CASE HISTORY
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.
GLOBAL HEALTH
PROBLEM ANALYSIS
Discussion:
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%.
DEEP TRIGGER POINT
STIMULATION (DTPS) also known as ELECTRICAL TWITCH OBTAINING INTRAMUSCULAR
STIMULATION
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.
DTPS Role in
CRMP
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.
LEARNING
POINTS/TAKE HOME MESSAGES
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.
PATIENT'S
PERSPECTIVE
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.
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