Schmechel DE, Edwards C. 2012. Fibromyalgia, mood disorders, and intense creative energy: A1AT polymorphisms are not always silent. Neurotoxicology. [Mar 10 Epub ahead of print]. "Persons with single copies of common alpha-1-antitrypsin polymorphisms such as S and Z are often considered 'silent carriers'. Published evidence however supports a complex behavioral phenotype or trait - intense creative energy ("ICE") -associated with A1AT polymorphisms. We now confirm that phenotype and present an association of fibromyalgia syndrome (FMS) and A1AT in a consecutive series of neurological patients....Our findings support the ICE behavioral phenotype for A1AT polymorphism carriers and the reported association with anxiety and bipolar spectrum disorders. We now extend that phenotype to apparent vulnerability to inflammatory muscle disease in a spectrum from JRA to fibromyalgia (FMS) and specific behavioral subsets of ADD, PTSD, and specific late onset neurological syndromes (FTD-PD and PPA). High and low risk FMS subsets can be defined using A1AT, MTHFR and APOE genotyping. Clinical diagnoses associated with A1AT polymorphisms included fibromyalgia, JRA/JIA, bipolar disorder, PTSD, primary progressive aphasia and FTDPD, but not most Alzheimer Disease subtypes. These results support an extended phenotype for A1AT mutation carriers beyond liver and lung vulnerability to selective advantages: ICE phenotype and disadvantages: fibromyalgia, affective disorders, and selected late onset neurological syndromes."
Schmelz M. 2006. [Interactions between itch and pain.]
Hautarzt [Apr 5 Epub ahead of print] [German] “Chronic
inflammatory diseases can locally sensitize nerve endings and thereby
contribute to itch. ….there is increasing evidence that also
central processing of itch can be sensitized in pruritus patients.
Interestingly, this pattern of peripheral and central sensitization in
pruritus has striking similarities to the one observed in chronic pain
patients. The presumed similarities in underlying sensitizing
mechanisms between itch and pain has major therapeutic consequences as
successful therapies for chronic pain might be used also in chronic
Schmelz, M., R. Schmidt, A. Bickel, H. E. Torebjork and H. O.
Innervation territories of a single sympathetic C-fibers in human skin. J Neurophysiol
Schmelz, M., R. Schmidt, A. Bickel, H. O. Handwerker and H. E.
Specific C-receptors for itch and human skin. J Neurosci 17(20:8003-8008.
Schmid M, Schieppati M. 2004. Neck muscle fatigue and spatial
orientation during stepping in place in humans. J Appl Physiol.
[Epub ahead of print] “Neck proprioceptive input, as elicited by
muscle vibration, can produce destabilizing effects on stance and
locomotion. Neck muscle fatigue produces destabilizing effects on
stance, too. Neck muscle fatigue can also perturb the orientation
in space during a walking task. The neck represents a complex
source of inputs capable of modifying our orientation in space during a
Schmid, P. 1999. [No title available}. Schwiz Med Wochenschr 129(38):1368-80.
Schmidt, C. W. 1999. Poisoning young minds. Environ Health Perspect
Schmidt-Wilcke T, Luerding R, Weigand T et al. 2007.
Striatal grey matter increase in patients suffering from fibromyalgia – a
voxel-based morphometry study. Pain [Jun 21 Epub ahead of
print]. “Our data suggest that fibromyalgia is associated with
structural changes in the CNS of patients suffering from this chronic pain
disorder. They might reflect either a consequence of chronic
nociceptive input or they might be causative to the pathogenesis of
Schneider C, Palomba D, Flor H. 2004.
Pavlovian conditioning of muscular responses in chronic pain patients:
central and peripheral correlates. Pain 112(3):239-247. “These
data confirm the hypothesis of enhanced muscular responding in chronic pain
patients and suggest a dissociation of muscular and central processes during
aversive conditioning in the patients that might contribute to the
Schneider, M. J. 1996. Chiropractic management of myofascial and muscular disorders. Advances
in Chiropractic 3:55-85.
Schneider, M.. J. 1995. Tender Points/fibromyalgia vs. trigger points/myofascial pain
syndrome: a need for clarity in terminology and differential diagnosis. J Manip.
Physiol Ther 18(6):398-406.
Schneider, M. J. 1992. Soft tissue effects of sacroiliac and lumbosacral join
manipulation. Chiropractic Technique 136-142.
Schneider, M. J. 1991. The traction methods of Cox and Leander: the neglected role of
the multifidus muscle in low back pain. Chiro Tech 3(3):109-115.
Schneider W, Dvorak J. 1996.
[Functional treatment of diseases and injuries of the cervical spine]
Orthopade. 25(6):519-523. [German] “The clinical findings and
pain symptoms determine the functional treatment of the cervical spine
disorders. Acute pain syndromes are to be approached by passive
procedures, such as massage, electrotherapy, trigger point treatment.
Could the pain reaction be reduced, the mobilizing techniques, including
manipulation are indicated, followed by training therapy/reconditioning of
shoulder girdle muscles. The patients are also to be instructed to
perform home exercise program aiming the stabilization of cervical spine.”
Schneider-Helmert D. 2003. [Do we need polysomnography in
insomnia?] Schweiz Rundsch Med Prax. 92(48):2061-2066.
[German] “In the field of differential diagnosis, overlapping of
insomnia with other disturbances within and outside the range of sleep
medicine is frequent. Special problems arise in chronic
non-organic pain. It is clear from all these aspects that PSG [polysomnography–sleep
study] is indispensable in insomnia.” [This is an important study.
Lack of restorative sleep plays an important role in many cases of
fibromyalgia, and not enough is done to track down the causes of
non-restorative sleep. Too often it is just dismissed as part of
FMS, when there often may be components that are treatable. DJS]
Schneider-Helmert D, Whitehouse I, Kumar A et al. 2001. Insomnia
and alpha sleep in chronic non-organic pain as compared to primary
insomnia. Neuropsychobiology 43(1):54-58. This study indicates
that insomnia in chronic pain patients may not be due to the pain
itself. It should not be dismissed as a given part of the chronic pain
picture. “It is suggested that insomnia in chronic pain patients should
be taken seriously and treated by its specific methods.”
Schnurr, R. F. and M. R. MacDonald. 1995. Memory complaints in chronic pain. Clin J
Pain11(2):103-11. These finding suggest that memory complaints may be related not only
to depression but also to the presence of chronic pain.
Schochat T, Raspe H. 2003. Elements of
fibromyalgia in an open population. Rheumatology
42(7):829-835. “Subjects could be identified who met the tender
point criterion of the ACR without a history of widespread pain.”
[These patients were not screened for co-existing myofascial TrPs.]
Schochat T, Beckmann C. 2003. [Sociodemographic
characteristics, risk factors and reproductive history in subjects with
fibromyalgia — results of a population-based case-control study]
[German] Z Rheumatol. 62(1):46-59. The factors of low
social level, low alcohol intake, rare pregnancy and late start of first
menstruation were more common among FMS patients than other chronic pain
patients or people without chronic pain.
Schochat T, Beckmann C
2003. [Sociodemographic characteristics, risk factors and reproductive
history in subjects with fibromyalgia – results of a population-based
case-control study.] Z Rheumatol 62(1):46-59.
[German] “The associations with a low social level, low alcohol
intake, late menarche and rare pregnancies are specific for subjects with
fibromyalgia. These factors distinguish subjects with fibromyalgia from
subjects with other chronic pain conditions as well as from subjects with no
chronic pain. The same hormonal factors responsible for a delayed
menarche and a reduced fertility may be relevant in the development of
Schoenberger NE, Shif SC, Esty ML et al. 2001.
Flexyx neurotherapy system in the treatment of traumatic brain injury: an
initial evaluation. J Head Trauma Rehabil 16(3):260-274.
This type of brain wave modulation neurotherapy appears to be a promising
therapy for traumatic brain injury.
Schonen J. 2004. Tension-type
headache and fibromyalgia: what’s common, what’s different?
Neurol Sci 25 (Suppl 3):S157-159.
Schoofs N, Bambini D, Ronning P et al. 2004. Death of a lifestyle:
the effects of social support and healthcare support on the quality of
life of persons with fibromyalgia and/or chronic fatigue syndrome.
Orthop Nurs. 23(6):364-374. “Social support, unlike
healthcare support, is related to quality of life (QOL). Subjects
suffering from CFS and/or FMS do not experience high levels of social
Schraer, CD, SO Ebbesson, AI Adler, JS Cohen, EJ Boyko and ED Nobmann. 1998. Glucose tolerance and insulin-resistance syndrome among St. Lawrence Island
Eskimos. Int J Circumpolar Health 57 Suppl 1:348-54.
Schreuder, BJ. 1999. [Cognitive ego-disturbances in the elderly who have become
victims of organized violence]. Z Gerontol Geriatr 32(4):266-272 [German].
Schrier M, Amital D, Arnson Y et al. 2011. Association of fibromyalgia characteristics in patients with non-metastatic breast cancer and the protective role of resilience. Rheumatol Int. [Sep 8 Epub ahead of print]. "Women with breast cancer tend to develop chronic widespread pain syndromes more often than do healthy women."
Schroeder B, Sanfilippo JS, Hertweck SP. 2000.
Musculoskeletal pelvic pain in a pediatric and adolescent gynecology
practice. J Pediatr Adolesc Gynecol. 13(2):90. “MS
(musculoskeletal) etiologies of pelvic pain are common in the adolescent age
group and respond well to physical therapy. Physical therapy might be
employed as an early intervention prior to surgery in adolescent girls with
unexplained pelvic pain.” Research indicates that these patients are NOT
good candidates for surgery as often the pain is myofascial in origin, and
surgery is seldom needed if the cause of the pain can be found.
Schroder, H, E Navarro, A Tramullas, J
Mora and D Galiano. 2000. Nutrition antioxidant status and oxidative stress in professional basketball players: effects of a
three compound antioxidative supplement. Int J Sports Med 21(2):146-50.
Schubert MS. 2004. Allergic fungal sinusitis.
Otolaryngol Cli North Am. 37(2):301-326.
Schuler M, Njoo N, Hestermann M et al. 2004. Acute
and chronic pain in geriatrics: clinical characteristics of pain and the
influence of cognition. Pain Med. 5(3):253-262.
Schultz, R. L. and Feitis R. 1996. The Endless Web: Fascial Anatomy and Physical
Reality. North Atlantic Books, Berkeley, CA.
Shultz SP, Driban JB, Swanik CB. 2007. The evaluation of electrodermal properties in the identification of myofascial trigger points. Arch Phys Med Rehabil 88(6):780-784. The area of a TrP, either active or latent, has significant increased skin electrical resistance that decreases as with the distance from the TrP.
Avellana-Adalid V., Baron-Van Evercooren A. et al. 2002. Steroid
synthesis and metabolism by glia: tropic and protective effects. Glia
(Suppl 1):S4 [Abstract].
Schwabe, C. and E. E. Bullesbach. 1990. Relaxin. Comp Biochem Physiol [B] 96(1):15-21.
Schwarcz, R., C. Speciale and E. D. French. 1987. Hippocampal kynurenines as
etiological factors in seizure disorders. Pol J Pharmacol Pharm 39(5):485-494.
Schwartz M.J., Offenbacher
M., Neumeister A. et al. 2002. Evidence for an altered tryptophan metabolism
in fibromyalgia. Neurobiol Dis 11(3):434-442. This study shows
an altered tryptophan metabolism in a subgroup of fibromyalgia patients.
Schwarz MJ, Offenbaecher M,
Neumeister A et al. 2003. Experimental evaluation of an altered
tryptophan metabolism in fibromyalgia. Adv Exp Med Biol.
527:265-275. “These data demonstrate an altered TRP metabolism in a
subgroup of FM patients, where the TD seems to activate 5-HT metabolism
and IL-6 production.”
Schwarz, M. J., M. Spath, H. Muller-Bardorff, D. E. Pongratz, B. Bondy and M.
Ackenheil. 1999. Relationship of substance P, 5-hydroxyindole acetic acid and tryptophan in
serum of fibromyalgia patients. Neurosci Lett 259(3):196-8.
Schwartz RG, Gall NG, Grant AE. 1984.
Abdominal pain in quadriparesis: myofascial syndrome as unsuspected cause.
Arch Phys Med Rehabil. 65(1):44-46. “This is a case report of a
47-year-old man with C6 quadriparesis who presented with tenderness in the
right lower quandrant of his abdomen which was diagnosed as iliocostalis
myofascial syndrome. Diagnosis of nephrolithiasis and appendicitis
were considered, but the complete blood count, abdominal x-ray, intravenous
pyelogram, and sonogram were all normal. His symptoms became
progressively more severe over the ensuing 2-week period. Examination
at that time revealed extreme tenderness to light touch in the right lower
quandrant, right flank, and right posterior subcostal area. A trigger
point in the right iliocostalis muscle referred pain to the right lower
quandrant. In the absence of evidence of internal derangement a
diagnosis of iliocostalis myofascial syndrome was made. A 3-day course
of ‘spray and stretch’ to the iliocostalis cleared the symptoms. This
case illustrates that myofascial syndrome should be considered in the
differential diagnosis of soft tissue pain in the patient with spinal cord
injury and sensory sparing.”
Schweinhardt P, Lee M, Tracey I. 2006. Imaging
pain in patients: is it meaningful? Curr Opin Neurol.
19(4):392-400. “Results to date strongly support the notion that
neuroimaging will aid our understanding of basic mechanisms contributing to
the generation of chronic pain states.”
Sciotti V.M. , Mittak V.L.
, DiMArco L.M. et al. 2002. Clinical precision of myofascial trigger point
location in the trapezius muscle. Pain 93(3)259-226.
Scott NA, Guo B, Barton PM et al. 2009.
Trigger point injections for chronic non-malignant musculoskeletal pain: a
systematic review. Pain Med. 10(1):54-69. “TPI (trigger
point injection) is a safe procedure when used by clinicians with
appropriate expertise and training. It relieved symptoms when used as
a sole treatment for patients with chronic head, neck, shoulder, and back
pain or whiplash syndrome, regardless of the injectant used, and may be a
useful adjunct to intra-articular injection in the treatment of
osteoarthritis pain. Although the addition of TPI to stretching
exercises augments treatment outcomes, this was also true of other therapies
such as ultrasound and laser.” “The only advantage of injecting
anesthetic into trigger points may be to reduce the pain of the needling
process, which may not be an insignificant benefit.”
Seaman, D. R. and C. Cleveland 3rd. 1999. Spinal pain syndromes:
nociceptive, neuropathic, and psychologic mechanisms. J Manipulative Physiol Ther
Sears, Barry. 1999. The Anti-Aging Zone HarperCollins Inc New York.
Seas, K. L. and H. W. Clark. 1993. Opioid use in the treatment of chronic pain:
assessment of addiction. J Pain Symptom Manage 8(5):257-264.
Seed SM, Dunican KC, Lynch AM et al. 2012. An update in options for the treatment of pain: a review of new opioid formulations. Hosp Pract (Minneap). 40(1):166-175. "This article reviews new opioid options for the treatment of pain management and requirements of the Risk Evaluation and Mitigation Strategies program."
Seegal, R. F., J. R. Wolpaw and R.
Dowman. 1989. Chronic exposure of primates to 60-Hz
electric and magnetic fields: II. Neurochemical effects. Bioelectromagnetics
Seematter G, Binnert
C, Martin JL et al. 2004. Relationship between stress, inflammation
and metabolism. Curr Opinion Clin Nutr Metab Care 7(2):169-173.
The HPA axis stress response mobilizes neuroendocrine response systems that
can institute a metabolic cascade with far-reaching consequences.
“They also exert anti-insulin actions and may in the long-term induce a
state of insulin resistance. In addition, stress stimulates
inflammatory mediators in mononuclear cells. Given the possible role
of low-grade inflammation in chronic metabolic disorders, this suggests that
stress may be a factor in the development of insulin resistance and the
metabolic syndrome.” Stress and causes of same, including pain, must be
Seematter G, Binnert C, Martin JL et al. 2004. Relationship
between stress, inflammation and metabolism. Curr Opin Clin
Nutr Metab Care 7(2):169-173. “Recent work performed in the
field has indicated that stress may be a significant factor in the
pathogenesis of metabolic disorders. Nutritional intervention or
pharmacological agents targeted at modulating stress should be
Seers, K. 1996. "The patients experiences of their chronic non-malignant
pain." J Adv Nurs 24(6):1160-1168.
Sees, K. L. and H. W. Clark. 1993. Opioid use in the treatment of chronic pain:
assessment of addiction. J Pain Sympt Manage 8(5):257-64.
Segerstrom SC, Miller GE. 2004. Psychological stress and the human
immune system: a meta-analytic study of 30 years of inquiry.
Psychol Bull 130(4):601-630. “Acute stressors (lasting
minutes) were associated with potentially adaptive upregulation of some
parameters of natural immunity and downregulation of some functions of
specific immunity. Brief naturalistic stressors (such as exams)
tended to suppress cellular immunity while preserving humoral immunity.
Chronic stressors were associated with suppression of both cellular and
humoral measures. Effects of event sequences varied according to
the kind of event (trauma vs. loss). In some cases, physical
vulnerability as a function of age or disease also increased
vulnerability to immune change during stressors.”
Segura-Jimenez V, Carbonell-Baeza A, Aparicio VA et al. 2012. A Warm Water Pool-Based Exercise Program Decreases Immediate Pain in Female Fibromyalgia Patients: Uncontrolled Clinical Trial. Int J Sports Med. [Dec 20 Epub ahead of print]. Fibromyalgia is characterized by chronic and extended musculoskeletal pain. The combination of exercise therapy with the warm water may be an appropriate treatment. However, studies focusing on the analysis of immediate pain during and after an exercise session are rare. This study aimed to determine the immediate changes of a warm water pool-based exercise program (12 weeks) on pain (before vs. after session) in female fibromyalgia patients. 33 Spanish women with fibromyalgia were selected to participate in a 12 week (2 sessions/week) low-moderate intensity warm water pool-based program. We assessed pain by means of a Visual Analogue Scale before and after each single session….a warm water pool-based exercise program for 12 weeks (2 times/week) led to a positive immediate decrease in level of pain in female patients with fibromyalgia. Improvements were higher in older women and in those with more intense pain.
Segura-Jimenez V, Romero-Zurita, Carbonell-Baeza A et al. 2013. Effectiveness of Tai-Chi for Decreasing Acute Pain in Fibromyalgia Patients. Int J Sports Med. [Nov 7 Epub ahead of print]. "Tai-Chi has shown benefits in physical and psychological outcomes in diverse populations. We aimed to determine the changes elicited by a Tai-Chi program (12 and 24 weeks) in acute pain (before vs. after session) in fibromyalgia patients. We also assessed the cumulative changes in pain brought about by a Tai-Chi program….In conclusion, a low-moderate intensity Tai-Chi program for 12 weeks (3 times/week) decreased levels of acute pain in fibromyalgia patients. A longer period is necessary (e. g. 24 weeks) for observing cumulative changes in pain."
Seibold, J. R., P. J. Clements, D. E.
Furst, M. D. Mayes, D. A. McCloskey, L. W.
Moreland, B. White, F. M. Wigley, S. Rocco, M. Erikson, J. F. Hannigan, M. E. Sanders and
E. P. Amento.1998. Safety and pharmacokinetics of recombinant human relaxin in systemic
sclerosis. J Rheumatol 25(2):302-307.
Seidel MF, Weinreich GF, Stratz T et al. 2007. 5-HT3 receptor
antagonists regulate autonomic cardiac dysfunction in primary
fibromyalgia syndrome. Rheumatol Int. [Jul 19 Epub ahead of
print]. “Tropisetron reduced not only pain perception but also had a
favorable effect on cardiac dysfunction during treatment.” [This
medication seems to be effective for both FM and myofascial pain, as
well as cardiac dysfunction. DJS]
Sendur OF, Gurer G, Bozbas GT. 2006. The
frequency of hypermobility and its relationship with clinical
findings of fibromyalgia patients. Clin Rheumatol. [Apr
25 Epub ahead of print] “...more severe clinical findings were
observed in FM patients with hypermobility when compared with ones
Senior BA, Khan M,
Schwimmer C et al. 2001. Gastroesophageal reflux and obstructive sleep
apnea. Laryngoscope 111(112):2144-6. “These results suggest a
potential relationship between OSA and GER...” Treatment of one may
significantly impact the other in some patients.
Seo HG, Bang MS, Chung SG et al. 2012. Effect of electrical stimulation on botulinum toxin A therapy in patients with chronic myofascial pain syndrome: A 16-week randomized double-blinded study. Arch Phys Med Rehabil. [Oct 31 Epub ahead of print]. Short-term electrical stimulation may affect reduction in pain after BTX-A injection at TrPs in patients with chronic MPS on the neck and shoulder regions. Based on the results, it seems that sensory electrical stimulation was superior to motor electrical stimulation as an adjuvant therapy of BTX-A injection in the patients with chronic MPS. Further studies are warranted to investigate the method facilitating the effect of BTX-A on MPS.
Seok J, Warren HS, Cuenca AG et al. 2013. Genomic responses in mouse models poorly mimic human inflammatory diseases. Proc Natl Acad Sci USA. [Feb 11 Epub ahead of print]. This study shows that the commonly used mouse as an experimental model does not translate well to human applications in the context of inflammatory disease. How a mouse responds in an experiment does not indicate how a human will respond. [One very small step for mouse-kind. DJS]
Sephton SE, Salmon P, Weissbecker I et al. 2007.
Mindfulness meditation alleviates depressive symptoms in women with
fibromyalgia: results of a randomized clinical trial. Arthritis
Rheum. 57(1):77-85. “This meditation-based intervention alleviated
depressive symptoms among patients with fibromyalgia.”
Sepici V, Tosun A, Kokturk O. 2007.
Obstructive sleep apnea syndrome as an uncommon cause of fibromyalgia: a
case report. Rheumatol Int. [Jun 23 Epub ahead of print].
Sergey A, Dzugan R, Arnold Smith R.
2002. Hypercholesterolemia treatment: a new hypothesis or just an
accident? Med Hypoth 59(6):751-756. This team’s
“...findings support the hypothesis that hypercholesterolemia is a
compensatory mechanism for life-cycle related down-regulation of steroid
hormones and that broadband steroid hormone restoration is associated with a
substantial drop in serum TC in many patients.”
This may be very important in treating FMS patients who often have
many hormonal axes imbalanced. It is vital that the hormone levels be
tests and the normal amounts restored using natural hormones.
Sergi, M., M. Rizzi, A. Braghiroli, P. S.
Puttini, M. Greco, M. Cazzola and A. Andreoli. 1999. Periodic breathing during sleep in patients affected by fibromyalgia
syndrome. Eur Respir J 14(1):203-8.
Serra E, Spaeth M, Carbonell J et al. 2010. Development of the Fibromyalgia Burden Assessment: measuring the multifaceted burden of fibromyalgia. Clin Exp Rheumatol. 28(6 Suppl 63):S87-93. "The FMBA is a self-reported questionnaire allowing the assessment and a better understanding of the impacts of fibromyalgia and the burden associated with these on patients' daily lives. It is available in UK English, French, German and Spanish. Its scoring and validation remain to be undertaken."
Serra J, Collado A, Sola R et al. 2013. Hyperexcitable C nociceptors in fibromyalgia. Ann Neurol. [Nov 16 Epub ahead of print]. "Microneurography was used to record from C nociceptors of 30 female patients meeting criteria for fibromyalgia and compared with recordings from 17 female patients with small fiber neuropathy and 9 female controls…. The mechano-sensitive nociceptors in the fibromyalgia patients behaved normally, but the silent nociceptors in 76.6% of fibromyalgia patients exhibited abnormalities. Spontaneous activity was detected in 31% of silent nociceptors in fibromyalgia, 34% in small fiber neuropathy, and 2.2% in controls. Sensitization to mechanical stimulation was found in 24.2% of silent nociceptors in fibromyalgia, 22.7% in small fiber neuropathy, and 3.7% in controls. Abnormally high slowing of conduction velocity when first stimulated at 0.25 Hz was more common in fibromyalgia. Interpretation: We show for the first time that the majority of fibromyalgia patients have abnormal C nociceptors. Many silent nociceptors exhibit hyperexcitability resembling that in small fiber neuropathy, but high activity-dependent slowing of conduction velocity is more common in fibromyalgia patients, and may constitute a distinguishing feature. We infer that abnormal peripheral C nociceptor ongoing activity and increased mechanical sensitivity could contribute to the pain and tenderness suffered by patients with fibromyalgia."
Settipane, R. A. 1999. Complications of allergic rhinitis. Allergy Asthma Proc
Dobkin PL, Bernatsky S. et al. 2004. Medication non-adherence in
women with fibromyalgia. Rheumatology (Oxford)
43(5):648-654. ”Overall non-adherence was predicted by higher
patient-physician discordance...The therapeutic relationship, in
addition to clinical and psychosocial characteristics, influenced
non-adherence to medication.”
Shadmehr A, Jafarian Z, Tavakol K et al. 2013. Effect of pelvic compression on the stability of pelvis and relief of sacroiliac joint pain in women: A case series. J Musculoskel Pain. 21(1):31-36. "Pelvic compression significantly reduced the EMG (electromyographic) activity from six muscles....pelvic compression can improve both the motor control and stability of the pelvis, while reducing joint pain in women suffering from sacroiliac symptoms."
Shah MA, Feinberg S, Krishnan E. 2006. Sleep-disordered breathing
among women with fibromyalgia syndrome. J Clin Rheumatol.
12(6):277-281. “A large proportion of women with fibromyalgia in a
general rheumatology practice had sleep-disordered breathing, which can
be detected using sleep polysomnograms.”
Shah JP, Parikh S, Danoff J et al.
2007. Re: the myofascial trigger point region: correlation
between the degree of irritability and the prevalence of
endplate noise. Am J Phys Med Rehabil. 86(12
Danoff JV, Desai MJ et al. 2008. Biochemicals associated
with pain and inflammation are elevated in sites near to and
remote from active myofascial trigger points. Arch Phys
Med Rehabil. 89(1):16-23. “We have shown the
feasibility of continuous, in vivo recovery of small molecules
from soft tissue without harmful effects. Subjects with
active MTPs in the trapezius muscle have a biochemical milieu of
selected inflammatory mediators, neuropeptides, cytokines, and
catecholamines different from subjects with latent or absent
MTPs in their trapezius. These concentrations also differ
quantitatively from a remote, uninvolved site in the
gastrocnemius muscle. The milieu of the gastrocnemius in
subjects with active MTPs in the trapezius differs from subjects
without active MTPs.”
Shah J. 2007. Uncovering the
biochemical milieu of myofascial trigger points using in-vivo
microdialysis. J Musculoskel Pain 15 (Supp 13):2
item 2. [Myopain 2007 Poster] The use of in-vivo
sampling by microdialysis acupuncture needle “...provides us the
unprecedented ability to safely explore and measure the local
biochemical milieu of TrPs before, during and after a local
twitch response.” “...the local biochemical milieu does
appear to change after a LTR.” “...the vicinity of the
active TrP exhibits a unique biochemical milieu of substances
associated with pain and inflammation .... analyte abnormalities
may not be limited to local areas of active TrPs.”
Shah JP, Phillips TM, Danoff JV et al.
2005. An in-vivo microanalytical technique for measuring the
local biochemical milieu of human skeletal muscle. J
article describes a ground-breaking technique for measuring
minute amounts of biochemicals in the body. In this case,
the biochemicals released in the interstitial fluid surrounding
myofascial TrPs during TrP twitch were analyzed. They found a
sensitized and sensitizing soup of over 30 biochemicals
released. In the active TrP patient group, bradykinins,
calcitonin gene-related peptide, IL-$,
serotonin, tumor necrosis factor-",
and norepinephrine were significantly higher and the pH dropped
significantly than in the control group or the group with latent
TrPs. Substance P and CGRP dropped significantly after the
TrP twitch release. This study may indicate some of the
cause of TrP pain, and also highlight promising targets for TrP
pain relief. [It also indicates some ways active TrPs can
aggravate the central sensitization of fibromyalgia. DJS]
Shaheen NJ, Madanick RD, Alattar M et al. 2007.
Gastroesophageal Reflux Disease as an etiology of sleep disturbance in
subjects with insomnia and minimal reflux symptoms: a pilot study of
prevalence and response to therapy. Dig Dis Sci. [Nov 6
Epub ahead of print]. “Despite the lack of GERD symptoms, a
significant minority of subjects with sleep disturbance have abnormal
acid exposures. These preliminary data suggest that aggressive
treatment of GERD in such patients may result in improvement in sleep
efficiency.” [Care providers should first attempt to normalize the
gut flora with the use of healthy diet, probiotics, prebiotics,
supplements and non-invasive care such as frequency specific
Shan G, Daniels D, Gu R. 2004.
Artificial neural networks and center-of-pressure modeling: a practical
method for sensorimotor-degradation assessment. J Aging Phys Act.
12(1):75-89. “Tai Chi slowed down the effects of sensorimotor aging.”
Shanahan, F. 1999. Brain-gut axis and mucosal immunity: a perspective on mucosalpsychoneuroimmunology. Semin Gastrointest Dis 10(1):8-13.
Shankar H, Cummings C. 2012. Ultrasound Imaging of Embedded Shrapnel Facilitates Diagnosis and Management of Myofascial Pain Syndrome. Pain Pract [Oct 24 Epub ahead of print]. "Trigger points can result from a variety of inciting events including muscle overuse, trauma, mechanical overload, and psychological stress....A veteran was referred to the pain clinic for management of his severe headache following a gunshot wound to the neck with shrapnel embedded in the neck muscles a few years prior to presentation. He had no other comorbid conditions. Physical examination revealed a taut band in the neck. An ultrasound imaging of the neck over the taut band revealed the deformed shrapnel located within the levator scapulae muscle along with an associated trigger point in the same muscle. Ultrasound guided trigger point injection, followed by physical therapy resolved his symptoms."
Shankar H, Reddy S. 2012. Two- and Three-Dimensional Ultrasound Imaging to Facilitate Detection and Targeting of Taut Bands in Myofascial Pain Syndrome. Pain Med. [Jun 8 Epub ahead of print]. This is a case report using ultrasound elastography. Conservative TrP therapy had been insufficient to resolve pain and reduced range of motion of the shoulder. "Three-dimensional ultrasound images provided evidence of aberrancy in the architecture of the muscle fascicles around the taut bands compared to the adjacent normal muscle tissue during serial sectioning of the accrued image. On two-dimensional ultrasound imaging over the palpated taut band, areas of hyperechogenicity were visualized in the trapezius and supraspinatus muscles. Subsequently, the patient received ultrasound-guided real-time lidocaine injections to the trigger points with successful resolution of symptoms....This is a successful demonstration of utility of ultrasound imaging of taut bands in the management of myofascial pain syndrome. Utility of this imaging modality in myofascial pain syndrome requires further clinical validation." [This method is a research method and not presently accessible for clinical applications. DJS]
Shankland II W. E. 1995. Craniofacial pain syndromes that mimic temporomandibular joint
disorders. Ann Acad Med Singapore 24(1):83-112.
Shankland, II W. E., J. A. Negulesco and B. OBrian. 1996. The pre-anterior belly
of the temporalis muscle; a preliminary study of a newly described muscle. Cranio
Shankland, II W. E. 1995. Craniofacial pain syndromes that mimic temporomandibular
joint disorders. Ann Acad Med Singapore 24(1):83-112.
Shanks, N., R. J. Windle, P. Perks, S. Wood, C. D. Ingram and S. L.
Lightman. 1999. The
hypothalamic-pituitary-adrenal axis response to endotoxin is attenuated during lactation. J
Shannon, C. N. and A. P. Baranowski. 1997. Use of opioids in non-cancer pain. Br J
Shanoudy H, Soliman A, Moe S, Hadian D et al.
2001. manifestations of
syndrome in patients with compensated chronic heart failure. J
Card Fail 7(2):146-52. "Patients
with compensated CHF display the derangements in thyroid hormone
metabolism of impaired peripheral conversion of T(4) and t(3) and
increased production of rT(3) in the presence of normal dynamic
function of the hypothalamic-pituitary-thyroid axis, which are
consistent with early manifestations of a sick euthyroid state."
Shapir E, Cohen H,
Calzolari A et al. 2008. Electronic structure of single DNA molecules
resolved by transverse scanning tunnelling spectroscopy. Nat Mat
(7):68-74. The DNA molecule is laterally electrically conductive
across the helix. [This may be a method whereby some electroceutical
devices, such as frequency specific microcurrent and electroacupuncture,
change the body chemistry even below the cellular level, effecting healing
through the DNA. DJS]
Shapiro, R. S. 1994. Legal bases for the control of analgesic drugs. J Pain Symptom
Sharan D, Ajeesh PS, Rameshkumar R et al. 2012. Risk factors, clinical features, and outcome of treatment of work related musculoskeletal disorders in on-site clinics among IT companies in India. Work. Suppl 1:5702-5704. This study focused on the IT (information technology) profession and workplace risk in India. It found poor office ergonomics; lack of keyboard and/or mouse tray and foot rest; and improper monitor height to be the most common risk factors. The most common musculoskeletal disorders were myofascial pain syndrome (49.2%), thoracic outlet syndrome (25%), and fibromyalgia (8.5%). The body regions affected mostly were neck (64.9%), shoulder 42.1%), lower back (56.5%), and thigh (34.2%). The patients were treated with the RECOUP protocol designed by Dr. Sharan, and the patients were satisfied with their progress.
Sharan D, Jacob BN, Ajeesh PS et al. 2011. The effect of cetylated fatty esters and physical therapy on myofascial pain syndrome of the neck. J Bodyw Mov Ther. 15(3):363-374. Myofascial pain patients were treated with either a combination of cetylated fatty ester complex (CFEC) and 1.5% menthol or a control cream of 1.5% menthol. The patients treated with the compound containing the CFEC experienced significantly improved symptoms compared with those who used the menthol cream. [Patients on guaifenesin should be aware that the cream available in the USA, Celadrin, has significant peppermint oil and would be contraindicated due to the salicylates in it. DJS]
Sharkey SW, Lesser JR,
Zenovich AG et al. 2005. Acute and reversible cardiomyopathy provoked
in stress in women from the United States. Circulation.
111(4):472-479. Profound psychological stress can trigger reversible
cardiac events including chest pain and cardiac dysfunction.
Sharpe, M. H. and T. S. Miles. 1993. Position sense at the elbow after fatiguing
contractions. Exp Brain Res 94(1):179-82.
Sharpley, A., A. Clements, K. Hawton and M. Sharpe. 1997. Do patients with
"pure" chronic fatigue syndrome (neurasthenia) have abnormal sleep? Psychosom
Shaver, J. L. , M. Lentz, C. A. Landis, M. M.
Heitkemper, D. S. Buchwald and N. F.
Woods. 1997. Sleep, psychological distress, and stress arousal in women with fibromyalgia.
Res Nurs Health 20(3):247-257.
Shaw S, Lee A. 2010. Student nurses'
misconceptions of adults with chronic nonmalignant pain. Pain Manag Nurs.
11(1):2-14. Earlier research has identified chronic pain as a leading cause
of disability..... The knowledge and attitudes of nurses have been found to
affect patient experience and treatment..... The student nurses who
participated in this study demonstrated that they held misconceptions about
adults with chronic nonmalignant pain to a considerable degree. Students
enrolled in semester six held the misconceptions to a slightly lesser degree
than those enrolled in semesters one and four. The process of undergraduate
education needs to equip nursing students with accurate knowledge about
chronic nonmalignant pain and encourage them to develop the appropriate
attitudes for working with patients experiencing it.
Shaywitz, S. E., B. A. Shaywitz, K. R. Pugh, R. K. Fulbright, Skudlarski P, W. E.
Mencl, R. T. Constable, F. Naftolin, S. F. Palter, K. E. Marchione, L. Katz, D. P.
Shankweiler, J. M. Fletcher, C. Lacadie, M. Keltz, J. C. Gore. 1999. Effect of estrogen on
brain activation patterns in postmenopausal women during working memory tasks. JAMA
Shear, D. A., J. Dong, K. L. Haik-Creguer, T. J. Bazzett, R. L. Albin and G. L. Dunbar.
1998.Chronic administration of quinolinic acid in the rat striatum causes spatial learning
deficits in a radial arm water maze task. Exp Neurol 150(2):305-311.
Sheehan, J., J. McKay, M. Ryan, N. Walsh and D. OKeefe. 1996. "What cost
chronic pain?" Ir Med J 89(6):218-219.
Sheon, R. P. 1997. Repetitive strain injury. 2. Diagnostic and treatment tips on six
common problems. The Goff Group. Postgrad Med 102(4):72-78.
Sherman KJ, Cherkin DC, Deyo RA et al. 2006.
The diagnosis and treatment of chronic back pain by acupuncturists,
chiropractors, and massage therapists. Clin J Pain.
22(3):227-234. “Information on the care patients routinely received
from CAM (complementary and alternative) providers will help physicians
better understand these increasingly popular forms of care.”
Sherwin, B. B. 1998. Estrogen and cognitive functioning in women. Proc Soc Exp Biol
Sherwin, B. B. 1997. Estrogens effects on cognition in menopausal women. Neurology
48(5 Suppl 7):A21-6.
Shi, D., O. Nikodijevic, K. A. Jacobson and J. W. Daly. 1994. Effects of chronic
caffeine on adenosine, dopamine and acetylcholine systems in mice. Arch Int Pharmacodyn
Shilo, L., Y. Dagan, Y. Smorjik, U. Weinberg, S. Dolev, B. Komptel, H. Balaum and L.
Shenkman. 1999. Patients in the intensive care unit suffer from severe lack of sleep
associated with loss of normal melatonin secretion pattern. Am J Med Sci
Shinozaki T, Sakamoto E, Shilba S et al. 2006.
Cervical plexus block helps in diagnosis of orofacial pain originating from
cervical structures. Tohoku J Exp Med. 210(1):41-47.
Shmushkevich Y, Kalichman L. 2013. Myofascial pain in lateral epicondylalgia: A review. J Bodyw Mov Ther. 17(4):434-439. "There is an ongoing debate about the myofascial component, characterized by the presence of myofascial trigger points (MTrPs) in lateral epicondylalgia (LE)…." The objectives of this study were: "To review current evidence of the association between myofascial pain and LE, including efficacy of treatment, focusing on myofascial pain….PubMed, Google Scholar and PEDro databases were searched without search limitations from inception until October 2012 for terms relating to LE and MTrPs….Two observational studies showed a high prevalence of MTrPs in LE patients compared to healthy controls. Three randomized controlled trials demonstrated significant improvement in pain and functional outcomes after application of soft tissue techniques, focusing on the myofascial component. Myofascial pain and MTrPs may be part of the LE etiology. Treatment focusing on the myofascial component seems to be effective in reducing pain and improving function in patients with LE. Additional trials are essential to attain a solid conclusion." [Since some studies still use the term "myofascial pain" to mean TMJD, and so very many researchers are not even aware of myofascial trigger points or lack the training and experience needed to palpate them, previous research is only as good as the training. There should be no "ongoing debate" about the myofascial component of LE. There are only those experienced and well-trained in the techniques of palpating TrPs and those who are not. Disagreements between those who are trained and those who are not, does not constitute a true debate. To have a controversy, there must be science on both sides. Researchers who do not understand the ubiquity of TrPs are churning out incomplete and often flawed research. Quantity does not equal quality. The "debate" will continue until they all become enlightened. Until then, bad research will beget more bad research. This study is not bad, but reflects the need for education. DJS]
Shoaib, M., L. S. Swanner, S. Yasar and S. R. Goldberg. 1999. Chronic caffeine exposure
potentiates nicotine self-administration in rats. Psychopharmacology (Berl) 142(4):327-33.
Shochat, T., I Haimov and P. Lavie. 1998. Melatoninthe key to the gate of sleep. Ann
Shoskes DA, Berger R, Elmi A et al. 2007.
Muscle tenderness in men with chronic prostatitis/chronic pelvic pain
syndrome: the chronic prostatitis cohort study. J Urol. [Dec 12
Epub ahead of print]. "Myofascial pain is a possible etiology for
category III chronic prostatitis/chronic pelvic pain syndrome, either
secondary to infection/inflammation or as the primary cause."
"Abdominal/pelvic tenderness is present in half of the patients with chronic
pelvic pain syndrome…."
Sidell, N. L. Adult adjustment to chronic illness: a review of the literature. Health
Soc Work 22(1):5-11.
Sido B, Dumoulin FL, Homann J et al. 2013. [Surgical interventions in patients with mast cell activation disease: Aspects relevant for surgery using the example of a cholecystectomy.] Chirurg. [Dec 15 Epub ahead of print.] [Article in German] "Systemic mast cell activation disease (MCAD) is characterized by an increased and unregulated release of mast cell mediators which can evoke a multifaceted clinical picture often resembling irritable bowel syndrome or fibromyalgia. Because of the considerable prevalence (~ 17 %) of MCAD surgeons are frequently unwittingly confronted with MCAD patients in whom unexpected intraoperative and postoperative complications may occur. Therefore, knowledge of the particular requirements is of relevance for surgical treatment of MCAD patients….Due to the high prevalence of MCAD in the general population it can be assumed that the frequency in the surgical patient population is similar. If a patient has MCAD, specific characteristics should be taken into account in the surgical procedure to avoid increased operative and complication risks resulting from MCAD."
Siedentopf F. 2009. [Chronic pelvic pain in
women from a gynecologic viewpoint] Urologe A.
48(10):1193-1194, 1196-1198. [German] It is rather amazing that the
most common cause of chronic pelvic pain, the myofascial trigger point, is
not included in this article.
Siegan, J. B., A. T. Hama and J. Sagen. 1997. Suppression of neuropathic pain by a
naturally derived peptide with NMDA antagonist activity. Brain Res 755(2):331-334.
Siegel, D. M. , D. Janeway and J. Baum. 1998. Fibromyalgia syndrome in children and
adolescents: clinical features at presentation and status at follow-up. Pediatrics
101(3 Pt 1):377-382.
Siegmeth, W. 1999. [No title available]. Wien Med Wochenschr 149(19-20):558-60
Siegmund G.P., Brault J.R.,
Chimich D.D. 2002. Do cervical muscles play a role in whiplash
injury? J Whiplash and Rel Dis 1(1):23-40. “...initially-relaxed
cervical muscles have the potential to alter the head and neck kinematics
and Kinematics resulting from whiplash events.”
Sigal, L. H. , D. J. Chang and V. Sloan.1998. 18 tender points and the "18
wheeler" sign: clues to the diagnosis of fibromyalgia. JAMA 279(6):434.
Sigmundsson H. 2005. Disorders of motor development (clumsy child
syndrome). J Neural Transm Suppl. (69):51-68.
“Research has shown that about 6-10% of children have motor competences
well below the norm. It is unusual for motor problems to simply
disappear over time. In the absence of intervention the syndrome
is likely to manifest itself.” “...clumsiness must be seen as a
Sigmundsson H. 2003. Perceptual deficits in clumsy children:
inter- and intra-modal matching approach — a window into clumsy
behavior. Neural Plast. 10(1-2):27-38. There are many
informational deficits that can contribute to clumsy behavior.
Sensory integration dysfunction must be considered as well as
proprioception and visual-perceptual and visual motor deficits.
Sikdar S, Ortiz R, Gebreab T et al. 2010. Understanding the vascular environment of myofascial trigger points using ultrasonic imaging and computational modeling. Conf Proc IEEE Eng Med Biol Soc. 1:5302-5305. "Recently, our research group has developed new ultrasound imaging methods to visualize and characterize MTrPs and their surrounding soft tissue. The goal of this paper was to quantitatively analyze Doppler velocity waveforms in blood vessels in the neighborhood of MTrPs to characterize their vascular environment.... 16 patients with acute neck pain were recruited for the study and the blood vessels in the upper trapezius muscle in the neighborhood of palpable MTrPs were imaged using Doppler ultrasound. Preliminary findings show that symptomatic MTrPs have significantly higher peak systolic velocities and negative diastolic velocities compared to latent MTrPs and normal muscle sites. Using compartment modeling, we show that a constricted vascular bed and an enlarged vascular volume could explain the observed flow waveforms with retrograde diastolic flow."
Sil S, Lynch-Jordan A, Ting TV et al. 2012. The influence of family environment on long-term psychosocial functioning of adolescents with juvenile fibromyalgia. Arthritis Care Res (Hoboken). [Dec 19 Epub ahead of print]. "Results indicated that family environment during early adolescence significantly predicted greater depressive symptoms in early adulthood for both the JFM group and healthy controls. In particular, a controlling family environment (use of rules to control the family and allowing little independence) during early adolescence was the driving factor in predicting poorer long-term emotional functioning for patients with JFM. Family environment did not significantly predict longer-term physical impairment for either group."
Siler AC, Gardner H, Yanit K et al. 2010. Systematic Review of the Comparative Effectiveness of Antiepileptic Drugs for Fibromyalgia. J Pain. [Dec 9 Epub ahead of print]. "Fibromyalgia is a difficult-to-treat chronic pain syndrome that affects 2% of the US population. Pregabalin is an antiepileptic recently FDA approved for fibromyalgia treatment. Other antiepileptics have been suggested for treatment. This systematic review examines the relative benefits and harms of antiepileptic drugs in the treatment of fibromyalgia. A literature search was conducted and 8 studies matched criteria (7 studies of pregabalin, 1 of gabapentin). Both drugs reduced mean pain scores more than placebo at a modest rate (pregabalin, 38% to 50%; gabapentin, 51%). In a 6-month trial of pregabalin responders, 32% continued to have response at 6 months, with a mean time to loss of response of 34 days. Compared to placebo, the drugs had similarly high rates of adverse events and withdrawals. Without a head-to-head trial it is not possible to conclude if 1 antiepileptic is more effective or harmful than the other, although limited evidence suggests potential differences. Future studies must directly compare the drugs, include a more broadly defined population, examine long term benefits and harms, and include cointerventions. We conclude that pregabalin and gabapentin are modestly effective for the treatment of fibromyalgia but that their long-term safety and efficacy remain unknown….This systematic review evaluates the benefits and harms of using the antiepileptic drugs gabapentin and pregabalin for the treatment of fibromyalgia. Conclusions from this paper can help clinicians to more effectively treat the pain associated with fibromyalgia."
Silva KM, Tucano SJ, Kumpel C et al. 2012. Effect of hydrotherapy on quality of life, functional capacity and sleep quality in patients with fibromyalgia. Rev Bras Reumatol. 52(6):851-857. [English, Portuguese]. "Hydrotherapy improves sleep quality, physical function, professional status, psychological disorders and physical symptoms in patients with fibromyalgia."
Silva MP, Barrett JM, Williams JD. 2004. A
retrospective review of outcomes of fibromyalgia patients following physical
therapy treatments. J Musculoskel Pain 12(2):83-92.
Upledger’s cranio-sacral release therapy may be effective to decrease pain
levels and medication and increase quality of life for FMS patients.
Silver DS, Wallace DJ.
2002. The management of fibromyalgia-associated syndromes.
Rheum Dis Clin North Am 28(2):405-17. "Most
of the six million Americans with fibromyalgia have at least one
associated syndrome which mandates specialized attention in
addition to traditional therapeutic approaches. The successful
treatment of fibromyalgia-associated syndromes improves the
symptoms, quality of life, and prognosis of fibromyalgia."
Silver, I. A., J. Deas and M. Erecinska. 1997. Ion homeostasis in brain cells:
differences in intracellular ion responses to energy limitation between cultured neurons
and glial cells. Neuroscience 78(2):589-601.
Simeonova M, Gimsa J. 2006. The influence of the molecular
structure of lipid membranes on the electric field distribution and
energy absorption. Bioelectromagnetics [Aug 17 Epub ahead
Simms, R. W. 1998. Fibromyalgia is not a muscle disorder. Am J Med Sci
Simms, R. W. , C. A. Zerbini, N. Ferrante, J. Anthony, D. T. Felson and D. E. Craven.
1992. Fibromyalgia syndrome in patients infected with human immunodeficiency virus. the
Boston City Hospital Clinical AIDS Team. Am J Med 92(4):368-374.
Simon, J., E. Klaiber, B. Wiita (yes 2 "i"s), A. Bowen and H. M. Yang. 1999.
Differential effects of estrogen-androgen and estrogen-only therapy on vasomotor symptoms,
gonadotropin secretion, and endogenous androgen bio availability in post menopausal women.
Simonnet G. 2005. [Complexity and
physiological logic of analgesic effects of opioids]
Rev Med Suisse. 1(25):1682-1685. [French] “NMDA receptor
antagonists and specific diets able to negatively modulate NR2B
subunit containing NMDA receptors prevented abnormal pain
hypersensitivity, partially reversed chronic pain and restored
the opioid effectiveness on opioid-resistant pain models.”
Simons DG. 1991.
Symptomatology and clinical pathophysiology of myofascial pain.
Schmerz. 5(Supp 1):S29-37. “Myofascial pain
syndromes, fibromyalgia, and articular dysfunctions may all be
contributing to our patients’ ubiquitous musculoskeletal pain
problems that generally are poorly understood and poorly
managed.” [So many years later, and this is still the case.
One must wonder what it will take for the medical world to be
equal to the paradigm change that it will take to bring
myofascial pain into mainstream medicine, reducing so much
needless pain, misery and cost. DJS]
Simons DG, Hong CZ, Simons LS.
2002. Endplate potentials are common to midfiber
myofascial trigger points. Am J Phys Med Rehabil.
81(3):212-222. “Endplate noise was significantly more
prevalent in myofascial trigger points than in sites that were
outside of a trigger point but still within the endplate zone.
Endplate noise seems to be characteristic of, but is not
restricted to, the region of a myofascial trigger point.”
Simons DG. 2004. New aspects of
myofascial trigger points: etiological and clinical. J
Musculoskeletal Pain 12(3/4):15-21. This article clearly
explains the evidence backing the integrated hypothesis for TrP
formation, including information on biopsies and on the release
of sensitizing substances documented by the work of Shah (see
Shah JP, Phillips TM, Danoff JV et al. 2005. et al.). It
explains that it is a ...“serious mistake to consider the TrP in
isolation.” Patients often have clusters or chains of TrPs, and
clinicians need to be on the alert that when one TrP is present
in a patient with chronic symptoms (not always pain–TrPs can
cause muscle dysfunctions including weakness as well as other
symptoms before they cause pain), it is important to take into
account the possible presence of other TrPs adding to the
symptom load and maintaining chronicity.
Simons DG. 1981. Myofascial trigger points: a need for
understanding. Arch Phys Med and Rehab. 62:97-99. We need
to clear up the terminology associated with myofascial TrPs. There
are neurophysiological mechanisms that can explain the TrP.
Simons DG, Mense S. 1998. Understanding and measurement of muscle
tone as related to clinical muscle pain. Pain 75(1):1-17.
“Thixotropy of muscle is a ubiquitous and functionally important
phenomenon that is not commonly recognized. A clinical pain
condition associated with increased muscle tension is tension-type
headache, which is largely muscular in origin; it is often caused by
myofascial trigger points.” Diagnoses of muscle tension and muscle
spasm must be differentiated.
Simons DG. 1995.
Myofascial pain syndrome: One term but two concepts; a new understanding.
J Musculoskeletal Pain 3(1):7-14. This paper is of vital importance.
It explains how some researchers have been using the term “myofascial pain
syndrome (MPS)” as synonymous with temporomandibular dysfunction (TMJD),
without explaining the definition. [This practice is common in papers
written by dentists. This dangerous practice can lead to misleading or
erroneous conclusions. Others build on these conclusions, not
realizing that authors are using the term MPS to mean TMJD, and may assume
that they refer to myofascial pain due to trigger points that may occur in
all four quadrants of the body. Authors must be careful to define
their terms. DJS]
DG, Mense S.
Diagnosis and therapy of myofascial trigger points. Schmertz
17(6):419-424. This verifies by muscle biopsy the segmental shortening
of sarcomere groupings in individual muscle fibers, suggesting the mechanism
behind myofascial trigger point taut band formation. It presents an
integrated hypothesis for the pathophysiology of myofascial trigger points,
beginning with the release of excess acetylcholine from dysfunctional motor
Simons D. G. 2001. Do
endplate noise and spikes arise from normal motor endplates? Am J.
Phys Med Rehabil 80(2):134-40. Endplate noise may be a commonly
misunderstood phenomenon and needs to be more carefully assessed in regards
to association with myofascial trigger points.
Simons, DG. 1999. Diagnostic criteria of myofascial pain caused by trigger points. J
Musculoskel Pain 7(1-2):111-120.
Simons, D. G. 1993. Examining for myofascial trigger points. Arch Phys Med Rehabil
Simons, D. G. and W. C. Stolov. 1976. Microscopic features and transient contraction of
palpable bands in canine muscles. Am J Phys Med 55:65-88.
Simpson, J. J. and W. E. Davies. 1999. Recent advances in the pharmacological treatment
of tinnitus. Trends Pharmacol Sci 20(1):12-8.
Simpson KH. 2002. Individual choice of opioids and formulations:
strategies to achieve the optimum for the patient. Clin
Rheumatol 21 Suppl 1:S5-S8. “Recent years have seen a gradual
shift towards the use of opioid therapy in chronic non-malignant pain (CNMP)
following recognition that at least a subpopulation of such patients
appears to benefit from long-term opioid treatment. Misconceptions
about opioids and the associated risk of dependence stemmed from older
research that was fundamentally flawed. Opioid treatment must
therefore be individualized for each patient, based on a clear
understanding of drug absorption, metabolism, toxic and binding
characteristics, using opioid switching strategies where appropriate.
Practical guidelines for opioid therapy in MNMP include regular and
systematic checks of treatment results to adjust therapy or each
individual patient and to ensure optimum benefit.”
Simunovic, Z., T. Trobonjaca and Z. Trobonjaca. 1998. Treatment of medial and
lateral epicondylitistennis and golfers elbowwith low level laser
therapy: a multicenter double-blind, placebo-controlled clinical study on 324 patients. J
Clin Laser Med Surg 16(3):145-51.
Simunovic, Z. 1996. Low level laser therapy with trigger points technique: a clinical
study on 243 patients. J Clin Laser Med Surg 14(4):163-167.
Sinaii N, Cleary S.D,
Ballweg M.L. et al. 2002. High rates of autoimmune and endocrine
disorders, fibromyalgia, chronic fatigue syndrome and atopic diseases among
women with endometriosis: a survey analysis. Hum Reprod
Singh, B. B., B. M. Berman, V. A. Hadhazy and P. Creamer. 1998. A pilot study of
cognitive behavioral therapy in fibromyalgia. Altern Ther Health Med 4(2):67-70.
Singh, G., D. R. Ramey, D. Morfeld, H. Shi, H. T. Hatoum and J. F. Fries. 1996.
Gastrointestinal tract complications of nonsteroidal anti-inflammatory drug treatment in
rheumatoid arthritis. A prospective observational cohort study. Arch Intern Med
Singh RB, Kartik C, Otsuka K et al. 2002. Brain-heart connection
and the risk of heart attack. Biomed Pharmacother. 56 Suppl
2:257s-265s. This article connects recent research linking conditions
such as diabetes, ambient pollution, insulin resistance and mental
stress with heart attack risk, gives some perpetuating factors of chest
pain, and lists some possible protective mechanisms.
Sinz, E. H., P. M. Kochanek, M. P. Heyes, S. R. Wisniewski, M. J. Bell, R. S. Clark, S.
T. DeKosky, A. R. Blight and D. W. Marion. 1998. Quinolinic acid is increased in CSF and
associated with mortality after traumatic brain injury in humans. J Cereb Blood Flow
Sirvent P, Mercier J, Vassort G et al. 2005.
Simvastatin triggers mitochondria-induced Ca2+ signaling altercation in
skeletal muscle. Biochem Biophys Res Commun 329:1067-1075.
This article is vitally important for physicians who have patients with
myofascial TrPs. Simvastatin, and, by biochemical inference, statin
medications, triggers flood of intra-cellular calcium. Increased
release of Ca2+ is an essential part of the formation of myofascial TrPs,
according to Simons’ integrated hypothesis. The addition of statins
could cause a flare of TrP symptoms that would not abate until statins are
discontinued. [This would mesh with personal observations and
communications from myofascial pain specialists who have observed that many
of their patients do not improve until they are off statins. DJS]
Sist T, Wong C. 2000. Difficult
problems and their solutions in patients with cancer pain of the head and
neck areas. Curr Rev Pain. 4(3):206-214. Often, pain in cancer
patients is attributed to tumor regrowth when it is due to something else.
These authors urge careful consideration of alternatives and the possibility
of mixed pain generators, including myofascial trigger points.
Sist, T., Miner, M.., Lema,
M.,. 1999. Characteristics of postradical neck pain syndrome: a
report of 25 cases. These results indicate that postoperative
neuropathic pain and postoperative TrP pain can be present
concurrently, that TrPs can be a common cause of postoperative
pain, and that each type of pain requires its own specific
treatment for relief.
Sitges C, Garcia-Herrera M, Pericas M et
al. 2007. Abnormal brain processing of affective and sensory pain
descriptors in chronic pain patients. J Affect Disord. [Apr
13 Epub ahead of print]
Siu AM, Chan CC, Poon
PK. 2006. Evaluation of the chronic disease self-management
program in a Chinese population. Patient Educ Couns. [Jul
25 Epub ahead of print] “The CDSMP participants demonstrated
significantly higher self-efficacy in managing their illness, used more
cognitive methods to manage pain and symptoms, and felt more energetic
than the subjects in the comparison group.”
Sivri, A., A. Cindas, F. Dincer and B. Sivri. 1996. Bowel dysfunction and irritable
bowel syndrome in fibromyalgia patients. Clin Rheumatol 15(3):283-286.
Sjogren P, Christrup LL, Petersen MA et al. 2005.
Neuropsychological assessment of chronic non-malignant pain patients treated
in a multidisciplinary pain centre. Eur J Pain 9(4):453-0462.
“MMSE [Mini Mental State Examination] seems to be too insensitive for
detecting the milder forms of cognitive impairment found in chronic
Sjolund, K. F., M. Segerdahl and A. Sollevi. 1999. Adenosine reduces secondary
hyperalgesiain two human models of cutaneous inflammatory pain. Anesth Analg
Skargren, E. I. , B. E. Oberg, P. G. Carlsson and M. Gade. 1997. Cost and effectiveness
analysis of chiropractic and physiotherapy treatment for low back and neck pain. Six-month
follow-up. Spine 22(18):2167-2177.
Skootsky, S. A., B. Jaeger and R. K. Oye. 1989. Prevalence of myofascial pain in
general internal medicine practice. West J Med 151(2):157-160.
Skrabek RQ, Galimova L, Ethansand
Daryl K. 2007. Nabilone for the treatment of pain in
fibromyalgia. [Oct 30 Epub ahead of print]. “To our knowledge,
this is the first randomized, controlled trial to assess the benefit of
nabilone, a synthetic cannabinoid, on pain reduction and quality of life
improvement in patients with fibromyalgia. As nabilone improved
symptoms and was well-tolerated, it may be a useful adjunct for pain
management in fibromyalgia.” [Cannabinoids are increasingly being
researched for chronic pain, with positive results. DJS]
Slater ME, De Lima J, Campbell K et al.
Opioids for the management of severe chronic nonmalignant pain in children:
a retrospective 1 year practice survey in a children’s hospital.
Pain Med. [Epub ahead of print] Function was improved in these
children when they received adequate pain control. Pediatric patients
with severe nonmalignant chronic pain should not be denied opioids if they
are needed as part of a pain management strategy.
Sloan P. 2008. Review of oral oxymorphone in the management of pain. Ther Clin Manag 4(4):777-787. Oxymorphone is available in both sustained-release and immediate release forms. This opioid does not have an NSAID or acetaminophen included, and has been successful for relief of chronic pain.
Slocumb, J. C. 1984. Neurological factors in chronic pelvic pain: trigger points and
the abdominal pelvic pain syndrome. Am J Obstet Gynecol 149(5):536-43.
Slotkoff, A. T., D. A. Radulovic and D. J. Clauw. 1997. The relationship between
fibromyalgia and the multiple chemical sensitivity syndrome. Scand J Rheumatol
Smania N, Corato E, Fiaschi A et al. 2005.
Repetitive magnetic stimulation - a novel therapeutic approach for
myofascial pain syndrome. J Neurol. [Epub ahead of print]
“Our results strongly suggest that at medium and longer term intervals
peripheral rMS may be more effective than TENS for the treatment of
Smania N., Corato E.,
Fiaschi A. et al. 2003. Therapeutic effects of peripheral repetitive
magnetic stimulation on myofascial pain syndrome. Clin Neurophysiol.
This study indicated that peripheral repetitive magnetic stimulation may
have therapeutic effects on myofascial head and neck TrP pain and ROM.
The improvement noted lasted at least one month.
Smart, P. A., G. W. Waylonis and K. V. Hackinshaw. 1997. Immunologic profile of
patients with fibromyalgia. Am J Phys Med Rehabil 76(3):231-4.
Smith, D. L. 1986. Patient education: tuning in to the needs of the elderly. Medical
Smith EK, Magarey M, Argue S et al. 2009.
Muscular load to the therapist’s shoulder during three alternative
techniques for trigger point therapy. J Bodyw Mov Ther.
13(2):171-181. “While there is evidence that the TTT (treatment-tool
technique) decreases the muscular load to the shoulder of the contact arm,
there is no indication of where this load is redistributed.”
Smith H, Elliott J. 2001. Alpha2 receptors and
agonists in pain management. Curr Opin Anaesthesiol.
14(5):513-518. “It has been noted that these agents can enhance analgesia
provided by traditional analgesics, such as opiates, and may result in
opiate-sparing effects. This has important implications for the
management of acute postoperative pain and chronic pain states…”
Smith, H.S., Audette J.,
Royal M.A. 2002. Botuminum toxin in pain management of soft tissue
syndrome. Clin J Pain. These authors suggest that because
botulinum toxin has been used successfully for pain associated with myofascial
trigger points, and it admits that central sensitization may be part of many
chronic pain syndromes, it suggests that botulinum toxin therapy may be “particularly
useful” in many soft tissue syndromes such as fibromyalgia when other
approaches have failed. [This paper ignores the specific mechanism of
the myofascial trigger point (MTrP), as we believe it to be, with a release of
excess acetylcholine at the motor endplate causing the release of excess
calcium and the formation of MTrPs. Botulinum toxin specifically
interrupts acetylcholine in this process. Logic indicates that one
cannot extrapolate that the use of botulinum locally would be of any benefit
in the control of a chronic central pain state, unless the peripheral pain
generators perpetuating that state are MTrPs. In that case, the MTrPs
must first be shown to respond to local injection using the proper technique
incorporating positioning of involved muscles, palpation for TrPs, injection
of all related MTrPs, and full ROM stretch. If this releases the muscle,
but the release does not hold for a significant time in spite of the
identification and control of all perpetuating factors, it would then be the
time for consideration of more aggressive methods.]
Smith J.A., Lumley M.A., Longo D.J. 2002. Contrasting emotional approach
coping with passive coping for chronic myofascial pain. Ann Behav Med
24(4):326-35. Emotional-approach coping (emotional processing and emotional
expression) was related to less pain in myofascial pain patients, especially
women, and less depression in men. The use of passive pain coping
strategies are associated with worse pain and adjustment. Some
emotion-focused types of pain coping may be adaptive.
Smith JD, Terpening CM, Schmidt SO et al.
2001. Relief of fibromyalgia symptoms following discontinuation of
dietary excitotoxins. Ann Pharmacother 35(6):702-706.
A subset of FMS patients may improve significantly with the elimination
of excitotoxins such as monosodium glutamate and aspartame from their
Smith MT, Moore BJ. 2012. Pregabalin for the treatment of fibromyalgia. Expert Opin Pharmacother. 13(10):1527-1533. "This review addresses pregabalin pharmacokinetics, efficacy and adverse event (AE) profiles from randomized controlled trials and open-label extension studies in patients with FM. These effects are compared with those of the serotonin norepinephrine reuptake inhibitors, duloxetine and milnacipran that also have FDA approval for the treatment of fibromyalgia….At the approved dosages, oral pregabalin has at most a moderate therapeutic benefit above placebo with tolerable side-effects, in no more than 50% of patients with FM. Durability of clinically meaningful...pain relief in pregabalin-responders has been demonstrated for at least 6-months, but longer-term studies are required as most patients have symptoms for decades. Exclusion of patients with common co-morbidities from the pregabalin RCTs in FM raises questions on the generalizability of the RCT findings to the typical patient seen in clinical practice and so additional investigation is required."
Smith MT, Perlis ML, Haythornthwaite JA. 2004.
Suicidal ideation in outpatients with chronic musculoskeletal pain:
an exploratory study of the role of sleep onset insomnia and pain
intensity. Clin J Pain. 20(2):111-118. “Chronic
pain patients who self-reported severe and frequent initial insomnia
with concomitant daytime dysfunction and high pain intensity were
more likely to report passive suicidal ideation, independent from
the effects of depression severity.” More attention needs to
be focused on controlling factors leading to suicidal ideation in
chronic pain patients.
Smith MT, Edwards RR, Robinson RC et al. 2004.
Suicidal ideation, plans, and attempts in chronic pain patients:
factors associated with increased risk. Pain
111(1-2):201-208. “Demographics, pain severity, and depression
severity were not associated with suicidal ideation in multivariate
Smith MT, Edwards RR, Robinson RC et al. 2004. Suicidal ideation,
plans, and attempts in chronic pain patients: factors associated with
increased risk. Pain 111(1-2):201-208. “These
findings highlight the need for routine evaluation monitoring of
suicidal behavior in chronic pain, especially for patients with
histories of suicide, those taking potentially lethal medications, and
patients with abdominal pain.”
Smith PF. 2012. Dyscalculia and vestibular function. Med Hypotheses. [Jul 21 Epub ahead of print]. "A few studies in humans suggest that changes in stimulation of the balance organs of the inner ear (the 'vestibular system') can disrupt numerical cognition, resulting in 'dyscalculia', the inability to manipulate numbers. Many studies have also demonstrated that patients with vestibular dysfunction exhibit deficits in spatial memory....It is suggested that there may be a connection between spatial memory deficits resulting from vestibular dysfunction and the occurrence of dyscalculia, given the evidence that numerosity is coupled to the processing of spatial information (e.g., the 'spatial numerical association of response codes ('SNARC') effect')."
Smith PF, Darlington CL. 2013. Personality changes in patients with vestibular dysfunction. Front Hum Neurosci. 7:678. "The vestibular system is a sensory system that has evolved to detect linear and angular acceleration of the head in all planes so that the brain is not predominantly reliant on visual information to determine self-motion. Since the vestibular system first evolved in invertebrate species in order to detect gravitational vertical, it is likely that the central nervous system has developed a special dependence upon vestibular input. In addition to the deficits in eye movement and postural reflexes that occur following vestibular dysfunction, there is convincing evidence that vestibular loss also causes cognitive and emotional disorders, some of which may be due to the reflexive deficits and some of which are related to the role that ascending vestibular pathways to the limbic system and neocortex play in the sense of spatial orientation. Beyond this, however, patients with vestibular disorders have been reported to experience other personality changes that suggest that vestibular sensation is implicated in the sense of self. These are depersonalization and derealization symptoms such as feeling "spaced out", "body feeling strange" and "not feeling in control of self". We propose in this review that these symptoms suggest that the vestibular system may make a unique contribution to the concept of self through information regarding self-motion and self-location that it transmits, albeit indirectly, to areas of the brain such as the temporo-parietal junction (TPJ)." [I have observed that many patients with fibromyalgia and chronic myofascial pain also have co-existing (and often undiagnosed) vestibular dysfunction. This co-existing condition may be a cause of significant symptoms. DJS]
Smith PF, Zheng Y. 2013. From ear to uncertainty: vestibular contributions to cognitive function. Front Integr Neurosci. 7:84. "In addition to the deficits in the vestibulo-ocular and vestibulo-spinal reflexes that occur following vestibular dysfunction, there is substantial evidence that vestibular loss also causes cognitive disorders, some of which may be due to the reflexive deficits and some of which are related to the role that ascending vestibular pathways to the limbic system and neocortex play in spatial orientation. In this review we summarize the evidence that vestibular loss causes cognitive disorders, especially spatial memory deficits, in animals and humans and critically evaluate the evidence that these deficits are not due to hearing loss, problems with motor control, oscillopsia or anxiety and depression. We review the evidence that vestibular lesions affect head direction and place cells as well as the emerging evidence that artificial activation of the vestibular system, using galvanic vestibular stimulation (GVS), can modulate cognitive function."
Smith, W. A. 1998. Fibromyalgia Syndrome. Nurs Clin North Am 33(4):653-669.
Smith WR, White PD,
Buchwald D. 2006. A case control study of premorbid and currently
reported physical activity levels in chronic fatigue syndrome.
BMC Psychiatry 6:53. “Patients with chronic, unexplained, disabling
fatigue reported being more active before becoming ill than healthy
controls. This finding could be explained by greater premorbid
activity levels that could predispose to illness, or by an
overestimation of previous activity.”
Smith-Coggins, R., M. R. Rosekind, K. R. Buccino, D. F. Dinges and R. P. Moser. 1997.
Rotating shift work schedules: can we enhance physician adaptation to night shifts? Acad
Emerg Med 4(10):951-61.
Smythe HA. 2004. Fibromyalgia
among friends. J Rheumatol 31(4):627-630. This editorial
describes anti-fibromyalgia bias that is blatant in material from some
medical authors, in spite of scientific evidence that it is real.
Legal advocates should take note of this.
Smythe, H. 1998. Examination for tenderness: learning to use 4 kg force. J Rheumatol
Snyder-Mackler L, Barry AJ, Perkins AI et
al. 1989. Effects of helium-neon laser irradiation on skin resistance
and pain in patients with trigger points in the neck or back. Phys
Ther. 69(5):336-341. “The purpose of this double-blind study was
to ascertain the effects of helium-neon (He-Ne) laser irradiation on skin
resistance and pain in patients with trigger points in the neck or low
back.” “Results indicated a statistically significant increase in skin
resistance and a decrease in pain following laser treatment.”
Snyder-Mackler, L., A. Delitto, S. W. Stralka and S. L. Bailey. 1994. Use of electrical
stimulation to enhance recovery of quadriceps femoris muscle force production in patients
following anterior cruciate ligament reconstruction. Phys Ther 74(10):901-907.
Soderberg, S., B. Lundman and A. Norberg. 1999. Struggling for dignity: the meaning of
womens experiences of living with fibromyalgia. Qual Health Res 9(5):575-87.
Soderberg, S., B. Lundman and A. Norberg. 1997. Living with fibromyalgia: sense of
coherence, perception of well-being, and stress in daily life. Res Nurs Health
Sohn W. 2001. [The path to pain management on
WHO. Step III. Towards a better understanding of the treatment of
severe chronic pain] Fortschr Med Orig. 119 Suppl 2:81-89. [German]
“Many patients with severe chronic pain continue to receive inadequate
treatment. The reason is often a lack of proper communication between
patient and physician.”
Soin A, Cheng J, Brown L et al. 2008.
Functional outcomes in patients with chronic nonmalignant pain on long-term
opioid therapy. Pain Pract. 8(5):379-384. “We conclude
that judicious use of opioids therapy may lead to improvement in perceived
quality of life and certain aspects of functional capacity and daily
activities in a highly selected group of patients with CNMP (chronic
nonmalignant pain) who have not responded to other therapeutic modalities
for over 6 months.”
Sok SR, Erien JA, Kim KB. 2003. Effects of
acupuncture therapy on insomnia. J Adv Nurs 44(4):375-384.
Acupuncture may have a significant effect on insomnia.
Solberg Nes L, Carlson CR, Crofford LJ et al. 2010. Self-regulatory deficits in fibromyalgia and temporomandibular disorders. Pain. [Jun 17 Epub ahead of print].
"Chronic pain conditions such as fibromyalgia (FM) and temporomandibular disorders (TMDs) are accompanied by complex interactions of cognitive, emotional, and physiological disturbances. Such conditions are complicated and draining to live with, and successful adaptation may depend on ability to self-regulate. Self-regulation involves capacity to exercise control and guide or alter reactions and behavior, abilities essential for human adjustment. Research indicates that self-regulatory strength is a limited source that can be depleted or fatigued, however, and the current study aimed to show that patients with FM and TMD are vulnerable to self-regulatory fatigue as a consequence of their condition…. Patients displayed significantly less capacity to persist on the subsequent task compared with controls. In fact, patients exposed to low self-regulatory effort displayed similar low persistence to patients and controls exposed to high self-regulatory effort, indicating that patients with chronic pain conditions may be suffering from chronic self-regulatory fatigue….Impact of chronic pain conditions on self-regulatory effort was mediated by pain, but not by any other factors. The current study suggests that patients with chronic pain conditions likely suffer from chronic self-regulatory fatigue, and underlines the importance of taking self-regulatory capacity into account when aiming to understand and treat these complex conditions. "
Solerte, S. B., M. Rondanelli, R. Giacchero, M. Stabile, E. Lovati, L. Cravello, B.
Pontiggia, G. Vignati and E. Ferrari, MF. 1999. Serum glucagon concentration and
hyperinsulinaemia influence renal haemodynamics and urinary protein loss in normotensive
patients with central obesity. Int J Obes Relat Metab Disord 23(9):997-1003.
Solomon, C. G., J. S. Carroll, K. Okamura, S. W. Graves and E. W. Seely. 1999. Higher
cholesterol and insulin levels in pregnancy are associated with increased risk for
pregnancy-induced hypertension. Am J Hypertens 12(3):276-82.
Solomon, D. H. and M. H. Liang. 1997. Fibromyalgia: scourge of humankind or bane of a
rheumatologist's existence? Arthritis and Rheumatism 40:1553-1555.
Solomon L, Schnitzler CM, Browett JP. 1982.
Osteoarthritis of the hip: the patient behind the disease. Ann
Rheum Dis. 41(2):118-125. “...appearances of hip OA are determined
by 3 interacting factors: mechanical stress, cartilage degeneration, and
bone response.” [Mechanical stress could be supplied by the presence
of myofascial TrPs, especially in the attachment regions. DJS]
Sommer C. 2013. [Neuropathic pain: Pathophysiology, assessment, and therapy.] Schmerz. [Nov 13 Epub ahead of print]. [Article in German] "Neuropathic pain is caused by lesions in the somatosensory system. Characteristic but not exclusive features are spontaneous burning pain, electrifying and shooting pain, hyperalgesia, and allodynia. The basic concept of the pathophysiology of neuropathic pain is the combination of peripheral and central sensitization. Knowledge on the molecular mechanisms has grown exponentially in recent years. The problem lies in identifying the individual mechanisms and in determining a comprehensive concept. Progress has also been made in assessment, e.g., methods for detecting dysfunction of nociceptors have significantly improved. In addition, there are many more therapeutic options available than 15 years ago. The drugs available include antidepressants, anticonvulsants, opioids, and topical medications."
Soppi, M. and E. Beneforti. 1999. Muscular pain in some rheumatic diseases. J
Musculoskel Pain 7(1-2):225-229
Sorensen, J., A. Bengtsson, J. Ahlner, K. G. Henriksson, L. Ekselius, and M. Bengtsson.
1997. Fibromyalgia--are there different mechanisms in the processing of pain? A double
blind crossover comparison of analgesic drugs. J Rheumatol 24(8):1615-1621.
Sorensen, J., A. Bengtsson, E. Backman, K. G. Henriksson and M. Bengtsson. 1995. Pain
analysis in patients with fibromyalgia. Effects of intravenous morphine, lidocaine, and
ketamine.Scand J Rheumatol 24(6):360-365.
Sorg, B. A. and T. Hochstatter. 1999. Behavioral sensitization after repeated
formaldehyde exposure in rats. Toxicol Ind Health 15(3-4):346-55.
Sorond FA, Hurwitz S, Salat De et al. 2013. Neurovascular coupling, cerebral white matter integrity, and response to cocoa in older people. Neurology Aug 7 [Epub ahead of print] Neurovascular coupling is associated with cognitive function. Both can be improved in individuals with impaired cognitive function between the ages of about 67 to 78 if they consume cocoa every day.
Sorrell MR. 2010. Myofascial examination
leads to diagnosis and successful treatment of migraine headache. J
Musculoskel Pain. 18(1). “The myofascial examination of the head and
neck reproduced the headache pain of most patients having migraine. The
PTS (physical therapist supervised stretching of involved muscles along
their lengths) is effective in treating these headaches. The myofascial
examination should be used to determine treatment for migraineurs.”
Sorrell MR, Flanagan W. 2003.
Treatment of chronic resistant myofascial pain using a
multidisciplinary protocol [The Myofascial Pain Program]. J
Musculoskel Pain 11(1):5-9. Multidisciplinary treatment including
myofascial technique physical therapy, surface electromyography and
biofeedback training, medication and trigger point injections can
significantly produce pain relief, mood elevation and increase ability to
function, even in patients who have symptoms resistant to other therapies.
Sorrell MR, Flanagan W,
McCall JL. 2003. Symptom duration affects the outcome of
multidisciplinary treatment of myofascial pain. The method of assessment
influences the understanding of the results. J Musculoskel Pain 11(1):11-16.
The earlier the patient enters a multidisciplinary treatment program that
understands myofascial pain, the better the results.
MR, Flanagan W, McCall JL. 2003. The effect of depression and anxiety on
the success of multidisciplinary treatment of chronic resistant myofascial
pain. J Musculoskel Pain 11(1):17-20. Co-existing depression
significantly reduced positive outcome of this treatment
Sousa RF, Gazzola JM, Gananca MM et al. 2011. Correlation between the body balance and functional capacity from elderly with chronic vestibular disorders. Braz J Otorhinolaryngol. 77(6):791-798. [Article in English, Portuguese] "Vestibular disorders are common among the elderly, mainly resulting in dizziness and imbalance - symptoms which can impact daily routine activities.....There is a positive correlation between body balance and functional capacity in elderly patients with peripheral vestibular disorders, that is: the better the balance, the better the individual's functional capacity. In addition, a worse functional capacity increases the individual's risk of falling." [Vestibular dysfunction is also common in FM patients, and must be considered. DJS]
Southwick, S. M., C. A. Morgan 3rd, D. S. Charney and J. R. High. 1999. Yohimbine use in a natural setting: effects on posttraumatic stress disorder. Biol
Sowers, J. R. and B. Draznin. 1998. Insulin, cation metabolism and insulin resistance. J
Basic Clin Physiol Pharmacol 9(2-4):223-33.
Soyupek F, Guney M, Kaplan O et al. 2013. Is fibromyalgia syndrome common in the patients with primary dysmenorrhea? J Musculoskel Pain 21(2):156-160. Fibromyalgia was more frequent in primary dysmenorrhea patients, especially symptomatic ones. [These patients were not checked for co-existing chronic myofascial pain. Since trigger points can cause dysmenorrhea and drive FM central sensitization, these patients may have had primary myofascial pain due to trigger points that caused the dysmenorrhea and subsequently, the FM. DJS]
Soyupek F, Soyupek S, Akkus S et al. 2007. The
coexistence of the fibromyalgia syndrome and the overactive bladder
syndrome. J Musculoskel Pain 15(3):31-37. “Our findings
suggest that there is an association between OBS and FMS, especially in
female patients.” The authors remind readers that both FM and OBS are
Soyupek F, Yildiz S, Akkus S et al. 2010. The frequency of fibromyalgia syndrome in patients with polycystic ovary syndrome. J Musculoskel Pain 18(2):120-126. This interesting article reports that 32% of FM patients in the study had polycystic ovary syndrome (PCOS). Only 7.7% of the healthy controls had PCOS. Insulin resistance is a common co-existing condition in FM patients, and PCOS is common in insulin resistance. It would be most interesting to learn what percentage of these patients also had insulin resistance. It is suspected that FM and insulin resistance are interactive diagnoses. DJS]
Spaeth M, Alegre C, Perrot S et al. 2013. Long-term tolerability and maintenance of therapeutic response to sodium oxybate in an open-label extension study in patients with fibromyalgia. Arthritis Res Ther. 15(6):R185. "The long-term safety and therapeutic response of sodium oxybate (SXB) in fibromyalgia syndrome (FM) patients were assessed for a combined period of up to 1 year in a prospective, multicenter, open-label, extension study in patients completing 1 of 2 phase 3 randomized, double-blind, controlled, 14-week trials that examined the efficacy and safety of SXB 4.5 g, SXB 6 g, and placebo for treatment of FM….Maintenance of SXB therapeutic response was demonstrated with continued improvement from controlled-study baseline in pain VAS, Fibromyalgia Impact Questionnaire (FIQ) total scores, and other measures. Responder analyses showed that 68.8% of patients achieved ≥ 30% reduction in pain VAS and 69.7% achieved ≥ 30% reduction in FIQ total score at study endpoint….The long-term safety profile of SXB in FM patients was similar to that in the previously reported controlled clinical trials. Improvement in pain and other FM clinical domains was maintained during long-term use."
Spaeth M. 2011. [Fibromyalgia]. Z Rheumatol. 70(7):573-587. [German]. "Although chronic musculoskeletal pain represents the main symptom of fibromyalgia, those affected usually experience many and various accompanying symptoms of differing frequency and extent. While symptoms such as non-restful sleep, daytime fatigue, impaired memory and concentration, morning stiffness, as well as digestive and urination disorders help to establish the diagnosis, they represent a particular disease burden on patients, those around them and on the social system. Pathogenetic research is focused increasingly on a central dysregulation in pain perception and pain processing, leading to the concept of 'central sensitization' as a final common pathway for fibromyalgia and similar syndromes. This supports the recommendations for prompt multimodal therapy based on pharmaco-, functional and behavioral therapy."
Spaeth M. 2010. Fibromyalgia syndrome treatment from a multidimensional perspective. J Musculoskel Pain. 18(4):373-379. "Fibromyalgia syndrome (FMS) is a pain syndrome which is not due to tissue damage or inflammation, and is thus fundamentally different from rheumatic disorders and many other pain conditions. Presenting as a 'prototype' of a 'central pain' disease, FMS widespread pain is often associated with a wide range of other symptoms such as sleep disturbance, fatigue, cognitive disturbance, stiffness, and depressive symptoms. The underlying mechanisms involved in the development of central sensitization both explain the clinical variety of symptoms (heterogeneity) and provide targets for pharmacologic and nonpharmacologic treatment strategies." "Nonpharmacologic therapies include education, exercise, cognitive behavioral therapy, and other multidimensional therapeutic approaches. These should enable the patient to develop his or her own disease management strategies, in which drugs can be incorporated. Pharmacologic treatment targets several mechanisms involved in the development of central sensitization." "The role of nonrestorative, unrefreshing sleep has been underestimated for many years. Recently, clinical trials have been published, emphasizing the important role of improved sleep quality. There was significant benefit on many disease domains by giving sodium oxybate. The complex symptomatology of FMS will continue to require a multidisciplinary approach including education and exercise, in addition to drug therapy to achieve the most efficient management of FMS, thus indicating a strong need for further and more extended studies targeting the benefits from using combinations of pharmacologic and nonpharmacologic treatments….Comorbid mood and anxiety disorders have often led to the misconception that FMS is a pure psychiatric illness. Now there is increasing evidence that FMS subgroups exist, presenting with a broad variety of different comorbidities and a varying extent of these comorbidities." "There is increasing evidence that nonrestorative sleep and its influence on peripheral functions promote hyperalgesia, fatigue and bodily hypersensitivity….The fragmentation of slow-wave sleep increases sensitivity to pain as well as to nonpainful stimuli such as loud sounds and bright light. Fragmented sleep is a result of periodic arousal disturbances and has been demonstrated in FMS patients using polysomnography; the high index of such arousal disturbances in FMS patients is an indicator of sleep instability and is associated with unrefreshing, less efficient sleep, and is correlated to the severity of clinical symptoms in FMS patients….Neurotransmitter functions and dysfunctions in FMS patients also contribute to hypersensitivity and disordered sleep. Sodium oxybate increases slow-wave sleep decreases alpha intrusions into nonrapid eye movement slow-wave sleep and reduces pain and fatigue associated with FMS. The most recent study with sodium oxybate in FMS could demonstrate significant improvement in a composite score including pain, rated on a visual analog scale, the fibromyalgia impact questionnaire score, and patient global assessment." [It is extremely sad, seeing the evidence supporting the ability of sodium oxybate to provide restorative, refreshing sleep, that the FDA has denied its use for FM patients. The denial was due to admitted fear that it would be abused by patients who might sell it for use as a date-rape drug rather than use it. That is quite a commentary on our focus on the "War on Drugs," which, in this instance, has become a "War on Chronic Pain Patients." They say they need more studies. Perhaps they should read this article. DJS]
Spaeth M. 2009. Epidemiology, costs,
and the economic burden of fibromyalgia. Arthritis Res Ther.
11(3):117. “Despite the differences between healthcare and
sociopolitical systems in various countries, more recent results from
epidemiological research now clearly demonstrate the socioeconomic burden of
fibromyalgia and its comorbidities. The costs of the disease,
calculated in single studies and countries, allow estimates for populations
in other countries. The alarming results highlight the urgent need
both for more research (including pathophysiology and epidemiology) and for
the acceptance of emerging treatment challenges.” [The central
sensitization of fibromyalgia occurs worldwide, and is a significant burden
on the patient and the health care system. Most cases of FM are
preventable. It’s long past time for the medical community to devote
resources to research and vigorous treatment, rather than wasting resources
in denying the existence of FM. DJS]
Spaeth M, Bennett RM, Benson BA et al. 2012. Sodium oxybate therapy provides multidimensional improvement in fibromyalgia: results of an international phase 3 trial. Ann Rheum Dis. [Jan 31 Epub ahead of print]. "Along with pain and fatigue, non-restorative sleep is a core symptom of fibromyalgia." This study of 573 FM patients meeting the 1990 ACR criteria... .."were randomly assigned to placebo, SXB (sodium oxybate) 4.5 g/night or SXB 6 g/night." Assessment included pain, ..."function, sleep quality, effect of sleep on function, fatigue, tenderness, health-related quality of life and subject's impression of change in overall wellbeing....Significant improvements in pain, sleep and other symptoms associated with fibromyalgia were seen in SXB treated subjects compared with placebo....These results, combined with findings from previous phase 2 and 3 studies, provide supportive evidence that SXB therapy affords important benefits across multiple symptoms in subjects with fibromyalgia.
Spaeth M, Rizzi M, Sarzi-Puttini P. 2011. Fibromyalgia and sleep. Best Pract Res Clin Rheumatol. 25(2):227-239. "Chronic pain in fibromyalgia patients, together with its associated symptoms and co-morbidities, is now considered a result of dysregulated mechanisms in the central nervous system (CNS). As fibromyalgia patients often report sleep problems, the physiological processes that normally regulate sleep may be disturbed and overlap with other CNS dysfunctions. Although the mechanisms potentially linking chronic widespread pain, sleep alterations and mood disorders have not yet been proven, polysomnography findings in patients with fibromyalgia and non-restorative sleep and their relationships with clinical symptoms support the hypothesis of a conceptual common mechanism called 'central sensitization'. Food and Drug Administration (FDA)-approved drugs for the treatment of fibromyalgia may benefit sleep, but their label does not include the treatment of fibromyalgia-associated sleep disorders. Non-pharmacological therapies (including a thorough sleep assessment) can be considered in the first-line treatment of non-restorative sleep, although they have not yet been fully investigated in patients with fibromyalgia. Both pharmacological and non-pharmacological treatments should be used cautiously in patients with fibromyalgia, bearing in mind the patients' underlying disorders and the potential interactions of the therapies."
Spaggiari, M. C., F. Granella, L. Parrino, C. Marchesi, I. Melli and M. G. Terzano.
1994. Nocturnal eating syndrome in adults. Sleep 17(4):339-44.
Spath M, Stratz T, Farber L et al. 2004.
Treatment of fibromyalgia with tropisetron — dose and efficacy
correlations. Scand J Rheumatol Suppl (119):63-66.
Tropisetron therapy may need to be tailored to subgroups of FMS
Spath M, Stratz T, Neeck G et al. 2004.
Efficacy and tolerability of intravenous tropisetron in the treatment of
fibromyalgia. Scand J Rheumatol. 33(4):267-270.
Intravenous tropisetron, a 5-HT3 receptor blocker, provided significant
pain relief for the FMS patients in this prospective trial.
M, Neeck G. 2002. [The expert assessment of fibromyalgia.] Z
Rheumatol 61(6):661-6. [German]
Pain amplification syndromes are well documented and have been
researched for a decade. The validity of the reality of fibromyalgia has
no place in an expert assessment. “The sociomedical implications (of
fibromyalgia) are obvious and considerable...” Assessments must be
specific to the individual, focusing on evaluation of specific impairments and
disabilities and how these handicaps affect function.
Sperber, A. D., S. Carmel, Y. Atzmon, I. Weisberg, Y. Shalit, L. Neumann, A. Fich and
D. Buskila. 1999. The sense of coherence index and the irritable bowel syndrome. A
cross-sectional comparison among irritable bowel syndrome patients with and without
coexisting fibromyalgia, irritable bowel syndrome non-patients, and controls. Scand J
Sperber, A. D., Y. Atzmon, L. Neumann, I. Weisberg, Y. Shalit, M. Abu-Shakrah, A. Fich
and D. Buskila. 1999. Fibromyalgia in the irritable bowel syndrome: studies of prevalence
and clinical implications. Am J Gastroenterol 94(12):3541-6.
Sperber AD, Dekel R. 2010. Irritable Bowel Syndrome and Co-morbid Gastrointestinal and Extra-gastrointestinal Functional Syndromes. J Neurogastroenterol Motil. 16(2):113-119. "Many IBS patients have at least one co-morbid somatic complaint and many meet diagnostic criteria for other functional disorders. Patients with IBS and another functional disorder, in comparison with patients with IBS only, have more severe IBS symptoms, a higher rate of psychopathology, greater impairment of quality of life, and more illness-related work absenteeism. Estimates of the prevalence of IBS in patients with fibromyalgia range from 30-35% to as high as 70%. Studies of IBS among patients with chronic fatigue syndrome have reported a prevalence ranging from 35-92%.....It has been suggested that the presence of multiple co-morbid disorders may be a marker for psychological influences on etiology. This raises the question of whether the functional syndromes represent the same pathophysiological process, i.e., are the same entity that has been separated into different clinical entities because of medical sub-specialization, or are indeed separate disorders. While the answer to this question awaits further research, it would appear that most functional patients who meet formal diagnostic criteria for more than one functional disorder manifest one disorder clinically more that the others and seek consultation differentially for that set of symptoms.
Spevak C. 1997. Asystole during
trigger point injections in a patient with panic disorder. Reg
Anesth. 22(6):583. [This article is a vital reminder that TrP
injections can be painful and complex, and that it takes more than a glance
at a TrP diagram to be able to perform them adequately. Patients must be
carefully assessed and pain and anxiety must be brought under control, and
the protocol followed, with the pain and anxiety level kept below danger
level. One must always monitor for symptoms of shock or other severe
reaction and be ready to handle whatever may come. The best
preventative is a well-educated and prepared patient and care provider.
Spiro, H. 1992. What is empathy and can it be taught? Ann Intern Med
Spitzer AR, Boyle JT, Tuchman DN et al. 1984. Awake apnea
associated with gastroesophageal reflux: a specific clinical syndrome.
J Pediatr 104(2):200-205.
Spitzer AR, Broadman M. 2010. Treatment of the narcoleptiform sleep disorder in chronic fatigue syndrome and fibromyalgia with sodium oxybate. Pain Pract. 10(1):54-59. "Sixty percent of patients treated with oxybate experienced significant relief of pain, while 75% experienced significant relief of fatigue. We postulate that the response to oxybate in CFS and FM suggests a disturbance of sleep similar to narcolepsy. These findings support this novel approach to intervention and further research."
Sprott H, Salemi S, Gay RE et al. 2004.
Increased DNA fragmentation and ultrastructural changes in fibromyalgic
muscle fibres. Ann Rheum Dis. 63(3):245-251. This study found
a significantly high rate of DNA fragmentation in FMS patient samples
(55.4%) compared with healthy controls (4.1%). Myofibers and actin
filaments were disorganized, and the number of mitochondria were
significantly lower in FMS patients.
Sprott, H., L. A. Bradley, S. J. Oh, W. Wintersberger, G. S. Alarcon, H. G. Mussell, A.
Tseng, R. E. Gay and S. Gay. 1998. Immunohistochemical and molecular studies of serotonin,
substance P., galanin, pituitary adenylyl cyclase-activating polypeptide, and
secretoneurin in fibromyalgia to muscle tissue. Arthritis Rheum 41(9):1689-94.
Sprott, H., A. Muller and H. Hartmut. 1997. Collagen crosslinks in fibromyalgia.
Srbely JZ, Dickey JP, Bent LR et al. 2009.
Capsaicin-induced central sensitization evokes segmental increases in
trigger point sensitivity in humans. J Pain. [Dec 14 Epub ahead
of print] “This study investigated whether inducing central
sensitization evokes segmental increases in trigger point pressure
sensitivity.” “These results demonstrate that increases in central
sensitization evoke increases in trigger point pressure sensitivity in
segmentally related muscles.” “Myofascial pain is the most common form
of musculoskeletal pain. Myofascial trigger points play an important
role in the clinical manifestation of myofascial pain syndrome.
Elucidating the role of central sensitization in the pathophysiology of
trigger points is fundamental to developing optimal strategies in the
management of myofascial pain syndrome.”
Srbely JZ, Dickey JP. 2007. Randomized
controlled study of the anti-nociceptive effect of ultrasound on trigger
point sensitivity: novel applications in myofascial therapy? Clin
Rehabil. 21(5):411-417. “Ultrasound may be a useful clinical
tool for the treatment and management of trigger points and myofascial pain
Srbely JZ, Dickey JP, Lee D et al. 2010. Dry needle stimulation of myofascial trigger points evokes segmental anti-nociceptive effects. J Rehabil Med. 42(5):463-468. "One intervention of dry needle stimulation to a single trigger point (sensitive locus) evokes short-term segmental anti-nociceptive effects. These results suggest that trigger point (sensitive locus) stimulation may evoke anti-nociceptive effects by modulating segmental mechanisms, which may be an important consideration in the management of myofascial pain."
Srbely JZ, Vernon H, Lee D et al. 2013. Immediate effects of spinal manipulative therapy on regional antinociceptive effect in myofascial tissues in healthy young adults. J Manipulative Physiol Ther. 36(6):333-341. This study had as its participants healthy students from Guelph University with identifiable (assumedly latent) trigger points in the infraspinatus and gluteus medius myofascia. They tested the effects on pain sensitivity in these muscles after one single high-velocity, low amplitude rotary spinal thrust spinal manipulative therapy on the C5-C6. The treatment resulted in short-term increases in pain sensitivity in the muscles tested. This did not occur in students in a control group who received sham treatment. [The effects on pain sensitivity in the buttocks and shoulder after a chiropractic technique performed on the spinal area of the neck (in healthy students who probably had latent trigger points) are interesting. I'd like to see a study with comparison of Activator and manual techniques compared, using patients with active trigger points in the same muscles, including patients who have central sensitization. DJS]
Srdic, F., Sarhus, M., Topuz, O.
2002. Comparisons of two different techniques of electrotherapy on
myofascial pain. J Back Musculoskel Rehab 16:11-16.
Electrotherapy can be useful to treat myofascial pain.
Srikuea R, Symons TB, Long DE et al. 2012. Fibromyalgia is associated with altered skeletal muscle characteristics which may contribute to post-exertional fatigue in post-menopausal women. Arthritis Rheum. [Nov 1 Epub ahead of print]. "Peripheral mechanisms i.e. altered muscle fiber size distribution and decreased capillary density may contribute to post-exertional fatigue in subjects with FM. Understanding these defects in fibromyalgic muscle may provide valuable insight for treatment." [The authors of this study from Thailand may have been looking at co-existing myofascial trigger points. DJS]
Srinivasan AK, Kaye JD, Moldwin R. 2007. Myofascial dysfunction
associated with chronic pelvic floor pain: management strategies.
Curr Pain Headache Rep. 11(5):359-364.
Staedt, J., H. Hunerjager, E. Ruther and G. Stoppe. 1998. Pergolide: treatment of
choice in restless legs syndrome (RLS) and nocturnal myoclonus syndrome (NMS). Long term
follow up on pergolide. Short communication. J Neural Transm 105(2-3):265-8.
Staedt, J., G. Stoppe, A. Kogler, H. Riemann, G. Hajak, D. L. Munz, D. emrich and E.
Ruther. 1995. Nocturnal myoclonus syndrome (periodic movements in sleep) related to
central dopamine D2-receptor alteration. Eur Arch Psychiatry Clin Neurosci
Stahl SM, Briley M. 2009. Why
psychiatrists should not ignore pain in their patients – focus on
fibromyalgia? Hum Psychopharmacol. 24 Suppl 1:S1-2.
St. Amand, R. Paul and Claudia C. Marek. 1999. What Your Doctor May Not Tell You
About Fibromyalgia. Warner Books: New York.
Stair S., K. Carlson, S. Shuster et
al. 2002. Mystixin peptides reduce hyaluran deposition and edema formation.
Eur J Pharmacol 450(3):291.
Stamer UM, Bayerer B, Stuber F. 2005.
Genetics and variability in opioid response. Eur J Pain.
9(2):101-104. “In pain therapy, the genetic background influencing
the efficacy of opioid therapy is of special interest. CYP2D6
genetic variability is supposed to be a major factor of adverse drug
reaction, possibly influencing hospital stay and total costs.
Further candidate genes involved in pain perception, pain processing and
pain management like opioid receptors, transporters and other targets of
pharmacotherapy are under investigation. Aspects of genetic
differences influencing efficacy, side effects and adverse outcome of
pharmacotherapy will be of importance for future pain management.”
Stander S, Schmelz M. 2006. Chronic itch
and pain – similarities and differences. Eur J Pain
[May 4 Epub ahead of print] “Classical inflammatory mediators such
as bradykinin have been shown to sensitize nociceptors for both itch
and pain. Also regulation of gene expression induced by
trophic factors, such as NGF, plays a major role in persistently
increased neuronal sensitivity for itch and pain. Finally,
itch and pain exhibit corresponding patterns of central
S, Steinhoff M, Schmetz M et al. 2003. Neurophysiology of pruitis:
cutaneous elicitation of itch. Arch Dermatol 139(11):1463-1470.
This article is important because it indirectly explains how itch can
be a manifestation of both fibromyalgia and/or myofascial pain. It
covers receptor systems, itch generation by both peripheral and central
nervous systems, as well as mechanical, chemical (including biochemical)
triggers. This paper may be of help in documenting itch associations with
the above-mentioned conditions.
Stark, F. M. and H. M. Sobetzko. 1999. Approaches to coping with chronic fatigue
syndrome. Zentralbl Hyg Umweltmed 202(2-4):179-90.
Starlanyl DJ. 2006. Comment on Canadian consensus
document on fibromyalgia syndrome. J Musculoskel Pain.
14(4):75-81. In the original document, there seemed to be confusion between
symptoms due to FMS and those that were due to co-existing myofascial TrPs.
This offers clarifications.
Starlanyl DJ, Jeffrey JL, Roentsch G, Taylor-Olson C.
The effect of transdermal
T3 (3,3,5-triiodothyronine) on geloid masses found in patients with both
fibromyalgia and myofascial pain: double-blinded, N of 1 clinical study.
review Aug 15, 2001.]
Starlanyl, D. Tai Chi Chuan and Musculoskeletal Pain.
Tai Chi Magazine. [Accepted for publication July 2001.]
Starlanyl DJ and Jeffrey JL. 2001.
The presence of geloid masses in a patient with both
fibromyalgia and chronic myofascial pain. Phys Ther Case Rep 4(1):22-31.
Starlanyl D. J. and M. E. Copeland. 2001. Fibromyalgia and Chronic Myofascial Pain:
A Survival Manual. Edition 2. Oakland: New Harbinger Publications.
Starlanyl DJ. 1999. The Fibromyalgia Advocate. Oakland: New Harbinger
Starlanyl D J 1997. Chronic Myofascial Pain Syndrome: A Guide to the Trigger Points.
Oakland: New Harbinger. 2 hour video.
Starlanyl DJ. 1997. Fibromyalgia and Myofascial Pain Syndrome: A Special Challenge. Clin
Bull Myofas Ther 2 (2/3): 75-89.
Starlanyl DJ. 1995. "Comment on Granges and Littlejohn's. "Prevalence of
myofascial pain syndrome in fibromyalgia and regional pain syndrome: A comparative
study." J Musculoskel Pain 3 (1):129-132.
Starlanyl DJ 1994. "Comment on article by Hong, Chen, Pon and Yu,
"Intermediate effects of various physical medicine modalities on pain threshold of an
active myofascial trigger point." J Musculoskel Pain 2 (2):141-142.
Staud R. 2012. Peripheral and Central Mechanisms of Fatigue in Inflammatory and Noninflammatory Rheumatic Diseases. Curr Rheumatol Rep. [Jul 17 Epub ahead of print].
"Whereas many studies have focused on disease activity as a correlate to these patients' fatigue, it has become apparent that other factors, including negative affect and pain, are some of the most powerful predictors for fatigue. Conversely, sleep problems, including insomnia, seem to be less important for fatigue. There are several effective treatment strategies available for fatigued patients with rheumatologic disorders, including pharmacological and nonpharmacological therapies."
Staud R. 2011. Evidence for Shared Pain Mechanisms in Osteoarthritis, Low Back Pain, and Fibromyalgia. Curr Rheumatol Rep. [Aug 11 Epub ahead of print]. "Osteoarthritis (OA), low back pain (LBP), and fibromyalgia (FM) are common chronic pain disorders that occur frequently in the general population. They are a significant cause of dysfunction and disability. Why some of these chronic pain disorders remain localized to few body areas (OA and LBP), whereas others become widespread (FM), is unclear at this time. Genetic, environmental, and psychosocial factors likely play an important role...... Ineffective endogenous pain control and central sensitization are important features of OA, LBP, and FM patients."
Staud R. 2011. Sodium oxybate for the treatment of fibromyalgia. Expert Opin Pharmacother. [Jun 16 Epub ahead of print]. "Introduction: Gamma-hydroxybutyrate (GHB) is a short-chain fatty acid that is synthesized within the CNS, mostly from its parent compound gamma amino butyric acid (GABA). GHB acts as a neuromodulator/neurotransmitter to affect neuronal activity of other neurotransmitters and so, stimulate the release of growth hormone. Its sodium salt (sodium oxybate: SXB) was approved by the Food and Drug Administration (FDA) for the treatment of narcolepsy. SXB has shown to improve disrupted sleep and increase NR3 (slow-wave restorative) sleep in patients with narcolepsy. It is rapidly absorbed and has a plasma half-life of 30 - 60 min, necessitating twice-nightly dosing. Most of the observed effects of SXB result from binding to GABA-B receptors. Areas covered: Several randomized, controlled trials demonstrated significantly improved fibromyalgia (FM) symptoms with SXB. As seen in narcolepsy trials, SXB improved sleep of FM patients, increased slow-wave sleep duration as well as delta power, and reduced frequent night-time awakenings. Furthermore, FM pain and fatigue was consistently reduced with nightly SXB over time. Commonly reported adverse events included headache, nausea, dizziness and somnolence. Despite its proven efficacy, SXB did not receive FDA approval for the management of FM in 2010, mostly because of concerns about abuse. Expert opinion: Insomnia, fatigue and pain are important clinical FM symptoms that showed moderate improvements with SXB in several large, well-designed clinical trials. Because of the limited efficacy of currently available FM drugs additional treatment options are needed. In particular, drugs like SXB - which belong to a different drug class than other Food and Drug Administration (FDA)-approved FM medications such as pregabalin, duloxetine and milnacipran - would provide a much-needed addition to presently available treatment options. However, the FDA has set the bar high for future SXB re-submissions, with requirements of superior efficacy and improved risk mitigation strategies. At this time, no future FDA submission of SXB for the fibromyalgia indication is planned."
Staud R. 2011. Peripheral pain mechanisms in chronic widespread pain. Best Pract Res Clin Rheumatol. 25(2):155-164. "Clinical symptoms of chronic widespread pain (CWP) conditions like fibromyalgia (FM), include pain, stiffness, subjective weakness, and muscle fatigue. Muscle pain in CWP is usually described as fluctuating and often associated with local or generalized tenderness (hyperalgesia and/or allodynia). This tenderness related to muscle pain depends on increased peripheral and/or central nervous system responsiveness to peripheral stimuli, which can be either noxious (hyperalgesia) or non-noxious (allodynia). For example, patients with muscle hyperalgesia will rate painful muscle stimuli higher than normal controls, whereas patients with allodynia may perceive light touch as painful, something that a 'normal' individual will never describe as painful. The pathogenesis of such peripheral and/or central nervous system changes in CWP is unclear, but peripheral soft tissue changes have been implicated. Indirect evidence from interventions that attenuate tonic peripheral nociceptive impulses in patients with CWP syndromes like FM suggest that overall FM pain is dependent on peripheral input. More importantly, allodynia and hyperalgesia can be improved or abolished by removal of peripheral impulse input. Another potential mechanism for CWP pain is central disinhibition. However, this pain mechanism also depends on tonic impulse input, even if only inadequately inhibited. Thus, a promising approach to understanding CWP is to determine whether abnormal activity of receptors in deep tissues is fundamental to the development and maintenance of this chronic pain disorder.....Most CWP patients present with focal tissue abnormalities including myofascial trigger points, ligamentous trigger points or osteoarthritis of the joints and spine. While not predictive for the development of CWP, these changes nevertheless represent important pain generators that may initiate or perpetuate chronic pain. Local chemical mediators, including lactic acid, adenosine triphosphate (ATP) and cytokines, seem to play an important role in sensitizing deep tissue nociceptors of CWP patients. Thus, the combination of peripheral impulse input and increased central pain sensitivity may be responsible for widespread chronic pain disorders including FM."
Staud R. 2010. Is It All Central Sensitization? Role of Peripheral Tissue Nociception in Chronic Musculoskeletal Pain. Curr Rheumatol Rep. [Sep 30 Epub ahead of print].
"Fibromyalgia syndrome (FM) is a highly prevalent musculoskeletal disorder that is often accompanied by somatic hyperalgesia (enhanced pain from noxious stimuli). Neural mechanisms of somatic hyperalgesia have been analyzed via quantitative sensory testing of FM patients. Results of these studies suggest that FM pain is associated with widespread primary and secondary cutaneous hyperalgesia, which are dynamically maintained by tonic impulse input from deep tissues and likely by brain-to-spinal cord facilitation. Enhanced somatic pains are accompanied by mechanical hyperalgesia and allodynia in FM patients as compared with healthy controls. FM pain is likely to be at least partially maintained by peripheral impulse input from deep tissues. This conclusion is supported by results of several studies showing that injection of local anesthetics into painful muscles normalizes somatic hyperalgesia in FM patients." [This work agrees with the research showing the FM patients have TrPs, and that TrP-pain generation is a common factor sustaining central sensitization. DJS]
Staud R. 2008. Heart rate variability as a
biomarker of fibromyalgia syndrome. Fut Rheumatol.
3(5):475-483. “HRV (heart rate variability) has been shown to correlate with
FM pain and is sensitive to change; in particular, pain related to physical
and mental stressors. Thus, ANS (autonomic nervous system) dysfunction
as assessed by HRV analysis may serve as a useful biomarker, and may become
part of future FM diagnostic criteria and serve as a surrogate end point in
Staud R. 2010. Pharmacological treatment
of fibromyalgia syndrome: new developments. Drugs.
70(1):1-14. “Duloxetine and milnacipran, two highly selective
serotonin-norepinephrine (noradrenaline) reuptake inhibitors, and the
alpha(2)delta agonist pregabalin have been approved by the US FDA for
the treatment of fibromyalgia symptoms. In general, about half of
all treated patients seem to experience a 30% reduction of symptoms,
suggesting that many patients with fibromyalgia will require additional
therapies. Thus, other forms of treatment, including exercise,
cognitive behavioral therapies and self-management strategies, may be
necessary to achieve satisfactory treatment outcomes. Despite
promising results of pilot trials, RCTs (randomized controlled trials)
with dopamine receptor agonists and sodium channel antagonists have so
far been disappointing for patients with fibromyalgia. However,
new pharmacological approaches for the treatment of fibromyalgia pain
and insomnia using sodium oxybate appear to be promising.”
Staud R. 2009. Abnormal pain
modulation in patients with spatially distributed chronic pain:
fibromyalgia. Rheum Dis Clin North Am. 35(2):263-274.
“Many chronic pain syndromes are associated with hypersensitivity to
painful stimuli and with reduced endogenous pain inhibition. These
findings suggest that modulation of pain-related information may be
linked to the onset or maintenance of chronic pain. The
combination of heightened pain sensitivity and reduced pain inhibition
seems to predispose individuals to greater risk for increased acute
clinical pain. It is unknown whether such pain processing
abnormalities may also place individuals at increased risk for chronic
Staud R. 2007.
Mechanisms of acupuncture analgesia: effective therapy for musculoskeletal
pain? Curr Rheumatol Rep. 9(6):473-481. Acupuncture relief
may take some time “...to develop and resolve." “…some forms of AP are
more effective for providing analgesia than others.” Particularly,
electro-AP seems best to activate powerful opioids and non-opioid analgesic
Staud R. 2007. The role of peripheral input
for chronic pain syndromes like fibromyalgia. J Musculoskel Pain
15 (Supp 13):7 item 8. [Myopain 2007 Poster] Indications are
that the diffuse, bodywide pain of FM is maintained by peripheral pain
stimuli. “Most FMS patients present with focal tissue abnormalities
including myofascial trigger points [TrPs], ligamentous trigger points, or
osteoarthritis of the joints and spine. While not predictive for the
development of FMS, these changes nevertheless represent important pain
generators that may initiate or perpetuate chronic pain. Thus
spatially limited forms of musculoskeletal pain, including MPS, may develop
in some patients into widespread chronic pain syndromes like FMS.”
Staud R. 2006. Biology and therapy of
fibromyalgia: pain in fibromyalgia syndrome. Arthritis Res
Ther. 8(3):208 “Many recent studies have emphasized the role of
central nervous system pain processing abnormalities in FM,
including central sensitization and inadequate pain inhibition.
However, 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. “Importantly, after central
sensitization has been established only minimal nociceptive input is
required for the maintenance of the chronic pain state.”
Staud R. 2004. Fibromyalgia pain: do we know the source?
Curr Opin Rheumatol 16(2):157-63. This review brings together studies that show that the mechanism behind FMS may be biochemicals released due to acute or repetitive injury (traumatic or biochemical) “...may be responsible for long-term activation of spinal cord glia and dorsal horn neurons, thus resulting in central sensitization.”
This conceptual understanding may aid us in discovering more effective therapies and treatment strategies in the future.
It is also an important step in defining the mechanism of FMS, and this may lead to a change in classification from syndrome to
Staud R. 2004. Predictors of
clinical pain intensity in patients with fibromyalgia syndrome. Curr
Rheumatol Rep. 6(4):281-286. “The magnitude of wind-up
after-sensations appeared to be one of the best predictors for clinical
pain intensity of fibromyalgia syndrome patients (27%).”
Staud R. 2002. Evidence
of involvement of central neural mechanisms in generating
fibromyalgia pain. Curr Rheumatol Rep 4(4):299-305. "Fibromyalgia
syndrome (FMS) is characterized by widespread pain, fatigue, sleep
abnormalities, and distress. Abnormal temporal summation of
second pain (wind-up) and central sensitization have been
described recently in patients with FMS. Wind-up and central
sensitization, which rely on activation of nocicepto-specific
neurons and wide dynamic range neurons in the dorsal horn of the
spinal cord. Other abnormal central pain mechanisms recently
detected in patients with FMS include diffuse noxious inhibitory
controls. These pain inhibitory mechanisms rely on spinal cord
and supraspinal systems involving pain facilitatory and pain
inhibitory pathways. Brain-imaging techniques that can detect
neuronal activation after nociceptive stimuli have provided
additional evidence for abnormal central pain mechanism in FMS.
Brain images have corroborated the augmented reported pain
experience of patients with fibromyalgia during experimental pain
stimuli. In addition, thalamic activity, which contributes
significantly to pain processing, was decreased in fibromyalgia.
However, central pain mechanisms of fibromyalgia may not depend
exclusively on neuronal activation. Neuroglial activation has
been found to play an important role in the induction and
maintenance of chronic pain."
Staud R, Cannon RC, Mauderli AP et al.
2003. Temporal summation of pain from mechanical
stimulation of muscle tissue in normal controls and subjects
with fibromyalgia syndrome. Pain
102(1-2):87-95. “Temporal summation for FMS subjects
occurred at substantially lower forces and at a lower
frequency of stimulation. Furthermore, painful
after-sensations were greater in amplitude and more
prolonged for FMS subjects.” “Abnormal input from muscle
nociceptors appears to underlie production of central
sensitization in FMS that generalizes to input from
Staud R, Koo E, Robinson ME et al. 2007.
Spatial summation of mechanically evoked muscle pain and painful
aftersensations in normal subjects and fibromyalgia patients. Pain.
[Apr 23 Epub ahead of print]. “…decreasing pain in some muscle areas by
local anesthetics or other means may improve overall clinical pain of FM
patients.” [This is another indication that control of peripheral pain
stimuli such as caused by myofascial trigger points and arthritis can be a
significant part of chronic pain treatment in FM. DJS]
Staud R, Nagel S, Robinson ME et al. 2009.
Enhanced central pain processing of fibromyalgia patients is maintained by
muscle afferent input: a randomized, double-blind, placebo-controlled study.
Pain. [Jun 18 Epub ahead of print]. “Lidocaine injections
increased local pain thresholds and decreased remote secondary heat
hyperalgesia in FM patients, emphasizing the important role of peripheral
impulse input in maintaining central sensitization in this chronic pain
syndrome; similar to other persistent pain conditions such as irritable
bowel syndrome and complex regional pain syndrome.” [This is yet another
study showing that peripheral pain sensations such as those caused by
myofascial TrPs are sufficient to maintain the central sensitization state
of FM and may be important to maintaining other chronic conditions. DJS]
Staud R, Price DD, Robinson ME et al. 2004.
Body pain area and pain-related negative affect predict clinical
pain intensity in patients with fibromyalgia. J Pain
5(6):338-343. “The number of painful body areas obtained by
body pain diagrams is a better predictor of clinical pain
intensity than TPS in FM patients.” [It would be helpful
if these patients were checked for co-existing myofascial TrPs.
It could be that the presence of co-existing myofascial TrPs is
the better predictor of clinical pain intensity. DJS]
Staud R, Price DD, Robinson ME et al. 2004. Body pain area and
pain-related negative affect predict clinical pain intensity in
patients with fibromyalgia. J Pain 5(6):338-343. The
combination of charts showing painful body areas, tender point
counts, and pain-related negative emotions gave a much more accurate
representation of pain intensity in FMS patients than did simple
counting of tender points.
Staud R, Price DD, Robinson ME et
al. 2004. Maintenance of windup of second pain requires less frequent
stimulation in fibromyalgia patients compared to normal controls.
Pain 110(3):689-696. “Unlike NC (normal control) subjects, FM
subjects showed enhanced second pain during WU-M (wind-up maintenance)
stimuli at very low stimulus frequencies, indicating central
sensitization. Increased WU sensitivity, enhanced WU-M, and increased
WU-related aftersensations help account for persistent pain conditions
in FM subjects.” [Patients with FMS may respond to lower stimuli
to maintain a state of central sensitization. Myofascial trigger points
that would not cause central sensitization in healthy individuals may be
sufficient to maintain central sensitization in patients with FMS. DJS]
Staud R, Robinson ME, Goldman CT et al. 2011. Attenuation of experimental pain by vibro-tactile stimulation in patients with chronic local or widespread musculoskeletal pain. Eur J Pain. [Feb 19 Epub ahead of print]. "One form of endogenous pain inhibition, diffuse noxious inhibitory controls (DNIC), has been found to be abnormal in some chronic pain patients and evidence exists for deficient spatial summation of pain, specifically in FM. Similar findings have been reported in patients with localized musculoskeletal pain (LMP) disorders, like neck and back pain. Whereas DNIC reduces pain through activation of nociceptive afferents, vibro-tactile pain inhibition involves innocuous A-beta fiber.....To assess endogenous analgesic mechanisms of study subjects, vibro-tactile conditioning stimuli were simultaneously applied with test stimuli either homotopically or heterotopically. Additionally, the effect of distraction on experimental pain was assessed. Homotopic vibro-tactile stimulation resulted in 40% heat pain reductions in all subject groups.....Conclusions: Vibro-tactile stimulation effectively recruited analgesic mechanisms not only in NC (normal pain-free controls) but also in patients with chronic musculoskeletal pain, including FM. Distraction did not seem to contribute to this analgesic effect."
Staud R, Robinson ME, Price DD. 2007. Temporal
summation of second pain and its maintenance are useful for characterizing
widespread central sensitization of fibromyalgia patients. J Pain.
[Aug 1 Epub ahead of print]. “Perspective: The pain of FM seems to be
accompanied by generalized central sensitization, involving the length of
the spinal neuroaxis. Thus, widespread central sensitization appears
to be a hallmark of FM and may be useful for the clinical case definition of
this prevalent pain syndrome. In addition, measures of widespread
central sensitization, like TSSP-M (temporal summation of second pain and
maintenance), could also be used to assess treatment responses of FM
Staud R, Robinson ME, Weyl EE et al. 2010.
Pain variability in fibromyalgia is related to activity and rest: role
of peripheral tissue impulse input. J Pain. [May 6 Epub ahead of
print]. “FM is a pain-amplification syndrome that depends at least in
part on peripheral tissue impulse input. Whereas muscle activity
increased overall pain, short rest periods produced analgesic effects.”
[This indicates that in cases of FM, short rest periods may enable us to
accomplish some activities. This agrees with Travell and Simons’
recommendations for myofascial trigger points, which often cause the
peripheral pain stimuli maintaining FM central sensitization. We must
remember to rest every 20 minutes, or whatever our time limit is for
each task. DJS]
Staud R, Smitherman
ML. 2002. Peripheral and central sensitization in fibromyalgia:
pathogenetic role. Curr Pain Headache Rep 6(4):259-66. "Patients
with fibromyalgia show psychophysical evidence of mechanical,
thermal and electrical hyperalgesia. Peripheral and central
abnormalities of nociception have been described in fibromyalgia.
Important nociceptor systems in the skin and muscles seem to
undergo profound changes..." "These include sensitization of
vanilloid receptor, acid-sensing ion channel receptors, and purino-receptors.
Tissue mediators of inflammation and nerve growth channel
receptors can excite these receptors and cause extensive change in
pain sensitivity, but patients with fibromyalgia lack consistent
evidence for inflammatory soft tissue abnormalities."
Staud R, Vierck CJ, Robinson ME et al. 2006.
Overall fibromyalgia pain is predicted by ratings of local pain and
pain-related negative affect – possible role of peripheral tissues.
Rheumatology (Oxford) [Apr 18 Epub ahead of print] “We
hypothesized that the overall clinical pain is largely determined by
the pain intensity of local body areas. Thus, we assessed the
role of local body pains as predictors of overall clinical pain in
FM patients.” “Peripheral factors (maximal/average local pain and
number of painful body areas) predicted most of the variance of
overall clinical FM pain, suggesting that the input of pain by the
peripheral tissues is clinically relevant. About 19% of the
pain variance was predicted by PRNA. Thus, peripheral pain and
negative affect appear to be particularly relevant for overall FM
pain and may represent important targets for future therapies.”
Staud R, Vierck CJ,
Robinson ME et al. 2005. Effects of the N-Methyl-D-Aspartate receptor
antagonist Dextromethorphan on temporal summation of pain are similar in
fibromyalgia patients and normal control subjects. Jour Pain
Staud R, Weyl EE, Bartley E et al. 2013. Analgesic and anti-hyperalgesic effects of muscle injections with lidocaine or saline in patients with fibromyalgia syndrome. Eur J Pain. [Nov 5 Epub ahead of print.] This double-blind controlled study of 62 women with fibromyalgia utilized injection into trapezius and gluteal trigger points with either saline or lidocaine. The results indicate that injection of peripheral trigger point pain generators can reliably and significantly reduce clinical fibromyalgia pain. This research strongly suggests that, at least in women, it is the input from peripheral pain generators such as trigger points that maintain the mechanical and heat hyperalgesia of fibromyalgia. "…effects of muscle injections on hyperalgesia were greater for lidocaine than saline; the effects on clinical pain were similar for both injectates."
Staud R, Weyl EE, Price DD et al. 2012. Mechanical and Heat Hyperalgesia Highly Predict Clinical Pain Intensity in Patients with Chronic Musculoskeletal Pain Syndromes. J Pain. [Jun 26 Epub ahead of print]. "Multiple abnormalities in pain processing have been reported in patients with chronic musculoskeletal pain syndromes. These changes include mechanical and thermal hyperalgesia, decreased thresholds to mechanical and thermal stimuli (allodynia), and central sensitization, all of which are fundamental to the generation of clinical pain.....we hypothesized that quantitative sensory tests may provide useful predictors of clinical pain intensity of such patients..... Using either heat or pressure pain ratings as well as tender point counts and negative affect as predictors, up to 49.4% of the patients' variance of clinical pain intensity could be estimated....Simple tests of mechanical and heat hyperalgesia can predict large proportions of the variance in clinical pain intensity of chronic musculoskeletal pain patients and thus are feasible to be included in clinical practice and clinical trials."
Stearns, V., C. Isaacs, J. Rowland, J. Crawford, M. J. Ellis, R. Kramer, W. Lawrence,
J. J. Hanfelt and D. F. Hayes. 2000. A pilot trial assessing the efficacy of paroxetine
hydrochloride(Paxil) in controlling hot flashes in breast cancer survivors. Ann Oncol
Stecco A, Gesi M, Stecco C et al. 2013. Fascial components of the myofascial pain syndrome. Curr Pain Headache Rep. 17(8):352. "Myofascial pain syndrome (MPS) is described as the muscle, sensory, motor, and autonomic nervous system symptoms caused by stimulation of myofascial trigger points (MTP). The participation of fascia in this syndrome has often been neglected. Several manual and physical approaches have been proposed to improve myofascial function after traumatic injuries, but the processes that induce pathological modifications of myofascial tissue after trauma remain unclear. Alterations in collagen fiber composition, in fibroblasts or in extracellular matrix composition have been postulated. We summarize here recent developments in the biology of fascia, and in particular, its associated hyaluronan (HA)-rich matrix that address the issue of MPS."
Stecco A, Stecco C, Macchi V et al. 2011. RMI study and clinical correlations of ankle retinacula damage and outcomes of ankle sprain. Surg Radiol Anat. [Feb 9 Epub ahead of print]. Alterations shown by MRI in ankle retinacula from trauma or chronic ankle instability corresponds to proprioceptive damage noted by photography and clinical exam. This indicates that the ankle reticulinum are not passive stabilizers but also involved in proprioceptive function. Deep massage of the ankle retinacula alleviated these symptoms. The authors state that adaptive fibrosis may develop as a consequence of unremitting non-physiological tension in a fascial segment. The deep friction massage changes the nature of the ground substance, restoring glide. They believe this to be due to changes in the myofascia rather than to bones or ligaments. [Correspondence with the authors revealed that they also have found trigger points in retinacula. DJS]
Stecco C, Gagey O, Belloni A et al. 2007. Anatomy of the deep fascia of the upper limb. Second part: study of innervation. Morphologie 91(292):38-43. This study indicates that the flexor retinaculum has more proprioceptive functions, whereas the tendons were primarily mechanical in function. "…the fascia is a membrane that extends throughout the whole body and numerous muscular expansions maintain it in a basal tension. During a muscular contraction these expansions could also transmit the effect of the stretch to a specific area of the fascia, stimulating the proprioceptors in that area."
Stecco C, Macchi V, Porzionato A et al. 2010. The ankle retinacula: morphological evidence of the proprioceptive role of the fascial system. Cells Tissues Organs 192(3):200-210. "The retinacula are not static structures for joint stabilization, like the ligaments, but a specialization of the fascia for local spatial proprioception of the movements of the foot and ankle. Their anatomical variations and accessory bundles may be viewed as morphological evidence of the integrative role of the fascial system in peripheral control of articular motility."
Stecco C, Stern R, Prozionato A et al. 2011. Hyaluronan within fascia in the etiology of myofascial pain. Surg Radiol Anat 33(10):891-896. This study focused on hyaluronic acid in the fascial layers. "The HA within the deep fascia facilitates the free sliding of two adjacent fibrous fascial layers, thus promoting the normal function associated with the deep fascia. If the HA assumes a more packed confirmation, or more generally, if the loose connective tissue inside the fascia alters its density, the behavior of the entire deep fascia and the underlying muscle would be compromised, This, we predict, may be the basis of the common phenomenon known as "myofascial pain." This study describes the fascial reservoir as a "…reservoir of water and ions for surrounding tissues. It may also function as a reservoir to accumulate and remove various degradation products and toxic substances…A fundamental element of the loose connective tissue (ground substance) is the HA, and its concentration determines, together with the temperature and other physical parameters, the density of the matrix. " The study proposes the mechanism of increasing viscosity of ground substance, and proposes a new type of cell they call the "fasciacyte." [This study confirms increased hyaluronic acid in myofascial pain areas (what we found in the geloid mass over areas of resistant TrPs), and gives new anatomical fascial insights and a new direction in what may be a promising way to relieve and even reverse myofascial pain. DJS]
Stejskal V, Ockert K, Bjørklund G. 2013. Metal-induced inflammation triggers fibromyalgia in metal-allergic patients. Neuro Endocrinol Lett. 34(6):559-565. "Fifteen female FM patients were included in the study. Metal allergy was measured by a lymphocyte transformation test, MELISA®….All FM patients tested positive to at least one of the metals tested. The most frequent reactions were to nickel, followed by inorganic mercury, cadmium and lead. Some healthy controls responded to inorganic mercury in vitro but most of the tests were negative. Objective examination 5 years later showed that half of the patients no longer fulfilled the FM diagnosis, 20% had improved and the remaining 30% still had FM. All patients reported subjective health improvement."
Sterling M, Jull G, Vicenzino B et al. 2003. Sensory
hypersensitivity occurs soon after whiplash injury and is associated
with poor recovery. Pain 104(3):509-517. “These
findings suggest that those with persistent moderate/severe symptoms at
six months display, soon after injury, generalized hypersensitivity
suggestive of changes in central pain processing mechanisms. This
phenomenon did not occur in those who recover or those with persistent
Sterling M, Jull G, Vicenzino B et al. 2003. Development of motor
system dysfunction following whiplash injury. Pain
103(1-2):65-73. “This study identifies, for the first time,
deficits in the motor system, as early as one month post whiplash
injury, that persisted not only in those reporting moderate/severe
symptoms at three months but also in subjects who recovered and those
with persistent mild symptoms.”
Sterling M, Jull G, Wright A. 2001. The effect of musculoskeletal
pain on motor activity and control. J Pain 2(3):135-145.
“Aberrant movement patterns and postures are obvious to clinicians
managing patients with musculoskeletal pain. Some changes in motor
function that occur in the presence of pain are less apparent.
Clinical and basic science investigations have provided evidence of the
effects of nociception on aspects of motor function. Recent
research has seen the emergence of a new model in which patterns of
muscle activation and recruitment are altered in the presence of pain
(neuromuscular activation model). These changes seem to
particularly affect the ability of muscles to perform synergistic
functions related to maintaining joint stability and control.
These changes are believed to persist into the period of chronicity.
It is apparent that people experiencing musculoskeletal pain exhibit
complex motor responses that may show some variation with the time
course of the disorder.”
Sterling M, Kenardy J, Jull G et al. 2003. The development of
psychological changes following whiplash injury. Pain
106(3):481-489. “This study identifies, for the first time,
deficits in the motor system, as early as 1 month post whiplash injury,
that persisted not only in those reporting moderate/severe symptoms at 3
months but also in subjects who recovered and those with persistent mild
M., Jull G, Wright A. 2001. The effect of musculoskeletal pain on
motor activity and control. J Pain 2(3):135-145. This
article relates how muscle activation and recruitment patterns are
influenced by pain, affecting the ability of muscles to perform
synergistically. This can
affect joint stability and control of muscle function. This is important, as it isn’t only the specific pain that must be
treated, but associated muscle weakness and dysfunction must also be
recognized and addressed for function to be restored.
Sterling M., Treleven J.,
Edwards S. et al. 2002. Pressure pain thresholds in chronic Whiplash
Associated Disorder: further evidence of altered central pain processing.
Central sensitization may occur after whiplash. J Musculoskel Pain
Sterling M, Jull G, Wright A. 2001. The
effect of musculoskeletal pain on motor activity and control. [No
journal listed] 2(3):135-145. Patterns of muscle activation and
recruitment are altered in the presence of pain. "These
changes seem to particularly affect the ability of muscles to
perform synergistic functions related to maintaining joint
stability and control. It is apparent that people experiencing
musculoskeletal pain exhibit complex motor responses that may show
some variation with the time course of the disorder."
Stella, N., P. Schweitzer and D. Piomelli. 1997. A second endogenous cannabinoid that
modulates long-term potentiation. Nature 388(6644):773-778.
Stelmack, R. M. 1990. Biological bases of extraversion: psychophysiological evidence. J
Stephan AH, Madison DV, Mateos JM et al. 2013. A dramatic increase of C1q protein in the CNS during normal aging. J Neurosci. 33(33):13460-13474. "The decline of cognitive function has emerged as one of the greatest health threats of old age. Age-related cognitive decline is caused by an impacted neuronal circuitry, yet the molecular mechanisms responsible are unknown. C1q, the initiating protein of the classical complement cascade and powerful effector of the peripheral immune response, mediates synapse elimination in the developing CNS. Here we show that C1q protein levels dramatically increase in the normal aging mouse and human brain, by as much as 300-fold. This increase was predominantly localized in close proximity to synapses and occurred earliest and most dramatically in certain regions of the brain, including some but not all regions known to be selectively vulnerable in neurodegenerative diseases, i.e., the hippocampus, substantia nigra, and piriform cortex. C1q-deficient mice exhibited enhanced synaptic plasticity in the adult and reorganization of the circuitry in the aging hippocampal dentate gyrus. Moreover, aged C1q-deficient mice exhibited significantly less cognitive and memory decline in certain hippocampus-dependent behavior tests compared with their wild-type littermates. Unlike in the developing CNS, the complement cascade effector C3 was only present at very low levels in the adult and aging brain. In addition, the aging-dependent effect of C1q on the hippocampal circuitry was independent of C3 and unaccompanied by detectable synapse loss, providing evidence for a novel, complement- and synapse elimination-independent role for C1q in CNS aging." [The microglial cells that help prune developing brain cells early in life may be part of the problem of aging. Dysfunctional glial cells could be responsible for some of the symptoms of fibromyalgia that seem to be an advanced aging process. If so, the ability of this C1q deficient mouse may hold some clues to a work-around of fibromyalgia cognitive deficits in the future. DJS]
Stevensen, C. 1995. The role of shiatsu in palliative care. Complement Ther Nurs
Stewart, D. P., J. Kaylor and E. Koutanis. 1996. Cognitive deficits in presumed minor
head injured patients. Acad Emerg Med 3 (1):21-26.
Stewart, J. M., M. H. Gewitz, A. Weldon and J. Munoz. 1999. Patterns of orthostatic
intolerance: the orthostatic tachycardia syndrome and adolescent chronic fatigue. J
Pediatr 135(2 Pt 1):218-25.
Stewart WF, Ricci JA, Chee E et al.
2003. Lost productive time and cost due to common pain conditions in
the US workforce. JAMA 290(18):2443-2454. Pain is not only a
common disability keeping people from the workforce, but AMost of the
pain-related lost productive time occurs while employees are at work and is
in the form of reduced performance.@
Stiasny-Kolster K, Magerl W, Oertel
WH et al. 2004. Static mechanical hyperalgesia without dynamic
tactile allodynia in patients with restless legs syndrome.
Brain [Epub Feb 25 ahead of print]
Stoll, B. A. 1999. Western nutrition and the insulin resistance syndrome: a link to
breast cancer. Eur J Clin Nutr 53(2):83-7.
Stormorken H, Brosstad F. 2005. [Frequent urination—an important
diagnostic marker in fibromyalgia] Tidsskr Nor Laegeforen
125(1):17-19. [Norwegian] “An abnormally high frequency of
urination is a characteristic feature in fibromyalgia and a useful
diagnostic variable. The pattern is that of urge, sometimes with
incontinence.” [This study would have been more useful had the
patients been screened for co-existing myofascial TrPs that can cause
the same symptoms and yet can respond immediately to appropriate
Straub, T. A. 1999. Endoscopic carpal tunnel release: a prospective analysis of factors
associated with unsatisfactory results. Arthroscopy 15(3):269-74.
Stratz T, Fiebich B, Haus U et al. 2004. Influence of tropisetron
on the serum substance P levels in fibromyalgia patients. Scand
J Rheumatol Suppl (119):41-43. “It is possible that the
responders to tropisetron represent a subgroup of FM patients for whom
substance P and 5-HT3 receptors play key roles in the development of the
Stratz T, Muller W. 2004. Treatment of chronic low back pain with
tropisetron. Scand J Rheumatol Suppl (119):76-78.
Some patents with myofascial pain syndromes and painful tendinopathies
were helped by tropisetron injections.
Stricker, R. B., B. Goldberg and W. L. Epstein. 1997. Topical immune modulation (TIM):
a novel approach to the immunotherapy of systemic disease. Immunol Lett
Striffler, J. S., J. S. Law, M. M. Polansky, S. J. Bhathena, and R. A. Anderson. 1995.
Chromium improves insulin response to glucose in rats. Metabolism 44(10):1314-1320.
Strimpakos N. 2011. The assessment of the cervical spine. Part 1: Range of motion and proprioception. J Bodyw Mov Ther. 15(1):114-124. "Neck pain and headache of cervical origin are complaints affecting an increasing number of the general population. Mechanical factors such as sustained neck postures or movements and long-term "abnormal" physiologic loads on the neck are believed to affect the cervical structures and compromise neck function. A comprehensive assessment of neck function requires evaluation of its physical parameters such as range of motion, proprioception, strength and endurance/fatigue. The complicated structure of the cervical spine however, makes it difficult for any clinician to obtain reliable and valid results. The aim of the first part of this systematic critical review is to identify the factors influencing the assessment of range of motion and proprioception of the cervical spine."
Strobel, E. S., M. Krapf, M. Suckfull, W. Bruckle, W. Fleckenstein and W. Muller. 1997.
Tissue oxygen measurement and 31 P magnetic resonance spectroscopy in patients with muscle
tension and fibromyalgia. Rheumatol Int 16(5):
Stryła W, Pogorzała AM, Stępień J. 2013. Proprioception exercises in medical rehabilitation. Pol Orthop Traumatol. 78:5-27. "Proprioception, or kinesthesia, is the sense of orientation responsible for perception of body and relative position of its parts. Kinesthesia is received by receptors located in muscles and tendons. In this study a set of proprioception developing exercises was presented. Proprioception should be restored in case of musculoskeletal and neurological disorders. Proprioception training can also be used as a prophylaxis before starting various sporting activities. Proprioception developing exercises have significant meaning for the elderly, who are at risk of balance disorders. These exercises help developing motor memory and at the same time protect from falls." [All care providers must understand that myofascial TrPs can have associated proprioceptive and/or autonomic dysfunction. DJS]
Stuifbergen AK, Phillips L, Carter P et al. 2010. Subjective and objective sleep difficulties in women with fibromyalgia syndrome. J Am Acad Nurse Pract. 22(10):548-556. "Sleep problems are a major concern among women with FMS. Those with concurrent depressive symptoms, high pain, and limited functioning may be candidates for in-depth sleep assessment and behavioral programs to improve sleep." [When pain is a major cause of sleep impairment, the causes of pain must be addressed. Co-existing sleep dysfunctions, such as obstructive sleep apnea, must also be addressed. Myofascial trigger points may be major components of these. Often, the psychological support is needed to address the failure of medicine to promptly and adequately address the causes of pain and dysfunction and support the patients with these conditions. DJS]
Stuifbergen AK, Phillips L, Voelmeck W et al. 2006.
Illness perceptions and related outcomes among women with fibromyalgia
syndrome. Womens Health Issues 16(6):353-360. “Emotional
representations explained 41% of the variance in mental health scores and
17% in reported health behaviors. Overall, this sample of women with
FMS had fairly negative perceptions of their illness. As suggested by
Leventhal’s model, cognitive and emotional representations predicted
Sturgeon JA, Yeung EW, Zautra AJ. 2014. Respiratory Sinus Arrhythmia: a Marker of Resilience to Pain Induction. Int J Behav Med. [Jan 14 Epub ahead of print.] There may be significant individual differences in physiological regulatory responses to the experience of pain and stress. Respiratory sinus arrhythmia is a physiological indicator that may have implications for efficient physiological responses to pain and stress….Fifty-nine women (33 with fibromyalgia and 26 healthy controls) were exposed to repeated thermal pain stimuli and were asked to rate their feelings of fatigue after each block of thermal pain exposures….Self-reported fatigue affect increased during pain induction, but greater respiratory sinus arrhythmia predicted less-pronounced increases in fatigue affect across induction trials. Respiratory sinus arrhythmia appears to be a promising indicator of physiological resilience to pain, predicting an attenuated effect of repeated pain exposure on self-reported fatigue. Implications of efficient regulation of pain, fatigue, and long-term physical health are discussed.
Sturnieks DL, Tiedemann A, Chapman K et al. 2004. Physiological
risk factors for falls in older people with lower limb arthritis.
J Rheumatol. 31(11):2272-2279. “A physiological falls-risk
profile based on mean test scores for the arthritis group highlights
deficits in muscular strength, knee proprioception, and standing
balance, indicating the need for targeted falls prevention intervention
in this population.”
Sturzenegger, M. G. Di Stefano, B. P. Radanow and A. Schnidrig. 1994. Presenting
symptoms and signed after whiplash injury: the influence of accident mechanisms. Neurology
Suarez-Almazor, M. E., L. Gonzalez-Lopez, J. I. Gamez-Nava, E. Belseck, C. J. Kendall
and P. Davis. 1998 Utilization and predictive value of laboratory tests in patients
referred to rheumatologists by primary care physicians. J Rheumatol 25(10:1980-5.
Subramaniam, V., M. W. Stewart and J. F. Smith. 1999. The development and impact of a
chronic pain support group: a qualitative and quantitative study. J Pain Symptom Manage
Sucher BM. 1995.
Palpatory diagnosis and manipulative management of carpal tunnel syndrome:
Part 2. ‘Double crush’ and thoracic outlet syndrome. J Am Osteopath
Assoc. 95(8):471-479. “The physician treating carpal tunnel
syndrome needs to be aware of the possible concomitant occurrence of
thoracic outlet syndrome, the so-called double crush syndrome.
Palpation is used to differentiate carpal tunnel syndrome from thoracic
outlet syndrome. Such palpatory examination assists the physician in
planning the initial treatment, including osteopathic manipulation and
self-stretching maneuvers, targeted specifically at the most clinically
significant pathologic region. Supplemental physical medicine
modalities such as ultrasound may enhance the treatment response. Some
illustrative cases are reported.” [Carpal tunnel syndrome often co-exists
with TOS. Myofascial trigger points can cause symptoms of both, so the
examining clinician needs to look for patterns, and for TrPs. DJS]
Sucher, B. M. 1993. Myofascial release of carpal tunnel syndrome. J Am Osteopath
Sugawa T, Fujiwara Y, Okuyama M et al. 2007.
[Prevalence, diagnosis and treatment of extraesophageal manifestation of
GERD] Nippon Rinsho. 65(5):946-950. [Japanese]
“Gastroesophageal reflux disease (GERD) is associated with a variety of
extraesophageal symptoms including asthma, chronic cough, laryngeal
disorders, and various ENT symptoms. Recent studies suggest that GERD
underlies or contributes to chronic sinusitis, chronic otitis media, dental
erosion and obstructive sleep apnea syndrome (OSAS).”
Sugimoto Y, Iba Y, Nakamura Y et al. 2004. Pruritus-associated response mediated by cutaneous histamine H3 receptors.
Clin Exp Allergy 34(3):456-459. Histamine 1 receptor antagonists have been a primary treatment for itching.
Histamine 3 receptor antagonists may also be useful.
Suleiman S, Johnston DE. 2001. The
abdominal wall: an overlooked source of pain. Am Fam Physician
64(3):431-438. “When abdominal pain is chronic and unremitting, with
minimal or no relationship to eating or bowel function but often a
relationship to posture (i.e., lying, sitting, standing), the abdominal wall
should be suspected as the source of pain. Frequently, a localized,
tender trigger point can be identified, although the pain may radiate over a
diffuse area of the abdomen. If tenderness is unchanged or increased
when abdominal muscles are tensed (positive Carnett’s sign), the abdominal
wall is the likely origin of pain. Most commonly, abdominal wall pain
is related to cutaneous nerve root irritation or myofascial irritation.
The pain can also result from structural conditions, such as localized
endometriosis or rectus sheath hematoma, or from incisional or other
abdominal wall hernias. If hernia or structural disease is excluded,
injection of a local anesthetic with or without a corticosteroid into the
pain trigger point can be diagnostic and therapeutic.”
Sullivan MD, Cahana A, Derbyshire S et al. 2013. What does it mean to call chronic pain a brain disease? J Pain. 14(4):317-322. "When considering the significance of neuroimaging results, it is important to remember that "disease" is a concept that arises out of clinical medicine, not laboratory science. Following Canguilhem, we believe that disease is best defined as a structural or functional change that causes disvalue to the whole organism. It is important to be cautious in our assertions about chronic pain as a brain disease because these may have negative effects on 1) the therapeutic dialogue between clinicians and patients; 2) the social dialogue about reimbursement for pain treatments and disability due to pain; and 3) the chronic pain research agenda.... We should not see pain caused by the brain alone. Pain is not felt by the brain, but by the person….conceiving of chronic pain as a brain disease can have negative consequences for research and clinical care of patients with chronic pain."
Sullivan SK, Petroski
RE, Verge G et al. 2004. Characterization of the interaction of
indiplon, a novel pyrazolopyrimidine sedative-hypnotic, with the GABA
receptor. J Pharmacol Exp Ther 311(2):537-546.
Indiplon had a higher binding to GABA A receptors than zolpidem or
zaleplon, according to this study. Indiplon may be a promising new
tool for the treatment of sleep disorders.
Suma S, Veerendra Kumar B. 2012. Temporomandibular disorders and functional somatic syndromes: Deliberations for the dentist. Indian J Dent Res. 23(4):529-536.
"Temporomandibular disorder (TMD) is an umbrella term for a collection of disorders affecting the temporomandibular joint (TMJ) and associated tissues…. Management is dictated by the cause. The most 'famed' causes include trauma, inflammation, aging, parafunctional habits, infections, neoplasms, and stress; and these are always considered in the differential diagnosis of TMJ pain. There are some less 'famed' causes of TMD, which are characterized by increased pain sensitivity due to psychosocial factors; these include myofascial pain syndrome and functional somatic syndromes (FSS) such as fibromyalgia and chronic fatigue syndrome. They present with chronic pain, fatigue, disability, and impairment in ability to perform daily activities."
Summers J, Johnson S, Pridmore S et al. 2004.
Changes to cold detection and pain thresholds following low and high
frequency transcranial magnetic stimulation of the motor cortex.
Neurosci Lett. 368(2):197-200. RTMS may reduce sensory threshold
changes that may benefit people in chronic pain.
Sundblom, D. M., S. Haikonen, J. Niemi-Pynttari and I. Tigerstedt. 1994. Effect of
spiritual healing on chronic idiopathic pain: a medical and psychological study. Clin J
Sundstrom I., D. Ashbrook and T. Backstrom. 1997. Reduced benzodiazepine sensitivity in
patents with premenstrual syndrome: a pilot study. Psychoneuroendocrinology
Sullivan, J. A. 1999. Pediatric flatfoot: evaluation and management. J Am Acad
Orthop Surg 7(1):44-53.
Suskind AM, Berry SH, Suttorp MJ et al. 2012. Health-related quality of life in patients with interstitial cystitis/bladder pain syndrome and frequently associated comorbidities. Qual Life Res. [Oct 7 Epub ahead of print]. "To estimate the association of chronic non-urologic conditions [i.e., fibromyalgia (FM), chronic fatigue syndrome (CFS), and irritable bowel syndrome (IBS)] with health-related quality of life (HRQOL) in patients with interstitial cystitis/bladder pain syndrome (IC/BPS).....In patients with IC/BPS, the presence of FM, CFS, and IBS has a significant association with HRQOL, equivalent in impact to the bladder symptoms themselves. These results emphasize the importance of a multidisciplinary approach to treating patients with IC/BPS and other conditions."
Sutbeyaz ST, Sezer
N, Koseoglu F et al. 2009. Low-frequency pulsed electromagnetic
field therapy in fibromyalgia: a randomized, double-blind,
sham-controlled clinical study. Clin J Pain. 25(8):722-728.
“Low-frequency PEMF (pulsed electromagnetic field) therapy might improve
function, pain, fatigue, and global status in FM patients.”
Suzuki R, A. H. Dickenson. 2002. The
pharmacology of Central Sensitization. J Musculoskel Pain 10(1/2):35-43. As
research discovers how the pain processing system works, we have a much
better chance of coming up with pharmacological methods to treat it.
Suzuki R, Dickenson AH. 2002.
Neuropharmacologic targets and agents in fibromyalgia. Curr
Pain Headache Rep 6(4):267-73. Fibromyalgia pain is commonly
poorly managed. Patients often have fatigue, sleep disturbances
and anxiety. Some medications that target the central nervous
system may help a number of these symptoms.
Svebak S, Hagen K, Zwart JA. 2006. One-year
prevalence of chronic musculoskeletal pain in a large adult Norwegian county
population: relations with age and gender – the HUNT study. J
Musculoskel Pain 14(1):21-28. “Nearly half of the adult population
reported chronic MSCs during the last year. The high degree of
interference with daily activities and work capacity should be motivation
for better preventive strategies in the future.”
B 2004. Use less cosmetics – suffer less from fibromyalgia? J
Womens Health 13(2):187-194. Reduced
use of cosmetics resulted in a reduction in FMS symptoms.
Svendsen KB, Andersen S, Arnason S et al. 2005.
Breakthrough pain in malignant and non-malignant diseases: a review
of prevalence, characteristics and mechanisms. Eur J Pain.
9(2):195-206. “Breakthrough pain or transient worsening of
pain in patients with an ongoing steady pain is a well known feature
in cancer pain patients, but it is also seen in non-malignant pain
conditions with involvement of nerves, muscles, bones or viscera.
We suggest that peripheral and/or central sensitization (hyperexcitability)
may play a major role in many causes of BTP.”
Swenson CJ. 2002. Ethical issues in pain management.
Semin Oncol Nurs 18(2):135-142. “The oncology patient
continues to have inadequate pain control. With the acknowledgment
that we have the technical skills and the physiological knowledge to
reduce pain, yet it is not being done, health care professionals have
begun to explore the ethics behind pain.”
Swerdlow B, Dieter JN. 1992. An
evaluation of the sensitivity and specificity of medical thermography for
the documentation of myofascial trigger points. Pain.
Swezey RL and J Adams. 1999. Fibromyalgia: a risk factor for osteoporosis. J
Swick TJ. 2011. Sodium oxybate: a potential new pharmacological option for the treatment of fibromyalgia syndrome. Ther Adv Musculoskelet Dis. 3(4):167-178. "Fibromyalgia syndrome (FMS) is a common disorder, characterized by diffuse pain and tenderness, stiffness, fatigue, affective disorders and significant sleep pathology. A new set of diagnostic criteria have been developed which should make it easier for a busy clinician to diagnose the condition. US Food and Drug Administration (FDA) approved medications for the treatment of FMS have, for the most part, been geared to modulate the pain pathways to give the patient some degree of relief. A different kind of pharmacological agent, sodium oxybate (SXB), is described that is currently approved for the treatment of excessive daytime sleepiness and cataplexy in patients with narcolepsy. SXB, an endogenous metabolite of the inhibitory neurotransmitter gamma-hydroxybutyrate, is thought to act independently as a neurotransmitter with a presumed ability to modulate numerous other central nervous system neurotransmitters. In addition SXB has been shown to robustly increase slow wave sleep and decrease sleep fragmentation. Several large clinical trials have demonstrated SXB's ability to statistically improve pain, fatigue and a wide array of quality of life measurements of patients with fibromyalgia. SXB is not FDA approved to treat fibromyalgia."
FR, Serra CR, Rodrigues MC et al. 2001. [Rheumatic diseases in
adolescence.] J Pediatr 77 Suppl 2:S234-244. This review
lists many conditions, including fibromyalgia and growing pains, but does
not specifically mention myofascial trigger points. It does state:
“It is important that health professionals diagnose these diseases as
early as possible so that prompt action can be taken and prognosis can be
Szygula-Jurkiewicz B, Hudzik B, Nowak J et al. 2004. [Sleep apnea
syndrome in patients with chronic heart failure] Wiad Lek.
57(3-4):161-165. [Polish] “Sleep apnea syndrome (SAS) in patients
with chronic heart failure (CHF) increases the risk of death.
Obstructive apneas (OSAHS) may lead to central apneas by frequent
arousals, decreased left ventricular function and prolongation of
Taccola, A., D. Miotti and M. Zambelli. 1998. [Occupational exposure to vibration:
Raynauds phenomenon and the vascular response to methacholine iontophoresis]. G
Ital Med Lav Ergon 20(4):243-8 [Italian].
Taddio A, Katz J. 2005. The effects of
early pain experience in neonates on pain responses in infancy and
childhood. Paediatr Drugs 7(4):245-257. “Pre-term
infants that are hospitalized as neonates and subjected to painful
procedures appear to have a dampened response to painful procedures
later in infancy. Full-term neonates exposed to extreme stress
during delivery, or to a surgical procedure, react to later noxious
procedures with heightened behavioral responsiveness. Studies
in which analgesic agents (local anesthetics or opioids) have been
administered prior to noxious procedures demonstrate less procedural
pain and a reduction in the magnitude of long-term changes in pain
behaviors.” [Adequate pain control from infancy may prevent
sensitizing the central nervous system and lessen the chance of
developing FMS. DJS]
Taggart HM, Arslanian CL, Bae S et
al. 2003. Effects of T’ai Chi exercise on fibromyalgia symptoms and
health-related quality of life. Orthop Nurs 22(5):353-60.
“T’ai Chi is potentially beneficial to patients with FM.” [The
high drop-out rate in the study may be due to lack of modification of the
training, or to co-existing myofascial trigger points. See reference
article under “Starlanyl DJ, published in T’ai Chi Magazine.”
Tagoe CE, Zezon A, Khattri S et al. 2013. Rheumatic manifestations of euthyroid, anti-thyroid antibody-positive patients. Rheumatol Int. [Jan 5 Epub ahead of print]. The aim of this study is to define the rheumatic manifestations of euthyroid patients with chronic lymphocytic thyroiditis (CLT) but without a well-defined connective tissue disease…..[This study found that] Rheumatic manifestations frequently occur in patients with CLT in the absence of overt thyroid dysfunction and mimic the presentation of the well-defined connective tissue diseases."
Taguchi T. 2005. [The indication and clinical value of neural
blocks for low back pain.] Clin Calcium 15(3):337-342.
[Japanese] Trigger point blocks are included in this article.
Tague SE, Smith PG. 2010. Vitamin D receptor and enzyme expression in dorsal root ganglia of adult female rats: Modulation by ovarian hormones. J Chem Neuroanat. [Oct 20 Epub ahead of print]. "Vitamin D insufficiency impacts sensory processes including pain and proprioception, but little is known regarding vitamin D signaling in adult sensory neurons. These findings (in rats) imply that vitamin D signaling may play a specialized role in a neural cell population that is primarily nociceptive."
Tai CF, Baraniuk JN. 2003. A tale of two neurons in the upper
airways: pain versus itch. Curr Allergy Asthma Rep.
3(3):215-220. Connections between itch and pain and unmyelinated type C
Tai CF, Baraniuk JN. 2002. Upper airway neurogenic mechanisms.
Curr Opin Allergy Clin Immunol. 2(1):11-19. This article
links dysfunctional Type C nociceptive nerves, involved in some types of
chronic pain and itch, as contributors of “...allergic rhinitis,
infectious rhinitis, nasal hyperresponsiveness, and possibly sinusitis.”
Taimela, S., M. Kankaanpaa and S. Luoto. 1999. The effect of lumbar fatigue on the
ability to sense a change in lumbar position. A controlled study. Spine
Takagi, A. 1999. [Effect of caffeine on tension development of skeletal muscle of mdx
mouse]. Rinsho Shinkeigaku 39(2-3):311-5. [Japanese]
Talebian S, Otadi K, Ansari NN et al. 2012. Postural control in women with myofascial neck pain. J Musculoskel Pain. 20(1):25-30.Patients with myofascial TrPs in the neck area had difficulty standing on foam flooring, both with one-foot standing and bipedal standing. Foam flooring affected both the control group and the patient group, but the patients had a faster sway velocity and significantly greater displacement distance. The study revealed that patients with cervical TrPs have standing deficits in standing balance with the eyes open or closed. Postural impairments could be from proprioceptor dysfunction associated with neck TrPs. The use of foam flooring as a standing surface significantly worsened postural control, both during one-legged and bipedal stances. The foam disrupts the sensory information from cutaneous mechanoreceptors on the soles of the feet, contributing to postural instability that increased with TrP-related neck pain. Patients did recruit the ankle tissues in an attempt to compensate for the postural imbalance, stressing those muscles. [This has direct application for those patients who exercise on foam matted surfaces, for t'ai chi chuan, yoga and other forms in which postural balance is of importance. DJS.]
Tamim H, Castel ES, Jamnik V et al. 2009.
Tai Chi workplace program for improving musculoskeletal fitness among female
computer users. Work. 34(3):331-338. “Results showed that
the TC (Tai Chi) program was effective in improving musculoskeletal fitness
and psychological well-being.” “Significant improvements in
physiological and psychological measures were observed, even at the large
class sizes tested here, suggesting that TC has considerable potential as an
economic, effective and convenient workplace intervention.”
Tamimi MA, McCeney MH, Krutsch J. 2009.
A case series of pulsed radiofrequency treatment of myofascial trigger
points and scar neuromas. Pain Med. 10(6):1140-1143. “…PRF
(pulsed radiofrequency) could be a minimally invasive, less neurodestructive
treatment modality for these painful conditions and that further systematic
evaluation of this treatment approach is warranted.”
Tamisier R, Pepin JL, Wuyam B et al. 2004. Expiratory changes in
pressure: flow ratio during sleep in patients with sleep-disordered
breathing. Sleep 27(2):240-248.
Tampin B, Briffa NK, Slater H. 2012. Self-reported sensory descriptors are associated with quantitative sensory testing parameters in patients with cervical radiculopathy, but not in patients with fibromyalgia. Eur J Pain. [Oct 26 Epub ahead of print]. "The painDETECT questionnaire (PD-Q) has been used as a tool to characterize sensory abnormalities in patients with persistent pain. This study investigated whether the self-reported sensory descriptors of patients with painful cervical radiculopathy (CxRAD) and patients with fibromyalgia (FM), as characterized by responses to verbal sensory descriptors from PD-Q (sensitivity to light touch, cold, heat, slight pressure, feeling of numbness in the main area of pain), were associated with the corresponding sensory parameters as demonstrated by quantitative sensory testing (QST)....Clinicians and researchers should be cautious about relying on PD-Q (as a stand-alone screening tool to determine sensory abnormalities in patients with FM."
Tampin B, Slater H, Hall T. 2012. Quantitative sensory testing somatosensory profiles in patients with cervical radiculopathy are distinct from those in patients with nonspecific neck-arm pain. Pain. [Sep 11 Epub ahead of print]. The aim of this study was to establish the somatosensory profiles of patients with cervical radiculopathy and patients with nonspecific neck-arm pain associated with heightened nerve mechanosensitivity (NSNAP). Sensory profiles were compared to healthy control (HC) subjects and a positive control group comprising patients with fibromyalgia (FM)....Despite commonalities in pain characteristics between the two neck-arm pain groups, distinct sensory profiles were demonstrated for each group. [It would be extremely helpful to discover what percentage of these patients had co-existing myofascial trigger points referring to the upper limb and/or neck. DJS]
Tander B, Atmaca A, Aliyazicioglu Y et al. 2007.
Serum ghrelin levels but not GH, IGF-1 and IGFBP-3 levels are altered in
patients with fibromyalgia syndrome. Joint Bone Spine. [Jun
29 Epub ahead of print] “Our results suggest that low levels of ghrelin
in FMS are not related to the changes in hypothalama-pituitary-IGF-1
axis but may be related to some symptoms of FMS. Our results need
to be clarified by further studies.” [This may explain some of the
abdominal fat pad, some of the glycolysis abnormalities, and some
overeating issues in some patients with FM. DJS]
Tang B, Ji Y, Traub RJ. 2007.
Estrogen alters spinal NMDA receptor activity via a PKA signaling
pathway in a visceral pain model in the rat. Pain [Dec 7
Epub ahead of print]. “Pain symptoms in several chronic pain
disorders in women, including irritable bowel syndrome, fluctuate with
the menstrual cycle..” The estrogen beta receptor may be in part
Tang S, Calkins H, Petri M. 2004.
Neurally mediated hypotension in systemic lupus erythematosus patients
with fibromyalgia. Rheumatology (Oxford) 43(5):609-614. In
SLE patients, “...NMH has no impact on quality of life above that
determined by FM, and has no significant association with FM status.
Identification of NMH may be important in selected patients with SLE who
have chronic fatigue, but NMH cannot explain the increased prevalence of
FM in SLE.”
Tanrikut A, Nadire O,
Huseyin AK et al. 2001. High voltage galvanic stimulation in
myofascial pain syndrome. J Muscoloskel Pain 11(2):11-15.
HGVS can be a useful treatment for myofascial pain.
Imamura M, Kaziyama HH et al. 2002. Pain treatment with
acupuncture for patients with fibromyalgia. Curr Pain
Headache Rep. 6(5):379-383. This review is a comparison of
acupuncture and other therapies in the relief of FMS.
Traditional acupuncture resulted in FMS improvement.
Leproult R, Ehrmann DA et al. 2008. Slow-wave sleep and the risk of type
2 diabetes in humans. Proc Natl Acad Sci U S A
105(3):1044-1049. “These findings demonstrate a clear role for SWS
in the maintenance of normal glucose homeostasis. Furthermore, our
data suggest that reduced sleep quality with low levels of SWS
(slow-wave sleep), as occurs in aging and in many obese individuals, may
contribute to increase the risk of type 2 diabetes.”
Tassain V, Attal N, Fletcher D et al. 2003.
Long term effects of oral sustained release morphine on
neuropsychological performance in patients with chronic non-cancer pain.
Pain 104(1-2):389-400. “...twelve months treatment with oral
morphine does not disrupt cognitive functioning in patients with chronic
non-cancer pain and instead results in moderate improvement of some
aspects of cognitive functioning as a consequence of the pain relief and
concomitant improvement of well-being and mood.”
Tauben DJ, Loeser JD. 2013. Pain education at the University of Washington School of Medicine. J Pain. 14(5):431-437. "There is a compelling need for implementation of new approaches to pain medicine education in both medical and other health science schools in response to the increasing evidence of inadequate and insufficient pain medicine education in both the U.S. and elsewhere. The UWSOM has recently increased pain curriculum time spent and the future practice relevance of its pain education by implementing a 4-year integrated curriculum tailored to match both the learning level and clinical experience, including most of the ISAP's recommended content, while emphasizing the educational needs of future primary care physicians, those who are and will continue to manage the vast majority of patients seeking medical advice and treatment of both acute and chronic pain."
Taubes G. 2003. Neuroscience.
Insulin insults may spur Alzheimer's disease. Science
301(5629):40-41. Patients with type II diabetes and insulin resistance may have an increased incidence of Alzheimer’s disease.
Any diet that increases insulin levels may also predispose toward the development of Alzheimer’s.
Tawfik VL, Nutile-McMenemy N, Lacroix-Fralish ML,
DeLeo JA. Efficacy of propentofylline, a glial modulating agent, on
existing mechanical allodynia following peripheral nerve injury.
Brain Behav Immun 2006 [Aug 30 Epub ahead of print].
Taylor AG, Anderson JG, Riedel SL et al. 2013. A randomized, controlled, double-blind pilot study of the effects of cranial electrical stimulation on activity in brain pain processing regions in individuals with fibromyalgia. Explore (NY). 9(1):32-40. "The observed decrease in activation in the pain processing regions may indicate a decrease in neural activity in these regions that may be related to decreased pain. This is the first randomized, controlled trial of CES in patients diagnosed with fibromyalgia to report functional magnetic resonance imaging data."
Taylor-Piliae RE, Froelicher ES. 2004.
Effectiveness of T'ai Chi exercise in improving aerobic capacity: meta-analysis.
J Cardiovasc Nurs 19(1):48-57. T'ai chi may be considered aerobic exercise.
"The greatest benefit was seen from the classical Yang style T'ai Chi when performed for
one year by sedentary adults with an initial low level of physical activity
Teachey WS. 2004. Otolaryngic myofascial pain syndromes.
Curr Pain Headache Rep. 8(6):457-462. Many unexplained ear,
nose, throat, head and neck dysfunctions that cannot be explained
otherwise fit the diagnosis of myofascial dysfunction, and TrP therapy
is effective for these symptoms.
Tecco S, Marzo G, Crincoli V et al. 2012. The prognosis of myofascial pain syndrome (MPS) during a fixed orthodontic treatment. Cranio. 30(1):52-71. "Among treatments in the literature for myofascial pain syndrome (MPS), the most reliable therapies in dentistry are spray and stretch, and, although less frequently used, anesthetic injection. Adult MPS subjects are often treated using fixed orthodontic therapy for resolution of malocclusion....The purpose of this study was to analyze the prognosis of MPS during orthodontic treatment of subjects with malocclusion, initially diagnosed as having MPS. The analysis covered the medical records of 91 young adult Caucasians scheduled for orthodontic treatment for various malocclusions. Thirty-seven of the patients were initially diagnosed as also having MPS (T0). Thirty patients began the orthodontic treatment and were recalled for a re-evaluation of MPS after dental alignment and dental class correction was achieved (T1). A wait-and-see strategy was applied in seven subjects who were included as the control subjects. They received no treatment for MPS. At T1, a statistically significant decrease was observed in the study group in the presence of any clicking or creaking noises from the jaw joint, a significant jaw joint and jaw muscle pain reduction, and a quality of life improvement. Among patients who were depressed at the beginning of treatment, the majority felt better at the follow-up evaluation. On muscular palpation, a statistically significant decrease was found on the visual analogic scale value of the middle fibers of the temporalis muscle, temporalis tendon, clavicular and sternal division of the sternocleidomastoid muscle, masseter muscles, and posterior cervical muscles. The temporalis and the masseter muscles showed a significant decrease in the number of subjects with trigger points (TrPs) in all areas in the study group, after treatment. The digastric and sternocleidomastoid muscles also showed a significant reduction in the number of subjects with TrPs. Subjects with MPS and malocclusion were treated using a fixed orthodontic treatment. They showed improvement, although no resolution, in the signs and symptoms of MPS, compared with the untreated control group."
Costigan M, Griffin RS et al. 2006. GTP cyclohydrolase and
tetrahydrobiopterin regulate pain sensitivity and persistence.
Nat Med. 12(11):1269-1277. This study indicates a genetic
rate-limiting essential cofactor that influences neuropathic and
inflammatory pain, as well as the formation of several biochemicals such
as serotonin. “BH4 is therefore an intrinsic regulator of pain
sensitivity and chronicity, and the GTP cyclohydrolase haplotype is a
marker for these traits.” Researchers are searching for potential GTP
Johnson C, St Cyr J. 2006. The use of D-ribose in chronic
fatigue syndrome and fibromyalgia: a pilot study. J Altern
Complement Med. 12(9):857-862. “D-ribose significantly reduced
clinical symptoms in patients suffering from fibromyalgia and
chronic fatigue syndrome.”
Teixeira MJ, Yeng LT, Garcia OG et al. 2011. Failed back surgery pain syndrome: therapeutic approach descriptive study in 56 patients. Rev Assoc Med Bras. 57(3):286-291. [English, Portuguese] "The authors show the clinical evaluation and follow-up results in 56 patients diagnosed with a failed back surgery pain syndrome. ... In patients with a post-laminectomy syndrome, postoperative pain was more severe than preoperative pain from a herniated disk. A myofascial component was found in most patients."
Tekin L, Akarsu S, Durmuṣ O et al. 2012. The effect of dry needling in the treatment of myofascial pain syndrome: a randomized double-blinded placebo-controlled trial. Clin Rheumatol. [Nov 9 Epub ahead of print]. "The present study shows that the dry needling treatment is effective in relieving the pain and in improving the quality of life of patients with MPS."
Tekkok S.B., Ye Z.C., Brown
A.M. et al. 2002. Glutamate and aspartate are released from mouse
optic nerve during oxygen/glucose deprivation. Glia (Suppl
Tennant F. 2009. Brain atrophy with
chronic pain – A call for enhanced treatment. Pract Pain Manage.
9(2):12-14,44. Chronic pain can cause areas of the brain to shrink by
as much as 11%, similar to that lost by 1-2 decades of aging. “The decrease
in the prefrontal cortex and the thalamus…was related to the duration of
time spent in pain. Every year of pain appeared to decrease grey
matter by 1.3 cubic centimeters….Brain atrophy, along with altered brain
physiology and neurochemistry, now joins the risk profile of undertreated
chronic pain.” [This study was done on chronic back pain patients.
It indicates that undertreated pain is an interactive condition of itself,
although a preventable one. DJS]
Tennant F, Hermann L. 2001. (231) use of
transmucosal fentanyl in non-malignant, chronic pain. Pain
Med. 2(3):252-253. “Reported reasons for widespread
patient acceptance included TF’s fast action, fewer bed-bound days,
increased energy, decreased use of other opioids, less depression,
and fewer emergency room visits. This pilot study indicates
that TF is effective and desired as a preferential opioid for
breakthrough pain by a high percentage of chronic, non-malignant
Tepper S J. 2004. New
thoughts on sinus headache. Allergy Asthma Proc
25(2):95-96. “Sinus headaches are usually severely disabling migraines,
misdiagnosed and mistreated, with 61% of patients receiving antibiotic
prescriptions for noninfectious causes, thus failing the patients and,
in addition, contributing to a serious public health problem.”
Terman, M. and J. S. Terman. 1999. Bright light therapy: side effects and benefits
across the symptom spectrum. J Clin Psychiatry 60(11):799-808.
Ternov, K., M. Nilsson, L. Lofberg, L. Algotsson and J. Akeson. 1998. Acupuncture for
pain relief during childbirth. Acupunct Electrother Res 23(1):19-26.
Tershner SA, Mitchell JM, Fields HL. 2000. Brainstem pain
modulating circuitry is sexually dimorphic with respect to mu and kappa
opioid receptor function. Pain 85(1-2):153-159. “There are
sex differences in the pain modulating potency of the opioid
Theadom A, Cropley M, Humphrey KL. 2007.
Exploring the role of sleep and coping in quality of life in
fibromyalgia. J Psychosom Res. 62(2):145-151. “Sleep
quality was significantly predictive of pain, fatigue, and social
functioning in patients with FMS....Interventions designed to improve
sleep quality may help to improve health-related quality of life for
patients with FMS.”
Theoharides TC. 2007. Treatment approaches
for painful bladder syndrome/interstitial cystitis. Drugs.
67(2):215-235. “Lack of early diagnosis and treatment [of painful
bladder] can affect outcomes and leads to the development of
Thieme K, Gracely RH. 2009. Are
psychological treatments effective for fibromyalgia pain? Curr
Rheumatol Rep. 11(6):443-450. This is a review based on literature
search, and so based on studies that do not take into consideration the
co-existing conditions including TrPs, which now have been found to
occur in all FM patients. This may have something to do with the
FM heterogenicity mentioned in this review. It basically compared
the effects of different types of psychological treatments.
Remembering the above caveats, relaxation as a single therapy was shown
to be not helpful, hypnotherapy and writing intervention were mildly
effective, but operant-behavioral therapy and cognitive behavioral
therapy were considered effective for FM pain. [Although psychological
mechanisms can be helpful adjuncts, if FM pain is being maintained by
myofascial TrPs, and they are due to defects in calcium channels,
psychological methods cannot be considered treatment of FM pain, but
they can help people with FM cope with the pain, the other symptoms, and
the lack of support and understanding by others, often including the
medical care team. Adequate pain control and identification and control
of TrP perpetuating factors might do a great deal more to help “FM”
Thieme K, Turk DC. 2005. Heterogeneity of
psychophysiological stress responses in fibromyalgia syndrome patients.
Arthritis Res Ther. 8(1):R9 “The identification of low baseline
muscle tension in FMS is discrepant with other chronic pain syndromes
and suggests that unique psychophysiological features may be associated
with FMS. The different psychophysiological response patterns
within the patient sample support the heterogeneity of FMS.”
Thimineur M, De Ridder D. 2007. C2
area neurostimulation: a surgical treatment for fibromyalgia.
Pain Med. 8(8):639-646. “C2 area scalp stimulation
may diminish pain and related symptoms in patients with FM.”
Thomas CH. 2010. Spinal cord
mechanisms of chronic pain and clinical implications. Curr Pain
Headache Rep. 14(3):213-220. “In chronic pain states, painful
stimuli trigger afferent fibers in the dorsal horn to release
neuropeptides and neurotransmitters. These events induce multiple
inflammatory and neuropathic processes in the spinal cord dorsal
horn, and trigger modification and plasticity of local neural
circuits. As a result, ongoing noxious signals to the brain are
amplified and prolonged, a phenomenon known as central
Thomas HV, Stimpson NJ, Weightman AL et al.
2006. Systematic review of multi-symptom conditions in Gulf
War veterans. Psychol Med. 36(6):735-747. “Studies
were included if they compared the prevalence of chronic fatigue
syndrome, multiple chemical sensitivity, CDC-defined chronic
multi-symptom illness, fibromyalgia, or symptoms of either fatigue
or numbness and tingling…” “The results support the hypothesis that
deployment to the Gulf War is associated with greater reporting of
Thomas K, Shankar H. 2013. Targeting myofascial taut bands by ultrasound. Curr Pain Headache Rep. 17(7):349. "Myofascial pain syndrome (MPS) is a frequent diagnosis in chronic pain and is characterized by tender, taut bands known as trigger points. The trigger points are painful areas in skeletal muscle that are associated with a palpable nodule within a taut band of muscle fibers. Despite the prevalence of myofascial pain syndrome, diagnosis is based on clinical criteria alone. A growing body of evidence that suggests that taut bands are readily visualized under ultrasound-guided exam, especially when results are correlated with elastography, multidimensional imaging, and physical exam findings such as local twitch response."
Thomas M., Sing H., Belenky
G., Holcomb H., Mayberg H., Dannals R., Wagner H., Thorne D., Popp
K., Rowland L., Welsh A., Balwinski S., Redmond D. 2000. Neural
basis of alertness and cognitive performance impairments during
sleepiness. I. Effects of 24 h of sleep deprivation on waking
human regional brain activity. J Sleep Res 9(4):335-352.
Sleep deprivation can cause dysfunction in the brain, primarily in
the thalamus. Short-term sleep deprivation produces global
decreases in brain activity and dsyfunction in higher-order
Thomas RJ. 1995. Excitatory amino acids in health and disease.
J Am Geriatr Soc. 43(11):1279-1289. “Pharmacological
manipulation of the excitatory amino acid receptors is likely to be of
benefit in important and common diseases of the nervous system.” Only a
few neurotransmitter modulators now available have acceptable
therapeutic indices. New medications in this field may have
applications in chronic pain therapy.
Thomas RJ, Terzano MG, Parrino L et al. 2004. Obstructive
sleep-disordered breathing with a dominant cyclic alternating pattern —
a recognizable polysomnographic variant with practical clinical
implications. Sleep 27(2):229-234. “This variant of
sleep apnea may reflect a dominant component of respiratory instability
and periodic breathing coupled with upper-airway obstruction.
Besides positive airway pressure, measures to treat periodic breathing
may be required.
Thomas, S. A. and R. D. Palmiter. 1997. Disruption of the dopamine beta-hydroxylase
gene in mice suggests roles for norepinephrine in motor function, learning, and memory. Behav
Thomas, S. A. and R. D. Palmiter 1997b. Impaired maternal behavior in mice lacking
norepinephrine and epinephrine. Cell 91(5):583-592.
Thomas, S.P., 2000. A
phenomenologic study of chronic pain. West J Nurs Res
22(6):683-99. This paper called chronic nonmalignant pain "a force or monster
that cannot be tamed", in which "time seemed to stop; the future
Thomas, T. J. 1988. Fibrositis in men. West Virginia Med J 84:235-6.
Thomason HC 3rd, Bos GD, Renner JB. 2001. Calcifying
tendinitis of the gluteus maximus. Am J Orthop.
Thompson JM. 2012. Exercise in muscle pain disorders. PM R. 4(11):889-893. "Muscle pain disorders range from local or regional (myofascial pain) to widespread (fibromyalgia). Many people with muscle pain have decreased fitness. Exercise intolerance is a common feature as well, and yet exercise plays an important role in the treatment of muscle pain disorders. Results of studies have shown repeatedly, via multiple modes and methods of delivery, that exercise is at least as effective as the best pharmacologic treatments. An understanding by clinicians and their patients of the unique benefits of a carefully crafted exercise program is one step in the successful management of these often frustrating muscle pain disorders." Mayo School of Graduate Medical Education
Thompson JM, Luedtke CA, Oh TH. 2010. Direct medical costs in patients with fibromyalgia: Cost of illness and impact of a brief multidisciplinary treatment program. Am J Phys Med Rehabil. [Oct 21 Epub ahead of print]. "Patients with clinically diagnosed fibromyalgia incur direct medical costs about twice that of their matched controls. This increased cost is related to the severity of their symptoms as measured by the Fibromyalgia Impact Questionnaire and was not impacted by participation in a brief cognitive behaviorally based fibromyalgia treatment program."
Thornton EW, Sykes KS, Tang WK. 2004.
Health benefits of T'ai Chi exercise: improved balance and blood pressure in middle-aged women.
Health Promot Int 19(1):33-38. “Elderly T'ai chi practitioners attained the same level of balance control performance as did young, healthy subjects when standing under reduced or conflicting somatosensory, visual, and vestibular
Thorson, K. 1999. Is fibromyalgia a distinct clinical entity? The patients
evidence. Baillieres Best Pract Res Clin Rheumatol 13(3):463-7.
Thoss, F., B. Bartsch, D. Tellschaft and M. Thoss. 1999. Periodic inversion of the
vertical component of the Earths magnetic field influences fluctuation of visual
sensitivity in humans. Bioelectromagnetics 20(7):459-461.
Tiedemann AC, Sherrington C, Lord SR. 2007. Physical and
psychological factors associated with stair negotiation performance in
older people. J Gerontol A Biol Sci Med Sci.
62(11):1259-1265. “An inability to negotiate stairs is a marker of
disability and functional decline and can be a critical factor in loss
of independence in older people.” “In community-dwelling older people,
impaired stair negotiation is associated not only with reduced strength
but also with impaired sensation, strength, and balance; reduced
vitality; presence of pain; and increased fear of falling.” [T’ai chi
chuan may be useful to prevent or improve this problem. Improvement of
proprioception and muscle function, including range of motion, through
the treatment of co-existing MTPS should also be considered. Latent
MTPs may be common but unsuspected in elderly patients with restricted
range of motion. DJS]
Tietjen GE, Brandes JL,
Peterlin BL et al. 2009. Allodynia in migraine: association with
comorbid pain conditions. Headache. 49(9):1333-1344.
“Symptoms of CA (cutaneous allodynia) in migraine were associated with
current anxiety, depression, and several chronic pain conditions. A
graded relationship was observed between number of allodynic symptoms and
the number of pain conditions, even after adjusting for confounding factors.
This study also presents the novel association of CA symptoms with younger
age of migraine onset, and with cigarette smoking, in addition to confirming
several previously reported findings.”
Tiidus PM. 2010. Skeletal muscle damage and repair: classic paradigms and recent developments. J Musculoskel Pain. 18(4):396-402. This article explains the processes involved in muscle damage and repair, including muscle swelling, delayed onset muscle soreness, secondary injury related to the inflammatory response, and effects of sex hormones (and the loss of same on the aging), NSAIDS, and the arachidonic cascade on muscle repair. For example, NSAIDS may reduce the rate of post-injury repair, and estrogens and testosterone may enhance muscle recovery in multiple ways. The latter can be of significance to those of older years.
Tiihonen, M., M. Partinen and S. Narvanen. 1993. The severity of obstructive sleep
apnea is associated with insulin resistance. J Sleep Res 2(1):56-61.
Tikiz C, Muezzinoglu T, Pirildar T et al. 2005. Sexual dysfunction
in female subjects with fibromyalgia. J Urol.
174(2):620-623. “Female patients with FM have distinct sexual
dysfunction compared with healthy controls and coexistent MD has no
additional negative effect on sexual function. Thus, female
subjects with FM should be evaluated in terms of sexual function to
provide better quality of life.”
Timmerman GM, Calfa NA, Stuifbergen AK. 2013. Correlates of body mass index in women with fibromyalgia. Orthop Nurs. 32(2):113-119. "The findings support a growing body of evidence that excess weight is negatively related to quality of life and pain in women with FMS."
Ting TV, Hashkes PJ, Schikler K et al. 2012. Pediatr Rheumatol Online J. 10(1):16.
The role of benign joint hypermobility in the pain experience in Juvenile Fibromyalgia: an observational study. "Juvenile Fibromyalgia (JFM) is characterized by chronic widespread musculoskeletal pain and approximately 40% of children and adolescents with JFM also suffer from benign joint hypermobility (HM)....The presence of HM among adolescent patients with JFM appears to be associated with enhanced physiologic pain sensitivity, but not self-report of clinical pain. Further examination of the mechanisms for increased pain sensitivity associated with HM, especially in adolescents with widespread pain conditions such as JFM is warranted."
Tishler, M., Smorodin, T.,
Vanzina-Amit, M., et al. 2003. Fibromyalgia in diabetes mellitus. Rheumatol
Int [***epub ahead of print]. “Fibromyalgia is a common finding
in patients with types 1 and 2 diabetes, and its prevalence could be related
to control of the disease. As with other diabetes complications, FM
might be prevented by improved control of blood glucose levels.”
Tishler, M., Y. Barak, D. Paran and M. Yaron. 1997. Sleep disturbances, fibromyalgia
and primary Sjogren's syndrome. Clin Exp Rheumatol 15(1):71-74.
Tizabi, Y., R. L. Copeland Jr., R. Brus and R. M. Kostrzewa. 1999. Nicotine blocks
quinpirole-induced behavior in rats: psychiatric implications. Psychopharmacology
Tobbackx Y, Meeus M, Wauters L. 2012. Does acupuncture activate endogenous analgesia in chronic whiplash-associated disorders? A randomized crossover trial. Eur J Pain. [Sep 11 Epub ahead of print]. "It was shown that one session of acupuncture treatment results in acute improvements in pressure pain sensitivity in the neck and calf of patients with chronic WAD. Acupuncture had no effect on conditioned pain modulation or temporal summation of pressure pain. Both acupuncture and relaxation appear to be well-tolerated treatments for people with chronic WAD. These findings suggest that acupuncture treatment activates endogenous analgesia in patients with chronic WAD."
Toda K. 2007. The prevalence of
fibromyalgia in Japanese workers. Scand J Rheumatol.
36(2):140-144. “FM is a common musculoskeletal disorder among
Japanese adult workers, especially among female workers.”
Toda K, Harada T, Ishizaki F et al. 2006.
Parkinson disease patient with fibromyalgia: a case report.
Parkinsonism Relat Disord. [Jul 5 Epub ahead of print]. This
report indicates that pain in Parkinson’s disease patients may be from
other sources, including FMS. [The pain could also be due to
myofascial TrPs. DJS]
Todisco T, Todisco C, Bruni L et al. 2004.
Chin stimulation: a trigger point for provoking acute hiccups.
Tolk J, Kohnen R, Muller W. 2004. Intravenous
treatment of fibromyalgia with the 5-HT3 receptor antagonist tropisetron in
a rheumatological practice. Scand J Rheumatol Suppl.
(119):72-75. “IV tropisetron treatment represents a promising option
for the treatment of FM even though the study design incorporated many
Toms J. 2012. [Updated view of fibromyalgia]. Cas Lek Cesk. 151(9):415-419 [Czech].
"Fibromyalgia is a chronic syndrome characterized by dysfunction of pain processing and regulation....The absence of objective diagnostic tests often results in delayed diagnosis and patient fluctuation among a number of specialists with uncertainty and fear of a serious disease. The treatment is based on the individually adjusted and multidisciplinary approach to the patient, combining pharmacological and non-pharmacological therapy."
Ton E, Bakker MF, Verstappen SM on behalf of the Utrecht Rheumatoid Arthritis Cohort Study. 2011. Look Beyond the Disease Activity Score of 28 Joints (DAS28): Tender Points Influence the DAS28 in Patients with Rheumatoid Arthritis. J Rheumatol. [Oct 15 Epub ahead of print].
"DAS28 is influenced by tender points, even in the non-fibromyalgia range, falsely suggesting higher disease activity and decreasing the sensitivity of the DAS28 criterion of low disease activity or remission. When applying DAS28-guided "tight control" or "treat-to-target" treatment strategies in RA, evaluation of not only the DAS28, but also its individual components along with a full joint and physical evaluation including assessment of TP is required to reliably estimate the individual's disease activity, which guides therapeutic decisions."
Torma LM, Houck GM, Wagnild GM et al. 2012. Growing Old with Fibromyalgia: Factors That Predict Physical Function. Nurs Res. 62(1):16-24.
"Resilience, a novel variable in fibromyalgia research, was a unique predictor of physical function. Further research is needed to learn more about the relationships between resilience, fibromyalgia impact, and the aging process."
Torpy, D. J. and G. P. Chrousos. 1996. The three-way interactions between the
hypothalamic-pituitary-adrenal and gonadal axes and the immune system. Baillieres Clin
Torres Lacomba M, Mayoral del Moral O,
Coperias Zazo JL et al. 2010. Incidence of myofascial pain syndrome in
breast cancer surgery: a prospective study. Clin J Pain.
26(4):320-325. “Pain after breast cancer therapy is a recognized
complication found to have an adverse impact on patient's quality of life,
increasing psychosocial distress.....The objective of this study was to
assess the incidence of myofascial pain syndrome prospectively 12 months
after breast cancer surgery....Each participant was assessed preoperatively,
postoperatively between day 3 and day 5, and at 1, 3, 6, and 12 months after
surgery. A physical therapist, expert in the diagnosis of myofascial pain
syndrome, performed follow-up assessments. Pain descriptions by the patients
and pain pattern drawings in body forms guided the physical examination. The
patients were not given any information concerning myofascial pain or other
muscle pain syndromes....One year follow-up was completed by 116 women. Of
these, 52 women developed myofascial pain syndrome.... CONCLUSION:
Myofascial pain syndrome is a common source of pain in women undergoing
breast cancer surgery that includes axillary lymph node dissection at least
during the first year after surgery. Myofascial pain syndrome is one
potential cause of chronic pain in breast cancer survivors who have
undergone this kind of surgery.”
Torres M, Mayoral del Moral O, Yuste MJ et al. 2007.
Prevalence of myofascial pain syndrome in breast cancer. J
Musculoskel Pain 15 (Supp 13):29 item 47. [Myopain 2007 Poster]
“The prevalence of regional MPS in breast cancer suggests that it may be an
important cause of pain following cancer treatment such as surgery,
radiotherapy, chemotherapy or hormonal therapy.”
Torres-Oviedo G, Bastian AJ. 2010. Seeing is believing: effects of visual contextual cues on learning and transfer of locomotor adaptation. J Neurosci. 30(50):17015-17022. "Devices such as robots or treadmills are often used to drive motor learning because they can create novel physical environments. However, the learning (i.e., adaptation) acquired on these devices only partially generalizes to natural movements. What determines the specificity of motor learning, and can this be reliably made more general? Here we investigated the effect of visual cues on the specificity of split-belt walking adaptation. ….We evaluated the adaptation of temporal and spatial features of gait (i.e., timing and location of foot landing), their transfer to walking over ground, and washout of adaptation when subjects returned to the treadmill. Removing vision during both training (i.e., on the treadmill) and testing (i.e., over ground) strongly improved the transfer of treadmill adaptation to natural walking. Removing vision only during training increased the transfer of temporal adaptation, whereas removing vision only during testing increased the transfer of spatial adaptation. This dissociation reveals differences in adaptive mechanisms for temporal and spatial features of walking. Finally training without vision increased the amount that was learned and was linked to the variability in the behavior during adaptation. In conclusion, contextual cues can be manipulated to modulate the magnitude, transfer, and washout of device-induced learning in humans. "
Torresani C, Bellafiore S, De Panfilis G.
2009. Chronic urticaria is usually associated with fibromyalgia
syndrome. Acta Derm Venereol. 89(4):389-392. “A total of
126 patients with chronic urticaria were investigated for fibromyalgia
syndrome. The corresponding proportion for 50 control dermatological
patients was 16%, which is higher than previously published data for the
Italian general population (2.2%). It is possible that dysfunction
cutaneous nerve fibers of patients with fibromyalgia syndrome may release
neuropeptides, which, in turn, may induce dermal microvessel dilatation and
plasma extravasation. Furthermore, some neuropeptides may favor mast
cell degranulation, which stimulates nerve endings, thus providing positive
feedback. Chronic urticaria may thus be viewed in many patients, as a
consequence of fibromyalgia syndrome; in fact, skin neuropathy (fibromyalgia
syndrome) may trigger neurogenic skin inflammation (chronic urticaria).”
Toto BJ. 1993. Chiropractic
correction of congenital muscular torticollis. J Manipulative
Physiol Ther. 16(8):556-559. “Treatments included chiropractic
manipulation, trigger point therapy, specific stretches, pillow positioning
and exercises. Excellent results were obtained. Conclusion:
Suggests that chiropractic intervention is a viable treatment option for
congenital muscular torticollis. Further studies should be performed
to compare the effectiveness of other treatment options.”
Touch EA, White AR, Richards S et al. 2007.
Variability of criteria used to diagnose myofascial trigger point pain
syndrome-evidence from a review of the literature. Clin J Pain.
23(3):278-286. [While it is true that far too many authors of papers
confuse myofascial pain as TMJ, it is unfortunate that these authors did not
differentiate between the two, in spite of the clear distinction in the
articles: Simons DG. 1995. Myofascial pain syndrome: One term but two
concepts; a new understanding. J Musculoskeletal Pain 3(1):7-14 and
Simons DG. 2004. New aspects of myofascial trigger points: etiological
and clinical. J Musculoskeletal Pain 12(3/4):15-21. The authors
have noted an important truth. Far too many articles purporting to be
on myofascial pain do not specify the criteria that have been used.
Also, I believe that far too many articles on any kind of pain, including
fibromyalgia, do not take into consideration co-existing myofascial trigger
points may be influencing their research and lead to faulty or biased
Tough EA, White AR, Richards SH et al. 2010. Myofascial trigger point needling for whiplash associated pain - A feasibility study. Man Ther. [Jun 24 Epub ahead of print].
Forty-one patients with recent whiplash injury were tested in this study to see if phase III study specific needling therapy of myofascial TrPs was warranted. It is, and is being planned.
Townsley P, Ravenscroft A, Bedforth N. 2011. Ultrasound-guided spinal accessory nerve blockade in the diagnosis and management of trapezius muscle-related myofascial pain. Anaesthesia. [Mar 18 Epub ahead of print]. "We report the first description of ultrasound-guided spinal accessory nerve blockade using single-shot and subsequently continuous infusion (via a perineural catheter) local anesthetic techniques, for the diagnosis and treatment of myofascial pain affecting the trapezius muscle.... We have demonstrated that the spinal accessory nerve is identifiable in the posterior triangle of the neck and can be blocked successfully using ultrasound guidance. This technique can aid the diagnosis and treatment of myofascial pain originating from the trapezius muscle."
Trampas A, Kitsios A, Sykaras E et al. 2010. Clinical massage and modified Proprioceptive Neuromuscular Facilitation stretching in males with latent myofascial trigger points. Phys Ther Sport. 11(3):91-98.
Tran MT, Arendt-Nielsen L, Kupers R et al. 2012. Multiple chemical sensitivity: On the scent of central sensitization. Int J Hyg Environ Health. [Apr 7 Epub ahead of print]. "Increased capsaicin-induced secondary punctate hyperalgesia was demonstrated in MCS patients without comorbid, overlapping disorders, suggesting facilitated central sensitization in MCS."
Travell J. 1981. Identification of
myofascial trigger point syndromes: a case of atypical facial neuralgia.
Arch Phys Med Rehabil. 62(3):100-106. “A case report describes
in detail the treatment of a patient who, for 13 years, had suffered from a
medically enigmatic, intense right facial pain with severe dysfunction and
who is now pain-free, with a full schedule of unrestricted activities 23
years later.” [One cannot help but grieve for the patient’s 13 years lost
to needless intense pain. DJS]
Travell JG. 1977. A trigger point for hiccup.
J Am Osteopath Assoc. 77(4):308-312. This TrP is found in the
uvula, and can be treated by stimulation with the end of a cold spoon.
[Spray with appropriate anesthetic or application of oral anesthetic can
often work as well. DJS]
Tremblay A, Pelletier C, Doucet E et
al. 2004. Thermogenesis and weight loss in obese individuals: a primary
association with organochlorine pollution. Int. Jour Obesity
28(7):936-939. Many toxic chemicals can be stored in fat. Weight loss
may release toxic chemicals that slow and otherwise affect the body’s
metabolism, contributing to feelings of malaise and difficulty losing
Triadafilopoulos, G. , R. W. Simms and D. L. Goldenberg. 1991. Bowel dysfunction in
fibromyalgia syndrome. Dig Dis Sci 36(1):59-64.
Triano, J. J., M. McGregor and D. R. Skogsbergh. 1997. Use of chiropractic manipulation
in lumbar rehabilitation. J Rehabil Res Dev 34(4):394-404.
Trimble, M. H. and R. M. Enoka. 1991. Mechanisms underlying the training effects
associated with neuromuscular electrical stimulation. Phys Ther 71(4):273-280.
Trujillo KA, Akil H. 1994. Inhibition of
opiate tolerance by non-competitive N-methyl-D-aspartate receptor
antagonists. Brain Res. 633(1-2):178-188. “...NMDA
receptors may have a fundamental role in the development of opiate
tolerance....non-competitive NMDA receptor antagonists may be effective
adjuncts to opiates in the treatment of chronic pain.”
Trujillo, K. A. and H. Akil. 1994. Inhibition of opiate tolerance by
non-competitiveN-methyl-D-aspartate receptor antagonists. Brain Res
Tsai CT, Hsieh LF, Kuan TS et al. 2009.
Injection in the cervical facet joint for shoulder pain with myofascial
trigger points in the upper trapezius muscle. Orthopedics.
32(8). “This study demonstrates that intra-articular or
peri-articular injection into the cervical facet joint region can
effectively inactivate the upper trapezius myofascial trigger point
secondary to the facet lesion.” [Trigger points have perpetuating
factors. If the TrPs return in spite of appropriate treatment, the
perpetuating factor must be identified and brought under control.
In this case, the perpetuating factor was a facet joint problem. DJS]
Tsai CT, Hsieh LF, Kuan TS et al. 2009.
Remote effects of dry needling on the irritability of the myofascial trigger
point in the upper trapezius muscle. Am J Phys Med Rehabil.
[Apr 28 Epub ahead of print]. “This study demonstrated the remote
effectiveness of dry needling. Dry needling of a distal myofascial
trigger point can provide a remote effect to reduce the irritability of a
proximal myofascial trigger point.”
Tsang WW, Wong VS, Fu SN et al. 2004.
T'ai Chi improves standing balance control under reduced or conflicting sensory conditions.
Arch Phys Med Rehabil 85(1):129-137. "…T'ai Chi exercise can be a good choice of exercise for middle-aged adults, with potential benefits for
ageing as well as the aged."
Tsao JC, Meldrum M, Kim SC et al. 2007. Treatment preferences for
CAM in children with chronic pain. Evid Based Complement
Alternat Med. 4(3):367-374. “This study examined treatment
preferences in chronic pediatric pain patients offered a choice of CAM
therapies for their pain. Participants were 129 children (94
girls) (mean age = 14.5 years +/- 2.4; range = 8-18 years) presenting at
a multidisciplinary, tertiary clinic specializing in pediatric chronic
pain.” “Patients with a diagnosis of fibromyalgia (80%) were the
most likely to try CAM versus those with other pain diagnoses.”
“When given a choice of CAM therapies, this sample of children with
chronic pain, irrespective of pain diagnosis, preferred non-invasive
approaches that enhanced relaxation and increased somatic control.
Longer duration of pain and greater impairment in functioning,
particularly during family activities increased the likelihood that such
patients agreed to engage in CAM treatments, especially those that were
categorized as mind-based modalities.” [Children get FM. They also get
MTPs. Many suffer needlessly because of the mistaken belief that
they do not. Pediatricians need to become aware that many children are
suffering needlessly and perhaps unknowingly, because they have no frame
of reference. They have always hurt. Seek and ye shall find.
Tschopp, K. P. and C. Gysin. 1996.
Local injection therapy in 107 patients with
myofascial pain syndrome of the head and neck. ORL J Otorhinolaryngol Relat Spec 58(6):306-310.
Tsen, L. C. and W. R. Camann. 1997. Trigger point injections for myofascial pain during
epidural analgesia for labor. Reg Anesth 22(5):466-468.
Tsigos C, Chrousos G.
2002. Hypothalamic-pituitary- adrenal axis, neuroendocrine factors and
stress. J Psychosom Res 53(4):865. When the stress response system is
disrupted, many other hormones and informational substances can be affected,
including sex hormones, growth hormone and thyroid hormone.
Tsuchie H, Miyakoshi N, Kasukawa Y et al. 2013. High prevalence of abdominal aortic aneurysm in patients with chronic low back pain. Tohoku J Exp Med. 230(2):83-86. "The prevalence of LBP (low back pain) is high in AAA (abdominal aortic aneurysm) patients, and doctors who treat chronic LBP should be aware of AAA as a potential cause of LBP." [This study is included here to alert readers that abdominal aortic aneurysm is common in low back pain patients and must be assessed and can mimic symptoms of spinal or myofascial pain. DJS]
Tu CH, Niddam DM, Chao HT et al. 2010. Brain morphological changes associated with cyclic menstrual pain. Pain.150(3):462-468. "Primary dysmenorrhea (PDM) is the most prevalent gynecological disorder for women in the reproductive age. PDM patients suffer from lower abdominal pain that starts with the onset of the menstrual flow. Prolonged nociceptive input to the central nervous system can induce functional and structural alterations throughout the nervous system. In PDM, a chronic viscero-nociceptive drive of cyclic nature, indications of central sensitization and altered brain metabolism suggest a substantial central reorganization.... Our results demonstrate that abnormal GM volume changes are present in PDM patients even in the absence of pain. These changes may underpin a combination of impaired pain inhibition, increased pain facilitation and increased affect. Our findings highlight that longer lasting central changes may occur not only in sustained chronic pain conditions but also in cyclic occurring pain conditions." [The most common cause of menstrual pain is myofascial TrPs. It is to be hoped that greater awareness will be focused on the pain generators, as well as on the pain amplifier. DJS]
Tu CH, Niddam DM, Yeh TC et al. 2013. Menstrual pain is associated with rapid structural alterations in the brain. Pain. [May 18 Epub ahead of print]. "Dysmenorrhea is the most prevalent gynecological disorder for women in the childbearing age. Dysmenorrhea is associated with central sensitization and functional and structural changes in the brain. Our recent brain morphometry study disclosed that dysmenorrhea is associated with trait-related abnormal gray matter (GM) changes even in the absence of menstrual pain, indicating that the adolescent brain is vulnerable to menstrual pain. Here we report rapid state-related brain morphological changes, i.e. between pain and pain-free states, in dysmenorrhea. We used T1-weighted anatomical magnetic resonance imaging to investigate regional GM volume changes between menstruation and peri-ovulatory phases, in 32 dysmenorrhea subjects and 32 age- and menstrual cycle-matched asymptomatic controls. An optimized voxel-based morphometry analysis was conducted to disclose the possible state-related regional GM volume changes across different menstrual phases. A correlation analysis was also conducted between GM differences and the current menstrual pain experience in the dysmenorrhea group. Compared to the peri-ovulatory phase, the dysmenorrhea subjects revealed greater hypertrophic GM changes than controls during the menstruation phase in regions involved in pain modulation, generation of the affective experience and regulation of endocrine function while atrophic GM changes were found in regions associated with pain transmission. Volume changes in regions involved in regulation of endocrine function and pain transmission correlated with the menstrual pain experience scores. Our results demonstrated that short-lasting cyclic menstrual pain is associated not only with trait-related but also rapid state-related structural alterations in the brain. Considering the high prevalence rate of menstrual pain, these findings mandate a great demand to revisit dysmenorrhea regarding its impact on the brain and other clinical pain conditions."
Tuchman M, Barrett JA, Donevan S et al.
2010. Central sensitization and Ca(V)alpha(2)delta ligands in chronic pain
syndromes: pathologic processes and pharmacologic effect. J Pain.
[May 14 Epub ahead of print]. “This focus article discusses how the central
nervous system plasticity phenomenon, central sensitization, is established
in the induction and maintenance of chronic pain, allodynia, and
hyperalgesia. In addition, it explores the neurophysiologic actions of the
calcium-channel ligands gabapentin and pregabalin in limiting pathological
manifestations of central sensitization.”
Tugnet N, Williams R. 2012. "My bones hurt." An unusual cause of fibromyalgia syndrome. J Musculoskel Pain 20(3):208-221. This excellent case report documents fibromyalgia caused by multiple bony hemangiomatosis. [This is a good reminder that when the central nervous system is sensitized, it has been sensitized by something. One must look for the cause. DJS]
Tuncer, T., B. Butun, M. Arman, A. Akyokus and A. Doseyen. 1997. Primary fibromyalgia
and allergy. Clin Rheumatol 16(1):9-12.
Tullberg M, Ernberg M. 2006. Long-term effect on tinnitus by
treatment of temporomandibular disorders: a two-year follow-up by
questionnaire. Acta Odontol Scand. 64(2):89-96. “The
results of this study showed that TMD symptoms and signs are frequent in
patients with tinnitus and that TMD treatment has a good effect on
tinnitus in a long-term perspective, especially in patients with
Tuo KS, Cheng YY, Kao CL. 2006.
Vestibular rehabilitation in a patient with whiplash-associated
disorders. J Chin Med Assoc. 69(12):591-595.
Prompt comprehensive rehabilitation, including TrP injection,
coordination and vestibular rehab, may successfully treat some cases
of whiplash syndrome
Turk DC, Robinson
JP, Burwinkle R. 2004. Prevalence of fear of pain and activity
in patients with fibromyalgia syndrome. J Pain
5(9):483-490. “Fear of movement is a significant concern for
chronic pain sufferers because these behaviors maintain pain and
increase disability.” [While this is true of itself, care must
be taken in interpreting this behavior. It is not abnormal to
avoid movements that cause pain, and to consider this as
pathological shows disregard for the pain level of the patient and
lack of understanding and justice. DJS]
Turk DC. 1997. Evaluating the role of physical, operant,
cognitive, and affective factors in the pain behaviors of chronic pain
patients. Behavior Modification 21(3):259-280. “63
chronic pain patients diagnosed with the disorder fibromyalgia underwent
medical, physical, and psychological evaluations. The physical,
cognitive, and affective factors, but not operant factors, were
significantly related to observed pain behaviors. Pain behaviors
should be conceptualized as behavioral manifestation of pain based on a
complex interaction of various psychological and physical factors.”
Turk, D. C., A. Okifuji, J. D. Sinclair and T. W. Starz. 1998. Interdisciplinary
treatment for fibromyalgia syndrome: clinical and statistical significance. Arthritis
Care Res 11(3):186-95.
Turk, D. C., A. Okifuji, T. W. Starz and J. D. Sinclair. 1996. Effects of type of
symptom onset on psychological distress and disability in fibromyalgia syndrome patients. Pain
Turkyilmaz AK, Kurt EE, Capkin E et al. 2012. Assessment of neuropathic pain in patients with fibromyalgia syndrome: A pilot study. J Musculoskel Pain. 20(3):170-176. [This study indicated that many patients with fibromyalgia have neuropathic pain syndromes that are associated with pain severity. Since many if not all fibromyalgia patients also have myofascial trigger points, and trigger points can cause nerve entrapment and these symptoms, it is to be hoped that future studies will include co-existing trigger points as a possible cause of these symptoms. DJS]
Turner, R. A., M. Altemus, T. Enos, B. Cooper and T. McGuiness. 1999. Preliminary
research on plasma oxytocin in normal cycling women: investigating emotion and
interpersonal distress. Psychiatry 62(2):97-113.
Turo D, Otto P, Gebreab T et al. 2013. Shear wave elastography for characterizing muscle tissue in myofascial pain syndrome. J Acoust Soc Am. 133(5):3358. "Myofascial pain syndrome (MPS) affects 85% of chronic pain sufferers in a specialty pain center. Neck and low-back are commonly affected by MPS. Myofascial trigger points (MTrPs) are characteristic findings of MPS and are palpable tender nodules in the muscles of symptomatic subjects. Mechanical characterization of MTrPs and surrounding tissue can offer important insight about the pathophysiology of the MPS, which is currently poorly understood. In this study, we propose an inexpensive technique, based on ultrasound shear wave elastography, to objectively measure mechanical properties of MTrPs and surrounding tissue in the upper trapezius. In an ongoing clinical study, we recruited 34 subjects: 12 healthy controls, 10 with not spontaneously painful MTrPs (latent) and 12 with symptomatic chronic neck pain (>3 months) and active (spontaneously painful) MTrPs. Shear wave elastography was performed on the upper trapezius of all subjects using the Ultrasonix RP system and an external vibrator. Voigt's model was used to estimate shear modulus G and viscosity µ of the interrogated tissue. Preliminary analysis demonstrates that symptomatic muscle tissue in subjects with neck pain is stiffer …compared to muscle in control subjects… and that active MTrPs are more viscous …than surrounding tissue…. Latent MTrPs …and surrounding tissue … are more viscous than normal tissue …."
Turo D, Otto P, Shah JP et al. 2013. Ultrasonic characterization of the upper trapezius muscle in patients with chronic neck pain. Ultrason Imaging. 35(2):173-187. "Localization, diagnosis, and clinical outcome measures of painful MTrPs (myofascial trigger points) can be improved by objectively characterizing and quantitatively measuring their properties. The goal of this study was to evaluate whether ultrasound imaging and elastography can differentiate symptomatic (active) MTrPs from normal muscle.....results suggest that active MTrPs have more homogeneous texture and heterogeneous stiffness when compared with normal, unaffected muscle. Our methods enabled us to improve the imaging contrast between suspected MTrPs and surrounding muscle. Our results indicate that in subjects with chronic neck pain and active MTrPs, the abnormalities are not confined to discrete isolated nodules but instead affect the milieu of the muscle surrounding palpable MTrPs. With further refinement, ultrasound imaging can be a promising objective method for characterizing soft tissue abnormalities associated with active MTrPs and elucidating the role of MTrPs in the pathophysiology of MPS."
Turo D, Otto P, Shah JP et al. 2012. Ultrasonic tissue characterization of the upper trapezius muscle in patients with myofascial pain syndrome. Conf Proc IEEE Eng Med Biol Soc. 2012:4386-4389. Myofascial trigger points (MTrPs) are palpable, tender nodules in skeletal muscle that produce symptomatic referred pain when palpated…. Objective characterization and quantitative measurement of the properties of MTrPs can improve their localization and diagnosis, as well as lead to clinical outcome measures. MTrPs associated with soft tissue neck pain are often found in the upper trapezius muscle. We have previously demonstrated that MTrPs can be visualized using ultrasound imaging. The goal of this study was to evaluate whether texture-based image analysis can differentiate structural heterogeneity of symptomatic MTrPs and normal muscle.
Turton, E. P., P. J. Kent and R. C Kester. 1998. The aetiology of Raynauds
phenomenon. Cardiovasc Surg 6(5):431-40.
Tutoglu A, Boyaci A, Koca I et al. 2014. Quality of life, depression, and sexual dysfunction in spouses of female patients with fibromyalgia. Rheumatol Int. [Jan 9 Epub ahead of print.] "Being a spouse of a patient with fibromyalgia might significantly interfere with quality of life and lead to a high rate of sexual dysfunction. Spouses of patients with fibromyalgia might also be investigated for sexual dysfunction and quality of life. Treatment programs for this group should be considered."
Tuttle N. 2005. Do changes within a
manual therapy treatment session predict between-session changes for
patients with cervical spine pain? Aust J Physiother.
51(1):43-48. “The results support the use of within-session
changes in ROM [range-of-motion], centralization, and possible pain
intensity as predictors of between-session changes for
musculoskeletal disorders of the cervical spine.”
Tuunainen E, Poe D, Jantti P et al. 2011. Presbyequilibrium in the oldest olds, a combination of vestibular, oculomotor and postural deficits. Aging Clin Exp Res. [Mar 29 Epub ahead of print]. "Progressive loss of balance in the aged, or "presbyequilibrium," is a complex and incompletely understood process involving vestibular, oculomotor, visual acuity, proprioception, motor, organ system and metabolic weaknesses and disorders. These factors provide some potential basis for streamlining the diagnostic evaluation and aiding in planning for effective therapy. In the oldest olds, these problems are magnified, raising the need for additional expertise in their care that could be met by training specialized health care staff." [This study makes a good point. It would be interesting to include myofascial TrPs, a common cause of balance dysfunction, as part of this process. DJS]
Uceyler N, Valenza R, Stock M
et al. 2006. Reduced levels of anti-inflammatory cytokines in
patients with chronic widespread pain. Arthritis &
Rheumatism. 54(8):2656-2664. “Chronic widespread pain is
associated with a lack of anti-inflammatory and analgesic Th2
cytokine activity, which may contribute to its pathogenesis.”
Uceyler N, Zeller D, Kahn AK et al. 2013. Small fibre pathology in patients with fibromyalgia syndrome. Brain. [Epub Mar 9]This case control study of 25 patients investigated shape and function of small nerve fibers through punch biopsies of the upper thigh and lower leg, plus patient neurological assessment. FM patients had increased neuropathic findings in questionnaires. Compared with healthy controls and patients with depression, FM patients had impaired small fiber function with increased cold and warm sensation thresholds and increased reaction to touch/pain stimuli. There were a smaller number of unmyelinated nerve fiber bundles in the skin of FM patients compared to the others, although mylinated nerve fibers were equal in all groups. This study indicates that pain in FM has a neuropathic nature.[These patients were not screened for co-existing myofascial trigger points and related microcirculation abnormalities and nerve entrapment. DJS]
Ueda HM, Kato M, Saifuddin M et al. 2002.
Differences in the fatigue of masticatory and neck muscles between male
and female. J Oral Rehabil. 29(6):575-582. “The
purpose of this study was to investigate the nature of fatigue and
recovery of masticatory and neck muscles and the differences between
sexes in normal subjects during experimentally induced loading.
Significant differences in the recovery ratios between both sexes were
more prominent in the masseter muscle than in the SCM. These
results suggest that the differences in muscle endurance between sexes
may have some association with higher susceptibility of craniomandibular
disorders in females than in males.”
Uemoto L, Antonio C Garcia M, Vinicius D et al. 2013. Laser therapy and needling in myofascial trigger point deactivation. J Oral Sci. 55(2):175-181. Twenty-one women patients with bilateral masseter TrPs were divided into groups to receive either laser therapy, needling with local anesthetic or no treatment (control). The laser and needling groups experienced a significant decrease of pain by visual analogue scale. A significant decrease in pressure pain threshold was experienced by the local anesthetic needling group only. This study indicates that four sessions of needling with 2% lidocaine without vasoconstrictor, with intervals between 48 and 72 hours between treatments, or laser therapy at a dose of 4 J/cm2, effectively deactivated the TrPs.
Uemoto L, Nascimento de Azevedo R, Almeida Alfaya T et al. 2013. Myofascial trigger point therapy: laser therapy and dry needling. Curr Pain Headache Rep. 17(9):357. "The aim of the present review is to discuss two forms of treatment for myofascial pain: laser therapy and dry needling. Although studies have reported the deactivation of myofascial trigger points with these two methods, clinical trials demonstrating their efficacy are scarce. The literature reports greater efficacy with the use of laser over dry needling. It has been suggested that improvements in microcirculation through the administration of laser therapy may favor the supply of oxygen to the cells under conditions of hypoxia and help remove the waste products of cell metabolism, thereby breaking the vicious cycle of pain, muscle spasm and further pain. While laser therapy is the method of choice for patients with a fear of needles and healthcare professionals inexperienced with the dry needling technique, further controlled studies are still needed to prove the greater efficacy of this method."
Ulas UH, Unlu E, Hamamcioglu K et al. 2005.
Dysautonomia in fibromyalgia syndrome: sympathetic skin
responses and RR Interval analysis. Rheumatol Int.
[Epub ahead of print June 30] “Sympathetic as well as
parasympathetic nervous system dysfunction occurs in FM patients
and this abnormality could be determined by SSR [sympathetic
skin response] and RRIV [R-R interval variation] analysis.”
Brodsky L. Nasal pain disrupting sleep as a presenting
symptom of extraesophageal acid reflux in children. Int
J Pediatr Otorhrinolaryngol 69(11):1555-1557. Acid
reflux caused nasal pain and disrupted sleep in a 4 year old
boy. Treated with acid suppression. Not tested for
Uludag M, Kaparov A, Sari H et al. 2011. Osteopoikilosis associated with fibromyalgia and active myofascial trigger point in upper trapezius muscles. J Back Musculoskel Rehabil. 24(4):257-261. "The sclerosing bone dysplasia known as osteopoikilosis can be associated with fibromyalgia and trigger points." [This is another case of interactive diagnoses. DJS]
Umeda M, Corbin LW, Maluf KS. 2013. Pain mediates the association between physical activity and the impact of fibromyalgia on daily function. Clin Rheumatol. [Sep 13 Epub ahead of print].
"This study quantified the association between recreational physical activity and daily function in women with fibromyalgia, and determined if this association is mediated by symptoms of pain, depression, or body mass….These results indicate that the intensity of musculoskeletal pain, rather than depressive symptoms or body mass, mediates the association between physical activity and daily function among women with fibromyalgia." This study shows that pain itself is the driving factor determining the amount of activity and function in FM women, and it is not the "sedentary nature" or depression that drives the pain.
Umstadt HE. 2002. [Botulinum toxin in
oromaxillofacial surgery] Mund Kiefer Gesichtschir.
6(4):249-260. [German] “Abnormal activity of the masticatory or
mimic muscular system, whether acquired or congenital, leads to
aesthetic and/or functional impairments for the patient. Subsequently,
pathological changes of the tissue structure caused by persistent
dysfunction can entail chronic pain and progressive aesthetic reduction
can induce psychopathological conditions in a patient. Use of
botulinum toxin A can achieve short-term correction of muscular
activities with very few side effects if applied in an accurate and
controlled manner.” [Trigger points should be treated with
standard management techniques before botulinum toxin is considered.
Unno N, Fink MP 1998. Intestinal epithelial
hypermobility. Mechanisms and relevance to disease.
Gastroenterol Clin North Am 27(2):289-307. Mechanisms and
relevance of leaky gut syndrome.
Urata M, Fukuno H, Nomura M et al. 2006.
Gastric motility and autonomic activity during obstructive sleep apnea. Aliment
Pharmacol Ther. 24 Suppl 4:132-140. “The present study suggested that,
in addition to decreased pressure on the pleural cavity, factors affecting
the development of RE might include abnormal gastric motility, low oxygen,
and increased sympathetic nervous activity during sleep apnea.”
Urban, M. O. and G. F. Gebhart. 1999. Central mechanisms in pain. Med Clin North Am
Uremovic M, Cvijetic S, Pasic MD et al. 2007.
Impairment of proprioception after whiplash injury. Coll Antropol.
31(3):823-827. “…subject with recent cervical spine injury have
incorrect perception of their head position. Therefore, their
rehabilitation should include the correction of proprioception and head
coordination.” [Assessment for associated MTPs in the head and neck,
which may adversely affect priprioception, as well as restrict range of
motion and cause other symptoms, should be done promptly, and treatment
continued until the MTPs are resolved to avoid chronicity if possible. DJS]
Urresti F, Perez LG, Cueco RT. 2007. Effectiveness of deep dry
needling of trigger points in lateral pterigoid muscle. J
Musculoskel Pain 15 (Supp 13):40 item 69. [Myopain 2007
Poster] “LPTM (lateral pterygoid muscle) MTP appears to be a common
cause of temporomandibular pain.”
Urschitz, MS, Guenther, A,
Eggebrecht, E et al. Snoring, intermittent hypoxia and academic
performance in primary school children. Am J Resp Crit Care Med
168:464-468. Habitual snoring is significantly associated with poor
Ursin, R., I. Endresen, H. Vaeroy and A. M. Hjelmen. 1999. Relations among muscle pain,
sleep variables, and depression. J Musculoskel Pain 6(4):59-72.
Ustun N, Arslan F, Mansuroglu A et al. 2013. Efficacy of EMLA cream phonophoresis comparison with ultrasound therapy on myofascial pain syndrome of the trapezius: a single-blind, randomized clinical study. Rheumatol Int. [Oct 23 Epub ahead of print]. This study from Turkey took 50 myofascial pain syndrome patients (42 female and 8 male), and separated them into groups where they received either phonophoresis (PH) with EMLA local anesthetic (2.5% lidocaine, 2.5% prilocaine) cream, or ultrasound (US). The groups received treatment 10 minutes a day for 15 sessions on all active trapezius trigger points. The study found: "EMLA cream phonophoresis is more effective than conventional ultrasound therapy in terms of pain and associated neck disability…"
Usui C, Hatta K, Doi N et al. 2010. Brain
perfusion in fibromyalgia patients and its differences between responders
and poor responders to gabapentin. Arthritis Res Ther. 12(2):R64.
“The present study revealed brain regions with significant hyperperfusion
associated with the default-mode network, in addition to abnormalities in
the sensory dimension of pain processing and affective-attentional areas in
fibromyalgia patients. Furthermore, hyperperfusion in these areas was
strongly predictive of poor response to gabapentin.”
Usui C, Doi N, Nishioka M et al. 2006.
Electroconvulsive therapy improves severe pain associated with fibromyalgia.
Pain. 121(3):276-280. “Several reports have recently suggested
the novel concept that fibromyalgia is due to the central nervous system
becoming hyper-responsive to a peripheral stimulus....Our study clearly
demonstrated that pain was significantly less severe after ECT, as indicated
by the VAS scale for pain and the evaluation of TPs. A further notable
observation was that thalamic blood flow was also improved.”
Usui C, Doi N, Nishioka M et al. 2006.
Electroconvulsive therapy improves severe pain associated with fibromyalgia.
Pain [Feb 20 Epub ahead of print].
Uvnas-Moberg, K. 1997. Physiological and endocrine effects of social contact. Ann N
Y Acad Sci 807:146-163.
Vadivelu N, Mitra S, Narayan D.
Recent advances in
postoperative pain management. Yale
J Biol Med. 83(1):11-25. “Good pain control after surgery is
important to prevent negative outcomes such as tachycardia,
hypertension, myocardial ischemia, decrease in alveolar ventilation, and
poor wound healing. Exacerbations of acute pain can lead to neural
sensitization and release of mediators both peripherally and centrally.
Clinical wind up occurs from the processes of N-Methyl D-Aspartate (NMDA)
activation, wind up central sensitization, long-term potentiation of
pain (LTP), and transcription-dependent sensitization. Advances in the
knowledge of molecular mechanisms have led to the development of
multimodal analgesia and new pharmaceutical products to treat
postoperative pain. The new pharmacological products to treat
postoperative pain include extended-release epidural morphine and
analgesic adjuvants such as capsaicin, ketamine, gabapentin, pregabalin
dexmetomidine, and tapentadol. Newer postoperative patient-controlled
analgesia (PCA) in modes such as intranasal, regional, transdermal, and
pulmonary presents another interesting avenue of development.” [This
paper stresses the importance of acute pain control to help prevent
central sensitization. When patients already are in a central
sensitization state such as FM, such pain control is critical. DJS]
Vadivelu N, Hines RL.
2008. Management of chronic pain in the elderly: focus on
transdermal buprenorphine. Clin Interv Aging. 3(3):421-430.
“The transdermal buprenorphine matrix allows for slow release of
buprenorphine and damage does not produce dose dumping. In
addition, the long-acting analgesic property and relative safety profile
makes it a suitable choice for the treatment of chronic pain in the
elderly. Its safe use in the presence of renal failure makes it an
attractive choice for older individuals. Recent scientific studies
have shown no evidence of a ceiling dose of analgesia in man but only a
ceiling effect for respiratory depression, increasing its safety
profile. It appears that transdermal buprenorphine can be used in
clinical practice safely and efficaciously for treating chronic pain in
Vaeroy, H., T. Sakurada, O. Forre, E. Kass and L. Terenius. 1989. Modulation of pain in
fibromyalgia (fibrositis syndrome): cerebral spinal fluid (CFS) investigation of pain
related neuropeptides with special reference to calcitonin gene related peptide (CGRP). J
Rheumatol Suppl 19:94-97.
Vaeroy, H., A. Abrahamsen, O. Forre and E. Kass. 1989. Treatment of fibromyalgia
(fibrositis syndrome): a parallel double-blind trial with carisoprodol, paracetamol and
caffeine (Somadrilcomp) versus placebo. Clin Rheumatol 8(2):245-250.
Valance, A. K. 1998. Can biological activity be maintained at Ultra-High Dilution? An
overview of homeopathy, evidence, and bayesian philosophy. J Altern Complement Med
Valdés M, Collado A, Bargalló N et
al. 2010. Increased glutamate-glutamine compounds (Glx) in the brain of
patients with fibromyalgia: A MR spectroscopy study. Arthritis Rheum.
[Feb 26 Epub ahead of print] Fibromyalgia (FM) has been defined as a
systemic disorder clinically characterized by pain, cognitive deficit
and the presence of associated psychopathology, all of which are
suggestive of a primary brain dysfunction. In order to identify the
nature of this cerebral dysfunction, brain metabolites of FM patients
have been studied through MR spectroscopy techniques. METHODS: Brain
metabolites in amygdala, thalami and prefrontal cortex were studied
through MR spectroscopy techniques in a sample of 28 women with FM, and
in a control group of healthy women (n=24) of the same age. RESULTS::
Compared to healthy controls FM patients showed higher levels of
glutamate compounds (Glx) (11,9+/-1,6 vs. 13,4+/-1,7 arbitrary
institutional units respectively, t= 2.517, df 35, p=0.03) and a higher
glutamine-glutamate/creatine ratio (Glx/Cr) (2,1+/- 0,4 in controls vs.
2,4 +/- 1,4 in FM patients, t=2.373, df 35, p=0.04) in the right
amygdala. In FM patients with more pain, fatigue and depressive symptoms
inositol (Ins) levels were significantly higher in the right amygdala
and right thalamus. CONCLUSIONS: The distinctive metabolic features
found in the right amygdala of FM patients suggest the possible
existence of a neural dysfunction in emotional processing, this being a
prolongation of the dysfunction in pain processing previously proposed
by some authors.
Valencia-Flores M, Cardiel MH, Santiago
V et al. 2004. Prevalence and factors associated with fibromyalgia in Mexican patients with systemic lupus erythematosus.
Lupus 13(1):4-10. “Fibromyalgia is not common in Mexican patients with SLE and has a different pattern of symptoms in RP (regional pain) and NP (no pain) patients.
These data add evidence that ethnicity can play an important role in FM manifestations.”
Valenza MC, Rodenstein DO, Fernandez-de-las-Penas C. 2011. Consideration of sleep dysfunction in rehabilitation. J Bodyw Mov Ther. 15(3):262-267. Patients with whiplash commonly have neck pain that is contributory to sleep disturbance. There is a direct relationship between pain intensity and worsening sleep quality. It is essential to treat both the causes of the pain and the sleep dysfunction components as part of management of these patients.
Valenza MC, Valenza G, Gonzalez-Jimenez E et al. 2011. Alteration in sleep quality in patients with mechanical insidious neck pain and whiplash-associated neck pain. Am J Phys Med Rehabil. [Dec 14 Epub ahead of print]. "Sleep disturbances are a common finding in individuals with neck pain and are associated with the intensity of ongoing pain in WAD (whiplash)." Inadequate sleep quality and quantity can contribute to multi-system effects. "It seems essential to address the ongoing cycle of pain and sleep disturbances as an integral part of the treatment of patients with neck pain."
Valim, V., Oliveira, L., Suda, A.,
et al. 2003. Aerobic fitness effects in fibromyalgia. J
Rheumatol 30(5):1060-1069. “...aerobic exercise is beneficial to
patients with FM, but the cardiorespiratory gain is not related to
improvement of FM symptoms.”
Valkeinen H, Hakkinen A, Alen M et al. 2007.
Physical fitness in postmenopausal women with fibromyalgia. Int J
Sports Med. [Oct 24 Epub ahead of print]. “A lower maximal load in
the aerobic test suggests the patients’ unsatisfactory ability to stand
physical loading and resist overall fatigue. Moreover, fatigue rather
than pain was the main factor to decrease the quality of life in women with
fibromyalgia. Additional efforts should be addressed to strength
training, when planning health promotion and rehabilitation programs in
fibromyalgia.” [These results may be suspect as there is no allowance
for co-existing MTPs that could be affecting the results. Also,
strength training, if there are MTPs, will only make them worse. You
can’t strengthen a muscle that is physiologically inhibited by MTPs.
Vallbona, C., C. F. Hazelwood and G. Jurida. 1997. Response of pain to static magnetic
fields in post-polio patients: a double-blind pilot study. Arch Phys Med Rehabil
Vallejo M, Martinez-Martínez LA, Grijalva-Quijada S et al. 2013. Prevalence of fibromyalgia in vasovagal syncope. J Clin Rheumatol. 19(3):111-114. "Fibromyalgia was relatively frequent in these women with vasovagal syncope and could be associated with dysautonomic symptoms. Therefore, it seems important to search for dysautonomic comorbidities in patients with vasovagal syncope and/or fibromyalgia, to provide a patient-centered holistic approach, instead of the often currently used therapeutic partition."
Valouchova P, Lewit K. 2009. Surface
electromyography of abdominal and back muscles in patients with active
scars. J Bodywork Move Ther. 13(3):262-267. Abdominal
scars may significantly impair back mobility and add to clinical symptoms.
These scars and the tissue around them can often be treated successfully
with manual methods, and this study gives objective data of surface
electromyography to show this. The “…muscles surrounded by active scar
tissue are likely to harbour trigger points.”
Valrie CR, Bromberg MH, Palermo T et al. 2013. A systematic review of sleep in pediatric pain populations. J Dev Behav Pediatr. 34(2):120-128. "Findings from this review highlight the need to assess and treat sleep problems in children presenting with persistent pain. Health care providers should consider conducting routine sleep screenings, including a comprehensive description of sleep patterns and behaviors obtained through clinical interview, sleep diaries, and/or the use of standardized measures of sleep. Future research focusing on investigating the mechanisms associating sleep and pediatric persistent pain and on functional outcomes of poor sleep in pediatric pain populations is needed."
Van Cauter E,
Holmback U, Knutson K et al. 2007. Impact of sleep and sleep loss on
neuroendocrine and metabolic function. Horm Res. 67 Suppl
1:2-9. “Laboratory studies in healthy young volunteers have shown that
experimental sleep restriction is associated with a dysregulation of the
neuroendocrine control of appetite consistent with increased hunger and with
alterations in parameters of glucose tolerance suggestive of an increased
risk of diabetes. Epidemiologic findings in both children and adults
are consistent with the laboratory data.” Deep sleep has a significant
effect on hormones.
Van Cauter E, Latta F, Nedeltcheva A
et al. 2004. Reciprocal interactions between the GH axis and sleep.
Growth Horm IGF Res. 14 Suppl A:S10-7. “Preliminary data show decreased
total sleep time and increased sleep fragmentation in GH-deficient patients
as compared with normal controls.”
Van Cauter, E., L. Plat and G. Copinschi. 1998. Interrelations between sleep and the
somatotropic axis. Sleep 21(6):553-66.
Van Daele DJ, McCulloch TM, Palmer PM et al. 2005.
Timing of glottic closure during swallowing: a combined electromyographic
and endoscopic analysis. Ann Otol Rhinol Laryngol.
114(6):478-487. [This article indicates why TrPs in some of the area
muscles could have some patients choking on their own saliva, “swallowing
the wrong way". In such cases, it may be wise to check the thyroarytenoid
and other area muscles for TrPs.]
van de Glind G, de Vries M, Rodenburg R et al. 2007. Resting
muscle pain as the first clinical symptom in children carrying the MTTK
A8344G mutation. Eur J Paediatr Neurol. [Feb 9 Epub ahead
of print] “Fatigue in combination with recurrent resting muscle pain
occurs frequently in the initial phase of various hereditary muscle
disorders and in several autoimmune, endocrine and metabolic syndromes.
In the absence of obvious biochemical/metabolic abnormalities and in the
lack of neurological symptoms, the complaints are frequently labeled as
fibromyalgia or chronic fatigue syndrome.” [We certainly need more
research into genetic mitochondrial defects. DJS]
van Denderen, J. C. , J. W. Boersma, P. Zeinstra, A. P. Hollander and B. R. van
Neerbos. 1992. Physiolgical effects of exhaustive physical exercise in primary
fibromyalgia syndrome (PFS): is PFS a disorder of neuroendocrine reactivity? Scand J
Vanderweeen L, Oostendorp RA, Vaes P et al.
1996. Pressure algometry in manual therapy. Man Ther.
Van de Ven TJ, John Hsia HL. 2012. Causes and prevention of chronic postsurgical pain. Curr Opin Crit Care [Jun 22 Epub ahead of print]. "Surgical incision invariably causes some measure of nerve damage and inflammatory response that, in most cases, heals quickly without long-term negative consequence. However, a subset of these patients go on to develop lasting neuropathic pain that is difficult to treat and, in many cases, prevents the return to normal activities of life. It remains unknown why two patients with identical surgical interventions may go on to develop completely divergent pain phenotypes or no pain at all. Aggressive, early analgesic therapy has been shown to reduce the incidence of chronic postsurgical pain (CPSP), but no specific regional anesthetic technique or systemic pharmacologic therapy has been shown to prevent CPSP....Inflammation and glial cell activation have recently been shown to be just as important in the transition from normal acute pain to pathologic chronic pain as nerve injury itself and that central sensitization may not be solely due to repetitive nociceptive firing at the time of nerve injury. This has opened a number of new therapeutic possibilities for prevention of CPSP....Here, we discuss the causes of CPSP and current useful preventive strategies in the perioperative period. We also discuss future potential disease-modifying treatments of CPSP." [Since glial cells in the spinal cord have been implicated in the development of central sensitization states such as fibromyalgia, this is of interest. Histamine levels, microcirculation, and other factors affecting TrP development may be part of the answer to this puzzle. DJS]
Van Gheluwe B, Dananberg HJ, Hagman F et al. 2006.
Effects of hallux limitus on plantar foot pressure and foot kinematics
during walking. J Am Podiatr Med Assoc 96(5):428-436.
[Stiffness or contracture of the hallicis muscles, such as that due to
myofascial TrPs, although largely ignored in the literature, could be a
major source of gait irregularities and foot dysfunction. DJS]
Van Handel D, Fass R. 2005. The
pathophysiology of non-cardiac chest pain. J Gastroenterol Hepatol.
20 Suppl 3:S6-S13. Gastroesophageal reflux disease (GERD) is the most
common cause of non-cardiac pain. [But what is causing the GERD? It
would have been helpful if these patients had been checked for abdominal
Van Houdenhove B, Luyten P. 2006. Stress,
depression and fibromyalgia. Acta Neurol Belg. 106(4):149-156.
Van Houdenhove B,
Neerinckx, E, Onghena P et al. 2002. Daily hassles reported by
chronic fatigue syndrome and fibromyalgia patients in tertiary
care: a controlled quantitative and qualitative study.
Psychother Psychosom 71(4):207-13. Patients with Chronic
Fatigue Syndrome and FM show "a higher frequency of hassles,
higher emotional impact and higher fatigue, pain depression and
anxiety levels than patients with RA or MS." The cause of the
hassles are "dissatisfaction with oneself, insecurity and a lack
of social recognition." "An optimal therapeutic approach of CFS
and FMS should take account of this heavy psychosocial burden,
which might refer to core themes of these patients' experiences."
Van Koulil S, Kraaimaat FW, van Lankveld W
et al. 2009. A patient’s perspective on multidisciplinary treatment gain
for fibromyalgia: an indicator for pre-post treatment effects?
Arthritis Rheum. 61(12):1626-1632. “Results suggest that the
patient’s perception of treatment gain and pre-post changes in outcomes
during treatment assess different aspects of the patient’s perception of
treatment gain as an independent and clinically relevant outcome, in
addition to standardized trial data of pre-post assessments of health
van Laarhoven A, Kraaimaat F, Wilder-Smith O. 2007.
Generalized and symptom-specific sensitization of chronic itch and pain.
J Eur Acad Dermatol Venereol. 21(9):1187-1192. “The present
study provides preliminary support that both generalized and
symptom-specific sensitization processes play a role in the regulation and
processing of somatosensory stimulation of patients with chronic itch and
Van Middendorp H, Lumley MA, Moerbeek M et
al. 2009. Effects of anger and anger regulation styles on pain in
daily life of women with fibromyalgia: a diary study. Eur J
Pain. [Apr 16 Epub ahead of print]. “Our study suggests that
anger and a general tendency to inhibit anger predicts heightened pain
in the everyday life of female patients with fibromyalgia.
Psychological intervention could focus on healthy anger expression to
try to mitigate the symptoms of fibromyalgia.”
van Oosterwijck J, Meeus M, Paul L et al. 2013. Pain physiology education improves health status and endogenous pain Inhibition in fibromyalgia: A double-blind randomized controlled trial. Clin J Pain. [Jan 30 Epub ahead of print]. "These results suggest that FM patients are able to understand and remember the complex material about pain physiology. Pain physiology education seems to be a useful component in the treatment of FM patients as it improves health status and endogenous pain inhibition in the long term."
Van Oosterwijck J, Nijs J, Meeus M et al. 2012. Evidence for central sensitization in chronic whiplash: A systematic literature review. Eur J Pain. [Sep 25 Epub ahead of print]. "It has been suggested that sensitization of the central nervous system plays an important role in the development and maintenance of chronic (pain) complaints experienced by whiplash patients. According to the PRISMA guidelines, a systematic review was performed to screen and evaluate the existing clinical evidence for the presence of central sensitization in chronic whiplash....These studies evaluated the sensitivity to different types of stimuli (mechanical, thermal, electrical). Findings suggest that although different central mechanisms seem to be involved in sustaining the pain complaints in whiplash patients, hypersensitivity of the central nervous system plays a significant role.....international guidelines for the definition, clinical recognition, assessment and treatment of central sensitization are warranted."
van Uden-Kraan CF,
Drossaert CH, Taal E et al. 2010. Patient-initiated online support
groups: motives for initiation, extent of success and success factors.
J Telemed Telecare. 16(1):30-34. “We studied the success and
success factors of online support groups (OSGs) for patients, and the
motives and goals of people who start such groups. We interviewed 23
webmasters of OSGs for patients with breast cancer, fibromyalgia and
arthritis. The majority were women (n = 20) and most were patients (n =
21). Analysis of the interviews revealed that webmasters had altruistic
and intrinsic motives for initiating an online support group. They
defined success as the fulfillment of the goals they had in mind when
they initiated their groups. To be able to make a group successful,
decisions about its organization and management need to be coherent with
these goals. Most webmasters stressed that promoting the group, keeping
it alive and moderating the messages were vital success factors during
the evolution stage. Management of the OSGs took up much of the
webmasters' time and energy. On average webmasters were occupied with
the group for 10-15 hours a week. Our study provides an overview of the
pros and cons of differing decisions that have to be made when
initiating an OSG.”
van Uden-Kraan CF,
Drossaert CH, Taal E et al. 2008. Empowering processes and outcomes of
participation in online support groups for patients with breast cancer,
arthritis, or fibromyalgia. Qual Health Res. 18(3):405-417.
“Empowering outcomes mentioned were being better informed; feeling confident
in the relationship with their physician, their treatment, and their social
environment; improved acceptance of the disease; increased optimism and
control; enhanced self-esteem and social well-being; and collective
action.” “...participation in online support groups can make a valuable
contribution to the emergence of empowered patients.” [It is vitally
important that the support groups be positive and empowering. Negative
groups that are exclusive or stressful can have an equally undermining
effect on patient quality of life. DJS]
Wilgen CP, Dijkstra PU, Van Der Laan BF et al. 2004. Morbidity of the
neck and head and neck cancer therapy. Head Neck 26(9):785-791.
The authors found that 46% of the post-surgery cancer patients had
myofascial pain. [This indicates that at least some of the pain, loss
of range of motion and muscle weakness the patients with co-existing
myofascial pain sustained could be either eliminated or minimized by
adequate treatment of the myofascial component. DJS]
van Wilgen CP, Keizer D. 2012. The sensitization model to explain how chronic pain exists without tissue damage. Pain Manag Nurs. 13(1):60-65. "The interaction of nurses with chronic pain patients is often difficult. One of the reasons is that chronic pain is difficult to explain, because no obvious anatomic defect or tissue damage is present. There is now enough evidence available indicating that chronic pain syndromes such as low back pain, whiplash, and fibromyalgia share the same pathogenesis, namely, sensitization of pain modulating systems in the central nervous system. Sensitization is a neuropathic pain mechanism in which neurophysiologic changes may be as important as behavioral, psychological, and environmental mechanisms. The sensitization model provides nurses with an opportunity to explain pain as a physical cause related to changes in the nervous system. This explanation may improve the patient's motivation to discuss the importance of psychosocial factors that contribute to the maintenance of chronic pain. In this article, sensitization is described as a model that can be used for the explanation of the existence of chronic pain. The sensitization model is described using a metaphor. The sensitization model is a useful tool for nurses in their communication and education toward patients."
Vanhala, M. 1999. Childhood weight and metabolic syndrome in adults. Ann Med
Varani, K, F Portaluppi, S Merighi,
F Ongini, L Belardinelli and PA Borea.
1999. Caffeine alters A2A adenosine receptors and their function in human platelets. Circulation
Vargas A, Vargas A, Hernandez-Paz R et al. 2006.
Sphygmomanometry-evoked allodynia – a simple bedside test indicative of
fibromyalgia: a multicenter developmental study. J Clin Rheumatol.
12(6):272-274. “Sphygmomanometry is a simple bedside test that may be
useful in the recognition of patients with FM….Based on our results, we
suggest searching for FM features in any person who has sphygmomanometry-evoked
allodynia.” [This article unfortunately fails to recognize that this
method, possibly an easy, inexpensive way to diagnose FMS, was discovered
and developed by JB Eisenger. DJS]
Vargas A, Vargas A,
Hernandez-Paz R et al. 2006. Sphygmomanometry-evoked allodynia – a
simple bedside test indicative of fibromyalgia: a multicenter
developmental study. J Clin Rheumatol. 12(6):272-274.
“Sphygmomanometry is a simple bedside test that may be useful in the
recognition of patients with FM. Blood pressure testing is a
universal procedure in all clinical environments. Based on our
results, we suggest searching for FM features in any person who has
sphygmomanometry-evoked allodynia.” [This supports the work of JB
Eisinger and his discovery that FMS may be diagnosed by blood pressure
test evoked pain. DJS]
Vargas-Alarcon G, Alvarez-Leon E, Fragoso JM et al. 2012. A SCN9A gene-encoded dorsal root ganglia sodium channel polymorphism associated with severe fibromyalgia. BMC Musculoskel Disord. 13(1):23. "A consistent line of investigation suggests that autonomic nervous system dysfunction may explain the multi-system features of fibromyalgia (FM); and that FM is a sympathetically maintained neuropathic pain syndrome....The aim of this study was to search for an association between fibromyalgia and several SCN9A sodium channels gene polymorphisms....We studied 73 Mexican women suffering from FM and 48 age-matched women who considered themselves healthy....In this ethnic group; a disabling form of FM is associated to a particular SCN9A sodium channel gene variant. These preliminary results raise the possibility that some patients with severe FM may have a dorsal root ganglia sodium channelopathy."
Vargas-Alarcon G, Fragoso JM, Cruz-Robies
D et al. 2009. Association of adrenergic receptor gene
polymorphisms with different fibromyalgia syndrome domains.
Arthritis Rheum. 60(7):2169-2173. “AR (adrenergic
receptor) gene polymorphisms are related to the risk of developing
FM and are also linked to different domains of the FM syndrome.”
Vaz C, Couto M, Duarte C et al. 2009.
[An unusual case of generalized pain: paramyloidosis simulating
fibromyalgia] Acta Reumatol Port. 34(2B):431-435.
[Portuguese] [Fibromyalgia central sensitization is maintained by
something, whether it be myofascial TrP pain or another underlying
co-existing condition. Diagnosis does not stop with a FM label
but must include searching for the cause of the central sensitization.
Vecchiet L, Vecchiet J, Giamberardino MA.
1999. Referred muscle pain: clinical and pathophysiologic aspects.
Curr Rev Pain 3(6):489-498. Referred pain is common in medicine,
and the average practitioner in general practice encounters it
frequently. [One wonders why the concept of referred pain from
myofascial TrPs is met with such resistance. DJS]
Vecchiet, L, J Vecchiet, R Bellomo, and MA Giamberardino. 1999. Muscle pain from
physical exercise. J Musculoskel Pain 7(1-2):43-63.
Vecsei, L., G. Dibo and C. Kiss. 1998. Neurotoxins and neurodegenerative disorders. Neurotoxicology
Velazquez KT, Mohammad H, Sweitzer SM. 2007.
Protein kinase C in pain: involvement of multiple isoforms.
55(6):578-589. “Protein kinase C
isozymes are under investigation as potential therapeutics for the
treatment of chronic pain conditions.” “…protein kinase C may function
as a master regulator of the peripheral and central sensitization that
underlies many chronic pain conditions.”
Veldhuijzen DS, Sondaal SF, Oosterman JM. 2012. Intact cognitive inhibition in patients with fibromyalgia but evidence of declined processing speed. J Pain. 13(5):507-515. "Patients with fibromyalgia frequently report cognitive complaints. In this study we examined performance on 2 cognitive inhibition tests, the Stroop Color-Word Test (SCWT) and the Multi-Source Interference Test (MSIT), in 35 female patients with fibromyalgia and 35 age-matched healthy female controls....For patients, pain ...correlated significantly to several indices of cognition. Psychosocial variables were not related to cognitive test performance. Fibromyalgia patients performed worse on both tests but to a similar extent for the neutral condition and the interference condition, indicating that there is no specific problem in cognitive inhibition. Evidence of decreased mental processing and/or psychomotor speed was found in patients with fibromyalgia. PERSPECTIVE: Fibromyalgia patients performed worse on interference tests, but no specific problem in cognitive inhibition was found. Decreased reaction time performance may instead point to an underlying problem of psychomotor or mental processing speed in fibromyalgia. Future studies should examine potential deficits in psychomotor function in fibromyalgia patients in more detail."
Velly AM, Look JO, Schiffman E et al.
2010. The effect of fibromyalgia and widespread pain on the clinically
significant temporomandibular muscle and joint pain disorders – a
prospective 18-month cohort study. J Pain. [May 11 Epub ahead of
print]. “Fibromyalgia and widespread pain should receive important
consideration when evaluating and developing a treatment plan for
patients with TMJD (temporomandibular muscle and joint disorders).”
[Consistent with current research, any chronic pain generator may
promote central sensitization. What is needed is to look for the causes
of the chronic pain, such as trigger points (often cause or contributor
to TMJD), and treat them as promptly and effectively as possible and
bring perpetuating factors under control. DJS]
Vendrig, A. A., P. F. van Akkerveeken and K. R. McWhorter. 2000. Results of a
multi-modal treatment program for patients with chronic symptoms after a whiplash injury of
the neck. Spine 25(2):238-44.
Venancio Rde A, Alencar FG Jr, Zamperini C.
2009. Botulinum toxin, lidocaine, and dry-needling injections in
patients with myofascial pain and headaches. Cranio.
27(1):46-53. “Statistically, all the groups showed favorable results
for the evaluated requisites…, except for the use of rescue medication and
local post injection sensitivity….” “Considering its reduced cost,
lidocaine could be adopted as a substance of choice, and botulinum toxin
should be reserved for refractory cases, in which the expected effects could
not be achieved, and the use of a more expensive therapy would be
Vera-Portocarrero LP, Zhang ET, Ossipov MH et
al. 2006. Descending facilitation from the rostral
ventromedial medulla maintains nerve injury-induced central
sensitization. Neuroscience [Apr 27 Epub ahead of
print] “The results demonstrate the novel concept that once
initiated, maintenance of nerve injury-induced central sensitization
in the spinal dorsal horn requires descending pain facilitation
mechanisms arising from the rostral ventromedial medulla.”
[Researchers are zeroing in on the mechanisms behind central
sensitization. This may give us more of a chance to control
Vergne-Salle P, Dufauret-Lombard C, Bonnet C et al. 2010. A randomized, double-blind, placebo-controlled trial of dolasetron, a 5-hydroxytryptamine 3 receptor antagonist, in patients with fibromyalgia. Eur J Pain. [Oct 29 Epub ahead of print]. "Reduction in pain intensity... was significantly greater in dolasetron-treated patients...compared with placebo controls..... The most common adverse events were constipation, nausea, dizziness and headache, with no significant differences between the two groups. Intermittent IV dolasetron was safe and efficacious for the reduction of pain intensity associated with FM at 3months."
Verne GN, Robinson ME, Vase L et al.
2003. Reversal of visceral and cutaneous hyperalgesia by local rectal
anesthesia in irritable bowel syndrome (IBS) patients. Pain
105(1-2):223-30. This article
deals with altered visceral perception in IBS. The researchers found
that using topical anesthetic (lidocaine) rectally effectively decreased
visceral and cutaneous hyperalgesia in these patients. They concluded
that this was a central blockade, but perhaps topical application of
lidocaine on area myofascial trigger points could have been involved.
More medical researchers need to become aware of the reality and scope of
myofascial trigger points.
Vgontzas A.N., Papanicolaou
D.A., Bixler, E.O., Hopper K., Lotsikas A., Lin H.M., Kales A.,
Chrousos G.P. 2000. Sleep apnea and daytime sleepiness and
fatigue: relation to visceral obesity, insulin resistance, and
hypercytokinemia. J. Clin Endocrinol Metab. 85(3):1151-8.
Sleep apnea is associated with daytime sleepiness and fatigue,
abdominal obesity, and insulin resistance.
Vgontzas, A. N. and A. Kales. 1999. Sleep and its disorders. Annu Rev Med
Vgontzas, A. N. , G. Mastorakos, E. O. Bixter, A. Kales, P. W. Gold and G. P. Chrousos.
1999. Sleep deprivation effects on the activity of the hypothalamus-pituitary-adrenal and
growth axes: potential clinical implications. Clin Endocrinol
Viane I, Crombez G, Eccleston C et al.
2003. Acceptance of pain is an independent predictor of mental
well-being in patients with chronic pain: empirical evidence and
reappraisal. “Acceptance of chronic pain is best conceived of as
the shift away from pain to non-pain aspects of life, and the shift away
from a search for a cure with an acknowledgment that pain may not
Vicennati, V., Pasquali R.
2000. Abnormalities of the hypothalamic-pituitary-adrenal axis in
nondepressed women with abdominal obesity and relations with
insulin resistance: evidence for a central and a peripheral
alteration. J. Clin Endocrinol Metab 85(11):4093-8.
HPA-axis dysfunction is associated with abdominal obesity and
insulin resistance. [HPA-axis dysfunction is also associated with
Vierck CJ Jr. 2006.
Mechanisms underlying development of spatially distributed chronic pain
(fibromyalgia). Pain [Jul 12 Epub ahead of print] “It
appears that central mechanisms of FM pain are dependent on abnormal
peripheral input(s) for development and maintenance of this condition.”
Vierck CJ Wong F, King CD et al. 2013. Characteristics of Sensitization Associated With Chronic Pain Conditions. Clin J Pain. [Apr 25 Epub ahead of print]. "The widespread sensitization for irritable bowel syndrome and TMD participants does not rely on mechanisms of spatial and temporal summation often invoked to explain widespread hyperalgesia associated with chronic pain. Increased sensitivity during descending series of stimulation of an arm or leg but not the face indicates a propensity for sensitization of nociceptive input to the spinal cord. Abnormally prolonged sensitization for FM participants reveals a unique influence of widespread chronic pain referred to deep somatic tissues."
Vilar B, Busserolles J, Ling B et al. 2013. Alleviating Pain Hypersensitivity through Activation of Type 4 Metabotropic Glutamate Receptor. J Neurosci. 33(48):18951-18965. "Hyperactivity of the glutamatergic system is involved in the development of central sensitization in the pain neuraxis, associated with allodynia and hyperalgesia observed in patients with chronic pain. Herein we study the ability of type 4 metabotropic glutamate receptors (mGlu4) to regulate spinal glutamate signaling and alleviate chronic pain. We show that mGlu4 are located both on unmyelinated C-fibers and spinal neurons terminals in the inner lamina II of the spinal cord where they inhibit glutamatergic transmission through coupling to Cav2.2 channels. Genetic deletion of mGlu4 in mice alters sensitivity to strong noxious mechanical compression and accelerates the onset of the nociceptive behavior in the inflammatory phase of the formalin test. However, responses to punctate mechanical stimulation and nocifensive responses to thermal noxious stimuli are not modified. Accordingly, pharmacological activation of mGlu4 inhibits mechanical hypersensitivity in animal models of inflammatory or neuropathic pain while leaving acute mechanical perception unchanged in naive animals. Together, these results reveal that mGlu4 is a promising new target for the treatment of chronic pain."
Villa, M., P. Mustarelli and M. Caprotti. 1991. Biological effects of magnetic fields.
Life Sci 49(2):85-92.
Villalon P, Arzola JF, Valdivia J et al. 2013. The occlusal appliance effect on myofascial pain. Cranio. 31(2):84-91. "There are limited studies about the effects of occlusal appliance (OA) after three months of use. This study aimed to compare myofascial pain (MP) according to RDC/TMD, craniocervical relationships (CR) and masseter and temporalis bilateral electromyographic (EMG) activity, before and after three months of occlusal appliance use. Nineteen patients participated in this study. Cephalometric and RDC/TMD diagnostics were performed previously (baseline) and at the end of the study period (three months). EMG recordings at clinical mandibular rest position (MRP), during swallowing of saliva (SW) and during maximum voluntary clenching (MVC) were performed as follows: after one hour of use of an OA; after three months of using the OA for a minimum of 16 hours each day; and immediately after removal from the mouth. MP was relieved in all patients at the end of the study period. CR did not change significantly between baseline and after removal of the OA at the end of the study period. EMG activity during MRP, SW, and MVC decreased in both muscles after one hour using the OA and maintained the same level for the three-month period. When comparing baseline versus final EMG activity without OA, a significant decrease was only observed in the masseter muscle. The results observed in the present study are relevant to clinicians because they imply that the therapeutic effect of OA does not significantly affect the homeostasis of the craniocervical system."
Vincent A, Whipple MO, Luedtke CA et al. 2011. Pain and other symptom severity in women with fibromyalgia and a previous hysterectomy. J Pain Res. 4:325-329. "Pain and other fibromyalgia symptom severity were worse in women who had had a hysterectomy with or without an oophorectomy." [It would be interesting if the Mayo Clinic did a companion study, taking into account the reason for the surgery. Many FM patients have significant pelvic pain and other symptoms due to a variety of co-existing conditions. DJS]
Viola-Saltzman M, Watson NF, Bogart A et al. 2010. High prevalence of restless legs syndrome among patients with fibromyalgia: a controlled cross-sectional study. J Clin Sleep Med. 6(5):423-427. "There is a higher prevalence and odds of RLS in those with FM compared to controls. Clinicians should routinely query FM patients regarding RLS symptoms because treatment of RLS can potentially improve sleep and quality of life in these patients." [One must wonder how many of these patients also have TrPs, as TrPs have been shown to be a factor in RLS, and these patients were not checked for co-existing TrPs. DJS]
Vitton O, Gendreau M, Gendreau J et al. 2004.
A double-blind placebo-controlled trial of milnacipran in the treatment
of fibromyalgia. Hum Psychopharmacol. 19(S1):S27.
Mililcipran may have the potential to reduce several FMS symptoms,
including pain. [Minilcipran, affecting norepinephrine and serotonin as
an SNRI, has a 3:1 effect ratio of norepinephrine to serotonin. Effexor
has a 1:3 ratio. DJS]
Vitali, C., A. Tavoni, B. Rossi, E. Bibolotti, C. Giannini, L. Puzzuoli, R. Cacialli
and G. Pasero. 1989. Evidence of neuromuscular hyperexcitability features in patients with
primary fibromyalgia. Clin Exp Rheumatol 7(4):385-390.
Vizi, E. S. and B. Lendvai. 1999. Modulatory role of presynaptic nicotinic receptors in
synaptic and non-synaptic chemical communication in the central nervous system.
Res Brain Res Rev 30(3):219-35.
Volkmann, H., J. Norregaard, S. Jacobsen, B. Danneskiold-Samsoe, G. Knoke and D.
Nehrdich. 1997. Double-blind, placebo-controlled cross-over study of intravenous
A-adenosyl-L-methionine in patients with fibromyalgia. Scand J Rheumatol
Vollestad NK, Mengshoel AM. 2005. Relationships between
neuromuscular functioning, disability and pain in fibromyalgia.
Disabil Rehabil. 27(12):667-673.
Volonte C, Amadio S, Cavaliere F et al. 2003.
Extracellular ATP and neurodegeneration. Curr Drug Targets
CNS Neurol Disord. 2(6):403-412. “...extracellular ATP
plays a very complex role not only in the repair, remodeling and
survival occurring in the nervous system, but even in cell death and
this can occur either after normal developmental conditions, after
injury, or acute and chronic diseases. [Extracellular ATP and
neurodegeneration may be involved in biochemical traumatic brain
injury, a factor I believe is often unrecognized in FMS and other
chronic pain patients.]
Volonte C, Amadio S, Cavaliere F et al.
2003. Extracellular ATP and neurodegeneration. Curr Drug
Targets CNS Neurol Disord. 2(6):403-412. “Extracellular ATP
plays a very complex role not only in the repair, remodeling and
survival occurring in the nervous system, but even in cell death and
this can occur either after normal developmental conditions, after
injury, or acute and chronic diseases.” [This mechanism may be involved
in the development of some chronic pain states. DJS]
Volz MS, Medeiros LF, Tarrago MD et al. 2013. The Relationship between Cortical Excitability and Pain Catastrophizing in Myofascial Pain. J Pain. [Jun 27 Epub ahead of print]. "Pain catastrophizing regularly occurs in chronic pain patients. ….this study explored the relationship between a neurophysiological marker of cortical excitability, as assessed by transcranial magnetic stimulation, and catastrophizing, as assessed by the Brazilian Portuguese Pain Catastrophizing Scale, in patients with chronic myofascial pain syndrome. …Our results did not suggest that these findings were influenced by other factors, such as age or medication use. Furthermore, short intracortical inhibition showed a significant association with pressure pain threshold….This study highlights the relationship between cortical excitability and catastrophizing. Cortical measures may illuminate how catastrophizing responses may be related to neurophysiological mechanisms associated with chronic pain."
Vondrackova D, Leyendecker P, Meissner W et
al. 2008. Analgesic efficacy and safety of oxycodone in combination
with naloxone as prolonged release tablets in patients with moderate to
severe chronic pain. J Pain. 9(12):1144-1154. “Not only does
oxycodone PR/naloxone PR demonstrate analgesic efficacy comparable with
oxycodone PR, but it also improves opioids-induced bowel dysfunction, and
may therefore improve the acceptability of long-term opioids treatment for
von Klitzing, L. 1991. A new encephalomagnetic effect in human brain generated by
static magnetic fields. Brain Res 540(1-2):295-6.
Von Stulpnagel C, Reilich P, Straube A et
al. 2009. Myofascial trigger points in children with tension-type
headache: a new diagnostic and therapeutic option. J Child Neurol.
24(4):406-409. “These preliminary findings suggest a role for active
trigger points in children with tension-type headache. Trigger
point-specific physiotherapy seems to be an effective therapy in these
Von Stulpnagel C, Blaschek A, Lee SH et al. 2006.
[Primary headache in children] MMW Fortschr Med. 148(46):39-41.
[German] “...treatment of headaches is integrative and multimodal, and
includes pharmacotherapy, psychological interventional measures,
modification of the daily routine (e.g., drinking, sleeping) and trigger
Vranesh, J. G., G. Madrid, J. Bautista, P. Ching and R.A. Hicks. 1999. Time perspective
and sleep problems. Percept Mot Skills 88(1):23-4.
Vulfsons S, Ratmansky M, Kalichman L. 2012. Trigger point needling: techniques and outcome. Curr Pain Headache Rep. 16(5):407-412. "In this review we provide the updates on last years' advancements in basic science, imaging methods, efficacy, and safety of dry needling of myofascial trigger points (MTrPs). The latest studies confirmed that dry needling is an effective and safe method for the treatment of MTrPs when provided by adequately trained physicians or physical therapists. Recent basic studies have confirmed that at the site of an active MTrP there are elevated levels of inflammatory mediators, known to be associated with persistent pain states and myofascial tenderness and that this local milieu changes with the occurrence of local twitch response. Two new modalities, sonoelastography and magnetic resonance elastography, were recently introduced allowing noninvasive imaging of MTrPs. MTrP dry needling, at least partially, involves supraspinal pain control via midbrain periaqueductal gray matter activation. A recent study demonstrated that distal muscle needling reduces proximal pain by means of the diffuse noxious inhibitory control. Therefore, in a patient too sensitive to be needled in the area of the primary pain source, the treatment can be initiated with distal needling."