Focus on Pain (Travell) Seminar
Orlando, 2003 (notes by Devin J. Starlanyl)

One of the best seminars with new research in the fields of fibromyalgia syndrome (FMS) and chronic myofascial pain (CMP) for care providers is the Focus on Pain (Travell) Seminar.  The following is an account of some of the highlights of the March 6-9, 2003, Focus on Pain Seminar in Orlando, Florida.  This seminar series has been organized by Robert Gerwin, MD.  Dr .Gerwin, a neurologist with vast experience in myofascial pain, was one of the first doctors to recognize the importance of the work of Travell and Simons.  He offers continuing seminars in myofascial medicine, as well as the Travell seminars.  The seminars are packed with exciting presenters and new research, but not enough attendees.  The days are full, and conversation is lively.  The National Association of Myofascial Trigger Point Therapists holds its national convention in conjunction with this seminar.  Attendees have a wealth of knowledge that they share freely.  There are interesting exhibits. There is a danger that the seminar series may be discontinued due to lack of attendance.  The seminar information is at www.painpoints.com.  I pray there will be enough interest to keep this series going.  At best, I can only give you a brief taste of what was presented.  Was your doctor there? 

Chronic pain is not the same as acute pain.  At this seminar one paper called chronic nonmalignant pain "a force or monster that cannot be tamed” (Thomas, 2000).  Powerful words.  Changes take place in the pain system of the body when pain is chronic.  Your body produces less endorphins, and the grind of daily and nightly pain wears out your resources.  With both FMS and myofascial trigger points (TrPs), symptoms can vary from hour to hour and day to day, and they are, to the unpracticed eye, invisible.  “The opinion that fibromyalgia syndrome (FMS) is a psychiatric disorder or can be caused by stress or abuse is unproven and can be of potential harm to patients.”  Care providers should be aware of "possible undue influences on medical opinion by agencies providing health care and research funding" (Nielson WR, Merskey H, 2001).

Some of the work presented comes into greater focus due to the findings of Roland Staud, MD, a physician at the University of Florida in Gainesville.  He has studied a phenomenon called "wind-up" in FMS patients.  Wind-up occurs due to the lack of normal central nervous system (CNS) pain filtering processes, both in the pain facilitatory and pain inhibitory pathways.  Brain-imaging techniques that can detect neuronal activation after pain stimuli have provided additional evidence for abnormal central pain mechanism in FMS.  These changes provide a constant stressor to the body.  Dr. Staud and his team published a paper in March of 2003 indicating that abnormal input from muscle pain receptors (i.e., TrPs) perpetuates FMS central sensitization.  Pain onset can be delayed from the stimulus.

The start of each case of FMS probably has multiple causes.  "A combination of multiple, mild impaired responses may lead to more profound physiologic and clinical consequences as compared with a defect in only one system and could contribute to the symptoms of fibromyalgia” (Adler, Manfredsdottir, Creskoff, 2002).  FMS is not progressive (Wolfe, Anderson, Harkness et al, 1997).  If it is getting significantly worse with time, there is at least one perpetuating factor that is not being addressed.  No two FMS patients are alike.  We don’t even all share the same pain processing dysfunctions (Sorensen, Bengtsson, Ahlner, et al, 1997).  Each patient is a unique individual, with unique needs, and must be so treated.  There are many subsets of FMS.  One study has separated some subsets into meaningful categories (Eisinger, Starlanyl, Blotman et al, 2000), and this separation may help decide which treatment regimens are more likely to help specific patients.

The hypothalamus-pituitary-adrenal (HPA) axis dysfunction of FMS has important consequences.  Nothing can be excessively stressed continually without damage.  Our stress response system floods us with adrenalin and other biochemicals, and it suppresses immune, reproductive and digestive systems so that our efforts can be focused on readiness to fight or to run away.  Cortisol released during stress increases blood pressure, heart rate and cholesterol.  Continued release of stress hormones can cause osteoporosis, damage to memory, damage to blood vessels in the heart, and increase the chance of stroke and heart attack.  FMS must be taken seriously.  Research suggests that FMS is a risk factor for osteoporosis (Swezey, Adams, 1999).  HPA axis dysfunction is associated with insulin resistance (Vicennati V, Pasquali R, 2000).  Prolonged stress raises risk factors for cerebrovascular disease (Kakojic, Demarin, Kadojic et al, 1999).

Directions in the Study of Soft Tissue Pain  

I. Jon Russell, MD, PhD, editor of the Journal of Musculoskeletal Pain, emphasized the importance of FMS subsets to treatment.  FMS is not an “it,” it is a “they.”  He predicts that treatments will become more effective as medical science understands the causes.  FMS subsets may be significant in that these differing causes may help determine the best medications and therapies for each subset.  Much of the FMS costs to the medical system could be diminished if there were prompt and effective diagnosis and treatment.  There is on-going research on genetic links to FMS that has already confirmed gene abnormalities.  Dr. Russell is working with Dr. Nancy Olson and teams of researchers on the FMS genome project.  The research is underway and not yet published.  Many laboratory abnormalities documented in FMS research can be due to genetics.  Much enzymatic function and even hormonal response is genetically determined.  A candidate gene that can cause abnormal serotonin receptors has already been confirmed in FMS patients.  Fifty percent of FMS patients have abnormal C-reactive protein.   There are some indications that in secondary FMS, an inflammatory process may be the initial cause, although FMS is not inflammatory of itself.  [Dr. Linda Watkins later presented on this connection.]  One of the problems right now is that the inflammatory cytokine cascade that is part of the start of FMS is complicated.  The biochemicals called cytokines are synergistic and redundant.  They work together, sometimes in different combinations, and some research may be valid but not relevant.  The Food and Drug Administration (FDA) does not easily allow combination medications through its approval process.  This can complicate the treatment of FMS, in which there may be multiple biochemicals out of balance, and that balance may vary in different individuals.  This variety may cause confusion for care providers and patients alike and may lead to expensive and unnecessary treatments and misinformation.  Dr. Russell mentioned a number of recent papers questioning the validity and existence of FMS.  While some doctors are working very hard to deny the existence of FMS, other doctors, such as Dr. Russell, are uncovering the varied causes of FMS and possible treatments.  Some of Dr. Russell’s interesting predictions for FMS include subgroup FMS classification and treatment based on pathogenesis (cause), the use of biologicals in the treatment of FMS, and the medication of FMS patients before exercise.  There will be more prevention of CNS sensitization, thus resulting in fewer FMS patients.

Integration of Pain Research into Clinical Management

David Butler, BPhty, GDAMT, MAppSC, came from Australia to provide a lively presentation on the integration of pain sciences into clinical management.  His books were available as well.  He spoke about how the doctors “on the battlefield” are not getting information from the latest research.  “There is a revolution in chronic pain research, but does the clinician even care?”  The current diagnostic classification of chronic pain states is not helping the patient or the doctor.  He quoted a passage from Revelations, “Neither shall there be any more pain.”  Also a 1998 quote from Patrick Wall, “If we are so good, why are patients so bad?”  There are a lot of hurting patients out there, yet there are adequate means to control pain.  Doctors learn anatomy, but we don’t treat anatomy.  Anatomy is the vehicle for the pathobiological process.  The two new categories to manage patient pain are pathobiology and dysfunction.  Doctors must consider tissue mechanisms and pain mechanisms.  Doctors who treat pain, and that includes most doctors, need to understand ion channel upregulation and mid axon ion channel crosstalk.  Myelin surrounding nerves can be affected by biochemical toxins.  Pain management needs to include this understanding, plus environmental, immunological and endocrine management.  One of the things that must be done is to find a way to stop processes before they ignite central pain.  This can be as simple as better pacing of activities in some cases.

If your brain thinks that you need heightened sensitivity and more adrenalin to succeed in this society, your DNA will provide them.  An injured peripheral nerve can have a delayed firing two weeks after the stimuli.  The neuron experience may be: stimuli, stimuli, stimuli.  FIRE.  If the pain is not adequately treated, your body will cry out louder and louder until you listen and do something to stop the pain.  The body finally lets you know that it has had enough.  It may take a while for the central sensitization to build up after a trauma.  Doctors must understand that it can be a latent pain. Insurance companies don’t understand that concept either.  David Butler said that when he asked their patients, “When do the pains come on?”, they reply, “They come on when they want to.”  That is central sensitization.  He laughs grimly when he sees a patient arrive with the diagnosis of “atypical FMS.”  He said that he’s never seen a “typical” case of FMS.  Doctors are trained in the anatomy concept.  When they see patients with pain they don’t understand, they take the part of anatomy that is hurting the most and put an “itis” on the end.  That gives it a label.  There are issues in the CNS and issues in the tissues, and they must be addressed.  One of the problems is that there are no cheap, reliable and specific tests for FMS.  He noted that it is an exciting time in pain management, and clinicians must not “forget to make it exciting for patients as well.”

Beyond Neurons: Implications of Immune and Glial Activation for Chronic Pain  

Linda Watkins, PhD, is Director of the Interdepartmental Neuroscience PhD program at the University of Colorado.  Her team is investigating the onset of chronic pain.  They are zeroing in on the mechanism behind central sensitization.  It is the activation of the type of CNS cells called glial cells.  Dr. Watkins gave a fascinating presentation on what may eventually prove to be the key mechanism behind FMS.  It may offer clues to treatment options as well.

An important part of the instigation and maintenance of chronic pain is glial cell activation.  Glial cells account for almost 90% of the cells in the CNS.  In many ways, they are to the CNS what fascia is to the rest of the body.  Glial cells, like myofascia, are more than just scaffolding.  In the first edition of the Survival Manual, I wrote that I believed glial cells were important in FMS and CMP.  Since then, we’ve learned that some glial cells affect mineral ion concentrations.  Nerve cells can regenerate and glia are a key to this nervous system renewal.  Glia surround every nerve fiber and every group of nerve fibers, providing elasticity and support.

Glial cells also provoke a sickness response after an infection, trauma or other threat to the body.  This response includes activation of the immune system.  The immune system talks to the brain and the brain talks back.  You may run a fever, which is very energy intensive.  [There is 10-15% more energy used for every degree of fever.]  Your ions alter, you need more sleep, your hypothalamus-pituitary-adrenal system — the HPA system — is activated, and so is the sympathetic nervous system.  This sickness response starts in a part of the brain called the nucleus tractus solitarius.  This is an important link in the chain of evidence, and, just like crime scene investigators, researchers are discovering how central sensitization (which can be a real crime if you have it) takes place. 

The sickness response of the brain occurs after it is signaled by the immune system.  It causes, among other things, reduced activity and desire for exploration of new things, reduced social and sexual behavior, disrupted learning and memory, anxiety, and an enhanced pain response.  Pro-inflammatory cytokines are both necessary and sufficient to provoke the sickness response.  Certain types of glial cells, called astrocytes and microglia, release all sorts of biochemicals when they are activated.  Some of these biochemicals are responsible for allodynia (pain from normally nonpainful stimuli) and hyperalgesia (amplification of pain response).  The substance fractalkine seems to be important to central sensitization.  The neurocircuitry of this process proceeds from the nucleus tractus solitarius through to the spinal pain transmission nerves.  Angry spinal glial cells cause enhanced pain neurotransmitter release as well as enhanced neuronal excitability.  The glial cells upset the immune functions which further upsets the glia.  This can result in increased pain, as well as memory and learning disruptions resulting from a facilitated pain state.

Glial cells don’t care if you stub your toe, but with repeated or massive injury or other trauma (which may be biochemical), they can become activated.  Glial activation is necessary and sufficient to produce enhanced pain.  The glia that are responsible for a lot of central sensitization are spinal cord glia.  That means that we can treat spinal glia without disrupting the healthy glia that provide important functions in the rest of the body.  Research suggests that substances released by glia counteract the effect of chronic opioids.  These pro-inflammatory cytokines trigger the production of each other, and then they act synergistically.  Substances released by glia excite pain transmission neurons (PTNs).  Fractalkine is the substance used as a signal from the neuron to the glia, after the glia have turned on the neurons. 

Right now Dr. Watkin’s team has been able to completely eliminate central sensitization in rats using IL-10 (interleukin-10), an anti-inflammatory cytokine.  The sensitized rats’ pain levels dropped quickly if their spinal cords were infused with IL-10.  [One recent study showed an association of low IL-10 in women with metabolic syndrome.  Metabolic syndrome is a common perpetuating factor of both FMS and CMP.]  Glial cell loss may contribute to cognitive deficits such as memory impairment (Kurosinski P, Gotz J, 2002).  Dr. Watkins says that even glial cell activation can cause cognitive deficits.  Right now isn’t the time to drop the pain meds and demand a spinal cord (intrathecal) injection of IL-10 from your primary care physician.  I had lunch with Linda Watkins at the seminar (attendees can have lunch with speakers), and know that even if I showed up at her lab in a rat suit, however well-made, I could not be treated with IL-10 at this time.  But the FDA is very interested in this research, and it brings us hope.  

The Future Research Needs in Muscle Pain Syndromes

FMS is not the same as CMP (Gerwin 1999).  It is fundamentally different in an important way (Simons, Travell and Simons, 1999, p 18.)   There is no such thing as a fibromyalgia trigger point.  TrPs cause myofascial pain, not FMS, and you and your care provider must understand this.  Even if you have never heard of myofascial TrPs, you will recognize them when you see the pain patterns and may be able to identify one of the chief sources of your symptoms.  When someone says, “I have Thoracic Outlet Syndrome, Carpal Tunnel Syndrome, Tarsal Tunnel Syndrome, Dysmenorrhea, Plantar Fasciitis, Piriformis Syndrome, Frozen Shoulder, TMJD, Tennis Elbow, etc.”, the neon sign starts flashing.  These things can be caused by myofascial TrPs.  They aren’t always.  But if this pattern is there, this person probably has CMP. They probably also have multiple perpetuating factors.  CMP, like central sensitization, is often iatrogenic.  Patients can develop CMP because their doctors don’t recognize single TrPs and treat them promptly.  Myofascial medicine is swimming upstream, with a constant flow of medical school graduates without myofascial training.  

David G. Simons, MD, gave a presentation on progress and prospects in myofascial TrP research.  Thirty-eight percent of the general population is in pain at any one time (White K et al, 1996).  Ninety-eight percent of that pain is musculoskeletal.  Muscles make up half of the body.  Yet the muscle is an orphan organ.  No medical specialty concentrates on it.  Most clinicians, doctors “in the trenches” treating patients, are not familiar with or trained in myofascial medicine.  Palpation is no longer a common skill, and many doctors don’t understand that weakness in a muscle and restriction of range of motion may be the first signs of a TrP, long before pain occurs.  There is a credible integrated hypothesis that explains the mechanisms behind  myofascial TrP pain [see Fibromyalgia and Chronic Myofascial Pain: A Survival Manual ed. 2], but it is widely ignored.  We still need to discover why acetylcholine causes sarcomere contraction and taut bands.  We may need TrP biopsy research.  We don’t know how the energy crisis feedback causes sarcomere shortening.  There are more pieces of the puzzle to put into place.  Some of these may indeed be known, but the researchers who know them don’t know about TrPs and this possible application of their research.  

PhD researchers often know nothing about TrPs.  Myofascial TrP-trained clinicians are often untrained in research.  Thus, clinicians now focus on treating symptoms rather than causes.  They also neglect to treat early TrPs aggressively, so the untreated or under-treated TrPs can develop satellites and secondary TrPs.  The patient can develop CMP, especially if he or she has one or more perpetuating factors.  This progression is largely preventable.  There have been studies showing high interrater reliability identifying myofascial TrPs (Gerwin RD, Shannon S, Hong C-Z et al, 1997; Sciotti VM, Mittak VL, DiMarco L, et al, 2001).  If two people disagree on a TrP, they should go back to the TrP and find out why.  They might learn something.  Palpation identification of myofascial TrPs requires both training and experience.  TrPs can be imaged by ultrasound and tissue impedance.  A week before the seminar, Dr. Simons was contacted on the phone by Wolfgang Baumeister in Germany.  He had been successful in using a shock wave generator, such as used to crush kidney stones, to find TrPs.  He could scan the tissue, and pain would be generated at the TrP.  Doctors who cannot palpate might be able to use this method to map TrPs.  There is a great need to "find and train people with high innate palpation ability and who care more about relieving suffering than $".  Many people lack the kinetic intelligence, the “touch instinct,” to learn palpation.  It takes patience...and a good teacher.  Many people are working to get myofascial TrPs incorporated as a part of training curriculum.  

You know by now what a TrP feels like.  The contraction knots are what you can often feel beneath your fingers, often like BB shot.  The taut band of muscle fibers extends from the Central TrPs in the belly of the muscle to the Attachment TrPs.  The band forms and the dysfunction starts before the pain is even evident.  You may have wondered why some TrPs are small and some are large.  It depends on how many contraction knots are in place, as well as how much infiltration of biochemicals and excess fluid is in the area.  Spacing between the muscle striations varies.  Each of these spaces is the length of one sarcomere, the small contractile unit of the muscle.  In myofascial TrPs, some sarcomeres are elongated and thin, some are contracted and fat.  The stresses cause biochemical changes.  The central TrP may contain many contraction knots.  

We know from vol I ed. 2 of the Trigger Point Manual, “Any attempt to passively stretch the muscle beyond this limit produces increasingly severe pain because the involved muscle fibers are already under substantially increased tension at rest length.”  EMG studies indicate “...in muscles with active TrPs, the muscle starts out fatigued, it fatigues more rapidly, and it becomes exhausted sooner than normal muscles.”  Myofascial TrPs may have many perpetuating factors.  For example, “Myofascial TrPs are aggravated by high histamine levels and active allergies.”  Biochemical sensitizing substances may have a lot to do with the reason that patients with both FMS and CMP have more than twice the trouble than if they had only one of these conditions.

The Use of a New Method to Assess Biochemicals Surrounding TrPs  

During the formation of the TrP, at the nerve endplates in the muscle there is a release of nerve irritant substances, including histamine, bradykinin and cytokines.  This causes more pain, which causes more muscle contraction and dysfunction, and so forth.  Much of chronic pain may be preventable if the components causing it are identified and dealt with.  Jay P. Shah, MD, Director, Medical Rehabilitation Training Program, Rehab Medicine Dept. Clinical Center, NIH, has come up with a novel way to sample the biochemicals that are produced in the area of a myofascial TrP using a hollow, specially-designed microdialysis acupuncture needle.  [None of the participants in the study had FMS as well as CMP.]  The biochemicals change dramatically with the twitch response when a TrP is activated, and there may be more than one twitch response per TrP.  The pH drops, and his team has found 31 different biochemicals involved.  It is a “sensitized and sensitizing soup.”  The amount of substance P generated around a TrP is enormous, ditto serotonin, cytokines, tumor necrosis factor, norepinephrine — very high.  I can’t give you quotes or pictures, because the data are still being accumulated for eventual publication.  Analysis of the substances released during the TrP twitch (and sometimes there is more than one twitch per TrP) is time-intensive.  Dr. Shah stressed that, as with real estate and location, myofascial examination of the body is palpation, palpation, palpation.  “Kinesthetic intelligence of the examiner must be high.”  He started his talk at the seminar with the I Ching trigram of unification, and he tells his myofascial patients to study t’ai chi.  [T’ai chi was often mentioned at the seminar as one of the best exercises for chronic pain patients.  There was sufficient room at the seminar at the pool and hot-tub area for me to practice my t’ai chi long form every day.]

Myofascial and Neurological Effects of Breathing Pattern Disorders  

Leon Chaitow, DO, ND, spoke on the importance of breathing correctly.  Breathing pattern disorders can cause myofascial and neurological effects, as well as change the whole body chemistry.  There are many accessory muscles that may be involved in breathing dysfunction, such as the iliopsoas, and they should not be overlooked.  Any TrPs must be successfully treated before the muscles can work properly.  Treatment must include identification and control of perpetuating factors, including a review of dietary habits, sleep pattern disturbances and exercise.  [Dr. Chaitow also advocated t’ai chi.]  He emphasized that quality breathing depends on freeing the “tethered and restricted structures,” as well as the learning and application of proper breathing technique.                

Tissue Histopathological Changes from Repeated Strain Injuries 

William Stauber, PT, PhD, spoke on the cause and mechanism of work-related muscle pain and a strategy to reduce it.  He had some very interesting information on the possible role of the extracellular matrix (ECM) in pain.  FMS patients have a changed ECM, and that may set them up for repetitive damage.  The ECM is where the nerve endings and pain receptors are.  “Chronic repeated strains can alter muscle ECM, causing receptors to be encased and resulting in ‘force-threshold’ pain and increased muscle stiffness.”  Fibrosis, a hardening of the tissue, can develop with expansion of ECM with repeated strain.  The amount of ECM increases drastically, and this increase continues after 6 weeks from a repeated strain injury and does not recover fully after 3 months of rest.  This change does not get better with time.  There is an increase in collagen crosslinks, which can result in stiffer muscles.  Collagen struts occur after chronic overuse or repetitive strain.  The dysfunctional tissue created is more difficult to break down than healthy tissue.  The thickened ECM can be a barrier to nutrients, and the dysfunctional tissue created by repetitive strain can form the matrix for calcification.  The calcification does not show up on imaging because it is too diffuse.  Increased connective tissue in skeletal muscles could cause increased pain and stiffness, decreased shock absorption, and a decrease in endurance.  Rest for muscle tissue recovery between repetitions in exercise is of vital importance to avoid these tissue changes.  Clinicians need to be aware of the magnitude of these tissue changes and their implications in chronic pain states.  

Abnormal Pain Sensitivity in Fibromyalgia:  Physiological and Psychosocial Factors     

Lawrence Bradley, PhD, gave a presentation on abnormal pain sensitivity in FMS.  He mentioned that there was no difference between FMS patients and healthy controls in psychological illness when factors of chronic pain are taken into consideration.  Much research is skewed in that it uses FMS patients in tertiary facilities.  Patients in tertiary facilities have often been misdiagnosed for years, have co-existing conditions, and have been subjected to many therapies and medications.  These patients require extreme care and are very ill.  If they are in tertiary facilities their symptoms are out of control.  These are not typical FMS patients.  By the time they reach this state they often do have psychological problems.  Yet this research is often used to justify linking FMS with psychological illness.  There is greater affective pain response in FMS patients in tertiary care facilities, but not in the open population of FMS.  The research presented indicates that “psychological distress and psychiatric illness do not account for abnormal pain sensitivity in women with FM”.  As FMS research develops, it may have implications in the treatment of other chronic pain conditions.  

Sex, Gender and Pain:  Are the Differences Clinically Relevant?

Roger Fillingim, PhD, presented on the effect gender and sex have on pain.  Quantitative differences in pain sensitivity between sexes are smaller than those differences that occur within each sex.  The neurochemistry underlying male and female stress analgesia is different, but we don’t know why.  The more prolonged and intense the stimulus, the more robust the changes are between the sexes in perception of pain.  In a process called temporal summation of pain, “Repetitive brief stimuli lead to enhanced pain perception due to an NMDA receptor-mediated enhancement of responses...”  Women exhibit greater temporal summation [wind-up] of pain than men.  Anxiety is more commonly tied to pain responses in men than in women.  Morphine seems to work better in women than men.  Topical lidocaine seems to help pressure pain better in men.  Ibuprofen helps electrical pain tolerance in men, but not in women.  Research done on one sex may not be applicable to the other.  Animal research often provides very different conclusions than those shown in human studies.              

Psychological Rehabilitation: Getting Back on Track

Lack of restorative sleep is a major perpetuating factor for both FMS and CMP.  You may not be getting enough sleep, or the right quality of sleep.  You must feel refreshed when you wake up, or you are not getting sufficient quality of sleep.  In FMS, the normal sleep pattern is fragmented (Drewes, Kielson,Taagholt et al, 1995).  Edward Kelty, PhD, APP, warned that much sleep research is not pertinent to the fragmented sleep of FMS.  Stressors of many varieties can trigger FMS, and any stressor changes the neurohormonal structure, the CNS, the immune system, and the pain response network.  Patients with fairly recent FMS development are fortunate in that they may be able to reverse the changes relatively easily.  One of the most important things is accepting the illness and having others recognize it.  

Weight management may help sleep management.  It may help patients to try to lose from one to five pounds at a time.  Small increments of weight loss are much more doable.  Exercise is also helpful in sleep management, but pacing is important.  It isn’t unusual to have waking periods during the sleep span.  Even if you get up for 30 minutes, that is not abnormal.  If you wake up groggy, it is often a sign that the sleep cycle has been interrupted, and you need to go back to sleep and finish that cycle if possible.  Dr. Kelty also advocated t’ai chi as part of pain and sleep management.     

Pain and Sleep Interaction  

Gilles Lavigne, DMD, MSc, spoke on pain and sleep interaction.  We still don’t understand how humans process pain during sleep.  It is normal to have 14 microarousals per hour during sleep, as an environmental check and reset.  It is not normal to have frequent arousal events, such as can happen in sleep apnea.  [Our local sleep clinic found that I had arousal events every 2 minutes all night because I stopped breathing, with no stage 3 and 4 sleep.  This is not normal.]  According to Dr. Lavigne, “All sleep stages are needed in succession to recover normal memory function.”  If there is a lack of restorative sleep, look into contributing causes such as Restless Leg Syndrome (RLS) and Sleep Apnea.  RLS is often helped by small doses of Mirapex (dopamine enhancer that works at the hypothalamus).  The first third of the night should be dominated by restorative sleep — stages 3 and 4.  Vivid dreams often occur during the last REM (rapid eye movement) sleep of the night.  The paralysis, or atonia, that occurs during REM sleep in humans does not occur in all species (or cats would be very fat).  After 40 years of age, there is an increase in sleep fragmentation and an decrease in sleep quality.  Sleep pressure increases during the day to reach peaks at 4:00 p.m. and 4:00 a.m.  Pain perception and a circadian cycle link is not demonstrated in pain-free subjects.  Generally, FMS and myofascial pain are worst from 3:00 p.m. to evening hours.  Arthritis is worst in the morning.  Bruxism, or teeth grinding, is largely limited to sleep arousal states only.  

Dr. Lavigne stated, “The sleeping area should not be a working area or a negotiation site.  There should be no TV, no scent of cigarette smoke, no noise.  Avoid intense exercise at least 3 to 4 hours before bed.  Ditto heavy meals.  Try having your main meal at lunch.  A late dinner is terrible for sleep quality.”  Sleep is necessary to avoid memory problems and recharge batteries.  Sleep apnea can result in problems that mimic Alzheimer’s.  One snorer in 5 has sleep apnea.  Symptoms of lack of restorative sleep can start with dysthesias and then move on to chronic pain.  Cardiac activity in sleep may hold the key to normalizing sleep.  Stage 1 and 2 light sleep are stages of reduced sympathetic dominance of the wakened state.  Deep sleep stage 3 and 4 are stages of parasympathetic dominancy and are dysfunctional in FMS, insomnia and diabetes.  REM sleep is a time of sympathetic overshoot.  FMS patients remain under high sympathetic dominance.  What we need is a safe drug to reduce autonomic function such as heart rate without danger or unwanted side-effects.  Chronic pain patients do not slow their heart rate normally when they sleep.  

There are many kinds of fatigue.  It is important to find out what kind you have.  You may have more than one kind.  Contributors could include fatigue post-exercise, boredom, depression, anxiety, life style, medications, use of cigarettes, alcohol and caffeine.  Hormone Replacement Therapy can sometimes change sleep for the better [but it must approximate human hormone.  Horses sleep standing up. :-} ]  Sleep deprivation can cause and affect pain.      

New Diagnosis and Management Technique for Neuro-Musculoskeletal Pain  

A new protocol for the quantified diagnosis of neuromuscular pain and more efficient treatment has been developed by Andrew A. Fischer, MD, PhD, (Great Neck, N. Y.) and Marta Imamura MD, PhD, ( Sao Paolo, Brazil).  Dr. Imamura gave two presentations on this topic, and I spoke with Dr. Fischer about it as well.  It is based on the diagnosis and treatment of spinal segmental sensitization (SSS).  It treats both the central sensitization of the spinal segment and the associated TrPs.  There is a separate information sheet on SSS on the website, written by Dr. Fischer.  Some of that information is used here.  This technique requires special training for doctors, but the training is available now and can offer immediate relief for patients.  Dr. Fischer said it is not unusual for a patient to come in with a cane and go striding out after therapy.

Trigger points and other pain generators such as areas of muscle spasms, nerve inflammation and other dysfunctions are identified.  Spinal segmental sensitization (SSS) therapy requires that the specific spinal segment corresponding to the peripheral generator be treated.  SSS represents a state of central hyperactivity and sensitization that develops in the spinal cord as a response to peripheral nociceptive impulses.  This facilitation spreads from the spinal sensory component to the anterior horn cells and the sympathetic centers in the sensitized spinal segment.  Drs. Fischer and Imamura have developed improved specific diagnostic techniques of palpation, neurological examination and pain diagnostic instruments.  Dysfunction in the dermatome, myotome, sclerotome and sympathetic hyperactivity is identified. 

Treatment for SSS consists of a paraspinous block (in the space between the spinous processes, with local anesthetic in spinal ligaments) to desensitize the SSS, a pre-injection block of the hypersensitive area to be infiltrated followed by needling and infiltration of the taut band and TrPs.  This is an office procedure.  Injections are followed by specific physical therapy (including heat, cold, electrical stimulation, postural correction, relaxation exercises and stretching).  Diagnosis and control of perpetuating and causative factors are required, as always.  

Drs. Fischer and Imamura say that this form of therapy can relieve not only FMS and TrP pain, but also can be effective for arthritis pain in the back, neck, hip or knee; bursitis and tendinitis; sport injuries such as tennis elbow, golf shoulder, or running injuries; repetitive motion injuries; whiplash; nerve root compression; Reflex Sympathetic Dystrophy (RSD) also called Complex Regional Pain Syndrome (CRPS); rotator cuff problems and many other conditions. 

Chronic Pelvic Pain, Interstitial Cystitis and Prostadynia:  A Myofascial Connection 

I was already familiar with the work done by Raggi Doggweiler-Wiygul, MD, on pelvic pain and myofascial dysfunction, and was delighted to have some time to speak with her.  Her presentation on chronic pelvic pain, interstitial cystitis, prostadynia and the myofascial connection was important.  I wish every doctor, nurse and other care provider involved with pelvic pain had heard it.  Dr. Doggweiler-Wiygul reminded us that urinary voiding is a learned behavior, and dysfunction can be learned as well.  Dysfunction can begin from not being allowed to interrupt work or school to go to the bathroom.  Using pelvic floor muscles the wrong way has consequences.  Trauma, such as surgical wounding or even sustained sitting, can cause dysfunction.  

It is important to take a comprehensive history.  Interstitial cystitis is not an isolated disease.  There are often contributory TrPs, leaky gut syndrome, and/or pain on intercourse.  There may be a history of sinusitis from childhood with periodic antibiotic use, dysmennorhea, IBS, drug hypersensitivity, candida, FMS or migraines.  It is important to get the whole picture, because that will give you the clues to possible causes or contributors and possible treatments.  She believes, as I do, that if intervention is successful at the beginning of urethral syndrome (often during childhood), interstitial cystitis may often be prevented.  In one of the studies she has co-authored (Interstitial cystitis, pelvic pain, and the relationship to myofascial pain and dysfunction: a report on four patients. World J Urol 20):310-4), the authors concluded that “Referred motor activity to the pelvic floor muscles (sphincters), as well as to the pelvic organs, due to TrPs can be the sole cause of IC, CPP (chronic pelvic pain), prostadynia, and irritative voiding dysfunction...”   Myofascial TrPs must be recognized and treated.  Comprehensive treatment often includes dietary changes (including avoidance of acidic foods and caffeine), physical therapy (postural analysis, breathing technique, relaxation, myofascial release, pelvic floor exercises), and stress reduction.  She uses a combination of medications including alpha blockers, muscle relaxants, antidepressants, antihistamines, anticholergic medications and analgesics.  Some of these she uses compounded in topical form.  

Movement Impairment Syndromes  

Shirley Sahrmann, PT, PhD, gave a presentation on movement impairment syndromes.  She has written a book on this topic.  The clinician must be like a detective, looking for the cause of dysfunction.  There may or may not be a pathological state to begin with, but the initial dysfunction can lead to a series of interrelated problems.  For example, someone with stiff hips may have a walking pattern that causes hyperflexibility in the spinal rotation, because the hip joints are stiffer than the lumbar spine.  (The lumbar spine is not designed to rotate.)  Repeated movements and sustained postures result in tissue changes.  People get the way they are by what they do.  Adaptive tissue changes may contribute to the condition.  At times, muscles may be too long or too weak.  If muscles are maintained in a static position, sarcomeres may be added in a series to the muscle tissue.  One interesting perpetuating factor for muscle dysfunction mentioned by Dr. Sahrmann is a height of 5'3" or less.  Furniture doesn’t fit and the thigh muscles are compressed unless a proper footrest is provided.  She has found that it is not muscle shortness per se, but relative stiffness across the joints, that drives most muscle impairment syndromes.      

Myofascial Trigger Points:  Their Effects on Muscle Activation Patterns

Karen Lucas, BAppSc, AdDip, PhD candidate, and a myotherapist from Australia, gave a detailed analysis of the effects of myofascial TrPs on muscle activation patterns.  Latent TrPs are frequently overlooked.  Patients with latent TrPs find that if they don’t move, they don’t hurt.  Latent TrPs don’t cause pain.  They restrict range of motion and cause muscle weakness and other problems.  Muscles are designed to move, and if you don’t move, your range of motion continues to lessen.  You accumulate latent TrPs as other muscles are recruited to contribute to the work of the muscle that is weakened by TrPs.  Then an infection, a fall, or some other stressor activates all the TrPs, and suddenly you are in a world of pain and wondering how you got so bad so fast.  By measuring muscle function with surface EMG (electromyography), Karen Lucas studied just how important treating latent TrPs is.  If the patient is treated before the pain results, when there is dysfunction but no active TrPs, treatment is effective and fast.  Latent TrPs change the temporal sequencing of muscle recruitment, further stressing the muscle and the surrounding muscles.                           

Even brief exposure to considerable pain can cause long-lasting changes in the spinal cord that enhance pain.  Insulin resistance seems to be common and contributes to several frequent health problems including sleep apnea, obesity and type 2 diabetes.  Possible perpetuating factors include faulty diet, lack of proper exercise, smoking and stress (Kelly 2000).  Respect your muscles.  They are designed to contract, relax, and be kept mobile through full range of motion.  Develop a home therapy program.  Don’t be over-enthusiastic.  Do exercises correctly.  Try to recover function, with some pain relief.  Avoid perpetuating movements.  Teach your body healthy sleeping positions.  

Myofascial Disorders and Visceral Diseases of the Pelvis

John Jarrell, MD, Msc, FRCSC, CSPO, from Calgary, Canada, gave a presentation on myofascial disorders and visceral diseases of the pelvis.  There are so many TrPs that can be associated with visceral disease, and many cause symptoms that can be misdiagnosed.  The TrPs can cause symptoms to persist long after the original cause is gone.  Common TrPs can occur in the vaginal cuff, in scar tissue or in dense fibrotic tissue.    

It was very interesting to note that TrPs can be present in the perineal area, causing pain, with or without visceral disease.  He has found that there is a unique relationship between the vaginal apex and the lower abdominal quadrants, and that if vaginal fibrotic nodules are treated after a hysterectomy, abdominal TrPs will be eliminated and there will not be pain during intercourse.  Dr. Jarrell noted that there is a remarkable variation in TrP appearance, reminding us that the Trigger Point Manuals only give us guidelines as to the most common TrPs.  It is important to realize that there may be underlying visceral disease or dysfunction and not to just continue to treat the TrP.  

Mast Cells and Histamine:  A Possible Cause of FMS?

Alice Larson, PhD, presented on a possible cause of FMS.  Trauma, surgery and infection can set up FMS.  Serotonin and tryptophan are low, dynorphin is increased in the CNS, and substance P is elevated in the cerebrospinal fluid (CSP).  Nerve growth factor (NGF) is elevated centrally in primary FMS but not in secondary FMS.  This suggests a different causative mechanism.  So where does the NGF come from?  Potential sources are central damage from trauma or infection, physical damage such as spinal stenosis, and mast cells in the thalamus.  We don’t know why there are mast cells in the CNS.  The thalamus is part of pain transmission, sleep modulation, hypervigilance, etc.  The thalamus looks like an attractive target for FMS dysfunction.  

Mast cells in tissue degranulate (expel their histamine granules) when they are activated and then can regranulate (form more histamine granules) again and again.  Mast cells in the CNS are located exclusively in the thalamus.  In FMS, there is decreased thalamic activity following pain.  Mast cells are influenced by stress.  Histamine, released by mast cells, is a stimulant.  Recent research indicates that histamine increases local vasopermeability and chances of varicose veins (Haviarova, Weismann, Pavlikova, et al, 2002).  Blood histamine is also associated with coronary artery disease and cardiac events (Clejan, Japa, Clemetson, et al, 2002). 

Stress activates the HPA axis which eventually activates mast cells.  There are many more VPL (pain nuclei) mast cells in the thalamus of females.  There is a dramatic difference in mast cell distribution of these nuclei between males and females.  There are cyclic changes in the number of mast cells throughout the estrus cycle.  What are mast cells doing involved in reproduction?  We don’t know.  Mice treated intrathecally with cromalin, a mast cell stabilizer, improved.  Cognitive learning depends on synaptogenesis.  You need blood flow to support learning activities.  Mast cells are recruited to the thalamus in response to pain and stress.  Mast cell function may be to increase blood flow in areas necessary for appropriate modulation of pain and stress responses.  Dr. Larson’s working hypothesis is that patients with FMS may have "inappropriate mast cell/vascular responses necessary to suppress pain, cope with stress, regulate sleep, etc.". 

Edited by Barb Zweber, with appreciation.  DJS

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