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Aarflot, T. and D.
Bruusgaard. 1996. Association between
chronic widespread musculoskeletal complaints and thyroid autoimmunity. Results from
a community survey. Scand J Prim Health Care 14(2):111-115.
Abajo, F.J., Rodriguex L.A.G.,
Montero, D. 1999. Association between selective serotonin reuptake
inhibitors in gastrointestinal bleeding: population based control
study. The concomitant use of NSAIDs or aspirin with SSRIs poses a
significantly increased risk of GI bleeding. The possible
etiological mechanism is the lower level of platelet serotonin in
patients on SSRIs.
Abbasi, F., T. McLaughlin, C. Lamendola and G. M. Reaven.
2000. Insulin regulation of plasma free fatty acid concentrations is abnormal in
healthy subjects with muscle insulin resistance. Metabolism 49(2):151-4.
Abbott RB, Hui KK, Hays RD et al. 2007. A
randomized controlled trial of Tai Chi for tension headaches. Evid
Based Complement Alternat Med. 4(1):107-113. “A 15 week intervention of
Tai Chi practice was effective in reducing headache impact and also
effective in improving perceptions of some aspects of physical and mental
health.”
Abdel-Moty E, Khalil T, Rosomoff H. 1999. The
effects of the Aqua-PT on myofascial pain. Paper presented at the 18th
Annual Scientific Meeting of the American Pain Society, Oct 21-24, Greater
Fort Lauderdale/Broward County Convention Center. This paper, studying 123
patients with myofascial pain as a primary diagnosis, indicates that 15
minute therapy sessions on an aqua massage unit may provide some relief from
myofascial pain.
Abeles AM, Pillinger MH, Solitar BM et al. 2007.
Narrative review: the pathophysiology of fibromyalgia. Ann Intern
Med. 146(10):726-734.
Abitbol, J., P. Abitbol and B. Abitbol. 1999. Sex
hormones and the female voice. J Voice 13(3):424-46.
Acasuso-Diaz, M. and E. Collantes-Estevez. 1998. Joint
hypermobility in patients with fibromyalgia syndrome. Arthritis Care Res
11(1):39-42.
Achermann, J. C. and J. L. Jameson. 1999. Fertility and
infertility: genetic contributions from the hypothalamic-pituitary-gonadal axis.
Mol Endocrinology. 13(6):812-8.
Acheson DW, Luccioli
S. 2004. Microbial-gut interactions in health and disease.
Mucosal immune responses. Best Pract Res Clin Gastroenterol
18(2):387-404. This is a good review, including functions of the
GI mucosal barrier and permeable membrane, or Leaky Gut Syndrome.
Adak B, Tekeoglu I, Ediz L et al. 2005.
Fibromyalgia frequency in hepatitis B carriers. J Clin
Rheumatol. 11(3):157-159. “The present study suggests that
chronic hepatitis B carriage appears to increase the risk of FM and many
of the typically associated symptoms.”
Adam TC, Epel ES. 2007. Stress, eating and the reward system.
Physiol Behav. 91(4):449-458. Chronic stress may be worsening
the obesity epidemic due to the loss of glucocorticoid regulation by
insulin and leptin.
Adams PJ, Snutch
TP. 2007. Calcium channelopathies: voltage-gated calcium channels.
Subcell Biochem. 45:215-251. Genetically caused minute
changes in calcium ion channels can have a wide spectrum affect on
“...mammalian developmental, physiological and behavioral functions.”
Agents that act on selective calcium channel activity may be important
medications for the future.
Adams, W. R., K. J. Spolnik and J. E.
Bouquot. 1999.
Maxillofacial osteonecrosis in a patient with multiple idiopathic facial
points. J Oral Pathol Med 28(9):423-32. Called NICO (neuralgia-inducing
cavitational osteonecrosis). The underlying problem is vascular insufficiency.
Adcock KG, Kyle PB, Deaton JS et al. 2007.
Pharmacokinetics of intranasal and intratracheal pentoxifylline in rabbits.
Pharmacotherapy. 27(2):200-206. “The pharmacokinetic profiles after
intranasal and intratracheal administration of pentoxifylline appear similar
to those after intravenous administration.” [Since intrathecal glial
cell modulation works well in rats to diminish or relieve central
sensitization, this use of intranasal pentoxifylline may have potential for
FMS. DJS]
Adiguzel O, Kaptanoglu E, Turgut B
et al. 2004. The possible effect of clinical recovery on regional cerebral
blood flow deficits in fibromyalgia: a prospective study with
semi-quantitative SPECT. South Med J. 97(7):651-655. “...these
findings could indicate that deficits in cerebral blood flow in fibromyalgia
improve parallel to clinical recovery.”
Adler GK, Geenen R. 2005.
Hypothalamic-pituitary-adrenal and autonomic nervous system functioning
in fibromyalgia. Rheum Dis Clin North Am 31(1):187-202.
“In general, there seems to be a reduction in some neuroendocrine and
autonomic nervous system (ANS) responses to applied stresses in
individuals who have fibromyalgia.”
Adler GK,
Manfredsdottir VF, Creskoff KW. 2002. Neuroendocrine abnormalities
in fibromyalgia. Curr Pain Headache Rep 6(4): 289-98. "A
combination of multiple, mild impaired responses may lead to more
profound physiologic and clinical consequences as compared with a
defect in only one system, and could contribute to the symptoms of
fibromyalgia."
Adler, G. K., B. T. Kinsley, S. Hurwitz, C. J. Mossey and D. L.
Goldenberg. 1999. Reduced hypothalamic pituitary and sympathoadrenal responses
to hypoglycemia in women with fibromyalgia syndrome. Am J Med 106(5):534-43.
Adler MW, Rogers TJ. 2005. Are chemokines the third
major system in the brain? J Leukoc Biol. [Oct 4 Epub ahead
of print] The authors propose that the endogenous chemokine system
in the brain interacts with the neurotransmitter and neuropeptide
systems to govern brain function. [There are abundant chemokine
receptors in the glial cells, and activated intrathecal glia have been
implicated in the inception and maintenance of chronic pain states.
Imbalance of specific neuopeptides, and neurotransmitters and cytokines
have been implicated in fibromyalgia, and biochemicals belonging to
these systems are released during myofascial trigger point twitch. DJS]
Adriaensen H, Vissers K, Noorduin H et al.
2003. Opioid tolerance and dependence: an inevitable consequence of
chronic treatment? Acta Anaesthesiol Belg. 54(1):37-47.
“Although opioids provide effective analgesia, largely unsubstantiated
concern about opioid-induced tolerance, physical dependence and
addiction have limited their appropriate use. As a consequence, many
patients receive inadequate treatment for both malignant and
non-malignant pain. However, it has been shown that analgesic tolerance
develops less frequently during chronic opioid administration in a
clinical context than in animal experiments.”
Aftimos, S. 1989. Myofascial pain in children. N Z Med J 102(874):440-441.
Agargun, M. Y. , I. Tekeoglu, A. Gunes, B. Adak, H. Kara and M.
Ercan. 1999. Sleep quality and pain threshold in patients with fibromyalgia. Compr
Psychiatry 40(3):226-8.
Ahmadpour, S. and U. M. Kabadi. 1997. Pancreatic
alpha-cell function in idiopathic reactive hypoglycemia. Metabolism 46(6):639-643.
Aikins, Murphy P. 1998. Alternative therapies for nausea
and vomiting of pregnancy. Obstet Gynecol 91(1):149-155.
Airaksinen, O. and P. J. Pontinen. 1992. Effects of
electrical stimulation of myofascial trigger points with tension headache. Acupunct
Electrother Res 17(4):285-290.
Akassoglou K., Strickland S. 2002.
Fibrin inhibits nerve regeneration by arresting schwann cell
differentiation. Glia (Suppl 1):S42 [Abstract]. “These results
provide the first indication that fibrin, a blood-derived protein, which
becomes a component of the extracellular matrix of the
nervous system in pathological states, can affect repair by negatively
regulating myalination. Dysregulation of fibrin clearance and/or deposition
could play a role in traumatic injuries of the nervous system, as well as in
demyelinating diseases such as multiple sclerosis.”
Akkasilpa S, Goldman D, Magder LS et al. 2005.
Number of fibromyalgia tender points is associated with health
status in patients with systemic lupus erythematosus. J
Rheumatol. 32(1):48-50. “A strong association between the
number of FM TPs and health status was found in patients with SLE.
The number of TPs, and not just the presence/absence of FM, is
associated with health status in SLE.”
Al-Alawi A, Mulgrew A, Tench E et al.
2006. Prevalence, risk factors and impact on daytime
sleepiness and hypertension of periodic leg movements with
arousals in patients with obstructive sleep apnea.
J Clin Sleep Med. 2(3):281-287. “Risk factors
for PLMS include preexisting medical conditions --
particularly depression, fibromyalgia, and diabetes mellitus
-- increasing age, predisposing medications, obesity and OSA.”
Al-Shenqiti AM, Oldham JA. 2005.
Test-retest reliability of myofascial trigger point detection in
patients with rotator cuff tendonitis. Clin Rehabil.
19(5):482-487. “The presence or absence of the taut band, spot
tenderness, jump sign and pain recognition was highly reliable
between sessions. Referred pain and local twitch response
reliability varied depending on the muscle being studied.”
[Again, both training and experience are vital to reliably
diagnose and treat TrPs. DJS]
Alanoglu E, Ulas UH, Ozdag F. et
al. 2004. Auditory event-related brain potentials in fibromyalgia
syndrome. Rheumatol Int. [Epub Feb 21 ahead of print].
“...FM affects quality of life and dysfunction in cognitive abilities
can be determined by brain event-related potentials.”
Alarcon, G. S., and L. A. Bradley. 1998. Advances in the treatment
of fibromyalgia: current status and future directions. Am J Med Sci 315
(6):397-404.
Albright, G. L. and A. A. Fischer. 1990. Effects of
warming imagery aimed at trigger-point sites on tissue compliance, skin temperature, and
pain sensitivity in biofeedback-trained patients with chronic pain: a preliminary
study. Percept Mot Skills 71(3 Pt 2):1163-70.
Album D, Westin S. 2007. Do diseases have a
prestige hierarchy? A survey among physicians and medical students.
Soc Sci Med. [Sep 10 Epub ahead of print] Medical specialties and
illnesses are considered to have a ranking among doctors and medical
students. “Myocardial infarction, leukemia and brain tumor were among
the highest ranked, and fibromyalgia and anxiety neurosis were among the
lowest.” “Low prestige scores are given to diseases and specialties
associated with chronic conditions located in the lower parts of the body or
having no specific bodily location, with less visible treatment procedures,
and with elderly patients.” [It seems we have a lot of educating to
do, and it is no wonder FM patients are considered to have a self-esteem
problem. See: “Bennett RM. 2007. Do patients’ perceptions of negative
physician attitudes influence fibromyalgia symptoms and status?” This would
seem to indicate that some doctors could be major perpetuating factors.
DJS.]
Aldridge, R., E. B. Cady, D. A. Jones and G. Obletter.
1986. Muscle pain after exercise is linked with an inorganic phosphate increase as
shown by 31P NMR. Biosci Rep 6(7):663-7.
Alexander, R. W. , L. A. Bradley, G. S. Alarcon, M.
Triana-Alexander, L. A. Aaron, K. R. Alberts, M. Y. Martin and K. E. Stewart. 1998.
Sexual and physical abuse in women with fibromyalgia: association with outpatients health
care utilization and pain medication usage. Arthritis Care Res 11(2):102-15.
Alford, F. P., F. L. Hew, M. C. Christopher and C. Rantzau.
1999. Insulin sensitivity in growth hormone (GH)-deficient adults and effect of GH
replacement therapy. J Endocrinol Invest 22(5 Suppl):28-32.
Alix ME, Bates DK. 1999. A proposed etiology of cervicogenic
headache: the neurophysiologic basis and anatomic relationship between
the dura mater and the rectus posterior capitis minor muscle. J
Manipulative Physiol Ther. 22(8):534-539. This study found bridges
formed of connective tissue at the atlanto-occipital junction between
the rectus capitis posterior and the dorsal spinal dura. Tightness
of these connections may be associated with headache. “The dura-muscular,
dura-ligamentous connections in the upper cervical spine and occipital
areas may provide anatomic and physiologic answers to the cause of the
cervicogenic headache.”
Allcock N, McGarry J, Elkan R. 2002.
Management of pain in older people within the nursing home: a
preliminary study. Health Soc Care Comm. 10(6):464-471.
“It has been estimated that approximately two-thirds of people aged 65
years and over experience chronic pain, and that the prevalence of
chronic pain in nursing home residents is between 45% and 80%.
Overall, 37% of nursing home residents were identified as experiencing
chronic non-malignant pain.”
Allegrante, J. P. 1996. The role of adjunctive therapy
in the management of chronic nonmalignant pain. Am J Med 101(1A):33S-39S.
Allen, G., B. S. Galer and L. Schwartz. 1999.
Epidemiology of complex regional pain syndrome: a retrospective chart review of 134
patients. Pain 80(3):539-44
Almeida, TF, Roizenblatt, S,
Benedito, Silva AA, et al. 2003. The effect of combined therapy
(ultrasound and interferential current) on pain and sleep in
fibromyalgia. Pain 104(3):665-672. Combined therapy with pulsed
ultrasound and interferential current can be an effective therapy for pain
and sleep dysfunction in fibromyalgia patients.
Alonso-Ruiz, A., A. De la Hoz-Martinez and A. C. Zea-Mendoza. 1985.
Fibromyalgia syndrome as a late complication of toxic-oil syndrome. J Rheumatol
12(6):1207-1208.
Altindag O, Gur A, Calgan N et al. 2007. Paraoxonase
and arylesterase activities in fibromyalgia. Redox Rep.
12(3):134-138. “Patients with fibromyalgia might be prone to
development of atherosclerosis with reduced paraoxonase and arylesterase
activities.”
Altindag O, Celik H. 2006. Total antioxidant
capacity and the severity of the pain in patients with fibromyalgia.
Redox Rep. 11(3):131-135. “Increased oxidative stress may play
a role in the etiopathogenesis of the disease.” Antioxidant
supplements may be a useful part of therapy.
Alvarez DJ, Rockwell PG. 2002. Trigger
points: diagnosis and management. Am Fam Physician
65(4):653-660. “Trigger points are discrete, focal, hyperirritable
spots located in a taut band of skeletal muscle. They produce
pain locally and in a referred pattern and often accompany chronic
musculoskeletal disorders. Acute trauma or repetitive
microtrauma may lead to the development of stress on muscle fibers
and the formation of trigger points. Patients may have
regional, persistent pain resulting in a decreased range of motion
in the affected muscles. These include muscles used to
maintain body posture, such as those in the neck, shoulders, and
pelvic girdle. Trigger points may also manifest as tension
headache, tinnitus, temporomandibular joint pain, decreased range of
motion in the legs, and low back pain. Palpation of a
hypersensitive bundle or nodule of muscle fiber of harder than
normal consistency is the physical finding typically associated with
a trigger point. Palpation of the trigger point will elicit
pain directly over the affected area and/or cause radiation of pain
toward a zone of reference and a local twitch response.
Various modalities, such as the Spray and Stretch technique,
ultrasonography, manipulative therapy and injection, are used to
inactivate trigger points. Trigger-point injection has been
shown to be one of the most effective treatment modalities to
inactivate trigger points and provide prompt relief of symptoms.”
Alvarez, L. B. , J Teran, J. L. Alonso, J. Alegre, I. Arroyo and J.
L. Viejo. 1992. Lack of association between fibromyalgia and sleep apnea syndrome. Ann
Rheum Dis 51(1):108-11.
Aly T.A., Tahaka Y., Aizawa
T. et al. 2002. Medial superior cluneal nerve entrapment neuropathy in
teenagers: a report of two cases. Tohoku J Exp Med 197(4):229-31.
Nerve entrapment causing pain radiating down the low back may be caused by
myofascial trigger points, but these are often misdiagnosed.
These two patients completely recovered after trigger point therapy,
even though they had been misdiagnosed and in pain for a long time.
Amador NJ, Shivers K, Weiner J et al. Program
51.16/M8. Estrus cycle effects on behavioral and physiological
responses to formalin-induced inflammatory pain. Georgia World
Congress Center Atlanta, GA. Society for Neuroscience, Presentation.:
Oct 14, 2006. Both physiological and behavioral changes to inflammatory
pain can vary significantly with the estrus cycle in rats. Hormones
may physically affect perceptions of pain.
Ambalavanar R, Moutanni A, Dessem D. 2006.
Inflammation of craniofacial muscle induces widespread mechanical allodynia.
Neurosci Lett. [Feb 27 Epub ahead of print]
Ambrogio, N., J. Cuttiford, S. Lineker and L. Li. 1998. A comparison
of three types of neck support in fibromyalgia patients. Arthritis Care Res
11(5):405-10.
Ames BN, Elson-Schwab I, Silver EA. 2002.
High-dose vitamin therapy stimulates variant enzymes with decreased coenzyme
binding affinity (increased K(m)): relevance to genetic disease and
polymorphisms. Am J Clin Nutr. 75(4):616-658. This
article concerns increasing developments in the science of genomics. They
have already found over 50 genetic diseases that can be helped by high doses
of the vitamin component of coenzymes, restoring metabolic paths.
[From what we have learned in the study of genomics and epigenomics, each
human being has significantly different nutrient requirements, and this may
be profoundly affected by differences in intestinal permeability. The use
of healthy food and supplements as medicine may become more accepted as
research unfolds. DJS]
Amital D, Fostik L, Polliack ML et al. 2006.
Posttraumatic stress disorder, tenderness, and fibromyalgia syndrome: are
they different entities? J Psychosom Res. 61(5):663-669. This
study concerned comorbidity of FMS in male patients with PTSD that occurred
after an intensive, initial combat-related traumatic event. [In these
patients, and not necessarily all male patients as the study concluded, the
occurrence, degree and impact of PTSD is often significantly related to
co-existing FMS. FMS may be amplifying more than pain. DJS]
Ammer, K. and P. Melnizky. 1999. [Medicinal baths for
treatment of generalized fibromyalgia.] Forsch Komplementarmed 6(2):80-5. [German]
.
Anand KJ. 2000. Pain, plasticity,
and premature birth: a prescription for permanent suffering?
Nat Med 6(9):971-973. Premature infants and other children
requiring medical procedures require adequate pain control.
Failure to provide it not only causes needless acute suffering but can
change the central nervous system and cause predisposition to chronic
pain.
Anand P, Aziz Q, Willert R et al. 2007.
Peripheral and central mechanisms of visceral sensitization in man.
Neurogastroenterol Motil. 19(1 Suppl):29-46.
Ancoli-Israel, S. and T. Roth. 1999. Characteristics of
insomnia in the United States: results of the 1991 National Sleep Foundation Survey.
I. Sleep 22 Suppl 2:S347-53.
Anderberg, UM, 2001.[Stress-related
syndromes-contemporary illnesses.] Lakartidningen
Dec;98(51-52):5860-3.[Swedish] The diagnoses of burnout, chronic
fatigue syndrome and fibromyalgia syndrome may represent reactions
to an overwhelming situation. The new diagnoses may indicate
preliminary stages of more serious diseases such as angina
pectoris or myocardial infarction. Other causes of death may be
related to stress. "These circumstances reflect not only
considerable suffering on the part of individuals, but also a
substantial economic burden for society".
Anderberg, U. M., Z. Liu, L Berglund and F. Nyberg.
1999. Elevated plasma levels of neuro-peptide Y in female fibromyalgia
patients. Eur J Pain 3(1):19-30.
Anderberg, U. M. , I. Marteinsdottir, J. Hallman and T. Backstrom.
1998. Variablility in cyclicity affects pain and other symptoms in female fibromyalgia
syndrome patients. J Musculoskel Pain 6(4):5-22.
Anderson H, Arendt-Nielsen L, Svensson P et al.
2007. Spatial and temporal muscle hyperalgesia induced by nerve
growth factor in humans. J Musculoskel Pain 15 (Supp 13):13
item 16. [Myopain 2007 Poster] “NGF intramuscular injection
causes a time-dependent enlargement of the hyperalgesic area that is
most prominent 24 hours after injection. The expansion of
hyperalgesia locally and in distinct area innervated by the same nerve
indicates that both peripheral and central mechanisms are involved in
the NGF-induced sensitization. These findings may add to the
current knowledge of the development of chronic pain conditions.”
Anderson, K. and J. M. Silver. 1998.
Modulation of Anger and Aggression. Semin Clin Neuropsychiatry
3(3):232-242.
Anderson RU, Wise D,
Sawyer T et al. 2005. Integration of myofascial trigger
point release and paradoxical relaxation training treatment of
chronic pelvic pain in men. J Urol. 174(1):155-160.
Myofascial release of trigger points combined with paradoxical
relaxation training can provide pain relief superior to
traditional therapy.
Andersson HI. 2004. The course of
non-malignant chronic pain: a 12-year follow-up of a cohort from the
general population. Eur J Pain 8(1):47-53. “Mortality was
significantly higher in the group initially reporting widespread pain
compared with the other groups. The chronicity of widespread
chronic pain supports early and intense intervention among individuals
with located pain. The association between chronic widespread pain
and increased mortality needs further investigation but may deepen the
view of chronic pain as a public health problem.”
Andersen, S. and G. Leikersfeldt. 1996. Management of
chronic non-malignant pain. Br J Clin Pract 50(6):324-330.
Anderson, R. A. 1992. Chromium, glucose tolerance, and
diabetes. Biol Trace Elem Res 32:19-24.
Anderson, R. C. and J. H. Anderson. 1999. Sensory
irritation and multiple chemical sensitivity. Toxicol Ind Health
15(3-4):339-45.
Anderson, R. C. and J. H. Anderson. 1998. Acute toxic
effects of fragrance products. Arch Environ Health 53(2):138-46.
Andersson HI. 2004. The course of
non-malignant chronic pain: a 12-year follow-up of a cohort from the
general population. Eur J Pain 8(1):47-53. “Mortality was
significantly higher in the group initially reporting widespread pain
compared with the other groups. The chronicity of widespread
chronic pain supports early and intense intervention among individuals
with located pain. The association between chronic widespread pain
and increased mortality needs further investigation but may deepen the
view of chronic pain as a public health problem.”
Andersson, M., J. R. Bagby, L. Dyrehag and C. Gottfries.
1998. Effects of staphylococcus toxoid vaccine on pain and fatigue in patients with
fibromyalgia/chronic fatigue syndrome. Eur J Pain 2(2):133-142.
Andersson, M., J. R. Bagby, L. E. Dyrehag and C. G. Gottfries. 1999. Effects of staphylococcus toxoid vaccine on pain and fatigue
in patients with fibromyalgia/chronic fatigue syndrome. Eur J Pain
2(2):133-142.
Andreu JL, Sanz J. 2005. [Fibromyalgia and its diagnosis.] Rev
Clin Esp. 205(7):333-336. [Spanish] “Although the
fibromyalgia classification criteria of the American College of Rheumatology are not diagnostic
criteria, they have been extensively used to diagnose FMS in patients
with chronic diffuse arthromyalgias. Fibromyalgia diagnosis
reduces the patient’s anxiety, avoiding complementary expensive and
unnecessary tests and it allows the patient to share his/her fears,
illnesses and expectations with other human beings who suffer the same
problem.”
Andrews R.C., Herlihy O.,
Livingstone D.E. 2002. Abnormal cortisol metabolism and tissue
sensitivity to cortisol in patients with glucose intolerance. J
Clin Endocrinol Metab 87(12):5587-93. “...in patients with
glucose intolerance, cortisol secretion, although normal, is inappropriately
high given enhanced central and peripheral sensitivity to glucocorticoids....altered
cortisol action occurs not only in obesity and hypertension but also in
glucose intolerance, and could therefore contribute to the link between
these multiple cardiovascular risk factors.”
Andrews, R. C. and B. R. Walker. 1999.
Glucocorticoids and insulin resistance: old hormones, new targets. Clin Sci
(Colch) 96(5):513-523.
Angarola, R. T. 1990. National and international
regulation of opioid drugs: purpose, structures, benefits and risks. J Pain
Symptom Manage 5(1 Suppl):S6-S11.
Angsuwarangsee T,
Morrison M. 2002. Extrinsic laryngeal muscular tension in
patients with voice disorders. J Voice 16(3):333-343.
“A strong relationship was found between thyrohyoid muscle tension
and both gastroesophageal reflux (GER) and muscle misuse dysphonia (MMD).”
[These patients were not checked for TrPs. TrPs may cause
muscle tension. This may be an important connection between
reflux as a perpetuating factor of myofascial TrPs. DJS]
Antoin H, Beasley RD. 2004. Opioids for
chronic noncancer pain. Tailoring therapy to fit the patient and
the pain. Postgrad Med. 116(3)37-40, 43-44. “…opioids can
be a viable option today for successful therapy for chronic non-cancer
pain.”
Anuradha, C. V. and S. D. Balakrishnan. 1999. Taurine attenuates
hypertension and improves insulin sensitivity in the fructose-fed rat, and animal model of
insulin resistance. Can J Physiol Pharmacol 77(10:749-54.
Apkarian AV, Sosa Y, Krauss BR et al. 2004.
Chronic pain patients are impaired on an emotional decision-making task.
Pain 108(1-2):129-136. “Performance on an emotional
decision-making task may be impaired in chronic pain since human brain
imaging studies show that brain regions critical for this ability are
also involved in chronic pain. Our evidence indicates that chronic
pain is associated with a specific cognitive deficit, which may impact
everyday behavior especially in risky, emotionally laden situations.”
Apkarian AV, Sosa Y, Sonty S et al. 2004.
Chronic back pain is associated with decreased prefrontal and thalamic gray
matter density. J Neurosci. 24(46):10410-10415. “Patients
with CBP showed 5-11% less neocortical gray matter volume than control
subjects. The magnitude of this decrease is equivalent to the gray
matter volume lost in 10-20 years of normal aging. The decreased
volume was related to pain duration, indicating a 1.3 cm3 loss of gray
matter for every year of chronic pain. Our results imply that CBP is
accompanied by brain atrophy and suggest that the pathophysiology of chronic
pain includes thalamocortical processes.”
Appelboom, T. and A. Schoutens. 1990. High bone turnover in
fibromyalgia. Calcif Tissue Int 46(5):314-317.
Arciero, P. J., M. D. Vukovich, J. O. Holloszy, S. B. Racette and W.
M. Kohrt. 1999. Comparison of short-term diet and exercise on insulin action
in individuals with abnormal glucose tolerance. J Appl Physiol 86(6):1930-5.
Arden Pope III, C., R. L. Verrier, E. G. Lovett, A. C. Larson, M. E.
Raizenne, R. E. Kanner, J. Schwartz, G. M. Villegas, D. R. Gold and D. W. Dockery.
1999. Heart rate variability associated with particulate air pollution. Am
Heart J 138(5):890-899.
Ardic F, Gokharman D, Atsu S et al. 2006.
The comprehensive evaluation of temporomandibular disorders seen in
rheumatoid arthritis. Aust Dent J. 51(1):23-28.
“...the myofascial pain of the temporomandibular system is an
important cause of pain in rheumatoid arthritis...”
Arendt-Nielsen L. 2007. Measuring muscle
pain. J Musculoskel Pain 15 (Supp 13):9 item 11. [Myopain
2007 Poster] “Referred muscle pain [and the possible related
hyperalgesia] is manifested in somatic structures [skin, muscles,
joints, tendons]. These manifestations are of significant clinical
importance for the diagnosis of pain pathologies.” “Recently we
have found that patients suffering from chronic musculoskeletal pains
have significantly larger referred pain areas to experimentally induced
muscle pain intramuscular injection of hypertonic saline, and at the
same time they show manifestations of muscle sensitization.
Furthermore they show facilitated responses to a variety of other
stimuli.”
Arendt-Nielsen L, Mense S, Graven-Nielsen T. 2003.
[Assessment of muscle pain and hyperalgesia. Experimental and
clinical findings] [German] Schmerz 17(6):445-449. “ An
important part of the manifestation of pain in chronic musculoskeletal
disorders may be due to peripheral and central sensitization processes,
which are also involved in the transition from acute to chronic pain.
Knowledge of these processes has expanded enormously in recent years; it
should be utilized when new intervention strategies are designed.”
Arendt-Nielsen, L, Graven-Neilsen,
T. 2003. Central sensitization in fibromyalgia and other
musculoskeletal disorders. Curr Pain Headache Rep.
7(5):355-361. Tenderness and referred chronic musculoskeletal pain may
be due to peripheral and central sensitization.
This sensitization may be part of what changes acute pain into
chronic pain.
Arendt-Nielsen, L., T.
Graven-Nielson. 2002. Deep tissue Hyperalgesia. J Musculoskel Pain
10(1/2):97-119. "increased muscle sensitivity is present in
musculoskeletal pain conditions and may play a role for chronification of
pain, and interventions should take this aspect into consideration".
Arendt-Nielsen, L., T. Graven-Nielsen and P.
Svensson. 1999.
Assessment of muscle pain in humansclinical and experimental aspects. J
Musculoskel Pain 7(1-2):25-41.
Argoff, C. E. 2002. A review of the
use of topical analgesics for myofascial pain. Curr Pain Headache Rep
6(5):375-8.
Arguelles LM, Afari N, Buchwald DS et al. 2006.
A twin study of posttraumatic stress disorder symptoms and chronic
widespread pain. Pain [May 13 Epub ahead of print]
“Our findings suggest that PTSD (posttraumatic stress disorder)
symptoms, as measured by IES (Impact Events Scale), are strongly
linked to CWP (chronic widespread pain), but this association is not
explained by a common familial or genetic vulnerability to both
conditions. Future research is needed.
Ariji Y, Sakuma S, Izumi M et al. 2004.
Ultrasonographic features of the masseter muscle in female patients with
temporomandibular disorder associated with myofascial pain. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod 98(3):337-341.
Masseter muscle pain in TMD might be associated with muscle edema.
Ariji
Y, Sakuma S, Izumi M et al. 2004. Ultrasonographic features of the masseter
muscle in female patients with temporomandibular disorder associated with
myofascial pain. Oral Surg. 98(3):337-341. [I found it
very interesting that the myofascial pain in patients in this study was
associated with muscle edema. DJS]
Arnold LM, Crofford LJ, Martin SA et al. 2007.
The effect of anxiety and depression on improvements in pain in a
randomized, controlled trial of pregabalin for treatment of fibromyalgia.
Pain Med. 8(8):633-638. “The pain treatment effect of
pregabalin did not depend on baseline anxiety or depressive symptoms,
suggesting pregabalin improves pain in patients with or without these
symptoms. Much of the pain reduction appears to be independent of
improvements in anxiety or mood symptoms.”
Arnold LM, Pritchett YL, D’Souza DN et al. 2007. Duloxetine for
the treatment of fibromyalgia in women: pooled results from two
randomized, placebo-controlled clinical trials. J Womens Health
16(8):1145-1156. “…duloxetine is a safe and efficacious treatment
for both the pain and functional impairment associated with fibromyalgia
in female patients, while significantly improving quality of life.”
Arnold L, Duan W, Young, Jr. J et al. 2007.
Efficacy of pregabalin monotherapy for relief of pain associated with
fibromyalgia syndrome: time course and durability of pain results of a
14-week, double-blind, placebo-controlled trial. J Musculoskel
Pain 15 (Supp 13):41 item 71. [Myopain 2007 Poster]
“Pregabalin was associated with relief of FMS pain.”
Arnold L, Russell IJ, Duan R et al. 2007.
Pregabalin monotherapy for relief of symptoms of fibromyalgia syndrome: two
double-blind, randomized, controlled trials. J Musculoskel Pain
15 (Supp 13):41 item 72. [Myopain 2007 Poster] “Pregabalin 300,
450, and 600mg/d [BID] therapy was associated with significant and
clinically relevant reduction of pain associated with FMS.”
Arnold LM,
Goldenberg DL, Stanford SB et al. 2007. Gabapentin in the treatment of
fibromyalgia: a randomized, double-blind, placebo-controlled, multicenter
trial. Arthritis Rheum. 56(4):1336-1344. “Gabapentin
(1,200-2,400 mg/day) is safe and efficacious for the treatment of pain and
other symptoms associated with fibromyalgia.” [It would be interesting
to see a comparison of the effectiveness and side-effect profile of
Gabapentin and Lyrica. DJS]
Arnson Y, Amital D, Fostick L et al. 2007.
Physical activity protects male patients with post-traumatic stress disorder
from developing severe fibromyalgia. Clin Exp Rheumatol.
25(4):529-533. “Physical exercise in male patients with combat-related
PTSD provides protection from the future development of fibromyalgia and is
related in this group of patients to a better perception of their quality of
life.”
Arnstein, P., M. Caudill, C. L. Mandle, A. Norris and R.
Beasley. 1999. Self efficacy as a mediator of the relationship between pain
intensity, disability and depression in chronic pain patients. Pain
80(3):483-91.
Arnstein, P. M. 1997. The neuroplastic phenomenon: a
physiologic link between chronic pain and learning. J Neurosci Nurs
29(3):179-186.
Arlt, W., F. Callies, J. C. van Vlijmen, I. Koehler, M. Reincke, M.
Bidlingmaier, D. Huebler, M. Oettel, M. Ernst, H. M. Schulte and B. Allolio. 1999.
Dehydroepiandrosterone replacement in women with adrenal insufficiency. N Engl J
Med 341(14):1013-20.
Arshad A, Ool KK. 2007. Awareness and
perceptions of fibromyalgia syndrome: a survey of Southeast Asian
rheumatologists. J Clin Rheumatol. 13(2):59-62.
Arshad A, Kong KO. 2007. Awareness and
perceptions of fibromyalgia syndrome: a survey of Malaysian and Singaporean
rheumatologists. Singapore Med J. 48(1):25-30. “This study
confirmed that there was a variation of perceptions and knowledge of FMS
among rheumatologists from Malaysia and Singapore.” [It is unfortunate that
neither the rheumatologists surveyed nor the authors themselves understand
that fibromyalgia is not a diagnosis of exclusion, and that FMS is often
present as a condition interacting with other diagnoses. DJS]
Asa, P. B., Y. Cao and R. F. Garry. 2000. Antibodies to
squalene in Gulf War syndrome. Exp Mol Pathol 68(1):55-64.
Asaki S, Sekikawa M, Kim YT. 2006. Sensory
innervation of temporomandibular joint disk. J Orthop Surg.
14(1):3-8. “Free nerve endings and sensory nerve end organs are
present in the disk parenchyma of the human temporomandibular joint and
are associated with sensation and proprioception, just as they are in
the acetabular labrum, glenoid labrum, triangular fibrocartilage
complex, and meniscus.”
Asbring P, Narvanen AL.
2003. Ideal versus reality: physicians perspectives on patients with
chronic fatigue syndrome (CFS) and fibromyalgia. Soc Sci Med 57(4):711-720.
“The results suggest that there is a discrepancy between the ideal role of
the physician and reality in the everyday work in interaction with these
patients.” “The results also illuminate the physician’s
interpretations of patients in moralising terms. Conditions given the
status of illness were regarded, for example, as less serious by the
physicians than those with disease status. Skepticism was expressed
regarding especially CFS, but also fibromyalgia. Moreover, it is shown how
the patients are characterized by the physicians as ambitious, active,
illness focused, demanding and medicalising. The patients in question
do not always gain full access to the sick-role, in part as a consequence of
the conditions not being defined as diseases.” [It is a sad
reflection on the state of medical practice that many practitioners do not
understand that syndromes can be every bit as serious and life-altering as
diseases. Just because we do
not understand the total mechanisms behind the illness does not mean the
patients with these illnesses do not deserve the care given to patients who
have illnesses that we do understand. DJS]
Asbring,
PJ, Chronic Illness-A Disruption in Life: Identity-Transformation
Among Women with Chronic Fatigue Syndrome and Fibromyalgia. Adv
Nurs 34(3):312-319, 2001. FMS can profoundly affect personal
identity, particularly in relation to work and social life. Some
of the change was positive. The first step toward successful
therapy is often the acceptance of diagnosis.
Ashburn, M. A. and P. S. Staats. 1999. Management of
chronic pain. Lancet 353(9167):1865-9.
Ashby, E.C. 1994.
Chronic obscure groin pain is commonly caused by enthesopathy:
'tennis elbow'
of the groin. Br J. Surg 81(11):1632-4. Groin pain
may be caused by myofascial trigger points in the groin ligaments.
Ashina S, Bendtsen L, Ashina M. 2005.
Pathophysiology of tension-type headache. Curr Pain Headache Rep.
9(6):415-422. “Increased excitability of the central nervous system
generated by repetitive and sustained pericranial myofascial input may be
responsible for the transformation of episodic tension-type headache into
the chronic form. Studies of nitric oxide (NO) mechanisms suggest that
NO may play a key role in the pathophysiology of tension-type headache and
that the antinociceptive effect of nitric oxide synthase inhibitors may
become a novel principle in the future treatment of chronic headache.”
[Nitric oxide is a focus of chronic pain research, and would give another
pathway to treat it. DJS]
Asmundson, G. J., P. J. Norton and G. R. Norton. 1999.
Beyond pain: the role of fear and avoidance in chronicity. Clin Psych Rev 19(1):97-119.
Assefi, N.P., Coy, T.V.,
Uslan, D. et al. Financial, occupational, and personal consequences of
disability patients with chronic fatigue syndrome and fibromyalgia compared
to other fatiguing conditions. J Rheumatol 30(4):804-8.
Patient evaluation at a chronic fatigue clinic indicated that the patients
with the most extensive loss of support by friends, family, and loss of job,
possessions, and recreational abilities were those with FMS alone or with
CFS, and yet there were “...no reliable difference between groups in use
of disability benefits.” The
authors recommend “Employers and personal relations of patients with
chronic fatigue should make a greater effort to accommodate the
illness-related limitations of these conditions, especially for those with
FMS and CFS.
Assimos, D. G., P. Langenstroer, R. F. Leinbach, N. S. Mandel, J. M.
Stern and R. P. Holmes. 1999. Guaifenesin- and ephedrine-induced stones. J
Endourol 13(9):665-7.
Attal, N., L. Brasseur, F. Parker, M. Chauvin and D.
Bouhassira. 1998. Effects of gabapentin on the different components of peripheral
and central neuropathic pain syndromes: a pilot study. Eur Neurol 40(4):191-200.
Audette JF, Wang F, Smith H. 2004.
Bilateral activation of motor unit potentials with unilateral
needle stimulation of active myofascial trigger points. Am
J Phys Med Rehabil. 83(5):368-374. TrPs on the
contralateral side of the body exhibited a local twitch response
after dry needling TrPs. The group with active TrPs had
motor unit potentials (MUPs) activated in a specific muscle on
both sides of the body when the TrP on one side was needled.
This did not happen if the TrP was latent. [If there are
active TrPs on one side of the body, the corresponding muscles
should be checked for latent TrPs and if those TrPs are present,
they may need to be treated. DJS]
Audette JF,
Ryan AH. 2004. The role of acupuncture in pain management.
Phys Med Rehabil Clin N Am. 15(4):749-772.
Audette JF, Blinder RA. 2003. Acupuncture
in the management of myofascial pain and headache. Curr Pain
Headache Rep. 7(5):395-401. Many practitioners and patients
have reported benefits from the treatment of myofascial pain and
headache by acupuncture.
Audette JF, Wang F, Smith H 2004.
Bilateral activation of motor unit potentials with unilateral needle
stimulation of active myofascial trigger points. Am J Phys Med
Rehabil. 83(5):368-374. “...perception of pain and muscle
dysfunction in active MTrPs may be related to abnormal central nervous
system processing of sensory input at the level of the spinal cord.”
Auleciems, L. M. 1995. Myofascial pain syndrome: a
multidisciplinary approach. Nurs Pract 20(4):18.
Austin, James H. 1999. Zen and the Brain. MIT
Press: Cambridge MA.
Auvenshine, R. C. 1997. Psychoneuroimmunology and its
relationship to the differential diagnosis of temporomandibular disorders. Dent
Clin North Am 41(2):279-296.
Auvinet B, Bileckot R, Alix AS et al. 2006.
Gait disorders in patients with fibromyalgia. Joint Bone
Spine. [Mar 15 Epub ahead of print] “Gait during stable walking
was severely altered in the patients. Walking speed was
significantly diminished as a result of reductions in stride length
and cycle frequency. The resulting bradykinesia was the best
factor for separating the two groups. Regularity was affected
in the patients; this variable is interesting because it is
independent of age and sex in healthy, active adults.
Measuring the variables that characterize relaxed walking provides
useful quantitative data in patients with fibromyalgia.”
[Unfortunately, these patients were not evaluated for co-existing
myofascial TrPs which are often the cause of gait disturbance. DJS]
Avery, D. H., K. Dahl, M. V. Savage, G. L. Brengelmann, L. H.
Larsen, M. A. Kenny, D. N. Eder, M. V. Vitiello and P. N. Prinz. 1997.
Circadian temperature and cortisol rhythms during a constant routine are phase-delayed in
hypersomnic winter depression. Biol Psychiatry 41(11): 1109-1123.
Azad SC, Huge V, Schops P et al. 2005. [Endogenous cannabinoid
system. Effect on neuronal plasticity and pain memory] Schmerz
19(6):521-527. [German] “The endogenous cannabinoid system is involved
in the control of neuroplasticity as part of pain processing.
Cannabinoids prevent the formation of LTP (long-term potentiation) in
the amygdala via activation of CBI receptors.”
Azuma, J., T. Kishi, R. H. Williams and K. Folkers. 1976.
Apparent deficiency of Vitamin B6 in typical individuals who commonly serve as normal
controls. Res Commun Chem Pathol Pharmacol 14(2):343-66
Babu AS, Mathew E, Danda D et al. 2007.
Management of patients with fibromyalgia using biofeedback: a randomized
control trial. Indian J Med Sci. 61(8):455-461. “Biofeedback
as a treatment modality reduces pain in patients with FMS, along with
improvements in FIQ (fibromyalgia impact questionnaire), SMWT (six-minute
walk test) and the number of tender points.”
Bach GL, Clement DB. 2007.
Efficacy of Farabloc as an analgesic in primary fibromyalgia. [Jan 11 Epub
ahead or print] Clin Rheumatol. This single-blind study suggests
that Farabloc, an electromagnetic shielding fabric, if used as material for
night clothes for fibromyalgia patients, has analgesic properties.
Bachmann, G. A. 1999. Vasomotor flushes in menopausal
women. Am J Obstet Gynecol 180(3):312-6.
Baconnier,
S., S. B. Lang, M. Polomska et al. Calcite microcrystals in the pineal gland
of the human brain: First physical and chemical studies. Bioelectromagnetics
23(7):488-495. A new form of crystallization that is separate and different
from the hydroxyapatite concretions often described has been found in the
pineal gland. This calcium, carbon and oxygen crystallization may have
piezoelectric properties. Tests are in progress to determine function and
formation of these crystals.
Bagge, E., B. A. Bengtsson, L. Carlsson and J. Carlsson. 1998. Low
growth hormone secretion in patients with fibromyalgia-a preliminary report on 10 patients
and 10 controls. J Rheumatol 25(1):145-148.
Bagis S., Tamer L., Sahin G. et al.
2003. Free radicals and antioxidants in primary fibromyalgia: an
oxidative stress disorder? Rheumatol Int. [Epub Dec 20
ahead of print]. This study indicates that free radical levels may
cause FMS.
Baik, H. W. and R. M. Russell. 1999. Vitamin B12
deficiency in the elderly. Annu Rev Nutr 19:357-77.
Bajaj
P, Bajaj P, Madsen H et al. 2003. Endometriosis is associated with
central sensitization: a psychophysical controlled study. J Pain
4(7):372-380.
Baker, B. A. 1986. The muscle trigger: evidence of
overload injury. J Neuro Ortho Med Surg 7(1):35-44. ISSN
0271-1575/86-0701.
Baker K, Barkhuizen A. 2006. Pharmacologic
treatment of fibromyalgia. Curr Psychiatry Rep. 8(6):464-469.
“Fibromyalgia is a syndrome of widespread pain, non-restorative sleep,
disturbed mood, and fatigue. Optimal treatment involves a
multidisciplinary approach with a team of health care providers using
pharmacologic and nonpharmacologic treatment. Because of the
heterogeneity of the illness, management should be individualized for the
patient. Pharmacologic treatment should address issues of pain
control, sleep disturbance, fatigue and any underlying coexisting mood
disorder. Nonpharmacologic treatment should include patient education,
a regular exercise and stretching program, and cognitive behavioral therapy.
All of these are essential to improving functional capacity and quality of
life. This review provides general guidelines in initiating a
successful pharmacologic treatment program for patients with fibromyalgia.”
Bakker, S. J., J. C. ter Maaten, C. Popp-Snijders, R. J. Heine and
R. O. Gans. 1999. Triiodo-thyronine: a link between the insulin
resistance syndrome and blood pressure? J Hypertens 17(12 Pt
1):1725-30.
Balasubramaniam R, Laudenbach JM, Stoopler ET. 2007. Fibromyalgia:
an update for oral health care providers. Oral Surg Oral Med
Oral Pathol Oral Radiol Endod. 104(5):589-602. “Oral health
care providers may be the first to recognize signs and symptoms of this
complex disorder and are often consulted to participate in the
management of FM patients.” “This review will also highlight
issues that are important to the oral health care provider, including
orofacial manifestations and dental considerations for patients with
FM.” [Many dentists and oral hygienists have no idea how much
their work can impact the life of their FM patients. They don’t
understand central sensitization and can cause significant needless pain
that can last for weeks or longer. Many dentists are also unaware
of MTPs, and thus unaware of the impact MTPs can have on equilibration.
If the bite is off due to MTPs, or there is dental pain or sensitivity
to pressure or cold, etc., due to MTPs, errors in “correcting” the bite
can ruin the patient’s mouth, cause needless dental work, and amount to
malpractice. Information has been available for a long time, and there
is no excuse for dentists (nor other care providers) “not wanting to
know.” DJS]
Balasubramanian V, Adalarasu K. 2007. EMG-based
analysis of change in muscle activity during simulated driving. J
Bodywork Move Ther. 11, 151-158. “Extensive usage of computers could
cause fatigue and even lead to musculo-skeletal injuries.”
Baldweg, S. E., A. Golay, A. Natali, B. Balkau, S. Del Prato and S.
W. Coppack. 2000. Insulin resistance, lipid and fatty acid concentrations in
867 healthy Europeans. Eur J Clin Invest 30(1):45-52.
Baldwin, C. M., I. R. Bell and M. K. ORourke.
1999. Odor sensitivity and respiratory complaint profiles in a community-based
sample of asthma, hay fever, and chemical odor intolerance. Toxicol Ind Health
15(3-4):403-9.
Baliki MN, Geha PY, Apkarian AV. 2007.
Spontaneous pain and brain activity in neuropathic pain: functional MRI and
pharmacologic functional MRI studies. Curr Pain Headache Rep
11(3):171-177. Functional MRI may be a valid method for studying
clinical pain. “...the latest results using this approach imply that
distinct clinical chronic pain conditions seem to involve specific brain
circuitry, which is also distinct from the brain activity commonly observed
in acute pain.”
Baliki MN, Chialvo DR, Geha PY. 2006. Chronic
pain and the emotional brain: Specific brain activity associated with
spontaneous fluctuations of intensity of chronic back pain. Chronic pain
seems to activate different areas of the brain than are activated during
acute pain. Chronic pain is associated with the insula, an area of the
brain that also is associated with negative emotions, response
conflict, emotional memories and self-image. Chronic back pain may
influence a person’s sense of being and may trigger emotional distress of
itself.
Balint G. 2002. Buprenorphine
treatment of patients with non-malignant musculoskeletal diseases.
Clin Rheumatol 21 Duppl 1:S17-S18. “When simple analgesics are
not sufficient, the use of opioid-type analgesics is justified.
Buprenorphine transdermal therapeutic system (TDS) is a novel
formulation of a well-tolerated and highly effective drug for
satisfactory pain control that can also be used in patients with chronic
non-malignant pain (CNMP) due to musculoskeletal diseases.”
Balousek S, Plane MB,
Fleming M. 2007. Prevalence of interpersonal abuse in primary care
patients prescribed opioids for chronic pain. J Gen Intern Med.
[Jul 20 Epub ahead of print]. This study, contrary to many others,
reported abuse of opioids in chronic pain patients. A large percentage
of these patients, however, had suffered lifetime physical abuse and suicide
attempts. The study concludes that understanding of patients' needs
may be better met by screening patients taking opioids for chronic pain for
a history of interpersonal abuse, and addressing those needs specifically.
Banahan, B. F. 3rd and E. M. Kolassa. 1997. A
physician survey on generic drugs and substitution of critical dose medications. Arch
Intern Med 157(18):2080-2088.
Bani, D., L. Ballati, E. Masini, M. Bigazzi and T. B. Sacchi.
1997. Relaxin counteracts asthma-like reaction indused by inhaled antigen in
sensitized guinea pigs. Endocrinology 138(5): 1909-1915.
Bani, D. 1997. Relaxin: a pleiotropic hormone. Gen Pharmacol
28(1):13-22.
Banic B, Petersen-Felix S, Andersen
OK et al. 2004. Evidence for spinal cord hypersensitivity in chronic
pain after whiplash injury and in fibromyalgia. Pain
107(1-2):7-15. This study gives evidence for spinal cord
hyperexcitability with hyperalgesia and allodynia in fibromyalgia patients
and in post-whiplash patients with chronic pain, in spite of the absence of
tissue damage.
Banisadr G, Rostene W, Kitabgi P et al. 2005.
Chemokines and brain functions. Curr Drug Targets Inflamm
Allergy 4(3):387-399. “Chemokines are small secreted proteins
that chemoattract and activate immune and non-immune cells both in
vivo and in vitro. Besides their well-established role in the
immune system, several recent reports have suggested that chemokines
and their receptors may also play a role in the central nervous
system. These proteins regulate the leukocyte infiltration in
the brain during inflammatory and infectious diseases.
Chemokines and their receptors are constitutively expressed by glial
and neuronal cells in the CNS, where they are involved in
intercellular communication. The implication of chemokines in
cellular communication could allow: i) to identify a new pathway for
neuron-neuron and/or glia-glia and/or neuron-glia communications
that are relevant to both normal brain function and
neuroinflammatory and neurodegenerative diseases; ii) to develop new
therapeutic approaches for still untreatable diseases further.”
Bannwarth, B. 1999. Risk-benefit assessment of opioids
in chronic noncancer pain. Drug Saf 21(4):283-96.
Banovac, K., K. Renfree, A. L. Makowski, L. L. Latta and R. D.
Altman. 1995. Fracture healing and mast cells. J Orthop Trauma
9(6):482-90.
Baran, H., K. Jellinger and L.
Deecke. 1999. Kynurenine
metabolism in Alzheimers disease. J Neural Transm 106(2):165-81.
Blockade of NMDA receptors by KYNA may be responsible for impaired memory, learning and
cognition in AD patients.
Baraniuk JN, Casado B, Maibach H. 2005. A
chronic fatigue syndrome-related proteome in human cerebrospinal fluid.
BMC Neurol Dec 1:5(1):22. “This pilot study detected an
identical set of central nervous system, innate immune and amyloidogenic
proteins in cerebrospinal fluids from two independent cohorts of subjects
with overlapping CFS (chronic fatigue syndrome), PGI (Persian Gulf War
Illness) and fibromyalgia.” The conditions are different, but they may
share the proteome and pathological mechanism. This study also gives an
objective neuropathophysiology shared by each of these conditions.
[Dr. Baraniuk stated that his research “ …provides initial evidence that
chronic fatigue syndrome and its family of illnesses (i.e., FMS and GWI) may
be legitimate, neurological diseases and that at least part of the pathology
involves the central nervous system.” Georgetown University Medical Center public press release 12/1/05. ]
Baraniuk JN,
Whalen G, Cunningham J et al. 2004. Cerebrospinal fluid levels
of opioid peptides in fibromyalgia and chronic low back pain.
BMC Musculoskel Disord 5(1):48. “Central nervous system
opioid dysfunction may contribute to pain in fibromyalgia.”
Baraniuk JN, Petrie KN, Le U et al. 2004.
Neuropathology in Rhinosinusitis. Am J Respir Crit Care Med [Epub]
Baraniuk, J. N. , D. Clauw, A. Yuta, M. Ali, E. Gaumond, N.
Upadhyayula, K. Fujita and T. Shimizu. 1998. Nasal secretion analysis in allergic
rhinitis, cystic fibrosis, and nonallergic fibromyalgia/chronic fatigue syndrome subjects.
Am J Rhinol 12(6):435-40.
Barbara G, Stanghellini V, DeGiorgio R et al. 2004.
Activated mast cells in proximity to colonic nerves correlate with abdominal pain in irritable bowel syndrome.
Gastroenterology 126(3):693-702. The pain of IBS may be in part provoked by release of mast cells in the colon.
Bardin L, Tarayre JP, Malfetes N et al. 2003. Profound, non-opioid
analgesia produced by the high-efficacy 5-HT(1A) agonist F 13640 in the
formalin model of tonic nociceptive pain. Pharmacology
67(4):182-194. “These results help to establish large-magnitude
5-HT(1A) receptor activation as a new molecular mechanism of profound,
central analgesia and suggest that F 13640 may be particularly effective
against pain arising from severe tonic nociceptive stimulation.”
[Although these studies are in early phases in rats, they provide hope
that a new type of medication for chronic pain will become available
that may be helpful for FMS. DJS]
Barkhuizen A. 2002. Rational and targeted pharmacologic treatment of fibromyalgia.
Rheum Dis Clin North Am 28(2):261-90. "Pharmacologic agents
remain an important component of FM management. Addressing the
main symptoms of pain, disturbed sleep, mood disturbances,
fatigue, and associated conditions is essential to improve patient
functioning and enhanced quality of life."
Barnes, J. 1996. Myofascial release for craniomandibular pain and
dysfunction. Int J Orofascial Myology 22:20-22.
Barnes, J. 1990. Myofascial Release. MFR Seminars, 10 S.
Leopard Road, Suite One, Paoli, PA. 19301.
Barton, A., B. Pal, P. J. Whorwell and D. Marshall.
1999. Increased prevalence of sicca complex and fibromyalgia in patients with
irritable bowel syndrome. Am J Gastroenterol 94(7):1898-901.
Barzilai, N., L. She, B. Q. Liu, P. Vuguin, P. Cohen, J. Wang and L.
Rossetti. 1999. Surgical removal of visceral fat reverses hepatic insulin
resistance. Diabetes 48(1):94-8.
Barzilai, N., J. Wang, D. Massilon, P. Vuguin, M. Hawkins and L.
Rossetti. 1997. Leptin selectively decreases visceral adiposity and enhances insulin
action. J Clin Invest 100(12):3105-3110.
Batterman S.D., Batterman
S.C. 2002. Delta-V, spinal trauma, and the myth of the minimal damage
accident. J Whiplash and Rel Dis 1(1):41-52.
Bassoe, C. F. 1995. The skinache syndrome. J R Soc
Med 88:565-569.
Bazzichi L, Rossi A, Massimetti G et al. 2007.
Cytokine patterns in fibromyalgia and their correlation with clinical
manifestations. Clin Exp Rheumatol. 25(2):225-230. “The higher
levels of cytokines found in FM patients suggest the presence of an
inflammatory response system (IRS) and highlight a parallel between the
clinical symptoms and biochemical data. They support the hypothesis
that cytokines may play a role in the clinical features of fibromyalgia.
In addition, the similar cytokine patterns found in FM patients with
different psychiatric profiles suggests that IRS impairment may play a
specific role in the disease.”
Bazzichi L, Rossi A, Giuliano T et al.
2007. Association between thyroid autoimmunity and
fibromyalgic disease severity. Clin Rheumatol. [May 9
Epub ahead of print]. “...autoimmune thyroiditis is present in an
elevated percentage of FM patients…”
Bazzichi L, Giannaccini G, Betti L et al. 2006.
Alteration of serotonin transporter density and activity in
fibromyalgia. Arthritis Res Ther. 8(4):R99. “A change in
SERT (specific serotonin transporter, and serotonin uptake) seems to
occur in fibromyalgia patients, and it seems to be related to the
severity of fibromyalgic symptoms.”
Beal, M. W. 1998. Womens use of complementary and
alternative therapies in reproductive health care. J Nurse Midwifery
43(3):224-34.
Beard, J. L., M. J. Borel and J. Derr. 1990. Impaired
thermoregulation and thyroid function in iron-deficiency anemia. Am J Clin Nutr
52(5):813-9.
Becker, N., A. B. Thomsen, A. K. Olsen, P. Sjogren, P. Bech and J.
Erikson. 1998. [No title available]. Ugeskr Laeger 160(47):6816-9.
[Danish].
Becker, N., A. Bondegaard Thomsen, A. K. Olsen, P. Sjogren, P. Bech
and J. Erikson. 1997. Pain epidemiology and health related quality of life in
chronic non-malignant pain patients referred to as Danish multidisciplinary pain
center. Pain 73(3):393-400.
Becker, N., P. Sjogren, P. Bech, A. K. Olsen and J. Eriksen.
2000. Treatment outcome of chronic non-malignant pain patients managed in a Danish
multidisciplinary pain center compared to general practice: a randomized controlled
trial. Pain 84(2):203-11.
Bell IR, Lewis DA 2nd, Lewis SE et
al. 2004. EEG alpha sensitization in individualized
homeopathic treatment of fibromyalgia. Int J Neurosci.
114(9):1195-1220.
Bell IR, Lewis II DA, Brooks AJ et al.
2004. Improved clinical status in fibromyalgia patients treated with
individualized homeopathic remedies versus placebo. Rheumatology
(Oxford) 43(5):577-582. This double-blind, randomized,
parallel-group, placebo-controlled study indicates that
“...individualized homeopathy is significantly better than placebo in
lessening tender point pain and improving the quality of life and global
health of persons with fibromyalgia.”
Bell, I. R., C. M. Baldwin, M. Fernandez and G. E. Schwartz.
1999. Neural sensitization model for multiple chemical sensitivity: overview of
theory and empirical evidence. Toxicol Ind Health 15(3-4):295-304.
Bell, I. R., M. J. Szarek, D. R. Dicenso, C. M. Baldwin, G. E.
Schwartz and R. R. Bootzin. 1999. Patterns of waking EEG spectral power in
chemically intolerant individuals during repeated chemical exposures. Int J
Neurosci 97(1):41-59.
Bell, I. R., C. M. Baldwin and G. E. Schwartz. 1998.
Illness from low levels of environmental chemicals: relevance to chronic fatigue syndrome
and fibromyalgia. Am J Med 105(3A):74S-82S.
Bell, I. R., C. M. Baldwin, L. G. Russek, G. E. Schwartz and E. E.
Hardin. 1998. Early life stress, negative paternal relationships, and chemical
intolerance in middle-aged women: support for a neural sensitization model. J
Womens Health 7(9):1135-47.
Bellamy N, Sothern RB, Campbell J. 2004. Aspects of diurnal rhythmicity in pain, stiffness, and fatigue in patients with fibromyalgia.
J Rheumatol 31(2):379-89. This study indicates that there are indications that pain, stiffness and fatigue show daily and possibly weekly patterns.
The awareness of these patterns can be useful for scheduling activities, measurement in clinical trials, and perhaps timing administration of medications for when they are most needed.
Bellastella, A., G. Pisano, S. Iorio, D. Pasquali, F. Orio, T.
Venditto and A. A. Sinisi. 1998. Endocrine secretions under abnormal light-dark
cycles and in the blind. Horm Res 49(3-4):153-7.
Bendiksen A, McGehee E, Handberg G. 2007.
[The use of methadone in the treatment of chronic non-malignant pain in an
out-patient setting] Ugeskr Laeger 169(17):1568-1572. [Danish]
“Opioid treated chronic pain patients with insufficient pain relief may
benefit from conversion to methadone, as 59% in our analysis achieved better
pain relief, while the rotation was generally opioid-saving at the same
time. The method used was safe and acceptable to the patients.
The analyses did not result in any fundamental changes to the procedure.”
Methodone may be a viable option for insufficiently relieved pain in chronic
non-malignant pain patients.
Bendtsen L. 2000. Central
sensitization in tension-type headache—possible pathophysiological
mechanisms. Cephalalgia 20(5):486-508. “The
stimulus-response function for palpation pressure vs. pain was found to be
qualitatively altered in chronic tension-type headache patients compared
with controls. The stimulus-response function was found to be
qualitatively altered also in patients with fibromyalgia. It was
concluded that the qualitatively altered nociception was probably due to
central sensitization at the level of the spinal dorsal horn/trigeminal
nucleus. Future basic and clinical research should aim at identifying
the source of peripheral nociception in order to prevent the development of
central sensitization and at ways of reducing established sensitization.
This may lead to a much needed improvement in the treatment of chronic
tension-type headache and other chronic myofascial pain conditions.”
Bendtsen, L., J. Norregaard, B. Jensen and J. Olesen.1997. Evidence
of qualitatively altered nociception in patients with fibromyalgia. J Rheumatol
40(1):98-102.
Benecke
R., Dressler D, Kunesch E et al. 2003. [No Title Given] Schmertz
17(6):450-458. Pain relief for myofascial pain has been reported with
botox injections, but “in fibromyalgia, there seems to be no analgesic
effect.”
Bengtsson, A., J. Ernerudh, M. Vrethem and T. Skogh. 1990. Absence
of autoantibodies in primary fibromyalgia. J Rheumatol 17(12:1682-3.
Bengtsson, A. and K. G. Henriksson. 1989. The muscle in
fibromyalgiaa review of Swedish studies. J Rheumatol Suppl Nov;(19)144-149.
Bengtsson, A. and M. Bengtsson. 1988. Regional sympathetic blockade
in primary fibromyalgia. Pain 33(2):161-7.
Bengtsson A., Henriksson KG, Larsson J. 1986. Reduced
high-energy phosphate levels in the painful muscles of patients with primary
fibromyalgia. Arthritis Rheum. 29:817-21.
Benjamin M, Toumi H, Ralphs JR et al. 2006.
Where tendons and ligaments meet bone: attachment sites (‘entheses’)
in relation to exercise and/or mechanical load. J Anat.
208(4):471-490. “Entheses (insertion sites, osteotendinous
junctions, osteoligamentous junctions) are sites of stress
concentration at the region where tendons and ligaments attach to
bone. Consequently, they are commonly subject to overuse
injuries (enthesopathies) that are well documented in a number of
sports.” [These areas are often sites of attachment TrPs and
these TrPs are frequently overlooked by orthopedic and surgical
consultants. DJS]
Benjamin, S., Morris, S.,
McBeth, J., MacFarland, G.J., Silman, A.J.. 2000. The association
between chronic widespread pain and mental disorder: A Population
Study. Epidemiological group has tended towards viewing FMS as a
somatization disorder. It was therefore important in this study
that they only found three cases of somatoform disorders and came
to the conclusion that somatoform disorders were uncommon in
people with chronic widespread pain.
Bennett GJ. 2000. Update on the
neurophysiology of pain transmission and modulation: focus on the NMDA-receptor.
J Pain Symptom Manage 19(1 Suppl):S2-S6. “NMDA-receptor
activation not only increases the cell’s response to pain stimuli, it
also decreases neuronal sensitivity to opioid receptor agonists.
In addition to preventing central sensitization, co-administration of
NMDA-receptor antagonists with an opioid may prevent tolerance to opioid
analgesia.”
Bennett, G. J. 2000. Update on the neurophysiology of
pain transmission and modulation: focus on the NMDA-receptor. J Pain Symptom
Manage 19(1 Suppl):S2-6.
Bennett R. 2007. Myofascial pain syndromes and
their evaluation. Best Pract Res Clin Rheum 21(3):427-445.
This outstanding summary of MTPs is a comprehensive, clearly written
overview of myofascial medicine. It explains why it is necessary for
doctors to be trained in diagnosis of MTPs, and that they frequently occur
in the presence of other conditions but, although they are exceedingly
common, are often undiagnosed or misdiagnosed. [Severe CMP with
central sensitization and multiple conditions are not explored, but the
treatments suggested are often adequate for mild cases. It is
significant that an article on MTPs written by such a respected scientist
and clinician has appeared in a rheumatology journal. It is hoped that
it is as well-read as it is well-written. DJS]
Bennett RM. 2007. Do patients’ perceptions of
negative physician attitudes influence fibromyalgia symptoms and status?
J Musculoskel Pain 15 (Supp 13):42 item 74. [Myopain 2007
Poster] “Current physicians were perceived to take the diagnosis of
FMS more seriously, which in turn was related to improved FMS symptomatology.
Perception that current or past physicians didn’t take FMS seriously was
associated with increased anxiety. Patients may improve both
physically and psychologically under the care of a physician who takes their
illness seriously, whereas a negative past attitude continues to adversely
influence their psychological health.” [Doctors can be serious
perpetuating factors. Use care in choosing your health care team. DJS]
Bennett R. 2007. Myofascial pain syndromes and
their evaluation. Best Pract Res Clin Rheumatol. 21(3):427-445.
“Myofascial pain refers to a specific form of soft tissue rheumatism that
results from irritable foci (trigger points) within skeletal muscles and
their ligamentous junctions. It must be distinguished from bursitis,
tendonitis, hypermobility syndromes, fibromyalgia and fasciitis. On
the other hand it often exists as part of a clinical complex that includes
these other soft tissue conditions, i.e., it is not a diagnosis of
exclusion.”
Bennett RM. 2004. Diagnostic criteria
and differential diagnosis of the fibromyalgia syndrome.
J Musculoskeletal Pain 12(3/4):59-64. This article
explains some of the difficulties arising from the use of 1990
ACR FMS Criteria for research as diagnostic criteria, the need
for clarification of terms and training in differential
diagnosis and treatment.
Bennett RM. 2004. Three years later:
presidential address to MYOPAIN ’04. J Musculoskeletal
Pain 12(3/4):1-12. [This is an excellent overview on
some of the current developments in FMS and myofascial pain,
including a summary of the reasons central sensitization is a
key to FMS, and a clear look at the increase in morbidity and
mortality for those with chronic pain. DJS]
Bennett R. 2005. The fibromyalgia impact
questionnaire (FIQ): a review of its development, current version,
operating characteristics and uses. Clin Exp Rheumatol.
23(5 Suppl 39):S154-162. The latest version of the
Fibromyalgia Impact Questionnaire can be found at
www.myalgia.com/FIQ/FIQ
Bennett RM, Schein J, Kosinski MR et al. 2005.
Impact of fibromyalgia pain on health-related quality of life before
and after treatment with tramadol/acetaminophen. Arthritis
Rheum. 53(4):519-527. “Moderate-to-severe fibromyalgia pain
significantly impairs HRQOL [health-related quality of life], and
effective pain relief in these patients significantly increases
HRQOL.”
Bennett R. 2004. Fibromyalgia: present to future.
Curr pain Headache Rep. 8(5):379-384. A review of the understanding
of FMS, including emerging clues and predictions on future developments.
Bennett RM.
2002. Adult growth hormone deficiency in patients with
fibromyalgia. Curr Rheumatol Rep 4(4):306-12. "There
is evidence that GH deficiency as defined in terms of a low
insulin-like growth factor-1 (IGF-1) level occurs in approximately
30% of patients with fibromyalgia and is probably the cause of
some morbidity. It seems most likely that impaired GH secretion
in fibromyalgia is related to a physiologic dysregulation of the
hypothalamic-pituitary-adrenal axis (HPA) with a resulting
increase in hypothalamic somatostatin tone. The severe GH
deficiency that occurs in a subset of patients with fibromyalgia
is of clinical relevance because it is a treatable disorder with
demonstrated benefits to patients."
Bennett RM. 2002. The
rational management of fibromyalgia patients. Rheum Dis Clin
North Am 2002. 28(2):181-99. "The
exponential increase in pain research over the last 10 years has
established fibromyalgia (FM) as a common chronic pain syndrome
with similar neurophysiologic aberrations to other chronic pain
states. As such, the pathogenesis is considered to involve an
interaction of augmented sensory processing (central
sensitization) and peripheral pain generators. The notion, the FM
symptomatology results from an amplification of incoming sensory
impulses, has revolutionized the contemporary understanding of
this enigmatic problem and provided a more rational approach to
treatment."
Bennett, R. M. 1999. Fibromyalgia Review. J
Musculoskeletal Pain 7(4):85.
Bennett, R. M. 1999. Emerging concepts in the neural biology
of chronic pain: evidence of abnormal sensory processing in fibromyalgia.. Mayo Clin
Proc 74(4):385-98.
Bennett, R. M. 1998. Disordered growth hormone secretion and
fibromyalgia: a review of recent findings and a hypothesized etiology. Z Rheumatol
57 Suppl 2:72-6.
Bennett, R. M., S. C. Clark and J. Walczyk. 1998. A
randomized, double-blind, placebo-controlled study of growth hormone in the treatment of
fibromyalgia. A J Med 104(3):227-231.
Bennett, R. M. , D. M. Cook, S. R. Clark, C. S. Burckhardt and
S. M. Campbell. 1997. Hypothalamic-pituitary-insulin-like growth factor-I axis dysfunction
in patients with fibromyalgia. J Rheumatol 24(7):1384-1389.
Bennett, R. M. 1995. Fibromyalgia: The commonest cause of
widespread pain. Frontiers 21(6):269-275.
Bennett, R. M. And S. Jacobsen. 1994. Muscle
function and origin of pain in fibromyalgia. Ballieres Clin Rheumatol 8(4):721-746.
Bennett, R. M., S. R. Clark, S. M. Campbell and C. S. Burckhardt. 1992. Low levels of somatomedin C in patients with the fibromyalgia
syndrome: a possible link between sleep and muscle pain. Arthritis Rheum
35(10):1113-6.
Bennett, R. M., S. R. Clark, S. M. Campbell, S. B. Ingram, C.
S. Burckhardt, D. L. Nelson and J. M. Porter. 1991. Symptoms of Raynauds syndrome in
patients with fibromyalgia. Arthritis Rheum 34(3):264-9.
Bennett, R.M., R. A. Gatter, S. M. Campbell, R. P. Andrews, S. R.
Clark and J. A. Scarola. 1988. A comparison of cyclobenzaprine and placebo in
the management of fibrositis. Arthritis Rheum 31(12):1535-1542.
Berga, S. L. 1998. Hypothalamus pituitary gonadal axis:
stress-induced gonadal compromise. J Musculoskel Pain 6(3):61-70.
Berger A, Dukes E, Martin S et al. 2007.
Characteristics and healthcare costs of patients with fibromyalgia syndrome.
Int J Clin Pract. [Jul 26 Epub ahead of print]. “Patients with FMS
have comparatively high levels of comorbidities and high levels of
healthcare utilization and cost.” [Researchers are realizing that FM
patients often have multiple conditions. What they do not yet
understand is that many of these conditions are interactive. DJS]
Berggren-Clive, K. 1998. Out of the darkness and into
the light: womens experiences with depression after childbirth. Can J
Commun Ment Health 17(1):103-20.
Bergholm U, Johansson BH. 2003. [No
title given] Lakartidningen 100(47):3842-3847. [Swedish]
“The late onset of symptoms can now be explained by the functional
stenosis of the spinal cord and brainstem due to scar formation around
the dens axis after injury. Modern neurophysiology can now explain
the background of the generalized and complex picture of chronic pain
and muscular and cognitive dysfunction. This new knowledge has
prepared the way for more specific therapy in patients suffering from
craniocervical instability symptoms and pain from disks and facet joints
in the cervical spine after whiplash trauma.”
Berman, B. M., J. P. Swyers and J. Ezzo. 2000. The
evidence for acupuncture as a treatment for rheumatologic conditions. Rheum Dis
Clin North Am 26(1):103-15, ix-x.
Berman, B. M. and J. P. Swyers. 1999. Complementary
medicine treatments for fibromyalgia syndrome. Baillieres Best Pract Res Clin
Rheumatol 13(3):487-92.
Berman, B. M, B. B. Singh, S. M. Hartnoll, B. K. Singh and D.
Reilly. 1998. Primary care physicians and complementary-alternative medicine:
training, attitudes, and practice patterns. J Am Board Fam Pract 11(4):272-81.
Berman, B. M. and J. P. Swyers. 1997. Establishing as research
agenda for investigating alternative medical interventions for chronic pain. Prim
Care 24(4):743-758.
Berman SM, Naliboff
BD, Suyenobu B et al. 2008. Reduced brainstem inhibition during
anticipated pelvic visceral pain correlates with enhanced brain response to
the visceral stimulus in women with irritable bowel syndrome. J
Neurosci. 28(2):349-359.
Bernardes AT, dos Santos RM. 1997. Immune
network at the edge of chaos. J Theor Biol. 186(2):173-187.
Chaos system, used in mathematics, corresponds in many ways to the state of
ill health, especially chronic illness.
Bernardis, L. L. and P. J. Davis. 1996. Aging and the
hypothalamus: research perspectives. Physiol Behav 59(3):523-36.
Bernatsky S, Dobkin P, DeCivita M et al. 2005.
Co-morbidity and physician use in fibromyalgia. Swiss Med Wkly
135(5-6):76-81. “Reported co-morbidity was classified into 4
categories: medical, psychiatric, ‘functional’ and unknown. The
category for ‘functional’ conditions included disorders that have been
classified by previous authors as medically unexplained symptoms such as
the irritable bowel and chronic fatigue syndromes. Co-morbidity
with other disorders, both functional and medical, was high in this
sample. Medical and psychiatric co-morbidity were stronger
determinants of high physician use than ‘functional’ co-morbidity.”
[It is illogical to classify conditions together merely because medical
science, or the authors, cannot explain them. DJS]
Bernstein J, Alonso DR, DiCaprio M et al. 2003.
Curricular reform in musculoskeletal medicine: needs, opportunities and
solutions. Clin Orthop Relat Res. (415):302-308.
“Musculoskeletal medicine is not taught adequately in American medical
schools and the predictable consequences are seen. Students cannot
show cognitive mastery of the subject and lack confidence in this topic.”
“…although inadequate education is neither new nor necessarily unique among
disciplines, the coming year or two, the beginning of the Bone and Joint
decade, was seen to be a particularly auspicious time for attempting
curricular reform.”
Berthold
U, Johansson BH. 2003. [No title given] Lakartidingen
100(47):3842-3847. [Swedish]
Late symptom onset may be due to scar formation around the dens axis
after whiplash injury. Functional magnetic resonance imaging (fMRI) may be a
valuable source of documentation in whiplash injuries. This may be causing
central pain, and muscular and cognitive dysfunctions. [Narrowing of the
spinal cord and brainstem area may also be due to constricting muscles due
to TrP contracture. DJS
Bezerra Rocha CA, Sanchez TG, Tesseroli de Siqueira
JT. 2007. Myofascial trigger point: a possible way of modulating
tinnitus. Audiol Neurootol. 13(3):153-160. “Temporary
modulation of tinnitus was frequently observed (55.9%) during digital
pressure, mainly in the masseter.” “An association between tinnitus and the
presence of myofascial trigger points was observed, as well as a laterality
association between the ear with the worst tinnitus and the side of the body
with more myofascial trigger points. Thus, this relationship could be
explained not only by somatosensory-auditory system interactions but also by
the influence of the sympathetic system.”
Biasi, G., A. Fioravani, A. Franci and R. Marcolongo. 1994. [The
role computerized telethermography in the diagnosis of fibromyalgia syndrome.] Minerva
Med 85(9):451-4. [Italian]
Bieber C, Muller KG, Blumenstiel K et al. 2008.
A shared decision-making communication training program for physicians
treating fibromyalgia patients: effects of a randomized controlled trial.
J Psychosom Res. 64(1):13-20. “SDM (shared decision making)
with FMS patients might be a possible means to achieve a positive quality of
physician-patient interaction. A specific SDM communication training
program teaches physicians to perform SDM and reduces frustration in
patients.”
Bieber C, Muller KG,
Blumenstiel K et al. 2006. Long-term effects of a shared decision-making
intervention on physician-patient interaction and outcome in fibromyalgia: A
qualitative and quantitative 1-year follow-up of a randomized controlled
trial. Patient Educ Couns. [Jul 25 Epub ahead of print]
Shared decision making can be a critical step in producing both doctor and
patient satisfaction in fibromyalgia care.
Billiard M, Bentley A. 2004. Is insomnia best
categorized as a symptom or a disease? Sleep Med. 5 Suppl
1:S35-40. It is important to discover if co-existing conditions are causing
the insomnia, or simply co-existing. If co-existing, it is important
to discover the cause of the insomnia and get that under control.
Binhi VN. 2005. Stochastic dynamics of
magnetosomes and a mechanism of biological orientation in the geomagnetic
field. Bioelectromagnetics [Nov 10 Epub ahead of print].
Magnetosomes embedded in the cytoskeleton (skeletal structure of the cells)
may be what allows migratory animals to orient themselves. They are
sensitive to the Earth’s magnetic field. [The possibility of magnetosomes
in cytoskeletons of those people electromagnetically sensitive or
electromagnetically sensible exists. DJS]
Birch, S. 2003. Trigger
point–acupuncture point correlations revisited. J Altern
Complement Med 9(1):91-103. Earlier research (Melzack et al 1977)
claimed 71% correspondence of trigger points to traditional acupuncture
points. This study finds that
result is “conceptually not possible,” and that there is no more than a
40% correlation and more likely 18% to 19% correlation between the two.
The author did find that another class of acupuncture points, “a
she” points, had a very high correlation to trigger points.
Birch, S. and R. N. Jamison. 1998. Controlled trial of
Japanese acupuncture for chronic myofascial neck pain: assessment of specific and
nonspecific effects of treatment. Clin J Pain 14(3):248-55.
Birdsall, T. C. 1998. 5-Hydroxytryptophan: a
clinically-effective serotonin precursor. Altern Med Rev 3(4):271-80.
Birkmayer W. and P. Riederer. 1989. Understanding the
Neurotransmitters: Key to the Workings of the Brain. Translated from German by Karl
Blau. NY: Springerer-Verlag.
Birketvedt, G. S. , J. Florholmen, J. Sundsfjord, B. Osterud, D.
Dinges, W. Bilker and A. Stunkard. 1999. Behavioral and neuroendocrine characteristics of
the night-eating syndrome. JAMA 282(7):657-63.
Bishnoi, A., H. E. Carlson, B. L. Gruber, L. D. Kaufman, J. L. Bock
and K. Lidonnici. 1994. Effects of commonly prescribed nonsteroidal anti-inflammatory
drugs on thyroid hormone measurements. Am J Med 96(3):235-8.
Bjorntorp P. 2001. Do
Stress reactions cause abdominal obesity and comorbidities?
Obes Rev 2(2):73-86. Long-term activation of the
Hypothalamus-Pituitary Adrenal (HPA) Axis and sympathetic nervous
system [commonly part of FMS DJS] may be the prelude to
many serious illnesses. This includes Metabolic Syndrome. It is
important to prevent and/or treat abnormal stress activation.
"...it is suggested that environmental, perinatal and genetic
factors induce neuroendocrine perturbations followed by abnormal
abdominal obesity with its associated comorbidities."
Bjorntorp, P., G. Holm and R. Rosamund. 1999. Hypothalamus arousal,
insulin resistance and Type 2 diabetes mellitus. Diabet Med 16(5):373-83.
Black, D. W., B. N. Doebbeling, M. D. Voelker, W. R. Clarke, R. F.
Woolson, D. H. Barrett and D. A. Schwartz. 1999. Quality of life and
health-services utilization in a population-based sample of military personnel reporting
multiple chemical sensitivities. J Occup Environ Med 41(10):928-33.
Black, K. M., P. McClure and M. Polansky. 1996. The
influence of different sitting positions on cervical and lumbar posture. Spine
21(1):65-70.
Blackman, J. D., V. L. Towle, G. F. Lewis, J. P. Spire and K. S.
Polonsky. 1990. Hypoglycemic thresholds for cognitive dysfunction in
humans. Diabetes 39(7):828-835.
Blacksher E. 2002. On being poor and
feeling poor: low socioeconomic status and the moral self. Theor Med
Bioeth. 23(6):455-470. “Persons of low socioeconomic status
generally experience worse health and shorter lives than their better
off counterparts. They also suffer a greater incidence of adverse
psychosocial characteristics, such as low self-esteem, self-efficacy,
and self-mastery and increased cynicism and hostility. Chronic
socioeconomic deprivation can create environments that undermine the
development of self and capacities constitutive to moral agency — i.e.,
the capacity for self-determination and crafting a life of one’s own.
This moral harm is particularly salient in modern Western societies,
especially in the United States, where success and failure is attributed
to the individual, with little notice of the larger social and political
realities that inform an individual’s circumstances and choices.”
Blanco I, Arbesu D, Al Kassam D et al. 2006.
Alphal-antitrypsin polymorphism in fibromyalgia syndrome patients from the
Asturias province in northern Spain: a significantly higher prevalence of
the PI*Z deficiency allele in patients than in the general population.
J Musculoskel Pain 14(3):5-12. A gene has been found that is
twice as high in FMS patients as in this general population. The gene
is associated with AT, an anti-inflammatory substance, and may indicate that
“...at least a subset of FMS subjects could suffer from an inflammatory
process, mediated by cytokines, proteases, and inflammation mediators
normally inhibited by AT.” [This study indicates that if there is a
triggering event that causes inflammation in the extra cellular matrix and
the patient lacks these anti-inflammatory modulators due to genetics, the
central sensitization process of FMS could begin. DJS]
Blashki G, McMichael T, Karoly DJ. 2007.
Climate change and primary health care. 36(12):986-989. “Climate
change has substantial potential health effects. These include heat
stress related to heat waves; injuries related to extreme weather events
such as storms, fires and floods; infectious disease outbreaks due to
changing patterns of mosquito borne and water borne diseases; poor nutrition
from reduced food availability and affordability; the psychosocial impact of
drought; and the displacement of communities. Primary health care has
an important role in preparing for and responding to these climate change
related threats to human health.” [Patients with weather-reactive
health conditions should be environmental activists. We are the canaries in
the mines. Sensitivity to pollution in all its forms has made us the
first to be aware, but we will not be the last to be affected. DJS]
Bliddal H, Danneskiold-Samsoe B. 2007. Chronic
widespread pain in the spectrum of rheumatological diseases. Best
Pract Res Clin Rheumatol. 21(3):391-402. “Evidence points to
central sensitization as an important neurophysiological aberration in the
development of FMS. Importantly, these neurological changes may result
from inadequately treated chronic focal pain problems such as osteoarthritis
or myofascial pain.” “Fibromyalgia patients need recognition of their
pain syndrome if they are to comply with treatment. Lack of empathy
and understanding by healthcare professionals often leads to patient
frustration and inappropriate illness behavior, often associated with some
exaggeration of symptoms in an effort to gain some legitimacy for their
problem.”
Blunz, K. L., M. H. Rajwani and R. C. Guerriero. 1997.
The effectiveness of chiropractic management of fibromyalgia patients: a pilot
study. J Manipulative Physiol Ther 20(6):389-399.
Blyth FM, March LM, Brnabic AJ et al. 2004. Chronic
pain and frequent use of health care. Pain 111(1-2):51-58.
“There was a strong association between pain-related disability and
greater use of services.”
Bohme K. 2002. Buprenorphine in a
transdermal therapeutic system — a new option. Clin Rheumatol
21 Suppl 1:S13-S16. “Typical opioid-related adverse events
were reported with a low incidence and mild intensity. Clinical
benefit, coupled with a high level of patient compliance and improved
quality of life, substantiate the usefulness of buprenorphine TDS in a
practical setting.”
Bolgla LA, Malone TR. 2004. Plantar fasciitis
and the Windlass Mechanism: A biochemical link to clinical practice.
J Alth Train 39(1):77-82. “This model provides a means for
describing plantar fasciitis conditions such that clinicians can formulate a
potential causal relationship between conditions and their treatments.
[This article is relevant to and can be useful in the treatment of
myofascial TrPs, and would have benefitted by their inclusion. DJS]
Bonadonna
R. Meditation’s impact on chronic illness. Holistic Nurs
Pract 17(6):309-319. This article points out that more research
needs to be done on the effect of living mindfully on chronic illness and
urges the practice of meditation as part of treatment regimens.
Bongers, K. M., J. P. ter Bruggen and C. L. Franke. 1991. [The
exploding head syndrome]. Ned Tijdschr Geneeskd 135(14):617-618. [Dutch]
Bonifazi M, Lisa Suman A, Cambiaggi C et al. 2006.
Changes in salivary cortisol and corticosteroid receptor-alpha mRNA
expression following a 3-week multidisciplinary treatment program in
patients with fibromyalgia. Psychoneuroendocrinology
31(9):1076-1086. “One of the active mechanisms underlying the
effects of our treatment is an improvement of HPA axis function,
consisting in increased resiliency and sensitivity of the stress system
probably related to stimulation of GR-alpha synthesis by the components
of the treatment.”
Boninger M.L., Cooper R.A.,
Fitzgerald S.G. et al. 2003. Investigati |