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Dynamic Chiropractic Canada – June 1, 2013, Vol. 06, Issue 06
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The Challenging 20%: Simplifying the Treatment of Chronic Pain

By Carolyn McMakin, MA, DC

After 18 years of diagnosing, treating, lecturing and writing about chronic pain, what was at first difficult to diagnose and treat has been simplified by experience into six conditions most clinicians miss because the presentations are not typical or do not generally respond to chiropractic.

If chiropractic care has not produced resolution of even chronic pain in 12 weeks, it is probably not going to. Ninety percent of the patients who contributed to my experience had failed with chiropractic care, physical therapy or medical treatment.1-2

There are six fairly straightforward conditions that turn out to have less than straightforward presentations in chronic pain patients. Disc and facet injuries, ligamentous laxity, myofascial trigger points and vestibular injuries all create chronic pain that often eludes diagnosis because it is not typical, surgical or readily responsive to traditional chiropractic care. With due respect to the miracles created by chiropractic treatment over the past century, chiropractic adjusting alone often will not correct these pain generators, and in some cases makes them worse. But combining chiropractic care with appropriate exercise and adjunctive therapies can help all of these conditions.

Disc Injuries

Disc injuries are created by a flexion or combined flexion-rotation mechanism of injury, or by long-term static posture that dehydrates the discs. The disc is like a sponge – it absorbs water when we recline and loses water when it is loaded by static standing or sitting. When repeated injuries to the disc annulus are repaired with inflammatory and sclerotic repair tissues, the disc annulus can be transformed into an atypical pain generator.3-4 Flexion will make the pain worse; extension will usually make the pain better unless the patient has co-existing facet-generated pain that is painful with extension.

When the disc annulus is cracked, the inflammatory material within the nucleus leaches out and irritates the adjacent nerve root, causing hyperesthesia in the dermatome, protective splinting in the muscles innervated by that nerve, and eventually myofascial trigger points in those muscles. The disc picture is confusing because there is no muscle weakness, no classic radiculopathy and no sensory loss. An MRI will often be read as normal because this is typically a small disc bulge that is simply chemically active.5-10

Treatment of Chronic Pain - Copyright – Stock Photo / Register Mark Don't depend on the radiology report. Look at the films yourself. A 2 mm bulge is a 2 mm bulge; it is not “normal.” There is no way to tell from an MRI whether a disc is a pain generator.

If flexion-extension X-rays show segmental translation at the same level as a disc bulge, it strongly suggests that this level has a damaged annulus. If this hypermobile level coordinates with the sensory exam showing hyperesthesia at the related dermatome, and if the muscles with myofascial trigger points receive their innervation from this nerve root, then this disc is the likely problem. The clinical picture puts the pieces of the puzzle together.

How to treat chronic disc pain: These chronic discs can recover with appropriate exercise to improve circulation and stabilize the injured segment. McKenzie extension exercises and classic spinal stabilization exercises are both essential to recovery. I also use frequency-specific microcurrent to eliminate the nerve irritation,11 treat the myofascial trigger points so the patient tolerates exercise, and reduce inflammation in the disc so that it can recover. Rotary chiropractic adjusting can make the disc worse when it shears the disc annulus. Using an adjusting instrument to keep the segments above and below the disc moving to remove the mechanical stress from the injured disc also is helpful.

Spinal Facet Joint Injuries

Spinal facet joints guide motion in flexion, extension and rotation, and absorb compressive loading in the spine. Facet joints are injured by ballistic or repeated extension and facet compression. These injuries bruise the cartilage and subchondral bone, and stretch the joint capsule and the medial branch nerve that lies along its edge.12-13

Facet joints become pain generators when the cartilage and bone repair with inflammatory scarring and calcification.14 Joint inflammation releases nerve growth factors that cause proprioceptive nerves to infiltrate the joint and change from proprioception to pain transmission.15

Nerve inflammation causes muscle splinting, which leads to myofascial trigger points.17-18 Facet joint referred pain patterns can mimic nerve pain patterns and overlap myofascial trigger point patterns.19 Adjusting will help temporarily, but rotary adjustments gap one joint while jamming the joint on the opposite side. If there is pain relief from adjusting, it is often temporary.

Treating facet joints: Chronic facet joints will respond to modified adjusting. For low back facets, try using a drop table and adjusting the low back from the front. Activating the upper thoracic paraspinal muscles to allow strengthening of the core lower abdominal muscles is essential to reducing the lumbar lordosis and alleviating the chronic postural compression of the lumbar facets. Cervical facets respond to exercise to activate the upper thoracic paraspinals and strengthen the anterior cervical muscle. I have also found that frequency-specific microcurrent helps reduce inflammation in the joint and the nerve, reduce adhesions between the nerve and the capsule, and soften the calcifications and scarring in the capsule and periosteum.20-21 Adopting an anti-inflammatory diet is also helpful.

Ligamentous Laxity

Ligamentous laxity is the most complicated of the chronic six to treat. The spinal ligaments are difficult to repair and the facets and discs are often injured by the same forces that damage the ligaments. The ligaments are stretched beyond their elastic range and don't recover easily.

Laxity in the anterior or posterior longitudinal ligaments allows a spinal vertebra to translate or slide forward or back during flexion and extension, instead of staying aligned and stable during movement. The instability causes muscles to splint, creating myofascial trigger points, but in my experience, treating the trigger points with manual therapy, massage, injections or dry needling gives only temporary relief and often makes the pain worse within hours of treatment.

The muscle relaxation allows the segmental translation to worsen. This worsening within four to six hours after treatment is diagnostic. Diagnosis can be confirmed by taking standing lateral flexion-extension X-rays in the neck or low back. Any cervical segmental translation that exceeds 3.5 mm requires a surgical consult because of potential risk to the spinal cord and nerves.

Treating ligament laxity can be accomplished in time and with careful treatment. Specific stabilization exercises to train the muscles to take over the job that should be performed by the ligaments are essential. Prolo or PRP therapy can be useful to create acute inflammation that will produce helpful repair tissue. The injections should be directed at the segments shown to be unstable by X-rays. Frequency-specific microcurrent reduces inflammation and increases collagen formation.21-22

Osseous adjusting usually makes ligamentous laxity worse. The unstable segment is almost impossible to protect, even with proper and careful setup. Once the X-rays have demonstrated the unstable segment, avoid osseous adjusting for at least a few months. Light-force instrument adjusting can be used to keep the stable segments above and below moving, but even that can be challenging. In many cases, skin taping superficial to the lax segment can be helpful. Treating ligamentous laxity takes time, but relief can usually be achieved within four months.

Myofascial Trigger Points

Myofascial trigger points accompany all of the other chronic pain problems, but in some cases can be their own problem. MTrP are small areas of hypercontractile tissue in a taut band within the muscle. They cause local and referred pain, and interfere with proper function and motor recruitment. The wide use of statins for cholesterol reduction has created a biochemical perpetuating factor because statins interfere with CoQ10 production essential for ATP production in the muscles.

Treating trigger points: Manual trigger-point therapy, frequency-specific microcurrent, dry needling, magnesium glycinate or malate, and gentle reconditioning exercises are all helpful in repairing trigger points, as long as the perpetuating factors such as disc and facet inflammation and ligamentous laxity have been addressed. Most patients on statins will be allowed to take a three- to six-month “statin vacation” to determine if the statins are contributing to the muscle dysfunction. It takes about 200 mcg of CoQ10 to compensate for the mitochondrial damage created by the statins.23

Neuropathic Pain

Neuropathic pain creates deep aching that feels as if it is in the joints or muscles and myofascial trigger points. It is usually caused by nerve traction injuries or disc injuries. The sensory area will most often be hypersensitive, not numb; muscle recruitment and reflexes will be normal in the hard-to-diagnose cases.

Nerve traction injuries are diagnosed when the history demonstrates force vectors that apply traction to the nerve. A simple sensory examination for sharp will show hyperesthesia in the painful area. Sensory loss and motor weakness only occur in those rare cases in which the nerve is torn.

Treating neuropathic pain: Reducing inflammation in the nerve will alleviate nerve pain. If the neuropathic pain is secondary to a disc injury, long-term improvement will depend on the disc repair strategies discussed above. X-ray=guided spinal epidural injections can be helpful, but are invasive, expensive and carry some risk. Frequency-specific microcurrent has been shown to treat neuropathic pain very effectively and is the only treatment shown to quickly repair nerve traction injuries.24-26

Epidurals are not effective in nerve traction injuries and without treatment, nerve traction injuries repair very slowly over months or years.

Vestibular Injuries

Vestibular injuries usually involve some mechanism of impact to the back or side of the head that damages the vestibular system in the inner ear or brain. This challenging group of patients is difficult to diagnose because they are not dizzy. They present with neck pain from muscle tightness.

They experience severe anxiety in visually complex places because without the vestibular system, the brain depends on a visual horizon for its location in space. Finding a simple visual horizon in a mall, grocery store, airport or warehouse shopping venue is difficult and the primitive brain center for balance becomes terrified when it doesn't know where it is in space.

These patients can awaken from sleep in a panic every 60 to 90 minutes for the same reason. Primitive brain centers govern function even during sleep and without input from the vestibular system they create anxiety when position changes during sleep. Patients have difficulty reading or using a computer because the eyes are ungoverned by the vestibular ocular reflex, move with saccadic pursuit and don't track smoothly. Horizontal eye movement to read produces fatigue, anxiety and a sense of disequilibrium.27

Screening for vestibular injuries can be done with a complete history, observation of eye movements during horizontal and vertical gaze, and lateralization of Weber's test with a tuning fork. Complete and accurate diagnosis of vestibular injuries requires a full vestibular testing laboratory, usually available in a metropolitan hospital.

Treating vestibular injuries: Vestibular injuries are very difficult to treat. Upper cervical adjusting can help in certain cases, but may make other cases worse. Vestibular rehabilitation helps to desensitize the brain to the loss of vestibular input and can improve balance and function. Motion sickness medications such as meclizine or Valium are helpful in some cases to reduce symptoms and help with sleep. Frequency-specific microcurrent has been found to help with brain injuries, but is not useful for peripheral vestibular injuries. For most patients, the diagnosis alone is helpful. Once they know the anxiety and disequilibrium have a physical cause, they are better able to develop and follow strategies to help manage their lives and their symptoms.28


  1. McMakin C. Microcurrent treatment of myofascial pain in the head, neck and face. Topics in Clinical Chiropractic, March 1998;5(1).
  2. McMakin C. Microcurrent therapy: a novel treatment method for chronic low back myofascial pain. Journal of Bodywork and Movement Therapies, 2004;8:143-153.
  3. Kraemer J. Natural course and prognosis of intervertebral disc diseases. Spine, 1995;20:635-639.
  4. Cloward RB. Cervical discography: mechanisms of neck, shoulder and arm pain. Annals of Surgery, 1959;150:1052-1064.
  5. Olmarker K, Rydevik B, Nordberg C. Autologous nucleus pulposus induces neurophysiologic and histologic changes in porcine cauda equina nerve roots. Spine, 1993;18:1425-32.
  6. Olmarker K, Blomquist J, Stromberg J, et al. Inflammatogenic properties of nucleus pulposus. Spine, 1995;20:665-669.
  7. Ozaktay AC, Cavanaugh JM, Blagoev DC. Phospholipase A2 – induced electrophysiologic and histologic changes in rabbit dorsal lumbar spine tissues. Spine, 1995;20:2659-68.
  8. Ozaktay AC, Kallakuri S, Cavanaugh JM. Phospholipase A2 sensitivity of the dorsal root and dorsal root ganglion. Spine, 1998;23(12):1297-1306.
  9. Marshall LL, Trethewie ER, Curtain CC. Chemical radiculitis. A clinical, physiological and immunological study. Clinical Orthopedics, 1977;129:61-67.
  10. Taylor JR, Twomey LT. Acute injuries to cervical joints. An autopsy study of neck pain. Spine, 1993;18(9):1115-1122.
  11. McMakin C. Non-pharmacologic treatment of neuropathic pain using frequency specific microcurrent. The Pain Practitioner, Fall 2010:68-73.
  12. Cavanaugh JM, Ozaktay AC, Yamashita HT, King AI. Lumbar facet pain; biomechanics, neuroanatomy and neurophysiology. J Biomechanics, 1996;29:1117-1129.
  13. Cavanaugh JM, Lu Y, Chen C, Kallakuri S. Pain generation in lumbar and cervical facet joints. J Bone Joint Surgery (Am), 2006;88 Suppl 2:63-67.
  14. Beaman DN, Graziano GP, Woitys EM, Chang V. Substance P innervation of lumbar spine facet joints. Spine, 1993;18:1044-1049.
  15. Lewis C. Physiotherapy and spinal nerve root adhesion: a caution. Physiotherapy Res Int, 2004;9:164-173.
  16. Chen C, Lu Y, Kallakuri S, Patwardhan A, Cavanaugh JM. Distribution of A-delta and C-fiber receptors in the cervical facet joint capsule and their response to stretch. J Bone and Joint Surgery (Am), 2006;88:1807-1816.
  17. Simons DG, Travell JG. Myofascial origins of low back pain: principles of diagnosis and treatment. Postgraduate Medicine, 1983;73(2):66, 68-70.
  18. Simons, DG, Mense, S, Russel, IJ, Muscle Pain: Understanding its Nature, Diagnosis and Treatment, 1st Edition. Lippincott Williams & Wilkins, 2001:205-288.
  19. Gerwin RD, Dommerholt J, Shah JP. An expansion of Simons' integrated hypothesis of trigger point formation. Current Pain and Headache Reports, 2004;8(6):468-475.
  20. Huckfeldt, Mikkelson, Larson, Hammond, Flick, McMakin. “The Use of Microcurrent and Autocatalytic Silver Plated Nylon Dressings in Human Burn Patients: A Feasibility Study.” Proceedings of John Boswick Burn and Wound Symposium in Maui, Hawaii, Feb. 21, 2003.
  21. Reilly WG, Reeve VE, McMakin CR. Anti-Inflammatory Effects of Interferential Frequency-Specific Applied Microcurrent.” Proceedings of the National Health and Medical Research Council, 2004.
  22. Suzuki D. Private communication regarding unpublished data. University of Washington, 2002.
  23. McMakin C. Frequency Specific Microcurrent in Pain Management: Textbook for Practitioners. Elsevier Science Press, Edinburgh, 2010.
  24. McMakin, Op Cit (reference #11).
  25. McMakin C, Gregory W. Phillips T. Cytokine changes with microcurrent therapy of fibromyalgia associated with cervical trauma.” Journal of Bodywork and Movement Therapies, July 2005.
  26. McMakin C, Op Cit (reference #23).
  27. Ibid.
  28. Ernst, et al. Management of posttraumatic vertigo. Otolaryngology – Head and Neck Surgery, April 2005:554-558.

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