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Patient Medical History Importance for Optimal Treatment

Patient Medical History Importance for Optimal Treatment

The first step in chiropractic care is getting the individual’s medical history. Many visit a chiropractor with certain expectations of how things will go. They will lay down on a table while the chiropractor adjusts the spine. There will be pops and cracks, and the tension will go away. And afterward, they�ll feel better. However, without an individual’s medical history, the treatment will not be as effective because of the lack of information. This means that a chiropractor is only able to perform general adjustments but is not able to get to the root cause and maximize the full potential of the adjustments. Patient education starts the moment someone walks into the clinic.  
11860 Vista Del Sol, Ste. 128 Patient Medical History Importance for Optimal Treatment
 

The nature of holistic medicine

Some questions a chiropractor might ask include:
  • What type of pain is presenting – shooting, burning, aching, throbbing, etc?
  • Have you had any recent surgeries?
  • Is there a history of chronic pain?
  • What medications are being taken?
Each will be explained in further detail and what they mean for the development of a treatment plan. An individual needs to understand how important their medical histories are for treatment progress. Patient history prevents executing the wrong treatment plan by having an informed understanding of the individual’s body. For example, a chiropractor can�t perform the same adjustments on a senior with osteoporosis that they do on a middle-aged athlete. And someone recovering from surgery will not have the range of motion when healthy. An adjustment can result in X, Y, or Z, depending on the factors at work. Medical history is vital as it eliminates any unknowns, so a chiropractor can solve for X, Y, or Z by being able to provide the best outcome for the individual.  
 

The more information, the better the treatment plan

When an individual has neck pain, a doctor is not going to prescribe immediate surgery, unless it is an emergency. Rather, they will perform a full examination, ask questions, try to find the cause, and analyze the intensity of the pain. A chiropractor is no different, and individual medical history is vital. Obtaining as much information as possible can help a chiropractor reach a proper diagnosis and ensures the right course of action is taken. Individuals often do not realize but for example,
  • An automobile accident that happened last year could be manifesting symptoms now.
  • Shoulder surgery five years ago could be limiting the range of motion, affecting the musculature around the cervical spine.
  • Chronic plantar fasciitis and self-medicating for a while can cause instability in the lumbar spine affecting the cervical spine.
Every little bit of information can help put the puzzle together to get a clear picture of what is going on. The biggest contributor of information is patient medical history, formally documented and informally spoken.  
11860 Vista Del Sol, Ste. 128 Patient Medical History Importance for Optimal Treatment
 

Informed care

A visit to Injury Medical Chiropractic Clinic is a collaboration between patient and chiropractor that leads to informed and the best treatment possible. Medical history informs optimal care. For more information or for more tips on chiropractic care, contact us today.

New Patient Chiropractic Care

 

Dr. Alex Jimenez�s Blog Post Disclaimer

The scope of our information is limited to chiropractic, musculoskeletal, physical medicines, wellness, and sensitive health issues and/or functional medicine articles, topics, and discussions. We use functional health & wellness protocols to treat and support care for injuries or disorders of the musculoskeletal system. Our posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate and support directly or indirectly our clinical scope of practice.* Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. We understand that we cover matters that require an additional explanation as to how it may assist in a particular care plan or treatment protocol; therefore, to further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900. The provider(s) Licensed in Texas& New Mexico*
References
Hunter, J. �Medical history and chronic pain.��The Clinical journal of pain�vol. 17,4 Suppl (2001): S20-5. doi:10.1097/00002508-200112001-00007
Chiropractic: A Brief History Of Its Origin

Chiropractic: A Brief History Of Its Origin

The history of chiropractic dates all the way back to 1895 when Daniel David (DD) Palmer, founder of chiropractic, did his first spinal adjustment on a janitor � restoring his hearing in the process. Palmer moved from what is now Ontario, Canada to the United States in 1865 and started practicing magnetic healing and other natural health practices in Davenport, Iowa in 1880. His interest in a more organic, less invasive approach to healing opened the door for the natural, whole body wellness that chiropractic provides.

Chiropractic

In 1895, Palmer encountered a janitor who claimed that he had lost his hearing when he moved and heard a �pop� in his back. Upon inspection, Palmer noted that the janitor had a vertebra out of place. He had the man lie on the floor, face down, while he manipulated the man�s spine, gently coaxing it into alignment. The next day the janitor claimed that he could hear again.

Two years later, after extensive research and development of the practice of what he called �chiropractic,� he opened the Palmer School of Cure where he began teaching others his techniques. After that first adjustment, word spread and this new, mysterious practice piqued the interest of the public, many who became students, including Palmer�s own son, Bartlett Joshua. Quite a few early students were practitioners of the healing arts of osteopathy and medicine. The school is still operational today as the Palmer School of Chiropractic.

The term was first coined by DD Palmer and is derived from two Greek words, the first cheir which means �hand� and praktos which means �done.� A literal translation is �done by hand� which is an apt moniker for this very hands on practice.

The first state to create laws licensing chiropractors was Kansas in 1913. By 1931, 39 states were on board, giving legal recognition to chiropractors. The last state was Louisiana in 1974.

chiropractic history el paso tx.

There are more than 60,000 active licenses in the U.S. alone. Several U.S. territories, including the U.S. Virgin Islands and Puerto Rico officially recognize the practice as a legitimate health care profession. Switzerland, Japan, Australia, Great Britain, Mexico, and Canada, as well as other countries, also recognize chiropractic and have created laws to regulate it.

Over the years, chiropractic has evolved and grown beyond the sole use of spinal adjustments as treatment. Other treatments and philosophies have been developed and introduced. Research was initiated in 1975 at a conference hosted by the National Institutes of Health.

Over the years, chiropractic was not met with much acceptance by many medical associations – initially anyway. Eventually, many have come on board once that have seen chiropractic�s benefits. In 1987, the American Medical Association filed and lost an antitrust case against chiropractic. Until that time, the AMA had been boycotting the practice. That ended when they lost their case.

Chiropractic successfully changed the landscape of health care and health care practitioners. By providing a whole body approach, it has been used to treat a variety of conditions from back pain to knee injuries to colic in infants. Research backing it as a legitimate medical practice is steadily mounting. Chiropractic is proving to be beneficial for a wide variety of health ailments that extend far beyond a painful back.

As chiropractic continues to develop and grow, even more doors are opened, allowing the practice to grow and evolve. Every year researchers are finding more uses for chiropractic treatment and discovering just how beneficial it can be for a myriad of health conditions. As fast as it has grown since its discovery, it is easy to envision continued, rapid advancement in the years to come.

Injury Medical Clinic: Chiropractor (Recommended)

Fibromyalgia History And Definition

Fibromyalgia History And Definition

Fibromyalgia History

Fibromyalgia History: Historically, fibromyalgia � or conditions very like it � have been reported for hundreds of years, under many names, including the most unsatisfactory term �fibrositis�. The fascinating history of what we now call fibromyalgia syndrome (FMS) and myofascial pain syndrome (MPS) has been catalogued by several modern clinicians working in the sphere of chronic muscle pain, from whose work the material summarized in Box 1.1 has been compiled. Thanks are due to these individuals (Peter Baldry, David Simons and Richard van Why in particular) for revealing so much about past studies into the phenomenon of chronic muscle pain. What we can learn from this information is just how long ago (well over 150 years) particular features were recognized, for example pain referral patterns and characteristics such as taut bands and �nodules�, as well as insights from many astute researchers and clinicians into the pathophysiology of these conditions.

American College Of Rheumatology Definition

Simply defined, fibromyalgia syndrome (FMS) can be said to be a debilitating illness, characterized primarily by musculoskeletal pain, fatigue, sleep disturbances, depression and stiffness (Yunus & Inanici 2002). It was not until the 1980s that a redefining took place of what was by then a confused � and confusing � picture of a common condition. In 1987, the American Medical Association recognized fibromyalgia as a distinct syndrome (Starlanyl & Copeland 1996), although at that time detailed knowledge of what the syndrome comprised was not as clear as the current, generally accepted American College of Rheumatology (ACR) definition, which was produced in 1990 (see Box 1.2 and Fig. 1.1). Russell (in Mense & Simons 2001) notes that defining the condition had profound effects on the scientific and medical communities:

fibromyalgia historyfibromyalgia historyfibromyalgia historyfibromyalgia history

fibromyalgia history

In the wake of successful classification criteria, a surge of investigative energy in the early 1990s led to a number of important new observations. FMS was found to be universally common. It was present in approximately 2% of the adult population of the USA and exhibited a similar distribution in most other countries where valid epidemiological studies had been conducted. Adult women were affected five to seven times more commonly than were men. In children the gender distribution was about equal for boys or girls.

When psychosocial and physical/functional factors of people with FMS were compared with those six different, predominantly chronic pain syndromes (upper extremity pain, cervical pain, thoracic pain, lumbar pain, lower extremity pain and headache), it was found that the fibromyalgia group experienced the most difficulties, by a significant margin. In regard to gender distribution of these seven chronic pain conditions, it was noted that fibromyalgia (and headache) are experienced by more females than males (Porter-Mofitt et al 2006).

fibromyalgia history

 

What can be said with certainty about fibromyalgia syndrome is that:

� It is a non-deforming rheumatic condition, and, indeed, one of the commonest such conditions.

� It is an ancient condition, newly defined (controversially � see below) as a disease complex or syndrome.

� There is no single cause, or cure, for its widespread and persistent symptoms (however, as will become clear, there do seem to exist distinct subsets of individuals with different aetiologies to their conditions, such as thyroid imbalance and whiplash injuries).

� Its complex causation often seems to require more than one essential aetiological factor to be operating, and there are numerous theories as to what these might be (see Ch. 4).

� There has been an explosion of research into the subject over the past decade (one data search on the internet revealed over 20 000 papers which mention fibromyalgia as a key word).

Despite its earlier medical meaning, which suggested involvement of both articular and non-articular structures, the word rheumatic has, through common usage, come to mean �a painful but nondeforming soft tissue musculoskeletal condition�, as distinct from the word arthritic which suggests articular and/or deforming features (Block 1993).

The Fibromyalgia Controversy

For the purposes of practicality this book accepts that the current widely used ACR definition is a hypothesis that is evolving, but that it may be flawed (see below). The definition as presented in Box 1.2 allows for the categorization of individuals with chronic pain and associated symptoms into subgroups, and offers clinicians a chance to begin to decipher the confusing patterns of symptoms displayed and reported by people who have been so labelled. However, not all experts, including many of the contributors to this text, accept the ACR definition. Nevertheless, since it forms the foundation for much of the research reported on in the book, the current definition needs to be given due consideration.

What Are The Arguments Against The ACR Definition?

Schneider et al (2006) sum up one major alternative view:

Recent data tend to support the notion that FMS is a disorder of the central nervous system pain processing pathways, and not some type of primary auto-immune disorder of the peripheral tissues. It is quite possible that the term FMS is a poor choice of words, for it implies that patients with a variable symptom complex all have the same singular disease or disorder.

As will be clear in subsequent chapters, this is precisely the message that this book will promote � that there are numerous aetiological influences relating to the symptom cluster represented by people with a diagnosis of FMS, and that within that population subgroups can be identified that demand quite distinctive therapeutic handling, compared with other subgroup cohorts. A logical extension of this multicausal scenario is a model that offers a variety of potential therapeutic interventions, none of which would have universal applicability, and most of which would be most usefully employed in treatment of specific subgroups within the overall diagnosis of FMS. The chapters in this book that reflect a variety of therapeutic approaches include those that evaluate and explain the use of acupuncture, endocrine issues, psychological influences, myofascial trigger points/ dry needling, use of microcurrent, hydrotherapy, therapeutic touch, manipulation, massage, exercise, nutrition and various other clinical methods. The issues surrounding FMS subsets, and of possible over(or mis-)diagnosis of FMS, are explored more fully in Chapters 3, 4 and 5.

Problems Arising From The ACR Definition

Useful as the defining of this condition has been, there are distinct and obvious problems with a definition as precise as that offered by the ACR:

� If pressure varies only slightly, so that on a �good day� a patient may report sensitivity and tenderness rather than �pain� when tender points are being tested, the patient may therefore not �qualify�; this could have very real insurance benefit implications, as well as leaving distressed individuals still seeking a diagnosis which might help them understand their suffering.

� If all other criteria are present, and fewer than 11 of the 18 possible sites are reported as �painful� (say only 9 or 10), what diagnosis is appropriate?

� If there are 11 painful sites but the �widespread� nature of the pain is missing (as per the definition in Box 1.2), what diagnosis is appropriate? Clearly, what is being observed in people with widespread pain and who also demonstrate at least 11 of the 18 test points as being painful is a situation which represents the distant end of a spectrum of dysfunction. Others who do not quite meet the required (for a diagnosis of FMS) number of tender points may well be progressing towards that unhappy state.

As reported earlier, approximately 2% of the population meet all the ACR criteria (Wolfe et al 1993). A great many more people, however, are advancing in that direction, according to both British and American research, which shows that about 20% of the population suffer �widespread� pain that matches the ACR definition, with almost the same number, but not necessarily the same people, demonstrating 11 of the specified 18 tender points as being painful on appropriate testing, also in accordance with the ACR definition. Some people have the widespread pain and not enough painful points, while others have the points but their generalized pain distribution is not sufficiently widespread.

What Condition Do They Have If It Is Not FMS (Croft et al 1992)?

If all the criteria are not fully met, and people with, say, 9 or 10 points (rather than the 11 needed) are offered a diagnosis of FMS (and therefore become eligible for insurance reimbursement or disability benefits, or suitable for inclusion in research projects), what of the person with only 8 painful points who meets all the other criteria?

In human terms this is all far from an academic exercise, for pain of this degree is distressing and possibly disabling, whether or not 11 (or more) points are painful. Clinically, such patients should receive the same attention, wherever they happen to be in the spectrum of disability, and whatever the tender point score, if their pain is sufficient to require professional attention.

As will become clear as examination of FMS unfolds in this and subsequent chapters, the frustration of the patient is matched in large degree by that of health care providers attempting to understand and offer treatment for the patient with FMS. This is largely because no single aetiological pattern has emerged from research efforts to date. Russell (in Mense & Simons 2001) sums it up as follows:

The cause of FMS is unknown, but growing evidence indicates that its pathogenesis involves aberrant neurochemical processing of sensory�signals in the CNS. The symptomatic result is lowering of the pain thresholds and an amplification of normal sensory signals until the patient experiences near constant pain.

As will also become clear, the components of the pathogenesis of the condition commonly include biochemical, psychological and biomechanical features. Somewhere in the combination of causal elements and unique characteristics of the individual may lie opportunities for functional improvement and the easing of the often intractable pain and other symptoms associated with FMS.

Symptoms Other Than Pain

In 1992, at the Second World Congress on Myofascial Pain and Fibromyalgia in Copenhagen, a consensus document on fibromyalgia was produced and later published in The Lancet (Copenhagen Declaration 1992). This declaration accepted the ACR fibromyalgia definition as the basis for a diagnosis, and added a number of symptoms to that definition (apart from widespread pain and multiple tender points), including persistent fatigue, generalized morning stiffness and non-refreshing sleep.

The Copenhagen document recognized that people with FMS may indeed at times present with fewer than 11 painful points � which is clearly important if most of the other criteria for the diagnosis are met. In such a case, a diagnosis of �possible FMS� is thought appropriate, with a follow-up examination suggested to reassess the condition.

There are practical implications for a cut-off point (of symptoms or tender point numbers, for example) in making such a diagnosis: these relate directly to insurance reimbursement and/or disability benefits, as well as, possibly, to differential diagnosis.

The Copenhagen document adds that FMS is seen to be a part of a larger complex which includes symptoms such as headache, irritable bladder, dysmenorrhoea, extreme sensitivity to cold, restless legs, odd patterns of numbness and tingling, intolerance to exercise, and other symptoms.

Mind Issues

The Copenhagen Declaration (1992) of the symptoms associated with FMS (over and above pain, which is clearly the defining feature) also addresses the psychological patterns often related to FMS, namely anxiety and/or depression.

The possible psychological component in FMS is an area of study fraught with entrenched beliefs and defensive responses. A large body of medical opinion assigns the entire FMS phenomenon � as well as chronic fatigue syndrome (CFS) � to the arena of psychosomatic/psychosocial illness. An equally well-defined position, occupied by many health care professionals as well as most patients, holds that anxiety and depression symptoms are more commonly a result, rather than a cause, of the pain and disability being experienced in FMS (McIntyre 1993a).

A 1994 review paper analysed all British medical publications on the topic of CFS from 1980 onwards and found that 49% favoured a non-organic cause while only 31% favoured an organic cause. When the popular press was examined in the same way, between 70% (newspapers) and 80% (women�s magazines) favoured an organic explanation (McClean & Wesseley 1994).

Typical of the perspective which holds to a largely �psychological� aetiology is a multicentre study by Epstein and colleagues, which was published in 1999. It concluded: �In this multicenter study, the persons with FMS exhibited marked functional impairment, high levels of some lifetime and current psychiatric disorders, and significant current psychological distress.� The most common disorders noted were major depression, dysthymia, panic disorder and simple phobia.

Many leading researchers into FMS who hold to an organic � biochemical � neurological explanation for the main symptoms are, however, dismissive of psychological explanations for the condition. Dr Jay Goldstein, whose detailed and important research and clinical insights into the care of patients with CFS and FMS will be outlined later in this book, uses the term �neurosomatic� to describe what he sees as a disorder of central information processing. He makes clear his position regarding the non-organic, psychosocial school of thought (Goldstein 1996):

Many of the illnesses [CFS, FMS] treated using this model [neurosomatic] are still termed �psychosomatic� by the medical community and are treated psychodynamically by psychiatrists, neurologists and general physicians. Social anthropologists also have their theories describing CFS as the �neurasthenia� of the 1990s, and a �culture bound syndrome� that�displaces the repressed conflicts of patients unable to express their emotions (�alexithymics�) into a culturally acceptable viral illness or immune dysfunction. Cognitive�behavioural therapy is perhaps more appropriate, since coping with the vicissitudes of their illnesses, which wax and wane unpredictably, is a major problem for most of those afflicted. Few investigators in psychosomatic illness (except those researching panic disorders) have concerned themselves about the pathophysiology of the patients they study, seeming content to define this population in psychosocial phenomenological terms. This position becomes increasingly untenable as the mind�body duality disappears.

Goldstein says that he only refers patients for psychotherapy if they are suicidally depressed. He emphasizes the normalization (using a variety of medications) of the biochemical basis for neural network dysfunction, which he has satisfied himself is the underlying cause of these (and many other) conditions.

When Is A Cause Not A Cause?

Goldstein�s methods will be examined in later chapters; however, it might prove useful at this stage to make a slight diversion in order to clarify the importance of looking beyond apparent causes to attempt to uncover their origins.

As we progress through the saga which is FMS (and CFS) we will come across a number of welldefined positions which maintain that the dominant cause is X or Y � or more usually a combination of X and Y (and possibly others). The truth is that in some important instances these �causes� themselves have underlying causes, which might usefully be therapeutically addressed.

An example � which will emerge in more detail later � is the suggestion that many of the problems associated with FMS (and CFS) are allergy related (Tuncer 1997). This may well be so in the sense that particular foods or substances can be shown, in given cases, to provoke or exacerbate symptoms of pain and fatigue. But what produces this increased reactivity/sensitivity? Are there identifiable causes of the (usually food) intolerances (Ventura et al 2006)?

In some cases this can be shown to result from malabsorption of large molecules through the intestinal wall, possibly due to damage to the mucosal surfaces of the gut (Tagesson 1983, Zar 2005). In some cases the mucosal damage itself can be shown to have resulted from abnormal yeast or bacterial overgrowth, resulting from prior (possibly inappropriate) use of antibiotics and consequent disturbance of the normal flora, and their control over opportunistic organisms (Crissinger 1990). Or the disturbed gut mucosa may be associated with endotoxaemia involving disturbed beneficial bacteria status (McNaught et al 2005).

The layers of the onion can be peeled away one by one, revealing causes which lie ever further from the obvious. The pain is aggravated by allergy, which results from bowel mucosa damage, which results from yeast overgrowth, which results from excessive or inappropriate use of antibiotics… and so on. The allergy in this example is not a cause per se but an exacerbating factor, a link in a chain, and while treating it might satisfactorily reduce symptoms, it would not necessarily deal with causes. Neither would treating the bacterial or yeast overgrowth, although this too might well assist in reducing overall symptom distress.

Where does the cause lie in this particular individual�s FMS? Probably in a complex array of interlocking (often historical) features, which may be impossible to untangle. Therefore, approaches such as those which direct themselves at the allergy or at the increased permeability, while possibly (in this instance) valid and helpful, are not necessarily dealing with fundamental causes.

Does this matter? In Goldstein�s model of FMS and CFS aetiology we are faced with a neural network which is dysfunctional. He acknowledges that the evolution of such a state requires several interacting elements:

� a basic susceptibility which is probably genetically induced

� some developmental factors in childhood (physical, chemical or psychological abuse/ trauma, for example)

� probably a degree of viral encephalopathy (influenced by �situational perturbations of the immune response�)

� increased susceptibility to environmental stressors resulting from reduction in neural plasticity.

The possibility that early developmental trauma or abuse is a feature is supported by research. For example, Weissbecker et al (2006) report that:

Adults with fibromyalgia syndrome report high rates of childhood trauma. Neuroendocrine abnormalities have also been noted in this population. Findings suggest that severe traumatic experiences in childhood may be a factor of adult neuroendocrine dysregulation among fibromyalgia sufferers. Trauma history should be evaluated and psychosocial intervention may be indicated as a component of treatment for fibromyalgia.

The �causes� within this model can be seen to be widely spread. Goldstein�s (apparently successful) interventions deal with what is happening at the end of this complex sweep of events when the neural network has, as a result, become dysfunctional. By manipulating the biochemistry of that end-state, many (Goldstein says most) of his patients� symptoms apparently improve dramatically and rapidly.

Such improvement does not necessarily indicate that underlying causes have been addressed; if these are still operating, future health problems may be expected to eventually emerge. The schematic representation of a �stairway to ill-health� (Fig. 1.2) indicates some of the possible features ongoing in complicated dysfunctional patterns such as FMS, where adaptive resources have been stretched to their limits, and the �stage of exhaustion� in Selye�s general adaptation syndrome has been reached (Selye 1952). See also the discussion of allostasis in Chapter 3, particularly Table 3.2.

Dysfunctional patterns such as CFS and FMS seem to have three overlapping aetiological features interacting with the unique inborn and subsequently acquired characteristics of individuals to determine their particular degree of vulnerability and susceptibility (Fig. 1.3):

1. Biochemical factors. These can include toxicity, deficiency, infectious, endocrine, allergic and other characteristics (Wood 2006).

2. Biomechanical factors. These might include:

a. structural (congenital � i.e. short leg or hypermobility features � postural or traumatically induced characteristics) (Gedalia et al 1993, Goldman 1991)

b. functional (overuse patterns, hyperventilation stresses on respiratory mechanisms, etc.)

c. neurological (sensitization, hypersensitivity � �wind-up�) (Staud et al 2005).

3. Psychosocial factors. These might include depression and/or anxiety traits, poor stress coping abilities, post-traumatic stress disorders, etc. (Arguellesa et al 2006).

Let us briefly consider Dr Goldstein�s model of dysfunction, which suggests neural network dysfunction as the �cause� of FMS, itself being a result of a combination of features as outlined above (Goldstein 1996). If we utilize the clinical options suggested in Figure 1.2, we can see that it is possible to attempt to:

1. reduce the biochemical, biomechanical or psychogenic �stress� burden to which the person is responding

2. enhance the defense, repair, immune functions of the person so that they can handle these stressors more effectively

3. palliate the symptoms, hopefully without producing any increase in adaptive demands on an already overloaded system.

Which of these tactics are being employed in Goldstein�s treatment approach in which drug-induced biochemical manipulation is being carried out, and does this address causes or symptoms, and does this matter, as long as there is overall improvement?

The particular philosophical perspective adopted by the practitioner/therapist will determine his judgement on this question. Some may see the rapid symptom relief claimed for the majority of these patients as justifying Goldstein�s particular therapeutic approach. Others might see this as offering short term benefits, not addressing underlying causes, and leaving the likelihood of a return of the original symptoms, or of others evolving, a probability. These issues will be explored in relation to this and other approaches to treatment of FMS in later chapters.

Associated Conditions

A number of other complex conditions exist which have symptom patterns which mimic many of those observed in FMS, in particular:

� chronic myofascial pain syndrome (MPS) involving multiple active myofascial trigger points and their painful repercussions

� chronic fatigue syndrome (CFS) which has among its assortment of symptoms almost all those ascribed to FMS, with greater emphasis on the fatigue elements, rather than the pain ones

� multiple chemical sensitivity (MCS)

� post-traumatic stress disorder (PTSD). MPS, FMS, MCS (for example, in relation to what has become known as Gulf War syndrome) and CFS � their similarities, and the sometimes great degree of overlap in their symptom presentation, as well as their differences � will be examined in later chapters. One feature of all of these conditions which has been highlighted is based on a toxic/biochemical hypothesis, involving �elevated levels of nitric oxide and its potent oxidant product, peroxynitrite� (Pall 2001).

 

fibromyalgia history

fibromyalgia history

 

Other Theories Of Causation

A variety of theories as to the causation of FMS have emerged, with many of these overlapping and some being essentially the same as others, with only slight differences in emphasis as to aetiology, cause and effect. FMS is variously thought to involve any of a combination of the following (as well as other) causative features, each of which raises questions as well as suggesting answers and therapeutic possibilities:

� FMS could be a neuroendocrine disturbance, particularly involving thyroid hormone imbalances (see Ch. 10) (Garrison & Breeding 2003, Honeyman 1997, Lowe 1997, Lowe & Honeyman-Lowe 2006) and/or hypophyseal growth hormone imbalances (possibly as a direct result of sleep disturbance � a key feature of FMS, and/or lack of physical exercise) (Moldofsky 1993). The question which then needs to be asked is, what produces the endocrine disturbance? Is it genetically determined as some believe, or is it the result of deficiency, toxicity, allergy, an autoimmune condition or infection?

� Duna & Wilke (1993) propose that disordered sleep leads to reduced serotonin production, and consequent reduction in the pain-modulating effects of endorphins and increased �substance P� levels, combined with sympathetic nervous system changes resulting in muscle ischaemia and increased sensitivity to pain (Duna & Wilke 1993). This hypothesis starts with a symptom, sleep disturbance, and the logical question is, what produces this?

� Dysautonomia, autonomic imbalance or dysfunction, characterized by �relentless sympathetic hyperactivity�, more prominent at night (Martinez-Lavin & Hermosillo 2005), have been proposed as foundational causes in a subgroup of individuals with FMS (and CFS). Many such patients have also been labelled with Gulf War-related illness (Geisser et al 2006, Haley et al 2004, van der Borne 2004).

� Muscle microtrauma may be the cause, possibly due to genetic predisposition (and/or growth hormone dysfunction), leading to calcium leakage, and so increasing muscle contraction and reducing oxygen supply. An associated decrease in mitochondrial energy production would lead to local fatigue and an inability for excess calcium to be pumped out of the cells, resulting in local hypertonia and pain (Wolfe et al 1992). The question as to why muscle microtrauma occurs more in some people than in others, or why repair is slower, requires investigation.

� FMS may be a pain modulation disorder resulting at least in part from brain (limbic system) dysfunction and involving mistranslation of sensory signals and consequent misreporting (Goldstein 1996). Why and how the limbic system and neural networks become dysfunctional is the key to this hypothesis (promoted by Goldstein, as discussed above).

� It has been suggested that what are termed idiopathic pain disorders (IPD) � such as temporomandibular joint disorders (TMJD), fibromyalgia syndrome (FMS), irritable bowel syndrome (IBS), chronic headaches, interstitial cystitis, chronic pelvic pain, chronic tinnitus, whiplash-associated disorders and vulvar vestibulitis (VVS) � are mediated by an individual�s genetic variability, as well as by exposure to environmental events. The primary pathways of vulnerability that underlie the development of such conditions are seen to involve pain amplification and psychological distress, modified by gender and ethnicity (Diatchenko et al 2006) (Fig. 1.4).

� FMS may be a congenitally acquired disorder, possibly related to inadequate thyroid regulation of gene transcription, with an autosomal dominant feature (Lowe et al 1997, Pellegrino et al 1989). As will be outlined, some research studies have found evidence of a genetically linked predisposition towards FMS. Congenital structural abnormalities, such as extreme ligamentous laxity (i.e. hypermobility (Karaaslan et al 2000)), and Chiari malformations (see further discussion of this in Ch. 3 (Kesler & Mandizabal 1999, Thimineur et al 2002)), certainly seem to predispose toward FMS. The questions this raises include: which factors exacerbate these predispositions, and can anything be done about them?

� Hudson et al (2004) have proposed that fibromyalgia is one member of a group of 14 psychiatric and medical disorders (attentiondeficit/hyperactivity disorder, bulimia nervosa, dysthymic disorder, generalized anxiety disorder, major depressive disorder, obsessive-compulsive disorder, panic disorder, post-traumatic stress�disorder, premenstrual dysphoric disorder and social phobia � plus four medical conditions: fibromyalgia, irritable bowel syndrome, migraine, and cataplexy), collectively termed affective spectrum disorder (ASD), hypothesized to share possibly heritable pathophysiological features. Following detailed analysis of data from 800 individuals with and without fibromyalgia (and the additional conditions under assessment), Hudson et al concluded that the present information added to evidence that the psychiatric and medical disorders, grouped under the term ASD, run together in families, raising the possibility that these disorders might share a heritable physiological abnormality.

fibromyalgia history

� The underlying cause of FMS is seen by some to result from the (often combined) involvement of allergy, infection, toxicity and nutritional deficiency factors which themselves produce the major symptoms of FMS (and CFS), such as fatigue and pain, or which are associated with endocrine imbalances and the various consequences outlined above, such as thyroid hormone dysfunction and/or sleep disturbance (Abraham & Lubran 1981, Bland 1995, Cleveland et al 1992, Fibromyalgia Network Newsletters 1990�94, Pall 2001, Robinson 1981, Vorberg 1985). The list of possible interacting features such as these, which frequently seem to coexist in someone with FMS, offers the possibility of intervention strategies which seem to focus on causes rather than effects. For example, specific �excitotoxins� such as monosodium glutamate (MSG) have been identified as triggering FMS symptoms (Smith et al 2001). These and other examples will be examined in later chapters.

� A central sensitization hypothesis suggests that central mechanisms of FMS pain are dependent on abnormal peripheral input(s) for development�and maintenance of the condition (Vierck 2006). A substantial literature defines peripheral�CNS� peripheral interactions that seem integral to fibromyalgia pain. The generalized hypersensitivity associated with the condition has focused interest on central (CNS) mechanisms for the disorder. These include central sensitization, central disinhibition and a dysfunctional hypothalamic�pituitary�adrenal (HPA) axis. However, it is asserted that the central effects associated with fibromyalgia can be produced by peripheral sources of pain. In this model, chronic nociceptive input induces central sensitization, magnifying pain and activating the HPA axis and the sympathetic nervous system. Chronic sympathetic activation then indirectly sensitizes peripheral nociceptors, and sets up a vicious cycle. (See also notes on facilitation later in this chapter, as well as further discussion of central and peripheral sensitization in Ch. 4.)

� Use of MRI and other scanning/imaging technology suggests that the central sensitization concept has objective evidence to support it. This subject is discussed further in Chapter 3 (see �The polysymptomatic patient�) and Chapter 4 (see �Central sensitization hypothesis� and Fig. 3.1). Two examples of imaging evidence, relating to altered brain morphology and/or behaviour in relation to FMS, are summarized in Box 1.3.

� Within the framework of �allergy� and �intolerance� as triggers to FMS symptoms lies a hypothesis which remains controversial, but worthy of discussion. This relates to the concept of blood-type specific intolerances resulting from an interaction between food-derived lectins (protein molecules) and specific tissue markers related to the individual�s blood type. D�Adamo (2002), who has done most to promote this concept, states (in relation to FMS sufferers who happen to be type O):

It has become obvious that those who are type O and suffering from fibromyalgia can see quite dramatic responses if they can stick to the wheat-free component of the diet for a long enough duration. A recent study indicates that dietary lectins interacting with enterocytes (cells lining�the intestines) and lymphocytes may facilitate the transportation of both dietary and gutderived pathogenic antigens to peripheral tissues, which in turn causes persistent immune stimulation at the periphery of the body, such as the joints and muscles (Cordain et al 2000). This, despite the fact that many nutrition �authorities� still question whether lectins even get into the systemic circulation! In genetically susceptible individuals, this lectin stimulation may ultimately result in the expression of disorders like rheumatoid arthritis and fibromyalgia via molecular mimicry, a process whereby foreign peptides, similar in structure to endogenous peptides, may cause antibodies or T-lymphocytes to cross-react and thereby break immunological tolerance. Thus by removing the general and type O specific lectins from the diet, we allow for the immune system to redevelop tolerance, the inflammation begins to ebb, and healing can begin.

fibromyalgia history

� Many FMS patients demonstrate low carbon dioxide levels when resting � an indication of possible hyperventilation involvement. The symptoms of hyperventilation closely mirror those of FMS and CFS, and the pattern of upper chest breathing which it involves severely stresses the muscles of the upper body which are most affected in FMS, as well as producing major oxygen deficits in the brain and so influencing its processing of information such as messages received from pain receptors (Chaitow et al 2002, Janda 1988, King 1988, Lum 1981). When hyperventilation tendencies are present, they can be seen in some instances to be a response to elevated acid levels (because of organ dysfunction perhaps) or they can be the result of pure habit. Breathing retraining can, in some FMS patients, offer a means of modifying symptoms rapidly (Readhead 1984).

� Psychogenic (or psychosomatic) rheumatism is the name ascribed to FMS (and other nonspecific chronic muscle pain problems) by those who are reluctant to see an organic origin for the syndrome. Until the 1960s it was suggested that such conditions be treated as �psychoneurosis� (Warner 1964). In FMS, as in all chronic forms of ill-health, there are undoubtedly elements of emotional involvement, whether as a cause or as an effect. These impact directly on pain perception and immune function, and, whether causative or not, benefit from appropriate attention, assisting both in recovery and rehabilitation (Melzack & Wall 1988, Solomon 1981).

� FMS is seen by some to be an extreme of the myofascial pain syndrome (MPS), where numerous active myofascial triggers produce pain both locally and at a distance (Thompson 1990). Others see FMS and MPS as distinctive, but recognize that �it is not uncommon for a patient with myofascial pain syndrome to progress with time to a clinical picture identical to that of FMS� (Bennett 1986a). Among the most important practical pain-relieving approaches to FMS will be the need to identify and deactivate myofascial trigger points which may be influencing the overall pain burden. A number of different approaches, ranging from electroacupuncture to manual methods, will be detailed (see Chs 6, 8 and 9 in particular).

� Trauma (e.g. whiplash) seems to be a key feature of the onset in many cases of FMS, and especially cervical injuries, particularly those involving the suboccipital musculature (Bennett 1986b, Curatolo et al 2001, Hallgren et al 1993). Recognition of mechanical, structural factors allows for interventions which address their repercussions, as well as the psychological effects of trauma. In Chapter 9 Carolyn McMakin presents compelling evidence for the use of microcurrents in treatment of FMS of traumatic (especially of the cervical region) origin.

� There is an �immune dysfunction� model for myalgic encephalomyelitis (ME) � that uniquely British name for what appears to be an amalgam of chronic fatigue syndrome and fibromyalgia. This proposes a viral or other (vaccination, trauma, etc.) initial trigger which may lead to persistent overactivity of the immune system (overproduction of cytokines). Associated with this there may be chemical and/or food allergies, hypothalamic disturbance, hormonal imbalance and specific areas of the brain (e.g. limbic system) �malfunctioning�. The primary feature of this model is the overactive immune function, with many of the other features, such as endocrine imbalance and brain dysfunction, secondary to this (Macintyre 1993b). In recent research, the presence of systemic bacterial, mycoplasmal and viral coinfections in many�patients with CFS and FMS has been a feature (Nicolson et al 2002).

The Musculoskeletal Terrain Of FMS

Current research and clinical consensus seem to indicate that FMS is not primarily a musculoskeletal problem, although it is in the tissues of this system that its major symptoms manifest: �Fibromyalgia is a chronic, painful, musculo-skeletal condition characterised by widespread aching and points of tenderness associated with: 1) changed perception of pain, abnormal sleep patterns and reduced brain serotonin; and 2) abnormalities of microcirculation and energy metabolism in muscle� (Eisinger et al 1994).

These characteristics, involving abnormal microcirculation and energy deficits, are the prerequisites for the evolution of localized areas of myofascial distress and neural hyper-reactivity (i.e. trigger points). As indicated, one of the key questions to be answered in any given case is the degree to which the person�s pain is deriving from myofascial trigger points, or other musculoskeletal sources, since these may well be more easily modified than the complex underlying imbalances which are producing, contributing to, or maintaining the primary FMS condition.

Fibromyalgia History: Early Research

A great deal of research into FMS (under different names � see Box 1.1), and of the physiological mechanisms that increase our understanding of the FMS phenomenon, has been conducted over the past century (and earlier) and is worthy of review. Additional research in parallel with that focused on chronic muscular pain may clarify processes at work in this complex condition.

Korr�s Work On Facilitation

Among the most important researchers in the area of musculoskeletal dysfunction and pain over the past half century has been Professor Irwin Korr, whose work in explaining the facilitation phenomenon offers important insights into some of the events occurring in FMS and, more specifically, in myofascial pain settings. Needless to say, these often overlap. As suggested above, in a clinical context it is vital to know what degree of the pain being experienced in FMS is the result of myofascial pain, since this part of the pain package can relatively easily be modified or eliminated (see Chs 8 and 9).

Neural structures can become hyper-reactive in either spinal and paraspinal tissues or almost any other soft tissue. When they are found close to the spine the phenomenon is known as segmental facilitation. When such changes occur in ligaments, tendons or periosteal tissues, they are called trigger points; if situated in muscles or in fascia they are termed �myofascial� trigger points. In early studies by the most important researcher into facilitation, Irwin Korr (1970, 1976), he demonstrated that a feature of unilateral segmental facilitation was that one side would test as having normal skin resistance to electricity compared with the contralateral side, the facilitated area, where a marked reduction in resistance was present. When �stress� � in the form of needling or heat � was applied elsewhere in the body, and the two areas of the spine were monitored, the area of facilitation showed a dramatic rise in electrical (i.e. neurological) activity. In one experiment volunteers had pins inserted into a calf muscle in order to gauge the effect on the paraspinal muscles, which were monitored for electrical activity. While almost no increase occurred in the normal region, the facilitated area showed greatly increased neurological activity after 60 seconds (Korr 1977) (Fig. 1.5). This and numerous similar studies have confirmed that any form of stress impacting the individual � be it climatic, toxic, emotional, physical or anything else � will produce an increase in neurological output from facilitated areas.

In Chapter 9, Carolyn McMakin describes how some forms of trauma, particularly those affecting cervical structures, can lead to chronic local facilitation, resulting in FMS-like pain. She reports that treatment utilizing microcurrent, manual modalities and nutritional support can frequently ease, or even remove, such symptoms.

Professor Michael Patterson (1976) explains the concept of segmental (spinal) facilitation as follows:

The concept of the facilitated segment states that because of abnormal afferent or sensory inputs to a particular area of the spinal cord, that area is kept in a state of constant increased excitation. This facilitation allows normally ineffectual or subliminal stimuli to become effective in producing efferent output from the facilitated segment, causing both skeletal and visceral organs innervated by the affected segment to be maintained in a state of�overactivity. It is probable that the somatic dysfunction with which a facilitated segment is associated, is the direct result of the abnormal segmental activity as well as being partially responsible for the facilitation.

fibromyalgia history

Wind-Up And Facilitation

The process known as wind-up (Fig. 1.6) supports the concepts of facilitation, in different terms. Staud (2006) has described the relationship between peripheral pain impulses that lead to central sensitization as follows:

Increasing evidence points towards peripheral tissues as relevant contributors of painful impulse input that might either initiate or maintain central sensitization, or both. It is well known that persistent or intense nociception can lead to neuroplastic changes in the spinal cord and brain, resulting in central sensitization and pain. This mechanism represents a hallmark of FM and many other chronic pain syndromes, including irritable bowel syndrome, temporomandibular disorder, migraine, and low back pain. Importantly, after central sensitization has been established only minimal nociceptive input is required for the maintenance of the chronic pain state. Additional factors, including pain related negative affect and poor sleep have been shown to significantly contribute to clinical FM pain.

The similarities between modern neurological observations and Korr�s original work are clear.

Arousal And Facilitation

Emotional arousal is also able to affect the susceptibility of neural pathways to sensitization. The increase in descending influences from the emotionally aroused subject would result in an increase in toxic excitement in the pathways and allow additional inputs to produce sensitization at lower intensities. This implies that highly emotional people, or those in a highly emotional situation, would be expected to show a higher incidence of facilitation of spinal pathways or local areas of myofascial distress (Baldry 1993).

fibromyalgia history

This has a particular relevance to fibromyalgia, where heightened arousal (for a variety of possible�reasons, as will become clear), in addition to possible limbic system dysfunction, leads to major influences from the higher centers (Goldstein 1996). Since the higher brain centers do influence the tonic levels of the spinal paths, it might be expected that physical training and mental attitudes would also tend to alter the tonic excitability, reducing the person�s susceptibility to sensitization from everyday stress. Thus the athlete would be expected to withstand a comparatively high level of afferent input prior to experiencing the self-perpetuating results of sensitization. This, too, has a relevance to fibromyalgia, where there exists ample evidence of beneficial influences of aerobic training programs (McCain 1986, Richards & Scott 2002).

Selective Motor Unit Recruitment

Researchers have shown that a small number of motor units, located in particular muscles, may display almost constant or repeated activity when influenced psychogenically. Low amplitude activity (using surface EMG) was evident even when the muscle was not being employed, if there was any degree of emotional arousal. �A small pool of lowthreshold motor units may be under considerable load for prolonged periods of time … motor units with Type 1 [postural] fibers are predominant among these. If the subject repeatedly recruits the same motor units, the overload may result in a metabolic crisis.� (Waersted et al 1993). The implications of this research are profound for they link even low grade degrees of emotional distress with almost constant sensitization of specific myofascial structures, with the implications associated with facilitation and pain generation. This aetiology parallels the proposed evolution of myofascial trigger points, as suggested by Simons et al (1999).

Not Only Myelinated Fibres

Research by Ronald Kramis has shown that, in chronic pain settings, non-nociceptive neurons can become sensitized to carry pain impulses (Kramis 1996). Hypersensitization of spinal neurons may actually involve non-nociceptive neurons altering their phenotype so that they commence releasing substance P. This, it is thought, may play a significant part in FMS pain perception, as increased levels of substance P in�the cerebrospinal fluid maintain heightened amplification of what would normally be registered as benign impulses. The research suggests that impulses from associated conditions such as ongoing viral activity, �muscular distress� or irritable bowel may be adequate to maintain the central pain perception.

Local Facilitation

Apart from paraspinal tissues, where segmental facilitation, as described above, manifests, localized areas of neural facilitation can occur in almost all soft tissues: these are called myofascial trigger points.

Much of the basic research and clinical work into this aspect of facilitation has been undertaken by doctors Janet Travell and David Simons (Simons et al 1999; Travell 1957; Travell & Simons 1986, 1992; see also Chs 6 and 8). Travell and Simons are on record as stating that if a pain is severe enough to cause a patient to seek professional advice (in the absence of organic disease), it usually involves referred pain, and therefore a trigger area is probably a factor. They remind us that patterns of referred pain are constant in distribution in all people, and that only the intensity of referred symptoms/pain will vary.

The implication for the fibromyalgia patient is the possibility (according to Travell and Simons this is a veritable certainty) that their pain has as part of its make-up the involvement of myofascial trigger points, which are themselves areas of facilitation (see Ch. 8 by Dommerholt & Issa). This suggests that trigger points, and the pain (and tingling, numbness, etc.) which they produce, will be exaggerated by all forms of stress influencing that individual patient. Travell has confirmed that her research indicates that the following factors can all help to maintain and enhance myofascial trigger point activity:

� nutritional deficiencies (especially vitamins C and B complex, and iron)

� hormonal imbalances (low thyroid hormone production, menopausal or premenstrual dysfunction)

� infections (bacteria, viruses or yeasts)

� allergies (wheat and dairy in particular)

� low oxygenation of tissues (aggravated by tension, stress, inactivity, poor respiration) (Simons et al 1999, Travell & Simons 1986, 1992).

This list corresponds closely with factors that are key aggravating agents for many (most) people with fibromyalgia, suggesting that the connection between facilitation (trigger point activity) and FMS is close (Starlanyl & Copeland 1996). Myofascial trigger points are, however, not the cause of fibromyalgia, and myofascial pain syndrome is not FMS, although they may coexist in the same person at the same time. Myofascial trigger points do undoubtedly frequently contribute to the painful aspect of FMS, and as such are deserving of special attention.

As will be explained in later chapters, there are a number of ways in which deactivation or modulation of myofascial trigger points can be achieved. Some practitioners opt for approaches that deal with them manually, while others prefer microcurrents or electro-acupuncture methods or variations on these themes, with yet others suggesting that reduction in the number and intensity of stress factors � of whatever type � offers a safer approach to reducing the influence of facilitation on pain.

Following this introduction to the concept of hyper-reactive, sensitized (facilitated) neural structures, it would be justifiable to enquire as to whether or not what is happening in the brain and in the neural network, as described by Goldstein, is not simply facilitation on a grand scale. The outline of some of the leading current hypotheses as to the aetiology of FMA in Chapter 4 may shed light on this possibility.

Additional Early Research Into FMS

Early FMS research has been presented in summary form in Box 1.1. Aspects of that research, and how some of it correlates with more recent findings, are outlined below.

R. Gutstein, a Polish physician who emigrated to the UK prior to the Second World War, was a remarkable researcher who published papers under different names (M. G. Good, for example) before, during and following the war. In them he clearly described the myofascial trigger point phenomenon, as well as what is now known as fibromyalgia, along with a great many of its predisposing and maintaining features.

Gutstein (1956) showed that conditions such as ametropia (an error in the eye�s refractive power occurring in myopia, hypermetropia and astigmatism) may result from changes in the neuromuscular component of the craniocervical area, as well as more distant conditions involving the pelvis or shoulder girdle. He stated: �Myopia is the long-term effect of pressure of extra-ocular muscles in the convergence effort of accommodation involving spasm of the ciliary muscles, with resultant elongation of the eyeball. A sequential relationship has been shown between such a condition and muscular spasm of the neck.�

Gutstein termed reflex areas he identified �myodysneuria� and suggested that the reference phenomena of such spots or �triggers� would include pain, modifications of pain, itching, hypersensitivity to physiological stimuli, spasm, twitching, weakness and trembling of striated muscles, hyper- or hypotonus of smooth muscle of blood vessels and of internal organs, and/or hyper- or hyposecretion of visceral, sebaceous and sudatory glands. Somatic manifestations were also said to occur in response to visceral stimuli of corresponding spinal levels (Gutstein 1944). In all of these suggestions Gutstein seems to have been in parallel with the work of Korr.

Gutstein/Good�s method of treatment involved the injection of an anaesthetic solution into the trigger area. He indicated, however, that where accessible (e.g. muscular insertions in the cervical area) the chilling of these areas combined with pressure would yield good results.

In this and much of what he reported in the 1940s and 1950s Gutstein was largely in agreement with the research findings of John Mennell (1952) as well as with Travell & Simons, as expressed in their major texts on the subject (Travell & Simons 1986, 1992). He reported that obliteration of overt and latent triggers in the occipital, cervical, interscapular, sternal and epigastric regions was accompanied by years of alleviation of premenopausal, menopausal and late menopausal symptoms (Good 1951). He quotes a number of practitioners who had achieved success in treating gastrointestinal dysfunctions by deactivating trigger areas. Some of these were treated by procainization, others by pressure techniques and massage (Cornelius 1903). He also reported the wide range of classic fibromyalgia symptoms and features, suggesting the name myodysneuria for this syndrome, which he also termed �nonarticular rheumatism� (Gutstein 1955). In describing myodysneuria (FMS), Gutstein demonstrated localized functional sensory and/or motor abnormalities of musculoskeletal tissues and saw the causes of such changes as multiple (Gutstein 1955). Most of these findings have been validated subsequently, in particular by the work of Travell and Simons. They include:

� acute and chronic infections, which he postulated stimulated sympathetic nerve activity via their toxins

� excessive heat or cold, changes in atmospheric pressure and draughts

� mechanical injuries, both major and repeated minor microtraumas � now validated by the recent research of Professor Philip Greenman of Michigan State University (Hallgren et al 1993)

� postural strains, unaccustomed exercise, etc., which could predispose towards future changes by lowering the threshold for future stimuli (in this he was agreeing with facilitation mechanisms as described above)

� allergic and/or endocrine factors which could cause imbalances in the autonomic nervous system

� congenital factors which make adaptation to environmental stressors difficult

� arthritic changes which could impose particular demands on the musculoskeletal system�s adaptive capacity

� visceral diseases which could intensify and precipitate somatic symptoms in the distribution of their spinal and adjacent segments.

We can see from these examples of Gutstein�s thinking strong echoes of the facilitation hypothesis in osteopathic medicine.

Gutstein�s diagnosis of myodysneuria was made according to some of the following criteria:

� a varying degree of muscular tension and contraction is usually present, although sometimes adjacent, apparently unaffected tissue is more painful

� sensitivity to pressure or palpation of affected muscles and their adjuncts

� marked hypertonicity may require the application of deep pressure to demonstrate pain.

In 1947 Travell & Bigelow produced evidence supporting much of what Gutstein (1944) had reported. They indicated that high intensity stimuli from active trigger areas produce, by reflex, prolonged vasoconstriction with partial ischaemia in localized areas of the brain, spinal cord, or peripheral nerve structures.

A widespread pattern of dysfunction might then result, affecting almost any organ of the body. These�early research findings correlate well with modern fibromyalgia and chronic fatigue research and the hypothesis of �neural network disorders� as described by Goldstein (1996), and in British and American research utilizing SPECT scans, which show clearly that severe circulatory deficits occur in the brainstem and in other areas of the brain of most people with CFS and FMS (Costa 1992).

Gutstein�s Suggested Pathophysiology Of Fibromyalgia/ Fibrositis/Myodysneuria

The changes which occur in tissue involved in the onset of myodysneuria/fibromyalgia, according to Gutstein, are thought to be initiated by localized sympathetic predominance, associated with changes in the hydrogen ion concentration and calcium and sodium balance in the tissue fluids (Petersen 1934). This is associated with vasoconstriction and hypoxia/ischaemia. Pain resulted, he thought, by these alterations affecting the pain sensors and proprioceptors.

Muscle spasm and hard, nodular, localized tetanic contractions of muscle bundles, together with vasomotor and musculomotor stimulation, intensified each other, creating a vicious cycle of self-perpetuating impulses (Bayer 1950). Varied and complex patterns of referred symptoms might then result from such �trigger� areas, as well as local pain and minor disturbances. Sensations such as aching, soreness, tenderness, heaviness and tiredness may all be manifest, as may modification of muscular activity due to contraction, resulting in tightness, stiffness, swelling and so on.

It is clear from this summary of his work that Gutstein was describing fibromyalgia, and many of its possible causative features.

Chapter 2 examines what FMS is, as well as what it is not, with suggestions for differential diagnosis.

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References:

Abraham G, Lubran M M 1981 Serum
and red cell magnesium levels in
patients with PMT. American
Journal of Clinical Nutrition 34(11):
2364�2366
American College of Rheumatology
1990 Criteria for the classification of
fibromyalgia. Arthritis and
Rheumatism 33: 160�172
Arguellesa L, Afarib N, Buchwald D et al
2006 A twin study of posttraumatic
stress disorder symptoms and
chronic widespread pain. Pain 124
(1�2): 150�157
Baldry P 1993 Acupuncture trigger
points and musculoskeletal pain.
Churchill Livingstone, London
Bayer H 1950 Pathophysiology of
muscular rheumatism. Zeitschrift fur
Rheumaforschung 9: 210
Bennett R 1986a Fibrositis: evolution of
an enigma. Journal of Rheumatology
13(4): 676�678
Bennett R 1986b Current issues
concerning management of the
fibrositis/fibromyalgia syndrome.
American Journal of Medicine
81(S3A): 15�18
Bland J 1995 A medical food
supplemented detoxification
programme in the management of
chronic health problems. Alternative
Therapies 1: 62�71
Block S 1993 Fibromyalgia and the
rheumatisms. Controversies in
Rheumatology 19(1): 61�78
Chaitow L, Bradley D, Gilbert C 2002
Multidisciplinary approaches to
breathing pattern disorders.
Churchill Livingstone, Edinburgh
Cleveland C H Jr, Fisher R H, Brestel
E P et al 1992 Chronic rhinitis: an
underrecognized association with
fibromyalgia. Allergy Proceedings 13
(5): 263�267
Copenhagen Declaration 1992
Consensus document on FMS: the
Copenhagen declaration. Lancet 340
(September 12)
Cordain L, Toohey L, Smith M J,
Hickey M S 2000 Modulation of
immune function by dietary lectins in
rheumatoid arthritis. British Journal
of Nutrition 83(3): 207�217
Cornelius A 1903 Die Neurenpunkt
Lehre. George Thiem, Leipzig, vol 2
Costa D 1992 Report. European Journal
of Nuclear Medicine 19(8): 733
Crissinger K 1990 Pathophysiology of
gastrointestinal mucosal
permeability. Journal of Internal
Medicine 228: 145�154
Croft P, Cooper C, Wickham C,
Coggon D 1992 Is the hip involved in
generalized osteoarthritis? British
Journal of Rheumatology 31:
325�328
Curatolo M, Petersen-Felix S, ArendtNielsen
L et al 2001 Central
hypersensitivity in chronic pain after
whiplash injury. Clinical Journal of
Pain 17(4): 306�315
D�Adamo P 2002 <www.
dadamo.com>
Diatchenko L, Nackleya A, Slade G
2006 Idiopathic pain disorders �
pathways of vulnerability. Pain 123
(3): 226�230
Duna G, Wilke W 1993 Diagnosis,
etiology and therapy of fibromyalgia.
Comprehensive Therapy 19(2):
60�63
Eisinger J, Plantamura A, Ayavou T 1994
Glycolysis abnormalities in
fibromyalgia. Journal of the
American College of Nutrition 13(2):
144�148
Epstein S, Kay G, Clauw D 1999
Psychiatric disorders in patients with
fibromyalgia: a multicenter
investigation. Psychosomatics 40:
57�63
Fibromyalgia Network Newsletters
1990�94 Reports on nutritional
influences: October 1990�January
1992, Compendium No. 2, January
1993, May 1993 Compendium,
January 1994, July 1994 (Back issues
are available from the Network at PO
Box 31750, Tucson, Arizona
85761�1750)
Garrison R, Breeding P 2003 A
metabolic basis for fibromyalgia and
its related disorders: the possible role
of resistance to thyroid hormone.
Medical Hypotheses 61(2): 182�189
Gedalia A, Press J, Klein M, Buskila D
1993 Joint hypermobility and
fibromyalgia in schoolchildren.
Annals of the Rheumatic Diseases
52(7): 494�496
Geisser M, Williams D, Clauw D 2006
Impact of co-morbid somatic
symptoms above and beyond that of
pain in patients with fibromyalgia
and gulf war illnesses. Journal of Pain
7(4 Suppl 1): S28
Goldman J 1991 Hypermobility and
deconditioning: important links to
fibromyalgia. Southern Medical
Journal 84: 1192�1196
Goldstein J 1996 Betrayal by the brain:
the neurological basis of CFS and
FMS and related neural network
disorders. Haworth Medical Press,
New York
Good M G 1951 Objective diagnosis
and curability of non-articular
rheumatism. British Journal of
Physical Medicine and Industrial
Hygiene 14: 1�7
Gutstein R 1944 The role of abdominal
fibrositis in functional indigestion.
Mississippi Valley Medical Journal
66: 114�124
Gutstein R 1955 A review of
myodysneuria (fibrositis). American
Practitioner and Digest of
Treatments 6(4)
Gutstein R 1956 The role of
craniocervical myodysneuria in
functional ocular disorders. American
Practitioner�s Digest of Treatments
(November)
Haley R, Vongpatanasin W, Wolfe G
et al 2004 Blunted circadian variation
in autonomic regulation of sinus node
function in veterans with Gulf War
syndrome. American Journal of
Medicine 117(7): 469�478
Hallgren R, Greenman P, Rechtien J
1993 MRI of normal and atrophic
muscles of the upper cervical spine.
Journal of Clinical Engineering 18(5):
433�439
Honeyman G 1997 Metabolic therapy
for hypothyroid and euthyroid
fibromyalgia: two case reports.
Clinical Bulletin of Myofascial
Therapy 2(4): 19�49
Hudson J I, Arnold L M, Keck P E et al
2004 Family study of fibromyalgia
and affective spectrum disorder.
Biological Psychiatry 56(11):
884�891
Janda V 1988 Muscles and cervicogenic
pain and syndromes. In: Grant R (ed)
Physical therapy of the cervical and
thoracic spine. Churchill Livingstone,
London, pp 153�166
Karaaslan Y, Haznedaroglu S, Ozturk M
2000 Joint hypermobility and
primary fibromyalgia. Journal of
Rheumatology 27: 1774�1776
Kesler R, Mandizabal J 1999 Headache
in Chiari malformation. Journal of
the American Osteopathic
Association 99(3): 153�156
King J 1988 Hyperventilation � a
therapist�s point of view. Journal of
the Royal Society of Medicine 81
(September): 532�536
Korr I 1970 Physiological basis of
osteopathic medicine. Postgraduate
Institute of Osteopathic Medicine
and Surgery, New York
Korr I 1976 Spinal cord as organiser of
disease process. Academy of Applied
Osteopathy Yearbook 1976, Carmel
Korr I (ed) 1977 Neurobiological
mechanisms in manipulation. Plenum
Press, New York
Kramis R 1996 Non-nociceptive aspects
of musculoskeletal pain. Journal of
Orthopaedic and Sports Physical
Therapy 24(4): 255�267
Lowe J 1997 Results of open trial of T3
therapy with 77 euthyroid female
FMS patients. Clinical Bulletin of
Myofascial Therapy 2(1): 35�37
Lowe J, Honeyman-Lowe B 2006
Female fibromyalgia patients: lower
resting metabolic rates than matched
healthy controls. Medical Science
Monitor 12(7): 282�289
Lowe J, Cullum M, Graf L, Yellin J
1997 Mutations in the c-erb-Ab1
gene: do they underlie euthyroid
fibromyalgia? Medical Hypotheses 48
(2): 125�135
Lum L 1981 Hyperventilation and
anxiety state. Journal of the Royal
Society of Medicine 74(January): 1�4
McCain G A 1986 Role of physical
fitness training in fibrositis/
fibromyalgia syndrome. American
Journal of Medicine 81(S3A): 73�77
McClean G, Wesseley S 1994
Professional and popular view of
CFS. British Medical Journal 308:
776�777
Macintyre A 1993a What causes ME?
Journal of Action for ME 14: 24�25
Macintyre A 1993b The immune
dysfunction hypothesis. Journal of
Action for ME 14: 24�25
McNaught C E, Woodcock N P,
Anderson A D, MacFie J 2005 A
prospective randomised trial of
probiotics in critically ill patients.
Clinical Nutrition 24(2): 211�219
Martinez-Lavin M, Hermosillo A 2005
Dysautonomia in Gulf War
syndrome and in fibromyalgia.
American Journal of Medicine
118(4): 446
Melzack R, Wall P 1988 The challenge
of pain. Penguin, New York
Mennell J 1952 The science and art of
manipulation. Churchill Livingstone,
London
Mense S, Simons D 2001 Muscle pain.
Lippincott/Williams and Wilkins,
Philadelphia
Moldofsky H L 1993 Fibromyalgia, sleep
disorder and chronic fatigue
syndrome. CIBA Symposium 173:
262�279
Nicolson G, Nasralla M, De Meirleir K
2002 Bacterial and viral co-infections
in chronic fatigue syndrome patients.
This article is available from: http://
www.prohealth.com/library/
showarticle.cfm?
id�3635&t�CFIDS_FM.
8 December 2008
Pall M L 2001 Common etiology of
posttraumatic stress disorder,
fibromyalgia, chronic fatigue
syndrome and multiple chemical
sensitivity via elevated nitric oxide/
peroxynitrite. Medical Hypotheses
57(2): 139�145
Patterson M 1976 Model mechanism for
spinal segmental facilitation.
Academy of Applied Osteopathy
Yearbook 1976, Carmel
Pellegrino M J, Waylonis G W, Sommer
A 1989 Familial occurrence of
primary fibromyalgia. Archives of
Physical Medicine and Rehabilitation
70(1): 61�63
Petersen W 1934 The patient and the
weather: autonomic disintegration.
Edward Brothers, Ann Arbor,
Michigan
Porter-Moffitt S, Gatchel R, Robinson R
et al 2006 Biopsychosocial profiles of
different pain diagnostic groups.
Journal of Pain 7(5):
308�318
Readhead C 1984 Enhanced adaptive
behavioural response in patients
pretreated by breathing retraining.
Lancet 22(September): 665�668
Richards S, Scott D 2002 Prescribed
exercise in people with fibromyalgia:
parallel group randomised controlled
trial. British Medical Journal 325:
185
Robinson M 1981 Effect of daily
supplements of selenium on patients
with muscular complaints. New
Zealand Medical Journal 93:
289�292
Schmidt-Wilcke T, Luerding R,
Weigand T 2007 Striatal grey matter
increase in patients suffering from
fibromyalgia � a voxel-based
morphometry study. Pain 132:
S109�S116
Schneider M J, Brady D M, Perle S M
2006 Commentary: differential
diagnosis of fibromyalgia syndrome:
proposal of a model and algorithm for
patients presenting with the primary
symptom of chronic widespread
pain. Journal of Manipulative and
Physiological Therapeutics 29:
493�501
Selye H 1952 The story of the
adaptation syndrome. ACTA,
Montreal, Canada
Simons D 1988 Myofascial pain
syndromes: where are we? Where are
we going? Archives of Physical
Medicine and Rehabilitation 69:
207�211
Simons D, Travell J, Simons L 1999
Myofascial pain and dysfunction: the
trigger point manual. Vol 1. Upper
half of body, 2nd edn. Williams and
Wilkins, Baltimore
Smith J D, Terpening C M, Schmidt S
O, Gums J G 2001 Relief of
fibromyalgia symptoms following
discontinuation of dietary
excitotoxins. Annals of
Pharmacotherapy 35(6):
702�706
Solomon G 1981
Psychoneuroimmunology. Academic
Press, New York
Starlanyl D, Copeland M E 1996
Fibromyalgia and chronic myofascial
pain syndrome. New Harbinger
Publications, Oakland, California
Staud R 2006 Biology and therapy of
fibromyalgia: pain in fibromyalgia
syndrome. Arthritis Research and
Therapy 8: 208
Staud R, Robinson M, Price D 2005
New evidence for central
sensitization of fibromyalgia patients:
Windup maintenance is abnormal.
Journal of Pain 6(3): S6
Sundgren P, Petrou P, Harris R 2007
Diffusion-weighted and diffusion
tensor imaging in fibromyalgia
patients: a prospective study of
whole brain diffusivity, apparent
diffusion coefficient, and fraction
anisotropy in different regions of the
brain and correlation with symptom
severity. Academic Radiology 14:
839�846
Tagesson C 1983 Passage of molecules
through the wall of the intestinal
tract. Scandinavian Journal of
Gastroenterology 18: 481�486
Thimineur M, Kitaj M, Kravitz E,
Kalizewski T, Sood P 2002
Functional abnormalities of the
cervical cord and lower medulla and
their effect on pain. Clinical Journal
of Pain 18(3): 171�179
Thompson J 1990 Tension myalgia as a
diagnosis at the Mayo Clinic and its
relationship to fibrositis, fibromyalgia
and myofascial pain syndrome. Mayo
Clinic Proceedings 65: 1237�1248
Travell J 1957 Symposium on
mechanism and management of pain
syndromes. Proceedings of the
Rudolph Virchow Medical Society
Travell J, Bigelow N 1947 Role of
somatic trigger areas in the patterns
of hysteria. Psychosomatic Medicine
9(6): 353�363
Travell J, Simons D 1986 Myofascial
pain and dysfunction. Williams and
Wilkins, Baltimore, vol 1
Travell J, Simons D 1992 Myofascial
pain and dysfunction. Williams and
Wilkins, Baltimore, vol 2
Tuncer T 1997 Primary FMS and allergy.
Clinical Rheumatology 16(1): 9�12
van de Borne P 2004 Cardiac autonomic
dysfunction in Gulf War syndrome:
veterans� hearts don�t rest at night.
American Journal of Medicine 117
(7): 531�532
van Why R 1994 FMS and massage
therapy. Self published
Ventura M T, Polimeno L, Amoruso A C
et al 2006 Intestinal permeability in
patients with adverse reactions to
food. Digestive and Liver Disease 38
(10): 732�736
Vierck C Jr 2006 Mechanisms
underlying development of spatially
distributed chronic pain
(fibromyalgia). Pain 124(3):
242�263
Vorberg G 1985 Ginko extract � a longterm
study of chronic cerebral
insufficiency. Clinical Trials Journal
22: 149�157
Waersted M, Eken T, Westgaard R 1993
Psychogenic motor unit activity � a
possible muscle injury mechanism
studied in a healthy subject. Journal
of Musculoskeletal Pain 1(3/4):
185�190
Warner E (ed) 1964 Saville�s system of
clinical medicine, 14th edn. Edward
Arnold, London, p 918
Weissbecker I, Floyd A, Dedert E et al
2006 Childhood trauma and diurnal
cortisol disruption in fibromyalgia
syndrome.
Psychoneuroendocrinology 31(3):
312�324
Wolfe F, Simons D G, Fricton J et al
1992 The fibromyalgia and
myofascial pain syndromes: a
preliminary study of tender points
and trigger points. Journal of
Rheumatology 19(6): 944�951
Wolfe F, Anderson J, Ross K, Russel I
1993 Prevalence of characteristics of
fibromyalgia in the general
population. Arthritis and
Rheumatism 36: S48 (abstract)
Wood P 2006 A reconsideration of the
relevance of systemic low-dose
ketamine to the pathophysiology of
fibromyalgia. Journal of Pain 7(9):
611�614
Yunus M, Inanici F 2002 Fibromyalgia
syndrome: clinical features,
diagnosis, and biopathophysiologic
mechanisms. In: Yunus M B, Yunus I
(eds) Myofascial pain and
fibromyalgia. Mosby, St Louis
Zar S 2005 Food-specific serum IgG4
and IgE titers to common food
antigens in irritable bowel syndrome.
American Journal of
Gastroenterology 100: 1550�1557

Close Accordion

Genetically Modified (GM) Food Nation: The History

Genetically Modified (GM) Food Nation: The History

The late nineties were an era of strong debate on the issue of genetically modified food and organisms in the UK. Controversy surrounded both the scientific and political aspects of GM, with government advisory bodies being accused of biased behavior and concerns being raised over the ethical issues of the science behind GM. At lunch, a bowl of good vegetable-based soup (home-made or Simply Organic�s naturally!) counts for another 1 or 2 portions and each one of our Pure & Pronto ready meals counts for a whopping 3 portions. Add a piece of fruit or two during the day and a salad or veg in the evening and you�re already at 6 or 7 portions of fruit and veg for the day � well above the 5.

At the same time there was substantial media coverage of scientific advances including cloning and the BSE crisis that fueled public concern into the governance of such issues. It was in this climate of debate, concern and contestation that the UK Government launched GM Nation, a national debate about the future of genetically modified crops and food in the UK.

Objectives: Genetically Modified Foods

geneticallyThe stated aims of the GM Nation debate were twofold: to promote an innovative, effective and deliberative program of debate on GM issues, framed by the public, against the background of the possible commercial production of GM crops in the UK and the options for possibly proceeding with this; and through the debate provide meaningful information to Government about the nature and spectrum of the public views, particularly at grass roots level, on the issue to inform decision-making.

We aim to develop business performance by ensuring the effectiveness and efficiency of people development relevant to our industry.

Eat your fruit and veg � you�re aiming for at least 5 portions a day but it�s not as hard as you might think. A glass of pure fruit juice and a handful of dried fruit added to your cereal at breakfast each count as 1 portion.

The focus of the debate was very much on empowering the public to lead the discussion and enabling wide participation, not just involving the usual suspects. The Agriculture and Environment Biotechnology Commission were clear in their recommendations for a wider public debate that it should not require a simple yes or no decision. Instead it stated it should “establish the nature and full spectrum of the public�s views on GM and the possible commercialization of GM crops, and any conditions it might want to impose on this”.

If you�re a journalist but you don�t like talking to pr people (even though ours are very nice), you can e-mail Chris or Gerry direct:

Is it time we faced up to the reality of GM in modern world?

The Government has given the go-ahead for the first growing trials of GM wheat. Farming Editor Peter Hall looks at the latest developments in this highly emotive topic.

The Question: Why So Much Disagreement?

There is so much disagreement about the benefits and risks of GM because there are so many different views surrounding it. Some focus on the benefits and view it as a natural development of existing plant breeding, while others say that such views do not take into account the genuine concerns of the public and that risks and benefits have not been scrutinized enough.

The debate was criticized for not having enough time or funding to give it the publicity it would need in order to reach a truly representative cross-section of the UK public, including at grass roots level. The lack of results from the scientific and economic studies meant that there was no new information available to feed into the debate. However feedback forms were generally positive about the debate and the chance to express views on such a controversial issue.

Details of Parliamentary and other events, including Labour Party Conference, the All Party Group on Advertising and the Debating Group.

Results:�Genetically Modified Foods

Those who had strong opposing views on GM and surrounding issues tended to agree with the outcomes and some did not pay too much attention to the process issues. However, independent evaluators tended to disregard the outcomes as not valid and focused on the process. The general view was therefore not a positive one. Taking these together, the Food Standards Agency outlined a precautionary, evidence-based approach, taking a case-by-case methodology for the future development of GM crops in the UK which was a component of all these different reports. They said that whilst there was no scientific case for a blanket approval of all the uses of GM, there was also no scientific case for a blanket ban on the use of genetic modification.

Written by:�History Of GM Nation Website

Chiropractic Care For The Boomers

The American Chiropractic Care History | Eastside Chiropractic

The American Chiropractic Care History | Eastside Chiropractic

Since its beginning in 1895, chiropractic has offered treatment for individuals with aggravating neck and back pain. Throughout American chiropractic history, some chiropractors have promised the connection between the spine, nervous system and brain to be as essential to one’s health and have held the belief that structural imbalances in the spine can affect the spinal cord, nerves, muscles, bones and joints of the human body.

 

What is the history behind American chiropractic care?

 

Over the years, according to evidence from literature and research studies, healthcare professionals have increasingly concentrated on treatment of spine-related disorders as well as other problems.

 

Chiropractic care has traditionally been predicated on spinal manipulation, which normally involves implementing a manual, controlled push into joints that have been restricted by tissue injury with the objective of restoring the joint’s distress, relieving related stiffness and pain, and allowing the tissues to heal. It is one of the most commonly used forms of treatment, while spinal manipulation has gotten more specialized because of its applications in chiropractic care.

 

However, because doctors of chiropractic have evolved together with the signs as to the most effective approaches to chronic pain, neck pain and back pain, they’ve embraced many different evidence-based treatment approaches. Quite a few healthcare professionals have got degrees, such as PhD’s, and have begun to investigate the effects of chiropractic adjustments and manual manipulations, in addition to other alternative treatment options.

 

Spinal Manipulation in Chiropractic History

 

Spinal manipulation, or chiropractic adjustment, was not invented by a chiropractor, nor is it even a method. Manipulation of the spine dates back to the beginning of time, together with Hippocrates imagining it.

 

Spinal manipulation is frequently associated with chiropractic care due to a man called Daniel David (D.D.) Palmer, the founder of chiropractic in the United States. Prior to the 20th century, learning more about using spinal manipulation in early times, Palmer maintained an interest towards the function of the spine on health and began to study its basic foundations, thus teaching himself the way to control and manipulate the spine.

 

In 1895, Palmer was approached by a janitor who was deaf in one ear. Palmer theorized that the condition was likely related to the spine, possibly a displaced vertebra. According to many accounts, the man’s back was examined by Palmer, where he manipulated the region, and noticed a bulge near the spine. Palmer reported the adjustment to restore the hearing loss of the man. This event is considered the start of chiropractic history.

 

A combination of the Greek words “cheir” (hand) and praktos (“done”), chiropractic means “Done by Hand”, though it’s essential to be aware that contemporary spinal manipulation has expanded beyond just hands-based adjustments.

 

In 1907, Palmer added the term “subluxation” into the chiropractic vocabulary. Palmer clarified “subluxations” in terms of the spinal vertebrae and joints putting pressure on the nerves, thus impairing operation, and then detailed how spinal alterations may be used to decrease subluxation and enhance patient symptoms. The term subluxation is still used today by some chiropractors to characterize certain misalignments of the spinal vertebrae and joints as well as to determine the proper treatment options to follow. At least one chiropractic school (National University of Health Sciences) has begun to refer to this word “subluxation” from a historical view only.

 

American Chiropractic History in the 20th and 21st Century

 

In 1897, Palmer founded the Palmer School of Chiropractic (which still exists today) to teach students about chiropractic principles and instruct them in chiropractic manipulation.

 

Palmer’s son Bartlett Joshua (B.J.) further developed and promoted chiropractic in the first half of the 20th century. B.J. Palmer not only provided training in chiropractic care, but aided in the education of both the medical community and the general public on the livelihood.

 

For patients seeking alternatives to traditional therapies using drugs, chiropractic slowly grew during this time period, and its own core fundamentals gained acceptance with continued research. By the late 20th century, chiropractic treatment emerged as one of the most accessible and popular forms of health care, to date.

 

The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
 

By Dr. Alex Jimenez

 

Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

blog picture of cartoon paperboy big news

 

TRENDING TOPIC: EXTRA EXTRA: About Chiropractic

 

 

1918 Flu Epidemic & Chiropractic Care

1918 Flu Epidemic & Chiropractic Care

Historical Chiropractic News

Editors Note: The information provided here was forwarded to Planet Chiropractic by a chiropractor in Texas. Far too many people (including chiropractors) are not aware of historical events that took place during the 1917 � 1918 Spanish Flu years, which involved chiropractors caring for thousands that suffered influenza infection during those times. With such a firestorm of media coverage and fear surrounding the Swine Flu Pandemic, it would be irresponsible not to attempt seeking knowledge regarding influenza events of the past.

The Official History of Chiropractic in Texas
By Walter R. Rhodes, DC
Published by the Texas Chiropractic Association � 1978

CHAPTER VI:
THE THREE GREAT SURVIVAL FACTORS
[Excerpts by Dan Murphy, DC]

�The 1917 � 1918 influenza epidemic swept silently across the world bringing death and fear to homes in every land. Disease and pestilence, especially the epidemics, are little understood even now and many of the factors that spread them are still mysterious shadows, but in 1917-1918 almost nothing was known about prevention, protection, treatment or cure of influenza. The whole world stood at its mercy, or lack of it.�

�But out of that particular epidemic, the young science of chiropractic grew into a new measure of safety. While many struggles would lie ahead this successful passage of the profession into early maturity assured its immediate survival and made the eventual outcome of chiropractic a matter for optimism. If there had been any lack of enthusiasm among the doctors of chiropractic, or a depleting of the sources of students then the epidemic took care of them too. These chiropractic survivors of the flu epidemic were sure, assured, determined, and ready to fight any battle that came up. The effect of the epidemic becomes evident in interviews made with old-timers practicing in those years. The refrain comes repeatedly,�

�I was about to go out of business when the flu epidemic came � but when it was over, I was firmly established in practice.�

�Why? The answer is reasonably simple. Chiropractors got fantastic results from influenza patients while those under medical care died like flies all around.� �Statistics reflect a most amazing, almost miraculous state of affairs. The medical profession was practically helpless with the flu victims but chiropractors seemed able to do no wrong.�

�In Davenport, Iowa, 50 medical doctors treated 4,953 cases, with 274 deaths. In the same city, 150 chiropractors including students and faculty of the Palmer School of Chiropractic, treated 1,635 cases with only one death.�

�In the state of Iowa, medical doctors treated 93,590 patients, with 6,116 deaths � a loss of one patient out of every 15. In the same state, excluding Davenport, 4,735 patients were treated by chiropractors with a loss of only 6 cases � a loss of one patient out of every 789.�

II.

�National figures show that 1,142 chiropractors treated 46,394 patients for influenza during 1918, with a loss of 54 patients � one out of every 886.�

�Reports show that in New York City, during the influenza epidemic of 1918, out of every 10,000 cases medically treated, 950 died; and in every 10,000 pneumonia cases medically treated 6,400 died. These figures are exact, for in that city these are reportable diseases.�

�In the same epidemic, under drugless methods, only 25 patients died of influenza out of every 10,000 cases; and only 100 patients died of pneumonia out of every 10,000 cases. This comparison is made more striking by the following table:�

Influenza Cases Deaths � Under medical methods � Under drugless methods �In the same epidemic reports show that chiropractors in Oklahoma treated 3,490 cases of influenza with only 7 deaths. But the best part of this is, in Oklahoma there is a clear record showing that chiropractors were called in 233 cases where medical doctors had cared for the patients, and finally gave them up as lost. The chiropractors saved all these lost cases but 25.�

�Statistics alone, however, don�t put in that little human element needed to spark the material properly. Dr. S. T. McMurrain [DC] had a makeshift table installed in the influenza ward in Base Hospital No. 84 unit stationed in Perigau, in Southwestern France, about 85 kilometers from Bordeaux [during WWI]. The medical officer in charge sent all influenza patients in for chiropractic adjustments from Dr. McMurrain [DC] for the several months the epidemic raged in that area. Lt. Col. McNaughton, the detachment commander, was so impressed he requested to have Dr. McMurrain [DC] commissioned in the Sanitary Corps.�

III.

�Dr. Paul Myers [DC] of Wichita Falls was pressed into service by the County Health Officer and authorized to write prescriptions for the duration of the epidemic there � but Dr. Myers [DC] said he never wrote any, getting better results without medication.�

Dr. Helen B. Mason [DC], whose �son, when only a year old, became very ill with bronchitis. My husband and I took him to several medical specialists without any worthwhile results. We called a chiropractor, as a last resort, and were amazed at the rapidity of his recovery. We discussed this amazing cure at length and came to the decision that if chiropractic could do as much for the health of other individuals as it had done for our son we wanted to become chiropractors.�

Dr. M. L. Stanphill [DC] recounts his experiences: �I had quite a bit of practice in 1918 when the flu broke out. I stayed (in Van Alstyne) until the flu was over and had the greatest success, taking many cases that had been given up and restoring them back to health. During the flu we didn�t have the automobile. I went horseback and drove a buggy day and night. I stayed overnight when the patients were real bad. When the rain and snow came I just stayed it out. There wasn�t a member of my family that had the flu.�

When he came to Denison he said: �I had a lot of trouble with pneumonia when I first came. Once again took all the cases that had been given up. C. R. Crabetree, who lived about 18 miles west of Denison, had double pneumonia and I went and stayed all night with him and until he came to the next morning. He is still living today. That gave me a boost on the west side of town.�

�And when interviews of the old timers are made it is evident that each still vividly remembers the 1917-1918 influenza epidemic. We now know about 20 million persons [recent estimates are as high as 100 million deaths] around the world died of the flu with about 500,000 Americans among that number. But most chiropractors and their patients were miraculously spared and we repeatedly hear about those decisions to become a chiropractor after a remarkable recovery or when a close family member given up for dead suddenly came back to vibrant health.�

�Some of these men and women were to become the major characters thrust upon the profession�s stage in the 20�s and 30�s and they had the courage, the background and the conviction to withstand all that would shortly be thrown against them� [including being thrown in jail for practicing medicine without a license].

�The publicity and reputation of such effectiveness in handling flu cases also brought new patients and much acclaim from people who knew nothing of chiropractic before 1918.�

IV.

�The first survival factor for chiropractic: they were the legal and legislative salvation. But the fabulous success of chiropractic in combating the 1917-1918 influenza outbreak was the public relations breakthrough that can certainly be called the second great survival factor. Better acceptance by the public followed and more patients meant financial safety for practicing chiropractors. Dedicated chiropractors came into the profession in increasing numbers and they had a sure sense of certainty, heady conviction, and a great willingness to fight for the cause.�

Other Texas Chiropractic History (view more at chirotexas.com)

1916 � Texas State Chiropractic Association Formed

1916 � First TSCA annual convention held at the St. Anthony Hotel in San Antonio

1917 � First chiropractic bill introduced into Texas Legislature

1923 � Second chiropractic bill introduced into Texas Legislature

Source:

PlanetChiropractic.com

What’s Chiropractic?

What’s Chiropractic?

Modern chiropractic started in the late 1800s when Daniel David Palmer, a self-educated teacher and healer, performed the very first spinal manipulation on a patient. Chiropractic is the third largest area of medicine today. The word chiropractic comes from Greek words meaning “treatment by hand”, which is exactly what chiropractors do�they use their hands to manipulate the body and promote healing and wellness.

The chiropractic philosophy is dependant on the following belief statements:

  • All bodily functions are connected as well as the healing process requires the entire body.
  • A healthy nervous system, especially the spine, is the important thing to your healthier body. The spinal cord carries advice throughout the body and is accountable for many bodily functions including voluntary movements (such as walking) and involuntary functions (like respiration). When the systems of the body have been in equilibrium, it is called homeostasis. Disorders of the bones, muscles, and nerves increase the risk of disorder along with other health problems and can disrupt homeostasis.
  • When body systems are in harmony, the human anatomy gets the extraordinary ability to keep well-being and treat itself.

 

Chiropractors

They use traditional diagnostic testing strategies (like x-rays, MRI, and laboratory work) along with specific chiropractic techniques that involve hands-on manipulation of the articulations (joints) of the body. Nutrition and healthful lifestyle counseling is also offered by chiropractors. Chiropractors elect to not prescribe drugs, plus they do not perform operation; however, many chiropractors work with medical doctors and certainly will refer a patient when needed.

Chiropractors believe among the chief reasons for pain and disease is the misalignment of the vertebrae in the spinal column (this is known as a chiropractic subluxation). Through the usage of manual detection (or palpation), carefully applied pressure, massage, and manual manipulation of the vertebrae and joints (called adjustments), chiropractors are able to alleviate pressure and irritation on the nerves, restore joint mobility, and help return the body’s homeostasis.

Some chiropractors dedicate their practices exclusively to finding and removing subluxations. But in addition to using manual adaptations, most chiropractors offer other treatment modalities such as the following:

  • Physiotherapy
  • Herbal therapy
  • Heat/cold therapy
  • Ultrasound
  • Electric muscle stimulation
  • Acupuncture
  • Manipulation under anesthesia
  • Traction
  • Massage
  • Exercise programs and teaching
  • Lifestyle and nutrition counselling
  • Physical rehabilitation

Additionally, many chiropractors have considerable postgraduate training and become board certified in some specific regions of interest such as for instance:

  • Neurology
  • Orthopaedics
  • Sports medicine
  • Physical rehabilitation
  • Nourishment
  • Diagnostic radiology

In Overview

Chiropractic has come a long way since its beginnings. Due to its success in treating back and neck problems and as a consequence of changing approaches and recent research, chiropractic has become more accepted and is currently considered by many to be a piece of mainstream Western medicine. Actually, many hospitals finally have chiropractors on staff. Chiropractors will also be recognized by the court system as expert witnesses inside their field.

 

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The History Of Chiropractic

The History Of Chiropractic

The understanding the spine is somehow involved in health and wellness, in addition to the practice of utilizing manual manipulation as a way to obtain healing, dates back to the time of the ancient Greek philosophers. In fact, Hippocrates once said, “Get understanding of the back, for this is the requisite for several ailments.”

The First�Chiropractic Adjustment

Modern chiropractic, however, indicates its beginnings in the late 1800s, �when a Canadian living in the US, Daniel David Palmer, a self educated teacher and healer, performed the very first spinal manipulation on a patient.

That patient was Harvey Lillard, a janitor who worked in Palmer’s building. Lillard was almost totally deaf and mentioned to Palmer that he lost his hearing many years before when he was bending over and felt a “pop” in his upper back.

Palmer, who had been a practitioner of magnet therapy (a common therapy of the time) was fairly learned in physiology and incredibly interested in how a spine interacts with all the remainder of the entire body’s systems.

He found a difficulty with one of his vertebra and examined Lillard’s back. Palmer manipulated Lillard’s vertebra and an amazing event occurred�Lillard’s hearing was restored. Today, this process is referred to as a chiropractic adjustment.

Palmer soon found that alterations could alleviate patients’ pain as well as other symptoms. These problems with vertebrae are called chiropractic subluxations.

He started to use these “hand treatments” to treat many different ailments, including sciatica, migraine headaches, stomach complaints, epilepsy, and heart trouble. In 1898, he started the Palmer School & Infirmary in Davenport, Iowa, and began teaching his chiropractic techniques.

 

Initial Resistance In The Medical Community

The medical community failed to immediately embrace techniques and Palmer’s chiropractic theories. The called him a “quack” and refused to recognize his achievements. At one point, Palmer spent time in jail because of his violation and was indicted for practicing medicine with no license.

Research has shown that Palmer was not the fish monger that was unlearned that some in the health care profession claim. An investigation of this library, which he quoted in his letters, showed that he was up to date in his knowledge at the turn of the 20th century. Obviously, his theories, in the light of 21st century knowledge, seem uneducated.

Chiropractic Today

Today, chiropractors are licensed in most European countries, Canadian provinces, all the US states, Australia and New Zealand. There tend to be more than 50,000 practicing chiropractors in the US alone . Despite its North American roots, there are more chiropractic educational programs beyond North America.

 

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