver-tebral misalignment before the client experiences pain.While commonly associated with the spine, pinchednerve compressive lesions are actually rare. Researcherssuggest that only 10–15 percent of spine related prob-lems are caused by direct pressure of bone on nerve tis-sue. Clients with this type of nerve occlusion usuallyreport numbness, burning, or a pins and needles feeling.

More frequently, nerve roots become agitated fromprolonged exposure to chemical or mechanical irrita-tion. This condition develops slowly as the nerve’sdural sheath is rubbed, scraped, or over-stretched. Ifsuch neurocompression does exist, referrals should bemade to appropriate medical professionals for anorthopedic work-up.

What makes the bone-on-nerve pinched nerve theo-ry so popular is that therapists viewing anatomy textsor cadavers can easily visualize how spinal nervescould become entrapped as they make their waythrough the bony little holes between vertebrae. Formost of humankind, it is far easier to believe some-thing we can see versus something invisible to thenaked eye. Despite this human tendency, today’s touchtherapist must understand that spinal joints and mus-cles have massive nociceptive and mechanoreceptiveinnervation that is profoundly affected by sustainedcompressional loading due to tension, trauma, andpoor posture. While not clearly apparent, sensoryreceptors are the primary reason for client visits.

Erik Dalton, PhD, originator of the Myoskeletal Alignment Techniquesand founder of the Freedom From Pain Institute, shares a broad therapeu-tic background in Rolfing and manipulative osteopathy in his innovativepain-management workshops. Visit www.erikdalton.com to view addition-al Myoskeletal Alignment Technique articles and new products and to reg-ister for a free monthly technique newsletter. Call 800-709-5054 for moreinformation.

Notes1.T. Melzack and P. D.Wall, “Pain Mechanisms:A New Theory,” Science 150 (1965): 971.2. R. Melzack and P. D.Wall, “The Challenge of Pain,” (United Kingdom: Penguin, 2004), 35.3. S. C. Mackey and F. Maeda,“Functional imaging and the neural systems of chronic pain,”

North American Journal of Clinical Neurosurgery 15, no. 3 (2005): 269–88.4.V. Janda,“Treatment of chronic back pain,” J Man Med 6 (1992): 166–168.5. J. Mennell, Joint Pain, (Boston: Little Brown & Company, 1964), 224–259.6.A. M. Burt, Textbook of Neuroanatomy, (Philadelphia:WB Saunders, 1996), 311.7. R. F. McLain,“Mechanoreceptor endings in human cervical facet joints,” Spine 19 (1998):

495–501.

M&B

Figure 9.The therapist’s left palm braces the client’sright anteriorly rotated ilium while his right handpulls the left posteriorly rotated ilium to barrier.Theclient inhales to a count of five while gently pulling hisleft hip toward the table against the therapist’s resist-ance.As the client exhales, the therapist pulls with hisright hand while pushing with the left to level theiliosacral joints. Courtesy of Erik Dalton.

p a i n g a m e