Chronic Refractory Myofascial Pain and Denervation Supersensitivity As Global Public Health Disease


A 63 year old successful entrepreneur/mountaineer suffered disabling chronic LBP and left buttock pain after an 8 feet (2.4 metres) fall in 2011 with pain aggravation 5 months later from a physically-challenging expedition. He had laminotomy with lumbar disc removal when contrast MRI in 2013 showed L4-L5 broad-based left paracentral disc extrusion with central canal narrowing and mass effect on bilateral L5 roots. Other MRI findings included L4-L5 retrolisthesis, C5-C7 degenerative disc changes, lower thoracic Schmorl’s nodes, L1-S1 small broad-based disc bulges, moderate sacro-iliac joint arthritis bilaterally, left hip labral tear and old right total hip arthroplasty. Spine X-Rays showed 24° lumbar levoscoliosis.

Post-spinal surgery, pain worsened, not alleviated with physical therapy, manual stretching, inversion spinal traction, epidural injectionsx3, chiropractic/osteopathic manipulations, anti-inflammatory medications, short and long-acting opioides, acupuncture and alternative methods. Pain severely compromised going up inclines/steps and ambulation to 500-1000 feet (150-300 metres) necessitating back and hip muscle stretches every 5-10 minutes. Pain-scale was 6/10 on presentation on August 7, 2014. Examination showed moderate range of motion limitation of neck, back, shoulders and hips with core muscle weakness, especially  on the left. There were no sensory deficits or upper motor neuron signs.

Pain-scale reduced from 6/10 to 2/10 with first DTPS session stimulating the MTrPs confirming predominant myofascial involvement. He continued with DTPS. Nine months into treatment, he successfully completed travelling in an expedition, his first since 2011 during which he walked 4-6 miles (6.4-9.6 km) on most days. During the 60 day vacation hiatus beginning June 1, 2015 to July 30, 2015, he performed self DTPS but due to frequent, strenuous activities, pain-scale increased to 6/10. In the 45 day period prior to and after the expedition his treatment sessions lasted 115+12.9 minutes and 120+6.6 minutes respectively indicating more difficulty in eliciting large force twitches due to tightness of muscles. Electrical supersensitivity related twitching at remote sites gradually returned but he lost ability to mechanically provoke autonomous twitch-trains.

For further improvement and/or maintenance of QOL, he requires and still receives ongoing, self-applied and professionally-applied DTPS.



Scope of chronic pain

Chronic pain (CP) is a world-wide public health problem affecting physiological, psychological and social well-being. There are 1.5 billion CP sufferers worldwide (American Academy of Pain Medicine web-site), including 100 million American adults. In the United States, annual CP care is estimated at $635 billion, which is more than cost/year for cancer, heart disease and diabetes, costing $243, $309 and $188 billion respectively. Total incremental cost of pain health-care is $261-$300 billion, private insurers paid the largest share ($112-$129 billion), government programs (Medicare and Medicaid) bore 25% ($66-$76 billion) and 8% ($20-$23 billion) respectively with individuals paying an additional $44-$51 billion in out-of-pocket health-care expense. CP negatively impacts annual number of work-days, work-hours and wages resulting in lost productivity of $299-$334 billion.

With global child survival improvement and increasing aging populations, the number of people experiencing LBP and NP will escalate since CP increases with age. CP dominate patients’ lives, causing disabilities in family/home responsibilities, occupational, social, recreational, sleep and sexual activities. Pain-related investigations and treatments often make CP worse affecting patients’ interactions with coworkers, physicians, family and social network creating alienation and isolation.

Constant pain interferes with ability to concentrate, impairs cognition with mood/memory alterations from effects of medications. World Health Organization data obtained in primary care centres worldwide show that 22% of all primary care patients suffer from CP. They are four times more likely to have co-morbid anxiety/depression than pain-free patients.

LBP causes more global disability than any other condition. NP and LBP have no associated mortality but morbidity rate for CP is higher than the general population. YLD and disability adjusted life years (DALY) is high. In 2010, DALY for NP rose to 33.6 million and 83.0 million for LBP. Systematic reviews of LBP treatments utilized in developed countries and treatments available in developing countries, heat/ice/ultrasound/traction, are discussed later.

Spine XRays and imaging studies for establishing presence of intervertebral disc pathology or spinal degenerative diseases for diagnosis of NP and LBP are not available/feasible in resource poor settings. Despite significant multilevel spine imaging abnormalities, our patient had objective improvements in pain and QOL with DTPS indicating that XRays/imaging studies correlate poorly with clinical symptoms.

It is essential to authenticate CRMP, the most common type of CP, as a ubiquitous neuromusculoskeletal disease resulting from spondylotic radiculopathies induced partial denervation with denervation supersensitivity (DS). Public health priorities necessitate an urgent need for a safe, efficacious, practical and objective cost-effective system with potential for prevention (pre-rehabilitation) with simultaneous real-time ability to clinically diagnose, treat (rehabilitation) and provide prognosis in of acute and CRMP management.

MTrPs/Motor Point Identification

MTrPs are pathognomonic of MP, clinically identifiable when pressure at this point causes referred pain and snapping palpation of the myofascial band produces local twitch response. Meta-analysis does not recommend physical examination as a reliable test for diagnosis of MTrPs.

Electrophysiologically, motor point is where single muscle contractions can occur with minimum intensity and short duration electrical pulses. Anatomically it is the area where motor endplates, namely terminal area of motor nerve fibres are dense. Electrically-evoked single muscle twitch contractions precisely locate MTrPs.

Twitches in Denervation Supersensitivity (DS)

Within 6-8 days of denervation, DS develops due to acetylcholine (Ach) receptor increase and decrease in acetylcholinesterase activity. DS can also occur in prolonged conduction block.

Twitches exercise and stretch individual muscles promoting local blood flow specifically to that muscle. Rat skeletal muscle experiments show that twitch contractions from 1Hz stimulation increase muscle blood flow by 240%.


Twitches in DS

Force, firing pattern, ease/difficulty of twitch elicitation of deep MTrPs objectively aids clinical differentiation of normal condition from partial denervation of spondylotic radiculopathy. Grade1 twitches result from focalized, partial contraction of stimulated muscle(s) at MTrP. Stronger twitch force on the electrode overlying MTrP with DS gives an asymmetrical, bouncy feedback on the bipolar probe with 6 inches (15 cm) separation between two water-wetted surface electrodes. Grade 2 twitches additionally show rocking/shaking limb and/or trunk movements from stimulation of MTrPs of deep muscles apposed to bone and joint. Grade 3 twitches produce anti-gravity limb movements due to whole muscle(s) contraction. This indicates proximal stimulus spread to many and/or larger nerves from antidromic/ephaptic/direct stimulation, and/or distal spread of the current front due to DS. Grade 4 twitches produce antigravity limb movements with firing rate slower than applied pulses due to erratic stimulation of MTrPs with DS from filter effect of tight and stiff overlying tissues. Ability to elicit Grade 4 twitches is recognized when joint movements suddenly become stronger. On halting DTPS, joint movements continue autonomously lasting from a few seconds to >10 minutes before fatiguing. Grade 5 twitches produce anti-gravity movements with firing rate faster than applied pulse-frequency and rapidly fatigue within a few seconds indicating full, instantaneous depolarization of MTrPs with DS in non-tight muscle.

A pre-fatigue phenomenon heralds onset of Grade 5 twitches as multiple twitches/pulse instead of normal single-twitch/pulse. On continuing stimulation, sudden increase in twitch-rate, rhythm and force occurs before erupting into autonomous fatigable twitches. When the twitch-cascade ends, DTPS can be re-applied repeatedly for 1-5 minutes at this motor end plate zone until the entire muscle becomes refractory at which time another patient position is used for stimuli to reach other MTrPs with DS within same muscle.

Pathophysiology of autonomous twitches is similar to cardiac dysrhythmias.

Deep MTrPs are difficult to seek in CRMP due to muscle stiffness, tightness, tenderness and poor tolerance to electrical stimulation. In normal muscles, finding MTrPs is immediate, pleasant and painless. There is non-forceful symmetrical feedback on both electrodes and Grades 3-5 twitches do not occur.

To facilitate twitching, relaxed muscle(s) is positioned at slight stretch advantageous for contraction, stimulating along less electrically-resistive intermuscular/intramuscular grooves. If elicited twitches are Grade 1 force, patient re-positioning in supine/prone/side-lying, sitting, standing, etc., and/or clinician repositioning is necessary to obtain the correct angle to locate/effectively stimulate the MTrP with DS. To obtain pain relief, minimum Grade 2 force is essential. Grade 3-5 forces in CRMP will not occur until many professional hours of consecutive treatments. Such twitches are elicitable at acute MTrPs with DS within non-tight muscles.

Stimulus parameters used for evoking twitches are similar to those used in electrodiagnostic medicine for peripheral nerve conduction studies. Repetitive stimulation at 2-3 Hz tests stability of neuromuscular transmission by temporarily depleting Ach at diseased or immature endplates causing fatigue in neuropathic conditions. Similarly, using 2-3 Hz, fatigable autonomous twitches elicited with DTPS signify neurogenic involvement with unstable neuromuscular transmission in CRMP.

MP Theories

Muscle trauma, overload, or strain causes endplate damage, resulting in excessive Ach release. This provokes local, partial muscle fibre contraction beneath the endplate and muscle fibre contracture leads to ischemia and pain. The neuromuscular junction is the site most susceptible to acute ischemia. Dysfunctional end plate exhibiting increased ACh release may be the starting point for abnormal regional contractions, which may be essential for the formation of MTrPs.

Spondylotic radiculopathies causes MP from intramuscular entrapment of nerves and blood vessels. Partial denervation induced shortened/tightened muscle fibres produce tension on pain sensitive regions, e.g. annulus fibrosus, bones and joints. Others have also found MTrPs in radiculopathies. Intervertebral disc degeneration, with nerve root compression/angulation from reduced intervertebral space, causing neuropathy which leads to distal muscle spasm in radicular distribution. Pain results from shortened/tight muscle fibres compressing small/large blood vessels leading to ischemia. Bradykinin and other neurochemical release sensitizes and/or excites nociceptors.

Systematic Reviews of Treatments for CRMP

Many methods are available to directly treat MTrPs to inactivate, disrupt or suppress MTrP activity. Systematic reviews have not shown MTrPs treatments with Botox, steroids, acupuncture or dry needling to be effective. In order to improve dry needling results in CRMP, the corresponding author first developed Automated Twitch-Obtaining Intramuscular Stimulation, which employs mechanical stimulation with a monopolar needle oscillated 3 times in 2 seconds. To facilitate twitching, she then created/engineered needle DTPS device that could deliver electrical pulses through a single automatic insertion and retraction of the monopolar needle. These methods were discontinued when she implemented the safe, efficacious, non-traumatic and non-invasive DTPS.  Needling methods cause pain, bleeding, bruising and tissue trauma and thus not indicated for repetitive/frequent applications throughout the body in CRMP patients requiring life-long regular treatments.

Systematic Reviews of LBP Treatments

Therapies for chronic LBP not showing high quality evidence for improving pain intensity, functional status, global improvement and return to work include lumbar supports, traction, superficial heat and cold, ultrasound, transcutaneous electrical nerve stimulation, low level laser therapy, muscle energy techniques, spinal manipulation techniques and chiropractic treatments.

In acute and chronic LBP, massage improves pain and function only short-term. Direct manual/mechanical stimulation mobilizes superficial muscles but deep massage can produce pain as an adverse event. DTPS accurately focalizes stimulation to MTrPs with DS and has minimal tendency to cause post-treatment pain which can be resolved with longer/more treatment sessions.

In neuropathic conditions, in hypertensive patients, and the elderly with significant tightness and stiffness, it is necessary that DTPS be applied essentially pain-free using only stimulation parameters that the patient can tolerate and settling for Grade1-2 twitches. The probe must be lifted off the skin every 2-4 twitches so that the stimulus on the non-twitching/poor twitching muscle does not undergo repetitive sub-threshold stimulation leading to spasm and pain during and after treatment. Patients may tolerate pain during treatment thinking erroneously that enduring strong stimulation will obtain larger twitches. Contrarily, pain-induced involuntary tightening of muscles during DTPS will inhibit deep penetration of electricity into the tissues causing pain during and after treatment. The clinician must watch patients’ facial expressions and listen for sighs/moans or objective physical distress signs related to increased sympathetic tone such as pilomotor, vasomotor and sudomotor reflexes and reduce stimulation strength accordingly.

Blood pressure and pulse rate reduction have been noted after pain relieving massage attributable to increased parasympathetic tone and sympathetic tone inhibition. Regular exercise in older active individuals lowers both SBP and PP compared to sedentary counterparts. Similarly regular DTPS sessions are useful aerobic exercises that reduce blood pressure and pulse proportional to twitch force.

There is insufficient evidence to support use of epidural injection to facet joints and nerve blocks in LBP. US Food and Drug Administration reports paraplegia, quadriplegia, spinal cord infarction, and stroke from technique-related problems such as intrathecal injection, epidural hematoma, direct spinal cord injury, and embolic infarction after inadvertent intra-arterial injection.

Systematic reviews on medications do not show clear evidence that anti-depressants, are more effective than placebo in chronic LBP. Non-steroidal anti-inflammatory drugs (NSAIDs) are effective for short-term symptomatic relief in patients with acute and chronic LBP without sciatica. Muscle relaxants are effective in management of non-specific LBP, but adverse effects require cautious use. Opioids compared to NSAIDs or antidepressants did not show differences regarding pain and function. There are no placebo-randomized controlled trials (RCTs) supporting effectiveness and safety of long-term opioid therapy for treatment of chronic LBP.

Gabapentin at doses of 1200 mg or more is effective for some people with some painful neuropathic pain conditions. Gabapentin (1200 mg) use on this patient an hour before DTPS reduced pain which facilitated twitch elicitation.

Conflicting evidence exists on short-term effect of radiofrequency lesioning in chronic LBP and disability of zygapophyseal origin. Intradiscal radiofrequency thermocoagulation is not effective for chronic discogenic LBP.

Evidence for minimally invasive discectomy (MID) although associated with shorter hospital stay has been found inferior in terms of relief of leg pain, LBP and re-hospitalization and our patient fits this profile. More research is needed to define appropriate indications for MID as alternative to standard open discectomy.

Systematic review of RCTs on stretching suggests that before, after, or before-after exercise stretching, does not produce clinically important reductions in delayed-onset muscle soreness in healthy adults. Chronic MP patients who did stretching for three weeks did not demonstrate effectiveness in improving muscle extensibility, although stretching increased tolerance to stretch-associated discomfort. When stiff hamstrings are subjected to eccentric exercise, strength loss, pain, muscle tenderness, and increased creatine kinase activity occurs. This is consistent with the sarcomere strain theory of muscle damage showing experimental evidence of association between flexibility and tendency to muscle injury.

Mechanical stretch forces delivered from the surface occur to many muscles simultaneously and are not effective in stretching shortened muscle fibres at deep MrTPs. The solution to make stretching consistently more effective lies in finding new methods including DTPS. Effective summation of twitch-induced stretch forces focused to MTrPs are best with repetitive 1-3 Hz stimulation.

Not commonly recognized is thixotropy of muscle which is a ubiquitous and functionally important phenomenon since it results from tendency of actin and myosin filaments to stick together when inactive for a period of time. Passive properties of thixotropy can be reduced with previous movements as evident with preventive warm-up activities of athletes before strenuous sports. Overcoming thixotropy may be the basis by which DTPS is able to clinically improve function in muscle tightness without pain, fibromyalgia, stroke or Parkinsonism. Reduced muscle thixotropy/stiffness persists as long as motion persisted but will return to its previous state. Stiffness reduction afforded by twitch exercise allows more mobility and the increased mobility and increased blood flow perpetuates to improve muscle function and QOL.

Improving Denervation Supersensitivity Related CRMP

Partial denervation and/or conduction block in the presence of DS leads to ongoing MTrPs formation in many myotomes at various times daily with ADL. Morphologic and electromyographic studies have demonstrated atrophy and delayed activation of deep muscles of the spine in patients with chronic NP and chronic LBP. Decrease in maximum force of deep back muscles improve resultant joint moments and reduce the stabilization function provided by these muscles to the lumbar spine. Exercise therapy appears to be slightly effective at decreasing pain and improving function in adults with chronic LBP. There is conflicting evidence for effectiveness of exercise in reducing the number of recurrences or the recurrence rate.

DTPS is aerobic exercise therapy to individual muscles. If there is no pain relief with the first DTPS session, the primary diagnosis of CP is not CRMP and other causes need consideration, e.g. neuropathic, inflammatory, psychiatric or nociceptive. Further DTPS sessions are advised even in such patients to treat co-morbid CRMP and/or muscle tightness to facilitate management of the primary pain.

For best functional results optimal treatment in CRMP includes these 5 muscle areas: trapezius, latissimus dorsi, gluteus maximus, adductor magnus, and paraspinal muscles from neck to sacral areas. This is needed even if patient presents only with NP/upper limb pain or LBP/lower limb pain as in this patient. Additionally, other muscles connected to the thoracolumbar fascia and along the kinetic chain must be treated proximo-distally starting with the largest muscles that cross multiple joints to small muscles of hands and feet as needed. Treatments begin with weakened muscles exposed to injurious eccentric contractions before directing treatments to strong muscles used primarily for concentric contractions. In the presence of weak symptomatic-side muscles, asymptomatic-side muscles are stronger by default and from overuse developing MTrPs that need treatment. This balances chronic strong pull of muscles toward asymptomatic side that more weakens symptomatic side. Treatments begin on the symptomatic-side starting with upper trapezius MTrPs with DS which can be easily located. Through its myofascial connections, other muscles on the symptomatic side become easier to treat. Provided MTrPs with DS are stimulated, Grades 3-5 twitch elicitation is facilitated by aged neuromuscular junctions exhibiting enhanced pre-synaptic nerve terminal branching, post-synaptic distribution of neurotransmitter receptor sites, increased Ach quantal content and more rapid decline of endplate potential strength during continuous pre-synaptic neuron stimulation.

Additionally, central sensitization amplifies DS. Noxious stimuli and/or misinterpretation of non-noxious stimuli (secondary hyperalgesia and allodynia) can induce chronic pain. Injury induced functional and adaptive changes include ineffective synapses unmasking, receptive field shifts and reorganization or altered effectiveness of surviving neural networks at the brain cortex level as well at peripheral nerves and receptors.


With DTPS we have originated an algorithm with consistent pain/discomfort relief and reproducible results without concurrent use of multiple medications or other therapies. Presence of DS in CRMP requires that treatments be safe and effective for regular life-long use on the entire body. We studied our case with statistical process control (SPC). Studying one case in detail sequentially over time can produce statistical results superior to that of a RCT. In these circumstances SPC has greater statistical power to exclude chance as an explanation.

DTPS is suitable for use in developing countries since it is cost effective.


1. CRMP is a neuromusculoskeletal disease caused by spondylotic radiculopathies following acute or chronic cumulative trauma with DS induced peripheral and central, mechanical and electrical hyper-excitability.

2. The mediate cause of CRMP is neuromuscular ischemia at deep MTrPs in tightened/shortened/stiffened muscles from spondylotic radiculopathy related partial denervation that maintains/aggravates CRMP.

3. Systematic reviews show lack of effective treatments for CRMP. As CRMP is a global public health problem with huge economic toll on society, governments of developed and developing nations should invest in safe, efficacious, cost effective novel systems such as DTPS for its prevention and management.

4. DTPS is a safe and efficacious innovation for repetitive, life-long whole body treatments for CRMP management as a real-time preventive, diagnostic, therapeutic and prognostic armamentarium. It empowers patients in their own health-care since it can also be self-performed.

5. Commonly available sphygmomanometer is useful as an inexpensive, practical, objective, real-time pain monitor for clinical follow-up of DTPS treatments.


I, Crawford Hill, had a spinal surgery two years ago in July 2013. The hypothesis was that my inability to walk uphill effectively was severely compromised by a herniated disc at L4-L5. I had had several injuries and trauma which probably contributed to the problem, whether it was a herniated disc or some other cause of compromising function- especially walking uphill. One of these was an expedition trip to Ecuador during which I was on a boat which slammed up and down for four hours. I had to tighten my buttock intensely and hold on for the entire boat-ride. The next day I was on a horse which trotted causing me more bouncing effects on my spine for four hours. This was an extreme challenge as I had to tighten my buttock again to endure the bouncing up-and down. These two back to back incidents followed about five months after I fell from a rock climb gym wall. After that fall, I laid on the padded mat for several minutes thinking I had severely hurt myself. However I was able to get up and I seemed to be okay. I thought that these injuries did not apparently compromise my function. However on hindsight it probably did – especially in conjunction with the traumatic incidents in Ecuador which I mentioned. Going further back in time about 10 years ago I attempted to water ski and ended up in a very compromised position and felt some tremendous strain on my hamstrings. I let go of the rope and thought that I had damaged my hamstrings severely. However again I was able to function and forgot about the injury.

Going further back in time I did “pull my groin” as they say, in high school football. There was no good treatment available. Lots of heat and inappropriate exercise probably contributed to the injury. However once again I moved on because I was generally very fit and probably have a high tolerance for pain and compromised function. I have tried just about every treatment possible including many versions of physical therapy, gravity-assisted traction, yoga, Feldenkrais exercises, spinal manipulations, acupuncture with four different practitioners, chiropractic release, medications, epidural injections, many anti-inflammatory medications including opioids and even spinal surgery. In addition I have a stretching and myofascial release program which does give me relief. Pain is on my mind 23 hours/day and I sought relief with eToims. After treatment with DTPS within six months, I can feel my affected musculature namely the gluteal and hamstrings muscles returning to function. The deep twitching has released most of the spasms and the muscles feel more functional and I’m ready to start light exercise. In June of 2015, I went on my first expedition since 2011. I went to Crete and I was able to walk on level and inclines for 3-6 miles daily for two weeks. This has been a dramatic development after years of frustration with all the other modalities I tried.