DRS. DAVID & JANNICE BOWLER
  • Home
  • Contact
  • About Us
  • FAQ
    • Cancellation policy
    • Your first visit
    • Prolotherapy
    • Trigger Point Injections
    • Perineural Injection Treatment
    • Platelet Rich Plasma (PRP)
    • Botox for migraines
    • Botox for postural correction
    • Ozone Injections
    • Neurofeedback
    • Clinical Hypnosis
    • Pain Reprocessing Therapy
    • Gut-Directed Hypnotherapy
  • Clinical Hypnosis
  • For Physicians
  • Links
  • COVID-19 information
  • Research
  • Blogs
    • Dr. Jannice's blog
    • Dr. David's blog
  • Telephone and Telemedicine appointments


​Dr. ​David's Corner

March 08th, 2021

8/3/2021

 
This Might Hurt is a documentary describing the work of Dr Howard Schubiner. Viewers follow the moving stories of a group of chronic pain patients for whom conventional medicine had little to offer other than opiates and other drugs or potentially harmful unnecessary surgery. Most of them found significant relief using a structured program examining the underlying emotions contributing to their physical symptoms. 

This approach has been used at our office for many years. 

Fibromyalgia - what it is and how to manage it.

15/6/2020

 
Fibromyalgia
Fibromyalgia is a common long-term condition, affecting 2-4% of the population, more commonly women than men, that causes pain all over the body along with many other symptoms.  People with fibromyalgia often have:
  • Tenderness to touch or pressure affecting the skin or soft-tissues – this is the most obvious complaint and often is misdiagnosed as tendonitis, tennis elbow, or arthritis.   This tenderness is generally in a fairly symmetrical pattern over the shoulders, neck, base of the skull, upper chest, arms, legs, lower back, buttocks, hips, thighs, and lower legs - in short, all over. 
  • Severe fatigue – fibromyalgia is often thought to be related to chronic fatigue syndrome – there is debate about whether they are different conditions or both on the same spectrum of illnesses
  • Sleep problems (waking up unrefreshed) – called non-restorative sleep
  • Problems with memory, concentration, or thinking clearly (cognitive symptoms, often referred to as “fibro-fog”)
  • Depression or anxiety
  • Migraine or tension headaches
  • Irritable bowel syndrome (commonly called IBS) with cramps, bloating, constipation or diarrhea
  • Gastroesophageal reflux disease (often referred to as GERD) or heartburn
  • Irritable or overactive bladder, often labelled as interstitial cystitis
  • Pelvic pain
  • Temporomandibular disorder - often called TMJD that may include face or jaw pain, jaw clicking, and ringing in the ears. 
While not part of fibromyalgia itself, it is not unusual for patients to also complain of multiple chemical sensitivities. They may be told they have costochondritis because the upper chest is tender.They may also have numbness or tingling in the hands and feet suggestive of a nerve disorder. 

Books and articles often say that the causes of fibromyalgia are unknown. It may be that it is the final destination arrived at from a variety of different starting points. For some people it occurs after an illness such as influenza; for others after an accident or other traumatic event. For many it develops gradually after an overwhelming incident or as the culmination of years of accumulated stressful events, often dating back to childhood. Numerous studies have found that between 50 and 63% of patients with fibromyalgia also meet the criteria for post-traumatic stress disorder, frequently reporting adverse childhood events or subsequent physical or emotional trauma. Adverse childhood events (such as the loss of a parent, abusive or chaotic households, early hospitalizations, accidents, neglect etc), and later traumas all can prime the nervous system's fight/flight/freeze response, giving rise to a sense of being unsafe in the world, and cause the body to respond with physical symptoms. Chronically elevated stress hormones change the way our glucose metabolism and digestive function work, cause increased muscular tone (tight muscles), and affect our immune system function. 

There is a complex inter-relationship between our nervous systems, our hormones, immune systems, gastrointestinal system, and our muscular function, including how the energy powerhouses (mitochondria) in our cells function. In other words, although it is a very real physical condition, the pain is being produced in the nervous system in response to (usually prolonged and cumulative) internal (such as the demands or expectations we place on ourselves) and external sources of stress. It can also be triggered by sleep deprivation in some people.  

For this reason, it is possible to turn the pain down or even off, by means of techniques that address past trauma, anxiety, stress, beliefs and expectations, as well as by optimizing nutrition, sleep and general well-being through regular exercise (while avoiding extreme of activity).  Coming to an understanding of the condition reduces fear, which in turn can substantially reduce pain intensity.


Fibromyalgia can be best thought of as a central nervous system condition in which the brain and spinal cord are sensitized and therefore respond to sensations which are perceived as much more painful than the same sensation would be experienced by someone without fibromyalgia. It is sometimes referred to as a Central Pain Amplification Disorder. Similarly, people with irritable bowel syndrome will perceive the same degree of gaseous intestinal distension as being much more painful than someone without IBS would do. It is as though the pain ‘thermostat’ or dial has been turned up to a very high level. 

Unlike rheumatoid arthritis or lupus, fibromyalgia is not an autoimmune or inflammatory condition. It can co-exist with arthritis but it is not primarily a joint condition. It does not lead to any ilife-threatening disease.

Fibromyalgia may run in families to some extent but whether this is genetic or due to a common environment (similar stresses) or a learned response to adverse circumstances is not clear. A small subset of people with symptoms suggestive of fibromyalgia have been found on skin biopsy to have an abnormality of small nerve fibres. Genetics alone cannot explain fibromyalgia. Symptoms tend to be worse with stress, over-work, excessive exercise, or sleep deprivation. 

Diagnosing Fibromyalgia

1. symptoms as mentioned above, present for more than 3 months with no other explanation
2. pressure at certain common soft tissue points on physical exam can be helpful to detect tenderness and to exclude other causes of muscle pain.

There is no specific blood test or X-ray that can diagnose fibromyalgia. Commonly tests will be ordered to exclude other conditions, for example, sleep apnea, an underactive thyroid, or polymyalgia rheumatica, anemia, iron-deficiency, rheumatoid arthritis or lupus. 

Treating fibromyalgia

While there is no one specific cure for fibromyalgia, approaching it from a number of different angles – certain medications, carefully structured aerobic exercise within one’s capabilities, and mind-body approaches such as relaxation, stress-reduction, Cognitive Behavioural Therapy, mindfulness, Tai Chi, and clinical hypnosis or guided imagery, can be helpful. Ensuring adequate sleep is essential. Some people have co-existent anxiety, depression, PTSD, panic disorder, all of which can also be treated.  Proper nutrition is also important. Anecdotally, some patients report a correlation between pain intensity and diet, such as refined carbohydrates, gluten, nightshades, or meat. This may be an individual response. 

A number of medications are often tried to reduce symptoms. Most of these are “off-label”. 


Low doses of an antidepressant called amitriptyline (Elavil) or related medications (such as nortriptyline or trazodone) can often be very helpful for pain, sleep, and to reduce migraines. 
A muscle relaxant such as cyclobenzaprine (Flexeril) can be helpful.  This is structurally similar to tricyclic antidepressants (TCAs) such as amitriptyline. 
A newer SNRI medication, duloxetine (Cymbalta) can sometimes help. 
Additional medications include pregabalin (Lyrica) and gabapentin (Neurontin) can be used. 
Another off-label medication is low dose naltrexone. 

Opioid narcotic medications are best avoided as they have significant side-effects, are largely ineffective, addictive and can lead to a conditions known as opiate-induced hyperalgesia, a parodoxical increase in pain the more opiates one cosumes. Of the opiates Tramadol may be better than the others but shares all the same risks as other opiates and interacts with other medications. 

Acetaminophen and anti-inflammatories (such as ibuprofen) are generally not effective for fibromyalgia but may help other co-existing pain. Sleeping tablets such as Zopiclone and benzodiazepines are not recommended. 

One small study published in December 2018 suggested that some patients with fibromyalgia may respond to treatment with a diabetes drug called metformin if their average sugar level (HBA1C) was in the high normal or elevated range. 

Gaining an understanding of fibromyalgia, engaging in self-care, ensuring good sleep, reducing stress, modifying behaviour, counselling, dietary modifications and supplements, and a judicious exercise regimen can all be helpful. 

In my own practice a combination of tender point injections, counselling, relaxation techniques, clinical hypnosis, medication and nutritional advice, and patient-education (which may include recommended reading and journalling) can lead to a significant reduction in symptoms, periods of remission, or even resolution. 






Psychophysiologic Disorders - a new book

13/6/2020

 
Experts in managing stress-induced illness and pain have produced a new book titled Psychophysiologic Disorders. It is available from Amazon in paperback and Kindle formats and free to subscribers of Kindle Unlimited. It is a comprehensive, in-depth, and up to date approach, reflecting the latest in neuroscience. 

​It describes a host of different stress-induced conditions and how they can be managed. 

Psychophysiologic Disorders: Trauma Informed, Interprofessional Diagnosis and Treatment Paperback – Nov. 13 2019 by David Clarke MD, Howard Schubiner MD, et al.



Picture

Curable App for managing your pain, especially for stress-related pain

13/6/2020

 
Physicians and allied mental health professionals have created an App that you can use gradually over time to help both educate yourself and manage the symptoms you have, once your condition has been properly evaluated medically. The Curable App can be downloaded from the appropriate App Store for your device and requires an annual subscription. 

Understanding Fibromyalgia

7/11/2015

 
We are often asked whether we can help patients with fibromyalgia. While there is no quick cure for most people with fibromyalgia there are many ways in which the condition can be helped. Before getting into management of this very troublesome condition in a subsequent blog entry it may be helpful to first look at an excellent summary of the current scientific understanding of what is going on at a biochemical, physiological and neurological level in people with fibromyalgia. Her is an excellent article from the Mayo Clinic. It is quite technical but don't worry; I shall try to simplify this in another post soon. 


Fibromyalgia: A Unifying Neuroendocrinologic Model for Understanding Its
Pathophysiology
Peter T. Dorsher, MS, MD
From the Department of Physical Medicine and Rehabilitation, Mayo Clinic, Jacksonville,
Florida
Address reprint requests to Peter T. Dorsher, MD, Department of Physical
Medicine and Rehabilitation, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224.
E-mail: dorsher.peter@mayo.edu. Phone 904-953-2823 Fax 904-953-0276
Text word count: 1682 (2956 with references, tables, and legends)
Abstract word count: 121
Introduction word count: 246
Discussion word count: 273
No. of tables: 3
No. of figures/parts: 3
©2008 Mayo Foundation for Medical Education and Research
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
Abstract
Fibromyalgia is believed to affect at least 2% of the population. Despite advances in the
scientific understanding of the derangements of central and peripheral pain processing
mechanisms in fibromyalgia, no current models of its pathophysiology account for the
other clinical conditions associated with it such as fatigue, migraine headache, irritable
bowel syndrome, and sleep cycle abnormalities. A neuroendocrinologic model of
fibromyalgia is presented that accommodates both its known central and peripheral pain
mechanisms as well as the myriad of hormonal, visceral, and psychological symptoms
associated with that disorder. This model also provides a unifying pathophysiologic basis
of fibromyalgia and chronic muscle pain, and offers the potential for developing new
avenues of research and treatment for these enigmatic, frequently disabling medical
conditions.
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
Introduction
In 1852, Virchow first described “muscular rheumatism” 1 and five decades later
Gowers described persons with widespread pain symptoms he termed “fibrositis” 2. The
fibromyalgia and myofascial pain histories have overlapped, with Kelly 3 in 1945
discussing the concept of distant referred-pain produced by “fibrositis” nodules. The
historical overlap of these conditions is not surprising, since both the myofascial pain and
fibromyalgia syndromes are pain conditions characterized by tender soft tissue
(especially muscle) sites that may generate referred-pain distant to those sites.
There are significant clinical differences between the fibromyalgia and myofascial
pain syndromes, however. Fibromyalgia afflicts females seven times more frequently
than males, while myofascial pain syndrome afflicts genders equally 4. Myofascial pain
syndrome often affects only one body region, though widespread myofascial pain has
been described 5. In contrast, the diagnosis of fibromyalgia requires the presence of
widespread soft tissue tenderness in multiple body regions 6. Both conditions may be
associated with sleep disturbances, but fibromyalgia is also associated with other clinical
conditions (Table 1) including irritable bowel syndrome, interstitial cystitis, and migraine
headaches 7. These conditions are 4-25 times more common in individuals diagnosed
with fibromyalgia 7.
Widespread body pain affects approximately 3.6% of adults in the United States 8,
with fibromyalgia diagnosed in 5 million (2%) of adults 4. In terms of rheumatologic
disorders, only osteoarthritis and gout 9 have higher prevalence than fibromyalgia; yet
fibromyalgia is associated with the highest disability rate (up to 26.5%) of all
rheumatologic disorders 10, 11.
A Neuroendocrinologic Model of Fibromyalgia and Chronic Muscle Pain
The sympathetic autonomic nervous system (SANS) subserves the body’s “fight
or flight” responses to dangerous or stressful stimuli, while the parasympathetic
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
autonomic nervous system (PANS) subserves its vegetative, “rest and digest” functions
(S. Bakewell, http://www.nda.ox.ac.uk/wfsa/html/u05/u05_010.htm). Most body
structures, including muscle, have dual sympathetic and parasympathetic innervation. As
shown in Table 2, SANS and PANS responses have opposite physiologic effects, with the
hypothalamus controlling the balance of those responses (D. Molavi,
http://thalamus.wustl.edu/course/hypoANS.html). As an example relevant to
musculoskeletal pain, SANS activation increases resting skeletal muscle tone while
PANS activation reduces it 12.
The clinical conditions associated with fibromyalgia (Table 1) are postulated to
result from imbalance or instability of the autonomic nervous system (Table 3). SANS
abnormalities have been described for many of those conditions, including migraines 13,
irritable bowel syndrome 14, interstitial cystitis 15, endometriosis 16, idiopathic urethritis
17, chronic prostatitis 18, and temporomandibular joint pain 19. Thus, abnormal regulation
of SANS/PANS outflow balance by the hypothalamus could result in these clinical
conditions seen in fibromyalgia patients. The circadian rhythms of sleep 20, appetite
regulation 21, mood 22, and temperature 23 also are regulated at the hypothalamic level;
and the abnormalities of those physiologic functions often described by fibromyalgia
patients are also consistent with hypothalamic dysfunction.
Though the insular cortex is believed to be mainly a viscerosensory structure, the
right insular cortex is believed to provide sympathetic outflow to the hypothalamus and
the left insular cortex its parasympathetic outflow 24. The orbitofrontal and medial
prefrontal cortex areas of the limbic system have direct anatomic input to the
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
hypothalamus, allowing emotions to directly influence autonomic balance there 25. The
amygdala serves to integrate behavioral and autonomic responses from the
somatosensory cortex and limbic system structures including the medial prefrontal cortex,
orbitofrontal cortex, cingulate gyrus, hippocampus, anterior thalamic nuclei, and medial
thalamic nuclei 26. The amygdala is thought to have inhibitory influence on the
hypothalamus to attenuate SANS output 27. These thalamic and cortical influences on the
hypothalamus are demonstrated in Figure 1.
Hypothalamic SANS output arises from its posterolateral nuclei that ultimately
innervate the interomediolateral nuclei of the spinal cord, while its PANS output arises
from its anteromedial nuclei that ultimately course to peripheral structures via the vagus
nerve (D. Molavi, http://thalamus.wustl.edu/course/hypoANS.html). The hypothalamus
also regulates the release of cortisol and norepinephrine through the hypothalamicpituitary-
adrenal (HPA) axis, which provides systemic SANS activation with slower
onset and longer duration (D. Molavi, http://thalamus.wustl.edu/course/hypoANS.html).
Further, hypothalamic output regulates brainstem structures (rostroventral medulla,
periaqueductal gray, and locus ceruleus) whose descending pathways to the dorsal horn
of the spinal cord modulate pain transduction in nociceptive neurons there, as shown in
Figure 1 28.
The systemic norepinephrine release via the HPA axis, accentuated SANS tone
through hypothalamic output to the interomediolateral cells of the spinal cord, and
reduced descending pain inhibition at the spinal cord level are then postulated in this
neuroendocrinologic model to produce sensitization of primary nociceptors in
fibromyalgia patients. Clinical research supporting this includes documentation that
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
fibromyalgia patients have elevated plasma catecholamine levels, which are associated
with hyperalgesia 29,30. Approximately 8% of spinal nerve fibers are postganglionic
sympathetic fibers 31, which also invest the arteries that accompany spinal nerves and
their branches to the extremities 32 (H. Gray, http://www.bartleby.com/107/214.html).
Neurogenic inflammation is a physiologic phenomenon 33 in which efferent
outflow from the spinal cord (dorsal root reflexes) causes nociceptive C-fibers to release
substance P (sP), calcitonin gene related peptide (cGRP) and somatostatin from their
terminal axons. These substances then cause local vasculature (plasma), platelets, and
macrophages to release bradykinin, histamine, and serotonin, which serve to activate
those nociceptive neurons 34, as illustrated in Figure 2. Thus, a local positive feedback
loop is produced as neurogenic inflammation ultimately produces release of substances
from the terminal axons that activate the primary nociceptors. Efferent or systemic SANS
activation can further sensitize these nociceptive neurons (Figures 1 and 2). The
abnormally high metabolic activity seen in the thalamus, amygdala, hippocampus,
cingulate gyrus, and other limbic system structures in fibromyalgia patients 35 is
consistent with abnormal central nervous system (CNS) autonomic efferent activity
contributing to nociceptor sensitization and neurogenic inflammation peripherally.
Psychological stress alone can cause degranulation of mast cells (many of which are
estrogen receptor positive) to initiate neurogenic inflammation 36,37, which may help
explain the predominance of fibromyalgia in females. Neurogenic inflammation causes
local edema (fibromyalgia nodules) and tenderness without histological presence of
inflammatory cells 38. Continuing activation of dorsal root reflexes and propriospinal
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
pathways produces ascending and descending sensitization of nociceptors in adjacent
spinal levels, providing a mechanism for the spread of tender regions to increasingly
larger areas of the body 34. This is consistent with Shah’s findings 39 that trigger points
have markedly increased concentrations of inflammatory mediators, but also that muscle
sites distant from the trigger points in those subjects have lesser elevations of these
inflammatory mediators (higher than normal), suggesting systemic nervous system
sensitization as predicted by this neuroendocrinologic model. Efferent output of these
sensitized primary nociceptors also leads to activation of wide dynamic range neurons in
the deeper lamina of the spinal cord, which have wider cutaneous receptive fields and
visceral sensory input.
Primary nociceptors relay information through the lateral spinothalamic tract to
the lateral thalamus then on to the somatosensory cortex to localize painful stimuli, while
wide dynamic range neurons send information through the paleospinothalamic tract to the
anterior and medial thalamus then on to limbic system structures that subserve the
emotional and behavioral reactions to painful stimuli 34. These ascending pathways are
largely anatomically independent of each other. As shown in Figure 1, abnormal
activation of the neospinothalamic and paleospinothalamic pathways then forms the final
link in a positive feedback loop to produce excessive activation of the thalamus,
neocortex, and limbic system structures that regulate autonomic balance centrally.
Abnormal activation of hypothalamic and limbic system structures provides an anatomic
substrate that could account for the excessive behavioral reactions to noxious stimuli seen
in chronic pain patients 40,41. This may represent the central mechanism of the lowering
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
of pain perception threshold (“thermostat”) in chronic pain patients, which in its extreme
progresses from hyperpathia to allodynia.
There is also pharmacologic evidence that supports this neurogenic model of
fibromyalgia. Drugs that demonstrate the most efficacy for treating fibromyalgia are in
the anti-convulsant (e.g. pregabalin) and anti-depressant (e.g. duloxitene) classes, which
act on the central and peripheral nervous systems. Fibromyalgia symptoms are relatively
resistant to opioids and anti-inflammatory drugs, which are efficacious for treating
musculoskeletal pain conditions.
Discussion
Functional MRI and neurophysiologic studies have demonstrated objective
evidence of abnormal central nervous system pain sensitization in patients with
fibromyalgia, even though its cause remains enigmatic. The recent work of Shah 39
demonstrates physiologic evidence of similar central nervous system sensitization in
myofascial pain syndrome.
Though both fibromyalgia and myofascial pain syndrome share the phenomenon
of tender muscular regions, only fibromyalgia is associated with other conditions such as
chronic headaches, irritable bowel syndrome, interstitial cystitis, and temporomandibular
joint pain syndrome. Clinical and experimental evidence of the role of neurogenic
inflammation and autonomic nervous system dysfunction in those disorders continues to
accumulate.
This neuroendocrinologic model of fibromyalgia provides an anatomically and
physiologically based conceptualization of the central and peripheral physiologic
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
mechanisms that can produce the widespread muscular tenderness and visceral
dysfunction seen clinically in fibromyalgia patients. The model integrates the known
clinical and experimental findings of abnormal hypothalamic- pituitary- adrenal axis
activation and abnormal and/or unstable autonomic nervous system balance that are
associated with widespread pain and visceral dysfunction in fibromyalgia patients (Figure
3).
The clinical syndrome of fibromyalgia, then, can be initiated by excessive
noxious input at any point along this loop by a wide variety of causes. Excessive
psychological trauma or stress is postulated to initiate this positive feedback loop
centrally at the level of the paleocortex (limbic system). Visceral injury or recurrent insult
(myocardial infarct, “leaky gut syndrome” after antibiotic administration, recurrent
prostatitis) then initiates this positive feedback loop through severe or recurrent abnormal
visceral nociceptor activation. Similarly, severe and or recurrent musculoskeletal or
peripheral nerve injuries can activate this positive feedback loop through A-delta and Cfiber
activation with neurogenic inflammation.
Conclusion
The model of fibromyalgia presented herein as dysfunction of the autonomic
nervous system with sensitization of central nervous system nociception can unify the
multiple clinical findings noted in that disorder including cognitive impairment,
depression, sleep disturbance, widespread pain, and organ dysfunction such as irritable
bowel syndrome and interstitial cystitis. This model offers a novel view of the
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
pathogenesis of this enigmatic syndrome that causes substantial morbidity and not
infrequently disability, and may lead to new avenues of treatment.
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
References
1) Virchow, R. Über parenchymatöse entzündung. Arch. Pathol. Anat. 4, 261-
279 (1852).
2) Gowers, W.R. Lumbago: its lessons and analogues. Br. Med. J. 1, 117-121
(1904).
3) Kelly, M. The nature of fibrositis: 1. the myalgic lesion and its secondary
effects: a reflex theory. Ann. Rheum. Dis. 5, 1-7 (1945).
4) Wolfe, F., Ross, K., Anderson, J., Russell, I.J. & Hebert, L. The prevalence
and characteristics of fibromyalgia in the general population. Arthritis Rheum.
38, 19-28 (1995).
5) Bergman, S., Herrstrom, P., Jacobsson, L.T. & Petersson, I.F. Chronic
widespread pain: a three year follow up of pain distribution and risk factors. J.
Rheumatol. 29, 818-825 (2002).
6) Wolfe, F. et al. The American College of Rheumatology 1990 criteria for the
classification of fibromyalgia: report of the multicenter committee. Arthritis
Rheum. 133, 160-172 (1990).
7) Clauw, D. Fibromyalgia: more than just a musculoskeletal disease. Am. Fam.
Physician. 52, 843-851 (1995).
8) Hardt, J., Jacobsen, C., Goldberg, J., Nickel, R. & Buchwald, D. Prevalence of
chronic pain in a representative sample in the United States. Pain Med.
10.1111/j.1526-4637.2008.00425.x [doi] (2008).
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
9) Lawrence, R.C. et al. Estimates of the prevalence of arthritis and selected
musculoskeletal disorders in the United States. Arthritis Rheum. 41, 778-799
(1998).
10) Hoffman, D.L. & Dukes, E.M. The health status burden of people with
fibromyalgia: a review of studies that assessed health status with the SF-36 or
the SF-12. Int. J. Clin. Pract. 62, 115-126 (2007).
11) Wolfe, F. et al. Work and disability status of persons with fibromyalgia. J.
Rheumatol. 24, 1171-8 (1997).
12) Roatta, S., Windhorst, U., Ljubisavljevic, M., Johansson, H. & Passatore, M.
Sympathetic modulation of muscle spindle afferent sensitivity to stretch in
rabbit jaw closing muscles. J. Physiol. 540, 237–248 (2002).
13) Peroutka, S.J. Migraine: a chronic sympathetic nervous system disorder.
Headache. 44, 53-64 (2004).
14) Mazur, M. et al. Dysfunction of the autonomic nervous system activity is
responsible for gastric myoelectric disturbances in the irritable bowel
syndrome patients. J. Physiol. Pharmacol. 58 Suppl. 3:131-139 (2007).
15) Pacak, K. Increased plasma norepinephrine concentration in cats with
interstitial cystitis. J. Urol. 165, 2051-2054 (2001).
16) Possover, M., Rheim, K. & Chiantera, V. The “neurologic hypothesis”: a new
concept in the pathogenesis of the endometriosis? Gynecol. Surg. 2, 107-111
(2005).
17) Husmann, D.A. Use of sympathetic alpha antagonists in the management of
pediatric urologic disorders. Curr. Opin. Urol. 16, 277-282 (2006).
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
18) Yilmaz, U., Liu, Y., Berger, R. & Yang, C. Autonomic nervous system
changes in men with chronic pelvic pain syndrome. J. Urol. 177, 2170 – 2174
(2003).
19) Appelgren, A. Neuropeptides in temporomandibular joint arthritis.
Dissertations from Karolinska Institutet. kl. 9.00. Föreläsningssal 1, plan 4,
Odontologiska Institutionen, Huddinge (1999).
20) Saper, C.B., Scammell, T.E. & Lu, J. Hypothalamic regulation of sleep and
circadian rhythms. Nature. 437, 1257-1263 (2005).
21) Neary, N.M., Goldstone, A.P., & Bloom, S.R. Appetite regulation: from the
gut to the hypothalamus. Clin. Endocrinol. 60, 153-160 (2004).
22) Müller, M.B., Uhr, M., Holsboer, F. & Keck, M.E. Hypothalamic-pituitaryadrenocortical
system and mood disorders: highlights from mutant mice.
Neuroendocrinology. 79, 1-12 (2004).
23) Hammel, H.T., Jackson, D.C., Stolwijk, J.A., Hardy, J.D. & Stromme, S.B.
Temperature regulation by hypothalamic proportional control with an
adjustable set point. J. Appl. Physiol. 18, 1146-1154 (1963).
24) Oppenheimer, S.M., Gelb, A., Girvin, J.P. & Hachinski, V.C. Cardiovascular
effects of human insular cortex stimulation. Neurology. 42, 1727–32 (1992).
25) Cechetto, D.R. & Saper, C.B. in Central Regulation of Autonomic Functions.
(eds. Loewy, A.D. & Spyer, K.M.) 208–223 (Oxford University Press, Oxford,
UK, 1990).
26) Cechetto, D.R. & Gelb, A.W. The amygdala and cardiovascular control. J.
Neurosurg. Anesthesiology. 13, 285-287 (2001).
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
27) Palkovits, M. Interconnections between the neuroendocrine hypothalamus and
the central autonomic system. Front. Neuroendocrinol. 20, 270-295 (1999).
28) Benarroch, E.E. Descending monoaminergic pain modulation: bidirectional
control and clinical relevance. Neurology. 71, 217-21 (2008).
29) Khasar, S.G., McCarter, G. & Levine, J.D. Epinephrine produces a beta
adrenergic receptor-mediated mechanical hyperalgesia and in vitro
sensitization of rat nociceptors. J. Neurophysiol. 81, 1104-1112 (1999).
30) Torpy, D.J., et al. Responses of the sympathetic nervous system and the
hypothalamic pituitary adrenal axis to interleukin-6: a pilot study in
fibromyalgia. Arthritis Rheum. 43, 872-880 (2000).
31) McCorry, L.K. Physiology of the autonomic nervous system. Am. J.
Pharmacol. Educ. 71, Article 78 (2007).
32) Birch, D.J., Turmaine, M., Boulos, P.B. & Burnstock, G. Sympathetic
innervation of human mesenteric artery and vein. J. Vasc. Res. 45, 323-332
(2008).
33) Lin, Q., Wu, J. & Willis, W.D. Dorsal root reflexes and cutaneous neurogenic
inflammation after intradermal injection of capsaicin in rats. J. Neurophysiol.
82, 2602–2611 (1999).
34) Fields, H.L. Pain. 1-354 (McGraw Hill, San Francisco, 1987).
35)Williams, D.A. & Gracely, R.H.. Biology and therapy of fibromyalgia:
functional magnetic resonance imaging findings in fibromyalgia. Arthritis Res.
Ther. 8, 224 (2006).
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
36) Alexcaos, N. et al. Neurotensin mediates rat bladder mast cell degranulation
triggered by acute psychological stress. Urology. 53, 1035-40 (1999).
37) Eutamene, H., Theodorou, V., Fioramonti, J. & Bueno, L. Acute stress
modulates the histamine content of mast cells in the gastrointestinal tract
through interleukin-1 and corticotropin-releasing factor release in rats. J.
Physiol. 553, 959-966 (2003).
38) Huguenin, L.K. Myofascial trigger points: the current evidence. Phys. Ther.
Sports. 5, 2-12 (2004).
39) Shah, J.P. et al. Biochemicals associated with pain and inflammation are
elevated in sites near to and remote from active myofascial trigger
points. Arch. Phys. Med. Rehabil. 89, 16-23 (2008).
40) Bradley, R.A. et al. Abnormal regional cerebral blood flow in the caudate
nucleus among fibromyalgia patients and non-patients is associated with
insidious symptom onset. J Musculoskel. Pain. 7, 285-292 (1999).
41) Gracely, R.H., Petzke, F., Wolf, J.M. & Clauw, D.J. Functional magnetic
resonance imaging evidence of augmented pain processing in fibromyalgia.
Arthritis Rheum. 46, 1333-1343 (2002).
42) Lambert, G.W. et al. Internal jugular venous spillover of noradrenaline and
metabolites and their association with sympathetic nervous activity. Acta.
Physiol. Scand. 163, 155-163 (1998).
43) Quintner J. & Cohen M. Referred pain of peripheral nerve origin: an
alternative to the myofascial pain construct. Clin. J. Pain. 10, 243–251 (1994).
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
Table 1. Clinical Conditions Associated with Fibromyalgia
Clinical Condition % fibromyalgia patients % general populaton
Chronic headache 50% 5%
Dysmenorrhea 60% 15%
Endometriosis 15% 2%
Interstitial cystitis 25% <1%
Irritable bladder/ urethra 15% <1%
Irritable bowel syndrome 60% 10%
Mitral valve prolapse 75% 15%
Multiple chemical sensitivities 40% 5%
Restless legs syndrome 30% 2%
TMJ syndrome 25% 5%
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
Table 2. Autonomic Nervous System and Its Clinical Effects
SANS Effects PANS Effects
“fight or flight” “rest and digest”
↑ alertness/vigilance ↓ alertness/vigilance
↑ heart rate and contractility ↓ heart rate and contractility
↑ breathing rate with
bronchodilitation
↓ breathing rate with
bronchoconstriction
↑ cardiac and skeletal
muscle blood flow
↓ cardiac and skeletal
muscle blood flow
↓ gut blood flow ↑ gut blood flow
↓ cutaneous blood flow ↑ cutaneous blood flow
↑ blood sugar ↓ blood sugar
↑ temperature ↓ temperature
↓ gut contractility ↑ gut contractility
↓ bladder contractility ↑ bladder contractility
↓salivation ↑ salivation
↓lacrimation ↑ lacrimation
↓digestion ↑ digestion
SANS= sympathetic autonomic nervous system
PANS= parasympathetic autonomic nervous system
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
Table 3. Autonomic Nervous System Imbalance in Fibromyalgia (relative degree of tonus)
Clinical Condition SANS PANS
Migraine ↑ initial phase ↑later phase
IBS, diarrhea predominant ↓ ↑
IBS, constipation predominant ↑ ↓
Interstitial Cystitis ↑ ↑
Raynaud’s-like phenomenon ↑ ↓
Endometriosis ↑ ↓
Aseptic Prostatitis ↑ ↓
Idiopathic Urethritis ↑ ↓
Skeletal Muscle Tone ↑ -
IBS= irritable bowel syndrome
SANS= sympathetic autonomic nervous system
PANS= parasympathetic autonomic nervous system
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
Legends
Figure 1. Detailed Neurophysiology of Positive Feedback Loop in Fibromyalgia
Figure 2. Peripheral Sensitization Mechanisms
Figure 3. Simplified Positive Feedback Loop in Fibromyalgia
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008
Nature Precedings : hdl:10101/npre.2008.2595.1 : Posted 3 Dec 2008

    Author

    David is a fan of books and no doubt will be sharing some good reads here.

    Archives

    March 2023
    January 2023
    November 2022
    October 2022
    March 2022
    January 2022
    October 2021
    August 2021
    July 2021
    June 2021
    May 2021
    March 2021
    February 2021
    December 2020
    October 2020
    June 2020
    March 2019
    July 2018
    March 2018
    November 2015
    October 2015
    June 2015
    May 2015
    April 2015
    February 2015
    November 2014

    Categories

    All
    Acupuncture
    Acute Pain
    Acute Pain Victoria BC
    Alternative Therapies
    Anatomy Trains
    Brain Bargaining
    Chronic Pain
    Chronic Pain Victoria BC
    Counselling
    Dextrose D5W
    Dr John Lyftogt
    Dry Needling
    Eastern And Western Medicine
    Fascia
    Fear
    Fibromyalgia
    Gut Directed Hypnotherapy
    Gut-directed Hypnotherapy
    Human Givens
    Hypnosis
    Hypnotherapy
    Irritable Bowel Syndrome
    Literature Reviews
    Mannitol
    Meridians
    Mindbody Medicine
    Myofascial Pain
    Neural Prolotherapy
    Neurokinetic Therapy
    OldPain2Go
    Pain And The Brain
    Painful Scars
    Pain Neutralization Technique
    Perineural Subcutaneous Injections
    Phobias
    PNT
    Prolotherapy
    Psychophysiologic Disorders
    Research
    SFMA
    SFMA Selective Functional Movement Assessment
    Tension Myoneuronal Syndrome
    Tension Myositis Syndrome
    Topical Mannitol
    Trigger Point Injections
    Trigger Points

    RSS Feed

  • Home
  • Contact
  • About Us
  • FAQ
    • Cancellation policy
    • Your first visit
    • Prolotherapy
    • Trigger Point Injections
    • Perineural Injection Treatment
    • Platelet Rich Plasma (PRP)
    • Botox for migraines
    • Botox for postural correction
    • Ozone Injections
    • Neurofeedback
    • Clinical Hypnosis
    • Pain Reprocessing Therapy
    • Gut-Directed Hypnotherapy
  • Clinical Hypnosis
  • For Physicians
  • Links
  • COVID-19 information
  • Research
  • Blogs
    • Dr. Jannice's blog
    • Dr. David's blog
  • Telephone and Telemedicine appointments