Steven Blake, a therapist in the UK, has skillfully woven together a number of therapeutic techniques by which it is possible for one to persuade the unconscious or subconscious mind to reduce or eliminate chronic pain which has outlived its usefulness. 

This technique has a number of premises including the understanding that acute (new) pain is helpful and protective, even though unpleasant, inasmuch as it is a warning that something is amiss (like an alarm signal) and needs to be sorted out, whereas, chronic (old) pain in general no longer serves a purpose, rather like something that is past its "sell-by date", or like an alarm which has malfunctioned and continued to ring long after the cause has been dealt with. Once chronic pain has been appropriately and thoroughly investigated medically and it has been determined that conventional medical therapy is either not available, effective or needed, then alternative means of relieving the suffering are appropriate, provided they are safe and effective.

Steven describes this process on his website.  This technique does not require a formal trance or hypnotic induction though it does require deep relaxation and can be combined with other therapies. 

It goes without saying that cause of a pain needs to be appropriately investigated before using these kinds of techniques to relieve the pain. The advantages of this technique include its safety, speed of onset, and remarkable effectiveness, not to mention that no drugs are involved. This technique has been effectively used in my office for a number of patients with chronic pain. Not everyone responds but there is nothing to lose but your pain. 



​

There has  been extensive research into the use of hypnosis for pain management over the years. 

A brief google scholar search bears this out. 

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: [email protected]. 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

We so often think of pain as a problem, that we forget that it has a useful purpose, at least in acute situations. Pain is nature's warning signal that something is amiss. People who lose the ability to feel pain (as is the case with peripheral neuropathy in diabetes) can injure themselves without realizing it. These injuries can become infected, fester and lead to loss of limb. In his book Pain- the Gift Nobody Wants, the late Dr Paul Brand wrote of his experience in treating leprosy in India many years ago. He discovered that the serious deformities and loss of digits and limbs that leprosy sufferers experience are due to loss of sensation, leading to burns and other injuries going unnoticed. 

A few years ago our family was renting a  quaint cottage in the Yorkshire Dales. It was a picturesque spot and we enjoyed it immensely. One drawback, however, was that the cottage's fire alarm was situated over the kitchen stove. It rang every time we did any cooking. Exasperated, I eventually unplugged its batteries. When we left, I forgot to plug them back in and it has been on my conscience ever since then, as I have wondered whether there has ever been a fire. Unlike acute pain which warns us of injury, chronic pain is pain which has outlived its usefulness, continuing to  send its signals long after the injury which caused it has passed. Acute pain usually (though not always) has an identifiable physical cause. Pain does not always mean damage or harm.  Chronic pain becomes a problem in its own right. Sometimes it is due to ongoing "peripheral sensitization" in the skin or soft tissues. Other times it is due to "central sensitization" in the brain, or both. This is why there are so many different possible approaches to chronic pain. 

 A few years ago a lady came to the office and said: “Remember that chronic pain I had? It’s gone.”
“What happened? “ she was asked.
“ I read a book.”

The book she had read was Dr. Scott Brady’s Painfree for Life which describes how the unconscious mind can aggravate, perpetuate, or even produce physical pain through the action of the autonomic nervous system, that part of the nervous system which is involved in the ‘fight, flight or freeze’ response to perceived danger.

When we heard her story we read Brady’s book and over a short period of time acquired a number of other books based on the work of Dr. John Sarno, a rehabilitation specialist, who discovered the role of stress or tension in causing back pain, and later extended this concept to a much larger group of functional conditions.  We had known that pain always seems worse when one is frightened and that a lot of chronic pain sufferers had emotional trauma in their backgrounds, but we were not aware that the brain could reproduce or initiate physical pain in the absence of any actual disease process.

 Since then we have had several patients whose pain disappeared or substantially diminished once they became aware of aspects of their personality, past experience, present circumstances, or psychological issues which triggered their pain.

 Please note, I am not speaking here of malingering (faking the pain when you know that nothing is wrong), or of secondary gain (remaining in the sick role when it is to your advantage to do so because you can avoid work or something else unpleasant or obtain sympathy). Even secondary gain can be subconscious – it is well known, for instance, that the best predictor of a swift return to work after a back injury is whether or not the worker enjoys the job.

 We are talking of an entirely subconscious process of real physical pain being produced (or reproduced) by the brain as a distraction, which allows the conscious mind to avoid dealing with intolerable memories or feelings by focusing on the pain instead of those other experiences. We are also talking about physical pain being produced by alterations in muscle tension, posture and blood flow brought on by emotional stress. Of course, we all recognize that stress can produce physical symptoms: sweating, nausea and diarrhea from “nerves” prior to giving a speech or writing an exam, for instance, or a tight jaw or shoulder knots when we are angry or frustrated. The same applies to musculoskeletal pain. Consider for a moment the metaphors we use in every day language: he’s a pain in the neck, she gives me heartburn, this job is full of headaches etc.

 Causes:

 ·      Personality:  you don’t have to have a dreadful trauma in your background or a psychiatric illness for the subconscious mind to produce pain. If you are a perfectionist, a people-pleaser (always trying to please other people and never feeling you completely satisfy them), or having impossibly high standards for yourself, you can set the stage for pain.

·      Past: a past history of abuse, or severe emotional trauma or intolerable memories can be triggers for pain. 50% of people with fibromyalgia, for instance, have post-traumatic stress disorder (PTSD) and victims of assault or childhood abuse frequently develop a variety of chronic pain syndromes.  Old pains long cured can suddenly recur when a subconscious memory is triggered by a sound, sight, aroma, or similar experience.

·      Present: feeling trapped, vulnerable or powerless in the job from hell or an unhappy relationship or other circumstance can produce physiological changes, postures and muscular tension, leading to pain.

·      Psychiatric illness such as depression or anxiety can also produce physical symptoms.

 
Examples from our clinical practice:

 ·      One patient underwent counseling including EMDR by a skilled psychologist. When this was completed not only were her traumatic memories dealt with and her depression lifted, but her fibromyalgia was also gone. 

·      One young lady volunteered that her fibromyalgia resolved when she forgave her mother.

·      Another found that journaling controlled her neck pain which functioned as a barometer for stress.

·      An accomplished student athlete with a two-year history of incapacitating back pain despite multiple investigations, treatments and specialist consults, read up online about the personality traits that contribute to stress-related pain. After viewing some of the websites listed below the pain was gone.

We don’t suggest for a moment that all chronic pain fits into this category but simply that it is worth keeping an open mind about the possibility that stress may pay a large role in chronic pain.

 Over the next few blog entries I hope to outline in simple terms how pain is processed and modified by the nervous system.

 
Stress Illness (Mindbody Syndrome or Psychophysiological Disorder) Resources:

(Disclaimer: we do not have any proprietary interest in any of these resources). 

Books by John Sarno:

“Mind Over Back Pain”

“Healing Back Pain: the Mind-body Connection”

“The Mindbody Prescription: Healing the Body, Healing the Pain “ (also on video)

“The Divided Mind”  this one is the most comprehensive but is quite academic.

 Book and Video Course by Scott Brady: “Pain-free for Life”

 Book by Marc Sopher: “To Be or not to Be – Pain-free”: the simplest and shortest of these books. 

 Book and Online Course by Howard Schubiner:  “Unlearn Your Pain.”             

 Book by David D. Clark “They Can’t Find Anything Wrong.”

 Book by Steven Ray Ozanich “The Great Pain Deception”

 Workbook by David Schecter  “Mindbody Workbook.”

 Book by Nancy Selfridge and Franklynn Petersen  “Freedom from Fibromyalgia”

 Internet resource: www.tmswiki.org : multiple articles and links on this subject. 

 Journal article:

 Abbass, A.   Somatisation : diagnosing it sooner through emotion-focused interviewing   MARCH 2005 / VOL 54, NO 3 · The Journal” of Family Practice


Additional resources:

 Psychotherapy:

Fosha, D, et al “The Healing Power of Emotion”

EFT, Faster EFT, EMDR can all be researched online.

Pain: Management textbook:

Steven Waldman  (editor)  “Pain Management”

Understanding some of the chemistry:

A book by Candace Pert: “Molecules of Emotion “ explains the biochemical process behind emotion and pain.