Clinical Application of Neuromuscular Techniques The Upper Body Volume 1

7 The internal environ ment 1 31 In some situations, particularly those involving substan­ chronic, low-grade, systemic inflammation that becomes tialligamentous damage, prolotherapy might also be a useful self-perpetuating. Seaman (2006) explains: tool. Prolotherapy involves the placement of a prolific agent (dextrose), which is injected at the attachment site of ligament Tumor necrosisfactor-a: (TNF), one of many pro-inflamma­ or tendon to bone . The resultant localized inflammation in ton) C1)tokines, is released by both white cells and adipocytes, this weak area increases blood supply and nutrient flow, and as individuals gain additional fat, there's an increased thereby stimulating tissue repair. Mooney (2003) observes: release of adipocyte-derived TNF, which serves to inhibit 'The concept of creating scar to offer tissue stability goes back insulin receptor activity that leads to insulin resistance to Hippocrates' advice for using a hot poker for chronically (Fernandez-Real & Ricart 2003, Grimble 2002). As insulin cUslocating shoulders.' Various sclerosant agents have been resistance develops, it promotes glycosylation ofproteins and used since the 1800s to treat varicose veins, hemorrhoids and DNA, enhancesfree radical formation (Preuss et al 2002), hernias non-surgically. A general surgeon named Hackett, and leads to an upregulation of inflammatory protein pro­ having recognized the potential for injected agents to duction (Evans et al 2002), and through these mechanisms, strengthen ligaments, started performing this procedure in insulin resistance will lead to a worsening of inflammation, the 1950s. He changed the procedure name to proliferant ther­ which leads to a vicious cycle of chronic inflammation apy rather than sclerosant treatment because of the more pos­ (Fernandez-Real & Ricart 2003). itive implication of enhancing tissue strength through new tissue rather than changing it by scar. (See also the hormonal discussion below.) Richards & Richards (2003), in Mastering Leptin, explain WHEN INFLAMMATION BECOMES GLOBAL this process in greater detail, simplifying complex concepts, It is important to consider that the inflammatory process such as a triad of leptin, insulin and adrenaline resistance. seen in the patient may be more systemically oriented, i.e. a 'The concept of fat as a storage place has been transformed generalized proinflammatory state that leads to chronic to fat as a major endocrine organ, such as the thyroid gland, inflammation. Diet-related metabolic imbalances (such as adrenal glands, and sex glands.' In actuality, the picture is insulin resistance, a prediabetic state, and free radical mech­ much bigger than the statement implies. anisms) are implicated as a driving force in systemic inflam­ mation, which has far-reaching consequences on practically HORMONAL INFLUENCES all organs and systems in the body. Hormones are the chemical messengers to and from the Seaman (2006) notes: brain, cells, glands and organs, forming a complex commu­ nication system that drives respiration, reproduction, . . . inflammation is part of the healing process; however, growth, digestion, energy production and usage, and prac­ chronic inflammation represents lack of tissue healing and tically all functions of the human body. Concentration levels actually, promotes ongoing tissue damage. Cancer, heart of hormones in blood and extracellular fluid are crucial disease, hypertension, Alzheimer disease, endometriosis, factors in health that regulate innumerable physiological osteoarthritis, rheumatoid arthritis, diabetes, aging, effects. Concentration levels are determined by the: osteoporosis, chronic obstructive pulmonary disease, and menopause are examples of conditions that developed and • rate of production exist as a consequence of chronic inflammation and this is • rate of delivery, and likely the casefor chronic musculoskeletal pain. • rate of degradation and elimination. He further notes that these metabolic imbalances occur When hormone concentrations are either too high or too simultaneously, are interrelated, and appear to have a cumu­ low disease almost always results. lative effect. He implicates free radicals, inappropriate ratios of omega-6 to omega-3 fatty acids, deficiencies of potassium In the few years since its discovery, leptin has been linked and magnesium, and related pH disorders as primary cul­ to influences on body weight, insulin levels, cardiovascular prits in the development of chronic inflammation. He sug­ health, reproductive function, sexuality, immune function, gests that single interventions, such as taking individual adrenal function, effects of stress, bone health, cancer and supplements of magnesium or vitamin E, will not have an inflammation. Research regarding leptin is still in its infancy, appreciable effect, and that a broader approach will likely be although it was the focus of over 4200 scientific papers needed, including significant changes in dietary habits. between 1995 and 2003 (Tenenbaum 2003). With new infor­ mation regarding hormones and other chemical communi­ These diet-related metabolic imbalances, as also dis­ cators (such as cytokines) emerging almost daily, there are cussed by Haffner et al (1992), are usually referred to as obvious challenges for most physicians to stay current with 'syndrome X', which is directly linked to hyperinsulinemia the information load. Hormonal imbalances in general, and and/or insulin resistance. It is apparently promoted by a leptin, adrenaline and insulin dysfunction in particular, appear to play significant roles in widespread damage, destruction and devastation in health and in the lives of

1 32 CL I N ICAL A P PL I C AT I O N OF N E U R O M U SC U L A R T EC H N I QU ES: T H E U P P E R B O DY those who suffer with them, making it critical to have a While they may be secreted directly into the bloodstream, baseline understanding of their interface. they may also move by circulation or diffusion to their tar­ get cell, which may be nearby or in a distant organ or tissue. Although we normally think of hormones as being pro­ Once they reach their target cells, the hormones combine duced by endocrine glands (Box 7.1), they are also pro­ with their receptors to complete the signal, which might duced by most organ systems and tissue types in the body. Box 7 . 1 The endocri ne system 6. adrenocorticotropin (ACTH) - governs the nutrition. growth Endocrine glands are ductless glands that secrete specific messenger and function of the adrenal cortex molecules called hormones that are released directly into the bloodstream and travel to target organs, upon which they act. 7. somatotropin - promotes body growth. fat mobilization and Conversely, exocrine glands (salivary, sweat and digestive glands) secrete products that are passed outside the body. While both are important, inhibition of glucose utilization the endocrine system as a whole works in parallel with the nervous system to control growth and maturation along with hom eostasis. 8. melanotropin - causes dispersion of melanin. which results in Each hormone's shape is specific and can be recognized by the darkening of the skin corresponding hormone receptors on the target cells. Some hormones are supplied in antagonistic pairs that have opposing 9. oxytocin and prolactin- stimulated at the end of pregnancy effects on the target o rgans. For example, insulin lowers blood sugar levels whereas glucagon raises it. Hormonal regulation (balance and to induce labor and prepare the breasts for milk production, hom eostasis) usua l l y depends on feedback loops. respectively. Endocrine-related problems include overproduction of a hormone, • The thyroid gland produces thyroid hormones that regulate underproduction of a hormone and non-functional receptors that cause target cells to become insensitive to or unable to utilize hormones. metabolism, including body temperature and weight, as we l l as Functions controlled by hormones include: calcitonin, which helps regulate calcium (see Box 7.2). • The parathyroid glands play a significant role in the regulation of • activities of certain organs • growth and development the body's calcium balance. • reproduction • sexual characteristics • The pancreas has two functions: functioning as a ducted • usage and storage of energy • levels of fl uid, salt and sugar in the blood. (exocrine) gland, it secretes digestive enzymes into the small More than 50 human hormones have been identified and are intestine; as a ductless (endocrine) gland its islets of Langerhans categorized into general classes (groups) by chemical structure, not secrete insulin and glucagon to regulate blood sugar levels. function. These include: • The adrenal glands, located one on top of each kidney, consist of • steroid hormones - l ipids derived from cholesterol; these include sex hormones (such as testosterone, estradiol, progesterone) and two parts that work hand-in-hand with the hypothalamus and adrenal steroids (such as cortisol) pituitary gland. The outer cortex secretes corticosteroids such as cortisone, wel l known as being antiinflam matory. The medulla • amines - derived from the amino acid tyrosine; secreted from the secretes epinephrine, norepinephrine and other similar 'stress' thyroid and the adrenal medu l l a hormones that respond in fight or flight situations as well as to caffeine or low blood sugar. Several steroid hormones are also • peptide hormones -secreted b y the parathyroid, pituitary, heart, produced by the adrenal glands, classified in the fol lowing cate­ stomach, liver and kidneys gories: mineralocorticoids (electrolyte balance), glucocorticoids (breakdown of fats and proteins) and sex hormones. • eicosanoids - derived from pol yunsaturated fatty acids; the prin­ cipal groups of hormones of this class are prostaglandins, prosta­ • The gonads or sex organs secrete sex hormones. While both sexes cyclins, leukotrienes and thromboxanes. make some of each of the hormones, typically male testes secrete The glands primarily androgens (including testosterone) and female ovaries • The pituitarygland is considered the ' master gland'. H owever, it make estrogens and progesterone. should be borne in mind that the hypothalamus secretes hor­ • The pineal gland is stimulated by the optic nerves. It secretes mones that stimul ate or suppress the rel ease of hormones in the melatonin, which promotes sleep. It also affects reproductive, pituitary gland, in addition to controlling water balance, sl eep, thyroid and adrenal cortex functions. In some animals, melatonin temperature, appetite and blood pressure. Together, the hypothal­ affects skin pigmentation. amus and pituitary gland control many other endocrine functions and secrete a number of hormones, including: • The thymus gland is l ocated in the upper part of the chest and 1. fol licl e-stimulating hormone (FSH) - stimulates deve lopment produces T lymphocytes (white blood cells that fight infections and destroy abnormal cel l s). and m aturation of a fo l l icle in one of a woman's ovaries In addition to the above listed classic endocrine organs, many other 2. luteinizing hormone (LH) - causes ovulation and the forma­ cells in the body secrete hormones. Among these are the adipose cells, which were previously thought to only provide a storage site. In recent tion of a corpus luteum years, much has come to light regarding hormonal production by adipocytes, thereby establishing adipose as a true endocrine organ 3. antidiuretic hormone (ADH) - helps regulate water excretion (Kershaw Et Flier 2004) (see Box 7.3). If defined broadly, the term by the kidneys and blood pressure 4. enkephalins and endorphins (opiates) - serve to deaden pain 'hormone' can also include all secreted chemical messengers, which means virtual ly all cells can be considered part of the endocrine system. receptors 5. thyrotropin - thyroid stimulating hormone Though this discussion has appeared to simplify endocrinology, the study of the endocrine system remains one of most complex information. It is important to bear in mind that there are no cell types, o rgans or processes that are not influenced - usual l y profoundly - b y hormone signaling. Often multiple hormones are acting in relation to each other. Although many hormones are known, there is no doubt that others remain to be discovered. And of those that we know to exist, little is ful ly understood.

7 The i n ternal environment 1 33 then trigger a succession of secondary actions within the issues of underactive thyroid, which is undoubtedly linked celi, with a cascade effect being common. to myofasciaf trigger point formation (Simons et al 1999) and fibromyalgia (Chaitow 2003, Lowe 2000). Box 7.3 dis­ \\lVhile it is certainly not within the scope of this text to cusses the significant impact of leptin resistance and its rela­ include an in-depth discourse on hormonal issues, those tionship to insulin resistance and adrenaline resistance. Box that are of primary concern to chronic myofascial pain 7.4 outlines key concepts in the relation between adipose patients demand discussion. Box 7.2 is dedicated to the Box 7.2 U nderactive thyroid Functional h ypoth yroidism Another method of eva l uating subclinical sluggish thyroid activity is The most common symptoms of underactive thyroid function a re: by a fu nctional test developed by Barnes Et Ga lton ( 1 976), which measures thyroid hormone's effect on the body rather than looking • depression solely at blood thyroid hormone levels. This is achieved by measuring • difficulty in losing weight a person's resting metabolic rate, w h ich is control led by the thyroid • dry skin gland, by ta king an axil lary temperature prior to getting out of bed • musculoskeletal symptoms t h ree mornings i n a row. An average temperature below • headaches 36.55°C/97.8°F i s suggestive of hypothyroidism. Barnes Et Galton • lethargy or fatigue found that measuring basal body temperature was a good way of • memory problems assessing basal metabolic rate and thus the body's response to • menstrual problems thyroid hormones, reg a rd l ess of their blood level. When employi ng • hyperlipidemia this test, the incidence of hypothyroidism is a surprising 25% • recurrent infections (Barnes Et Galton 1 976). • sensitivity to cold. Pizzorno Et M u rray (2005, p 1 793-1 794) report: Different forms of u nderactive thyroid function The hormones of the thyroid gland regu late metabolism, therefore a Functional tests show a far greoter incidence oflow thyroid than deficiency of thyroid hormones ca n affect virtually a l l bod i ly blood tests largely because typical blood tests meosure thyroxine (T4), functions. which accounts for 90% afthe hormone secretion by the thyroid. However. the form that affects the cells the most is T3 (triiodothyro­ Pizzorno Et Murray (2005, p. 1 79 1 - 1 793) report: nine), which cells make from T4. lf the cells cannot convert T4 to the four-times-more-active T3, a person can have normal levels ofthyroid Deficiency of thyroid hormone may be due to lack ofstimulation by hormone in the blood yet be thyroid deficient. the pituitary gland, defective hormone synthesis, or impaired cellular conversion ofT4 to T3. The pituitary gland regulates thyroid octivity 'Wilson's syndrome' is a name used for the condition i n w h ich through the secretion of thyroid-stimulating hormone (TSH). The subcl in ica l hypothyroidism is thought to be associated with deficient combination oflow thyroid hormone and elevated TSH blood levels peripheral conversion ofT4 to T3 ( Ba novac et al 1 985). usually indicates defective thyroid hormone synthesis, which is defined as primary hypothyroidism. When TSH and thyroid hormone Cellular resistance to th yroid hormone levels are both low, the pituitary gland is responsible for the low An u nderstanding is emerging of another fo rm of hypothyroid ism, thyroid function, a situation termed secondory hypothyroidism. a genetically acq u i red condition in which cel ls become resista nt Normal blood thyroid hormone and TSH blood levels combined with to the infl uence of the hormone, known as thyroid hormone low functional thyroid activity (as defined by a low basal metabolic resistance syndrome. This problem is characterized by elevated rate) suggestcellular hypothyroidism {sometimes called 'cellular free thyroid hormone levels and partial resistance to this at resistance}. the cel lular level (Chatterjee et al 1 99 1 ) . This condition is said to be far more widespread than is genera l ly thought (Krysiak Most estimates on the rate ofhypothyroidism are based on the lev­ et al 2006). els of thyroid harmanes in the blaad ... Using blood levels of thyroid hormones as the criteria, it is estimated that between 1 0;0 and 4% of Clinical symptomato l ogy of hypothyroid ism (from any the adult population have moderate to severe hypothyroidism, and another 10% to 12% have mild hypothyroidism. The rate ofhypothy­ ca use) roidism increases steadily with advancing age. Metabolic Causes of hypothyroidism • General decrease in the rate of util ization of fat, protein and car- Overt h ypothyroidism About 95% of a l l cases of overt hypothyroid ism a re primary. In the bohydrate past, the most common cause of hypothyroidism was iodine • Moderate weight gain deficiency; however, this cause is now rare in the USA due to the • Sensitivity to col d weather (demonstrated by cold hands or feet) wide use of iodized table salt. • Cholesterol and triglyceride levels are increased • Ca pil lary permeability and slow lymphatic drainage Subclinical h ypoth yroidism In this condition, thyroid stimulating hormone (TSH) (from the Endocrine pituitary) is elevated while serum thyroid hormone levels a re normal. • Loss of libido (sexu a l d rive) in men In subclinical hypothyroidism, the body can compensate for • Menstru a l abnormal i ties in women decreased thyroid function by increasing TSH pituitary output. These cases may be caused by a m i ld a utoim mune thyroid destruction or Skin, hair, and nails may b e due t o d r u g or su rg ical interventions. Subclinical • Dry, rough skin covered with fi ne superficial scales hypothyroid ism is a relatively com mon finding in primary care, • Hair is coarse, d ry and brittle affecting 2-7% of adults (Evans 2003). • Hair loss can be q uite severe • Nails become thin and brittle, often with transverse g rooves box con tinues

1 34 CLI N I CAL APPLICATI ON O F N E U RO M U SCU LAR TEC H N I Q U E S : T H E U PP E R BODY Box 7.2 ((oMi n tled) • Sou rces of zinc include seafood (especia l ly oysters), beef, oat­ meal, chicken, l iver, spinach, n uts and seeds. Psychological (Gold et al 198 1) • Depression, along with wea kness and fatigue • Copper is found in l iver and other organ meats, eggs, yeast, • Difficulty concentrating and forgetful beans, nuts a n d seeds. Muscular and skeletal (Krupsky et a1 1 987) • The best sources of the B vitamins are yeast, whole g ra ins and • Muscle weakness and joint stiffness l iver. • Muscle and joint pain, as wel l as tenderness (Hochberg et a l • The best source of selenium is Brazil nuts, especially those that 1 976) are u nshelled at the time of purchase. Cardiovascular • Orga nica lly g rown foods shou l d be recom mended due to their • Atherosclerosis due to the increase in cholesterol and trig lyc- higher levels of trace minerals (Liel et a I 1 996). erides Supplementation (Be rry Et Larsen 1 992, Choudhury et a l • Hypertension 2003, Oeshpande et al 2002) Other common manifestations • Zinc: 25 mg/day • Shortness of breath • Copper: 5 mg/day • Constipation • Selen i u m : 200 /lg/day • I mpaired kidney function • Vitamin C: 1 -3 g/day in d ivided doses • Vitamin E: 400 IU/day Diet The diet for i nd ividuals with hypothyroid function should be low in Exercise goitrogens and high in foods rich in the trace minera ls needed for Invigorating activity such as water sports, avoidance of overheated thyroid hormone production and activation (see list below). environments, and cold hydrotherapy can stimulate thyroid function (Lennon et al 1 985). Goitrogens (to be l i m ited) include brassica fam i ly foods (turnips, cabbage, ca u l iflower, broccoli, brussel sprouts, rutabagas, mustard Thyroid dysfu nction is relatively com mon in adu lts and can be a greens, radishes, horseradishes), cassava root, soybeans, peanuts, major feature in muscu loskeletal dysfu nction and pain, including pine nuts and m i l let. When eaten, these foods should be cooked to encou raging the presence of active trigger poi nts. Standard medical break down their goitrogenic constituents. thyroid hormone replacement is one therapeutic option, others include consulting someone who is either a licensed naturopathic • Sou rces of iodine include sea fish, sea vegetables (kelp, du lse, practitioner or traditional Chinese medicine practitioner. a rame, h ijiki, nori, waka me, kombu) and iod ized sa lt. Box 7.3 Leptin and other chemical i nfl uences in systemic i nflam mation Note: The fol lowing details a re pa rt of newly emerging information characterized by a g roup of metabolic risk factors in one person. It regard ing a d ipose tissue as an endocrine organ . Much of the presents with a cascade of d isorders (abdominal obesity, research on leptin and other newly d iscovered hormones is sti l l in its dysl ipidemia, prothrombotic state, hypertension, insu lin resistance infancy. While the authors of this text a re intrigued with the and a proinflammatory state) that together render fa r greater concepts d iscussed i n this box, they caution that the d ieta ry card iovascul a r (CV) risk than any of its i nd ivid ual factors. The main suggestions might not be right for everyo ne, such as for professional featu res of this condition i nclude i ncreased visceral adipose tissue ath letes, diabetics and others with advanced patholog ies that may (VAT) mass, d isplayed as an inflated waistline, a pple-shaped figure requ i re additional food intake beyond that suggested. We have (android body type) and increased systemic infla mmation (Berg Et chosen to i nclude this i n formation on using natural methods to Scherer 2005). obtain hormonal bal ance d u e to our interest in seeing research va l idation regarding the suggested eating pattern as a possible Ell iott (2007) notes: sol ution fo r endocrine and other systemic dysfu nctions. Regional body {fat} composition has been linked to heart disease, Once thought to be an inert tissue mainly devoted to energy stroke, diabetes mellitus, hypertension, endometrial cancer, peptic storage, wh ite adi pose tissue (WAT) is now known to be an active ulcers, non-alcoholic hepatitis, ga/l bladder disease, Cushing 's syn­ participant in reg u lating physiological and pathologica l processes, drome, polycystic ovaries, menstrual disorders, Werner's syndrome, including i m m un ity and inflam mation (Ju ge-Aubry et al 2005). WAT psychosocial problems, and other health risks (Lean 2003, Janssen a lso plays a primary role in the development of a triad of hormonal et aI 2002). These established correlations are among the many good imbalance (Ieptin resistance, adrenaline resistance, insulin reasons to measure body composition. resistance) with a cascade of endocrine interfaces that have sign ificant health consequences. Weight gain in the a bdominal Si nce many of these conditions a lso mask, or present with, region is a primary indicator of accu mulation of WAT that is myofascial pain symptoms, and since central obesity a lso has associated not only with these hormonal d isorders, but a lso with postural i m pl ications, it is suggested that an awareness of central high risks of developing ca rd iovascu l a r disease. obesity and syndrome X is i m portant for all manual practitioners. Central obesity has been shown to be associated with various Waist circu mference (WC) measurement has long been morbidities that have collectively emerged as 'synd rome X', a determ ined as a simple indicator of abdominal visceral adi pose mass precipitator of cardiovascular disease. The American Heart and its related CV risk (Pou liot et al 1 994), with obesity defined as a Association (2007) defines syndrome X as a metabolic syndrome waist circu mference of 40 inches ( 1 0 1 .6 cm) or g reater in men and 35 i nches (88.9 cm) or greater in women. Elliott (2007) has discussed box con tinues

7 The i nternal environment 1 35 Box 73 (continlled) . '. . the pros and cons of a nu mber of methods for measu ring body A primary purpose of the hormone leptin is to coordinate the meta­ composition and ag rees that the WC measurement, when performed bolic, endocrine and behavioral responses to starvation (Wilding correctly, can be a simple, inexpensive and accurate gauge that the 2007J. This hormone has a powerful influence on the subconscious practitioner as well as the patient ca n util ize. mind that is programmed by the genetic survival level, completely taking over eating patterns ifthe circumstances from its point ofview While measu ring at a specific level with consistency a mong dictate that it should. . . . When a person gets thrown out ofnatural practitioners is challenging (especially with the moderately obese, balance [homeostasis}, the brain does not sense leptin levels correctly, whose waistline is certainly not obvious), Elliott (2007) suggests literally building up resistance to the hormone. This problem steadily that, with proper t raining, individuals should be able to self-measure gets worse as a person gets older. WC at a point half way between the inferior su rface of the ribs and the top of the i l iac crest. This assessment would have a n initial va lue Kershaw & Flier (2004) explore leptin's effects beyond energy in determ ining excess of WAT. Periodic remeasuring can also be homeostasis. They document that it: val uable as a n obvious indicator of changes associated with compliance or fa i l u re in fol lowing a prescribed hea lth improvement • regulates neuroendocrine function and traditional endocrine prog ram. sys te m s While a trim waist l i ne and decreased cardiova scular risk are fine • decreases hypercortisolemia by inhibiting cortisol (a hormone goa ls for many reasons, WAT contributes fa r more infl uences to keenly associated with stress) consider in health. Fantuzzi (2005) notes that WAT produces both pro- and antiinflammatory factors, including adipokines (cytoki nes, • normalizes suppressed thyroid hormone cell-signaling proteins, such as leptin, adiponectin and resistin) as • accelerates puberty and interfaces in reproductive function well as other chemicals, such as tumor necrosis factor-alpha (TNF-a) • has d i rect effects via peripheral leptin receptors in the ova ry, and interleu kin 6 ( I L-6) (see below for deta i ls on these). 'The cu rrent view of adipose tissue is that of an active secretory organ, sending testis, prostate and placenta out and responding to signals that modulate a ppetite, energy • assists in reg u lation of i m m u ne function, hematopoiesis (blood expenditure, insu l i n sensitivity, endocrine and reproductive systems, bone metabolism, and inflammation and i m m u n ity: cell formation), angiogenesis (blood vessel development) and bone development To begin to consider the influences of WAT and its associated • influences sympathetic nervous system (SNS) activities, and chemical soup, let us explore some of the hormones produce by WAT. • decreases bone mass indirectly via activation of the SNS. For instance, adi pocytes (fat cells) secrete a n u mber of substances (Havel 2002) that play crucial roles in the development of type 2 Budak et a l (2006) h i g h l ig h t yet a nother point. 'Leptin and g h re l i n diabetes, obesity and atherosclerosis (Reilly & Rader 2003). A close [a n appetite sti m ulator] a n d other adi pose tissue-secreted hormones look at one of these, leptin hormone, will begi n to offer a g l impse have significant effects on reproduction. Acting through the brain, as to the wide-ranging conseq uences that these hormones can have these hormones may serve a s links between adipose tissue and the on health. reproductive system to supply and regu late energy needs for normal reproduction and pregnancy: The many faces of leptin hormone First discovered in 1 994, leptin hormone may very we l l be the most As part of a complex com m u n ication system , energy ma intenance important hormone realized to date. Though first thought to signal system and even as an a ppetite reg u lator, leptin and its affi liate satiety (hu nger satisfaction), peripheral actions of leptin a re now hormones keep the machi nery run n i ng smooth ly and fuel burning known to interface i n insu l i n biosynthesis a nd, with leptin receptors efficiently. However, modern l ife, including magnified stress, excess present on the pancreas, in pancreatic secretion (Fehmann et al food ava i labil ity and consumption of excessive carbohydrates a n d 1 997). In return, i nsulin stimu lates leptin secretion from adipose inappropriate fats, has strained these systems. A breakdown in tissue (Havel 2002, Trayh u rn et al 1 999), establishing a hormonal com m u nication ensues and, for many, a cascade of serious health regu latory feedback loop, the 'adi po-insular axis' (Seufert 2004). consequences develops. Crucial to surviva l and fundamental core level energy, leptin is When a good plan goes bad - hormonal resistance now known to be secreted by wh ite adipose tissue that is found This system probably worked well in the years of hunting and primarily on the abdomen, thighs and buttocks, a nd to have a gathering, when food su ppl ies were erratic - the body stored when regulatory effect on a n u m ber of other hormones, including thyroid, there was plenty so that it cou l d take from the stores when there adrenal, pancreatic and sex hormones (Havel 2000, Wauters et al was less. However, today, when there a re food supplies on every 2000). I t plays a n i m porta nt part in body weight regu lation, eating corner, the body often may not have even digested (let a lone burned behavior and reproduction by acting on the central nervous system u p) the previously eaten food before more is consumed. Cutler et al and target reproductive organs (Budak et al 2006). (2003) suggest that extra ca lories from snacking a re the weight gain cul prit, reporting a 60% rise in the average n u mber of daily snacks One of leptin's primary jobs is to com m u nicate with the since the early 1 970s. While one study (Field et al 2004) reports that hypothalamus as to how m uch fat is stored in the body. This, in turn, snack intake in children may be less influential on their weight than can affect the metabolic rate for burning this 'stored fuel'. If working the mother's weight or the child's dieting status, Howarth et al normal ly, leptin levels rise when enough food has been consumed , (2006) show that i n both younger and older a du lts 'eating frequency which signals t h e brain to stop eating and increase metabol ism. was positively associated with energy intake, and eating more than When leptin levels drop because food is not being consu med, three times a day was associated with being overweight or obese'. appetite is stimu lated. If food is sti l l not consu med (incl uding when meals a re volu ntarily skipped) and leptin levels continue to Key triad in systemic problems d rop, this eventua lly signals metabolism to slow down and conserve The triad of leptin, adrenal ine and insu l i n resistance i nterface to body fat. create an overweight consequence, with gain being pri mari ly in the middle - in the company of da ngerous cardiovascular and diabetic Richards & Richards (2005) indicate that this is part of a consequences as a bdominal and visceral a d i pose tissue m ushrooms. primitive mechanism. U nlocking this triad requ i res a n u n derstanding of how these hormonal resistances develop and how they interface. box con tinues

1 36 CLI N I CA L A PP L I CATI O N OF N E U R O M U SC U LA R T EC H N I Q U E S : T H E U PP E R B O DY Box 7.3 (continued) Leplin resistance occurs in overweight people. � When food is available, it heads to fat cells to The brain thinks there is not enough fat in storage and conlinues to fill fat cells with fuel zy.r- replenish depleted reserves Leptin level is not detected by the • brain, thus the brain thinks there is not enough fat in storage Once the hypothalamus senses that leptin levels Metabolic rate stays low because are high enough and there the brain thinks that the body is is plenty of fuel in storage, slarving fat will stop being stored and melabolic rate will Food heads for fat storage, increase resulting in excess fal in the body As fat cells fill up, Food is sent Higher than normal leptin A leptin levels rise to fat cells 10 be levels stored as energy reserves B Excess fat in storage White adipose tissue Fig u re 7.3 The deve l o p m e n t of leptin resistance. A : Leptin fu nction w h en food i s a va i l a b l e. B : Leptin resistance associated with ove rweig ht. Drawn after Richards 8: R i c h a rds (2005). Leptin resistance high levels of adrena line and the eventual development of reduced sym pathetic sensitivity by the fat cel ls (adrenaline resistance) Fad d iets, eating d isorders and other problems (e.g. continual (Rayner 8: Trayhurn 2001 ). Over time, the changes in metabolism sympathetic a rousal) m ay confuse the metabolic system and produce abdominal weight gain in both genders, as well as thigh and interfere with normal com m u nication (Ha l le 8: Persson 2003, hip weight gain in females, chronic fatigue, sleep problems, Tenenba u m 2003). Breakdowns occur in signaling and the ca rdiovascular distress and a host of other changes. This additional hypothalamus, which relies on an accurate perception of leptin to adi pose, as mentioned previously, contributes further to leptin set the meta bolic rate, develops a resistance to the signa ls. Although resistance. the leptin levels may be high, the signal to stop eating simply does not get through to the brain, the cornerstone of leptin resistance. Insulin resistance and the type of food consumed This results in overeating and frequent snacking in an attempt to Not only is the a mount of food and frequency of eating l i nked to q uiet the 'false hunger' pains. leptin levels, the type of food consumed is also important. High g lycemic index foods cause increased production of insulin, resulting Bodosi et a l (2004) note that leptin levels rise with the inta ke of in an imbalance of these two hormones that normally have a food and 'suggest a strong relationsh ip between feeding and the balancing effect on each other. Once leptin levels a re elevated and di urnal rhythm of lepti n, and that feed ing a lso fu ndamenta l ly leptin resistance develops, insulin resistance is not far behind, with mod u lates the d i u rnal rhythm of g h relin', a concept also supported leptin playing a primary role a s a mediator of insulin secretion (Va n by Howarth et al (2006). Richa rds 8: Richards (2005) suggest that Gaal et al 1 999) and insul i n as a prominent regulator of leptin's even with a small amount of food, constant snacking and the expression i n the fat cel l (Spiegelman 8: Fl ier 2001 ). resultant consistently elevated leptin release a re powerful cu lprits in the development of leptin resistance. Richards 8: Richards (2005) depict this vicious cycle of hormonal resistance. Once leptin resistance is established, the hypothalamus no longer receives the signals from the hormone, which is stil l being produced [The] brain cannot sense leptin, so it keeps metabolism slow and calo­ and, in fact, exists in high levels in the blood. When the brain ries heading for storage. The pancreas cannot sense leptin, so it keeps becomes resistant to the signals, the food being consumed is sent to making excess insulin, setting the stage for insulin resistance. \" . storage. Excess insulin production leads to insulin resistance throughout the body. as well as erratic or no energy from food. \". The normal nervous Adrenaline resistance system signal to simulate fat cell metabolism is no longer received by fat cells. This causes weight gain, especially in the abdominal area, The brain's contin u a l attempts to sti m u late meta bolism by using adrenal ine, cou pled with the excessive adrena line being released as a box continues result of the constant stresses of daily l ife, can result in constant

7 The i nternal enviro n ment 1 37 Box 7.3 (continued) resistance of adrenaline, insu lin and leptin, TNF-a and inter­ leukin-6 (IL-6) act as the 'glue' that keeps them locked, producing the type of weight most associated with cardiovascular disease and a proinflammatory state. They note that d u ring insu l i n resistance, reproductive organ cancer. TNF-a tends to match exaggerated insu lin levels, directly pro­ pelling insu l i n resistance. Additional ly, ' Excess TNFa contributes This fat, in turn, produces more l eptin, thereby keeping the vicious to cancer, heart d isease, arthritis and n u merous other problems cycle intact. by provoking a highly i nflammatory state of a ffairs'. • Interleukin-6 (IL-6) is a proinfl a m matory cytokine involved in The leptin-hormonal interface acute phase response to tra u ma as well as the inflammatory With leptin receptor sites on the l iver, kidney, ovary, adi pose and response to stress. If stress is chronic, a general systemic infla m­ gastrointestinal tract, one can readily see that leptin's interface is mation can result. Yudkin et a l (2000) suggest that I L-6, I L- 1 and broad reaching. It has a d i rect effect on a n umber of other hormones TNF-n are intimately involved in the progression of atherosclerosis. and cytokines as well as the ones discussed a bove. As the reader They further note 'circulating I L-6 sti m u la tes the considers the fol lowing l ist that only touches on a few of the many hypothalam ic-pituita ry-adrenal (HPA) axis, activation of which is other chemica l s evident in this cascade, it should be borne in mind associated with central obesity, hypertension and insu l i n resist­ that each of these chemicals plays a vital role in health, as well as a a nce. Thus we propose a role for I L-6 in the pathogenesis of coro­ significant position in the development of disease. There are no 'bad nary heart d isease (CHO) t h rough a com bination of a utocrine, g uys' or 'good guys' when in a ppropriate levels. They form a team, paracri ne and endocrine mechanisms. Long-chain omega-3 oi ls, where their significance is based on interdependence and interface. such as found in fish oil, borage oil and flax oil, can significantly reduce TN F-n and I L-6 (Simopoulos 2002), thereby reducing the • Adiponectin (AD), which is involved in regu lation of g lucose and inflammatory immune signals that lock i n leptin-resistance metabolism of fatty acid, appears to help reduce insu l i n resist­ overeating. ance (Ou ntas et al 2004). Levels of this hormone are i nversely • Nuclear factor kappa-B (N FIi:B) is activated at times of stress to correlated with body mass index, being decreased in obesity and d i rect cells as to which proteins to m a ke to meet the immediate in type 2 diabetes (Duntas et a l 2004). Adiponectin seems to act needs of the stressful situation. Without this d i rection, cells as a n antiinflammatory molecul e (Fantuzzi 2005) and appears to would be h ig hly intolerant of any type of stress. It also responds be controlled, at least in part, by leptin (H uypens 2007). I n to cytokines, free rad icals, ultraviolet rad iation and infections by research that studied obese children and adolescents with a bacteria or vi ruses. Excessive production of NF,.,:B has been linked chronic, general ized inflam matory reaction, AD appeared to be to cancer, autoim m une d isease and septic shock, among other the best indicator of metabolic syndrome, and thus the higher cond itions. In the majority of serious health problems excessive risks of cardiovascula r d isease associated with it (Gilard i n i et al levels of N FIi:B and TN F-a coexist, such as that noted in a lcohol­ 2006). l iver inflam mation (Hill et a l 2000). Silymarin (milk th istle herb) can directly lower the production of N Ft.:B (Manna et al 1 999). • Cortisol, an antiinflammatory stress-related hormone secreted by • Ghrelin, a hormone stim u lated by N PY and agouti, and produced the adrenal cortex, is norm a l ly highest in the morning and lowest in the stomach (and to some degree in the small intestine, pan­ at night, d u ring sleep. I t is released i n response to stress and has creas and thyroid), rises when blood l evels of leptin and glucose a n effect on blood sugar levels and blood pressure, and can sig­ fa l l , sti m u lating a ppetite. It u sually increases before m eals and nificantly influence metabol ism. In non-stressfu l circu mstances, decreases after food is consumed (Shi iya et a l 2002). I t signals both cortisol and leptin fol low a 24-hour rhythm that is genera l ly the anterior pituitary gland to secrete g rowth hormone and per­ reciproca l, with one rising as the other fa lls (inverse circadian forms antagon istically to leptin when they are both functioning rhythm) (Leal-Cerro et al 2001 ). The peak for l eptin is between norm a l ly. A recent study (Taheri et a l 2004) showed that elevated midnight and 2 a.m. and for cortisol is about 6 a.m. Cortisol is not g h relin levels were observed in participants who had short sleep under the control of leptin. However, it can, as part of the stress d u ration. The a uthors concluded that this is l ikely to 'increase response, 'turn up the volu me' of leptin in fat cells (N ishiyama a ppetite, possibly explaining the increased BMI observed with et a l 2000), leading to l eptin resistance and a l l that goes with it. short sleep d u ration. I n Western societies, where chronic sleep restriction is com mon and food is widely ava i lable, changes in • Neuropeptide y (N PY), a neurotransmitter found in the b rain and a ppetite regulatory hormones with sleep curta ilment may con­ autonomic system, plays a significant role in energy balance. tribute to obesity: Being the key h unger signal in the brain, it is countered by leptin when both are working normally. As leptin rises, N PY fa l ls, signal­ Other consequences of this hormonal cascade i ng satiety. I n leptin resistance, N PY levels stay elevated, resulting Other studies have shown significant i m pact of leptin, g h relin and in a lack of satisfaction with food, constant hunger and resultant many of these chemica l factors. Only a few a re mentioned here to overeating. N PY interfaces with dopam ine, serotonin, agouti, h is­ show the d iverse i nfl uences that have been revealed. tamine and other chemicals in varying ways that have a high impact on this craving cycle. • W u rst et al (2006) note that 'elevated leptin levels a re associated with a lcohol craving in patients suffering from a lcoholism. • Agouti, a gene signal that is regulated by ca lcium i ntake, pro­ Furthermore, g h relin l evels seem to be increased d u ring a lcohol motes appetite. It amplifies the production of leptin (Claycombe abstinence'. Kiefer et a l (200 1 ) indicate that a lcohol craving may et al 2000) and blocks the ability of the hypothalamus to sense it, be mod u lated by leptin and verified a positive association thereby sti m ulating food i ntake while a lso slowing down metabo­ between elevated leptin plasma levels and craving for alcohol l ism. Richards 8: Richards (2005) a g ree and suggest that: 'Extra d u ring early alcohol withdrawal. It is possible that by lowering calci u m intake can cool off this agouti gene, and thereby remove leptin levels to norma l, recovery from alcohol addiction might be a stressor that enha nces the production of excessive leptin and supported. rei nforces h igher levels of N PY causing food cravings: box continues • Tumor necrosis factor-alpha (TNF-a) is produced by the WAT (Sewter et al 1 999) and, when at normal levels, is a powerful cancer-destroying com pound as well as a major reg u lator in the inverse relationship between adiponectin and leptin (Huypens 2007). Richards 8: Richards (2005) explain that in the triad of

1 38 CLI N I CA L A P PL I CAT I O N OF N E U RO M U SC U LA R T EC H N I Q U E S : TH E U P P E R B O DY [ Box 7 .3 (� n ued) leptin resistance might affect bone density is u nclear, but is cer­ ta inly of interest. ATHEROSCLEROSIS • Gonzalez et al (2006) has investigated the mechanism(s) by which leptin contributes to mammary tumor (MT) development Plaque rupturelthrombosis and found that leptin increases the expression of vascular endothelial g rowth factor (VEGF), its receptor (VEGF-R2) a nd CARDIOVASCULAR cyclin D 1 . EVENTS Although all the mechanism(s) by which leptin con tributes to Fig u re 7.4 Pathophysiology of atherosclerotic card iovascu l a r tumor development are unknown, it appears leptin stimulates an d isease i n t h e metabolic synd rome. BP, blood pressure; H DL, h i g h increase in cell numbers, and the expression af VEGFNEGF-R2. d ensity l i poprote i n ; TG, triglyceride. D rawn after Rei l ly Et Rader Together, these results provide further evidence suggesting leptin is (2003). a MTgrowth-promoting factor. The inhibition of leptin signaling could serve as a potential adjuvant therapy for treatmen t of breast • Women have a pproximately 40% higher leptin levels than men, cancer and/or provide a new target for the designing strategies to which is thought to be hormonally related rather than d riven by prevent MT development. fat composition differences (Saad et a I 1 997). Interesting ly, an inverse relationship between serum testosterone and leptin in • Beltowski (2005) notes: men was reported by Luu kkaa et al ( 1 998), who concluded that testosterone has a suppressive effect on leptin production. Ainslie Leptin exerts many potentially atherogenic effects such as induction et al (2001 ) suggest that estrogen deficiency contributes to of endothelial dysfunction [affecting fat cells that line the heart and impaired central leptin sensitivity a n d overproduction of NPY. blood and lymphatic vessels}, stimulation ofinflammatory reaction, Further research is needed to clarify the degree to wh ich leptin oxidative stress, decrease in paraoxonase activity [thereby promot­ may be involved in infertility, menopausal symptoms and sexua l ing oxidation oflow-density lipoprotein (LOL)}, platelet aggregation, dysfu nction. migration, hypertrophy and proliferation ofvascularsmooth muscle cells. ... Several clinical studies have demonstrated that high leptin • Ya mauchi et a l (200 1 ) suggest that 'circu lating leptin might play level predicts acute cardiovascular events, restenosis after coronary a physiological role in maintaining bone mass as well as better angioplasty, and cerebral stroke independently of traditional risk bone qual ity'. Thomas et al (200 1 ) expand this to propose that 'fat factors. In addition, plasma leptin correlates with markers ofsub­ mass, leptin, and insu lin appear to be highly interrelated in terms clinical atherosclerosissuch as carotid artery intima-media thick­ of their potential effects on the skeleton, wh erea? estrogen ness and coronary artery calcifications. appears to be an independent predictor of BM D'. To what degree Note that thickening of the i ntima and media (layers of the vessel wal ls) of the common and internal carotid artery are visible with high-resolution u ltrasonography. • Watkins Et Maier (2002) have investigated the development and perpetuation of both peri pheral and central neuropathic pain. They note: From animal models ofboth traumatic and inflammatory neu­ ropathies, a consistent picture is beginning to emerge for immune involvement in pain. . . . The importance ofpro-inflammatory cytokines (TNF, IL- I, IL-6) in the creation and maintenance of pathological pain is the most consistent finding across models. ... [they} have been repeatedly implicated in demyelination and degeneration ofperipheral nerves, increases in sensory afferent excitability. and creation ofneuropathic pain. . . . Taken together, numerous lines ofevidence suggest that prolonged localized release of proinflammatory cytokines may occur in body regions affected by CRPS [chronic regianal pain syndrome]. Although clearly speCUlative, ifthis does occur, it suggests that such perse­ verative proinflammatory cytokine release could, by stimulation of sensory nerves, be a contributing factor to the maintenance of centrol sensitization observed in CRPS patients. Since TNF-o: is excreted by WAT, any factors that increase WAT, such as leptin o r insulin resistance, may well be implicated in this p rofi l e. • Banks et al (2004) have addressed the role of triglycerides in inducing leptin resistance and suggest that triglycerides may impair the transport of leptin across the blood-brain barrier (BBB) in both obesity and starvation. 'Here, we show that m i l k, for which fats a re 980/0 trig lycerides, immed iately inhibited leptin box continues

7 The i nternal enviro nment 139 transport as assessed with in vivo, in vitro, and in situ models of the stomach and easily decrease overal l caloric consumption. the BBB. Fat-free m i l k and intra l ipid, a sou rce of vegetable • Rule 4 : Eat a breakfast containing protein. This helps set the hor­ trig lycerides, were without effect: • Banks & Farrell (2003) documented leptin transport rates across monal cycles for the day and for the night. CompromiSing this the BBB in obese a nd thin m ice, an important factor in leptin can have hormonal effects d u ring the day and into the nig ht, d is­ resistance. In regards to the obese mice, they report: 'With mod­ turbing sleep. Weigle et al (2005) have shown that an i ncrease in erate reductions in body weight, the leptin transport rate dietary protein from 15 to 30% of energy produced a sign ificant increased to levels seen in thin m ice. These results show that the weight loss, presumably 'mediated by increased central nervous obesity-related defects in leptin transport across the BBB are system leptin sensitivity'. acquired and that they can be reversed with reductions in body • Rule 5 : Reduce the overall amount ofcarbohydrates eaten. U n l ess weight induced by either fasting or leptin treatment: They note one is a l ready on a low carbohydrate plan, cha nces a re too many that short-term fasting resulted in a good outcome and that carbohydrates are routinely consumed. Regarding carbohydrate longer fasts inhibit the leptin transporter. influences, Garg et al ( 1 992) note: 'Compared with the low­ carbohydrate diet, the high-carbohydrate diet caused a 27.5% Ti ming is everything increase in plasma trig lycerides and a similar i ncrease in [very low Th is d iscussion is a simpl istic overview of the complex metabolic density lipoprotein) cholesterol levels; it a lso reduced levels of distu rbances that lead to, or w h ich a re i nvolved in, a plethora of HDL cholesterol by 1 1 Ofo: chronic d iseases. It does not begin to cover the m u ltitude of chemica l interactions involved. The chemica l imbalances have Exercise has been shown to im prove insulin resistance (Boga rdus consequences that are far-reaching, both in daily l ife and in the fu l l et a l 1 984). Additionally, the fol lowing provides evidence that life cycle. To fu lly u nravel t h e complexities is overwhel ming and to va rious forms of nutritional support m i g ht be beneficial. develop a recuperative plan might appear a l most impossible. Not so, say Richards & Richards (2005). • Melatonin, a hormone produced a t night that has a n effect on sleep, has been shown to decrease circulating leptin levels (Kus Timing is everything. Our bodies areeither regulated by a harmonic et a l 2004). I t can be taken at bedtime by those who a re symphony. a heavy-metal tune, orsomewhere in between. Biological experiencing sleep d isturbance or who have other evidence of rhythms are the guiding force of human metabolism and natural bal­ leptin resistance. ance. They are the essence underlying communication in the body. A person either feels in sync or out ofbalance. . . . Hormones are impor­ • A diet rich in fish oil (omega-3 fatty acids) has been shown to tan t communication signals in the body that seek to coordinate the reduce plasma leptin (Beltowski 2005). body's ability to stay in sync and meet the extra demands or pressures. As a person begins to have problems, the body is thrown out ofsync, • Carnosine (a combination of the amino acids beta-al a n i ne and and timing is off. h istidine), a non-protein com ponent of brain tissue, is found i n relatively high amou nts i n m uscle; it helps t o protect t h e brain In Mastering Leptin, Richards & Richards (2005) define a simple plan cel ls from the damage of stress (Kang et al 2002) and has been to help rega in normal leptin levels and, thereby, balance the shown to stop the effects of excess adrena line on the kidneys hormonal cascade discussed above. Although this plan may not be (Niijima et a l 2002). ideal for everyone, it is presented here for the majority who w i l l benefit from i t s use. The fou ndation of their p l a n conta ins five • Calcium helps to decrease agouti, a close associate of N PY, w hich cardinal rules, which they emphasize are a l l necessary to fol low. together block thyroid function, even though common thyroid Brea king a ny of the ru les can lead to a setback for one or severa l tests might appear normal (Fekete et al 2002). days. They are summarized as: • Vitamin 0 is a powerful inh ibitor of leptin secretion (Menendez • Rule 1 : Never eat after din ner, not even a snack or g l a ss of wine et al 2001 ) as well as a cofactor in calcium absorption. or j uice. Al low 1 1 - 1 2 hours between d inner and breakfast. Generally finish eating dinner at least 3 hours before bed. This • Pantethine (a coenzyme form of vita m i n B51. a fat metabolizer, ru le is designed to al low leptin, melatonin, cortisol and other can help lower LDL cholesterol, raise HDL cholesterol and lower chemicals to balance during the night. Night-eating syndrome triglycerides (McRae 2005). individuals have abnormal hormonal patterns apparently associ­ ated with nocturnal eating (Geliebter 2001). • Conjugated l inoleic acid (CLA), one of the most vigorously researched n utrients in the world, shows considerable evidence in • Rule 2 : Eat three meals a day. Allow 5-6 hours between meals. its ability to reduce cancer, hardening of the a rteries and body Timing is crucial so that insulin levels can drop, glucagon (pro­ fat, and prevent the development of diabetes (Belury 2002). d uced by the l iver) can rise and fat metabolism ca n kick in. If this occurs a couple of hours before more food is eaten, fats stores • Acetyl-L-ca rnitine (ALC) before bed encourages the hypothalamus can be util ized until the next food is eaten. Snacking between to sti mulate growth hormone during sleep. Research has a lso meals sends the insulin back up and fat stores remain untapped. shown ALC to be effective in reducing leptin resistance (lsso et a l Snacks are, therefore, to be avoided. Portions are estimated as 2002) and i n helping t h e bra i n sense t h e true a mount o f leptin. protein the size of the palm of the hand, carbohydrates to match that amount, and vegetables as desired except peas, carrots and Richards & Richards clearly point to the importance of lifestyle corn, which are taken in moderation. management. In addition to suggesting adequate sleep, good food choices and fol lowing the five ca rdinal rules, they a lso note: • Rule 3: Do not eat large meals. Eat slowly and, if overweight, always try to finish a meal when slightly less than full. Eating slowly al lows Stress is the wild card variable that magnifies any weakness in a per­ time for hormonal signals to reach the brain before overeating son's brain chemistry. Ifthe weakness is on the dopamine side, crav­ occurs. Smal ler meals allow for better digestion, do not overstretch ings are for calorie-laden and salty foods. The subconscious goal is to have an energetic feeling of metabolic drive. If the weakness is on the serotonin side, cravings are for carbohydrates. The subconscious goal is to have a relaxed state of feelings or more pleasant mood. When the overall natural balance in a person's life is not good, then there is much less tolerance forstress. A person is likely to experience the cravings based on brain chemistry imbalance triggering stress box continues

1 40 C L I N ICAL A P P L I CAT I O N O F N E U R O M U S C U LA R T EC H N I Q U E S : T H E U P P E R B O DY Box 7.3 (conti n ued) hormonal resistances, a simple th ree square meals a day might not only be beneficial to weight reduction, but a lso to ca rdiovascular eating, in turn causing a disruption in fuel utilization. This leads to and pancreatic health. leptin resistance, insulin resistance, and adrenaline resistance, a path ofincreased fatigue and bad moods no matter what is eaten. The authors of this text suggest that this newly brea king information on endocrinology is of crucial benefit to manual As is evident with this host of information (that only begins to tap practitioners since many of their patients undoubtedly present with into the latest data on hormonal influences), biochemistry can be these conditions. The fu l l role that these inflammatory processes significantly infl uenced not only by what we eat, but also by when play in myofascial pain, chronic fatigue, fibromya lgia and trigger and how much we eat, the proportions or fats, carbohydrates and point formation remains to be clearly defined, yet, hopeful ly, their proteins, our exercise habits and our sleep patterns. For those who relevance in chronic pain syndromes is apparent. have already developed a thick waist and potentially the triad of Box 7.4 Key concepts i n the relation between adipose result of marked or repetitive muscular tension dragging on the attachment and the evolution of periosteal pain tissue and infl a m mation (Fantuzzi 2005) points (Lewit 1992) • the joint, which can become restricted and overapproxi­ Cells mated, to the extent that osteoarthritic changes can result • Macrophages a re a normal component of adipose tissue from the repeated microtrauma of shortened and unbal­ • Obesity is associated with increased numbers of macrophages anced soft tissue structures • overapproximation of joint surfaces due to soft tissue in adipose tissue shortening, leading to uneven wear and tear, as for exam­ • Obesity is associated with the presence of activated ple when the tensor fasciae latae structure shortens and crowds both the hip and lateral knee joint structures macrophages in adipose tissue • neural irritation, which can be produced spinally or along • There is a cross-ta l k between adipocytes and lymphocytes in the course of the nerve, as a result of chronic muscular con­ tractions. These can involve disc, facet and general spinal lymph nodes mechanical faults (Korr 1976), fascial arcades (Simons et al 1999, p. 733) and bone-related enclosures, such as the Molecules greater sciatic foremen (Travel! & Simons 1992, p. 191) • Adipocytes produce many factors mod ulating immunity and • variations in pain threshold - possibly to do with percep­ tion (Melzack 1 983) and memory (Sandklihler 2000) - inflam mation which can make all these factors more or less significant • Leptin exerts mostly proinflammatory and i m m u ne-potentiat­ and obvious. ing effects The research into tendon-related pain discussed earlier • Adi ponectin exerts mostly antiinflammatory effects should not lead to an assumption that inflammation is not an important issue in many of these areas of pain. On the Diseases contrary, there are, for example, high levels of inflammatory • Low adiponectin levels in type 2 diabetes a re a possible link to cytokines (inflammatory mediators such as prostaglandins and leukotrienes) in facet joint tissue associated with insulin resistance degenerative lumbar spinal disorders. • Obesity seems to be associated with asthma, but the mecha­ • Inflammatory cytokines have a higher concentration rate in nism is unknown lumbar spinal canal stenosis than in lumbar disc herniation. • Severa l conditions are associated with a ltered adi pokine levels, • Research findings suggest that inflammatory cytokines in but the sign ificance of this observation is unclear degenerated facet joints may also relate to the cause of pain in degenerative lumbar disorders (Igarashi et aI 2004). tissue and inflammation. The endeavor to build a founda­ tion of understanding of the enormous role these and other There is a progression of normal muscle to one that is in hormones play in health and homeostasis may very wel! painful, chronic distress (Baldry 2005) commonly involving: result in a practical paradigm shift in the treatment of myofascial syndromes and other conditions . • initial or repetitive trauma (strain or excessive use) leading to MUSCLES, JO INTS AND PAI N • release of numerous chemical mediators capable of acti­ Where pain exists in tense musculature (in the absence of vating, sensitizing or arousing nociceptors, such as kinins, other pathology), Barlow (1959) suggests that it results from: proinflammatory and antiinflammatory cytokines, • the muscle itself through some noxious metabolic product ('factor P') (Lewis 1942) or an interference in blood circula­ tion due to spasm, resulting in relative ischemia (see below for more recent research into pain generation concepts) • the muscular insertion into the periosteum, such as that caused by an actual lifting of the periosteal tissue as a

7 The internal environment 1 41 prostanoids, lipooxygenases, neurotrophins and other understanding and modifying the processes involved, which growth factors, neuropeptides, nitric oxide, histamine, might include: serotonin, proteases, excitatory amino acids, adrenergic amines and opioids (Coutaux et al 2005) • altering sources of external biomechanical overload (pos­ • subsequent sensitization of A-delta and C (Group I V ) ture, habits of use in da ily life including work and leisure sensory nerve fibers with involvement o f the brain (lim­ activities, etc.) bic system and the frontal lobe). Pain signals are gener­ ated by peripheral sensory organs (nociceptors), which • cognition and modification of abnormal illness behavior are endings of small-diameter nerve fibers responsive to • improvement of normal function via self-applied the tissue environment. strengthening, stretching, fitness training, balance and These chemical mediators may act in combination, or at a coordination-enhancing strategies. given time in the inflammatory process, to produce subtle changes that result in increased sensitivity and pain (hyper­ As these patterns are appropriately being addressed, func­ algesia or allodynia). tional rehabilitation of the motor system, through appropri­ ate treatment and exercise, should be ongoing. When We can see in the following example a manifestation of reading the sections of this book that focus most on the an adaptive response by the nervous system, as well as the treatment aspects of neuromuscular pa in and dysfunction, mind of the individual, to a long-standing stressor, pain. In the reader should bear in mind the essential need for the this sequence pain is associated with a spinal strain but the person's active participation in the recovery process. model holds true elsewhere. These features lie at the heart of the transition from an acute to a chronic pain syndrome. REFLEX EFFECTS OF MUSCULAR PAIN • Adaptation occurs to a painful event involving altered Liebenson ( 1996) highlights the fact that muscular pain pro­ biomechanics. duces not just increased stiffness and tension but inhibition as well. He quotes from research that has demonstrated: • The demands on local functional capacity may be exceeded by such changes, leading to tissue fatigue, as the • in acute back pain, localized areas of the multifidus mus­ processes of hysteresis and creep evolve (see Chapter 1 on cle show signs of unilateral wasting in association with a fascia, for details of these phenomena). single dysfunctional vertebral segment (Hides et a1 1994) • In order to maintain accurate proprioception, type I and • as a result of chronic back pain, type I multifidus fibers type II afferents are stimulated. (postural) hypertrophy on the symptomatic side, while type 1I fibers (phasic) atrophy bilaterally (Stokes et al • The firing from muscle spindle, joint mechanoreceptor 1992) and Golgi tendon organ afferents helps the adapting tis­ sues avoid failure. • reciprocal inhibition occurs in the abdominal muscles when erector spinae are excessively 'stiff ' and they • These receptors are adaptive and therefore cease to dis­ become spontaneously stronger again (without rehabili­ charge if the adaptation process continues for a lengthy tation exercises) when the overactive erector spinae are period . stretched (Janda 1 978) • Ultimately, however, as in all stress situations, adaptive • myofascial trigger points in upper trapeZius inhibit the capacity is exhausted and a painful, chronic situation functional activity of the lower trapezius muscle slowly emerges. (Headley 1993) •. At this stage, inflammatory processes commence (see more • deltoid inhibition occurs as a result of myofascial trigger detail on inflammation in this chapter), as does stimulation point activity in the supraspinatus muscle (Simons 1993). of non-adaptive types III and IV nociceptive afferents lead­ ing to protective mechanisms that immobilize the area . McPartland et al (1997) hypothesize a cycle initiated by chronic somatic dysfunction, resulting in muscle atrophy • Immobilization is appropriate in acute injury situations and reduced proprioceptive output from atrophied suboc­ but can become memorized and influence the evolution cipital muscles. toward chronic behavior. Barker et al (2004) show evidence of coex isting atrophy • Biomechanical insult (trauma, overuse, strain), biochem­ of psoas and multifidus and an association between ical alterations (inflammation), facilitation of pain­ decrease in the cross-sectional analysis of multifidus and related pathways, and, finally, neuromuscular duration of symptoms . adaptation evolves. If continued biomechanical insult is not avoided, abnormal illness behavior develops, and Danneels et al (2004) showed evidence that only the mul­ deconditioning occurs. Inadequate neuromuscular adap­ tifidus (and only at the lower endplate of L4) was found to tation and chronic pain with central nervous system be statistically smaller than other lower back muscles in involvement (corticalization) can result . cross-section analysis. They suggest that: Rehabilitation from the adverse effects of such a pain . . . atrophy may be the consequence of LBP [Lower back pain]: cycle requires the individual to be actively involved in after the onset ofpain and possible long-loop inhibition ofthe

1 42 CLI N I CA L A PP L I CATI O N OF N EU RO M USCU LA R T E C H N I QU ES : T H E U PP E R B O DY multifidus a combination ofreflex inhibition and substitution In this form of dysfunction, the joint (segment of the spine) patterns of the trunk muscles may work together and could is seen to be the maintaining factor in a soft tissue manifes­ cause a selective atrophy of the multifidus. Since this muscle tation of pain. However, Dvorak & Dvorak also see altered is considered important for lumbar segmental stability, the mechanics in a vertebral unit as causing 'reflexogenic phenomenon of atrophy may be a reason for the high recur­ pathological change of the soft tissue, the most important rence rate ofLBP being the \"myotendinoses\", which can be identified by pal­ pation'. Many experts, including Lewit, cited above, would SOURCE OF PAIN argue that soft tissue changes frequently precede the altered vertebral states, as a result perhaps of poor posture and pat­ IS IT REFLEX OR LOCAL? terns of overuse. 'It is in chronic pain patients that mobility of fascia is frequently impaired; in such cases, joint (spinal) Palpation of an area that the person reports to be painful mobility is as a rule restored by moving the fascia. It also will produce increased sensitivity or tenderness if the pain follows that unless we restore normal mobility of the fascia, is originating from that area . If, however, palpation pro­ muscle and joint dysfunction will recur' (Lewit 1996). duces no such increase in sensitivity, then the chances are strong that the pain is being referred from elsewhere. The reader may reflect on the fact that, in these examples, the same phenomena are being observed (pain and joint But where is it coming from? If the pain is indeed coming dysfunction) and quite different interpretations as to cause from a myofascial trigger point, knowledge of the distribu­ and effect are being ascribed. Do the soft tissues determine tion patterns of probable trigger point target zones (see and maintain the joint restriction and the pain that follows? Chapter 6) can allow for a swift focusing on suitable sites to Or does the joint restriction produce and maintain the soft search for an offending trigger. Unless the pattern is a result tissue changes and the pain that follows? Or are both ele­ of combinations of several trigger point referrals, the pat­ ments (joint and soft tissue) so intermeshed in their func­ terns distributed by trigger points are fairly predictable and tional roles that this separation is artificial? The authors of well documented by research (Simons et aI 1999). this text take the view, based on clinical experience, that the soft tissues hold the primary role most of the time, but not RADICULAR PAIN always. The discomfort could, however, be a radicular symptom ARE THE REFLEXES NORMAL? WHAT IS THE coming from the spine. 'When pain is being referred into a limb due to a spinal problem, the greater the pain distally SOURCE OF THE PAIN? from the source, the greater the index of difficulty in apply­ ing quickly successful treatment', suggests Grieve (1984) . The referred pain may not be from either a trigger or the spine itself. Kellgren (1938, 1939) showed that: 'The superfi­ Dvorak & Dvorak (1984) state: 'For patients with acute cial fascia of the back, the spinous processes and the radicular syndrome there is little diagnostic difficulty, supraspinous ligaments induce local pain upon stimula­ which is not the case for patients with chronic back pain. tion, while stimulation of the superficial portions of the Some differentiation for further therapy is especially impor­ interspinous ligaments and the superficial muscles results tant, although not always simple.' Noting that a mixed clin­ in a diffused (more widespread) type of pain'. ical picture is common, they then say: 'when testing for the radicular syndrome, particular attention is to be paid to the Clearly ligaments and fascia must therefore also be motor disturbances and the deep tendon reflexes. When considered as sources of referred pain and this is made examining sensory radicular disorders, the attention should clearer by Brugger (1960), who describes a number of syn­ be towards the algesias. ' dromes in which altered arthromuscular components pro­ duce reflexogenic pain. These syndromes are attributed to Dvorak & Dvorak have charted a multitude of what they painfully stimulated tissues (origins of tendons, joint cap­ term 'spondylogenic reflexes' that derive primarily from sules and so on) producing pain in muscles, te.ndons and intervertebral joints. The palpated changes are character­ overlying skin. ized as: As an example, irritation and increased senSitivity in the ... painful swellings, tender upon pressure and detachable region of the sternum, clavicles and rib attachments to the with palpation, located in the musculofascial tissue in topo­ sternum, through occupa tional or postural strain, will cause graphically well-defined sites. The average size varies from pain in the intercostal muscles, scalenes, sternocleidomas­ 0.5 cm to 1 cm and the main characteristic is the absolutely toid, pectoralis major and cervical muscles. The increased timed and qualitative linkage to the extent ofthefunctionally tone in these muscles and the resultant stresses that they abnormal position (segmental dysfunction). As long as a dis­ produce may lead to spondylogenic problems in the cervi­ turbance exists, the zones oj irritation can be identified, yet cal region, with further spread of symptoms. Overall, this disappear immediately after the removal of the disturbance. syndrome can produce chronic pain in the neck, head, chest wall, arm and hand (even mimicking heart disease) (Brugger 1960).

7 The internal environment 1 43 DIFFERENTIATING BETWEEN SOFT TISSUE AND Examples .of a joint assessment involving compression are described by Blower & Griffin ( 1984) for sacroiliac dys­ J OINT PAIN function. They showed that pressure applied over the lower half of the sacrwn or over the anterior superior iliac spines Several simple screening tests have been proposed by were diagnostic of sacroiliac problems (possibly indicating Kaltenborn (1980). ankylosing spondylitis) if pain was produced in the sacnun and buttocks. Soft tissue dysfunction would not produce 1. Does passive stretching (traction) of the painful area painful responses with this type of compression test. increase the level of pain? If so, it is probably of soft tis­ sue origin (extraarticular). Note: Lwnbar pain is not significant if it occurs on sacral pressure, as this action causes movement of the lumbosacral 2. Does compression of the painful area increase the pain? If joint, as well as some motion throughout the whole lumbar so, it is probably of joint origin (intraarticular) involving spine. tissues belonging to that anatomic jOint. NEUROPATHIC PAIN (Co rd e rre 1 9 9 3 , M e rskey 1 9 8 8 , 3. If active (controlled by the person) movement in one direc­ Nachemson 1 992) tion produces pain (and/or is restricted), while passive (controlled by the operator) movement in the opposite Neuropathic pain is defined as a chronic pain condition that direction also produces pain (and/or is restricted), the con­ occurs or persists after a primary lesion or dysfunction of tractile tissues (muscle, ligament, etc.) are implicated. the peripheral or central nervous system. Traumatic injury Resisted movement tests, the principles of which are of peripheral nerves also increases the excitability of noci­ described below, can confirm the accuracy of this proposal. ceptors in and around nerve trunks and involves neuro­ genic inflammation at the nerve terminals. As a result 4. If active movement and passive movement in the same nociceptors and injured nerve fibers release excitatory neu­ direction produce pain (and/or restriction), joint dys­ rotransmitters at their synaptic terminals (such as L-gluta­ function is probable. This can be confirmed by use of mate) and substances that trigger cellular changes in the traction and compression (and gliding) of the joint. central nervous system (Zieglgansberger et al 2005). This is what is currently thought to be an aspect of what happens Resisted tests are used to assess both strength of, and in the local environment of the pain receptors involved in painful responses to, muscle contraction. These tests neuropathic pain. involve producing a maximal contraction of the suspected muscle while the joint is kept immobile, somewhere near Liebenson (2006) has commented on neuropathic pain the middle of its range. No joint motion should be allowed and central sensitization in the spectrum of musculoskeletal to occur during the contraction. If it is painful, contractile dysfunction. He notes: tissues are implicated in the painful problem. Pain casts a long shadow in the nervous system. Pain can be These resisted tests are done after test 3 (described 'learned' in the nervous system so that it is maintained inde­ above) to confirm a soft tissue dysfunction rather than a pendent of injury, pathology, expectations, or dysfunction. joint involvement. Before performing the resisted test, it is Such pain is called neuropathic and is an important unrec­ wise to perform the compression test (2 above) to clear any ognized dimension of the chronic problem. Failure to appre­ suspicion of joint involvement. ciate when pain has become conditioned will lead to an overemphasis on coincidental structural pathology, func­ Cyriax (1962) adds to this the following thoughts. tional deficits, and psychosocialfactors. • If, on resisted testing, the muscle seems strong and is also Neuropathic pain is centrally maintained and therefore painful, there is no more than a minor lesion/dysfunc­ does not require peripheral sources of painful irritation or tion of the muscle or its tendon. injury. Typically, it arises as a result of a prolonged, inten­ sive bombardment from peripheral nociceptive pathways. • If it is weak and painful, there is a more serious However, because ofcentral sensitization, altered processing lesion/dysfunction of the muscle or tendon. of input from secondary neurons (after exiting the dorsal horn) occurs so that pain can be experienced in the absence • If it is weak and painless, there may be a neurological of peripheral injury, inflammation, or irritation. The most lesion or the tendon has ruptured. obvious example of this is a phantom limb pain where the painful source is not present, but the central pathways that • A normal muscle tests strong and pain free. carried nociceptive information are not inhibited, so that even non-noxious stimuli are interrupted as painful! It is suggested that all these statements be tested on condi­ tions of known etiology. The concept of sensitization and facilitation has been dis­ cussed in Chapter 6. A similar, but more complex mechanism In many instances soft tissue dysfunction accompanies is proposed by those researchers and clinicians who advocate (precedes or follows) joint dysfunction. Joint involvement is less likely in the early stages of soft tissue dysfunction than (for example) in the chronic stages of muscle shortening. It is hard to conceive of joint conditions, acute or chronic, without accompanying soft tissue involvement. The tests described above will offer a strong indication as to whether the major involvement in such a situation is of soft tissue or osseous in nature.

1 44 C LI N I CA L A P P LICAT I O N O F N EU RO M U S C U LA R T EC H N I Q U E S : T H E U PP E R B O DY the view tha t neuropathic pain plays a major part in many N EUROTOX I C ELE MENTS AND chronic pain syndromes. This involves increased sensitiza­ tion of nerve cells as a cause of persistent regional pain and NEUROPAT H I C PAI N associated symptoms and is seen to explain the pain of many people who may have previously had a psychological As the name implies, a neurotoxin adversely affects the func­ etiology ascribed to their conditions (Corderre 1 993, tional or structural components of the nervous system, acting Merskey 1988, Nachemson 1992). specifically on neurons, either at a local or a systemic level. Obvious examples of neurotoxins found in nature are those Both of the authors of this text have been consulted by used in defense, such as the venom of bees, scorpions, spiders, patients whose symptoms have been labeled 'psychosomatic' snakes and some sea life. A common effect is swelling, extreme in origin but who have been successfully treated by attention pain and often a rapid onset of paralysis. Other effects on the to musculoskeletal (i.e. structural or functional) dysfunction nervous system from neurotoxins can include depolarization responsible for the presenting symptoms. The ascribing of a of nerve and muscle fibers due to increased sodium ion per­ psychological etiology to a biomechanical problem is not nec­ meability of the excitable cell membrane, and alteration of essarily inaccurate, but it may be, and the neuropathic normal activity of membrane potentials and ion chanen ls. The hypothesis offers a differen t view on chronic pain that could, Office of Technology Assessment, U.S. Congress (1990) in a different setting, a ttract a psychological diagnosis. reports: 'Neurotoxic substances play a significant causal role in the development of some neurological disorders, and may It is believed, by the proponents of this perspective, that be particularly harmful to the developing brains of children.' following biomechanical stress (overuse, etc.), a sustained degree of normaL neuroLogicaL input (from types III and IV Neurotoxins can be exogenous (taken in from the environ­ mechanoreceptors, for example) to the dorsal hom neurons ment) or endogenous (produced within the body). can sensitize the nerve cells and decrease their threshold to Exogenous neurotoxi.ns include gases (e.g. carbon monox­ pain. Once sensitized, a situation of aLLodynia evolves, in ide), metals (mercury, lead, arsenic, etc.), liquids (ethanol) which the pain threshold is lowered so that stimuli that or a variety of solids, the inunedi a te effects of all of these would previously not be perceived as painful, such as nor­ being largely dependent on dosage. For instance, ethanol mal physiological movement or light touch, become painful. (alcohol) in low dosage usually produces the mild neuro­ If this occurs the affected areas will have become hyperaLgesic. toxic effect of inebriation. However, a large dose can be fatal and it is well documented tha t problems related to alcohol As part of this process, which involves central misprocess­ use over time exert an enormous toll on the lives and com­ ing of received information, there may be a degree of cuta­ munities of many nations (WHO 2004). neous hypoesthesia in which, for example, pinprick sensations will be noted as reduced. The neuropathic pain pattern will One of the most harmful environmentally acquired neu­ usually also include poor motor control, malcoordination rotoxins is mercury. Clarkson et al (2003) explain that and balance control ('Can you stand on one leg with eyes although mercury is present in thermometers, batteries, flu­ closed for 10 seconds?'). There is also a strong likelihood of orescent light bulbs and some industrial projects, the gen­ referred pain from associa ted myofascial trigger points. eral population is primarily exposed to it by three sources: fish consumption, dental amalgams and vaccines. Liquid Another condition that may be considered in this context is metallic mercury, methyl mercury and ethyl mercury all complex regional pain syndrome (CRPS), which may develop carry risks of poisoning through exposure and some carry after limb tra uma, and that is characterized by pain, sen­ risks with removal as well. They note that: sory-motor and autonomic symptoms. A major mechanism for CRPS symptoms involves trauma-rela ted cytokine release, Exposure to mercury from dental amalgams and fish CO/1- exaggerated neurogenic inflanunation, sympathetically main­ sumption has been a concern for decades, but the possible tained pain and cortical reorganization in response to chronic risk associated with thimerosal [in vaccinations] is a much pain - a process known as neuropLasticity (Birklein 2005) . newer concern. Thesefears have been heightened by a recent recommendation by the EnvironmentaL Protection Agency In all of these neuropa thic conditions palpation of super­ (EPA) that the allowabLe or safe daily intake of methyl mer­ ficial tissues will demonstrate the classic increase in sympa­ cury be reducedfrom 0.5 J.lg ofmercury per kilogram ofbody thetic activity described in Chap ter 6, including greater weight per day, the threshold established by the World superficial hydrosis, reduced skin elasticity and tighter Health Organization in 1978 (WHO 1978) to 0.1 J.lg ofmer­ adherence of skin to underlying fascia . The reader may cury per kilogram per day (EPA 2001). reflect on the degree of Similarity and overlap between this neuropathic view of chronic pain etiology and the osteo­ The question as to just how much damage has been done to pathic facilitation concept, discussed in Chapter 6. There is developing infan t brains and nervous systems via the inclu­ also a degree of similarity with Nimmo's (Cohen & Gibbons sion of mercury (Hg) based preservatives in some vaccina­ 1 998, Schneider et al 2001 ) and Travell & Rinzler's (1952) tion products remains for future research to establish. While views on the way myofascial trigger points evolve, as well this text is not the place for a deep analysis of this question, a as chiropractic subluxa tion concepts and research evidence few key points can be found in Box 7.5. They may be relevant rela ting to facet (zygapophyseal) pain sources (Bogduk & Twomey 1991, Igarashi et aI 2004).

7 The i nternal enviro n ment 1 45 Box 7.5 Mercury - is there a 'safe' level? Lorscheider et al ( 1 995) voice a strong opinion question ing the safety of amalgam fi l l ings: Mercury is a h i g h ly reactive, neurotoxic metal with widely recognized toxic properties at high dose, i ncluding paresthesias, During the past decade medical research has demonstrated that cerebellar ataxia, dysarthria and constriction of the visual fields {mercury] Hg is continuously released as vaporinto mouth air; then it (Needleman 2006). Medicine is aware of its lethal effects and has is inhaled, absorbed into body tissues, oxidized to ionic Hg, and finally eliminated it as a disinfectant and antibiotic, and has abolished its covalently bound to cell proteins. Animal and human experiments use in contact lens solutions. It bioaccumulates in the envi ronment demonstrate that the uptake, tissue distribution, and excretion of and is disposed of as a biohazardous waste. I n recent years, the amalgam Hg is significan t, and that dental amalgam is the major American Public Hea l th Association, the Ca l ifornia Medical con tributing source to Hg body burden in humans. Current research Association, and Hea l th Care Without Harm have a l l cal led for the on the pathophysiological effects of amalgam Hg has focused upon e20lim01i)n.ation. of putting any mercu ry in the human body (Watson the immune system, renalsystem, oral and intestinal bacteria, repro­ ductive system, and the central neNOUS system. Research evidence Mercu ry is an element that cycles through several different does not support the notion of amalgam safety. chemica l forms throughout the environment, exposing l iving organisms to its potential effects in the process. Although there may After a thorough d iscussion of research and pathophysiology be a latent period of weeks or months after exposure, paresthesias of associated with mercury toxicity, they conclude: the circumoral a rea a nd hands and feet, visu a l -field constriction and ataxia a re some of the symptoms reported in adults who have had Although human experimental evidence is incomplete at the present mercury exposure. Lorscheider et a l ( 1 995) d isclose that the brain i s time, the recent medical research findings presented herein strongly t h e primary target tissue; however, reproductive, i m m u n e , renal, ora l contradict the unsubstantiated opinions pronounced by various den­ and intestinal bacteria may also be affected and reg ional destruction tal associations and related trade organizations, who offer assurances of neurons in the visual cortex and cerebellar g ranule cells may be of amalgam safety to dental personnel and their patients without revea led in neuropatholog ical exa mination. providing hard scien tific data, including animal, cellular and molecu­ lar evidence, to support their claims. Environmental exposure Modern industrial activity, especially fossi l fuel combustion and A word of caution in wa rranted to the reader who is driven by this waste incineration, is responsible for a n estimated threefold increase information to request immediate removal of all mercury-laden fillings. in environmental mercury levels in this century a lone (Bender Et The process of amalgam removal carries with it inherent risks of Williams 1 999). The major source of non-occu pational exposure is potentially generating substantially more mercury vapor than if the dietary intake of methyl mercu ry, with fish and seafood being the fillings were left alone. Significant protection of the patient (rubber main culprits because of their propensity to concentrate mercury dams, air tubes, etc.) during the removal process as well as chelation of from the water (Clarkson et al 2003). Through dietary intake and the mercury load prior to and after removal is required. It would be other sources, mercury is present at low concentrations in many practical to question the chronic pain patient regarding any dental tissues. procedures that may have exposed the patient to mercury vapor with in the year prior to the onset of chronic pain, particularly when the pain is Dental sources of unknown etiology. There is often a latent period of weeks or months Dental amalgam fillings are composed of a number of metals, between exposure and the onset of symptoms (Clarkson et al 2003). including silver, tin, copper and a trace a mount of zinc, m ixed with approximately 50% mercury. Since amalgam fi l l ings were first Vacci n e sou rces introduced, the assumed health risks of mercury have been a source Contributing to such exposures are pharmaceutical products of controversy a nd debate, often labeled as the 'amalgam wa rs'. Part including some vaccines that contain thiomersal (formerly and still of the controversy revolves around whether the degree of mercury commonly known i n t h e United States as thimerosa l), a mercury­ vapors produced by aging amalgam fil li ngs releases significant derived preservative in use since the 1 930s, which is composed of enough mercu ry to be a health risk. 49.6% mercury by weight in the form of ethyl mercury (Steuerwald et al 2000). Recogn izing that the inhaled dose from a malgams might be sma l l a n d that t h e potential ra mifications o f mercury exposure from dental 'No danger' from vaccine sources message sou rces a re inconclusive, Clarkson et a l (2003) point out: One study (Pichichero et a l 2002) suggests that administration of vaccines conta ining thiomersa l does not seem to raise blood Nevertheless, amalgam fillings are the chiefsource ofexposure concentrations of mercury above safe va l ues in infa nts, claiming that to mercury vapor in the general population (WHO 1990). Brain, ethyl mercury seems to be e l i m i nated from blood rapidly, via the blood, and urinary concentrations correlate with the number stools, after admi nistration of thiomersa l i n vaccines. The a u thors of ofamalgom surfaces present. It has been estimated that this text q uestion whether there is a ny 'safe' level of ethyl m e rcury. 10 amalgam surfaces would raise urinary concentrations by 1 M ofmercury per liter. roughly doubling the background If 'safe' why has this prod uct been withdrawn? concentrations (Kingman et al 1998). Higher urinary concentrations Although thiomersal has recently been removed from most children's are found in persons who chew a great deal. ... The removal of vaccines, it is still present in flu vaccines g iven to pregnant women, amalgam fillings can also cause temporary elevations in blood the elderly and to ch i l d ren in developing cou ntries. I t is h a rd to concentrations (Molin et al 1990), since the process transiently imagine why its use should have been curta i led if there is 'no increases the amount ofmercury vapor inhaled. What are the health danger'. Experts maintain that preservative-free vaccines a re not risks from such exposures? Cases ofpoisoning from inhalation ofmer­ always a n option and that a preservative should a lways be used in cury vapor have been recognized for centuries (Ramazzini 1 964). multidose vials to prevent bacterial and fu ngal contam ination, and Severe cases are characterized by a triad of intentional tremor. gin­ multidose vials a re as yet the only option in many parts of the givitis, and erethism. Erethism consists ofbizarre behavior such as developing world (Pless Et Risher 2000). excessive shyness and even aggression. box continues

1 46 C L I N I CA L A P PLICAT I O N O F N E U RO M U S C U LA R T E C H N I QU ES : T H E U P P E R B O DY Possible n utritional protection treatment has been to apply chelating agents in an attempt to As noted, environ mental methyl mercury has been shown to be extricate the mercury. Another option is utilization of the body's own highly neurotoxic, especially to the developing bra i n (James et al detoxification mechanisms - for example. the endogenous enteric 2005). Because mercury has a high affin ity for thiol (su lfhydryl (SH)) bacteria. High-dose probiotics have been suggested as a n adjuva n t g roups, the thiol-conta ining a ntioxida nt, g lutathione (GSH), provides for detoxification protocols w i t h an emphasis on u s e in autistics the major i ntracel lular defense against mercury-induced (Brudnak 2002). neu rotoxicity. Pretreatment with the n utrients 1 00 M g l u tathione or N-acetylcysteine (NAC) (but not methioni ne) has been shown to Caution regarding use of probiotics when mercu ry is produce a significant increase in intrace l l u l a r GSH. present Stud ies suggest that since ora l bacteria. yeast (such as Candida) and Possible probiotic protection? probiotics a l l methylate mercu ry. any contact between them should Autism is a developmental disease characterized by a spectrum of be m i n im ized. This may explain some adverse reactions reported by symptoms ra nging from decreased verbal skil l s and social parents a n d patients who have used probiotics to correct dysbiosis or withdrawal , to repetitive behavior and violent outbursts. I t has been fungal overgrowth (Heintze et a 1 1 983. Rowland et a1 1 975. Yannai suggested that the etiology of autism may involve multiple loci, and et a l 1 99 1 ) . It is therefore suggested that i t is important to attempt many different theories exist (Blaxi l l et a l 2004). One theory is that to e l iminate mercury first. before high-dose use of probiotics. via envi ronmentally acquired mercury may be the cul prit since it is heavy metal detoxification. chelation a nd/or carefully protected capable of exerting neurolog ical effects on the brain. A standard amalgam replacement. in relation to a patient's history and /or symptom picture and small amounts in food. William Pardridge, MD (1979) illus­ should be considered as potentially part of the chronic pain trated that ' . . . dietary glutamate does not enter the brain profile. because the blood-brain barrier maintains a transport sys­ tem for acidic amino acids, such as glutamate, to effectively Endogenous neurotoxins include those tha t at normal exclude circulating glutamate from the brain'. Pardridge levels may act as an excitatory neurotransmitter, but when also showed that the levels of brain glutamate do not rise or in excess can cause tissue damage. For instance, when con­ fall with changes in plasma glutamate levels. centration levels of glutama te, a primary neurotransmitter in the brain, reach critical levels, the neuron kills i tself by a Additionally, the American College of Allergy, Asthma process called apoptosis. This process of excitotoxicity, as it is and Immunology (ACAAI 1991), after reviewing the litera­ aptly named, may also be involved in stroke, traumatic ture on MSG, food allergy and safety, concluded that MSG is not an allergen and reaffirmed its safety as a food ingre­ brain injury and diseases of the CNS, such as multiple scle­ dient. More recently, Simon (2000) conducted a well­ rosis, Alzheimer disease, fibromyalgia, Parkinson's disease, designed, double-blind, placebo-controlled study of 65 and Huntington's disease (Kim et al 2002, Smith et aI 200l ). subjects with chronic urticaria. None of the subjects exhib­ i ted positive reactions to doses of 2.5 g of MSG. Glutamate (glu tamic acid) is one of the 20 amino acids that make up proteins and is a non-essential amino acid, since it In the face of continued public interest and consistent can be syntheSized in the body. It is a key molecule in cellular denial by researchers that MSG is the cause of food-related metabolism as the most abundant excita tory neurotransmitter symptoms, the FDA contracted the Federation of American in the nervous system and is believed to be involved in cogni­ Societies for Experimental Biology (FASEB), a body of inde­ tive functions such as learning and memory. In appropriate pendent scientists dedicated to safety concerns, to review amounts and present in a wide variety of foods, glutamic acid available scientific data surrounding MSG. FASEB (1995) is responsible for the fifth human sense of taste, umami conclusions follow, extracted from the U .S. Food and Drug (Box 7.6), which accompanies sweet, sour, salty and bitter Administration (FDA) website in regards to monosodium (Halpern 2002). In excess, glutamic acid triggers excitotoxicity, glutamate (MSG). which can cause neuronal damage and, eventually, cell death. The agency asked FASEB to address 18 questions dealing In i ts free form, i.e. when it is not bound to another amino with: acid, such as in protein, it has a flavor-enhancing effect in foods. Monosodium glutamate (MSG), the sodium salt of 1 . the possible role of MSG in eliciting MSG symptom glutamic acid, is commonly used in the food industry to complex enhance flavor. It has long been suspect by consumers as the cause of a bizarre array of symptoms, often reported 2. the possible role of dietary glutamates in forming brain after consumption of oriental food, hence the name lesions and damaging nerve cells in humans 'Chinese restaurant syndrome'. Since MSG is a product tha t is widely consumed throughout the world, i t has been the 3. underlying conditions that may predispose a person to focus of much research for many years. adverse effectsfrom MSG However, research does not point to MSG as a culprit in 4. the amount consumed and otherfactors that may affect causing a neurotoxic effect in the brain when consumed in a person's response to MSG 5. the quality of scientific data and previous safety reviews.

7 The internal environment 1 47 . .. . . ' <i . 4 , '. , .,.. The fol lowing letter, titled What's in a Name?Are MSG and Umami individual tastants a re not described as del icious. In isolation, the the Same? was written by Bruce Halpern (2002) while associated taste of neither NaCI nor MSG is delicious. In similar fashion, with the Departments of Psychology and Neurobiology and Behavior, naturally occu rring tastants, such as potassium ch loride or Uris Hall, Cornell University. phosphate salts, amino acids l ike g lycine, a rg i nine and alanine, and nucleotides such as adenosine 5'-monophosphate, taken alone, are The Japanese word \"umami\" has a long past. It was a l ready in use not described as delicious. However, these same tastants, com bined during the Edo period (Tokugawa Shogunate) of Ja panese h istory, in appropriate proportions with NaCI and g l utamic acid (or MSG), which ended in 1 868 (Mason, 1 993). In Japanese, \"umami\" often yield the flavor of boi led crab (Konosu et a/ 1 987), and may be connotes a cogn itive category (Ya maguchi and Ninomiya, 1 998) of characterized as delicious, perhaps with reports of \"umami\". taste, or perhaps flavor, with defin itions that include del iciousness, flavor, rel ish, gusto and zest (I noue, 1 983). In effect, the Ja panese References word \"umami\" can denote a rea lly good taste of somethi ng-a taste • Backhouse, A.E. ( 1 978) Japanese taste terms. Unpublished doc­ or flavor that is an especia lly appropriate exemplar of the flavor of that thing (Backhouse, 1978). toral dissertation, University of Edinburgh, Edinburgh. • Guiry, M.s. (2002) Seaweed site. http ://www.seaweed.ie/ Recog nition of a role for sod ium salts of g l utamic acid in flavor has a shorter h istory. In 1 909 Dr Kikunae I keda reported defa u ltfriday.html (cited August 24). the isolation of meta l lic salts of g lutamic acid from a brown kelp • Halpern, B.P. ( 1 997) Psychophysics of taste. I n Beauchamp, G.K. [tang le, genus Laminaria (Guiry, 2002), \"konbu\" or \"kombu\" in Japanese] commonly used in Japanese cuisine, and recog nition that and Ba rtoshu k, L.M. (edsl. Tasting and Smelling. Handbook of the (mono) sod i u m sa lt of g l u tamic acid imparted a fa m i l iar and Perception and Cognition, 2nd edn. San Diego, CA, Academic highly desirable flavor to foods (I keda, 1 909; M u rata et a/ 1 985). Press, pp. 77-1 23. Dr Ikeda noted that the flavor coul d be described as del icious, n ice or • Halpern, B.P. (2000) Gl utamate and the flavor of foods. J. Nutrit., pa latable (\"umai\" in Japa nese). I t seemed to h i m to be related to his impressions when he ate meat or bonito (dried marine fish flakes; 1 30,9 1 OS -91 4S. \"katsuobushi\" in Japa nese), and was based u pon a taste that differed • Halpern, B.P. (2002) Taste. In Pash ler, H. (series ed.) and Yantis, S. from genera l ly recogn ized basic tastes. He accepted the suggestion that this taste could tempora rily be ca lled \"umami\". In a later (vol. ed.l. Stevens' Handbook of Experimental Psychology, Vol. 1 . publ ication, i n Engl ish (Ikeda, 1 91 2), he chose to use the description Sensation and Perception, 3 rd edn. New York, W i ley, pp. 653-690. \"g lutamate taste\". • Ikeda, K. ( 1 909) New seasonings. J. Tokyo Chem. Soc., 30,820-836 The taste of monosod ium glutamate (MSG) by itself does not in [in Japanese]. any sense represent deliciousness. Instead, it is often described as • Ikeda, K. ( 1 9 1 2) On the taste of the salt of g lutamic acid. In unpleasant. and as bitter, salty or soapy (Yamaguchi, 1 998; Ha lpern, 2000, 2002). However, when MSG is added in low concentrations to Proceedings of the 8th I n ternational Congress in Applied a ppropriate foods, the flavor, pleasantness and acceptabil ity of the Chemistry, vol. 38, p. 1 47 . food increases (Hal pern, 2000). These differences illustrate the • I noue, J . ( 1 983) I noue's S m a l l e r Japanese-Engl ish Dictionary. d istinction between the taste of a single tasta nt and the effects Tokyo, Tuttle. upon flavor of tasta nts in a food (Lawless, 1 996). • Konosu, S., Yamaguchi, K. and Hayash i, T. ( 1 987) Role of extrac­ tive components of boi led crab in prod ucing the characteristic MSG is a tastant, as is sa lt (NaCI). We ca n study transduction flavor. I n Kawamura, Y. and Kare, M.R. (eds), Uma m i : a Basic mechanisms for NaCI or MSG, and peripheral and central gustatory Taste. New York, Dekker, pp. 23 5-253. neural responses, in a particu lar species, while recog nizing that the • Lawless, H.T. ( 1 996) Flavor. I n Friedman, M.P. and Ca rterette, E.C. gustatory mechanisms and responses discovered in one species may (edsl. Cog nitive Ecology. San Diego, CA, Academic Press, be q u i te different from those in a nother (Hal pern, 2002). For human pp. 325-380. responses to NaCl, we ta lk about sal t taste, or saltiness. I n similar • Mason, P. (1 993) History of Japanese Art. New York, Abrams. fashion, for MSG i t is appropriate to speak of g l u ta mate taste, a s • M u rata K., Shimosato, S., I nayama, Y., Ifuka, H., Nagam u ra, S., Dr I keda did (I keda, 1 9 1 2). Flavor, derived from human descriptions Suzuki, H., Suzuki, M. and Shiga, M. ( 1 985) Ten Japa nese g reat of foods and beverages, depends upon mixtures of tastants (and inventors. http://www.jpo.go.jp/shoukaie/judaie.htm (cited July odorants) but represents aspects that emerge from the array of 1 2, 2002). tastants and odorants, and their matrix (Halpern, 1 997). In general, • Yamaguchi, S. ( 1 998) Basic properties of u m a m i and its effects on food flavor. Food Rev. I nt., 1 4, 1 39- 1 76. • Yamaguchi, S., and Ninomiya, K. ( 1 998) What is umami? Food Rev. Int., 1 4, 1 23-1 38. FASEB held a 2-day meeting and convened an expert panel • numbness in the back of the neck, radiating to the arms that thoroughly reviewed all the available scientific litera­ and back ture on this issue. • tingling, warmth and weakness in the face, temples, FASEB concluded the following key findings: upper back, neck and arms An unknown percentage of the population may react to • facial pressure or tightness MSG and develop MSG symptom complex, a condition • chest pain characterized by one or more of thefollowing symptoms: • headache • nausea • burning sensation in the back of the neck, forearms and • rapid heartbeat chest • bronchospasm (difif culty breathing) in MSG-intolerant people with asthma

1 48 C L I N I CA L A PP L I C AT I O N O F N E U RO M U SC U LA R T E C H N I Q U E S : T H E U PP E R B O DY [ • drowsiness plasma levels of aspartate (aspartic acid) (Stegink et al • weakness. 1987a,b). Although the health hazards of aspartame use in • In otherwise healthy MSG-intolerant people, the MSG the general population remain controversial, the health haz­ ards to those people born with phenylketonuria, a genetic symptom complex tends to occur within one hour after inability to metabolize one of aspartame's components, the eating 3 grams or more of MSG on an empty stomach or amino acid phenylalanine, are indisputable. U.s. Food and without other food. A typical serving of glutamate­ Drug Administration (2004) documents that: 'High levels of treated food contains less than 0.5 grams of MSG. A [phenylalanine] in body fluids can cause brain damage: reaction is most likely if the MSG is eaten in a large Further research performed by Walton et al (1993) showed quantity or in a liquid, such as a clear soup. that ingestion of aspartame created a significant difference • Severe, poorly controlled asthma may be a predisposing in the number and severity of symptoms in individuals medical conditionfor MSG symptom complex. with mood disorders. Aspartame is abundantly used in a • No evidence exists to suggest that dietary MSG or glu­ variety of products, including a profusion of 'low calorie' tamate contributes to Alzheimer's disease, Huntington's and 'sugar-free' i tems (including medica tions) that might chorea, amyotrophic lateral sclerosis, AIDS dementia be consumed several times each day by people of all ages. complex, or any other long-term or chronic diseases. These products may be easily overlooked as the source of a • No evidence exists to suggest that dietary MSG causes bizarre array of symptoms. brain lesions or damages nerve cells in humans. • The level of vitamin B6 in a person 's body plays a role in Neurotoxicity can result from medical procedures such glutamate metabolism, and the possible impact of mar­ as chemotherapy, radiation treatment and drug therapies ginal 86 intake should be considered infuture research. (Mullenix et a1 1994, Shimoyama et al 2003). Heavy metals, • There is no scientific evidence that the levels of gluta­ such as arsenic, lead and mercury, are at the top of the list of mate in hydrolyzed proteins cause adverse effects or that toxic substances with the U.S. Department of Health and other manufactured glutamate has effects difef rent from Human Services (ATSDR 2005). The neurological effects of glutamate normallyfound infoods. exposure to pesticides (Davies 1990), industrial and/or cleaning solvents (Juntunen 1993), certain foods and food They further consider ingredient listing on packaging. Each addi tives, cosmetics (Bridges 1 999) and some naturally ingredient used to manufacture a food must be identified occurring substances can all produce neurotoxic effects. by its name on the ingredient list. Currently, when MSG is Wha t is particularly challenging to the clinician is tha t added to a food in manufacturing, it must be identified as symptoms may appear immediately after exposure, such as 'monosodium glutamate'. Consumers commonly use the alcoholic beverages or paint fumes, while others produce term MSG when referring to glutamate, although there are long-term effects tha t appear over weeks or even years and several forms of free glutama te. For this reason, the FDA may be irreversible. In some cases the level or exposure considers it 'misleading' to label a food as 'No MSG' or 'No time may be critical, with some substances only becoming Added MSG' if the food contains sources of free glutama tes, neurotoxic in certain doses or over periods of time. such as hydrolyzed protein or hydrolyzed soy. Symptoms may include headache, cognitive and behavioral problems, limb weakness or numbness, loss of memory, Although research does not point to MSG as a health haz­ vision and /or intellect, and sexual dysfunction. ard, it is clear from this excerpt tha t it can be problema tic to certain individuals. The authors of this tex t suggest tha t the Multiple chemical sensitivity (MCS), also known by a mul­ range and degree of symptoms commonly reported by con­ titude of names such as '20th century syndrome', 'environ­ sumers be influenced by other factors associated with the mental illness', 'sick building syndrome' and 'idiopathic consumption of MSG, such as alcohol intake, preexisting envirorunental intolerance', is a syndrome evidenced by a per­ levels of B6, sodium, potassium and other nutrient levels, son's inability to tolerate even low-level chemical exposure. and general body hydration. Since flavoring effects can also be achieved by adding ingredients rich in glutamate and DeHart (1998) shares his insights: other umami substances, avoidance of MSG by those who find it problematic (although not easy when dining out) is This newly named clinical phenomenon has three defining suggested. MSG has a number of legal names used in label­ characteristics: (1) it is an acquired disorder with multiple ing of packaged foods. It is suggested tha t the interested recurrent symptoms; (2) it is associated with diverse envi­ reader perform an Internet search to become familiar with ronmental factors tolerated by the majority of other people; the various sources and names of MSG. and (3) it is not explained by any known medical, psychiatric or psychologic disorder. . . . Symptoms of multiple chemical Neurotoxicity may also result from the use of a well­ sensitivity include, but are not limited to, headache, loss of known artificial sweetener, aspartame (also known as consciousness, poor memory, palpitations, shortness of Nutrasweet), which is broken down into phenylalanine and breath, dizziness, joint pain andfatigue. These symptoms did aspartic acid, an excitotoxin. Unlike aspartic acid-containing not originate with multiple chemical sensitivity. They were proteins in foods, aspartame is metabolized and absorbed common to a diseasefrequently encountered in the previous very qu ickly. It is known tha t aspartame can spike blood century-neurasthenia. Thus, the constellation ofsymptoms

7 The internal environment 1 49 described for multiple chemical sensitivity is not new and Hyperventilation is the extreme of a breathing pattern perhaps this is not a new phenomenon. disorder, although respiratory alkalosis commonly occurs in individuals who have not reached that extreme. Since prog­ MCS etiology is hotly debated, with some professions esterone is a respiratory accelerator, this condition seems to believing tha t it is a physical illness, some as a chemical affect mainly females (Loeppky et al 2001), particularly (irritant or toxic) injury and others convinced tha t it is psy­ those in the postovulation stages of the menstrual cycle chosomatic. Although the patients are unsure of the ca use, when progesterone levels rise (Damas-Mora et aI 1980). what is usual ly presented is that exposure to chemical irri­ tants precipitates the (sometimes disabling) symptoms. Foster et al (2001 ) point out that respiratory alkalosis is an Regardless of the pa thogenesis of this condition, avoidance extremely common and complicated problem affecting vir­ of further exposure to irritants is a number one priority. tually every organ system in the body, producing as it does multiple metabolic abnormalities, including changes in Magill & Suruda (1998) note: potassium, phosphate and calcium balance, and the devel­ opment of a mild lactic acidosis. There are many cardiac Several theories have been advanced to explain the calise of effects of respira tory alkalosis, including tachycardia and MCS, including allergy, toxic efef cts and neurobiologic sensi­ ventricular and atrial arrhythmias, as well as ischemic and tization. There is insufficient scientific evidence to confirm a non-ischemic chest pain. In the gastrointestinal system there relationship between any of these possible causes and symp­ are changes in perfusion, motility and electrolyte handling. toms. Patients with MCS have high rates ofdepression, anx­ iety and somatoform disorders, but it is unclear if a causal Due to the circulatory changes induced by alkalosis relationship or merely an association exists between MCS (including constriction of blood vessels and the Bohr effect) and psychiatric problems. Physicians should compassionately body tissues tend to become ischemic and this encourages evaluate and carefor patients who have this distressing con­ increased sensitization, as well as the evolution of trigger dition, while avoiding the use of unproven, expensive or points (Mogyros et a1 1997, Seyal et aI 1998). potentially harmful tests and treatments. The first goal of management is to establish an effective physician-patient DECONDITIONING AND UNBALANCED relationship. The patient's efforts to return to work and to a normal social life should be encouraged and supported. BREATHING EFFECTS OF pH CHANGES TH ROUGH Because the deconditioned indiv idual relies more on anaer­ obic metabolism for energy supply, such changes are far B REATHING more likely to occur in people who are out of cond ition, who do not perform regular aerobic exercise. In such indi­ Despite being critical in healthcare in general, and in body­ v iduals respiratory alkalosis leads to an accumula tion of work in particular, the biochemical and pathophysiological incompletely oxidized products of metabolism, due to the ramifications of the widespread feature of disturbed breath­ activa tion of anaerobic energy pathways (Nixon & ing are not generally appreciated, recognized or evaluated Andrews 1996). The products of the anaerobic pathway are by healthcare providers. Probably the most important bio­ acids, such as lactic acid and pyruvic acid (Fried 1987) . This chemical change deriving from disturbed breathing pat­ leads to accumulation of lactate in muscle cells and the terns results from al tered blood pH, the effects of which bloodstream, and a reduction in pH, which encourages range from reduced pain thresholds to altered motor con­ bicarbonate retention, resulting in increased CO2 produc­ trol, sympathetic arousal, disturbed balance, reduced oxy­ tion, a more rapid breathing rate and perpetuation of the genation of tissues and smooth muscle constriction with adaptation cycle described above. potential influence on fascial tone (Hastreite et al 2001), as well as overuse of key muscles associated with respiration Outcomes of deconditioning include: (Chaitow 2004). 1. loss of muscle mass AL KALOSIS AND THE BOHR EFFECT 2. decreased ability to use energy substra tes efficiently 3. decreased neuromuscular transmission An increased brea thing rate, such as occurs in obvious hyper­ 4. decreased efficiency in muscle fiber recrui tment with ventilation, can increase the rate of carbon dioxide (C02) exhalation so that it exceeds the rate of its accumulation in indications of disruption of normal motor control being the tissues. This produces respira tory alkalosis, which is apparent (Wittink & Michel 2002). characterized by the decrease in CO2 and an increase in pH (above the norm of 7.4) (Pryor & Prasad 2002). Nixon & Andrews (1996) have summarized the emerging symptoms resulting from overbrea trung in a deconditioned Due to the Bohr effect, respiratory alkalosis induces individual as follows: 'Muscular aching at low levels of smooth muscle (and therefore vascular) constriction, thereby effort; restlessness and heightened sympathetic activity; decreasing blood flow, as well as inhibiting transfer of oxygen increased neuronal sensitivity and constriction of smooth from hemoglobin to tissue cells (Pryor & Prasad 2002). muscle tubes (e.g. vascular, and gastrointestinal) can accompany the basic symptom of inability to make and sus­ tain normal levels of effort.'

1 50 CLI N I CA L APPLI CATI O N O F N E U RO M USCULAR TEC H N I QU E S : T H E U PPER B O DY These adaptation sequences may lead to physiologically The correction of this conunon pH imbalance is breathing unsustainable adaptive changes that result in chronic retraining, as discussed in Volume 2, Chapter 7, and myofascial and joint problems, almost inevitably including Chapter 14 of this text. trigger point development. CAFFEINE 1 1\\1 I TS VARIOUS FORMS As Litchfield (2003) explainS: Caffeine, as found in tea, coffee, cola, chocolate and in many Hypocapnia is the result of over-breathing behavior, the mis­ medications, may very well be the most widely used (and match of breathing rate and depth. Its consequence is an accepted) neuroactive drug in the world, being consumed increased level ofpH, or respiratory alkalosis, which may have by a majority of the adult popula tion in most countries. It profound immediate and long-tenn effects that trigger, exacer­ does not appear to in troduce any major social problems, bate, and/or cause a wide variety ofemotional, perceptual, cog­ and may, in fact, improve social interactions. Unlike smok­ nitive, attention, behavioral, and physical deficits that may ing, it does not appear to directly pollute the environment seriously impact health and performance. Although thefunda­ of others and has not been definitively linked to a potential mental importance of CO2 in body chemistry regulation is health hazard of the consumer (as have both alcohol and common knowledge to any pulmonary or acid-base physiolo­ smoking). Evidence shows that tea and coffee may, in fact, gist, it remains virtually unknown by most healthcare practi­ have significant health benefits (Box 7.7). tioners, health educators, breathing trainers, and laypeople. Caffeine in general has a bad press. Is this justified by research or d o Epidemiological research evidence presented by H igdon Et Frei potential benefits outweigh t h e possible ha rmful effects o f excessive (2006) suggests that: •...coffee consumption may help prevent stimulation deriving from caffeine intake? Or is the possible h a rm several chronic diseases. including type 2 diabetes mellitus. resulting from consumption of caffeine-rich beverages (tea. coffee. Parkinson's d isease and liver d isease (cirrhosis a nd hepatocellular cola. chocolate) more related to the oils. added sugar a nd/or carcinoma)'. They caution. however. that: a rtificial sweetening? Some groups, including people with hypertension, children, adoles­ Not all a nswers a re clear as yet. but since - apart from water - cents. and the elderly. may be more vulnerable to the adverse effects tea and coffee consumption represents the g reatest source of l i q u id of caffeine. In addition, currently available evidence suggests that it may be prudent for pregnant women to limit coffee consumption to 3 i ntake for most people it is important for practitioners to have as cups/dayproviding no more than 300 mg/day of caffeine to exclude clear an overview as possible. any increased probability ofspontaneous abortion or impaired fetal growth. Siddi q u i et a l (2006) confirm the vast intake of tea. and clarify some key points: ·Tea. next to water. is the most widely consumed Prevention of chronic d isease by tea beverage in the world. Depending u pon the level of fermentation. tea Zhu et al (2006) state the case for tea as fol lows: can be categorized into three types: g reen (u nfermented). oolong (pa rti a l ly fermented). and black (highly to fu l ly fermented). In During the period 1982-2002, 691 research papers related to tea and genera l . g reen tea has been found to be superior to black and oolong health have been published in 290 Chinesejournals. These studies tea in terms of antioxidant and hea lth promoting benefits: Herbal showed that tea and tea constituents have various biological activi­ teas that contai n no caffeine are not considered in this section. ties and suggested that tea drinking might be beneficial to human health. Tea has potential in the prevention or adjuvant treatment of General advice and cautions regarding caffeine several diseases including cancer, cardiovascular diseases and obesity. inta ke Detai led m u ltid iscipli nary research on the effect of tea. and the Caffeine is probably the most freq uently ingested pha rmacologica l ly associated tea polyphenols. has led to major advances on the underlying mechanisms. active substance in the world. It is found in common beverages In most stud ies. g reen and black tea have similar effects. (coffee. tea. soft drin ks). in prod ucts containing cocoa or chocolate. including the fol lowing. and in med ications. The possibility that caffeine ingestion adversely • Tea polyphenols a re powerful antioxidants that may play a role in lowering the oxidation of LDL cholesterol. with a consequent affects human health was investigated based on reviews of decreased risk of heart disease. and also diminish the formation of oxidized metabol ites of DNA. with an associated lower risk of (pri marily) publ ished human studies obtained through a specific types of cancer - for exam ple. involving the prostate. Tea and tea polyphenols selectively induce Phase I and Phase I I comprehensive l iterature search. Based on the data reviewed. it was metabolic enzymes that increase the formation and excretion of detoxified metabol ites of carcinogens. Tea a lso lowers the rate of concluded that for the healthy adult population. moderate daily cell replication and thus the growth and development of neo­ plasms (Siddiqui et al 2006). caffeine intake at a dose level up to 400 mg (3-4 cups) per day. is box continues not associated with adverse effects such as general toxicity. cardiovascular effects. effects on bone status and calcium bala nce. changes in adult behavior. i ncreased incidence of cancer or effects on male fertility. The data also show that reproductive-aged women and child ren are 'at risk' subg roups who may req u i re specific advice on moderating their caffeine intake. Based on available evidence. it is suggested that reproductive-aged women shou l d consume no more than ,,;;300 mg caffeine (approximately 3 cups) per day while children shou l d consume no more than \";;2.5 mg/kg1 b. ody weight per day (1 cup equiva lent) (Nawrot et al 2003).

7 The internal environment 1 51 • Tea helpfully mod ifies the intestinal microflora, red ucing Hegarty et al (2000) stud ied a g roup of 1 2 56 women aged 65-76 undesirable bacteria and increasing beneficial bacteria l iving near Cambridge, U K, of whom 1 1 34 were tea drin kers. (Weisburger 1 999). Skeletal measurements were taken at the l u mbar spine, femoral neck, greater trocha nter a nd Ward's triangle. Tea d rinking was • The health influences of g reen tea are claimed to include highly associated with greater BMD at all sites, with the excep­ prevention of cancer, hypercholesterolemia, a rtherosclerosis, tion of the femora l n eck. The beneficial effect of tea on BMD Parkinson's disease, Alzheimer's disease and other aging­ occu rred i ndependent of factors such as the addition of m i lk, cof­ related diso rders. There is, however, some q u estion as to the fee d rinking, smoking or the use of hormone replacement therapy. bioavailability of its active polyphenolic catech ins, suggesting The tea drinkers overa l l had a 5% g reater mean BMD than non­ more research is requ i red to esta blish the true health benefits tea d ri n kers. The a uthors eq uate this difference with a 1 0-20% (Zaveri 2006). decl ine in fracture risk. • Tea polyphenols protect the nervous system agai nst lead toxicity, Other polyphenol sources including antioxidant effects (Zhao 2006). Other beverages and foods conta i n ing polyphenols, such dark chocolate and wi ne, have a lso been eva l uated for their possible • Anti-obesity i nfl uences: Green tea, green tea catech ins, and epi­ benefits on health and 'anti-aging' potential. Menat (2006) has gallocatechin gallate (EGCG) have been demonstrated in cell cul­ researched these substances and states: ture and animal models of obesity to reduce adipocyte d ifferentiation and proliferation, l ipogenesis, fat mass, body Polyphenols are a family ofmolecules whose antioxidant properties weight, fat absorption, plasma levels of triglycerides, free fatty are widely documented. Fruit and vegetables aside, three particular acids, cholesterol, glucose, insulin and leptin, as well as to types of food containing polyphenols in large quantities have demon­ i ncrease beta-oxidation and thermogenesis. Adipose tissue, l iver, strated theirprotective role for human health. Tea is known for its intestine, and skeletal muscle are target organs of g reen tea, preventative action, for both cardiovascular diseases and certain can­ mediating its a nti-obesity effects. Studies conducted with h u man cers. Many studies about wine and cocoa concern the diminution of subjects report reduced body weight a nd body fat, as wel l as the overall risk ofcardiovascular problems. The antioxidant power of i ncreased fat oxidation a nd thermogenesis and thereby confirm polyphenols lead us to believe that theyplay a role in age (especially findings in cell culture systems and animal models of obesity cerebral) preven tion, and retrospective studies on tea and wine have (Wolfram et al 2006). already begun ta confirm this. A regular and moderate consumption of these three food types help to gain synergy and efficiency without • It is suggested that the mechanisms whereby obesity is affected any side effects. Apart from the usual promotion ofhealthy nutrition by tea i nclude: 'the modu lations of energy bala nce, endocrine concerning proteins, 'good' fats and complex sugars, we can now systems, food i ntake, lipid and carbohydrate metabolism, the advise moderated consumption of wine, chocolate and tea. redox status, and activities of different types of cel ls (i.e. fat, liver, muscle, and beta-pancreatic cel ls)' (Kao et al 2006). • Reduced fracture risk: H i p fractures related to poor bone m ineral density (BMD) a re a significant cause of i l l ness in elderly women. These statements may seem out of place in the face of (Bak & Grobbee 1989), or perhaps simply the fact that it was seemingly contradictory reports (Papadopoulos 1993) not 'in moderation' (Tofler et al 2001) that creates ill effects. about the ill effects of caffeine consumption. Caffeine's use in cancer research and cell life has been discussed in a favor­ W HEN S H OU L D PAIN AND DYS FUNCTION able light (Bode & Dong 2007) and its use as a stimulant for BE LEFT ALONE? the sleep deprived is common. Rosmarin (1989) notes that attention has been focused on caffeine and coffee's relation­ Splinting (spasm) can occur as a defensive, protective, ship to coronary heart disease and its potential to induce involuntary phenomenon associated with trauma (fracture, cardiac arrhythmias, yet concludes that: 'Until more con­ for instance) or pathology (osteoporosis, secondary bone v incing evidence against coffee is compiled, it appears that, tumors, neurogenic influences, etc.) (Simons et al 1999). at least in moderate amounts in otherwise healthy persons, Splinting-type spasm commonly differs from more com­ coffee is a safe beverage.' So where is the problem with this mon forms of spasm because it releases when the tissues it widely consumed beverage? is protecting or immobilizing are placed at rest. When splinting is long term, secondary problems may arise in If we closely examine the ways by which caffeine is associated joints as a result (e.g. contractures) and bone (e.g. ingested, we might readily see some of the potential for health osteoporosis). Travell & Simons (1983) note that, 'Muscle­ concerns. Perhaps it is the fats associated with chocolate, the splinting pain is usually part of a complex process. cream and sugar in coffee and tea, and the inordinate amount Hemiplegic and brain-injured patients do identify pain that of sugar (or artificial sweeteners) in the colas that pose poten­ depends on muscle spasm'. They also note 'a degree of mas­ tially more health problems than the caffeine itself. If the seteric spasm which may develop to relieve strain in trigger freshly brewed coffee in moderation is not the problem, then points in its parallel muscle, the temporalis', which sug­ perhaps it is that which has sat in a pot on a low heat burner gests that spasm is sometimes a way of relieving overload for hours that may produce gastrointestinal irritation. elsewhere or repositioning a body part. Perhaps it is the Styrofoam cup in which it is served (Ohyama et al 2001), or whether it ran through a filter or was boiled

1 52 CLI N I CAL APPLICATI O N O F N E U RO M U SC U LA R TECH N IQ U E S : TH E U PPER BODY Travell & Simons (1983) also note a similar phenomenon he most aptly described, 'Pain is a more terrible lord of in low back pain. mankind than even death itself.' The patient who has suf­ fered for days in pain is desperate for relief. However, those In patients with low back pain and with tenderness to pal­ who have suffered for weeks, months or years have restruc­ pation ofthe paraspinal muscles, the superficial layer tended tured their lives, their habits and their outlook around that to show less than a normal amount of EMC activity until pain. If no psychological factors, no psychosocial impact the test movement became painful. Then these muscles and no need for psychological support exist for a chronic showed increased motor unit activity or 'splinting' . . . This pain patient, this would truly be the exception. Stress, observation fits the concept of normal muscles 'taking over' mood, coping skills, functional habits of use and beliefs (protective spasm) to unload and protect a parallel muscle about the future would likely have all been impacted by the that is the site ofsignificant trigger point activity. debilitating effects of chronic pain. Depression may result due to, or may be a causal factor in, chronic pain. Either Recognition of this sort of spasm in soft tissues is a matter of way, biochemical changes in the CNS may be the result and training and intuition. Whether a ttempts should be made to should be considered in a comprehensive treatment plan. release, or relieve, what appears to be protective spasm depends on understanding the reasons for its existence. If HOW IS ONE TO KNOW ? splinting is the resu lt of a cooperative a ttempt to unload a painful but not pathologically compromised structure, then Karel Lewi t (1992) suggests that, 'In doubtful cases the treatment is obviously appropriate to ease the cause of the physical and psychological components will be distin­ original need to protect and support. If, on the other hand, guished during the treatment, when repeated comparison spasm or splinting is indeed protecting the structure it sur­ of (changing) physical signs and the patient's own assess­ rounds (or supports) from movement and further (possibly) ment of them will provide objective criteria'. In the main, he serious damage, then it should clearly be left alone. suggests, if the pa tient is able to give a fairly preCise Experience alone can assist in differen tiating between this description and localization of his pain, we should be reluc­ sort of cooperative spasm and the board-like rigidity of tant to regard it as 'merely psychological'. spasm associated with, say, osteoporosis. It is safe to caution that if any doubt exists, the spasm should be left intact, In masked depression, Lewit suggests, the reported symp­ especially in the acute phase of recovery. toms may be of vertebral pain, p articularly involving the cer­ vical region, with associated muscle tension and 'cramped' Prolonged immobilization after tissue insult can, how­ posture. The practitioner may be alerted by abnormal ever, lead to scar tissue formation, formation of adhesions responses during the course of treatment to the fact that there and lowered fatigue tolerance (Liebenson 2006). During the may be something other than biomechanical causes of the remodeling phase, orientation of fibers can be influenced problem. The history should also provide clues, especially if along lines of imposed stress with appropriate movement. this is a 'thick file' individual, someone who has consulted It is therefore necessary to plan intervention at the earliest many people before yourself. In particular, Lewit notes that, acceptable stage or to refer for evaluation should joint, disc 'The most important symptom [associated with psychological or pathological conditions be suspected. distress] is disturbed sleep. Characteristically, the patient falls asleep normally but wakes within a few hours and CaIU10t get SOMATIZATION back to sleep'. It is entirely possible for musculoskeletal symptoms to If a masked depression is treated appropriately the verte­ represent an unconscious attempt by the person to entomb brogenic pain will clear up rapid ly, he states. Pain and dys­ their emotional distress. As noted in the segment on emo­ function can be masking major psychological distress. tion and musculoskeletal distress (see Chapter 4) and most Awareness of if, how and when to crossrefer should be part cogently expressed by Philip Latey (1996), pain and dys­ of the responsible practitioner 's skills base. function may have psychological distress as the root cause. The person may be somatizing this distress and presenting Becker (1996) informs us that somatizers may go years with apparently somatic problems. The earlier discussion without an adequate diagnosis, with misdiagnosis being: relating to neuropathic pain suggested that sometimes a misattribution occurs as to the cause of pain being 'psycho­ the inevitable precursor to prolonged and ineffective treat­ somatic'. This should not lead the practitioner to ignore the ment, and frequently to multiple and inappropriate chemi­ fact that some very real and intense somatic pain involves cal, electrical and imaging studies; inappropriate roots in the psyche of the individual. medications, including narcotics (which frequently com­ pound the problem); or, worse yet, to invasive procedures, It is also important to remember that psychological factors including surgical intervention. may have played a role in the development of pain. However, they may have developed and become a perpetuating factor He reports tha t, 'Depressed and otherwise psychologically as a result of being in chronic pain. Dr Albert Schweitzer unwell persons frequently do not recognize the psychologi­ (1931 ) understood the psychological implications of pain as cal nature of their problem. In fact they usually deny vehe­ mently any psychological or emotional d imension to their

7 The internal enviro nm e nt 1 53 clinical picture . . . [this] makes them particularly difficult to • fail ure of reasonable treatments - patient may report trea t . ' worsening symp toms to bewilderment of practitioner Becker (1991) adds the important clue to recognizing • practitioner may start feeling anger toward patient somatizers, who need a special degree of help, not necessar­ (countertransference) ily relating directly to their musculoskeletal symptoms: 'Certain individuals, emotionally shortchanged or scarred • 'emotional hunger' may be masked by increased weight during their forma tive years, evidence a proclivity to soma­ gain and use of pain-relieving medica tion. tize in the face of stressful untoward events and circum­ stances of adult life, especially ones that awaken untoward Examination findings: feelings buried in the unconscious and rooted in the past.' • theatrical presentation (excessive limp, unnecessary use How are you to recognize such a patient? An abbreviated of walking stick, often in wrong hand, etc.) list of Becker 's suggested 'red flags' is as follows. • non-anatomic sensory findings (accentuating the need In the history look for: for careful testing) • vague and implausible history • non-anatomic motor findings such as suboptimal grip • symptoms which proliferate and link different body attempts (accentuating the need for careful testing) areas • inappropriate response to tests such as palpa tion and • highly emotionally charged descriptors (searing, blind­ percussion, especially if practitioner's hand is pushed away in an exaggerated manner. ing, cruel, etc.) • hyperbole ('I couldn't move') But, despite the importance of the warnings suggested by • discrepancies (patient reports 'cannot sit' but sits for Becker and others, it is as well to remember that a great many people with bodywide pain and virtual d isability do duration of interview) indeed have musculoskeletal (or associated) conditions and • passivity (e.g. acceptance of disabled status) that their psychological distress derives directly from the • evidence of deconditioning, weight gain and/or pain and disability they suffer. The truth is tha t we should not make a hard demarcation between 'mind' and 'body' as increased use of narcotic medication. origins of pain. This has been the folly of much medical practice in the past, although ever more apparent is a recog­ Psychosocial issues: nition of the need to deal with the whole person. If, as we know, psychological factors can influence the body (soma) • apportioning of blame for financial or employment or then the reverse is patently true (see Box 7.8 - Placebo personal problems to external sources power). It may well be tha t as part of the rehabilitation of someone with chronic pain and psychological distress, • feelings kept internally appropriate bodywork can contribute toward recovery. • tearfulness during interview What is needed, though, is recognition that the emotional • denial of link between symptoms and emotional status. side needs skillful expert attention, just as much as do the somatic manifestations of dysfunction. Mood disturbances: • anger directed at employer or doctors may be displaced anger at parents Box 7.8 Placebo power • Placebos work best against headache-type pain (over 50% effec­ tiveness). If someone believes a form of treatment w i l l relieve pain, it will do so far more effectively than if the belief is that the treatment cannot • In about a third of a l l people, most pains a re rel i eved by help. I n trials involving over 1 000 people suffering from chronic pain, placebo. d ummy medication reduced the levels of the pain by at least 50% of that achieved by any form of pain-killing d rug, including aspirin and • A placebo works more effectively if injected, rather than if ta ken morphine (Melzack & Wall 1 989). by mouth. Melzack & Wa l l ( 1 989) explain: Th is shows clea rly that the • Placebos work more powerful ly if acco m pa nied by the suggestion psychological context - particularly the physician's and patient's that they a re indeed powerful and that they will ra pidly produce expectations - contains powerful therapeutic value in its own right resul ts. in addition to the effect of the d ru g itself • Placebos that are in ca psu le or ta blet form work better if two are Placebo facts taken rather than one. • Placebos a re far more effective against severe pain than m i l d • Large ca psules work as placebos more effectively than do sma l l pain. ones. • Placebos a re more effective in people who a re severely anxious • Red placebos a re most effective of a l l in helping pain problems. and stressed than in people who are not, suggesting that the • Green placebos help anxiety best. 'antianxiety' effect of placebos accounts for a t least part of the • Blue placebos a re the most seda tive and ca lming. reason for their usefu lness. • Yel low placebos a re best for depression and pink a re the most sti m u la ting. box continues

1 54 CLI N ICAL A P P LICAT I O N O F N EU R O M U SC U LA R TECH N I Q U E S : T H E U P P E R B O DY • Placebos have been shown to be effective in a wide variety of more influenced than others. It is essential that we should not think con ditions including anorexia, depression, skin d iseases, diarrhea that because a placebo 'works' i n an individual that the person is not and palpitation. genuinely suffering pain or that the reported relief is false (Mil lenson 1 995). • Placebo effects do not only occur when taking something by mouth or injection; for exa mple, any form of treatment from A person's attitudes and emotions can be seen to be manipu lation to acupu ncture to su rgery carries with it a degree powerful aids (or h i ndrances) to recovery. The feeli ngs of hope of placebo effect. and expectation of i m provement, coupled with a relationship with caring helpers, professional or otherwise, assist in recovery a nd Recognition of the placebo effect a l lows us to rea l ize the i mportance co p i n g . of the power of suggestion on a l l of us, with some people being PAIN MANAGEMENT some pharmaceutical, some surgical, some electrical, some hydrotherapeutic and some manual Gerome 1997). GUNN' S VIEW • Local anesthetics (nerve blocks such as procaine, etc.). Pain expert Dr C Chan Gunn (1983) observes that pain man­ • Neurolytic blocks which destroy small-fiber afferent tis­ agement is simplified when it is realized tha t following injury, three sequential stages may be noted. sue and therefore in terfere with pain transmission (e.g. facet rhizotomy - thermocauterization which elimina tes 1. Immediate - a perception of noxious input that is tran­ small-fiber afferent activity). sient unless tissue damage is sufficient to cause the next • Dry needling, which inhibits ascending pain pathway stage. transmission. • Hot packs which increase blood flow (at least temporar­ 2. Inflammation - during which time a lgesic substances are ily; hot followed by cold would be more effective), reduc­ released which sensitize higher threshold receptors, fol­ ing nociceptive metabolites and decreasing segmental lowed by reflexes and sympathetic tone. • Ice or cold sprays (ethyl chloride) which increase small­ 3. Chronic phase - where there may be persistent nocicep­ fiber activity, flooding afferent pathways and causing tion (or prolonged inflammation). Hyperalgesia may brainstem inhibi tion of nociceptive input from trigger exist where normally non-noxious stimuli are rendered area. excessive due to hypersensitive receptors. • TENS, which is thought to achieve i ts pain-reducing effects via : Close similarities can be observed between facilitation con­ 1. preferential activation of large myelinated fibers inter­ cepts as ou tlined in Chapter 6, the neuropathic concept out­ lined above and the sequence described by Gunn. fering with pain perception and increasing tolerance 2. local axonal fatigue reducing small-fiber activity and QUESTIONS therefore pain input During palpation and evaluation, questions need to be 3. activating descending inhibitory influences including asked. opioid release. • Which of this person's symptoms, whether of pain or • Vibration, which differentially stimulates large proprio­ other forms of dysfunction, is the result of reflexogenic activity such as trigger points or possibly of spondylo­ ceptive afferent fibers interfering with pain perception. genic or neuropathic origin? • Direct inhibi tory pressure (as used in neuromuscular • What palpable, measurable, identifiable evidence con­ therapy), which offers a combination of influences nects what we can observe, test and palpate to the symp­ including: toms (pain, restriction, fatigue, etc.) of this person? 1. mechanical (stretching shortened myofascial fibers) 2. circulatory enhancement when ischemic compression • Is there evidence of a psychogenic influence to the per­ son's complaint? is released 3. neurological influence via mechanoreceptors inhibit­ • What, if anything, can be done to remedy or modify the situa tion, safely and effectively? ing pain transmission 4. endorphin and enkephalin release • What other practitioners might need to be incorporated? 5. and, possibly, energetic influences. • Restoration of normal physiological (using manual PAIN CONTROL methods) and psychological function, including: 1. reeduca tion (e.g. cognitive behavior modification - Elimination of myofascial trigger points and i.nhibition of pain transmission is possible via a number of approaches, see Chapter 8) 2. comprehensive management of associa ted muscu­ loskeletal dysfunction patterns (including HVT,

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1 60 C L I N I C A L A P P L I CAT I O N O F N E U R O M U S C U LA R T E C H N I Q U E S : T H E U P P E R B O DY Trayhurn P, Hoggard N, Mercer J G et al 1999 Leptin: fundamental WHO 2004 G loba l status report on a lcohol 2004. Department of aspects. International Journal of Obesity 23:22-28 Mental Health and Substance Abuse, World Hea lth Organization, Geneva U.s. Food and Drug Administration 2004 Food a l lergies rare but risky. FDA Consumer. Online. Available: http: / /www. Wilding J 2001 Leptin and the control of obesity. Current Opinions cfsan.fda .gov / -dms/wh-alrgl .hhnl in Pharmacology 1 (6):656-661 Va n Gaal L F, Wauters M A, Mertens I L et al 1999 Clinical Wilson J, Best T 2005 Common overuse tendon problems: a review endocrinology of h uman leptin. lnternational Journal of Obesity and recommendations for trea tment. American Family Physician and Related Metabolic Disorders 23(Suppl 1):29-36 72(5 ) : 8 1 1 -8 1 8 Wahl S 1989 Role of growth factors in inflammation and repair. Wittink H, Michel T 2002 Chronic pain management for physical Journal of Cell Biochemistry 40:343-351 therapists, 2nd ed n. Butterworth-Heinemann, Boston Walker A, Bundy R, Hicks S et a l 2002 Bromelain reduces mild Wolfram S, Wang Y, Thielecke F 2006 Anti-obesity effects of green acute knee pain and improves wel l-being in a dose-dependent tea: from bedside to bench. Molecular Nutrition and Food fashion in an open study of otherwise healthy adults. Research 50(2):176-187 Phytomedicine 9(8):681-686 Woolf C J, Doubell T P 1994 The pathophysiology of chronic pain ­ Wal ton R G, Hudak R, Green-Waite 1993 Adverse reactions to increased sensitivity to low threshold A beta-fibre inputs. aspartame: double-blind chal lenge in patients from a vulnerable Current Opinion in Neurobiology 4:525-534 population. Biological Psychiatry 34(1-2):13-27 Woolf C J, Bennett G J, Doherty M et al 1998 Towards a mechanism­ Wa tkins L, Maier S 2002 Beyond neurons: evidence that immune based classification of pain? Pain 77:227-229 and glial cel ls contribute to pathological pain states. Physiological Reviews (82):981-1001 Wurst F, JunghalU1s K, Lesch 0 et a l 2006 Leptin and g hrelin levels in a lcohol withdrawal, abstinence and in a drinking experiment. Watson D 2001 Mercury in dental filling disclosure and prohibition ISBRA 2006 World Congress on Alcohol Research act. Statement by Congresswoman Diane Watson, Los Angeles, California, November 5, 2001 Yamauchi M, Sugimoto T, Yamaguchi T et al 2001 Plasma leptin concentrations are associated with bone mineral density and the Wauters M, Considine R V, Va n Gaal L F 2000 Human leptin: from presence of vertebral fractures in postmenopausal women. an adipocyte hormone to an endocrine mediator. European Journal of Endocrinology 143(3):293-311 Clinical Endocrinology 55(3):341-347 Yannai S, Berdicevsky I, Duek L 1991 Transformations of inorganic Weigle D, Breen P, Matthys C et al 2005 A high-protein diet induces sustained reductions in appetite, ad l ibitum caloric intake, and mercury by Candida a lbicans and Saccha romyces cerevisiae. body weight despite compensatory changes in d i urnal plasma Applied and Environmenta l Microbiology 57(1):245-247 leptin and ghrelin concentrations. American Journal of Clinical Yud kin J, Kumari M, Humphries S et a l 2000 lnflammation, obesity, N utrition 82(1):41-48 stress and coronary heart disease: is interleukin-6 the link? Atherosclerosis 148(2):209-214 Weisburger J 1999 Tea and health: the underlying mechanisms. Zaveri N 2006 Green tea and its poIyphenolic catechins: med icinal Proceedings of the Society for Experimental Biology and uses in cancer and non-cancer applications. Life Sciences Medicine 220(4):271-275 78(18):2073-2080 Zhao B 2006 The health effects of tea polyphenols and their antioxi­ Werbach M 1991 Nutritional in.f1uences on illness. Third Line Press, dant mechanism. Journal of C linical Biochemistry and Nutrition Ta rzana, CA 38(2) :59-68 Zhu Y-X, Huang H, Tu Y-Y 2006 A review of recent studies in China WHO 1978 Evaluation of certain food additives and contaminants: on the possible beneficial health effects of tea. International twenty-second report of the Joint FAO/ WHO Expert Committee Journal of Food Science and Technology 41(4):333-340 on Food Add itives. World Health Organization Technical Report Zieglgansberger W, Berthele A, Tolle T 2005 Understanding neuro­ Series 631 :1-39 pathic pain. CNS Spectrums 10(4):298-330 WHO 1990 Methylmercury. Vol. 101 of Environmental Health Criteria. World Health Organiza tion, Geneva

161 Chapter 8 Assessment, treatment and rehabilitation CHAPTER CONTENTS In this chapter several interacting influences on health in general, and musculoskeletal dysfunction in particular, will Numerous influences 162 be considered, including biomechanical, biochemical and A biomecha n i ca l example 162 psychosocial factors. Awareness of the need to consider the range of health influences impacting an individual forms 'Looseness a n d tightness' as part of the the fOlmdation for sOlmd complementary health care. biomechanical model 163 An essential requirement for achieving a realistic under­ Lewit (1996) and 'loose-tight' thinking 164 standing of a patient's problems is an ability to see whatever Soft tissue treatment a nd barriers 164 symptoms are presented, or condition is manifested, as a part of a process, rather than as an end in itself. A person does not Pain and the ti ght-loose concept - a nd the trigger point have 'a bad/painful back'. The reality is that this 'back pain' represents the person's current state of adaptation to what­ controversy 164 ever biomechanical and other stressors are presently operat­ Three-d i mensional patterns 165 ing, a virtual 'snapshot' of a moment in a process that includes the person's entire inherited and acquired local and Methods for restoration of 'three-dimensionally patterned general history - involving features and factors such as age, gender, ethnic background/genetics, nutrition, emotions, functional symmetry' 165 habits of use, previous trauma/ surgery, chemical exposures, Neuromuscular management of soft t i ssue dysfunct i o n 166 patterns of posture, exercise, breathing - and more. Manipulating tissues 166 The practical (and philosophical) difference between see­ Nutrition and pa i n : a biochemical perspective 167 ing the 'bad back' as an entity, as a fixed state, and of under­ standing it, as a 'part of a process', is profound. Nutritional treatment strategies 167 Specific nutrients and myofa scial pa i n 167 Some practitioners/therapists treat 'bad backs', while others treat people with 'bad backs'. All will be aware that Allergy a nd intolerance: additional biochemical i nfluences on every single painful back problem is different from every other in some particulars, if not in symptom presentation, pain 168 then certainly in etiology. That said, there are commonali­ What causes this increase in permeability? 169 ties and patterns from which it is usually possible to estab­ Treatment for 'allergic myalgi a ' 169 lish features of the individual's condition, leading to an Antii nflammatory nutri tional (biochemical) strategie s 169 appropriate selection of therapeutic approaches. Psycho social factors in pain ma n a gement: What this text is urging is that individuals, and their unique characteristics, be considered, rather than named the cognitive d i mension 170 conditions, whether this is a joint or a soft tissue problem, a Guidelines for pain management 171 spasm or a trigger point, a local or a bodywide manifesta­ tion of adaptation exhaustion. Each symptom is a signpost, Group pain ma nagement 171 a clue, and just as an archeologist uses small, often appar­ The litigation factor 171 ently insignificant slivers and fragments of ancient materials Other ba rriers to progress in pa i n management 171 to piece together a picture of the past, so should the therapist Stages of change in behavior modification 171 attempt - using questioning, observation, palpation and Wellness education 172 Goal setting and pacing 172 Low back pai n rehabilitation 172 The biopsychosoci a l model of rehabilitation 172 Concordance 173 Patient advice a nd concord a n ce (complia n ce ) issues 173

1 62 C L I N I CA L APP L I CAT I O N O F N E U R OM U S C U LA R TE C H N I Q U ES: T H E UPP E R B O DY assessment - to detect and construct a valid picture of the against which the person's current status can be measured. past, relative to presenting symptoms. This might involve all or any of the following. As will be noted later in this chapter, this calls not only • Assessing muscles for strength or weakness. for attention to the structural and functional patterns asso­ • Evaluation of relative 'shortness' of muscles. ciated with pain or dysfunction but also to how well or • Testing range of motion of soft tissues and joints. poorly nourished the individual is; whether or not there • Evaluating for presence, absence or overactivity of neu­ may be food intolerances associated with their symptoms; how their beliefs and attitudes impact on their condition; rological reflexes. and their willingness and ability to undertake a rehabilita­ • Evaluating for presence of localized, reflexogenically active tion program. It is not within the scope of practice, or skills base, of many practitioners and therapists to handle all such structures, such as myofascial trigger points or spinal health influences but this should not prevent them being hyperreactivity (segmental facilitation). aware of their potential to affect recovery. At the least, advice • Assessment of postural (a)symmetry. can be offered regarding sources of information and appro­ • Gait function assessment. priate professional care. In chronic pain conditions a team • Evaluating respiratory function. approach is often ideaL as will be explained in the notes on • Consideration of nutritional and lifestyle influences. cognitive behavior therapy later in this chapter. • Consideration of hormonal influences and other meta­ bolic disturbances. • Awareness of psychosocial influences and attributes. N U MERO U S I N FLUENCES A BI O MECH A N I CA L EXA M P LE An appreciation of multiple influences on what may seem In the earlier discussion of the upper crossed syndrome to be an obvious problem emerges from recent research in (p. 82) we saw an example of a number of these elements of California in which a group of patients with chronic (over a assessment interacting. This particular (upper crossed syn­ year) low back pain were treated in one of two ways - either drome) dysfunctional postural pattern included: with what is described as 'gold-standard' physical therapy or with breathing retraining (Mehling et al 2005). • observable postural imbalance, with the head forward of its center of gravity, chin poked forward, increased cervical The study involved 16 patients (mean age 49.7 years, lordosis and dorsal kyphosis, and rounded shoulder stance 31 .3% male) with chronic low back pain, who underwent breathing retraining therapy, compared with 12 subjects with • identifiable shortness in postural muscles of the region, similar complaints (mean age 48.7 years, 41 .7% male) who using assessments described in a later chapter underwent physical therapy. • demonstrable malcoordination between muscles as those • Both groups received one introductory evaluation ses­ which have become hypertonic will be inhibiting their sion of 60 minutes and 1 2 individual therapy sessions of antagonists (e.g. levator scapula tight, serratus anterior equal duration of 45 minutes, over 6-8 weeks. weak), as demonstrated by Janda's (1982) functional assessment methods as described in Chapter 5 • It was found that patients improved in both groups regard­ ing pain, with a visual analog scale reducing by -2.7 with • the presence of active myofascial trigger points in key breathing therapy and -2.4 with physical therapy. predictable sites (for example, upper trapezius, sternoclei­ domastoid) that can be identified by means of palpation, • Breathing therapy patients improved more functionally, as described in Chapter 6, and utilizing neuromuscular physically and emotionally, while physical therapy evaluation palpation methods (modern American and patients improved more in vitality. However, average European approaches) described in the clinical applica­ improvements were no different between the two groups. tions section of this book • At 6-8 weeks, results showed a slight trend favoring • probable rotator cuff dysfunction due to altered position those receiving breathing therapy. of glenoid fossa in relation to the humerus • At 6 months, a slight trend favored those receiving phys- • upper thoracic, cervical, atlantooccipital, temporomandi­ ical therapy. bular restrictions or imbalances, that can be evaluated by normal palpation and assessment methods What we can learn from this is that direct treatment of obvious symptoms is not the only way to handle chronic • altered respiratory function that can be evaluated using problems. Since the ultimate improvement depends on self­ methods described in Chapter 14 regulation (homeostasis), a variety of therapeutic strategies can offer similar benefits. • in addition, there may be evidence of emotional or psy­ chosocial factors that might be directly or indirectly Making sense of what is happening in a body that is adapt­ linked with the presenting symptoms. ing to the stresses of life requires a framework (or several frameworks) of evaluation, and grids of (relative) normality, The person's history, as well as the presenting symptoms, should be laid against this accumulation of dysfunctional

8 Assessme nt. treatment and re h a b i l itation 1 6 3 patterns. When this is done a picture should emerge tha t I f the individual's presenting symptoms relate directly to a suggests a line of action designed to minimize present single injury/traumatic inciden t, or to repetitive micro­ symptoms, as well as to rehabilitate toward a more normal trauma, the individual characteristics of the trauma/micro­ status. This should also prevent or reduce the likelihood of trauma should, of course, be considered against the recurrence. background of the individual's unique characteristics, in much the same way as would be the case if the symptoms Unless the cause(s) of the person's problems relates to a had emerged from a background of gradual compensation/ specific tra uma, the present dysfunctional patterns are decompensation influences. likely to represent the body's attempts to adapt to wha tever overuse, misuse, abuse and disuse stresses to which it has In evaluating for musculoskeletal imbalances, specific been subjected. Treatment needs to deal with these adap tive tests and assessments are necessary (see Chapters 9 and 10). changes, as far as is possible, as well as assisting in regain­ Broader views are also useful, such as that previously ing an awareness of normal function, while also evalua ting described by Tom Myers (1997) which suggests 'chains' of ways of preventing a return to the very patterns that pro­ soft tissue connections in which the fascial structures are duced the symptoms. If all these elements are not incorpo­ key (see Chapter 1). rated into treatment, results will be short term at best. 'LOOSENESS AN D TIGHTNESS' AS PART OF In order to be truly successful, such a program would THE B I O MECHAN I CA L M O DEL include: A different conceptual model is offered by Robert Ward DO • attention to soft tissue changes (abnormal tension, fibro­ (1997). Ward discusses the 'loose-tight' concept as an image sis, etc.) - possibly involving massage, NMT, MET, MFR, required to appreciate three-dimensionality as the body, or PRJ, spray and stretch, and/or articulation/mobilization part of it, is palpated/assessed. This can involve large or small regions in which interactive asymmetry produces • deactivation of myofascial trigger points - possibly involv­ areas, or structures, which are 'tight and loose', relative to ing massage, NMT, MET, MFR, PRT, spray and stretch, each other. Ward illustrates this with the following examples: and/or articulation/mobiliza tion • a 'tight' sacroiliac/hip on one side and 'loose' on the other • releasing and stretching the shortened soft tissues - uti­ • a 'tight' SCM and 'loose' scalenes on the same side lizing spray and stretch, MFR, MET or other stretching • one shoulder area 'tight' and the other 'loose'. procedures, including yoga In positional release methodology (strain/counterstrain, • strengthening weakened structures - involving exercise functional technique, etc., see Chapters 9 and 10), the terms and rehabilitation methods, such as Pila tes 'ease' and 'bind' describe similar phenomena. Assessment of 'tethering' of tissues, and of the subtle qualities of 'end­ • proprioceptive reeducation - utilizing physical therapy feel' in soft tissues and joints, is a prerequisite for appropri­ methods (e.g. wobble board) as well as methods such as ate treatment being applied, whether this is of a direct or those devised by Feldenkrais (1 972), Hanna (1988), Fila tes indirect nature, or whether it is active or passive. Indeed, (Knaster 1996), Trager (1987) and others the awareness of these features (end-feel, tight/loose, ease/bind) may be the deciding factor as to which thera­ • postural and breathing reeducation - using physical ther­ peutic approaches are introduced and in what sequence. apy approaches as well as Alexander technique, yoga, tai chi and other similar systems Ward (1997) states: 'Tightness suggests tethering, while looseness suggests join t and/or soft tissue laxity, with or • ergonomic, nutri tional and stress management strate­ without neural inhibition.' These barriers (tight and loose) gies, as appropriate can also be seen to refer to the obstacles that are sought in preparation for direct (toward bind, tightness) and indirect • attention to any psychosocial elements that may be fac­ (toward ease, looseness) techniques. toring into the etiology or maintenance of symptoms Clinically it is always worth considering whether restric­ • occupational therapy specializing in activating healthy tion barriers ought to be released, in case they are offering coping mechanisms, determining functional capacity, some protective benefit. As an example, Van Wingerden increasing activity that will produce greater 'concordance' (1997) reports that both intrinsic and extrinsic support for than rote exercise, while developing adaptive strategies the sacroiliac jOint derives in part from hamstring (biceps to return the individual to a greater level of self-reliance femoris) status. Intrinsically, the i nfluence is via the close and quality of life (Lewthwaite 1990). anatomic and physiological relationship between biceps femoris and the sacrotuberous ligament ( they frequently The essence of all of these approaches can be characterized attach via a strong tendinous link) . as having a dual focus: 1. to reduce the adaptive load(s) (better ergonomics, exer­ cise, postural and breathing habits - as examples), i.e. what is being adapted to, and 2. to enhance the functionality of the tissues, area, person (improved mobility, stability, balance, etc.), so allowing the tissues/the person an improved ability to cope with the adaptive load, whatever it happens to comprise.

1 64 C L I N I CA L A P P L I CAT I O N O F N E U R O M U S C ULAR T E C H N I Q U ES: T H E U P P E R B O DY He states: 'Force from the biceps femoris muscle can lead HVLT manipulation can offer any benefit to chronically to increased tension of the sacrotuberous ligament in vari­ shortened, fibrosed, soft tissues, even if a reduction in ous ways. Since increased tension of the sacrotuberous liga­ hypertonicity is more than short term. These comments ment diminishes the range of sacroiliac joint motion, the are not meant to suggest that there is no value in such biceps femoris can play a role in stabilization of the SIr (Van manipulation, only that it is unlikely to have any influ­ Wingerden 1997; see also Vleeming et aI 1989). ence on chronically modified soft tissue status. • In contrast, pOSitional release methods seek the indirect, He also notes that in low back patients forward flexion is 'ease' or 'loose' barriers. This concept will be made often painful as the load on the spine increases. This hap­ explicit when positiona l release methods are described in pens whether flexion occurs in the spine or via the hip joints Chapter 10. (tilting of the pelvis). If the hamstrings are tight and short they effectively prevent pelvic tilting. 'In this respect, an PAIN AND THE TIGHT-LOOSE CONCEPT - AND increase in hamstring tension might well be part of a defen­ sive arthrokinematic reflex mechanism of the body to THE TRIGGER POINT CONTROVERSY diminish spinal load.' If such a state of affairs is long stand­ ing the hamstrings (biceps femoris) will shorten (see discus­ Pain is more commonly associated with tight and sion of the effects of stress on postural muscles in Chapters bound/ tethered structures, which may be due to local over­ 4 and 5), possibly influencing sacroiliac and lumbar spine use/misuse/ abuse factors, scar tissue, reflexively induced dysfunction. The decision to treat a tight (, tethered') ham­ influences or centrally mediated neural control. When a tight string should therefore take account of why it is tight, and tissue is then asked to either fully contract or fully lengthen, should consider that in some circumstances it might be pain is often experienced. Paradoxically, as pointed out by offering beneficial support to the SI}, or that it might be Lewit (1996), pain is also often noted in the 'loose' rather than reducing low back stress. the 'tight' areas of the body, which may involve hypermobil­ ity and ligamentous laxity at the 'loose' joint or site. These LEWIT (1996) AND 'LOOSE-TIGHT' THINKING (lax, loose) areas are vulnerable to injury and prone to recur­ rent dysfunctional episodes (SI joint, TM}, etc.). Lewit observes that pain is often noted on the 'loose' side when there is an imbalance in which a joint or muscle Myofascial trigger points may develop in either 'tight' or (group) on one side of the body differs from the other. 'loose' structures but usually appear more frequen tly, and are more stressed, in those which are tethered, restric ted or A 'tight and loose complex', i.e. one side is restricted and the tight. Myofascial trigger pOints will continue to evolve if the other side is hypotonic, is frequently noted. Shifting [Lewit etiological factors that created and / or sustained them are is referring to stretching offascial structures] is examined not corrected and, unless the trigger points are deactivated, and treated in a craniocaudal or caudocranial direction on they will help to sustain the dysfunctional postural patterns the back, but it should be assessed and treated in a circular which subsequently emerge. manner around the axis of the neck and the extremities. Sterling et al (2001) highlight an ongoing debate as to the SOFT TISSUE TREATMENT AND BARRIERS validity of what may be termed the 'trigger point hypothe­ sis'. They represent that group of clinicians and researchers • MET methods can be utili zed to identify the tight bind who question the model based on the work of Travell, barrier and, using isometric contractions of agonist or Simons and others (Simons et aI1 999). antagonist, attempt directly to push this barrier back or to pass through it. Box 8. 1 Tight-loose parpation exercise (Ward 1997) • Myofascial release (in its direct usage) also addresses its • Person is supine. directions of force directly toward the barrier of restriction. • Practitioner grasps person's wrists. • High-velocity, low-amplitude (HVLA) thrust manipula­ • A slow movement is made of both arms to full overhead tion, or 'adj ustment', as employed in chiropractic, osteopa­ thy and increasingly in physical therapy, also addresses extension as particular focused attention is paid to symmetry the restriction barrier, forcing motion through that barrier. One objective of this procedure is the invoking of a neuro­ of freedom of movement and any sense of restriction com­ logical response that produces a reduction in local soft tissue tone. In addition, such manipulation aims to mencing at the wrist contact but possibly i nvolving the body mechanically modify previously 'blocked' movement (Gibbons & Teahy 2000). Whether such changes in soft as a whole. tissue tone (as measured by surface EMG) actually occur • Attention needs to be paid to both quality and amplitude of other than transiently has been questioned (Herzog et al 1 995). It is reasonable to also question whether use of the passive movement. • The same exercise sh ould be performed on each arm inde­ pendently, as well as simultaneously, while attention is paid to any sensations of restriction and the end-feel associated with it. • Ward states, 'With practice, variable tension and loads are readily sensed from the h ands and wrists into the lumbodorsal fascia and pelvis'.

8 Assessment. trea tment and re h a b i l itation 1 65 They (Sterling et al) note that workers such as Simons & low back area (which ends up involving the entire trunk Mense (1998) maintain that palpable taut bands of trigger and cervical area) as 'tight' areas evolve to compensate for points make muscles feel tense, even though these phenom­ loose, inhibited areas (or vice versa) (Fig. 8.1). ena are not associated with propagated action potentials that would be identified as EMG activity. • 'Tightness' in the posterior left hip, SI joint, lumbar erec- tor spinae and lower rib cage. In relation to this concept Sterling et al (2001 ) state: 'Although this proposal may sound enticing to both patients • 'Looseness' on the right low back. and clinicians, the validity and reliability of the existence of • Tight lateral and anterior rib cage on the right. trigger points have not been established.' They cite a study • Tight left thoracic inlet, posteriorly. by Stohler (1999) that holds to a neurological, rather than a • Tight left craniocervical attachments (involving jaw trigger point, explanation for myofascial pain and dysfunc­ tion, to support that statement. To be sure, other clinicians mechanics). also hold to a different model to explain myofascial pain, and these issues are discussed in Chapter 6. At any given treatment session, as tight areas are freed or loosened, even if only to a degree, inhibiting influences on Sterling et al maintain that increased muscle activity may 'loose' weak areas diminish and allow a return of tone. It is at instead occur in the presence of pain, via the flexor with­ this time that rehabilitation, proprioceptive and educational drawal reflex (i.e. involving central sensitization), a process p atterns of use need to be introduced and practiced by the that offers a neurological interpretation for such changes person, so that what initially 'feels wrong' in terms of pos­ (Matre et aI 1999). They also consider the possibility, basing ture and usage (proper position and movement) becomes the assertion on the work of Simons & Mense ( 1998), that comfortable and starts to feel 'right'. painful, taut muscles that are palpated at rest in patients with musculoskeletal syndromes may be caused by changes METHODS FOR RESTORATION OF in the viscoelastic properties of the muscles themselves. 'THREE-DIMENSIONALLY PATTERNED Note: The authors of this text, having examined the evi­ dence (see Chapter 6), are not in complete agreement with FUNCTIONAL SYMMETRY' Sterling et aI's view, but feel that, in the interest of objectiv­ ity, their point of view should be reported. There seems to 1 . Identification of patterns of ease/bind-loose/ tight in a be every chance that various models are required to explain given body area or the body as a whole. This can emerge the pathophysiological changes noted in relation to muscu­ from sequential assessment of muscle shortness and loskeletal dysfunction and pain, involving variously, and restriction or palpation methods, such as those described possibly coincidentally, trigger point activity, neurological by Ward (1997), or any other comprehensive evaluation sensitization and/ or viscoelastic modifications - and per­ of the status of the soft tissues of the body as a whole. haps even factors that have not yet been considered. 2. Appropriate methods for release of areas identified as THREE-DIMENSIONAL PATTERNS tight, restricted, tethered (possibly involving myofascial release, spray and stretch, MET, NMT, PRT, singly or in Areas of dysfunction will usually involve vertical, horizon­ combination, plus other manual approaches) . tal and 'encircling' (also described as crossover, spiral or 'wrap-around') patterns of involvement. Ward offers a 3 . I f j oints fail t o respond adequately t o soft tissue mobiliza­ ' typical' wrap-around pattern associated with a tight left tion, the use of articulation/ mobilization or high-velocity thrust methods may be incorporated into this sequence as appropriate to the status (age, structural integrity, inflam­ matory status, pain levels, etc.) of the individual and the scope of practice and training of the practitioner. Figure 8.1 Muscular imbalance altering joint mechanics. A: Symmetrical muscle tone. B: Unbalanced muscle tone. C: Joint surface degeneration. Reproduced with permission from the Journal of Bodywork and Movement Therapies 1999; 3(3):154. c

1 66 C L I N I CA L APP LICAT I O N O F N E U R OM U S C U LA R TECH N I Q U E S: TH E UPP E R B O DY 4. Identification and appropriate deactivation (using NMT • spray and stretch techniques, and or other appropriate means) of myofascial trigger points • variations on these basic themes. contained within these structures. Whether step 2 pre­ cedes step 4 or vice versa is a matter of clinical judgment MAN IPU LATING TISSUES (and debate). They may happen simultaneously. Lederman (1997) points out that, in effect, there are only a 5. Trigger points always require the stretching of the affected limited number of ways of treating tissues ('modes of load­ tissues housing the trigger points after deactivation. In ing') and most of the various direct 'techniques' employed by addition, restoration of normal resting length to the mus­ manual therapists are variations of these (Carlstedt & Nordin cle housing the trigger point is seen to be an important 1989). Indirect approaches that 'unload' tissues (i.e. they objective of treatment. move away from any perceived restriction barrier), such as osteopathic functional technique and strain/ counterstrain, 6. Reeducation and rehabilitation (including homework) of are not included in this summary of direct approaches. posture, breathing and patterns of use (work, leisure activ­ ities, sitting, walking, lying down) in order to restore func­ Lederman's perspective on variations of possible appli­ tional integrity and prevent recurrence, as far as possible. cation of direct treatment forces (with additions from the authors) includes the following. 7. Exercise (homework) has to be focused, time efficient and within the person's easy comprehension and capabilities, 1 . Tension loading in which factors such as traction, stretching, if cooperation is to be achieved. extension and elongation are involved. The objective is to lengthen tissue. The effect, if sustained, is to encourage NEU RO M U S CU LA R M AN AGEMENT OF S OFT an increase in collagen aggregation and therefore denser TISSU E DYSFUNCTION and stronger tissues. Lengthening forms a major part of rehabilitation methodologies and, on a l ocal level, of trig­ There are many ways of usefully applying manual methods ger point deactivation. to the musculoskeletal system. Treatment approaches can be categorized as direct and indirect, active and passive, 2. Compression loading shortens and widens tissue, increasing gentle or mechanically invasive, and all have value in their pressure and influencing fluid movement significantly. appropriate settings. Over time, a degree of lengthening may also occur in the direction of pressure if the underlying structures allow A great many of the methods of manual treatment can this (i.e. limited by any bony surface beneath the compres­ cluster under a heading of 'neuromuscular ' inasmuch as sion). As well as affecting circulation, compression also they focus on the soft tissues, including musculature, and influences neurological structures (mechanoreceptors, they incorporate into their methodology influences on neu­ etc.) and encourages endorphin release. ral function. Methods that are seen to be natural allies of neuromuscular therapy (NMT), as applied in Europe and 3. Rotation loading produces a variety of tissue effects since the USA, include: it is effectively elongating (some fibers) and compressing simultaneously, with the circulatory and/ or neurological • muscle energy techniques (MET) (and other forms of influences outlined above. Techniques which produce a induced stretching or release) 'wringing' effect on soft tissues, or in which joints are rotated as they are articulated, will cause this form ofload­ • positional release techniques (PRT) (including strain/ ing on soft tissues. Manual methods such as 5' ' bends (in counterstrain (SCS), functional technique, craniosacral which tissues are stretched in two directions at the same techniques, etc.) time by, for example, the action of opposing thumbs; see Chapter 1 2) can be seen to be simultaneously compress­ • myofascial release (MFR) (varying from dynamic to ing, elongating and, in those fibers close to the transition, extremely gentle) applying rotation loading. • direct manual pressure (also called ischemic compres­ 4. Bending loading is in effect a combination of compression sion, trigger poin t pressure release, inhibition technique, (on the concave side) and tension (on the convex side). This acupressure) has both a lengthening and a circulatory influence. On a local soft tissue level a 'e'-shaped bending of tissues that • direct manual variations (such as crossfiber friction, spe­ can be held to encourage elongation is commonly applied. cific soft tissue mobilization, etc.) 5. Shearing loading, which translates or shifts tissue laterally • rhythmically applied release methods (including percus­ in relation to other tissue. This is most used in joint sion and harmonic technique) articulation but insofar as it involves soft tissues, has the effect of compression and elongation in the region of • mobilization of associated joints (including articulation, transition. All techniques that attempt to slide a more rhythmic pulsating approaches, e.g. Ruddy's technique superficial layer of soft tissue across underlying tissues (Ruddy 1962), high-velocity thrust (HVT» would be included here. • McKenzie methods to encourage centralization of periph­ eral pain (McKenzie & May 2003) • mobilization with movement methods deriving from the work of Mulligan (1999)

1 678 Assessment. treatment and reha bilita t i o n 6. Combined loading involves the application of combined biochemical abnormalities which interfere with the ability of the muscle to recover or which continuously stress m uscle, variations of the modes of loading listed above, leading reactivating the trigger point. to complex patterns of adaptive demands on tissues. For example, Lederman (1997) points out that a stretch that is Among the 'systemic biochemical abnormalities' identified combined with a sidebend is more effective than either a are 'hypothyroidism, folic acid insufficiency and iron insuf­ sidebend or a stretch alone, something which most man­ ficiency'. These deficiency states are seen to be important ual therapists will recognize. because of their influence on enzyme systems. 7. Apart from the varia tions in load ing that are chosen (push, pull, twist, bend, shift) additional permutations Gerwin continues: include the following. • How hard? What is the degree of force being employed Vitamins act as cofactors in different enzyme systems that may be functioning at different rates at any one time. The (from grams to kilos)? optimum level ofa vitamin is that which permits maximum • How large? What is the size of the area to which force function for each enzyme for which it is an essential cofac­ tor. The vitamin requirements therefore change with time is being applied (lentil-sized nodule or whole limb or and circumstances. The daily vitamin intake should thus even whole body)? support optimum function . . . [and is] affected by host fac­ • How far? What is the intended amplitude of the induced tors such as smoking or by competitive inhibition by drugs. movement? The degree of force largely determines the (Travell & Simons 1983, 1992) amplitude - how far the tissues are being taken (milli­ meters or centimeters) . Simons et al (1999, p. 212) are absolutely clear in their insis­ • How fast? What i s the speed with which force is tence that nutritional balance has to be restored if myofas­ applied (from extremely rapid to subtly slow)? cial pain is to be adequately addressed: • How long? What is the length of time force maintained (from milliseconds to minutes)? Patients with chronic myofascial pain are a select group • How rhythmic? What is the rhythmic quality of which, in our experience, has a remarkably high prevalence applied force (from rapid to deliberate to synchronous of vitamin inadequacies and deficiencies. When the patient with, for example, breath or pulse rate)? fails to respond to specific myofascial therapy 01' obtains • How steady? Does the applied force involve movement only temporary relief vitamin deficiencies must be ruled out or is it static (sustained pressure or gEding action)? as a major contributing cause and, ifpresent, corrected. • Active, passive or mixed? Is the patient active in any of the processes (assisting in stretching, for example, or SPECIFIC NUTRIENTS AND MYOFASCIAL PAIN resisting applied force)? Folic acid (associated with the enzyme The reader might usefully reflect on which of the variations tetrahydrofolate) of loading - and the permutations as to refining these as listed above - is involved in any particular method or tech­ It is suggested that levels should be measu red in serum nique currently employed. It will be rare indeed to find together with B1 2, as well as in red blood cells (Gerwin direct methods that do not incorporate these elements. 1993). When in the low normal range, symptoms may include: N UTR ITION AN D PA I N: A BI O CHEM I CAL PERS PECTIVE • feeling unnaturally cold (as in hypothyroidism but with low cholesterol levels rather than high) A variety of nutritional influences can be noted in relation to pain in general and myofascial trigger point evolution • a tendency to diarrhea (rather than constipation, which is and behavior in particular. These include: associated with B12 deficiency) • nutritional deficiency • a tendency to restless legs, headache and disturbed sleep • allergy/intolerance • type II muscle fibers in the upper body are most likely to • antiinflammatory tactics. develop trigger points. NUTRITIONAL TREATMENT STRATEGIES Iron (associated with various blood enzymes. Gerwin (1993) states that while manual methods (pressure, including cytochrome oxidase) needling, etc.) can deactivate myo£ascial trigger points: Serum ferritin levels should be measured to evaluate cur­ Management ofrecurrent myofascial pain syndrome (MPS) rent levels. Deficiency may be noted more frequently in per­ requires addressing the perpetuating factors of mechanical imenopausal women whose diet is inadequate to replace imbalances (structural, postural, compressive) and systemic iron lost during menstruation. Blood loss may also be asso­ ciated with taking NSAIDs. Gerwin (2005) notes that iron deficiency can be a factor in the development or perpetuation

1 68 CLINICAL APPLICATION OF NEUROM USCULAR TECHNIQ UES: THE UPPER BODY of trigger points due to its impact on local muscle energy. misguided and has serious consequences, ie, the risk of vita­ Symptoms include: min 0 deficiency and increased risk of many chronic diseases. There is little evidence that adequate sun exposure will sub­ • unnatural fatigue (iron is needed to convert thyroid hor­ stantially increase the risk of skin cancer; rather, long-term mone T4 into its active T3 form, which may be an added excessive exposure and repeated sunburns are associated fatigue factor if either is deficient) with nonmelanoma skin cancers. • exercise-induced muscular cramping Selenium and vitamin E • intolerance to cold • restless legs syndrome (Gerwin 2005). In a double-blind study 140 mg selenium and 100 mg alpha­ tocopherol were supplemented daily and compared with Vitamin D placebo. Glutathione peroxidase levels increased in 75% of 81 patients with disabling muscular and osteoarthritic pain. Vitamin 0 is an essential nutrient for utilization of dietary Pain score reductions were more pronounced in the treated calcium. When vitamin 0 is deficient, absorption of calcium patients (Jameson 1985). is inadequate to meet the demands of the body. To help cor­ rect this, the body increases its release of parathyroid hor­ Additional nutritional deficiencies, including vitamins C mone, a hormone that acts to increase calcium levels by and B complex, have been identified by Simons et al (1999) removing it from the bones and by enhancing absorption as being implicated in myofascial trigger point evolution and through the kidneys. Holick (2003a) notes that this result in activity. It is self-evident that the ideal source of nutrients is rickets, osteopenia and osteoporosis and 'may have serious well-selected and appropriately prepared food. Whether an adverse consequences, including increased risk of hyper­ omnivorous or a vegetarian (or other variant) dietary pattern tension, multiple sclerosis, cancers of the colon, prostate, is chosen, the key elements remain the need for adequate breast, and ovary, and type 1 diabetes. There needs to be a nutrient-rich protein, complex carbohydrate (fresh vegeta­ better appreciation of the importance of vitamin 0 for over­ bles, pulses and grains), essential fatty acids, fruit and liq­ all health and well being' (Holick 2003b). uid. Food choices may be limited by economic factors, food intolerance issues (see below), ignorance or, more commonly, In considering the prevalence of vitamin 0 deficiency: ignoring what is known to be appropriate, something most people are aware of as a personal issue at times. It is sug­ • Plotnikof & Quigley (2003) found vitamin 0 deficiency in gested that, at the very least, a well-formulated multivita­ 89% of subjects with chronic musculoskeletal pain. min mineral supplement should be incorporated into any self-care advice offered to patients with musculoskeletal • Glerup et al (2000) reported that 88% of women investi­ dysfunction. gated who presented with muscle pains and weakness were severely vitamin 0 deficient. ALLERGY AND INTOLERANCE: ADDITIONAL • Bischoff et al (2003) observed that adults with vitamin 0 BIOCHEMICAL INFLUENCES ON PAIN deficiency present with muscle weakness and are more likely to fall. In the 1920s and 1930s, Dr A H Rowe demonstrated that widespread chronic muscular pains - often associated with Gerwin (2005), citing Glerup et al (2000) and Mascarenhas & fatigue, nausea, gastrointestinal symptoms, weakness, Mobarhen (2004), discusses vitamin 0 deficiency in its asso­ headaches, drowsiness, mental confusion and slowness of ciation with musculoskeletal pain, loss of type II muscle thought as well as irritability, despondency and widespread fibers and proximal muscle atrophy. He notes: bodily aching - commonly had an allergic etiology. He called the condition 'allergic toxemia' (Rowe 1930, 1972). The deficiency state is easily corrected, but it takes up to six months of replacement to reverse changes caused by defi­ Theron Randolph (1976) described 'systemic allergic ciency states. People not exposed to the sun are at great risk, reaction' as being characterized by a great deal of pain, either including those whose clothes leave little skin exposed to the muscular and/ or joint related, as well as numerous associa­ sun, and those who spend little time out of doors. ted symptoms. He has studied the muscular pain phenome­ non in allergy and his plea for this possibility to be considered Holick (2003a) agrees, specifying that 90% of required vita­ by clinicians was based on his long experience of it being min 0 comes from exposure to sunlight: ignored. Anything that in terferes with the penetration of solar ultra­ The most important point in making a tentative working violet radiation into the skin, such as increased melanin pig­ diagnosis of allergic myalgia is to think of it. The fact remains mentation and su nscreen use, will diminish the clltaneous that this possibility is rarely ever considered and is even more production of vitamin 03, The most cost-effective and effi­ rarely approached by means of diagnostico-therapeutic meas­ cient method for preventing vitamin 0 deficiency is to have ures capable of identifying and avoiding the most common adequate exposure to sunlight. Some dermatologists advise that people of all ages and ethnicities should avoid all direct exposure to sunlight and should always use sun protection when outdoors. This message is not only unfortunate, it is

8 Assessment. treatment a n d reh a b i l i tation 169 ] environmental incitants and perpetuants of this condition - the brain level, and not peripheral (immunological) sensitiza­ namely, specific foods addictants, environmental chemical tion, is a major etiological mechanism by means of which exposures and house dust. various abdominal and other health complaints are gener­ ated and may be misinterpreted as 'food allergy' . Randolph points out that when a food allergen is with­ drawn from the diet it may take days for the 'withdrawal' TREATMENT FOR 'ALLERGIC MYALGIA' symptoms to manifest. Rather than attempting to heal the intestinal changes (pro­ During the course of comprehensive environmental control biotics, etc.) or deal with the stress-coping abilities of the [fasting or multiple avoidance] as applied in clinical ecol­ individual, Randolph (1976) sta tes his position - 'Avoidance ogtj, myalgia and arthralgia are especially common with­ of incriminated foods, chemical exposures and sometimes drawal effects, their incidence being exceeded only by lesser environmental excitants'. How this is achieved in a fatigue, weakness, hunger and headache. setting other than a clinic or hospital poses a series of major hurdles for the practitioner - and the person with the symp­ The myalgic symptoms may not appear until the second or toms. If foods or other irritants can be identified, it makes third day of avoidance and may start to recede after the fourth perfect sense for these to be avoided, whether or not under­ day. Randolph warned that in testing for (stimulatory) reac­ lying causes (such as possible gut permeability issues) can tions to food allergens (as opposed to the effects of with­ be, or are being, addressed. drawal), the precipitation of myalgia and related symptoms may not take place for between 6 and 12 hours after ingestion According to the Fibromyalgia Network, the official p ub­ (of a food which contains an allergen), which can confuse lication of fibromyalgia patient support groups in the USA, matters as other foods eaten closer to the time of the symp­ the most commonly identified foods that cause muscular tom exacerbation may then appear to be at fault. Other signs pain for many people are wheat and dairy products, sugar, which can suggest that myalgia is allied to food intolerance caffeine, aspartame, alcohol and chocolate (Fibromyalgia include the presence of a common associated symptom, Network Newsletter 1993). restless legs (Ekbom 1960). Maintaining a whea t-free, dairy-free diet for any length When someone has an obvious allergic reaction to a food, of time is not an easy task, although many manage it. Issues this may be seen as a causal event in the emergence of other involving concordance (a term currently suggested as being symptoms. If, however, the reactions occur many times every more appropriate than commonly used words such as day and responses become chronic, the cause-and-effect link 'compliance' or 'adherence', which denote passive obedi­ may be more difficult to make. If a connection between par­ ence) deserve special attention, since the way information is ticular foods and symptoms such as muscular pain can presented and explained can make a major difference to the indeed be made, the major question remains - what is the determination displayed by already distressed people as cause of the allergy? One possibility is that the gut mucosa they embark on potentially stressful modifications to their may have become excessively permeable ('leaky gut syn­ lifestyles. drome'), so allowing large molecules into the bloodstream where a defensive 'intolerance' or allergic reaction is both Summary predictable and appropriate (Martinez-Gonzalez et a1 1994, Mielants et al 1991, Paganelli et aI 1 99 1 ) . If muscle pain appears to relate to nutrition one or all of the following may be helpful: WHAT CAUSES THIS INCREASE IN • Deal with underlying stress factors through better stress PERMEABI LITY? management, or avoidance/elimination of the stressors. Changes in the local intestinal environment due to factors • Identify whether increased intestinal permeability is a such as infection or stress encourage antigens (large mole­ factor, and help to correct this by means of specific nutri­ cules from the gut) to penetrate the mucosa and induce ents, herbal products and /or medication, as well as pro­ allergic inflammation (Bhatia & Tandon 2005, Heyman biotics. 2005). Evidence suggests that supplementation with probi­ otic microorganisms (beneficiaL or 'friendly' bacteria) can • Identify and avoid (exclude/challenge) foods and food improve the gut barrier function, and may, therefore, both families that provoke symptoms. 'undo and prevent unfavorable intestinal microecological alterations in a llergic individuals' (Bongaerts & Severijnen Note: If any such approaches lie outside of the practitioner's 2005). scope of practice, suitable referral should be made. Alternatively, it has been suggested tha t prolonged or ANTIINFLAMMATORY NUTRITIONAL repetitive stress might create a sensitization of the brain, leading to what appear to be 'intolerance' symptoms. Berstad ( BIOCHEMICAL) STRATEGIES et al (2005) suggest that cognitiv�motional sensitization at If an underlying inflammatory process is ongOing it may be possible to modify or modulate this without recourse to

1 7 0 C L I N I CA L A P P L I CAT I O N O F N E U R O M U S C U LA R T EC H N I Q U E S : T H E U P P E R B O DY [ over-the-coLU\\ter antiinflammatory medication (non-steroidal Other safe antiinflammatory dietary strategies antiinflamma tory drugs - NSAIDs). Dietary strategies exist that have an antiinflammatory influence (Adam et al 2003) These include: because they reduce levels of arachidonic acid (a major leukotriene source tha t leads to superoxide release by neu­ • taking ginger extracts or eating ginger regularly (Grzanna trophils, and which is a major contributing factor to the et al 2005). This has been shown to be helpful even in degree of inflammation being experienced). The first priority severe arthritic conditions (Altman & Marcussen 2001) in an antiinflammatory diet is to cut down or eliminate dairy fat. • increasing dietary fiber (such as is found in oatmeal) (Scheppach et al 2004) • Fat-free or low-fat milk, yogurt and cheese should be eaten in preference to full-fat varieties, and butter avoided alto­ • supplementing with vitamin C, a powerful antioxidant gether (Moncada 1986). Meat fat should be completely (Jensen 2003). avoided and since much fat in meat is invisible, meat itself can be left out of the diet for a time (or permanently). PSYC H O SO C I A L FACTO RS I N PA I N Poultry skin should be avoided. MANAGEM ENT: T H E COGN ITIVE DI MENSION • Hidden fats in products such as biscuits, cookies and Chiropractor Craig Liebenson (1996), a n expert i n spinal other manufactured foods should be looked for on pack­ rehabilitation, sta tes that: ages and avoided. Motivating patients to share responsibility for their recov­ (See also the extensive discussion of inflammation in ery from pain or injury is chaLLenging. Skeptics insist that Chapter 7.) patient compliance with self-treatment protocols is poor and therefore should not even be attempted. However, in chronic Eating fish or taking fish oil is beneficial pain disorders where an exact cause of symptoms can only be identified 15% of the time the patien t's participation in Some fish, mainly those from cold-water areas such as the their treatment program is absolutely essential (WaddeLL North A tlantic or Alaska, contain high levels of eicosapen­ 1998). Specific activity modification advice aimed at reduc­ tenoic acid (EPA), which helps cut levels of arachidonic acid, ing exposure to repetitive strain is one aspect ofpatient edu­ so helping to reduce inflammation, whether this is in a joint cation (WaddeLL et al 1996). Another includes training in or the digestive tract or in a skin condition (such as eczema) specific exercises to perform to stabilize a frequently painful or any other violent allergic reaction involving inflammation. area (Liebenson 1996, Richardson & Jull 1995). Patients who Fish oil exerts these antiinflammatory effects without inter­ feel they have no control over their symptoms are at greater fering with the useful roles which some prostaglandins have, risk ofdeveloping chronic pain (Kendall et al 1997). Teaching such as protection of delicate stomach lining and maintain­ patients what they can dofor themselves is an essential part ing the correct level of blood clotting (unlike some anti­ of caring for the person who is suffering with pain. inflammatory drugs) (Mayer et al 2003, Mickleborough Converting a pain patientfrom a passive recipient ofcare to 2006). an active partner in their own rehabilitation involves a par­ adigm shiftfrom seeing the doctor as healer to seeing him or Research has shown that the use of EPA in rheumatic and her as helper (Waddell et al 1996). When healthcare arthritic conditions offers relief from swelling, stiffness and providers promise to fix or cure a pain problem they only pain although benefits do not usually become evident LU\\til perpetuate the idea that something is wrong that can be after 3 months of fish oil supplementation, reaching their fixed (i.e. put back in place) . In pain medicine the likelihood most effective level after aroLU\\d 6 months. An experimental of recurrence is high (over 70%) and therefore it is impor­ blinded study showed that a fter 6 months both pain and func­ tant to show a person how to carefor them selfin addition to tion of osteoarthritic patients (male and female, age range offering palliative care. Simple advice regarding activity is 52--85) improved with EPA (10 mg daily plus ibuprofen) com­ often better than more sophisticated forms of conservative pared with placebo, in patients who had not previously care including mobilization or ergonomics (Malmivaara responded to ibuprofen alone (1200 mg daily) (Ford­ et al 1995). Promoting a positive state of mind and avoiding Hutchinson 1 985, Stammers et aI 1989). To follow this strategy the disabling attitudes which accompany pain is crucial to (but not if there is an allergy to fish) the individual should: recovery (Liebenson 1996). People who are at the greatest risk of developing chronic pain often have poorly developed • eat fish such as herring, sardine, salmon and mackerel coping skills (Kendall et al 1997). They may tend to cata­ (but not fried) at least twice weekly strophize their illness andfeel there is nothing that they can do themselves. It is easy for them to become dependent on • take EPA capsules (10-15 daily) when inflammation is at manipulation, massage, medication and various physical its worst until relief appears and then a maintenance therapy modalities. A key to getting a person to become dose of six capsules daily active in their own rehabilitation program is to shift them • consider a vegetarian option with supplementa tion with flax seed oil (same quantities as fish oil above).

8 Assessment. treatment and re h a b i l itation 1 7 1 from being a pain avoider to a pain manager (Troup & improved health on their financial position and can demon­ Videman 1989, Waddell et aI 1996). In a severely painful or unstable acute injury it may be appropriate to equate hurt strate that they are sufficiently motivated to change, despite and harm. But, in less severe cases, or certainly in the suba­ cute or recovery phase, hurt should not be automatically these considerations and consequences (Watson 2000). associated with harm. Infact, the target of treatment may be Additionally, the litigation process itself, including depOSi­ the stiffness caused by the patients overprotecting them­ tions, medical improvement testing, court appearances and selves during the acute phase. Muscles and joints that lose other procedures, may impose stresses - and distresses - their mobility while the patient restricts their activities dur­ which create emotional challenges that stimulate and ing acute pain should be expected to cause discomfort and provoke the pain response. This situation often results in remobilizing them may hurt but certainly won 't harm. setbacks in the recovery process. G UIDE LINES FOR PAIN M ANAGEMENT OTHER BARRIERS TO PROGRESS IN PAIN (Brad l ey 1 99 6) MANAGEMENT (G i l et a 1 1 988, Keefe et a l 1 996) • Assist the person in altering beliefs that the problem is • Distorted perceptions of the person (and / or their partner unmanageable and beyond their control. or family) about the na ture of their pain and disabili ty. • Inform the person about the condition. • Beliefs based on previous (possibly incorrect) diagnosis • Assist the person in moving from a passive to an active and treatment failure (,But the specialist said . . . ') . role. • Lack o f hope created b y practitioners (who often d o not • Enable the person to become an active problem solver understand the myofascial pain responses) whose prog­ nosis was limiting (,You will have to learn to live with it'). and to develop effective ways of responding to pain, emotion and the environment. • Dysfunctional beliefs about pain and activity ('It's bound • Help the person to monitor thoughts, emotions and behav­ to get worse if I exercise'). iors, and to identify how internal and external events influence these. • Negative expectation about the future Cit's bound to get • Give the person a feeling of competence in the execution worse whatever I do'). of positive strategies. • Help the person to develop a positive attitude to exercise • Psychological disorders that may contribute to the expe­ and personal health management. rience of pain (e.g. depression and anxiety). • Help the person to develop a program of paced activity to reduce the effects of physical deconditioning. • The person's lack of awareness of the control they have • Assist the person in developing coping strategies that can over the pain. be continued and expanded once contact with the pain management team or healthcare provider has ended. • The possibility that disability offers secondary gains (what benefit does the person receive from maintaining the pain GROUP PAIN MANAGEMENT or limitations?). In pain clinics group work is often involved to achieve the STAGES OF CHANGE IN BEHAVIOR MODIFICATION objectives in the list immediately above. Possible reasons for excluding someone from group pain management include DiClementi & Prochaska (1982) have developed a useful the following (all these are better dealt with individually model that explains stages of change. rather than in group settings). • Those who do not see their current behavior as a problem • Major psychiatric or psychological problems (psychotic needing change or who are unwilling to change are pa tients, those with current major depressive illness, etc.). described as precontemplative. • Major substance abuse including prescription drugs. • A person who sees the need for change is in the stage of • Major cardiorespiratory disease. contemplation. • Severe structural deformity. • Precontemplative individuals are unlikely to change THE LITIGATION FACTOR their behavior. Ongoing litigation or the receipt of large sums in wages com­ • Those who are contemplating change need help to start pensation is not necessarily a barrier to pain management, to plan the necessary changes. provided that the person is aware of the consequences of • Program attendance is part of this process of change and individuals are expected to also plan to make changes in their home and social environment. • Putting these plans into action is the next stage, where behavioral change is enacted and agreed goals are set. • People often relapse into old patterns if faced by addi­ tional or new stresses and challenges, such as a pain flare-up, and should be prepared for this. • Healthcare providers need to enable the person to acquire the knowledge, skills and strategies to avoid slid­ ing back into old ways.

1 72 C L I N I CA L A P P L I CAT I O N O F N E U R O M U S C U LA R T E C H N I Q U E S : T H E U P P E R B O DY W E LLN ESS E D U CATI O N (Vlaeyen et a l 1 996) • Activities should be incorporated that are meaningful to the person, such as those related to hobbies or interests Education regarding illness and wellness starts at the first (e.g. gardening), with some adaptation, which will consultation. Initial education in pain management should increase activity levels and encourage more consistent give the person information to help them make an informed participation. decision about participating in a program. Such a program should offer the person a credible rationale for engaging in O bjectives of a physical activity pain management, as well as information regarding: • Overcome the effects of deconditioning. • the condition itself (a major factor in rehabilitation) • Challenge and reduce the person's fear of engaging in • a simple guide to pain physiology (how pain is transmit­ physical activity. ted; where it is felt; what it means) • Reduce physical impairment and focus on recoverable • separating the link between 'hurting' and 'harming' (a function. revelation for some people; 'I thought that if it hurt it was • Increase physical activity in a safe and graded manner. doing harm') • Help the person to accept responsibility for increasing • ergonomic influences on pain, including education and advice about safe lifting and working postures, how to sit functional capacity. and lie safely without creating strain • Promote a positive view of physical activity in the • the effects of deconditioning and the benefits of exercise and healthy lifestyles. self-management of health. • Introduce challenging, functional activities to G O A L S ETTIN G A N D PAC I N G (Bu cklew 1 994, Gil et al 1 988) rehabilitation. Pacing rehabilitation exercise is a strategy to enable people Exercise should be designed to: to control exacerbations in pain by learning to regulate activity and, once a regime of paced activity is established, • stretch, to increase soft tissue length/suppleness to gradually increase the activity level. Part of the process of • mobilize joints recovery necessarily involves empowerment, the sense of • increase fitness. being in control, and this can be rapid or slow. The control learned by experiencing the effect of rehabilitation exercises LOW BACK PAIN REHABILITATION on the condition is a powerful force in this empowerment process, since how often, how hard, how long, etc. the pro­ In regard to rehabilitation from painful musculoskeletal gram is applied will be under the individual's control and dysfunction (this text is related to low back problems but so, to a large extent, will the outcomes. the principles are universal), Liebenson (1996) states: Rehabilitation goals should be set in three separate fields. The basic progressions to facilitate a 'weak link' and improve motor control include the following: 1 . PhysicaL - the person follows and sets the number of exer­ cises to be performed, or the duration of the exercise, and • train awareness of postural (neutral range joint) control the level of difficulty. during activities 2. Functional tasks - this relates to the achievement of func­ • prescribe beginner ('no brainer') exercises tional tasks of everyday living, such as housework or • facilitate automatic activity in 'intrinsic' muscles by reflex hobbies and tasks learned on the program. stimulation 3. Social - where the person is encouraged to set goals relat­ • progress to more challenging exercises (i.e. labile surfaces, ing to the performance of activities in the wider social environment. Goals should be personally relevant, inter­ whole-body exercises) esting, measurable and, above all, achievable. • transition to activity-specific exercises • transition to health club exercise options. Physical exercise (Be n n ett 1 99 6) THE BIOPSYCHOSOCIAL MODEL OF • Physical exercise should aim to redress the negative effects REHABILITATION of deconditioning. Brewer et al (2000) have described elements now considered • The key to participation and acceptance of the beneficial important in rehabilitation from injury (or dysfunction), as effects of exercise is a reduction in the fear of activity ('It including characteristics of the injury (dysfunction), socio­ may hurt but it won't do harm'). demographic factors, as well as biological, social! contextual and psychological factors, along with intermediate biopsy­ chological and sports injury rehabilitation outcomes (Fig. 8.2). A variety of other injury/rehabilitation psychological mod­ els exist, including the grief response model, with its well­ known stages of denial, anger, bargaining, depression and acceptance (Gordon et al 1991 ). There is also a cognitive

8 Assessme n t, trea tment a n d reh a b i l itation 1 7 3 1--_Charactertstlcs of ...f�____ Socl odemognplch Figure 8.2 The biopsychosocial model of sports i njury and the fnjury fac:ton rehabilitation. Reproduced with permission from Kolt & Snyder­ , Type , Age , Course • Gender Mackler (2003). , Severity • Raceiethnicity , Location Psychological , Socioeconomic , History faclon status , Endocrine • Personality , Metabolism , Cognition , Neurochemistry ' Affect , TIssue repair , Behavior , Nutrition , Situational characteristics • Rehabilitation environment Intennedlate Sport Injury rehabDltatIon blopaychologlcal outc:omea oufIlonIeI • Functional performance • Quality of life , Range of motion • Treatment satisfaction , Strength • Readiness to retum to sport , Joint laxity , Pain , Endurance • Rate of recovery Set goals exercise programs (as well as other health enhancement self-help programs), even when the individuals felt that the Secure effort was producing benefits. Research indicates that most commitment rehabilitation programs report a reduction in participation in exercise (Lewthwaite 1990, Prochaska & Marcus 1994). Feedback on Develop goal attainment action plan Wigers et al (1996) found that 73% of pa tients failed to continue an exercise program when followed up, although Figure 8.3 The goal setting implementation process. Reprod uced 83% felt they would have been better if they had done so. with permission from Kolt & Snyder-Mackler (2003). There is no record of whether patient-centered goaJ setting was part of this research. Participation in exercise is more appraisal model that involves the individual's particular likely if the individual finds it interesting and rewarding. stress and coping responses (Horsley 1995). For a greater understanding of these issues the text by Kolt & Snyder­ Research into patient participation in their recovery pro­ Mackler (2003) is recommended. grams in fibromyalgia settings has noted that a key element is that wha tever is advised (exercise, self-treatment, dietary Rehabilitation demands a process of goal setting and change, etc.) needs to make sense to the individual, in their implementation as outlined by Liebenson above. This can own terms, and that this requires consideration of cultural, ethnic and educational factors (Burckhardt 1994, Martin 1996). be visualized in the charted elements in Figure 8.3. In general, most experts, including Lederman (1997), CONCORD ANCE Lewit (1992) and Liebenson (1996, 2006) (see Further read­ ing), highlight the need (in treatment and rehabilitation of It is of major concern that concordance (aka compliance, dysfunction) to move as rapidly as possible from passive adherence, participation) is extremely poor regarding (opera tor-controlled) to active (pa tient-controlled) methods. The rate at which this happens depends largely on the degree of progress, pain reduction and functional improvement. PATIENT ADVICE AND CONCORDANCE (COMPLIANCE) ISSUES Individuals should be encouraged to l isten to their bodies and to never do more than they feel is appropriate in order

1 74 CLIN I CAL APPLICATI O N O F N E U R O M U SCU LAR TECH N I Q U E S : T H E U P PER B O DY to avoid what can be severe setbacks in progress when they It is useful to explain that all trea tment makes a demand for exceed their current capabilities. It is vital that rehabilitation a response (or several responses) on the part of the body strategies are very carefully explained, as active participa­ tion is not high when novel routines or methods are sug­ and that a 'reaction' (something ' feels different') is normal and gested unless they are well understood. expected and is not necessarily a cause for alarm but that i t Routines and methods (homework) should be explained i s O K t o make contact for reassurance. in terms that make sense to the person and the practitioner(s). It may be useful to offer a reminder that symptoms are Written or printed notes, ideally illustrated, help greatly to support and encourage compliance with agreed strategies, not always bad and that change in a condition toward nor­ especially if simply translated examples of successful trials mal may occur in a fluctuating manner, with minor setbacks can be included as examples of potential benefit. Information offered, spoken or written, needs to answer in advance ques­ along the way. tions such as: It can be helpful to explain, in simple terms, that there are • Why is this being suggested? many stressors being coped with and that progress is more • How often, how much? • How can it help? likely to come when some of the 'load' is lightened, espe­ • What evidence is there of benefit? cially if particular functions (digestion, respiratory, circula­ • What reactions might be expected? tion, etc.) are working better. • What should I do if there is a reaction? • Can I call or contact you if I feel unwell after exercise (or A basic understanding of homeostasis is also helpful (,broken bones mend, cuts heal, colds get better - all exam­ other self-applied treatment)? ples of how your body always tries to heal itself') with par­ ticular emphasis on explaining processes at work in the patient's condition. References Ekbom K 1960 Restless legs syndrome. 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Paule-Sastre J, G6mez­ Travell J, Simons D 1992 Myofascial pain and dysfunction: the trig­ Magan J C, Salvatierra-Rios D 1994 Intestinal permeability in ger point manual, vol 2: lower extremities. Williams and patients with ankylosing spondylitis. British Journal of Wilkins, Baltimore Rheumatology 33:644-647 Troup J D G, Videman T 1989 Inactivity and the aetiopathogenesis of musculoskeletal disorders. Clinical Biomechanics 4:173-178 Mascarenhas R. Mobarhen S 2004 Hypovitaminosis D-induced Van Wingerden J-p 1997 The role of the hamstrings in pelvic and pain. Nutrition Reviews 62(9):354-359 spinal function. In: Vleerning A, Mooney V, Dorman T, Snijders C, Stoekart R (eds) Movement, stability and low back pain. Matre D, Sinkjaer T, Knardahl S et al 1999 The influence of experi­ Churchill Livingstone, Edinburgh mental muscle pain on the human soleus stretch reflex during sitting and wal king. Clinical Neurophysiology 110:2033-2043 Vlaeyen J W, Teeken-Gruben N J. Goossens M E et al 1996 Cognitive-educational treatment of fibromyalgia: a randomized Mayer K, Meyer S, Reinholz-Muh.ly M et al 2003 Short-time infu­ clinical trial. 1. Clinical effects. Journal of Rheumatology sion of fish oil-based lipid emulsions, approved for parenteral 23(7):1237-1245 nutrition, reduces monocyte proinfiammatory cytokine genera­ tion and adhesive interaction with endothelium in humans. Journal of Immunology 1 71 :4837-4843 Mehling W E, Hamel K A, Acree M et al 2005 Randomized, controlled trial of breath therapy for patients with chronic low­ back pain. Alternative Therapies in Health and Medicine 1 1 (4) :44-52

1 76 CLIN I CAL APPLICATI O N O F N E U RO M USCU LAR TECH N I Q U E S : T H E U P PER B O DY Vleeming A, Van Wingerden J, Snijders C 1989 Load application to Ward R (ed) 1997 Foundations of osteopathic medicine. Williams the sacrotuberous ligament: influences on sacroiliac joint and Wilkins, Baltimore mechanics. Clinical Biomechanics 4:204-209 Watson P 2000 Interdisciplinary pain management in fibromyalgia. In: Chaitow L (ed) Fibromyalgia syndrome - a practitioner's WaddeJi G 1998 The back pain revolution. Churchill Livingstone, guide. Churchill Livingstone, Ed inburgh Edinburgh Wigers S H, Stiles T C, Vogel P A 1996 Effects of aerobic exercise Waddell G, Feder G, McIntosh A, Lewis M, H utchinson A 1996 Low versus stress management treatment in fibromyalgia: a 4.5 year back pain: evidence review. Royal College of General prospective study. Scandinavian Journal of Rheumatology Practitioners, London 25:77-86 Further reading Lederman E 2005 The science and practice of manual therapy, 2nd edn. Churchill Livingstone, Edinburgh For more detailed descriptions of the functional organiza­ tion of the motor system and of therapeutic considerations Lewit K 1 999 Manipulative therapy in rehabilitation of the locomo­ the following are recommended for further reading. Note tor system. Butterworths, London that these texts do not always agree on which manual meth­ ods are most helpful! Liebenson C (ed) 2006 Rehabilitation of the spine, 2nd edn. Lippincott Williams and Wilkins, Philadelphia Kolt G, Snyder-Mackler L 2003 Physical therapies in sports and exercise. Churchill Livingstone, Edinburgh Morris C 2005 Low back pain syndromes: integrated clinical man­ agement. McGraw-Hili, New York Lederman E 1997 Fundamentals of manua l therapy. Churchill Livingstone, Edinburgh Vleeming A, Mooney V, Stoeckart R (eds) 2007 Movement, stability and lumbopelvic pai.n: i.ntegration of research and therapy, 2nd edn. ChurchilI Livingstone, Edinburgh

177 Chapter 9 Modern neuromuscular techniques CHAPTER CONTENTS NEUROMUSCULAR THERAPY - AMERICAN VERSION Neuromuscular therapy - American version 1 77 Biomechanical factors 178 Neuromuscular therapy (NMT) American version™, as pre­ Biochemical factors 179 sented in this volume, will attempt to address (or at least take Psychosocial factors 180 account of) a number of features that are all commonly Biomechanical, biochemical and psychosocial involved in causing or intensifying pain (Chaitow 2003a). interaction 180 These include, among others, the following factors that affect NMT techniques contraindicated in initial stages of the whole body: acute injury 181 NMT for chronic pain 182 • nutritional imbalances and deficiencies Palpation and treatment 182 • toxicity (exogenous and endogenous) Treatment and assessment tools 189 • allergic/intolerance reactions Pain rating tools 190 • endocrine imbalances Treatment tools 190 • stress (physical or psychological) • posture (including patterns of use) European (Lief's) neuromuscular • hyperventilation tendencies technique (NMT) 191 NMT thumb technique 192 as well as locally dysfunctional states such as: Liefs NMT finger technique 193 Use of lubricant 194 • hypertonia Variations 194 • ischemia Variable ischemic compression 194 • inflammation A framework for assessment 195 • sensitization Some limited NMT research 196 • myofascial trigger points Integrated neuromuscular inhibition • neural compression or entrapment. technique 197 These 'components of pain and dysfunction' are particu­ larly significant areas of influence on the perception of pain, its intensity and its spread throughout the body, as well as on the maintenance of dysfunctional states. These and other factors can be broadly clustered under the headings of: • biomechanical (postural dysfunction, hyperventilation ten­ dencies, hypertonicity, neural compression, trigger point activity) • biochemical (nutrition, ischemia, inflammation, heavy metal toxins, hyperventilation tendencies) • psychosocial (stress, hyperventilation tendencies). It is necessary to address whichever of these (or additional) influences on musculoskeletal pain can be identified in

178 C L I N I C A L APPLI C AT I O N OF N E U R O M U S C U LA R T E C H N I Q U E S : T H E UPP E R B O DY [ Neuromuscular therapy tech niq ues have emerged in both Europe and medical, dental, massage and other therapeutic com m u n ities with North America almost simulta neously over the last 50 years. Fi rst documen tation, research and references for a whole new field of developed by Stanley Lief and Boris Chai tow, European-style NMT study - myofascial trigger poi nts. was developed between the m id-1930s and ea rly 1940. Trained i n chiropractic and naturopathy, these cousins developed i n teg rated Several of N i m mo's students bega n teach ing their own NMT concepts learned from teachers l ike Dewa nchand Varma and Bernarr protocols, based on Ni mmo's work. I n the USA the acronym NMT M a c fa d d e n . sign i fied neurom uscular therapy rather than technique. NMT St John Method and NMT American version became two prominent systems Lief and Cha itow developed and refi ned what they called which today still retain a strong focus on Nimmo's original 'neuromuscular techniq ues' as a means of assessing and treating soft tech n i q u es. tissue dysfunction, i n Liefs world-famous health resort, Cham pneys, at Tring in Hertfordshire, England. Many osteopaths and naturopaths European and American versions of NMT have subtle differences have taken part in the evolution and development of European neuromuscular therapy, i n clu d i ng Peter Lief, Brian Youngs, Terry in their hands-on applications wh ile reta i n i ng sim ilar fou ndations in Moule, Leon Chaitow and others. NMT is now taught widely i n their theoretical platform. North America n-style neuromuscular osteopathic and sports massage settings in Britain and forms part of therapy uses a med i u m-paced thumb or finger glide to uncover the tra i n ing lead ing to the Bachelor of Science (BSc(Hons)) degree in contracted bands or m uscular nodules whereas European-style Com plementary Health Sciences, Un iversity of Westmi nster, London. n eu romuscu lar techn iques use a slow-paced, thumb drag method of discovery. They also have slightly d ifferent emphasis on the method A few years after neuromuscular techniq ues developed i n Eu rope, of application of ischemic compression in treating trigger poi nts. across the ocean in America, Raymond Nimmo and James Vannerson Both versions emphasize a home care program and the patient's began writing of their experiences with what they termed 'noxious participation in the recovery process. nod ules', i n their newsletter, Receptor-Tonus Techniques. A step-by­ step system began to emerge, supported by the writings of Janet In this text. the American version of NMT is offered as the Travell and David Simons. Travell and Simons' work i m pacted the fou ndation for developing palpatory skills and treatment techniques wh ile the European version accompa nies it to offer an alternative a p p ro a c h . Box 9.2 SemantJc torrfusion .' A confusing element relating to the term NMT emerges from its use already in general manual medicine and osteopathic texts. In reality, by some European a u thors when they describe what are, in effect, almost all man ual methods that add ress either soft tissue or joint variations on the theme of isometric contractions (Dvorak et al dysfunction involve a degree of both muscula r and neural elements 1988). These methods, all of which form part of what is known as and could therefore receive a 'neuromuscular' designation. However, m uscle energy technique (MET) in osteopathic medicine, will be there would seem to be little to be gained via such an exercise. outlined in Box 9 .10. In this text, when the letters NMT a re used in relation to the Dvorak et al (1988) have listed various MET methods as NMT, as American version, it should be understood to indicate neuromuscular follows. therapies as described in this book in general and this chapter i n particu lar (i.e. a broad a pproach t o addressing musculoskeletal • Methods that i nvolve active self-mobilization in o rder to encour­ dysfu nction, i ncluding myofascial trigger poi nts). age movement past a resistance barrier are called 'NMT l' by Dvorak et al. When NMT is used in relation to the European approach it should be understood to refer only to the technique of assessment and • Isometric contraction, i nvolving postisometric relaxation and sub­ treatment of local m usculoskeletal dysfunction, mainly i nvolving sequent passive stretching of agonist muscles is described as myofascial trigger points u tilizing finger and/or thumb techniques, 'NMT 2'. and not the eclectic selection of complementary approaches i n corporated under the American NMT label. • Isometric contraction of antagonists, i nvolving reciprocal inhibi­ tion followed by stretching is called 'NMT 3' by Dvorak et a l . Naming these methods NMT 1, 2 and 3 would seem to add to (rather than reduce) semantic confusion since they a re adequately named order to remove or modify as many etiological and perpet­ active), tenderness, motor disturbances and autonomic uating stressors and influences as possible (Simons et al responses in other body tissues (see Chapter 6). Myofascial 1999), without creating further distress or reguirement for trigger points may form in muscle bellies (central trigger excessive adaptation. Unless this is comprehensively and points) or tendons and periosteal attachments (attachment effectively achieved, results of therapeutic intervention may trigger points). Trigger points can also occur in skin, fascia, be unsatisfactory (DeLany 1999). ligaments, periosteum, joint surfaces and, perhaps, in vis­ ceral organs. However, none of these would be considered BIOMECHANICAL FACTORS to be true myofascial TrPs since the mechanisms associated with their formation are apparently different from those Trigger points (TrPs) are located primarily in myofascial tis­ associated with motor endplate dysfunction in myofascial sues. These points are hyperirritable ('sensitized') spots tissues (Simons et al 1999). found in taut bands that are usually painful on compression and give rise to referred pain and other sensations (when Although it is not yet fully understood how trigger points develop, their locations and referral patterns are

9 Modern neuromuscular techniques 179 fairly predictable. NMT identifies and deactivates trigger heading of 'postural influences', habits of use need to be points primarily by means of trigger point pressure release considered, whether these involve overuse, disuse or abuse (previously known as ischemic compression). Lengthening (repetitive strain, hyperventilation breathing tendencies, the shortened fibers in which the points lie (stretching) is also inappropriate sitting, standing or sleeping habits). part of the process of treating the trigger points as should also be the removal of the underlying factors that helped create BIOCHEMICAL FACTORS them (Simons et aI1999). Biochemical factors can be local or global, both of which are Nerve entrapment/compression can result from pressure on fully discussed in Chapter 7. Ischemia is an insufficiency of blood flow (therefore of oxygen and nutrients) commonly neural structures by soft tissue including muscle, tendon, caused by muscular spasm or contracture. While global disc, ligament, fascia or skin or via more direct osseous pres­ ischemia is associated with less common conditions, such as sure (arthritic spur, for example). The structure(s) interfering cerebral palsy or regional spasms associated with spinal cord with normal neural function are known as the 'mechanical injuries, localized ischemia is so common that it is found (to interface'. The underlying cause of these entrapment/com­ some degree) in virtually every person. If ischemia is pro­ pression situations may lie in traumatic incidents or they longed, metabolic waste products accumulate and pool may be the result of repetitive microtrauma due to overuse or within the ischemic tissues, increasing neuroexcitability misuse patterns (work, sport, postural habits, etc.). (Cailliet 1996). This may predispose toward a local energy crisis developing within the muscle tissue and a resultant In order to evaluate the possibility of such entrap­ decrease in ATP production just when the tissue's energy ment/compression, it is necessary to be aware of neural needs increase (Simons et a11999), so encouraging the evolu­ pathways as well as which hard tissues may crowd the tion of myofascial trigger points (see Chapter 6). Mense et al nerve and/or which soft tissues may entrap them (see notes (2001) note that, 'Ischemia is one of the most potent factors on Butler's work in Chapter 13, Box 13.11, p. 475, as it relates releasing bradykinin.' Bradykinin is capable of encouraging to shoulder and arm pain). For example, when considering nociceptor sensitization (Koltzenburg et al 1992), which pain in the arm, pressure may have been placed on nerve results in an enhanced response to peripheral stimuli. This roots at the cord level by herniated discs, osteophytes or process leads to prolonged production of ischemia which subluxations; by the scalene muscles, as the nerves travel can be self-perpetuating. between or through them; by the clavicle or first rib; by pec­ toralis minor; or by upper extremity tissues, such as the tri­ NMT assesses and treats ischemia by using effleurage ceps or supinator muscles. Additionally, the position of the (gliding techniques), pressure release methods and length­ upper extremity itself may create tension and drag on the ening of the shortened myofascial fibers (stretching), which brachial plexus and its fascial ensheathment (e.g. the inter­ all encourage blood flow and a return to a more normal face between the head of the humerus and the glenoid fossa muscle length. alters if the shoulders are protracted). NMT attempts to identify such entrapments and compressions and to use Nutrition is an area of consideration in musculoskeletal manual methods and rehabilitation exercises to modify or pain and dysfunction that includes all the processes involved correct them, when possible. in the intake of nutrients necessary for cellular metabolism, repair and normal reproduction of cells in the body as a Postural (and use) influences are innumerable. Debate con­ whole. It includes ingestion, digestion, absorption, assimila­ tinues as to the extent to which there is an anatomically 'cor­ tion and a multitude of processes associated with these func­ rect' degree of alignment of the musculoskeletal system, a tions. Sound nutrition also considers avoidance of exposure so-called 'correct' or 'perfect' posture. Experts, including to substances that may be irritating and stimulating to the Feldenkrais (1972) and Hanna (1988), suggest that a degree nervous system or toxic to the body (smoke, heavy metals, of asymmetry is, in fact, the norm but that within that asym­ chemical exposures, excessive caffeine, etc.). metry there ought to be a relatively 'normal' functional balance, range of motion, etc., taking account of genetic Nutritional imbalances may perpetuate the existence of characteristics (hyperflexibility, for example), body type ischemia, trigger points, neuroexcitation and the resultant and age. The common compensatory pattern described by postural distortions (Simons et al 1999). Vitamin and min­ Zink & Lawson (1979) helps to explain 'normal' (or at least eral status should be considered, adequate fluid intake common) postural deviations (see Chapter 1). ensured and breathing habits evaluated (since both oxygen and carbon dioxide are critical factors in the nourishment of Janda (1982) and Lewit (1992), among others, have iden­ the body) . Additionally, obvious or hidden (,masked') food tified patterns of dysfunction that modify regions in rela­ intolerances and allergies should be identified in order to tion to each other (see crossed syndrome discussion in minimize the numerous negative effects such reactions can Chapter 5). NMT seeks to correct dysfunctional postural have, including increased nociception and lymphatic con­ patterns by releasing stressful tension in muscular and fas­ gestion (Randolph 1976). cial tissues. An individualized home care program is usu­ ally developed, which includes awareness of undesirable as Additional biochemical influences that may require considera­ well as improved postural and use habits, appropriate tion include endocrine balance/imbalance (most particularly stretching and strengthening procedures. Under the general

180 CL INI CAL APP L I CAT I ON O F N E U R O M U SC ULA R T E C H N I Q U ES: T H E UPP E R B ODY thyroid in the case of myofascial pain) (Ferraccioli 1990, Within these categories - biochemical, biomechanical and Lowe & Honeyman-Lowe 1998) and inflammatory processes (discussed in more detail in Chapter 7). A critical biochemical psychosocial - are to be fOildl most major influences on influence on pain involves the balance between oxygen and health, with 'subdivisions' (such as ischemia, postural imbal­ carbon dioxide in the body, which is intimately connected ance, trigger point evolution, neural entrapments and com­ with breathing patterns - a biomechanical function with huge pressions, nutritional and emotional factors) being of psychosocial overlays. This 'three-way' interaction is dis­ particular interest in NMT. cussed in greater detail in Chapter 4. NMT attempts to identify these altered states, insofar as PSYCHOSOCIAL FACTORS they impact on the person's condition, and either offers ther­ apeutic intervention that reduces the 'load' and/or assists the The influence of emotional stress on the musculoskeletal self-regulatory filcl tions of the body (homeostasis) or, if this system is beyond doubt (see Chapter 4). It is sufficient at is inappropriate or outside the therapist/practitioner's scope this stage to restate that there exists a fundamental require­ of practice, opens the opportunity for referral to appropriate ment for stress factors, whether self-generated or externally healthcare professionals. derived, to be considered as a part of the 'load' to which the individual is adapting. The degree to which anyone can be A home care program should be designed for both physical helped in regard to emotional stress relates directly to how relief of the tissues (stretching, self-help therapies, hydrother­ much of the load can be removed, as well as to how effi­ apies, postural awareness) and removal of perpetuating fac­ ciently adaptation is occurring. The same can, of course, be tors, including nutritional choices, postural habits, work and said for biochemical and biomechanical stresses. recreational practices, stress and lifestyle factors (rest, exer­ cise, etc.) (see notes on concordance in Chapter 8, p. 173). The role of the practitioner may include teaching and Lifestyle changes are encouraged to eliminate influences encouraging the individual (and their self-regulating, homeostatic functions) to handle the load more efficiently, Injury Tensile as well as alleviating the stress burden as far as possible. strength This would involve improving functional efficiency and removing negative influences, manually and by means of Inflammation rehabilitation, and nowhere is this seen more graphically than in the changes associated with breathing dysfunction 8 '--- �p-has-e -�--Reg-ene-ratio-n ai�d-r-e- mo-del-ing --- Time (Chaitow 2003b, Selye 1956). Evidence shows that this may be best achieved by a combination of relearning diaphrag­ Time : About day : :From about day 5-14 Starts about day 21. lasting until matic respiration, structural mobilization of the thorax, (depends on stress management, and a lifestyle that encourages nutri­ extent of : 4...0. : May last a few weeks.: about day 60. tional excellence, adequate exercise and sleep (DeGuire et al damage) 1996, Gardner 1996, Mehling et al 2005). Physiotogicat : Initially : Increase in number : Fibroblasts remain active. BIOMECHANICAL, BIOCHEMICAL AND : of fibroblasts : Turnover of collagen still high. process : blood clot. PSYCHOSOCIAL INTERACTION : Predominantly : and myofibroblasts. : Myofibroblasts disappear, The influences of a biomechanical, biochemical and psy­ : Increase in collagen chosocial nature do not produce single changes. Their inter­ : immune : deposition and : contraction of the scar ceases. action with each other is profOlmd. For example: : cells and : After day 60 cellular content of scar • Hyperventilation modifies blood pH, induces hypoxia, : cells that modifies calcium and magnesium status, alters neural : removal. : decreases, with a reduclion in reporting (initially hyper and then hypo), creates feelings : clean up the of anxiety and apprehension, and directly impacts on the : Scar contraction. : collagen turnover. structural components (both muscles and joints) of the : wound site. thoracic and cervical region (Gilbert 1998). : Very litlle , , : collagen. , , • Altered chemistry (hypoglycemia, acidosis, alkalosis, etc.) , , affects mood directly while altered mood (depression, anxi­ , , ety) changes blood chemistry as well as altered muscle tone and, by implication, trigger point evolution (Brostoff 1992). Response to :: No tensile : Increase in tensile : Improved mechanical behavior of mechanical strength. • Altered structure (e.g. posture) modifies fillction (e.g. stress : Poor response : strength. : scar. breathing) and therefore impacts on chemistry (e.g. : to mechanical 02:C02 balance, circulatory efficiency and delivery of : stress. : Fibroblasts and nutrients, etc.) which impacts on mood (Gilbert 1998). : collagen align : along lines of stress. : Improved formation : of blood vessels : along lines of stress. : Normal turnover of : collagen. F igure 9.1 Stages of the repair process.