Facco
E, Ceccherelli F. 2005. Myofascial pain mimicking radicular
syndromes. Acta Neurochir 92:147-150. “Myofascial
pain is very often underscored and misunderstood in clinical practice.
In many cases the localization of myofascial pain may resemble other
diseases, such as radicular syndromes and even diseases of internal
organs. When vertebral abnormalities are present on CT or MRI, it
should be checked whether the cause of pain is radicular, myofascial, or
both. On the other hand, the conventional approach to painful
disorders may lead to errors and wrong diagnosis, depending on several
factors: a) pain is often considered a symptom of an organic disease; b)
the diagnosis is usually directed towards the structural cause of pain
only; c) the functional components of the suffering patient are
underscored; d) the site of pain may introduce some bias.”
Faerber L, Drechsler S, Ladenburger S et al. 2007.
The neuronal 5-HT(3) receptor network after 20 years of research –
evolving concepts in management of pain and inflammation. Eur J
Pharmacol. 560(1):1-8.
Falcao DM, Sales L, Leite JR et al. 2008.
Cognitive behavioral therapy for the treatment of fibromyalgia syndrome:
a randomized controlled trial. J Musculoskel Pain.
16(3):133-140. The psychological aspects of chronic pain seems to
respond positively to cognitive behavior therapy.
Falla D, Bilenkij G, Jull G. 2004. Patients
with chronic neck pain demonstrate altered patterns of muscle activation
during performance of a functional upper limb task.
Spine 29(13):1436-1440. “Patients with neck pain demonstrated
greater activation of accessory neck muscles during a repetitive upper
limb task compared to asymptomatic controls.”
Falla D, Jull G, Edwards S et al. 2004.
Neuromuscular efficiency of the sternocleidomastoid and anterior scalene
muscles in patients with chronic neck pain. Disabil Rehabil.
26(12):712-717. “Reduced NME in the superficial cervical flexor muscles in
patients with neck pain may be a measurable altered muscle strategy for
dysfunction in other muscles. This aberrant pattern of muscle
activation appears to be most evident under conditions of low load.
NME, when measured at 25% MVC, may be a useful objective measure for future
investigation of muscle dysfunction in patients with neck pain.”
Fang L., Wu J.,
Lin Q. et al. 2002. Calcium-calmodulin-dependent protein kinase II
contributes to spinal cord central sensitization. J Neurosci
22(10):4196-4204.
Fannelli
Jr., G. M. and I. M. Weiner. 1975. Species variations among primates
in responses to drugs which alter the renal excretion of uric acid.
J Pharmacol Exp Ther 193(2):363-375.
Farella M., Michelotti A., Gargano A et al.
2002. Myofascial pain syndrome misdiagnosed as odontogenic pain: a case
report. Cranio 20(4):307-11. When the cause of dental
pain cannot be clearly identified, consider all possible causes of dental
pain, including the nonodontogenic ones such as myofascial pain, before any
irreversible dental procedures are considered.
Farajidavar A, Gharibzadeh S, Towhidkhah F et al. 2006. A
cybernetic view on wind-up. Med Hypotheses [Mar 21 Epub
ahead of print] “Wind-up may aggravate the pain in clinical
hyperalgesic situations such as post-surgical states, some neuropathic
pains, fibromyalgia syndrome, and post-herpetic neuralgia. [This
work was based on wind-up in Abeta fibers, and other wind-up studies
have been based on afferent C-fibers. DJS]
Farina S, Casarotto M, Benelle M et al. 2004.
A randomized controlled study on the effect of two different treatments (FREMS
AND TENS) in myofascial pain syndrome. N Eura Medicophys.
40(4):293-301. Both methods appeared effective for myofascial pain,
although FREMS seemed better.
Farrell, J and G. O. Littlejohn. 1999. Pain, nature
of task, and body part used in fibromyalgia syndrome. J Musculoskel Pain
7(1-2):279-284.
Fasmer, B. 1990. [Do antidepressive agents have
analgesic effects?] Tidsskr Nor Laegeforen 110(18:2370-2. [Norwegian]
Fass R, Naliboff
BD, Fass SS et al. 2007. The effect of auditory stress on perception
of intraesophageal acid in patients with gastroesophageal reflux disease.
Gastroenterology [Dec 7 Epub ahead of print]. “Acute auditory
stress can exacerbate heartburn symptoms in GERD patients by enhancing
perceptual response to intraesophageal acid exposure. This greater
perceptual response is associated with greater emotional responses to the
stressor.” [For those of us with FM amplification and GERD, auditory
stress may be an even greater peril. DJS]
Fass, R, Quan SF, O’Connor GT et al. 2005.
Predictors of heartburn during sleep in a large prospective cohort
study. Chest 127:1658-1666. “Heartburn during sleep
is very common in the general population. Reports of this type of
symptom of GERD are strongly associated with increased BMI, carbonated
soft drink consumption, snoring and daytime sleepiness, insomnia,
hypertension, asthma, and usage of benzodiazepines. Overall,
heartburn during sleep may be associated with sleep complaints and
excessive daytime sleepiness.”
Fatoye F, Palmer S, Macmillan F et al.
2008. Proprioception and muscle torque deficits in children with
hypermobility syndrome. Rheumatology (Oxford). [Dec 16 Epub
ahead of print]. [This study has some fatal flaws.
Hypermobility syndrome is common in children with growing pains, which
includes those with myofascial trigger points. The ropy bands of TrPs
may indeed be the body’s attempt to stabilize the hypermobile joints.
The proprioceptive impairment noted in this study could be due to those
very same myofascial trigger points, and the proposed “...muscle
strengthening...” would only worsen these TrPs, causing further muscle
dysfunction, weakness and pain. It is to be hoped that these authors
learn about myofascial TrPs before a bad situation becomes worse.
DJS]
Faucett, J. A. 1994. Depression in painful
chronic disorders: the role of pain and conflict about pain. J Pain
Symptom Manage 9(8):520-526.
Faucett, J. A. and J. D. Levine. 1991.
The contributions of interpersonal conflict to chronic pain in the presence
of absence of organic pathology. Pain 44(1):35-43.
Faure A, Reynolds SM, Richard JM et al.
2008. Mesolimbic dopamine in desire and dread: enabling motivation to
be generated by localized glutamate in nucleus accumbens. J
Neurosci 28(28):7184-4192. Reactions to dopamine deficiency seem
to be exceedingly site-specific in the part of the brain called the nucleus
accumbens, and the same amount injected in different areas of this part can
generate appetite or fear.
Feder KP, Majnemer A. 2007. Handwriting
development, competency and intervention. Dev Med Child Neurol.
49(4):312-317. “Poor handwriting may be related to intrinsic factors,
which refer to the child’s actual handwriting capabilities, or extrinsic
factors which are related to environmental or biomechanical components, or
both.” “There is evidence to indicate that handwriting difficulties do
not resolve without intervention and affect between 10 and 30% of
school-aged children.” [Students with these problems should be
evaluated for myofascial TrPs. DJS]
Feinberg, B. I. and R. A. Feinberg. 1998. Persistent
pain after total knee arthroplasty: treatment with manual therapy and
trigger point injections. J Musculoskel Pain 6(4):85-95.
Feldman, D. and A. Krishnan. 1995.
Estrogens in unexpected places: possible implications for researchers and
consumers. Environ Health Perspect 103 Suppl 7: 129-33.
Feldman, R. D. and N. D. Schmidt. 1999.
Moderate dietary salt restriction increases vascular and systemic insulin
resistance. Am J Hypertens 12(6):643-7.
Ferencik, M., M. Novak and J. Rovensky. 1998.
[Relation and interactions between the immune and neuroendocrine systems].
Bratisl Lek Listy 99(8-9):454-64 [Slovak].
Ferguson AR, Crown ED, Grau JW. 2006.
Nociceptive plasticity inhibits adaptive learning in the spinal
cord. Neuroscience [May 5 Epub ahead of print]
“Recent data suggest links between the learning deficit and the
sensitization of pain circuits associated with inflammation or
injury (central sensitization).” “Central sensitization
enhances reactivity to mechanical stimulation (allodynia) and
depends on the N-methyl-d-aspartate receptor (NMDAR).”
Fernandez-Carnero J,
Fernandez-de-Las-Penas C, de la Liave-Rincon AI et al. 2007.
Prevalence of and referred pain from myofascial trigger points in
the forearm muscles in patients with lateral epicondylalgia.
Clin J Pain. 23(4):353-360. “Lower PPT (pressure pain
threshold) and larger referred pain patterns suggest that peripheral
and central sensitization exists in LE (lateral epicondamgia).”
Fernandez-de-las-Penas C, Alonso-Blanco C, Del
Amo-Perez A et al. 2007. Trigger points in the masticatory muscles
in subjects presenting with ankylosing spondylitis. J
Musculoskel Pain. 15(3):39-47. “Trigger points in the
masticatory muscles were more conspicuous in AS subjects than in HNCs.
Patients showed a reduced active mouth opening and cervical
flexion-extension motion than matched HNCs. The AS subjects with
lesser mouth opening showed a greater occiput-to-wall distance and a
greater number of TrPs in the masticatory muscles.”
Fernandez-de-las-Penas C,
Cuadrado ML, Arendt-Nielsen L et al. 2007. A pain model for
tension type headache based on muscle trigger points. J
Musculoskel Pain 15 (Supp 13):20 item 30. [Myopain 2007
Poster] “Our studies suggest that TTH (tension-type headache) can
be explained by referred pain from active TrPs in neck-shoulder muscles.
Since chemical mediators most likely are released by active TrPs,
nociceptive inputs from these TrPs may lead to increased afferent
barrage into the trigeminal nucleus caudalis. This updated pain
model proposes that TrPs may be primary hyperalgesic zones, while
referred pain areas in the head could be viewed as secondary
hyperalgesic zones.”
Fernandez-de-las-Penas C,
Cuadrado M, Pareja J. 2007. Referred pain from
extra-ocular muscle trigger points in chronic headache. J
Musculoskel Pain 15 (Supp 13):19 item 27. [Myopain 2007
Poster] “Nociceptive inputs from the extra-ocular
muscles may provoke a continuous afferent bombardment to the
trigeminal nerve nucleus caudalis in CTTH (chronic tension-type
headache). The prolonged nociceptive activation by such muscle
inputs might contribute to central sensitization.” [This
exciting research indicates that even constant pain from facial
muscles around the eye could be enough to contribute to body-wide
central nervous system sensitization. DJS]
Fernandez-de-las-Penas
C, Cuadrado ML, Pareja JA. 2007. Muscle atrophy of
the suboccipital muscles associated with active trigger points
in chronic tension type headache. J Musculoskel Pain
15 (Supp 13):19 item 28. [Myopain 2007 Poster]
“Muscle atrophy in the RCPmin, but not in the RCPmaj, was
associated to active TrPs in the suboccipital muscles in CTTH.
Nociceptive inputs originated in active TrPs might contribute to
a greater muscle atrophy of the involved muscles.” [This
study is interesting in that it suggests that pain from MTPs
could contribute to muscle atrophy. As MTPs can cause
nerve entrapment and blood vessel entrapment, this would be
logical. DJS]
Fernandez-de-las-Penas C, De-la-Llave-Rincon
A, Miangolarra J. 2007. Uncommon referred pain from
scalene muscle trigger points in chronic tension type headache.
J Musculoskel Pain 15 (Supp 13):21 item 31. [Myopain
2007 Poster] “Nine CTTH (chronic tension type headache)
patients had an uncommon referred pain pattern from scalene
muscle TrPs, so these headache patients may need examination for
scalene TrPs. It is known that CTH show sensitization of
central pathways, which may provoke larger referred pain areas
of active muscle TrPs. Further, there are examples of
neurologically related exceptional pain patterns in other
muscles [e.g. the soleus].” [I believe that this is not so
uncommon, and I have seen it several times before, but it may be
more common in patients with CMP and central sensitization. DJS]
Fernandez-de-las-Penas C, Fernandez-Carnero
J, Miangolarra J. 2007. Multifidus muscle trigger point
management and stabilizing exercises in low back pain.
J Musculoskel Pain 15 (Supp 13):21 item 32. [Myopain
2007 Poster] “In some CLBP (chronic low back pain)
patients, it would be necessary to treat lumbar multifidus TrPs
before starting a stability exercise program because it includes
voluntary contraction of this muscle. Nociceptive barrage
originated in active TrPs could act as a contributing factor for
muscle inhibition.” [Multifidi, especially with nerve
entrapment, is exceedingly common in patients with CMP and
central sensitization. Treatment of the nerve pain
is before the TPM will increase the efficacy of the TPM
treatment. DJS]
Fernandez-de-las-Penas C,
Perez-de-Heredia-Torres M, Miangolarra J. 2007. Trigger
point management in lateral epicondylalgia. J
Musculoskel Pain 15 (Supp 13):20 item 29. [Myopain
2007 Poster] “Referred pain from TrPs in these patients
was causing the usual pain reported by patients with lateral
epicondylalgia. Muscle tension provoked by TrP taut band
may play an important role in the genesis and relief of the pain
commonly seen in lateral epicondylalgia.”
Fernandez-de-Las-Penas C, Cuadrado M,
Arendt-Nielsen L et al. 2007. Myofascial trigger points and
sensitization: an updated pain model for tension-type headache.
Cephalalgia [Mar 14 Epub ahead of print] “Based on
available data, an updated pain model for CTTH is proposed in which
headache can at least partly be explained by referred pain from TrPs in
the posterior cervical, head and shoulder muscles. In this updated
pain model, TrPs would be the primary hyperalgesic zones responsible for
the development of central sensitization in CTTH.”
Fernandez-de-las-Penas C, Carratala-Tejada M,
Luna-Oliva L et al. 2006. The immediate effect of hamstring muscle
stretching in subjects’ trigger points in the masseter muscle.
J Musculoskel Pain 14(3):27-35. “The present study
demonstrated an increase in active mouth opening and a decrease in TrP
sensitivity in the masseter muscle in response to the stretch of the
hamstring muscles.” Treatment, and constriction, in the myofascia
of one area can significantly alter the myofascia in another area, even
long distance.
Fernandez-de-Las-Penas C, Alonso-Blanco C, Luz Cuadrado M et al. 2006.
Myofascial trigger points in the suboccipital muscles in episodic
tension-type headache.
Man Ther. 11(3):225-230.
Fernandez-de-Las-Penas C, Alonso-Blanco C, Miangolarra JC. 2006.
Myofascial trigger points in subjects presenting with mechanical neck
pain: a blinded, controlled study. Man Ther. [Jun 10 Epub
ahead of print] “Active TrPs were more frequent in patients
presenting with mechanical neck pain than in healthy subjects.”
Fernandez-de-Las-Penas C, Cuadrado M, Pareja J. 2006. Myofascial
trigger points, neck mobility and forward head posture in unilateral
migraine.
Cephalalgia. 26(9):1061-1070. “Active TrPs located ipsilateral
to migraine headaches might be a contributing factor in the initiation
or perpetuation of migraine.”
Fernandez-de-Las-Penas C, Ge HY, Arendt-Nielsen L et al. 2006.
Referred pain from trapezius muscle trigger points shares similar
characteristics with chronic tension type headache. Eur J Pain.
[Aug 17 Epub ahead of print] Patients with chronic tension type
headache may have spatial summation of perceived pain and mechanical
pain, with referral pain characteristics of myofascial TrPs.
Fernandez de las Penas CF, Carnero JF, Page JCM.
2005. Musculoskeletal disorders in mechanical neck pain: myofascial
trigger points versus cervical joint dysfunction – a clinical study.
J Musculoskeletal Pain 13(1). “There is a possible relationship
between the presence of TrPs in the upper trapezius muscle and the presence
of cervical dysfunctions at C3 and C4 vertebrae in patients suffering from
mechanical neck pain. However, it cannot be established as a
cause-effect relationship. Moreover, there is clinical evidence
showing that joint dysfunctions can induce TrP activity, and that TrP
activity can aggravate corresponding joint dysfunction.”
Fernstrom, J. D. 1994. Dietary amino
acids and brain function. J Am Diet Assoc 94(1):71-77.
Ferranninni, E. A. Q. Galvan, A. Gastaldelli, S.
Camastra, A. M. Sironi, E. Toschi, S. Baldi, S. Frascerra, F. Monzani, A.
Antonelli, M. Nannipieri, A. Mari, G. Seghieri, and A. Natali. 1999.
Insulin: New roles for an ancient hormone. Eur J Clin Invest
29(10):842-52.
Ferrari R., H. Schrader and D. Obelieniene. 1999.
Prevalence of temporomandibular disorders associated with whiplash injury in
Lithuania. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
87(6):653-7.
Fetler L, Amigorena S. 2005.
Neuroscience. Brain under surveillance: the microglia patrol.
Science 309(5733):392-393. Opioids can activate pain
inhibitory and facilitatory systems, but opioid-induced hyperalgesia
may be prevented by strategies such as concomitant administration of
NSAIDS or NMDA antagonists, use of combinations of opioids with
different receptor selectivity, and other methods.
Field T, Diego M, Cullen C et al. 2002.
Fibromyalgia pain and substance P decrease and sleep improves after
massage therapy. J Clin Rheumatol. 8(2):72-76.
Field T, Hernandez-Reif M, Diego M et al. 2007.
Lower back pain and sleep disturbance are reduced following massage
therapy. J Bodywork Move Ther. 11, 141-145. “…the
massage therapy group, as compared to the relaxation group, reported
experiencing less pain, depression, anxiety and sleep disturbance.
They also showed improved trunk and pain flexion performance.”
Field T, Diego M, Cullen C et al. 2002.
Fibromyalgia pain and substance P decrease and sleep improves after
massage therapy. J Clin Rheumatol. 8(2):72-76.
“Both groups showed a decrease in anxiety and depressed mood
immediately after the first and last therapy sessions.
However, across the course of the study, only the massage therapy
group reported an increase in the number of sleep hours and a
decrease in their sleep movements. In addition, substance P
levels decreased, and the patients’ physicians assigned lower
disease and pain ratings and rated fewer tender points in the
massage therapy group.”
Figueroa J. 2007. Multidrug therapy including gamma
hydroxybuterate as used in the treatment of fibromyalgia and associated
anxiety, depression and post traumatic stress disorder. J
Musculoskel Pain 15 (Supp 13):46 item 80. [Myopain 2007
Poster] “GHB, when used in a CMTM, can benefit FM but also
anxiety, depression and PTSD.”
Figueroa J, Kobus B. 2007. Tizanidine and tender point pain. J
Musculoskel Pain 15 (Supp 13):46 item 79. [Myopain 2007
Poster] “Of the 22 patients, 21 observed a decrease in sleep
duration, latency and fragmentation. Fatigue also decreased.
All 22 patients had a significant decrease in TeP pain [i.e. a mean
decrease of 2.09] which was continuous and sustained [mean of 11.9
months].” “These data suggest combination therapy of tizanidine
with analgesic/anti-inflammatory agents benefit sleep and additionally
result in reduced TeP pain.”
Filatova E, Latysheva N, Kurenkov A. 2008.
Evidence of persistent central sensitization in chronic headaches: a
multi-method study. J Headache Pain [Aug 9 Epub ahead
of print]. “CS is persistent and prevalent in patients with
various types of chronic headache. CS levels are unrelated to
the predominant side of pain, disease duration or depression.
Neither is CS related to the headache type, suggesting similar
mechanisms of headache chronification and chronicity maintaining and
possibly explaining clinical similarity of various forms of chronic
headache.”
Filipovic V, Viskic-stalec N. 2006. The
mobility capabilities of persons with adolescent idiopathic
scoliosis. Spine. 31(19):2237-2242. When there is
a lack of normal mobility functions, especially with weak postural
control mechanisms and proprioception, the body compensates and
scoliosis can result.
Fillingim RB, Gear RW. 2004. Sex differences in opioid analgesia:
clinical and experimental findings. Eur J Pain 8(5):413-425.
Filos, K.S. and C.E.Vagianos. 1999. Pre-emptive
analgesia: how important is it in clinical reality? Eur Surg Res
31(2): 122-32.
Finckh A, Berner IC, Aubry-Rozier B et al. 2005.
A randomized controlled trial of dehydroepiandrosterone in postmenopausal
women with fibromyalgia. J Rheumatol 32(7):1336-1340.
This study did not find that taking DHEA brought about any useful changes.
Fine, PG. 1987. Myofascial trigger point pain in children.
J Pediatr.111(4):547-548. This article is noteworthy in
that it misidentified myofascial pain syndrome as part of fibromyalgia.
This is too common a mistake. It does encourage early diagnosis
and treatment, but to do that doctors will have to know which condition
– or both – are involved.
Fink, G., B. Sumner, R. Rosie, H. Wilson and J.
McQueen. 1999. Androgen actions on central serotonin
neurotransmission: relevance for mood, mental state and memory.
Behav Brain Res 105(1):53-68.
Fishbain DA, Cutler RB, Rosomoff HL et al.
2000. Clonazepam open clinical treatment trial for myofascial
syndrome associated chronic pain. Pain Med. 1(4):332-339.
Clonazepam may help some myofascial pain.
Fishbain, D. A., H. L. Rosomoff and R. S. Rosomoff.
1992. Drug abuse, dependence, and addiction in chronic pain patients.
Clin J Pain
8(2):77-85.
Fishbain, D. A., M. Goldberg, R. S. Rosomoff and H.
Rosomoff. 1991. Completed suicide in chronic pain. Clin
J Pain 7(1):29-36.
Fischer, A. A. 1999. Treatment of myofascial pain.
J Musculoskel Pain 7(1-2):131-142.
Fischer, A. A. 1999. Algometry in diagnoses of
musculoskeletal pain and evaluation of treatment outcome: an update. J
Musculoskel Pain 6(1): 5-32.
Fischer, H. P., W. Eich and I. J. Russell.
1998. A possible role for saliva as a diagnostic fluid in patients
with chronic pain. Semin Arthritis Rheum 27(6):348-59.
Fischer, A. A. 1988. Documentation of
myofascial trigger points. Arch Phys Med Rehabil 69(4):286-91.
Fishman SM. 2006. The role of the pain
psychologist, trigger point injections, reflex sympathetic dystrophy.
J Pain Palliat Care Pharmacother. 20(4):93-97. “This feature
presents information for patients in a question and answer format. It
is written to simulate actual questions that many pain patients ask and to
provide answers in a context and language that most pain patients will
comprehend. Issues addressed in this issue are the role of the pain
psychologist, trigger point injections, and reflex sympathetic dystrophy.”
Fishman SM, Mahajan G, Jung SW et al. 2002. The trilateral opioid
contract. Bridging the pain clinic and the primary care physician
through the opioid contract. J Pain Symptom Manage.
24(3):335-344. “We have extended the traditional use of opioid contracts
to involve the primary care physician (PCP). The PCP was asked to
collaborate with the pain specialist’s decision to use opioids by
cosigning an opioid contract. Explicit in the agreement was the
understanding that the primary care physician would assume prescribing
the refills for these medications once the opioid regimen had become
stabilized. In all cases in which a contract was completed, the
patient successfully stabilized on an appropriate opioid regimen and
then discharged to the care of the PCP for long-term opioid treatment.
The opioid contract made an effective tool for networking specialty and
primary care services in…chronic opioid therapy.” [Too often the
physician is neglected as part of the contract, and very often the pain
is vastly undertreated.]
Fitzcharles M.A., Boulos P. 2003.
Inaccuracy in the diagnosis of fibromyalgia syndrome: analysis of referrals.
Rheumatology (Oxford) 42(2):263-7. “At the final evaluation the
accuracy of the diagnosis regarding FM by either the referring physician or
by the rheumatologist at the time of the initial visit was correct in 34% of
patients.” This finding may help explain the current high rates of FM
and caution physicians to consider other diagnostic possibilities when
addressing diffuse musculoskeletal pain.
Fitzcharles, M. A. and J. M. Esdaile. 1997. The
overdiagnosis of fibromyalgia syndrome. Am J Med 103(1):44-50.
Fitzgerald MP, Kotarinos R. 2003.
Rehabilitation of the short pelvic floor. I: Background and patient
evaluation. Int Urogynecol J Pelvic Floor Dysfunct.
14(4):261-268. (See next entry)
Fitzgerald MP, Kotarinos R. 2003.
Rehabilitation of the short pelvic floor. II: Treatment of the patient
with the short pelvic floor. Int Urogynecol J Pelvic Floor
Dysfunct. 14(4):269-275. These articles provide options for
patient care and help for the diagnoses and treatment of many common but
often misdiagnosed pelvic and lower abdominal pain cases. Care
providers are reminded that myofascial TrPs can cause dysfunction such
as muscle weakness as well as pain, and many cases of bladder and bowel
dysfunction, vulvodynia, and similar ailments may be greatly relieved by
TrP treatment.
Flanagan, D. E. , J. C. Vaile, G. W. Petley, V. M.
Moore, I. F. Godsland, R. A. Cockington, J. S. Robinson and D. I. Phillips.
1999. The autonomic control of heart rate and insulin resistance in young
adults. J Clin Endocrinol Metab
84(4):1263-7.
Flanagan, D., P. Wood, R. Sherwin, K. Debrah and D.
Kerr. 1998. Gin and tonic and reactive hypoglycemia: what is
important–the gin, the tonic, or both? J Clin Endocrinol Metab
83(3): 796-800.
Flato, B., A. Aasland, I. H. Vandvik and O. Forre.
1997. Outcome and predictive factors in children with chronic
idiopathic musculoskeletal pain. Clin Exp Rheumatol
15(5):567-577.
Flax, B. J. 1995. Myofascial pain
syndomes–the great mimicker. Bol Assoc Med P R
87(10-12):167-170.
Fleischmann R. 2007. Primer: establishing
a clinical trial unit – regulations and infrastructure. Nat
Clin Pract Rheumatol. 3(4):234-239. [This comprehensive
review would be very helpful for physicians interested in doing a
clinical trial. DJS]
Fleury B. 2000. [Pharyngeal musculature and
obstructive sleep apnea syndromes] Rev Mal Respir. 17 Suppl
3:S15-20. [French] “The caliber of the pharynx at the soft palate
depends on the action of the tensor veli, the palatoglossus, the
palatopharyngeus and the uvula muscles. At the lingual level, the
action of the genioglossus and the geniohyoideus predominate.
These different muscle groups contract in coordination before the
diaphragm contracts. Their activity is diminished and disorganized
during sleep. These muscles appear to have a histological
composition adapted to short duration intense contractions making them
vulnerable to fatigue. In apneic patients, these muscles are
solicited constantly. Muscular lesions related to overwork have
been suggested.” [Muscle tension can affect sleep apnea.
Myofascial TrPs can affect muscle tension. Therefore, myofascial
TrPs can affect sleep apnea. DJS]
Florian H, Young Jr. J, Haig G et al. 2007. Pregabalin is
effective for the long-term treatment of pain associated with
fibromyalgia syndrome: a 1-year, open-label study. J
Musculoskel Pain 15 (Supp 13):47 item 81. [Myopain 2007
Poster] “Pregabalin administered for up to 1 year was associated
with improvements in FM-related pain. Pregabalin was generally
well tolerated.”
Floyd, J. A. 1999. Sleep promotion in adults.
Annu Rev Nurs Res
17:27-56.
Fogel RB, Triner J,
White DP 2005. The effect of sleep onset on upper airway muscle
activity in patients with sleep apnoea versus controls. J Physiol
564(Pt 2):549-562. “Although CPAP eliminated differences in UAR (Upper
Airway Resistance) during wakefulness and sleep, GGEMG genioglossus
(activity) remained greater in the OSA patients.” [TrPs in the pharyngeal
dilator muscles can significantly affect OSA. Their previous work
indicated tensor palatini muscle activity is high in OSA patients as well.
DJS]
Ford, ES, Giles WH,
Dietz WH. 2002. Prevalence of the metabolic syndrome among US adults:
findings from the third National Health and Nutrition Examination Survey.
JAMA Jan16;287(3):356-9. About 47 million US residents have the
metabolic syndrome, according to 2000 census data.
Forrest JB, Schmidt S. 2004. Interstitial
cystitis, chronic nonbacterial prostatitis and chronic pelvic pain syndrome
in men: a common and frequently identical clinical entity. J Urol.
172(6 Pt 2):2561-2562. “Interstitial cystitis in males appears to be
more common than historically reported. Interstitial cystitis in males
and patients with chronic pelvic pain syndrome and chronic nonbacterial
prostatitis share many clinical findings. A higher incidence of
interstitial cystitis had been found in American Indian males of Cherokee
descent and deserves further investigation.”
Forseth KO, Mengshoel AM. 2007.
Multidimensional therapy in warm climate for patients with fibromyalgia
syndrome – a pilot study. J Musculoskel Pain 15 (Supp 13):47
item 82. [Myopain 2007 Poster] “The multiple improvements
indicate that multidimensional treatment in warm climate may have short and
long lasting effect in patients with FM. Further controlled studies
are needed to confirm these findings.” [FM patients are heterogenous.
Some patients do better in warm dry climates and some do better in cold dry
climates. Some patients are both cold and heat sensitive, some are
helped by humidity and others feel worse with humidity. There are so
many environmental variables that can affect a climate reactor that studies
such as this may be very difficult to interpret. DJS]
Forseth, K. O. , O. Forre and J. T. Gran. 1999. A
5.5 year prospective study of self-reported musculoskeletal pain and of
fibromyalgia in a female population: significance and natural history.
Clin Rheumatol 18(2):114-21.
Forseth, K. O. and J. T. Gran. 1992. The
prevalence of fibromyalgia among women aged 20-49 years in Arendal, Norway.
Scand J Rheumatol
21(2):74-78.
Forst R, Ingenhorst A. 2005. [Myofascial pain syndrome]
Internist [Oct 15 Epub ahead of print] [German] “Untreated,
the myofascial pain syndrome leads to a reduced extensibility of the
involved muscle with consecutive decrease of the range of motion and
development of a muscular imbalance resulting in a disturbance of
complex movement and evolution of a chronic pain disease. An early
started and aimed therapy can prevent effectively the chronification.”
Fourie WJ. 2008. Considering wider
myofascial involvement as a possible contributor to upper extremity
dysfunction following treatment for primary breast cancer. J
Bodywork Move Ther. 12(4):349-355. “Breast cancer treatment
results in tissues losing their shearing and gliding ability. Mapped
restrictive tissue gliding clearly shows wider than reported restrictions.
This pattern needs further research and investigation.” Breast cancer
patients may find significant symptom relief from treatment of co-existing
myofascial trigger points.
Fox, A. W. and R. L. Davis. 1998.
Migraine chronobiology. Headache 38(6):436-41.
Fraenkel, L., Y. Zhang, C. E. Chaisson, S. R. Evans,
P. W. Wilson and D. T. Felson. 1998. The association of estrogen
replacement therapy and the Raynaud phenomenon in postmenopausal women.
Ann Intern Med 129(3):208-11.
Fraenkel, L., Y. Zhang, C. E. Chaisson, H. R. Maricq,
S. R. Evans, F. Brand, P. W. Wilson and D. T. Felson. 1999.
Different factors influencing the expression of Raynaud’s phenomenon in men
and women. Arthritis Rheum 42(2):306-10.
Frampton M, Harvey RJ, Kirchner V. 2003.
Propentofylline for dementia. Cochrane Database Syst Rev
(2):CD002853. This study is
included on this website because this medication is being studied as a
spinal glial cell modulator for central sensitization. It crosses the
blood-brain barrier.
Franco C, Bengtsson BA, Johannsson G. 2001.
Visceral obesity and the role of the somatotropic axis in the
development of metabolic complications. Growth Horm IGF Res
11:S97-S102. “Several studies have described a range of metabolic
disturbances associated with abdominal obesity, including glucose
intolerance, hyperinsulinaemia, insulin resistance, hypertension and
dyslipoproteinaemia, now widely known as the metabolic syndrome.
Several abnormalities in the hypothalamic-pituitary axis have been
described associated with visceral obesity, suggesting a central
neuroendocrine dysregulation including increased cortisol concentration
and impaired gonadotropin and growth hormone (GH) secretion.”
Franco C, Bengtsson BA, Johannsson G. 2001.
Visceral obesity and the role of the somatotropic axis in the development of
metabolic complications. Growth Horm IGF 11:S97-S102.
“Several studies have described a range of metabolic disturbances associated
with abdominal obesity, including glucose intolerance, hyperinsulinaemia,
insulin resistance, hypertension and dyslipoproteinaemia, now widely known
as the metabolic syndrome. Several abnormalities in the
hypothalamic-pituitary axis have been described associated with visceral
obesity, suggesting a central neuroendocrine dysregulation including
increased cortisol concentration and impaired gonadotropin and growth
hormone (GH) secretion.”
Francois, P. P., K. T. Preissner, M. Herrmann, R. P.
Haugland, P. Vaudaux, D. P. Lew and K. H. Krause. 1999.
Frank, E. M. 1999. Myofascial trigger point
diagnostic criteria in the dog. J Musculoskel Pain 7(1-2):231-237.
Franklin DW, Burdet E, Tee KP et al. 2008.
CNS learns stable, accurate, and efficient movements using a simple
algorithm. J Neurosci. 28(44):11165-11173. The algorithm
proposed in this article may be very useful in understanding how the
dysfunctional musculoskeletal system with proprioceptive concomitants in
patients with chronic myofascial pain and the dysfunctional brain in FM can
combine to cause exceptional difficulties for movement in patients with both
of these conditions. DJS]
Franssen JLM, Beersma B, Bron C. 2007.
Shoulder pain during swallowing: the use of surface electromyography as a
valuable diagnostic and therapeutic tool in myofascial pain syndrome.
J Musculoskel Pain 15 (Supp 13):22 item 33. [Myopain 2007
Poster] “MPS should be considered as a possible cause of
musculoskeletal complaints in neck or shoulder disorders. Surface
electromyography can be of great benefit in the process of differential
diagnosis and may be illuminate non-physiological motor behavior, which is
one of the perpetuating factors in MPS. The knowledge of referred pain
patterns may be helpful in identifying the muscle to be treated.”
[This is a very interesting study, as the MTPs were initiated due to use of
endotracheal tube during surgery, and the referral pain pattern occurred
during swallowing. Having experienced TPM cascade from endotracheal
intubation myself, I know how difficult this can be and how unaware most
anesthesiologists and other medical team members are that this can occur.
DJS]
Franken P, Chollet D, Tafti M. 2001. The
homeostatic regulation of sleep need is under genetic control.
Jour of Neuroscience 21(8):2610-2621.
Fredheim OM, Kaasa S, Fayers P et al. 2007.
Chronic non-malignant pain patients report as poor health-related
quality of life as palliative cancer patients. Acta
Anaesthesiol Scand. [Nov 13 Epub ahead of print]. “CNMP
patients admitted to multidisciplinary pain centres report significantly
reduced HRQoL, in addition to severe pain. They consider their
HRQoL to be as poor as HRQoL reported from dying cancer patients and
substantially poorer than national norms.” [This leaves one to
wonder about the ethics of having a substantial group of patients, those
with chronic non-cancer pain, with a quality of life lower than terminal
cancer patients. How can any system allow this situation, and what will
it take to improve it? DJS]
Fredheim OM, Borchgrevink PC, Klepstad P et al. 2006. Long
term methadone for chronic pain: a pilot study of pharmacokinetic
aspects. [Nov 16 Epub ahead of print] Eur J Pain
“...a 3-day opioid switch from morphine to methadone followed by a
one week titration seems pharmacologically sound.” These
patients had chronic non-malignant pain. Methadone serum
concentrations did not change significantly from dose titration
through 9 months therapy.
Fredheim OM, Kaasa S, Dale O et al. 2006. Opioid switching
from oral slow release morphine to oral methadone may improve pain control
in chronic non-malignant pain: a nine-month follow-up study.
Palliat Med. 20(1):35-41.
Freedenfeld RN, Murray M, Fuchs PN et al. 2006.
Decreased pain and improved quality of life in fibromyalgia patients treated
with olanzapine, an atypical neuroleptic. Pain Pract.
6(2):112-118. “In general, the data provide strong support that
olanzapine can, in certain patients, improve symptoms associated with
fibromyalgia in patients who have had limited success with other treatment
modalities.” There were significant side-effects that caused
discontinuance of treatment in a number of patients.
Fregni F, Gimenes R, Valle AC et al. 2006. A randomized,
sham-controlled, proof of principle study of transcranial direct current
stimulation for the treatment of pain in fibromyalgia.
Arthritis Rheum. 54(12):3988-3998. “Our findings provide
initial evidence of a beneficial effect of tDCS in fibromyalgia, thus
encouraging further trials.”
Fricton, J. R. 2002. "Masticatory myofascial pain"
an explanatory model of regional muscle pain syndromes. J Musculoskel Pain
10(1/2)131-150. The presence of myofascial trigger points should be explored
in cases of masticatory pain.
Friedman, D. P. 1990. Perspectives on the
medical use of drugs of abuse. J Pain Symptom Manage 5(1
Suppl):S2-S5.
Friedman M, Gurpinar B, Lin HC et al. 2007.
Impact of treatment of gastroesophageal reflux on obstructive sleep
apnea-hypopnea syndrome. Ann Otol Rhinol Laryngol.
116(11):805-811. “Treatment of GERD had a significant impact on the
reduction of the apnea-hypopnea index, snoring, and daytime sleepiness.
Elimination of GERD should be part of a comprehensive treatment plan for
patients with OSAHS.”
Freitas, J. P. , P. Filipe, I. Emerit, P. Meunier,
C. F. Manso and F. Guerra Rodrigo. 1996. Hyaluronic acid in progressive
systemic sclerosis. Dermatology. 192(1):46-9.
Fricton, J. R. 1996. Myofascial pain of
the head and neck: diagnosis and management. J Back & Musculoskeletal
Rehab 6:177-194.
Friedberg F, Sohl SJ, Halperin PJ. 2008.
Teaching medical students about medically unexplained illnesses: a
preliminary study. Med Teach. [May 20 Epub ahead of print].
“A relatively brief exposure to factual information on specific medically
unexplained illnesses was associated with more favorable attitudes toward
CFS in fourth year medical students. Conclusion: This type of instruction
may lead to potentially more receptive professional attitudes toward
providing care to these underserved patients.” You can’t see the pain,
or the fatigue. Medical students are much more receptive to patients
with “invisible illnesses” if they are trained in their reality.
Friederich HC, Schellberg D, Mueller K et al.
2004. [Stress and autonomic dysregulation in patients with
fibromyalgia syndrome.] Schmerz [Epub May 12 ahead of
print] [German] This study indicates that the stress system in FM
patients is hyporeactive.
Frieri M. 2003. Identification of masqueraders of autoimmune disease
in the office.
Allergy Asthma Proc 24(6):421-9. Fibromyalgia is included as one of
the diseases that often masquerades as and may be misdiagnosed as an
autoimmune disease. [This may result in inappropriate medications and
therapies. DJS]
Fries E, Hesse J, Hellhammer J et al. 2005. A new view on
hypocortisolism. Psychoneuroendocrinology [Epub ahead
of print June 8]. “Low cortisol levels have been observed in
patients with different stress-related disorders such as chronic
fatigue syndrome, fibromyalgia, and post-traumatic stress disorder.
We propose that the phenomenon of hypocortisolism may occur after a
prolonged period of hyperactivity of the
hypothalamic-pituitary-adrenal axis due to chronic stress as
illustrated in an animal model. Despite symptoms such as pain,
fatigue and high stress sensitivity, hypocortisolism may also have
beneficial effects on the organism.”
Frokjaer JB, Andersen SD,
Gale J et al. 2005. An experimental study of viscero-visceral
hyperalgesia using an ultrasound-based multimodal sensory testing approach.
Pain [Nov 15 Epub ahead of print]. “Central mechanisms can explain
the remote hyperalgesia to mechanical visceral stimulation and the increase
in referred pain areas.”
Fruchwald-Schultes B, Kern W, Born J, et al.. 2001. Hyperinsulinemia
causes activation of the hypothalamus-pituitary-adrenal axis in humans.
Int J Obes Relat Metab Disord 25 Suppl 1:S38-40. Hyperinsulinemia
acutely increases HPA secretory activity in healthy men.
Fruth SJ. 2006. Differential diagnosis and treatment in a patient
with posterior upper thoracic pain. Phys Ther. 86(2):254-268.
“This case suggests that CV/CT mobilizations and active TrP release may
have been beneficial in reducing pain and restoring function in this
patient.” This case is interesting in that myofascial dysfunction
occurred after a 35-year old man had been on the bleachers at a
hockey game for 3 hours. Two days later he had pain in the right
scapular area and spine that increased during the next 6 weeks. He had
considerable pain, lost some function and range of motion and had
difficulty sleeping due to movement-triggered pain. He was subjected to
weeks of physical therapy including spine mobilization, and given many
expensive radiological tests. After months of this, trigger points were
found in multiple area muscles. After 4 weeks of specific treatment the
patient had full return to function. [How much pain is needless, and how
much time and other resources are wasted, because we do not have care
providers who are adequately trained in the diagnosis and treatment of
myofascial TrPs? DJS]
Frye, J. 1997. Homeopathy in office
practice. Prim Care 24(4):845-865.
Fugh-Berman, A. and J. M. Cott. 1999.
Dietary supplements and natural products as psychotherapeutic agents.
Psychosom Med
61(5):712-28.
Fujioka, M., K. Okuchi, K. I. Hiramatsu, T.
Sakaki, S. Sakaguchi and Y. Ishii. 1997. Specific changes in human brain
after hypoglycemic injury.
Stroke 28(3):584-587.
Fukuda, K., Straus, S. E. , Hickie I.,
Sharpe, M. , Dobbins J, G., Komaroff A., and the ICFSSG. 1994. The
Chronic Fatigue Syndrome: A Comprehensive Approach to Its Definition and
Study. Ann Int Med 121(12)953-959.
Fulle S., Mecocci P., Fano G., Vecchiet I., Vecchini
A., Racciotti D., Cherubini A., Pizzigallo E., Vecchiet, Senin U., Beal M.F.
2000. Specific oxidative alterations in vastus lateralis muscle of
patients with the diagnosis of chronic fatigue syndrome. Free Radic Biol
Med 29(12):1252-9. Patients with chronic fatigue syndrome have
differences in muscle membranes, fluidity and fatty acid composition
compared to patients with fibromyalgia and healthy patients.
Furlan AD, Sandoval JA, Mailis-Gagnon A et al.
2006. Opioids for chronic non-cancer pain: a meta-analysis of
effectiveness and side effects. CMAJ
174(11):1589-1594. “Weak and strong opioids outperformed
placebo for pain and function in all types of CNCP. Other
drugs produced better functional outcomes than opioids, whereas for
pain relief they were outperformed only by strong opioids.
Despite the relative shortness of the trials, more than one-third of
the participants abandoned treatment.” This study
included patients with fibromyalgia. “Among the side effects
for opioids, only constipation and nausea were clinically and
statistically significant.”
Ga
H, Choi JH, Park CH et al. 2007. Acupuncture needling versus lidocaine
injection of trigger points in myofascial pain syndrome in elderly patients
– a randomized trial. Acupunct Med. 25(4):130-136. “There
was no significant difference between acupuncture needling and 0.5%
lidocaine injection of trigger points for treating myofascial pain syndrome
in elderly patients.”
Ga H, Koh HJ, Choi JH et al. 2007.
Intramuscular and nerve root stimulation vs. lidocaine injection to trigger
points in myofascial pain syndrome.
J Rehabil Med. 39(5):374-378. “In managing myofascial pain
syndrome, after one month intramuscular stimulation resulted in more
significant improvements in pain intensity, cervical range of motion and
depression scales than did 0.5% lidocaine injection of trigger points.
Intramuscular stimulation is therefore recommended for myofascial pain
syndrome.”
Gadalla T. 2008. Association of
comorbid mood disorders and chronic illness with disability and quality
of life in Ontario, Canada. Chronic Dis Can. 28(4):148-154.
“Health care providers are urged to proactively screen chronically ill
patients for mood disorders, particularly among the subgroups found to
have elevated risk for these disorders.”
Gagliese,
L. and R. Melzack. 1997. Chronic pain in elderly people.
Pain 70(1):3-14.
Gagnon I, Swaine B, Friedman D et al. 2004.
Children show decreased dynamic balance after mild traumatic brain injury.
Arch Phys Med Rehabil 85(3):444-452.
Even mild traumatic brain injury can cause postural balance
dysfunction in children 10 weeks after the injury.
Galic MA, Persinger MA. 2007. Lagged
association between geomagnetic activity and diminished nocturnal pain
thresholds in mice. Bioelectromagnetics [Jul 26 Epub ahead of
print]. “If the geomagnetic activity was greater 3 days before a given
hotplate trial, subjects tended to exhibit shorter response latencies,
suggesting lower pain thresholds or less analgesia. These results are
supported by related experimental findings and suggest that natural
variations in geomagnetic intensity may influence nociceptive behaviors in
mice.” [This study, although done in mice, may have implications for
electromagnetic sensitivity observed in some FM patients. DJS]
Galinier, M., J. Fourcade, N. Ley, S.
Boveda, S. Solera, M. L. Solera, P. Massabuau, S. Elhabaj, J. M. Fauvel, P.
Valdiguie and J. P. Bounhoure. 1999. [No title available] Arch Mal Coeur
Vaiss 92(8):1105-9. [French]
Gallagher, R. M. 1999. Primary
care and pain medicine. A community solution to the public health
problem of chronic pain. Med Clin North Am 83(3):555-83,v.
Gallagher, R. M. and S. Verma. 1999.
Managing pain and comorbid depression: A public health challenge.
Semin Clin Neuropsychiatry 4(3):203-20.
Galland L. 2006. Patient-centered care:
antecedents, triggers and mediators. Altern Ther Health Med.
12(4):62-70. “Functional medicine
is essentially patient centered, rather than disease centered. A
structure is presented for uniting a patient-centered approach to diagnosis
and treatment with the fruits of modern clinical science (which evolved
primarily to serve the prevailing model of disease-centered care).
The core scientific concepts of disease
pathogenesis are antecedents, triggers, and mediators. Antecedents are
factors, genetic or acquired, that predispose to illness; triggers are
factors that provoke the symptoms and signs of illness; and mediators are
factors, biochemical or
psychosocial, that contribute to pathological changes and
dysfunctional responses.
Understanding the antecedents, triggers, and mediators that underlie illness
or dysfunction in each patient permits therapy to be targeted to the
needs of the individual. The conventional diagnosis assigned to the
patient may be of value in identifying
plausible antecedents, triggers or mediators for each patient, but is not
adequate by itself for the designing of patient-centered care.
Applying the model of person-centered diagnosis to patients facilitates the
recognition of disturbances that are
common in people with chronic illness. Diet, nutrition, and exposure
to environmental toxins play central roles in functional medicine because
they may predispose to illness, provoke symptoms, and modulate the activity
of biochemical mediators through a complex and diverse set
of mechanisms. Explaining those
mechanisms is a key objective of the Textbook of Functional Medicine (from
which this article is excerpted). A patient's beliefs
about health and illness are critically
important for self-care and may influence
both behavioral and physiological
responses to illness. Perceived self-efficacy is an important mediator
of health and healing. Enhancement of patients' self-efficacy
through information, education, and the development of a collaborative
relationship between patient and
healer is a cardinal goal in all clinical
encounters.” [ I strongly
recommend this textbook for any doctor who has patients with chronic
illness. It will help them get to the cause of some of the
metabolic dysfunctions. DJS]
Galski, T., J. B. Williams and H. T. Ehle.
2000. Effects of opioids on driving ability. J Pain Symptom
Manage
19(3):200-8.
Gambi F, DeBerardis D, Sepede G et al. 2005.
Cannabinoid receptors and their relationships with neuropsychiatric
disorders. Int J Immunopathol Pharmacol. 18(1):15-20.
“The endocannabinoids may represent the first members of a new class of
neuromodulators that are not stored in cell vesicles, but rather
synthesized by the cell on demand. The endogenous cannabinoid
system could play a central role in several neuropsychiatric disorders
and is also involved in other conditions such as pain, spasticity and
neuroprotection.”
Gandhi R, Ryals JM, Wright DE. 2004.
Neurotrophin-3 reverses chronic mechanical hyperalgesia induced by
intramuscular acid injection. J Neurosci. 24(42):9405-9413.
“NT-3 (neurotrophine-3) may suppress events that lead to secondary
hyperalgesia triggered by insult to muscle afferents.”
Gangi, S. and O. Johansson. 2000. A theoretical model
based on mast cells and histamine to explain the recent proclaimed
sensitivity to electric and/or magnetic fields in humans. Med Hypos
54(4):663-671. Electromagnetic energy can activate mast cells, a type of
connective tissue cell, causing the release of a number of informational
substances including hyaluronic acid, vasoactive intestinal polypeptide
(VIP, a substance which has been implicated in keeping our HPA-axis in the
"fight or flight" stress mode), histamine (which can add to swelling,
itching, pain, allergic manifestations and hypersensitivity,) and cause
other cells to release somatostatin (which can enhance sensations of
inflammation and light sensitivity).
Gamez-Nava, J. I., L. Gonzalez-Lopez, P.
Davis and M. E. Suarez-Almazor. 1998. Referral and diagnosis of
common rheumatic diseases by primary care physicians. Br J
Rheumatol 37(11):1215-9.
Gamsa, A. 1990. Is emotional
disturbance a precipitator or a consequence of chronic pain? Pain
42(2): 183-195.
Gansky SA, Plesh O. 2007. Widespread pain and
fibromyalgia in a biracial cohort of young women. J Rheumatol.
[Feb 1 Epub ahead of print] These conditions are common, and there may
be racial differences that seem to develop early.
Garbuzenko E, Nagler A, Pickholtz D et al. 2002.
Human mast cells stimulate fibroblast proliferation, collagen synthesis and
lattice contraction: a direct role for mast cells in skin fibrosis.
Clin Exp Allergy. 32(2):237-246. This study indicates that
co-existing allergies and the presence of more numerous mast cells may have
a significant affect on scarring, formation of adhesions and fibrosis.
One of the two main mast cell mediators involved is histamine, one of the
biochemicals produced during MTrP local twitch response. Allergies may
thus be interactive with other conditions in yet one more way.
Garbuzenko E., Nagler A, Pickholtz D et al. 2002.
Human mast cells stimulate fibroblast proliferation, collagen synthesis
and lattice contraction: a direct role for mast cells in skin fibrosis.
“...mast cells have a direct and potentiating role in skin remodeling
and fibrosis.” [Excess histamine in the system, from allergy,
fibromyalgia imbalance, myofascial TrP twitch response, and/or other
reasons may directly affect the formation of adhesion and scar tissue.
DJS]
Garcia, J. and R. D. Altman. 1997 a.
Chronic pain states: invasive procedures. Semin Arthritis Rheum
27(3):156-160.
--- 1997 b. Chronic pain states:
pathophysiology and medical therapy. Semin Arth Rheum
27(1):1-16.
Garcia R. Jr., and J. A. Arrington. 1996.
The relationship between cervical whiplash and temporomandibular joint
injuries: an MRI study. Cranio 14(3):233-9.
Gardner, J. R. and G. Sandhu. 1997.
The stigma and enigma of chronic non-malignant back pain (CNMBP) treated
with long-term opioids (LTO). Contemp Nurse 6(2):61-66.
Garg A. 2006. Adipose tissue dysfunction in
obesity and lipodystrophy. Clin Cornerstone 8 Suppl 4:S7-S13.
“Dysfunction of adipose tissue can result in insulin resistance and its
metabolic complications in patients with excess body fat (obesity) or
markedly reduced body fat (lipodystrophy). Alterations in free fatty
acid and adipocytokine release from adipose tissue may underlie metabolic
complications.” Adipose tissue is more than a mechanical
perpetuating factor.
Garrison RL, Breeding PC. 2003. A metabolic
basis for fibromyalgia and its related disorders: the possible role of
resistance to thyroid hormone. Med Hypotheses 61(2):182-189.
Thyroid resistance may be a key perpetuating factor of FM.
Gatchel RJ, Okifuji A. 2006. Evidence-based
scientific data documenting the treatment and cost effectiveness of
comprehensive pain programs for chronic nonmalignant pain. J Pain
7(11):779-793. “This review clearly revealed that CPPs offer the
most efficacious and cost effective treatment for persons with chronic pain,
relative to a host of widely used conventional medical treatment.” [Chronic
pain programs for patients with FM and CMP must include care providers with
the skills to diagnose and treat these conditions. DJS]
Gatts SK, Woollacott MH. 2006. Neural
mechanisms underlying balance improvement with short term Tai Chi training.
Aging Clin Exp Res. 18(1):7-19. “TC (t’ai chi) enhanced
neuromuscular responses controlling the ankle joint of the perturbed leg.
Fast, accurate neuromuscular activation is crucial for efficacious response
to slips or trips.”
Gavish A., Winocur E., Ventura Y.S. et al. 2002.
Effects of stabilization splint therapy on pain during chewing in patients
suffering from myofascial pain. Patients with masticatory myofascial
pain who used flat occlusal splints experienced less intense pain than the
control patients. [Part of the reduction in pain may be due to TrPs becoming
latent because of using the splint. DJS]
Ge HY, Fernandez-de-Las-Penas C, Madeleine
P et al. 2008. Topographical mapping and mechanical pain sensitivity of
myofascial trigger points in the infraspinatus muscle. Eur J
Pain. 12(7):859-865. Patients who have shoulder pain on one
side actually have mechanical hypersensitivity on both sides.
Also, this study indicates that peripheral sensitization plays a
significant role in chronic pain conditions. The study also showed
that the locations of TrPs correspond to the locations of pressure pain
thresholds.
Ge HY, Zhang Y, Boudreau S et al. 2008.
Induction of muscle cramps by nociceptive stimulation of latent
myofascial trigger points. Exp Brain Res. 187(4):623-629.
“These results suggest that latent MTrPs (myofascial trigger points)
could be involved in the genesis of muscle cramps.”
Ge HY,
Fernandez-de-Las-Penas C, Madeleine P et al. 2008. Topographical
mapping and mechanical pain sensitivity of myofascial trigger points in the
infraspinatus muscle. Eur J Pain. [Jan 17 Epub ahead of print].
“There exists bilateral mechanical hyperalgesia in patients with unilateral
shoulder pain. Further, the association of multiple active MTPs with
unilateral shoulder pain and the heterogeneity of mechanical pain
sensitivity distribution suggest a crucial role of peripheral sensitization
in chronic myofascial pain conditions.”
Ge HY, Serrao M, Anderson OK et al. 2007.
Increased H-reflex response induced by intramuscular electrical stimulation
at trigger points. J Musculoskel Pain 15 (Supp 13):22 item 34.
[Myopain 2007 Poster] “The data suggest that there exists increased
sensitivity of muscle spindle afferents at TrPs.” This study indicates
heightened H-reflex response at MTPs and gives additional data documenting
the nature of the increased motor endplate sensitivity.
Ge HY, Fernandez-de-Las-Penas C, Arendt-Nielsen
L. 2006. Sympathetic facilitation of hyperalgesia evoked from
myofascial tender and trigger points in patients with unilateral
shoulder pain. Clin Neurophysiol. [May 29 Epub
ahead of print] Myofascial pain can cause sympathetic system
facilitation, and this sensitization factor must be considered when
determining evaluation and treatment.
Gear, R. W., C. Miaskowski, N. C. Gordon,
S. M. Paul, P. H. Heller and J. D. Levine. 1999. The kappa opioid
nalbuphine produces gender- and dose-dependent analgesia and antianalgesia
in patients with postoperative pain. Pain
83(2):339-45.
Gear, R. W., C. Miaskowski, P. H. Heller,
S. M. Paul, N. C. Gordon and J. D. Levine. 1997. Benzodiazepine
mediated antagonism of opioid analgesia. Pain 71(1):25-29.
Gear, R. W., C. Miaskowski, N. C.
Gordon, S. M. Paul, P. H. Heller and J. D. Levine 1996.
Kappa-opioids produce significantly greater analgesia in women than in men.
Nat Med 2(11):1248-1250.
Gedalia A, Garcia CO, Molina JF et al. 2000. Fibromyalgia
syndrome: experience in a pediatric rheumatology clinic. Clin
Exp Rheumatol 18(3):415-419.
Gedalia, A., J. Press, M. Klein and D.
Buskila. 1993. Joint hypermobility and fibromyalgia in schoolchildren.
Ann Rheum Dis 52 (7):494-496.
Geddes, B. J. and A. J. Summerlee. 1995.
The emerging concept of relaxin as a centrally acting peptide hormone with
hemodynamic actions. J Neuroendocrinol 7(6):411-417.
Geenen R, Jacobs JW. 2001. Fibromyalgia:
diagnosis, pathogenesis and treatment. Curr Opin Anaesthesiol.
14(5):533-539. “Fibromyalgia is a multifaceted problem.” “…the
objective in future evaluations should be to try to find the combined
pharmacological or non-pharmacological treatment of choice for specific
subgroups of patients.”
Geisser ME, Strader Donnell C, Petzke F et al. 2008.
Comorbid somatic symptoms and functional status in patients with
fibromyalgia and chronic fatigue syndrome: sensory amplification as a common
mechanism. Psychosomatics 49(3):235-242. “Sensory
amplification may be an underlying pathophysiologic mechanism in these
disorders that is relatively independent of depression and depressive
symptoms.”
Geisser ME, Glass JM, Rajcevska LD et al. 2008.
A psychophysical study of auditory and pressure sensitivity in patients with
fibromyalgia and healthy controls. J Pain.
9(5):417-422.
“Muscle tenderness is the hallmark of FM, but the findings of this study and
others suggest that persons with FM display sensitivity to a number of
sensory stimuli. These findings suggest that FM is associated with a
global central nervous system augmentation of sensory information.
These findings may also help to explain why persons with FM display a number
of comorbid physical symptoms other than pain.” [As suspected and
noted in my books and on the website handouts, the sensory amplification of
FM does not stop with pain. This means that the autonomic and
proprioceptive symptoms of co-existing MTPS, such as dizziness, for example,
may be greatly amplified. Care providers and patients must be made
aware of this to avoid expensive and possibly unnecessary testing and
procedures. DJS]
Gelfand , M. M . 2000. Sexuality
among older women. J Womens Health Gend Based Med Suppl
1:S15-20.
Gemmell C, Leathem JM. 2006. A study
investigating the effects of Tai Chi Chuan: individuals with traumatic brain
injury compared to controls. “Tai Chi provides short-term benefits
after TBI, with rigorous outcome measurement needed to examine long-term
benefits.”
Genazzani, A. R., A. Spinetti, R. Gallo and
F. Bernardi. 1999. Menopause and the central nervous system:
intervention options. Maturitas 31(2):103-10.
Gendreau M, Hufford MR, Stone AA. 2003.
Measuring clinical pain in chronic widespread pain: selected methodological
issues. Best Pract Res Clin Rheumatol 17(4):575-592.
“Patients pain reports can be systematically biased by a number of
methodological factors.”
Genter, P. M. and E. Ipp. 1994.
Accuracy of plasma glucose measurements in the hypoglycemic range.
Diabetes Care
17(6):595-598. Any interpretation or comparison of critical clinical
and research measurements of glucose in different settings take into account
methodological differences, particularly in the hypoglycemic range.
Gentili, A. and J. D. Edinger. 1999.
Sleep disorders in older people. Aging (Milano) 11(3):137-41.
Gerdle
B, Ostlund N, Gronlund C et al. 2008. Firing rate and conduction
velocity of single motor units in the trapezius muscle in fibromyalgia
patients and healthy controls. J Electromyogr Kinesiol.
18(5):707-716. “CV (conduction velocity) was significantly higher in
FM than in healthy controls; this might be due to alterations in
histopathology and microcirculation.” [These might also be due to
co-existing myofascial TrPs, as this has already been shown in other
studies. DJS]
Germanowicz D, Lumertz MS, Martinez D et al. 2006.
Sleep disordered breathing concomitant with fibromyalgia syndrome.
J Bras Pneumol. 32(4):333-338. “…the more than ten-fold higher
proportion of fibromyalgia cases seen in this sample supports the hypothesis
that there is an association between sleep disordered breathing and
fibromyalgia syndrome.
Gerson LB, Fass R. 2008. A systematic
review of the definitions, prevalence, and response to treatment of
nocturnal gastroesophageal reflux disease. Clin Gastroenterol
Hepatol. [Dec 3 Epub ahead of print]. “Nocturnal GERD is
common and is associated with adverse sleep parameters. It can be
effectively managed with medical and surgical therapy.” [I disagree.
There is a subset of patients with GERD, especially those with FM and CMP,
who may not be adequately managed by medical and surgical therapy. I am one
of those patients. DJS]
Gerster, J. C. and A. Hadj-Djilani. 1984.
Hearing and vestibular abnormalities in primary fibromyalgia syndrome. J
Rheumatol
11(5):678-680.
Gervais Tougas G. 1999. The autonomic
nervous system in functional bowel disorders. Can J Gastroenterol 13
Suppl A:15A-7A. [ED, THIS NOTATION IS CORRECT]
Gerwin R.
2008. The taut band and other mysteries of the trigger point: An
examination of the mechanisms relevant to the development and maintenance of
the trigger point. J Musculoskel Pain 16(1-2):115-121.
Dr. Gerwin’s hypothesis may fill in the missing elements in the formation of
myofascial trigger points (MTPs). We did not have an explanation for
the excess release of acetylcholine, the excess release of calcium, and the
excessive motor endplate noise, nor did we understand why the taut band
forms. These phenomenon could be explained by a dysfunctional
ryanodine receptor calcium channel. This dysfunctional ion channel
could promote the excessive calcium release from the sarcoplasmic reticulum,
resulting in persistent muscle fiber contraction. Gates in the cell
wall, like tiny airlocks in a space station, allow charged particles such as
calcium, potassium and other minerals to flow in and out of the cell
membrane and affect the interior metabolism of the cell. The pathways
are called ion channels. An illness caused by dysfunction of the gate
mechanism is called a channellopathy. This important piece of
the puzzle indicates that myofascial pain due to trigger points could be a
channellopathy. Dysfunctional mitochondria and/or second messenger
dysfunction metabolically upstream could also be responsible or be
associated with the ryanodine dysfunction. [I found this to be one of the
most exciting revelations at the Myopain ‘07 Congress, offering great hope
to those of us with myofascial pain. This offers a whole new way of
looking at myofascial pain, and perhaps a whole new way of treating it.
I hope researchers will take note and mobilize forces to investigate this.
DJS]
Gerwin R. 2004. Differential diagnosis of
trigger points. J Musculoskeletal Pain 12(3/4):23-28.
“Trigger points pain can have many different causes that must be identified
and treated specifically.”
Gerwin RD. 2005.
A review of myofascial pain and fibromyalgia—factors that
promote their persistence. Acupunct Med.
23(3):121-134. Fibromyalgia and myofascial pain are common
and different conditions, although they may occur in the same
patient. “Fibromyalgia is a chronic, widespread muscle
tenderness syndrome, associated with central sensitization.
It is often accompanied by chronic sleep disturbance and
fatigue, visceral pain syndromes like irritable bowel syndrome
and interstitial cystitis. Myofascial pain syndrome is an
overuse or muscle stress syndrome characterized by the presence
of trigger points in muscle.” It is important to uncover
the cause of chronic muscle pain so that treatment will be
effective. “Chronic myalgia may not improve until
underlying precipitating or perpetuating factor(s) are
themselves managed.” These causes may include structural
and metabolic conditions. If the underlying
conditions are brought under control, the
chronic myalgia may resolve.
Gerwin RD,
Dommerholt J, Shah JP. 2004. An Expansion of Simons’
integrated hypothesis of trigger point formation. Curr Pain
Headache Rep 8:468-475. This paper further expounds on the
mechanism of TrP formation explained in Simons Travell and Simons
1999 in the light of new research. Individual irritating
substances released at the motor endplate have been sampled during
the TrP twitch response and subjected to microanalysis. This
research further substantiates the release of muscle damaging
biochemicals and a significant drop in pH at the TrP site. The pH
drop alone is sufficient to cause a change in the nociceptive
milieu, and the addition of proinflammatory mediators such as
substance P, bradykinin and cytokines may additionally aggravate
this change. The continual pain barrage can affect central
nervous system plasticity, resulting in hyperalgesia and allodynia
as well as referred pain.
Gerwin RD. 1993. The management of myofascial pain syndromes.
Jour Musculoskel Pain 1(3/4):83-94. “MPS is a condition
which is treatable by eliminating the specific trigger points that are
the immediate cause of pain, and correcting those factors that
predispose to recurrence.”
Gerwin RD. 1994. Neurobiology of the myofascial trigger point.
Bailliere’s Clin Rheumatology 8(4):747-762. “Myofascial pain
is pain of muscle origin, although the central feature, a painful
trigger point, can also be found in skin, tendon, periosteum and
ligament. The properties of MPS that define it clinically and
differentiate it from other painful muscle conditions are: (a) the
exquisitely tender trigger point in a taut band of muscle; (b) the
restriction of range of motion related to the taut band; (c) a local
twitch of the taut band within muscle when physically stimulated; (d)
the appearance of zones of referred pain; and (e) the development of
satellite trigger points within the zones of referred pain.”
Gerwin RD. 2001. Classification, epidemiology and natural history
of myofascial pain syndrome. Curr Pain Headache Rep
5(5):412-420. Myofascial pain can be primary or secondary to
another condition. When it becomes chronic myofascial pain, it can
become generalized, but according to this respected author [he is a
master of treating myofascial pain – DJS], does not turn into
fibromyalgia. It is treatable, but the perpetuating factors must
be treated. This includes mechanical factors such as structural
asymmetry and posture as well as metabolic, toxic or infectious
perpetuators.
Gerwin, R. D. 1999. Differential
diagnosis of myofascial pain syndrome and fibromyalgia. J Musculoskel
Pain 7(1-2):209-215.
Gerwin, R. D. 1999. Myofascial
pain syndromes from trigger points. Pain 3:153-159.
Gerwin, R. D. 1998. Myofascial
pain and fibromyalgia: Diagnosis and treatment. J Back &
Musculoskeletal Rehab 11:175-181.
Gerwin, R. D. and D. Duranleau. 1997.
Ultrasound identification of the myofascial trigger point. Muscle Nerve
20:767-768.
Gerwin, R. D. 1997. Myofascial
pain syndromes in the upper extremity. J Hand Ther 10: 130-136.
Gerwin, R. D., S. Shannon, C. Z. Hong, D.
Hubbard and R. Gevirtz. 1997. Interrater reliability in
myofascial trigger point examination. Pain 69(1-2):65-73.
Gerwin, R. D. 1995. A study of
96 subjects examined both for fibromyalgia and myofascial pain. J
Musculoskel Pain 3(Suppl 1):121.(Abstract).
Gerwin, R. D. 1991. Myofascial
aspects of low back pain. Neurosurgery Clin North Am2(4):761-782.
Geudj E, Cammilleri S, Niboyet J et al.
2008. Clinical correlate of brain SPECT perfusion abnormalities in
fibromyalgia. J Mucl Med. [Oct 16 Epub ahead of print].
“These results show that brain perfusion abnormalities in patients with
fibromyalgia are correlated with the clinical severity of the disease.”
Ghione S, Del Seppia C, Mezzasalma L et al.
2004. Human head exposure to a 37 Hz electromagnetic field: Effects on
blood pressure, somatosensory perception, and related parameters.
Bioelectromagnetics
25(3):167-175. Specific
electromagnetic field exposure can alter pain sensitivity in human beings.
Giamberardino MA, Vecchiet J, Affaitati G et al.
2007. Antioxidative treatment for muscle symptoms in chronic fatigue
syndrome. J Musculoskel Pain 15 (Supp 13):64 item 113.
[Myopain 2007 Poster] “In CFS, prolonged treatment with Vitamin E
produces parallel improvement of oxidative stress and muscle
fatigue/hyperalgesia. The results suggest an important
pathophysiologic role for OS in the genesis of muscle symptoms in CFS.”
Giamberardino, M. A., G. Affaitati, S.
Iezzi and L. Vecchiet. 1999. Referred muscle pain and hyperalgesia from
viscera. J Musculoskel Pain 7(1-2):61-69.
Giamberardino, M. A., K. J. Berkley, S.
Iezzi, P. de Bigontina, and L. Vecchiet. 1997. Pain threshold
variations in somatic wall tissues as a function of menstrual cycle,
segmental site and tissue depth in non-dysmenorrhic women, dysmenorrhic
women and men. Pain 71(2):187-97.
Giesecke T, Gracely RH, Williams DA et al.
2005. The relationship between depression, clinical pain,
and experimental pain in a chronic pain cohort.
Arthritis Rheum. 52(5):1577-1584. This study suggests
a parallel but different sensory matrix for pain and for
depression. In a patient with both pain and depression,
treating the depression alone is not adequate. The pain
must also be treated.
Giesecke T, Williams DA, Harris RE et al.
2003. Subgrouping of fibromyalgia patients on the basis of pressure-pain
thresholds and psychological factors. Arthritis Rheum 48
(10):2916-2922. The authors separate FM subsets based on several
factors.
Gil, I. A., C. M. Barbosa, V. M. Pedro, K.
C. Silverio, D. P. Goldfarb, V. Fusco and C. M. Navarro. 1998.
Multidisciplinary approach to chronic pain from myofascial pain dysfunction
syndrome: a four-year experience at a Brazilian center. Cranio
16(1):17-25.
Gill K. A., Woodroofe, M. N. 2002.
Effect of extracellular matrix components on the presentation of chemokines
and migration of microglia and astrocytes cell lines. Glia
(Suppl 1):S43 [Abstract]. These researchers “conclude that the effect of
chemokines is significantly influenced by the extracellular environment, and
the composition of the ECM may be important in the design of therapeutic
strategies for inflammatory conditions.”
Gilula MF. 2007. Cranial electrotherapy
stimulation and fibromyalgia. Expert Rev Med Devices.
4(4):489-495. “Future medicine for FM and related conditions may
increasingly involve multimodality treatment that features CES as one
significant part of the therapeutic regimen. Future medicine may also
include CES as an invaluable, cost-effective add-on to many facets of
clinical pharmacology and medical therapeutics.”
Giordano J, Schatman ME, Benedikter R.
2008. Pain care for a global community – Part 2. Pract
Pain Manag. 8(7):65-69. Although this article is about
the global undertreatment of chronic pain, the authors acknowledge a sad
fact: “...the inadequacy of chronic pain treatment in the United
States has been well documented, particularly with regard to the
inappropriate exercise (i.e., under-use and/or incorrect/excessive use)
of various diagnostic and therapeutic technologies, and a failure to
provide integrative treatment approaches that address psycho-social, as
well as biological, aspects of pain.” [ I spend a lot of my time
trying to help people who cannot find doctors who can diagnose and treat
fibromyalgia and chronic myofascial pain all over the world, but mostly
in the USA. Most hospital physical therapy departments
don’t understand myofascial trigger points. This is a good
article. I hope that some day we will see adequate and
comprehensive pain care in the USA as well as throughout the world.
DJS]
Giovengo, S. L. , I. J. Russell and A. A.
Larson. 1999. Increased concentrations of nerve growth factor (NGF) in
cerebrospinal fluid of patients with fibromyalgia. J Rheumatol
26(7):1564-9.
Giske L, Vollestad NK, Mengshoel AM et al. 2007.
Attenuated adrenergic responses to exercise in women with fibromyalgia – a
controlled study. Eur J Pain. [Sep 7 Epub ahead of print]
“...the exercise was perceived as being more painful and strenuous in the FM
group. Muscle performance was altered with increased muscle activity
during the exercise. Women with FM showed an attenuated Adr (plasma
adrenalin) response to repetitive isometric exercise.”
Glass JM. 2008. Fibromyalgia and
cognition. J Clin Psychiatry. 69 Suppl 2:20-24. “Patients
with fibromyalgia frequently complain of cognitive problems or ‘fibrofog’.
The existence of these symptoms has been confirmed by studies of the
incident of cognitive problems in fibromyalgia patients and by the results
of objective tests of metamemory, working memory, semantic memory, everyday
attention, task switching, and selective attention. The results of
these tests show that fibromyalgia patients have impairments in working,
episodic, and semantic memory that mimic about 20 years of aging.
These patients have particular difficulty with memory when tasks are complex
and their attention is divided. Cognitive symptoms in these patients
may be exacerbated by the presence of depression, anxiety, sleep problems,
endocrine disturbances, and pain, but the relationship of these factors to
cognitive problems in fibromyalgia patients is unclear. Standardized
tests and treatment have not yet been established for cognitive problems in
fibromyalgia patients.”
Glass JM. 2006. Cognitive dysfunction in
fibromyalgia and chronic fatigue syndrome: new trends and future directions.
Curr Rheumatol Rep. 8(6):425-429. “Fibromyalgia (FM) and
chronic fatigue syndrome (CFS) patients often have memory and cognitive
complaints. Objective cognitive testing demonstrates long-term and
working memory impairments. In addition, CFS patients have slow
information processing, and FM patients have impaired control of attention,
perhaps due to chronic pain. Neuroimaging studies demonstrate cerebral
abnormalities and a pattern of increased neural recruitment during cognitive
tasks. Future work should focus on the specific neurocognitive systems
involved in cognitive dysfunction in each syndrome.”
Glass JM,
Park DC, Minear M et al. 2005. Memory beliefs
and function in fibromyalgia patients. J Psychosom Res.
58(3):263-269. “Among the patients, perceived capacity,
achievement motivation, and self-efficacy were significantly
correlated with objective memory performance on a recall task.”
Glass JM, Lyden AK, Petzke F et al. 2004.
The effect of brief exercise cessation on pain, fatigue, and mood
symptom development in healthy, fit individuals. J
Psychosom Res. 57(4):391-398. “A subset of subjects
developed symptoms of pain, fatigue, and mood changes after exercise
deprivation. This cohort was different from the individuals
who did not develop symptoms in baseline measures of HPA axis,
immune, and autonomic function. We speculate that a subset of
healthy individuals who have hypoactive function of the biological
stress response systems unknowingly exercise regularly to augment
the function of these systems and suppress symptoms. These
individuals may be at risk for developing chronic multisymptom
illnesses when a ‘stressor’ leads to lifestyle changes that disrupt
regular exercise.”
Glass JM, Lyden AK, Petzke F et al. 2004. The effect of brief
exercise cessation on pain, fatigue, and mood symptom development in
healthy, fit individuals. J Psychosom Res 57(4):391-398.
“A subset of subjects developed symptoms of pain, fatigue, mood changes
after exercise deprivation. This cohort was different from the
individuals who did not develop symptoms in baseline measures of HPA
axis, immune, and autonomic function. We speculate that a subset
of healthy individuals who have hypoactive function of the biological
stress response systems unknowingly exercise regularly to augment the
function of these systems and suppress symptoms. These individuals
may be at risk for developing chronic multisymptom illnesses when a
'stress' leads to lifestyle changes that disrupt regular exercise.”
Gloth, F. M. 3rd. 1996.
Concerns with chronic analgesic therapy in elderly patients. Am J
Med101(1A):19S-24S.
Gluszek, J., L. Szczesniak, F. Banaszak, A.
Tykarski and T. Rychlewski. 1999. [No title available]. Pol
Arch Med Wewn 101(3):191-6 [Polish].
Gockel U, Tolle T. 2007. Fibromyalgic vs. neuropathic pain.
J Musculoskel Pain 15 (Supp 13):48 item 83. [Myopain 2007
Poster] “The pain experienced subjectively by FM patients is
conspicuously greater than that experienced by other patients with
typical neuropathic complaints. Furthermore, this pain is
associated with more severe co-morbidities such as depression/anxiety
and sleep disturbance.”
Godfrey, R. G. 1996. A guide to
the understanding and use of tricyclic antidepressants in the overall
management of fibromyalgia and other chronic pain syndromes. Arch Intern
Med156(10):1047-1052.
Goebal A, Buhner S, Schedel R et al. 2008.
Altered intestinal permeability in patients with primary fibromyalgia and in
patients with complex regional pain syndrome. Rheumatology [Jun
7 Epub ahead of print] Intestinal permeability is significantly
increased in both FM and CRPS patients. [It would be interesting to
check what factors these patients had in common, such as medications. DJS]
Goebel A, Buhner S, Schedel R et al. 2008.
Altered intestinal permeability in patients with primary fibromyalgia
and in patients with complex regional pain syndrome.
Rheumatology (Oxford). 47(8):1223-1227. FM patients in this study
showed significant increased intestinal permeability. [I have
observed that permeable gut is a common interactive diagnoses associated
with FM. It is to be hoped that further research will be done
concerning the possibility of intestinal permeability as an initiating
factor of central sensitization, and even more hope that there will be
more focus on healing permeable gut as an integral part of FM treatment.
DJS]
Gogas KR. 2005. Glutamate-based therapeutic
approaches: NR2B receptor antagonists. Curr Opin Pharmacol Dec
20; [Epub ahead of print] “...phosphorylation of the NR2B subunit
(-containing NMDA receptor) could be responsible for the initiation and
maintenance of the central sensitization seen in neuropathic pain states.”
Gold AR, Dipalo F, Gold MS et al. 2004.
Inspiratory airflow dynamics during sleep in women with fibromyalgia.
Sleep 27(3):459-466. “Inspiratory airflow limitation is a
common inspiratory airflow pattern during sleep in women with fibromyalgia.
Our findings are compatible with the hypothesis that inspiratory flow
limitation during sleep plays a role in the development of the functional
somatic syndromes.”
Gold, D. R., S. Rogacz, N. Bock, T. D.
Tosteson, T. M. Baum, F. E. Speizer and C. A. Czeisler. 1992. Rotating
shift work, sleep, and accidents related to sleepiness in hospital nurses.
Am JPublic Health 82(7):1011-4.
Goldenberg DL,
Burckhardt C, Crofford L. 2004. Management of fibromyalgia syndrome.
JAMA 292(19):2388-2395. “A number of commonly used FM therapies,
such as trigger point injections, have not been adequately evaluated.”
[This is a noteworthy quote, in so much as there are no such things as
fibromyalgia trigger points and thus no FM trigger point injections to be
evaluated. Myofascial trigger point injections, however, have been
adequately evaluated. It is fundamental that clinicians and
researchers need to understand that there are no fibromyalgia trigger
points, and that myofascial pain is not the same as fibromyalgia.
Until this happens, the research will be skewed and the conclusions reached
not viable. DJS]
Goldenberg DL,
Burchkardt C, Crofford L. 2004. JAMA 292(19):2388-2395.
“Despite the chronicity and complexity of FM, there are pharmacological and
nonpharmacological interventions available that have clinical benefit.”
[FM is treatable,]
Goldenberg, DL. 1999. Fibromyalgia
syndrome a decade later: what have we learned? Arch Intern Med
159(8):777-85.
Goldberg, G. M., R. D. Kerns and R.
Rosenberg. 1993. Pain-relevant support as a buffer from depression among
chronic pain patients low in instrumental activity. Clin J Pain
9(1):34-40.
Goldberg, R. T., W. N. Pachas and D. Keith.
1999. Relationship between traumatic events in childhood and chronic
pain. Disabil Rehabil 21(1):23-30.
Goldberg, R. L. , J. P. Huff, M. E. Lenz,
P. Glickman, R. Katz and E. J. Thonar. 1991. Elevated plasma levels of
hyaluronate in patients with osteoarthritis and rheumatoid arthritis.
Arthritis Rheum 34(7):799-807.
Goldstein, L. B., F. C. Last and V. M.
Salerno. 1997. Prevalence of hyperactive digastric muscles
during swallowing as measured by electromyography in patients with
myofascial pain dysfunction syndrome. Funct Orthod 14(3):18-22.
Golinski, M. A. and D. M. Fill. 1995.
Preemptive analgesia. CNRA 6(1):16-20.
Gonzalez-Viejo MA, Avellanet M,
Hernandez-Morcuende MI. 2005. [A comparative study of
fibromyalgia treatment: ultrasonography and physiotherapy versus
sertraline treatment.] Ann Readapt Med Phys.
[Epub ahead of print June 22] [French] “Patients treated with
sertraline had a better outcome in terms of pain, morning stiffness
and sleep disorders, than the group treated with ultrasonography and
physical therapy.”
Goodchild CS, Kolosov A, Tucker AP et al.
2008. Combination therapy with flupirtine and opioids: studies in rat
pain models. Pain Med. 9(7):928-938. “Flupirtine
increases morphine antinociception without causing an increase in sedation.
Flupirtine should be investigated as an adjunct analgesic with opioids for
the management of patients with pain states involving central
sensitization.” [Other available opioid “boosters” such as
dextromethorphan and pherngan need to be looked at closely as well. DJS]
Goon JA, Aini AH, Musalmah M et al. 2009.
Effect of tai chi exercise on DNA damage, antioxidant enzymes, and oxidative
stress in middle-age adults. J Phys Act Health. 6(1):43-54.
“Regular tai chi exercise stimulated endogenous antioxidant enzymes and
reduced oxidative damage markers.”
Gordon, D. A. 1999. Chronic
widespread pain as a medico-legal issue. Baillieres Best Pract Res
Clin Rheumatol
13(3):531-43.
Gordon, N. P., P. D. Cleary, C. E. Parker
and C. A. Czeisler. 1986. The prevalence and health impact of
shiftwork. Am J Public Health 76(10):1225-8.
Gotlin, R. S., S. Hershkowitz, P. M. Juris,
E. G. Gonzalez, W. N. Scott and J. N. Insall. 1994. Electrical
stimulation effect on extensor lag and length of hospital stay after total
knee arthroplasty. Arch Phys Med Rehabil
75(9):957-959.
Gottrup H, Juhl G, Kristensen AD et al.
2004. Chronic oral gabapentin reduces elements of central
sensitization in human functional hyperalgesia. Anesthesiology
101(6):1400-1408.
Goucke CR. 2001. Australian management
strategies for oral opioid use in non-malignant pain. Eur J Pain 5
Suppl A:99-101.
Govender C, Cassimjee N, Schoeman J et al. 2007.
Psychological characteristics of FM patients. J Musculoskel Pain
15 (Supp 13):55 item 98. [Myopain 2007 Poster] “The majority of
subjects exhibited secure attachment and the results questions the existence
of a single FM-prone psychological profile.”
Gowans SE, Dehueck A. 2007. Pool exercise for
individuals with fibromyalgia. Curr Opin Rheumatol.
19(2):168-173. “Pool exercise can be an effective intervention for
individuals with fibromyalgia.” [One must be careful of the
temperature of the pool and the type of exercise, especially if patients
have co-existing myofascial TrPs. DJS]
Gowans SE, DeHueck A. 2004.
Effectiveness of exercise in management of fibromyalgia. Curr Opin
Rheumatol 16(2):138-42. “Individuals with fibromyalgia also need
to be able to access community exercise programs that are appropriate for
them. This may require community instructors to receive instruction on
exercise prescription and progression for individuals with fibromyalgia.”
[ It is also vitally important that these individuals receive instruction on
the dangers of repetitive exercise for individuals with co-existing CMP.
DJS]
Gowing LR, Ali RL, Christie P et al. 1998.
Therapeutic use of cannabis: clarifying the debate. Drug
Alcohol Rev. 17(4):445-452. “The debate regarding therapeutic
use of cannabis is being confused by a lack of distinction between
therapeutic and social use of cannabis.” “At present the evidence
is limited, it mostly relates to the use of synthetic cannabinoids, and
much of it fails to compare cannabis with the best therapies available
for the conditions of interest.” “There is sufficient evidence of
potential therapeutic benefit to justify the facilitation of further
research.”
Gowri V, Krolikowski A. 2001. Chronic pelvic
pain. Laparoscopic and cystoscopic findings. Saudi Med J.
22(9):769-770. [Another study that failed to include myofascial
TrPs in the differential diagnosis. DJS]
Gracely RH, Geisser ME, Giesecke T et al. 2004.
Pain catastrophizing and neural responses to pain among persons with
fibromyalgia. Brain 127(Pt 4):835-843. [Epub ahead of print Feb
11] “Catastrophizing influences pain perception through altering
attention and anticipation, and heightening emotional responses to pain.
Activation associated with catastrophizing in motor areas of the brain may
reflect expressive responses to pain that are associated with greater pain
catastrophizing.”
Gracely R.H., Petzke F., Wolf J.M. et al.
2002. Functional magnetic resonance imaging evidence of augmented pain
processing in fibromyalgia. Arthritis Rheum
46(5):1333-43.
Gracely RH, Petzke F, Wolf JM, Clauw DJ.2002.
Functional magnetic resonance imaging evidence of augmented pain processing
in fibromyalgia.
Arthritis Rheum 46(5):1333-43. "Supports the hypothesis that FM is
characterized by cortical or subcortical augmentation of pain processing."
Gracovetsky, S. 2008. Is the
lumbodorsal fascia necessary? J Bodywork Move Ther.
12(3):194-197. “The role of the lumbodorsal fascia is
generally neglected in spine biomechanics. Yet it is perhaps
with most important structure insuring the integrity of the spinal
machinery. The viscoelastic property of its collagen has a
direct impact on the way the muscles are used and forces are
channeled from the ground to the upper extremities. As a
controller of the forces distribution between muscles and fascia,
lordosis is the prime candidate for rehabilitation in the event of
injury.” [An ounce of prevention is worth a pound of cure.
DJS]
Graff-Radford SB. 2004. Myofascial pain:
diagnosis and management. Curr Pain Headache Rep.
8(6):463-467. “Clinical understanding and management of
myofascial pain is overlooked frequently when dealing with pain.”
Graff-Radford SB. 2004. Myofascial pain: diagnosis and management.
Curr Pain Headache Rep. 8(6):463-467. Myofascial pain is an
often-neglected and treatable as a component of patients’ pain.
Graff-Radford, S. B. , J. L. Reeves, R. L.
Baker and D. Chiu. 1989. Effects of transcutaneous electrical nerve
stimulation on myofascial pain and trigger point sensitivity. Pain
37(1):1-5.
Grafe, A., U. Wollina, B. Tebbe, H. Sprott,
C. Uhlemann and G. Hein. 1999. Fibromyalgia in lupus
erythematosus. Acta Derm Venereol 79(1):62-4.
Graham, C. and M. R. Cook. 1999.
Human sleep in 60 Hz magnetic fields. Bioelectro-magnetics
20(5):277-83.
Grahmann PH, Jackson KC 2nd, Lipman AG. 2004. Clinician
beliefs about opioid use and barriers in chronic nonmalignant pain.
J Pain Palliat Care Pharmacother. 18(2):7-28. “There is
increasing acceptance of opioids for most of the listed types of chronic
nonmalignant pain, but the acceptance varies by types of pain
syndromes.”
Grant, J. A., L. Danielson, J. P.
Rihoux and C. DeVos. 1999. A double-blind, single-dose,
crossover comparison of cetirizine, ebastine, epinastine, fexofenadine,
terfenadine, and loratadine versus placebo: suppression of histamine-induced
wheal and flare response for 24 h in. Allergy
54(7):700-7.
Grassi, W., R. De Angelis, G. Lapadula, G.
Leardini and R. Scarpa. 1998. Clinical diagnosis found in
patients with Raynaud’s phenomenon: a multicenter study. Rheumatol
Int 18(1):17-20.
Grassi, W., P. Core, G. Corlino, F. Salaffi
and C. Cervini. 1994. Capillary permeability in fibromyalgia. J
Rheumatol
21(7):1328-1331.
Graven-Nielsen T. 2007. The interaction of musculoskeletal pain
and motor control. J Musculoskel Pain 15 (Supp 13):10 item
12. [Myopain 2007 Poster] “The functional adaptation to
muscle pain may also involve increased muscle activity reflecting
compensatory muscle coordination. Such adaptation in motor
function might evoke overload of other muscle groups and as such play a
role in the persistence, amplification and spread of pain, and
interventions should take this aspect into consideration.”
Graven-Nielsen T, Mense S, Arendt-Nielsen L. 2004. Painful and
non-painful pressure sensations from human skeletal muscle. Exp
Brain Res. [Epub ahead of print] Specific nerve fiber
contributions to peripheral pain.
Graven-Nielsen, T., K. S. Aspegren, K. G.
Henriksson, M. Bengtsson, J. Sorensen, A. Johnson, B. Gerdle and L.
Arendt-Nielsen. 2000. Ketamine reduces muscle pain, temporal
summation, and referred pain in fibromyalgia patients. Pain
85(3):483-491.
Greaves MW, Wall PD. 1996.
Pathophysiology of itching. Lancet 348(9032):938-940.
There is a strong central nervous system component to some forms of
itch, and the neurotransmitter histamine is frequently involved.
[The connection between itch and pain is involved and still being
explored. DJS]
Green CR, Anderson KO, Baker TA et al. 2003.
The unequal burden of pain: confronting racial and ethnic
disparities in pain. Pain Med. 4(3):277-294.
“Racial and ethnic disparities in pain perception, assessment, and
treatment were found in all settings (i.e., postoperative, emergency
room) and across all types of pain (i.e., acute, cancer, chronic
nonmalignant, and experimental). The literature suggests that
the sources of pain disparities among racial and ethnic minorities
are complex, involving patient (e.g., patient/health care provider
communication, attitudes), health care provider (e.g., decision
making), and health care system (e.g., access to pain medication)
factors. There is a need for improved training for health care
providers and educational interventions for patients.” [People
of color often seem to be treated as invisible people, just like
people with invisible illness. The combination may cause
untold and needless misery. DJS]
Green CR, Anderson KO, Baker TA et al. 2003.
The unequal burden of pain: confronting racial and ethnic disparities in
pain. Pain Med. 4(3):277-294. There are complex
variables in the sources of pain disparity among ethnic and racial
groups. Some of this pain is unnecessary and can be remedied.
Green JS, Stanforth PR, Rankinen T et al. 2004. The effects of
exercise training on abdominal visceral fat, body composition, and
indicators of the metabolic syndrome in postmenopausal women with and
without estrogen replacement therapy: the HERITAGE family study.
Metabolism 53(9):1192-1196. Exercise did not improve the
Metabolic Syndrome status of these study participants.
Greenblatt, D. J., J. S. Harmatz, L. L. von
Moltke, B. L. Ehrenberg, L. Harrel, K. Corbett, M. Counihan, J. A. Graf, M.
Darwish, P. Mertzanis, P. T. Martin, W. H. Cevallos and R. I. Shader.
1998. Comparative kinetics and dynamics of zaleplon, zolpidem, and placebo.
Clin Pharmacol Ther 64(5):553-61.
Greenburg, P.E., Leong, S. A., Birnbaum,
H.G. et al. 2003. The economic burden of depression with painful
symptoms. 64 Suppl 7:17-23. “When painful physical
symptoms accompany the already debilitating psychiatric and behavioral
symptoms of depression, the economic burden that ensues for patients and
their employers increases considerably.
On purely economic grounds, more aggressive outreach may be warranted
for patients with depression and comorbid pain to initiate treatment before
symptoms are allowed to persist.”
Greenfield, S., M. A. Fitzcharles and J. M
. Esdaile. 1992. Reactive fibromyalgia syndrome. Arthritis Rheum
35(6):678-681.
Greenlund, K. J., R. Valdez, M. L. Casper,
S. Rith-Najarian and J. B. Croft. 1999. Prevalence and
correlates of the insulin resistance syndrome among Native Americans.
Diabetes Care22:441-447.
Greenman, Philip E. 1996.
Principles of Manual Medicine. Baltimore MD: Williams and Wilkins.
Griffiths, R. D., C. J. Hinds and R. A. Little. 1999.
Manipulating the metabolic response to injury. Br Med Bull
55(1):181-95.
Greisen J, Juhl CB,
Grofte T et al. 2001. Acute pain induces insulin resistance in humans.
Anesthesiology. 95(3):573-4 “...pain relief in stress states is
important for maintenance of normal glucose metabolism.” [Chronic pain
patients may also be predisposed to insulin resistance. DJS]
Grichnik, K. P. and F. M. Ferrante.
1991. The difference between acute and chronic pain. Mt Sinai
J Med
58(3):217-220.
Griep, E. N., J. W. Boersma, E. G.
Lentjes, A. P. Prins, J. K. van der Korst and E. R. de Kloet. 1998. Function
of the hypothalamic-pituitary-adrenal axis in patients with fibromyalgia and
low back pain. J. Rheumatol 25(7):1374-81.
Griep, E. N., J. W. Boersma, and E. R. de
Kloet. 1994. Pituitary release of growth hormone and prolactin in the
primary fibromyalgia syndrome. J Rheumatol 21(11):2125-2130.
Griep, E. N. , J. W. Boersma, and E. R. de
Kloet. 1993. Altered reactivity of the hypothalamic-pituitary-adrenal axis
in the primary fibromylgia syndrome. J Rheumatol 20(3):469-74.
Griffin, L. D. and S. H. Mellon.
1999. Selective serotonin reuptake inhibitors directly alteractivity
of neurosteroidogenic enzymes. Proc Natl Acad Sci
96(23):13512-7.
Grigsby, J., N. L. Rosenberg and D.
Busenbark. 1995. Chronic pain is associated with deficits in information
processing. Percept Mot Skills
81(2):403-410.
Grigsby, J., N. L. Rosenberg and D.
Busenbark. 1995. Chronic pain is associated with deficits in
information processing. Percept Mot Skills
81(2):403-410.
Grinnell F. 2008. Fibroblast
mechanics in three-dimensional collagen matrices. J Bodywork Move
Ther. 12(3):191-193. “Fascia provides mechanical support and
frameworks for the other tissues of the body. Type 1 collagen is the
major protein component of fascia, and fibroblasts are the cell type
primarily responsible for its biosynthesis and remodeling. Research on
fibroblasts interacting with collagen matrices provides new insights
regarding how cell-matrix tension state and growth factor specificity
regulate cell migration and matrix remodeling.”
Grip H, Sundelin G, Gerdle B et al. 2007.
Variations in the axis of motion during head repositioning – a comparison of
subjects with whiplash-associated disorders or non-specific neck pain and
healthy controls. Clin Biomech [Jul 6 Epub ahead of print].
“Measuring variation in the axis of motion together with target performance
gives objective measures on proprioceptive ability that are difficult to
quantify by visual inspection. Repositioning errors were in general
small, suggesting it is not sufficient as a single measurement variable in a
clinical situation, but should be measured in combination with other tests,
such as range of motion.” [Pain at the end of range of motion
indicates the possibility of myofascial trigger points, and as MTrPs often
have proprioceptor components, this study would have been better for
including them. DJS]
Grisart, J., Van der Linden M., Masquelier E.
2002. Controlled processes and automaticity in memory functioning in
fibromyalgia patients: relation with emotional distress and hypervigilance.
J Clin Exp Neuropsychol 24(8):994-1009.
“...memory functioning in fibromyalgia patients is related to their painful
condition as a whole rather than to any particular patient’s
characteristics.”
Grisart, J. M. and L. H. Plaghki. 1999.
Impaired selective attention in chronic pain patients.Eur J Pain
3(4):325-333.
Grobli C, Dejung B. 2003. [Non-pharmacological
therapy of myofascial pain] Schmertz 17(6):475-480. Specific manual
therapy is effective for low back trigger point pain. Connective
tissue adhesions that may form in the regions of TrPs as a result of
localized edema may be key areas involved in myofascial pain. They
deserve prompt and thorough attention. [German]
Grobli C, Dejung B. 2003. [No Title Given]
Schmertz 17(6):475-480. Specific manual therapy is effective for low
back trigger point pain. [German]
Grodin MA, Piwowarczyk L, Fulker D et
al. 2008. Treating survivors of torture and refugee trauma: a
preliminary case series using qigong and t’ai chi. J Altern
Comp Med 14(7):801-806. This limited study found qigong
and t’ai chi effective for torture survivors. With the caveat
that there are many kinds of qigong and t’ai chi, this suggests to
me that these practices may also be helpful for the survivors of the
torture of chronic pain. I have found them most helpful.
DJS]
Grontved, A., T. Brask, J. Kambskard and E.
Hentzer. 1988. Ginger root against seasickness.A controlled
trial on the open sea. Acta Otolarygol (Stockh) 105(1-2):45-49.
Grossman P, Tiefenthaler-Gilmer U, Raysz A et al.
2007. Mindfulness training as an intervention for fibromyalgia:
evidence of postintervention and 3-year follow-up benefits in well-being.
Psychother Psychosom. 76(4):226-233. “…results indicate
mindfulness intervention to be of potential long-term benefit for female
fibromyalgia patients.”
Grotenhermen F. 2005. Cannabinoids. Curr Drug
Targets CNS Neurol Disord. 4(5):507-530. “Cannabinoid receptors
are distributed in the central nervous system and many peripheral tissues,
including immune system, reproductive and gastrointestinal tracts,
sympathetic ganglia, endocrine glands, arteries, lung and heart.” “The
current main focus of clinical research is their efficacy in chronic pain
and neurological disorders.”
Gruber, D. M. and J. C. Huber. 1999.
Gender-specific medicine: the new profile of gynecology.Gynecol
Endocrinol 13(1):1-6.
Grumbach, M. M. and R. J. Auchus.
1999. Estrogen: consequences and implications of human mutations in
synthesis and action. C Clin Endocrinol Metab 84(12):4677-94.
Grundy, S. M. 1999.
Hypertriglyceridemia, insulin resistance, and metabolic syndrome.
Am J Cardiol 83(9B):25F-29F.
Gruneberg C, Bloem BR, Honegger F et al.
2004. The influence of artificially increased hip and trunk
stiffness on balance control in man. Exp Brain Res.
[Epub May 12 ahead of print]. Trunk and hip stiffness
increases the possibility of falling. This has implications for people
with restricted range of motion due to myofascial TrPs.
Guedj E, Cammilleri S, Colavolpe C et al.
2007. Predictive value of brain perfusion SPECT for ketamine
response in hyperalgesic fibromyalgia. Eur J Nucl Med Mol
Imaging. [Mar 13 Epub ahead of print. “Brain perfusion SPECT
may predict response to ketamine in hyperalgesic FM patients.”
Guerrero-Romero F., Rodriguez-Moran M. 2002.
Low serum magnesium levels and metabolic syndrome. Acta
Diabetol 39(4):209-13. “This study reveals a strong
relationship between decreased serum magnesium and MS.”
Guilleminault C, Huang YS, Kirisoglu C et al. 2005.
Is obstructive sleep apnea syndrome a neurological disorder? A
continuous positive airway pressure follow-up study. Ann Neurol.
58(6):880-887. “Obstructive sleep apnea syndrome involves abnormal
upper airway sensory input, which may be responsible for the development
of apneas and hypopneas. These neurological lesions are persistent
despite nasal CPAP treatment.” Even with relatively successful
CPAP treatment for obstructive sleep apnea, heightened pharyngeal
sensation persists.
Guilleminault C, Kirisoglu C, Poyares D et
al. 2006. Upper airway resistance syndrome: a long-term
outcome study. J Psychiatr Res. 40(3):273-279.
“Many UARS patients remained untreated following initial
evaluation. Worsening of symptoms of insomnia, fatigue and
depressive mood were seen with absence of treatment of UARS.”
Sleep studies must include evaluation for UARS, and patients
diagnosed with UARS must be treated successfully. CPAP
therapy often is the most efficient treatment.
Guilleminault C, Lee JH, Chan A. 2005.
Pediatric obstructive sleep apnea syndrome. Arch
Pediatr Adolesc. 159(8):775-785. Pediatric OSA is not
uncommon and needs to be considered in the differential
diagnosis. Orthodontic treatment, CPAP and other options
may be preferable to adenotonsillectomy.
Gulec H. 2008. Normalizing attributions may
contribute to non-help-seeking behavior in people with fibromyalgia
syndrome. Psychosomatics 49(3):212-217. Some attempts to
“normalize” help-seeking behavior can backfire in tertiary care FM
patients, leading to a self-perception of helplessness and hopelessness
over symptoms, with subsequent lack of attempts to seek help for symptom
control.
Gulec H, Sayar K, Yazici Gulec M. 2007. [The
relationship between psychological factors and health care-seeking
behavior in fibromyalgia patients] Turk Psikiyatri Derg.
18(1):22-30 [Turkish]. “The rate of psychiatric and medical
history is not related to the FM syndrome. Expectations and a
normalizing attribution style may contribute to help-seeking behavior
for FM.
Gullacksen AC, Lidbeck J. 2004. The life
adjustment process in chronic pain: psychosocial assessment and clinical
implications. Pain Res. Manag. 9(3):145-153.
Gunduz B, Bayazit YA, Celenk F et al. 2008. Absence of
contralateral suppression of transiently evoked otoacoustic emissions in
fibromyalgia syndrome. J Laryngol Otol. [Mar 4 Epub ahead
of print]. “The mechanisms related to contralateral suppression of
transiently evoked otoacoustic emissions seem dysfunctional in
fibromyalgia syndrome.” Patients with FM had audio test results
equal to control patients on pure tones, but there was a dysfunction in
FM patients with transiently evoked otoacoustic emissions. [This
study indicates again that there is more to FM than pain. DJS]
Gunn, C. C. 1996. The Gunn Approach to
the Treatment of Chronic Pain. New York, New York: Churchill Livingstone
Gunter, H. H., H. J. Balks, U. Messner, M.
Meffert, U. Nitsche, N. F. Rath and F. Degenhardt. 1999. [No title
available. German]. Zentralbl Gynakol 121(8):357-66.
Gunthert E.A. 2002. [no title] Urologe A
41(6):602-10. [German] This article refers to urogenital symptoms due
to myofascial pain as the result of psychologically-induced muscular tension
and classifies it as a somatization disorder.
This is not consistent with the facts concerning the physiological
basis of myofascial trigger points as we know them.
The author implies that because the symptoms cannot be “...proven by
laboratory tests or common technical diagnostic methods...” they are
somatization disorders. Patients should not pay for their care
provider’s lack of myofascial TrP diagnostic training.
Gupta A, McBeth J, Macfarlane GJ et al. 2006.
Pain thresholds and tender point counts as predictors of new chronic
widespread pain in psychologically distressed subjects. Ann
Rheum Dis. [Sep 29 Epub ahead of print] Subjects who are
psychologically distressed but without chronic pain are not at increased
risk of its development. Low pain-threshold is probably a
secondary result of chronic widespread pain and not a primary condition.
Gupta V, Tiwari S, Agarwal CG. 2006. Effect
of short-term cigarette smoking on insulin resistance and lipid profile
in asymptomatic adults. Indian J Physiol Pharmacol.
50(3):285-290. “It appears that smokers are prone to develop
hyperinsulenemia, hyperglycemia and the metabolic syndrome.”
Another indication that smoking is a perpetuating factor for many
ailments, including those which can be perpetuating factors of FM and
CMP.
Gur A, Sarac AJ, Cevik R et al. 2004.
Efficacy of 904 nm gallium arsenide low level laser therapy in the
management of chronic myofascial pain in the neck: a double-blind and
randomize-controlled trial. Lasers Surg Med. 35(3):229.
Short-term LLLT may be useful to reduce pain and raise quality of life
in patients with cervical MPS.
Gur A, Cevik R, Nas K et
al. 2004. Cortisol and hypothalamic-pituitary-gonadal axis
hormones in follicular-phase women with fibromyalgia and chronic fatigue
syndrome and effect of depressive symptoms on these hormones.
Arthritis Res Ther. 6(3):R232-238.
Gur, A., M. Karakoe, K. Nas et al. 2002. Effects of low
power laser and low dose amitriptyline therapy on clinical symptoms and
quality of life in fibromyalgia: a single-blind, placebo-controlled trial.
Rheumatol Int 22(5):188-93. Active low-power gallium-arsenide laser therapy
and/or amitriptyline therapy may be effective for fibromyalgia patients.
Gurer G, Sendur OF, Ay C. 2005. Serum lipid
profile in fibromyalgia women. Clin Rheumatol. [Oct 1 Epub
ahead of print] “In the FM group, we could not find a significant
correlation between the serum lipid profile values and the FM parameters
(p>0.05).” [This research confirms the research of Dr. Salih Ozgocmen
and his team. They found that in patients with both fibromyalgia and
chronic myofascial pain who had high lipid profiles, the high lipid profile
was related to the myofascial pain component and not the fibromyalgia. DJS]
Gursoy S, Erdal E, Sezgin M et al. 2007. Which
genotype of MAO gene that the patients have are likely to be most
susceptible to the symptoms of fibromyalgia? Rheumatol Int.
[Sep 20 Epub ahead of print] “It seems plausible to say that
MAOA-dependent metabolism of the biological amines may be partly related to
high-activated MAO-A, allele 3, in the occurrence of FS among Turkish
population.”
Gursoy, S., Erdal, E., Herken, H., et al.
Significance of catechol-O-methyltransferase gene polymorphism in
fibromyalgia syndrome. Rheumatol Int 23(3):104-7. [This
research may have implications in the treatment of FM, as well as genetic
tendency to develop FM. It indicates that the metabolism of catechol
drugs in FM patients may be different. DJS]
Gusi N, Tomas-Carus P. 2008. Cost-utility of an 8-month aquatic
training for women with fibromyalgia: a randomized controlled trial.
Arthritis Res Ther. 10(1):R24. “The addition of an aquatic
exercise program to the usual care for fibromyalgia in women is
cost-effective in terms of both health care costs and societal costs.
However, the characteristics of facilities (distance from the patients’
homes and number of patients that can be accommodated per session) are
major determinants to consider before investing in such a program.”
[Care must be taken to remember that all aquatic therapy programs are
not the same, nor are all FM patients. After individualized
assessment, some FM patients may benefit from some aquatic programs, and
this is another treatment option that may be considered if there is a
nearby facility with a pool at the proper temperature and instructors
that understand the ramifications of FM and exercise plus any
co-existing conditions. The additional plus to this study is that
this treatment is shown as a cost-effective option. It must be
noted that the aquatic programs for arthritis may not be suitable for FM
patients either in water temperature or exercise, especially if there
are co-existing MTPs. Co-existing MTPs also complicate therapy for
arthritis patients. DJS]
Gusi N, Tomas-Carus P, Hakkinen A et al. 2006.
Exercise in waist-high warm water decreases pain and improves
health-related quality of life and strength in the lower extremities in
women with fibromyalgia. Arthritis Rheum. 55(1):66-73.
“The therapy relieved pain and improved HRQOL (health-related quality of
life) and muscle strength in the lower limbs at low velocity in patients
with initial low muscle strength and high number of tender points.
Most of these improvements were maintained long term.”
Gustafsson M, Ekholm J, Ohman A. 2004.
From shame to respect: musculoskeletal pain patients’ experience of a
rehabilitation programme, a qualitative study. J Rehabil Med.
36(3):97-103.
Gustaw K. 2000. Myofascial pain syndrome in farmers – a
comprehensive approach to treatment. Ann Agric Environ Med
7(2):95-99. “The MPS syndrome was found to be relatively common in
Polish farmers and formed 12.7% of all chronic pain syndromes diagnosed
in the Institute of Agricultural Medicine during 18 months.”
Gutierrez-Reyes G, Lopez-Ortal P, Sixtos S
et al. 2006. Effect of pentoxifylline on levels of
pro-inflammatory cytokines during chronic hepatitis C.
Scand J Immunol 63(6):461-467. Pentoxifylline may be
helpful in controlling cytokine storms such as may occur in
hepatitis C. [And FM, and avian influenza. DJS]
Guttu RL, Page DG, Laskin DM. 1990. Delayed healing of muscle
after injection of bupivicaine and steroid. Ann Dent
49(1):5-8. “Bupivicaine produces more tissue reaction than
procaine and that the addition of steroid to bupivicaine increases the
initial tissue damage and prolongs the healing phase.” [Some
physicians still use bupivicaine (Marcaine) for TrP injections, although
research shows that procaine or lidocaine are much less toxic and more
useful for these injections. DJS]
Guymer EK, Clauw DJ.2002 Treatment of fatigue in
fibromyalgia. Rheum Dis Clin North Am 2002 28(2):367-78.
"Clearly, fatigue is a large and challenging problem for those suffering
from fibromyalgia. It adds greatly to the morbidity and disability
associated with the disease. In the management of this specific
symptom in fibromyalgia, attention should first be focused on identifying
comorbidities that may be present and contribute to fatigue. As with
other symptoms of fibromyalgia, education is a critical component of
management. Easier access to well designed nonpharmacologic therapies
is essential, because these treatments are underutilized in clinical
practice at present."
Haak T, Scott
B. 2007. The effect of Qigong on fibromyalgia (FM): a controlled
randomized study. Disabil Rehabil. [Jun 15 Epub ahead of
print] “…Qigong has positive and reliable effects regarding FM.”
“…Qigong intervention could be a useful complement to medical treatment for
subjects with FM.”
Haanen, H. C. , H. T. Hoenderdos, L.
K. van Romunde, W. C. Hop, C. Mallee, H. P. Terwiel and G. B. Hekster. 1991.
Controlled trial of hypnotherapy in the treatment of refractory
fibromyalgia. J Rheumatol
18(1):72-75.
Hader, N., D. Rimon, A. Kinarty and N.
Lahat. 1991. Altered interleukin-2 secretion in patients with primary
fibromyalgia syndrome. Arthritis Rheum
34(7):866-71.
Hagglund, K. J., W. E. Deuser, S. P.
Buckelew, J. Hewett and D. R. Kay. 1994. Weather, beliefs about
weather, and disease severity among patients with fibromyalgia.
Arthritis Care Res7(3):130-135.
Hainaut, K. and J. Duchateau. 1992.
Neuromuscular electrical stimulation and voluntary exercise. Sports Med
14(2):100-113.
Hadjistavropoulos, H. D., F. K. MacLeod and
G. J. Asmundson. 1999. Validation of the Chronic Pain Coping
Inventory. Pain
80(3):471-81.
Hagen, NA. 2004. A multi-centre
open-label, dose-escalation study of intramuscular tetrodoroxin for
severe cancer pain. Second Joint Scientific Meeting of the
American Pain Society and the Canadian Pain Society. May 6-9.
Vancouver, B.C.
Hakguder A,
Birtane M, Gurcan S et al. 2003. Efficacy of low level laser therapy
in myofascial pain syndrome: An Algometric and thermographic evaluation.
Lasers Surg Med 33(5):339-343.
“LLLT seemed to be beneficial for pain in MPS...” documented by
algometry and thermography.
Hakonarson H, Thornorsson A. 2001. [Common
causes of sleep disturbances in Icelandic children who undergo sleep
studies.] Laeknabladid 87(10):799-804. [Icelandic]
“…both OSA and GER are common problems in children with sleep disturbances.
We conclude that sleep studies are important in the overall workup of
children with sleep disturbances….”
Hall, S. 1999. Common pain
scenarios. Aust Fam Physician 28(1):31-5.
Hallberg, L. R. and S. G. Carlsson.
1998. Anxiety and coping in patients with chronic work-related
muscular pain and patients with fibromyalgia. Eur J Pain
2(4):309-319.
Hameroff, S. R., J. L. Weiss, J. C. Lerman,
R. C. Cork, K. S. Watts, B. R. Crago, C. P. Neuman,J. R. Womble and T. P.
Davis. 1984. Doxepin’s effects on chronic pain and depression:
acontrolled study. J Clin Psychiatry 45(3 Pt2):47-53.
Hamilton NA, Affleck G, Tennen H et al. 2008.
Fibromyalgia: the role of sleep in affect and in negative event reactivity
and recovery. Health Psychol. 27(4):490-497. The amount
of pain and the affect on quality of life was significantly impacted on the
amount and quality of sleep the night before. Sleep duration and sleep
quality affected the mood, stress reactivity and stress recovery of the
patient the next day. “Furthermore, the effects of inadequate sleep on
negative affect were cumulative. In addition, an inadequate amount of
sleep prevented affective recovery from days with a high number of negative
events....These results lend support to the hypothesis that sleep is a
component of allostatic load and has an upstream role in daily functioning.”
Han HS, Suk K. 2005. The function and
integrity of the neurovascular unit rests upon the integration of the
vascular and inflammatory cell systems. Curr Neurovasc Res.
2(5):409-423. “In an effort to understand the pathogenesis and find
rational treatments against inflammatory disorders in brain, studies have
been separately carried out using either endothelial cells or microglia.
Increased evidence, however, indicates that a crosstalk between these two
cell types is important for the brain inflammation.”
Han SC, Harrison P. 1997. Myofascial pain syndrome and
trigger-point management. Reg Anesth 22(1):89-101. “A
multidisciplinary approach to treatment appears to be most beneficial
and may include such modalities as trigger-point injections, dry
needling, stretch and spray, and transcutaneous electrical nerve
stimulation.”
Han, S. C. and P. Harrison. 1997.
Myofascial pain syndrome and trigger-point management.Reg Anesth
22(1):89-101.
Han, Y., J. Wang, D. A. Fischman, H. F.
Biller and I. Sanders. 1999. Slow tonic muscle fibers in the
thyroarytenoid muscles of human vocal folds; a possible specialization for
speech. Anat Rec 256(2):146-57.
Hanani
M., T. Huang, P. Cherkas et al. 2002. Glial cell plasticity in sensory
ganglia induced by nerve damage. Neuroscience 114(2):279. Changes in glial
cells may contribute to neuropathic pain.
Handa, R., P. Aggarwal, J. P. Wali,
N. Wig and S. N. Dwivedi. 1998. Fibromyalgia in Indian patients with
SLE. Lupus
7(7):475-8.
Handwerker, H. O. , C. Forster and C.
Kirchhoff. 1991. Discharge patterns of human C-fibers into used by itching
and burning stimuli. J Neurophysiol 66(1):307-15.
Hanna, J. L. 1995. The power of
dance: health and healing. J Altern Complement Med 1(4):
323-31.
Hannonen, P., K. Malminiemi, U.
Yli-Kerttula, R. Isomeri and P. Roponen. 1998. A randomized,
double-blind, placebo-controlled study of moclobemide and amitriptyline in
the treatment of fibromyalgia in females without psychiatric disorder.
Br J Rheumatol 37(12):1279-86.
Hansen A, Bi P, Nitschke M et al. 2008.
The effect of heat waves on mental health in a temperate Australian city.
Environ Health Perspect. 116(10):1369-1375. “Conclusion: Our
results suggest that episodes of extreme heat pose a salient risk to the
health and well-being of the mentally ill. Relevance to clinical or
professional practice: Improvements in the management and care of the
mentally ill need to be addressed to avoid an increase in psychiatric
morbidity and mortality as heat waves become more frequent.” [ This
study is interesting, and I would like to see more work done on the effects
on chronic pain by extreme weather changes, ionic winds, and other phenomena
that will become more prevalent with climate change. DJS]
Hapidou, E. G. and G. B. Rollman.
1998. Menstrual cycle modulation of tender points. Pain 77(2):151-61
Haq SA, Darmawan J, Islam MN et al. 2005. Prevalence of rheumatic
diseases and associated outcomes in rural and urban communities in
Bangladesh: a COPCORD study. J Rheumatol. 32(2):348-353.
“Fibromyalgia is a common cause of morbidity, disability, and work loss
in rural and urban communities of Bangladesh.” [Fibromyalgia
syndrome occurs worldwide, irrespective of race, socioeconomic class, or
other variables. DJS]
Harden RN, Revivo G, Song S et al. 2007. A
critical analysis of the tender points in fibromyalgia. Pain Med.
8(2):147-156. “There was a significant difference in the ‘algometric
total score’ between patients with fibromyalgia and controls….” “The
points specified by the ACR were only modestly superior to sham points in
making the diagnosis.” [We clearly need a better definition of FM.
One is under development now. DJS]
Harden RN, Bruehl SP, Gass S, Niemiec C,
Barbick B 2000. Signs and symptoms of the myofascial pain syndrome: a
national survey of pain management providers.Clin J Pain 16(1):64-72.
Harding, S. M. 1998. Sleep in fibromyalgia
patients: subjective and objective findings. Am J Med Sci
315(6):367-376.
Harlow, B. L., L. B. Signorello, J. E.
Hall, C. Dailey and A. L. Komaroff. 1998. Reproductive correlates of
chronic fatigue syndrome. Am J Med 105(3A):94S-99S.
Haroutiunian S, Rosen G, Shouval R et al.
2008. Open-label, add-on study of tetrahydrocannabinol for chronic
nonmalignant pain. J Pain Plliat Care Pharmacother.
22(3):213-217. “Cannabinoids have been used for pain relief for
centuries and recent studies have investigated their analgesic and
anti-inflammatory mechanisms, as well as clinical efficacy, in treating
chronic pain. We report an open-label study addressed to evaluate the
effect and adverse events of orally administered
Delta-9-tetrahydrocannabinol (Delta-9-THC) in 13 patients with chronic
nonmalignant pain (CNMP) unresponsive to conventional pharmacotherapy.
The effect of the treatment was assessed on an eight-item HRQoL
questionnaire. Five out of 13 patients reported adequate response to
the treatment while eight patients reported inadequate or no response.
Seven patients did not experience any adverse events (AEs), six patients
reported AEs, two of which discontinued the treatment. We conclude
that oral THC may be a valuable therapeutic option for selected patients
with CNMP that are unresponsive to previous treatments, though further
research is warranted to characterize those patients.” [It is
interesting that other studies have indicated a dysfunctional
endocannabinoid system in FM patients. A study using cannabinoids on
patients with FM, TrPs and both CMP and central sensitization (Stage II CMP)
might be very useful. See McPartland JM on the cannabinoid/TrP connection.
DJS]
Harris, A. J. 1999. Cortical
origin of pathological pain. Lancet 354(9188):1464-6.
Harris RE, Clauw DJ, Scott DJ et al. 2007.
Decreased central mu-opioid receptor availability in fibromyalgia.
J Neurosci. 27(37):10000-10006. Positron emission
tomography indicates that FM patients have a decreased mu-opioid
binding potential in several areas of the brain associated with pain
modulation. This altered endogenous opioid activity may
explain why it takes a greater amount of opioids for some FM
patients to produce the same amount of pain control.
Harris RE, Clauw DJ. 2006. How do we know fibromyalgia is “real?”
Curr Pain Headache Rep
(10):403-407. There is now “overwhelming data” that indicate FM
is real, with genetic predisposition. Functional magnetic
resonance imaging (fMRI) and single photon emission computed tomography
(SPECT) show significant difference between FM patients and others.
It is not a psychological, functional or “somatic” disorder. A
variation in the gene that encodes the enzyme catechol-O-methyl
transferase, significantly affects pain sensitivity and pain-related
emotions and feelings. This enzyme also is related to development
of TMJD. The pain is real, and it can be shown by radiological
studies.
Harrison, D. E., R. Cailliet, D. D.
Harrison, S. J. Troyanovich and S. O. Harrison. 1999. A review of
biomechanics of the central nervous system–Part I: spinal canal deformations
resulting from changes in posture. J Manipulative Physiol Ther
22(4):227-34.
Hart FX. 2008. The mechanical transduction of physiological
strength electric fields. Bioelectromagnetics [Mar 31 Epub
ahead of print]. This article explains how physiological strength
electrical fields produce torque on the glycoproteins, which then signal
the cytoskeleton and transmit the signals throughout the interior of the
cell. This may be part of a network of orchestrated transduction
mechanisms including the opening and closing of ion channels in the
cellular membranes. [This process may explain one way
electromedical devices can change cellular biophysics and biochemistry.
This could be very important for those of us with altered metabolisms.
One medical hypothesis mentions myofascial trigger points as a result of
an ion channel dysfunction. DJS]
Hart, P., S. Townley, M. Grimbaldston et
al. 2002. Mast cells, neuropeptides, histamine, and prostagladins in
UV-induced systemic immunosuppression. Methods 28(1):79.
This article points out the direct correlation between dermal mast
cell prevalence and susceptibility to UVB-induced systemic immunosuppression
in mice. [Above normal counts of mast cells have been found in fibromyalgia
patients.] The authors propose histamine and prostaglandin E2 are important
in downstream immunosuppression.
Harty J, Soffe K, O'Toole G et al. 2005. The
role of hamstring tightness in plantar fasciitis. Foot Ankle Int.
26(12):1089-1092. [Hamstring tightness, such as that due to myofascial
TrPs, could be a major unrecognized factor contributing to plantar
fasciitis. DJS]
Harvey, A. G. and R. A. Bryant. 1999.
Predictors of acute stress following motor vehicle accidents. J
Trauma Stress
12(3):519-25.
Hashkes PJ, Friedland O, Jaber L et al.
2004. Decreased pain threshold in children with growing pains.
J Rheumatol 31(3):610-613. Growing pain may be indicative of
developing fibromyalgia tender points, according to this research, but they
did not check for co-existing myofascial TrPs. Growing pains are often
due to TrPs. Research that takes them into account would be more
valuable, because we can't know if the link between the tender points and
the growing pains is coincidental.
Hassett AL, Radvanski DC, Vaschillo EG et al. 2007.
A pilot study of the efficacy of heart rate variability (HRV) biofeedback in
patients with fibromyalgia. Appl Psychophysiol Biofeedback.
[Jan 12 Epub ahead of print] “These data suggest that HRV biofeedback
may be a useful treatment for FM, perhaps mediated by autonomic changes.
While HRV effects were immediate, blood pressure, baroreflex, and
therapeutic effects were delayed. This is consistent with data on the
relationship among stress, HPA axis activity, and brain function.”
Hauser W, Thieme K, Turk DC. 2009.
Guidelines on the management of fibromyalgia syndrome – a systematic
review. Eur J Pain [Mar 3 Epub ahead of print]. This
article illustrates the problems that can occur even with the best
researchers if the studies that they review are flawed. In this
overview, in the table on page 5, trigger point injections are included
(as they have been in some of the articles assessed) as treatment for
fibromyalgia. Since trigger points are not part of fibromyalgia,
it indicates that a lot of clinicians doing research don’t understand
the very basic differences between myofascial pain due to trigger points
and fibromyalgia, and the conclusions they reach are therefore suspect.
DJS]
Hauser W. 2005. [Fibromyalgia in the legal
procedures of the German Sozialgericht – psychosocial risk factors and
predictors of health care utilization] Psychother Psychosom Med
Psychol. 55(2):72-78 [German] “Former and current psychiatric
disorders, biographic adverse experiences, duration of generalized pain,
sex and social class had no substantial predictive value on the
extensive health care utilization (number of doctors, pain-related
hospital and rehabilitation stays and pain-related operations).”
[This is important, as other studies have indicated that some chronic
conditions, such as fibromyalgia, can impact health care utilization.
DJS]
Hautanen, A., K. Raikkonen and H.
Adlercreutz. 1997. Associations between pituitary-adrenocortical function
and abdominal obesity, hyperinsulinaemia and dyslipidaemia in normotensive
males. J Intern Med
241(6):451-61.
Havas M. 2006. Electromagnetic
hypersensitivity: biological effects of dirty electricity with emphasis on
diabetes and multiple sclerosis. Electromagn Biol Med.
25(4):259-268. “Several disorders, including asthma, ADD/ADHD,
diabetes, multiple sclerosis, chronic fatigue, and fibromyalgia, are
increasing at an alarming rate, as is electromagnetic pollution in the form
of dirty electricity, ground current, and radio frequency radiation from
wireless devices. The connection between electromagnetic pollution and
these disorders needs to be investigated and the percentage of people
sensitive to this form of energy needs to be determined.” [One might
want to add CMP to this list, especially if FM amplification is part of the
picture. DJS]
Hawk, C., C. Long and A. Azad. 1997.
Chiropractic care for women with chronic pelvic pain: a prospective
single-group intervention study. J Manip Physiol Ther 20 (2):
73-79.
Hayden RJ, Louis DS, Doro C. 2005.
Fibromyalgia and myofascial pain syndromes and the workers’
compensation environment: an update. Clin Occup Environ
Med. 5(2):455-469. “Controversy exists as to whether
fibromyalgia and myofascial pain syndromes represent a specific
pathology or are merely terms to describe clinical conditions that
provide patients with the reassurance that their symptoms are real
and help clinicians with therapeutic direction. In the
occupational health setting, this uncertainty can lead to
significant difficulty in determining short- and long-term
disability and assigning culpability to an individual’s work
environment.”
Hayes, J. A. 1998. TAC-TIC
therapy: a non-pharmacological stroking intervention for premature infants.
Complement Ther Nurs Midwifery 4(1):25-7.
Haythornthwaite, J. A., L. A. Menefee, L.
J. Heinberg and M. R. Clark. 1998. Pain coping strategies
predict perceived control over pain. Pain 77(1):33-9.
Haythornthwaite, J. A., L. A. Menefee, A.
L. Quatrano-Piacentini and M. Pappagallo. 1998. Outcome of chronic
opioid therapy for non-cancer pain. J Pain Symptom Manage
15(3):185-94.
Haythornthwaite, J. A., M. T. Hegel and R.
D. Kerns. 1991. Development of a sleep diary for chronic pain
patients. J Pain Symptom Manage 6(2):65-72.
Haythornthwaite, J. A., W. J. Sieber and R.
D. Kerns. 1991. Depression and the chronic pain experience.
Pain
46(2):177-184.
He
D, Veiersted KB, Hostmark AT et al. 2004. Effect of acupuncture
treatment on chronic neck and shoulder pain in sedentary female workers:
a 6-month and 3-year follow-up study. Pain 109(3):299-307.
“Adequate acupuncture treatment may reduce chronic pain in the neck and
shoulders and related headache. The effect lasted for 3 years.”
Heap, L. C., T. J. Peters and S. Wessely.
1999. Vitamin B status in patients with chronic fatigue syndrome.
J R Soc Med
92(4):183-5.
Heath KM, Elovic EP. 2006. Vitamin D
deficiency: implications in the rehabilitation setting. Am J Phys
Med Rehabil. 85(11):916-923. “Vitamin D deficiency should be
included in the differential diagnosis in the evaluation of musculoskeletal
pain complaints in the rehabilitation setting, and treatment of any
identified deficiency should be considered a potentially important component
of the treatment regimen.”
Hein G., Franke S. 2002. Are advanced
glycation end-product-modified proteins of pathogenetic importance in
fibromyalgia? Rheumatology (Oxford) 41(10):1163-7.
Heinrich, S. 1991. The role of
physical therapy in craniofacial pain disorders: an adjunct to dental pain
management. Cranio
9(1):71-75.
Helfenstein, M. and D. Feldman. 2000.
The pervasiveness of the illness suffered by workersseeking compensation for
disabling arm pain. J Occup Environ Med 42(2):171-5.
Heller, U., E. W. Becker, H. P. Zenner and
P. A. Berg. 1998. [Incidence and clinical relevance of antibodies to
phospholipids, serotonin and ganglioside in patients with sudden deafness
and progressive inner ear hearing loss]. HNO 46(6):583-6.
[German]
Hellstrom, O. , J. Bullington, G. Karlsson,
P. Lindqvist and B. Mattsson. 1999. A phenomenological study of
fibromyalgia. Patient perspectives. Scand J Prim Health Care
17(1):11-6.
Helme, R. D. , S. Gibson and Z. Khalil.
1990. Neural pathways in chronic pain. Med J Aust 153(7):400-406.
Helme, R. D. , G. O. Littlejohn and C.
Weinstein. 1987. Neurogenic flare responses in chronic rheumatic pain
syndromes. Clin Exp Neurol
23(1):91-94.
Hemmeter, U., R. Kocher, D. Ladewig, M.
Hatzinger, E. Seifritz, C. J. Lauer and E. Holsboer-Trachsler. 1995.
[Sleep disorders in chronic pain and generalized tendomyopathy].
Schweiz Med Wochenschr 125(49):2391-7 [German]
Henderson, D. J., B. S. Withington, J. A.
Wilson and L. M. Morrison. 1999. Perioperative dextromethorphan
reduces postoperative pain after hysterectomy. Anesth Analg
89(2):399-402.
Hendi A, Dorsher PT, Rizzo TD Jr et al.
2009. Subcutaneous trigger point causing radiating postsurgical
pain. Arch Dermatol. 145(1):52-54. “Surgeons and pain
management specialists should be aware of this potential cause of
immediate postoperative pain to prevent unnecessary medical or surgical
interventions in the postoperative period.” [They might assess
pre-surgical patients for possible TrPs “to prevent unnecessary medical
or surgical interventions.” DJS]
Hendler, N. 1984. Depression caused by
chronic pain. J Clin Psychiatry 45(3 pt 2):30-38.
Henriksson CM, Liedberg GM, Gerdle B. 2005.
Women with fibromyalgia: work and rehabilitation. Disabil
Rehabil. 27(12):685-694. “The total life situation, other
commitments, type of work tasks, the ability to influence the work
situation, and the physical and psychosocial work environment are
important factors in determining whether a person can remain in a
work role. More knowledge is needed about how to adjust work
conditions for people with partial work ability to the benefit of
society and the individual.”
Henriksson CM. 1995. Living with continuous
muscular pain — patient perspectives. Part I: Encounters and
consequences. Scand J Caring Sci 9(2):67-76. “The
contradiction between the patients’ perception of illness and the lack
of objective findings is stressful. The women feel rejected,
misunderstood, and disbelieved, which prevents them from dealing with
their situation constructively. Long investigation periods provoke
anxiety, and confirmation of the diagnosis is a relief. Daily
routines are disrupted, conflicts between life roles lead to additional
stress and the women experience loss of ability to perform valued
activities, lack of physical fitness and loss of future opportunities.
Patients need early and adequate information and the consequences of the
condition must be acknowledged and taken into consideration if secondary
economic and psychosocial consequences are to be minimized.”
Henriksson KG, Sorensen J. 2002. The promise
of N-methyl-D-aspartate receptor antagonists in fibromyalgia.
Rheum Dis Clin North Am. 28(2):343-351. “The combination of a
weak opioid and an
NMDA-receptor antagonist with few side effects is
presently a promise for treatment of pain in a subgroup of patients with
FM.”
Henriksson, K. G. 2001. Is fibromyalgia a central pain
state? J Musculoskel Pain 10(1/2):45:57. "There is strong support for the
notion that pain and allodynia/hyperalgesia in FM have an organic cause.
The hyperexcitability in the nociceptive nervous system is mainly due to
changes in the CNS." " The permanent changes constitute a disease.
There are methods for objectively diagnosing this disease." "Many
causes could initiate and maintain the disease: e.g., long-standing local or
regional musculoskeletal pain, changes in stress-regulating systems,
hormonal changes, changes in serotonin metabolisms, and genetic factors."
[This includes chronic myofascial pain as a perpetuating factor of
FM.]
Henriksson K. G., Sorensen J. 2002. The promise
of N-methyl-D-aspartate receptor antagonists in fibromyalgia. Rheum Dis
Clin North Am 28(2):343-51. "The combination of a weak opioid and an
NMDA-receptor antagonist with few side effects is presently a promise for
treatment of pain in a subgroup of patients with FM."
Henriksson, K. G. 1999. Muscle activity and
chronic muscle pain. J Musculoskel Pain 7(1-2):101-109.
Henriksson, K. G. 1999. Is
fibromyalgia a distinct clinical entity? Pain mechanisms in
fibromyalgia syndrome. A myologist’s view. Baillieres Best
Pract Res Clin Rheumatol 13(3):455-61.
Henriksson, C. and C.Burckhardt. 1996.
Impact of fibromyalgia on everyday life: a study of women in the USA
and Sweden. Disabil Rehabil 18(5):241-248.
Henriksson, C. M.1994. Longterm effects of
fibromyalgia on everyday life. A study of 56 patients. Scand J Rheumatol
23(1):36-41.
Henriksson, C., I. Gundmark , A. Bengtsson
and A. C. Ek. 1992. Living with fibromyalgia. Consequences for
everyday life. Clin J Pain
8(2):138-144.
Herald, J. and M.Pecenka. 1991. Pain
doctors: the real world of a pain practice. An interview with Lawrence
A. Funt. Dental Management March, 26-29.
Heredia Jimenez JM, Aparicio Garcia-Molina
VA, Porres Foulquie JM et al. 2009. Spatial-temporal parameters of
gait in women with fibromyalgia. Clin Rheumatol. [Jan 24 Epub
ahead of print]. “Gait parameters of women affected by FM were
severely impaired when compared to those of healthy women. Different
factors such as lack of physical activity, bradikinesia, overweight, fatigue
and pain together with a lower isometric force in the legs can be
responsible for the alterations in gait and poorer life quality of women
with FM.” [It is very likely that these gait abnormalities are due to the
presence of co-existing soft tissue dysfunctions including TrPs. It would
have been valuable to assess these patients for co-existing TrPs, as their
role in gait abnormalities has been carefully documented. DJS]
Hetrick DC, Ciol MA, Rothman I et al. 2003. Musculoskeletal
dysfunction in men with chronic pelvic pain syndrome type III: a
case-control study. J Urol. 170(3):828-831. “Men with
CPPS have more abnormal pelvic floor muscular findings compared with a
group of men without pain. Abnormalities of the pelvic muscles may
contribute to this pain syndrome.”
Heyes, M. P., K. Saito and S. P. Markey.
1992. Human macrophages convert L-tryptophan into the neurotoxin quinolinic
acid. Biochem J 283(Pt. 3):633-635.
Hicks. R. A., D. DeHaro, G. Inman and G. J.
Hicks. 1999. Consistency of hand use and sleep problems. Percept Mot
Skills 89(1):49-56.
Hill Jr., C. S. 1996.
Government regulatory influences on opioid prescribing and their impact on
the treatment of pain of nonmalignant origin. J Pain Symptom Manage
11(5):287-298.
Hill Jr., C. S. 1995. When will
adequate pain treatment be the norm? JAMA 274 (23):1881-2.
Hill, C. S. Jr. 1992 The intractable pain
treatment act of Texas. Tex Med 88(2):70-72.
Hilliard MJ, Martinez KM, Janssen I et al.
2008. Lateral balance factors predict future falls in community-living
older adults. Arch Phys Med Rehabil. 89(9):1708-1713.
“The findings identify new predictor variables for risk of falling that
underscore the importance of dynamic balance recovery performance through ML
stepping in relation to neuromusculoskeletal factors contributing to lateral
balance stability. The results also highlight focused risk factors for
falling that are amenable to clinical interventions for enhancing lateral
balance function and preventing falls.” [Any study on falls that fails
to incorporate an assessment for relevant myofascial TrPs is failing in its
purpose. The presence of myofascial TrPs are a major risk factor for
falls. DJS]
Hitchcock, L. S., B. R. Ferrell and M.
McCaffery. 1994 The experience of chronic non-malignant pain J Pain Sympt
Manage 9(5):312-318.
Hiyama S, Ono T, Ishiwata Y et al. 2003.
Effects of experimental nasal obstruction on human masseter and
suprahyoid muscle activities during sleep. Angle Orthod.
73(2):151-157. “Nasal obstruction could modulate the
activities of the masseter and suprahyoid muscles during sleep.”
Activity of the suprahyoid muscles tended to increase
significantly and the masseter tended to decrease significantly
with nasal obstruction during sleep. [This could affect
TrPs, and also CPAP therapy for co-existing sleep apnea.
For the latter, it may indicate need for automatically adjusting
CPAP set to maximum high equal to that of the sleep study need
of the patient, rather than standard CPAP in some patients. DJS]
Holman AJ, Neiman RA, Ettlinger RE. 2004.
Preliminary efficacy of the dopamine agonist, pramipexole for
fibromyalgia: the first, open label, multicenter experience. J
Musculoskel Pain 12(1):69-74. Dopamine agonists may be promising
pharmaceutical agents for the treatment of FM.
Hiyama S, Ono T, Ishiwata Y et al. 2003.
Effects of experimental nasal obstruction on human masseter and
suprahyoid muscle activities during sleep. Angle Orthod.
73(2):151-157. “Nasal obstruction could modulate the
activities of the masseter and suprahyoid muscles during sleep.”
[Could nasal obstruction cause or contribute to TrPs? DJS]
Hiyama S, Ono T, Ishiwata Y et al. 2003. Effects of experimental
nasal obstruction on human masseter and suprahyoid muscle activities
during sleep. Angle Orthod. 73(2):151-157. “Nasal
obstruction could modulate the activities of the masseter and suprahyoid
muscles during sleep.” [TrPs in the sternocleidomastoid muscle are
known for ability to cause congestion. Other muscles may be part
of the “cause and effect” spiral, and need to be checked as well,
especially in cases of sleep apnea and known myofascial pain. DJS]
Ho IK, Goldschneider KR, Kashikar-Zuck S
et al. 2008. Healthcare utilization and indirect burden among
families of pediatric patients with chronic pain. J Musculoskel
Pain. 16(3):155-164. Preliminary findings suggest that prompt
involvement with a multidisciplinary outpatient treatment program may
reduce significant direct and indirect costs of pediatric chronic pain
patients.
Ho KY, Tan KH. 2006. Botulinum toxin A for
myofascial trigger point injection: a qualitative systematic review.
[Oct 26 Epub ahead of print] Eur J Pain. This database study
concluded that evidence does not support the use of BTA injections for TrPs.
[Many variables could have influenced this conclusion. TrP injections
must be used wisely. BTA injections are experimental, should be
restricted to those patients who temporarily respond to TrP injections with
local anesthetics. Perpetuating factors must still be brought under
control. The clinician performing the injections must scrupulously
practice sound technique, including palpation for TrPs, proper positioning
of the patient and slow range of motion stretches as part of the procedure.
Clinicians who give trigger point injections must be trained and
experienced. Looking at photos of possible TrP sites and giving the
injections as if they were flu shots is not appropriate and can
significantly skew a paper study such as this. DJS]
Ho, M. and J. J. Belch. 1998.
Raynaud’s phenomenon: state of the art in 1998. Scand JRheumatol
27(5):319-22.
Hobson, J. A., R. Stickgold and E. F.
Pace-Schott. 1998. The neuropsychology of REM sleep dreaming.
NeuroReport
9(3):R1-R14.
Hocking G,
Cousins MJ. 2003. Ketamine in chronic pain management: an
evidence-based review. Anesth Analg 97(6):1730-1739. This
review indicates evidence of increase of fibromyalgia pain relief,
endurance, and decreased trigger point tenderness [one must assume that
tender points are meant] with ketamine therapy, but with a narrow
therapeutic window. Perhaps
other NMDA inhibitors such as dextromethorphan might have beneficial effect
without the narrow therapeutic window, and/or might be used to enhance
opioid treatment.
Hodgson, M. J. and H. M. Kipen. 1999.
Gulf War illnesses: causation and treatment. J Occup Environ Med
41(6):443-52.
Hoffman DL, Dukes EM. 2007. The health status
burden of people with fibromyalgia: a review of studies that assessed health
status with the SF-36 or the SF-12. Int J Clin Pract. [Nov 24
Epub ahead of print]. “FM groups had similar or significantly lower
(poorer) physical and mental health status scores compared to those with
rheumatoid arthritis, osteoarthritis, osteoporosis, systemic lupus
erythematosus, myofascial pain syndrome, primary Sjogren’s syndrome and
others. FM groups scored significantly lower than the pain condition
groups mentioned above on domains of bodily pain and vitality.”
“People with FM had an overall health status burden that was greater in
magnitude compared to people with other specific pain conditions that are
widely accepted as impairing.” [What does this indicate about those
patients with FM AND CMP (and perhaps multiple other conditions)? DJS]
Hojsted, J., A. Alban, K. Hagild and J.
Erikson. 1999. Utilization of health care system by chronic pain
patients who applied for disability pensions. Pain
82(3):275-82.
Holick MF, Chen TC, Lu Z et al. 2007. Vitamin D and skin
physiology: A d-lightful stody. J Bone Miner Res 22 (Suppl
2): V-28-33. This article indicates that it is extremely difficult
to get adequate vitamin D from dietary sources. Even foods
normally high in this vitamin are variable. For example, wild
caught salmon have between 75% and 90% more vitamin D(3) than farmed
salmon. [Now that the importance and relative commonality of vitamin D
insufficiency is being accepted, use of light on skin and
supplementation can be critical for patients with chronic pain. DJS]
Holick MF. 2004. Vitamin D:
importance in the prevention of cancers, type 1 diabetes, heart disease, and
osteoporosis.
Am J Clin Nutr 79(3):362-371. "Vitamin D deficiency is often
misdiagnosed as fibromyalgia."
Hollister, L. E. 2000. An
approach to the medical marijuana controversy. Drug Alcohol Depend
58(1-2):3-7.
Holman AJ. 2008. Positional cervical spinal
cord compression and fibromyalgia: a novel comorbidity with important
diagnostic and treatment implications. J Pain. [May 20 Epub
ahead of print]. Co-existing cervical cord compression may exist with
FM. [Much of this may be due to co-existing myofascial trigger points,
and can be treated noninvasively. DJS]
Holsten, F. and B. Bjorvatn. 1997.
[Phototherapy. An alternative for seasonal affective disordersor sleep
disorders. Tidsskr Nor Laegeforen 117(17):2484-2488
[Norwegian].
Holman AJ. 2009. Impulse control
disorder behaviors associated with pramipexole used to treat fibromyalgia.
J Gambl Stud. [Feb 25 Epub ahead of print]. “Objective:
Compulsivity has been associated with use of dopamine agonists used to treat
Parkinson’s disease (PD). Increasing use of these agents to treat
fibromyalgia (FM) raises concern for this unexpected toxicity in a new group
of patients. This is the first report of compulsive gambling and
shopping among patients taking dopamine agonists for treatment of FM.”
“While biologic aspects of PD and FM differ considerably, compulsive
gambling and shopping have become important, yet unexpected concern related
to use of dopamine agonists for patients with FM and their treating
clinicians.”
Holman AJ, Myers RR. 2005. A randomized,
double-blind, placebo-controlled trial of pramipexole, a dopamine
agonist, in patients with fibromyalgia receiving concomitant
medications. Arthritis Rheum. 52(8):2495-2505. “In a
subset of patients with fibromyalgia, approximately 50% of whom required
narcotic analgesia and/or were disabled, treatment with pramipexole
improved scores on assessments of pain, fatigue, function, and global
status, and was safe and well-tolerated.”
Holland, N. W. and E. B. Gonzalez.
1998. Soft tissue problems in older adults. Clin Geriatr Med
14(3):601-11.
Holzberg, A. D., M. E. Robinson, M. E.
Geisser and H. A. Gremillion. 1996. The effects of depression
and chronic pain on psychosocial and physical functioning. Clin J
Pain 12(2):118-125.
Homko, C. J. , E. Sivan, E. A. Reece and G.
Boden. 1999. Fuel metabolism during pregnancy. Semin Reprod Endocrinol
17(2):119-25.
Hong C. 2004. Myofascial pain therapy.
J Musculoskeletal Pain 12(3/4):37-43. “Myofascial pain should
be appropriately treated to inactivate TrPs completely and to avoid
recurrence permanently.” This is a good overview of common options in
the treatment of TrPs.
Hong CZ. 2000. Specific sequential myofascial
trigger point therapy in the treatment of a patient with myofascial pain
syndrome associated with reflex sympathetic dystrophy: commentary.
Australas Chiropr Osteopathy 9(1):7-11.
Hong CZ. 2002. New trends in myofascial pain
syndrome. Zhonghua Yi Xue Za Zhi 65(11):501-512. This is
a good overview of current findings in myofascial medicine.
Hong CZ. 2006. Treatment of myofascial pain
syndrome. Curr Pain Headache Rep. 10(5):345-349.
“Effective MTrP therapies include manual therapies, physical therapy
modalities, dry needling, or MTrP injection. It is also important to
eliminate any perpetuating factors and provide adequate education and home
programs to patients so that recurrent or chronic pain can be avoided.”
Hong CZ. 1994. Lidocaine injection versus
dry needling to myofascial trigger point. The importance of
the local twitch response. Am J Phys Med Rehabil
73(4):256-263. “Lidocaine reduces the intensity and duration
of postinjection soreness compared with that produced by dry
needling.” [This is important to remember for patients who
also have the central sensitization of FM. The pain of dry
needling may needlessly further sensitize the central nervous system
in some patients with both FM and TrPs. DJS]
Hong CZ. 2002. New trends in myofascial pain syndrome.
Zhonghua Yi Xue Za Zhi 65(11):501-512. Myofascial TrP
therapies include “...stretch, massage, thermotherapy, electrotherapy,
laser therapy, MTrP injection, dry needling, and acupuncture.”
[Dry needling is not recommended if the patient also has central
sensitization such as fibromyalgia. DJS]
Hong CZ. 1994. Lidocaine injection versus dry needling to
myofascial trigger point. The importance of the local twitch
response. Am J Phys Med Rehabil 73(4):256-263.
“Patients treated with dry needling had post-injection soreness of
significantly greater intensity and longer duration than those treated
with lidocaine injection. It is essential to elicit LTRs during
injection to obtain an immediately desirable effect. TrP injection
with 0.5% lidocaine is recommended, because it reduces the intensity and
duration of post-injection soreness compared with that produced by dry
needling.”
Hong C-Z. 2002. New trends in
myofascial pain syndrome. Zhonghua Yi Xue Za Zhi (Taipei)
65(11):501-12. Review article. “The pathogenesis of [myofascial
trigger points] MTrPs appears to be related to the integration in the spinal
cord (formation of MTrP circuits) in response to the disturbance of the
nerve endings and abnormal contractile mechanism at multiple dysfunctional
endplates.”
Hong, C-Z. 1999. Current research on
myofascial trigger points-pathophysiological studies. J Musculoskel Pain
7(1-2):121-129.
Hong C-Z and T-C Hsueh. 1996. “The
difference in pain relief after trigger point injections in myofascial pain
in patients with and without fibromyalgia.” Arch Phys Med Rehabil
77:1161-1166.
Hong, C-Z, and J. Yu. 1998.
Spontaneous electrical activity of rabbit trigger after transection of
spinal cord and peripheral nerve. J Musculoskel Pain 6(4):45-58.
Hong, C. Z. and D. G. Simons. 1998.
Pathophysiologic and electrophysiologic mechanisms of myofascial trigger
points. Arch Phys Med Rehabil 79(7):863-72.
Hong, C. Z., T. S. Kuan, J. T. Chen and S.
M. Chen. 1997. Referred pain elicited by palpitation and by
needling of myofascial trigger points: a comparison. Arch Phys Med
Rehabil 78(9):957-960.
Hong, C. Z. 1996.
Pathophysiology of myofascial trigger point. J Formos Med Assoc
92(2):93-104.
Hooper MM, Stellato TA, Hallowell PT et al.
2006. Musculoskeletal findings in obese subjects before and
after weight loss following bariatric surgery. Int J Obes
(Lond) [Apr 25 Epub ahead of print] “There was a higher
frequency of multiple MSK (musculoskeletal) complaints, including
non-weight-bearing sites compared to historical controls, before
surgery, which decreased significantly at most sites following
weight loss and physical activity. These benefits may improve
further, as weight loss may continue for up to 24 months. The
benefits seen with weight loss indicate that prevention and
treatment of obesity can improve MSK health and function.”
[Obesity can be a major perpetuating factor. DJS]
Hopman-Rock, M., F. W. Kraaimaat, E. Odding
and J. W. Bijlsma. 1998. Coping with pain in the hip or knee in
relation to physical disability in community-living elderly people.
Arthritis Care Res
11(4):243-52.
Hopwood, M. B. and S. E. Abram. 1994.
Factors associated with failure of trigger point injections. Clin J
Pain
10:227-234.
Horne,. J. and L. Reyner. 1999. Vehicle
accidents related to sleep: a review. Occup Environ Med 56(5):289-94.
Horning, M. R. 1997. Chronic opioids:
a reassessment. Alaska Med 39(4):103-110.
Horowits, R. 1999. The physiological
role of titin in striated muscle. Rev Physiol Biochem Pharmacol
138:57-96.
Horven, S., T. C. Stiles, A. Holst and T.
Moen. 1992. HLA antigens in primary fibromyalgia syndrome. J.
Rheumatol 19(8):1269-70.
Hoseini SS, Hoseini M, Gharibzadeh S. 2005.
Sprouting phenomenon, a new model for the role of A-beta fibers in wind up.
Med Hypotheses [Dec 12 Epub ahead of print] “In this study, we
have proposed a new model for the role of Abeta fibers in wind up, through
sprouting of nerve fibers in the dorsal horn of spinal cord. We named
it “sprouting phenomenon”. It has been reported that in some clinical
hyperalgesic states induced by peripheral injury or inflammation, wind up
may aggravate the pain. Studies have indicated the presence of
…fibromyalgia syndrome…. According to sprouting phenomenon, it seems
that some clinical interventions can be assessed to alleviate
post-inflammatory pains: (1) immediate and complete relief of inflammation
by anti-inflammatory agents to prevent repetitive excitation of C-fibers and
subsequent morphological changes of dorsal horn laminae; (2) using local
anesthetics in order to prevent pain signal transmission; (3) prevention of
sprouting by intrathecal injection of some anti-proliferation agents; (4)
using NMDA or NK1 receptor antagonists to prevent central mechanism of wind
up.” “Future clinical studies are needed…”
Hotamisligil GS. 2003. Inflammatory
pathways and insulin action. Int J Obes Relat Metab Disord.
27 Suppl 3:S53-55. “Obesity and type 2 diabetes are associated
with a state of abnormal inflammatory response. The state of
chronic inflammation typical of obesity and type 2 diabetes occurs
at metabolically relevant sites, such as the liver, muscle, and most
interestingly, adipose tissues. Interference with these
pathways improves or alleviates insulin resistance. The
abnormal production of tumor necrosis factor alpha (TNF-alpha) in
obesity is a paradigm for the metabolic significance of this
inflammatory response. When TNF-alpha activity is blocked in
obesity, either biochemically or genetically, the result is improved
insulin sensitivity.”
Hotamisligil GS. 2003. Inflammatory pathways and insulin action.
Int J Obes Relat Metab Disord. 27 Suppl 3:S53-55. “Obesity
and type 2 diabetes are associated with a state of abnormal inflammatory
response. The state of chronic inflammation typical of obesity and
type 2 diabetes occurs at metabolically relevant sites, such as the
liver, muscle, and most interestingly, adipose tissues. …interference
with these pathways improve or alleviate insulin resistance.
Recent years have seen a critical progress in this respect by the
identification of several downstream mediators and signaling pathways,
which provide the crosstalk between inflammatory and metabolic
signaling.”
Hou C.R., Chung K.C., Chen J.T. et
al. 2002. Effects of a calcium channel blocker on electrical activity
in myofascial Trigger spots in rabbits. Am J Phys Med Rehabil
81(5):342-9. Calcium channel
blockers are effective inhibitors of myofascial trigger point spontaneous
electrical activity.
Hou C.R., Tsai L.C., Cheng K.F. et al.
2002. Immediate effects of various physical therapeutic modalities on
cervical myofascial pain and trigger-point sensitivity. Arch Phys
Med Rehabil 83(10):1406-14. “Results suggest that therapeutic
combinations such as hot pack plus active ROM and stretch with spray, hot
pack plus active ROM and stretch with spray as well as TENS, and hot pack
plus active ROM and interferential current as well as myofascial release
technique, are most effective for releasing MtrP pain and increasing
cervical ROM.”
Hou, C-R, K-C Chung, J-T Chen. 1991. The effect
of calcium channel blocker on spontaneous potentials of trigger points in
rabbits: Clin J of Biomed Eng
18(3):143-149.
Houtmeyers, E., R. Gosselink, G.
Gayan-Ramirez and M. Decramer. 1999. Effects of drugs on mucus
clearance. Eur Respir J
14(2):452-67.
Hrebicek J, Janout
V, Malincilova J, Horakova D, Cizek L. Detection of insulin resistance by
simple quantitative insulin sensitivity check index QUICKI for
epidemiological assessment and prevention.
J Clin Endocrinol Metab Jan;87(1):144-7.
Hrycaj P, Stratz T, Mennet P et al. 1996.
Pathogenetic aspects of responsiveness to ondansetron
(5-hydroxytryptamine type 3 receptor antagonist) in patients with
primary fibromyalgia syndrome — a preliminary study. J
Rheumatol 23(8):1418-1423. “Ondansetron appears to be an
effective drug in about 50% of patients with FM. There may be two
subsets of patients with FM that differ clinically and pathogenetically
with regard to the disturbance in the 5-HT-3R system.”
Hsieh YL, Kao MJ, Kuan TS et al. 2007.
Dry needling to a key myofascial trigger point may reduce the irritability
of satellite MTrPs. Am J Phys Med Rehabil. 86(5):397-403.
“This study supports the concept that activity in a primary MTrP leads to
the development of activity in satellite MTrPs and the suggested spinal cord
mechanism responsible for this phenomenon.”
Hsieh C.Y., Hong C. Z., Adams A. H., Platt
K. J. , Danielson C. D. , Hoehler F. K., and Tobis JS 2000. Interexaminer
reliability of the palpation of trigger points in the trunk and lower limb
muscles. Arch Phys Med Rehabil 81(3):258-64.
Hsu HC, Hong CZ. 2008. Floating
kidney with chronic myofascial pain syndrome in the abdominal muscles as the
major clinical manifestation: a case report. J Musculoskel Pain.
16(3):199-204. “Myofascial pain syndrome in the abdominal muscles
may be caused by a floating kidney. Treating an underlying
pathological lesion is important when attempting to eliminate TrPs.” When
myofascial trigger point pain recurs after adequate treatment, the
perpetuating factor(s) must be found and brought under control.
Hsu J.C., Lee Y.S.., Chang C.N. et al.
2002. Sleep deprivation affects nitric oxide synthesis and glial
reactions in the rat hippocampus. Glia (Suppl 1):S51 [Abstract].
Hsueh, T. C., S. Yu, T. S. Kuan and C. Z.
Hong. 1998. Association of active myofascial trigger points and
cervical disc lesions. J Formos Med Assoc 97(3):174-180.
Hsueh, T-C. , P. T. Cheng, T. S. Kuan and
C-Z Hong. 1997. The immediate effectiveness of electrical nerve stimulation
and electrical muscle stimulation on myofascial trigger points. 1997.
Am J Phys Med Rehabil
76(6):471-476.
Hu, F. B., M. J. Stampfer, J. E. Manson, E.
Rimm, G. A. Colditz, F. E. Speizer, C. H. Hennekens and W. C. Willett.
1999. Dietary protein and risk of ischemic heart disease in women.
Am J Clin Nutr 70(2):221-7.
Hubbard, D. R. and G. M. Berkoff.
1993. Myofascial trigger points show spontaneous needle EMG activity.
Spine
18(13):1803-7. Sustained spontaneous EMG activity was found in the 1-2
mm nidus of all TrPs, and was absent in non-TrPs.
Hubbell, S. L. and M. Thomas. 1985.
Postpartum cervical myofascial pain syndrome: review of four patients.
Obstet Gynecol
65(3 Suppl):56S-57S.
Huber R, Ghilardi MF, Massimini M et al.
2004. Local sleep and learning. Nature
430(6995):78-81. The amount of slow-wave activity in right brain areas
can help consolidate new learning. It is important for medical
teams to help FM patients regain deep level sleep.
Hudson JL, Arnold LM, Keck PE et al. 2004.
Family study of fibromyalgia and affective spectrum disorder.
Biol Psychiatry 56(11):884-891. This study found that FM was
associated with the other medical and psychiatric disorders that are
proposed to be grouped as affective spectrum disorder. [Since FM
does not cover a homogenous group, lumping it as such with a group of
medical and psychiatric disorders could add to the confusion. DJS]
Hudson J.I., Mangweth B., Pope H.G. et al.
Family study of affective spectrum disorder. Arch Gen Psychiatry.
This study suggests that some disorders such as ADHD, IBS, migraine, OC,
PTSD, fibromyalgia and other conditions may share a genetic predisposition,
as these conditions are often found clustered in families.
Hudson, N., M. A. Fitzcharles, M. Cohen, M.
R. Starr and J. M. Esdaile. 1998. The association of soft-tissue
rheumatism and hypermobility. Br J Rheumatol 37(4):382-6.
Hudson, N., M. R. Starr, J. M. Esdaile and
M. A. Fitzcharles. 1995. Diagnostic associations with hypermobility in
rheumatology patients. Br J Rheumatol 34(12):1157-1161.
Hudson, T. 2000. Fibrocystic
breasts. Women’s Health Update. Townsend Letter for Doctors &
Patients
Jan:142-3.
Hughes G, Martinez C, Myon E et al. 2005. The
impact of a diagnosis of fibromyalgia on health care resource use by primary
care patients in the UK: an observational study based on clinical practice.
Arthritis Rheum. 54(1):177-183. “Being diagnosed as having FM
may help patients cope with some symptoms, but the diagnosis has a limited
impact on health care resource use in the longer term, possibly because
there is little effective treatment.” [This could also be because
insurance companies do not cover nor many health care resources provide
effective treatment regiments. DJS]
Humphreys BK, Kenin S, Hubbard BB et al. 2003. Investigation of
connective tissue attachments to the cervical spinal dura mater.
Clin Anat. 16(2):152-159. Common but previously unremarked
connective tissue attachments originating from the nuchal ligament and
rectus capitis posterior minor muscle to the dura may play a significant
role in neck pain.
Huppe A, Brockow T,
Raspe H. 2004. [Chronic widespread pain and tender points in low back
pain: a population-based study].
Z Rheumatol 63(1):76-83. [German] These researchers did
not find fibromyalgia to be a common and significant factor in low back
pain.
Hurtig IM, Raak RI,
Kendall SA, Gerdle B, Wahren LK. Quantitative sensory testing in
fibromyalgia patients and in healthy subjects: identification of subgroups.
Clin J Pain
Dec:17(4):316-22,2001. There are distinct subgroups of FM patients
that have different cold pain thresholds. These groups have differences in
sleep quality, pain intensity, and number of tender points.
Huysmans MA, Hoozemans MJ, van der Beek AJ et al.
2007. Fatigue effects of tracking performance and muscle activity.
[Jan 5 Epub ahead of print] J Electromyogr Kinesiol.
Hwang M,
Kang YK, Shin JY et al. 2005. Referred pain
pattern of the abductor pollicis longus muscle. Am J Phys Med Rehabil.
84(8):593-597. “Referred pain patterns of the abductor pollicis
longus resemble pain experienced in de Quervain’s tenosynovitis.
Thus, identification of the abductor pollicis longus trigger point
should be considered in pain of the radial aspect of the wrist and
thumb, especially when no other neurologic abnormalities or inflammatory
conditions are present.”
Hwang M, Kang YK, Kim DH. 2005. Referred
pain pattern of the pronator quadratus muscle. Pain
[Epub ahead of print June 16th] This paper
describes two main pain patterns of pronator quadratus myofascial
trigger points.
Ibanez-Garcia J,
Alburquerque-Sendin F, Rodriguez-Blanco C et al. 2008. Changes in
masseter muscle trigger points following strain-counterstrain or neuro-muscular
technique. J Bodywork Move Ther. 13(1):3-10. “Our
results suggest that neuromuscular or strain-counterstrain technique
might be employed in the management of latent MTrPs in the masseter
muscle.”
Igaz P, Novak I, Lazaar E et al. 2001.
Bidirectional communication between histamine and cytokines.
Inflamm Res. 50(3):123-128. “Histamine plays fundamental roles
in numerous immune reactions. In addition to its
well-characterized effects in the acute inflammatory and allergic
responses, histamine also influences the expression and actions of
several cytokines. Because antihistamines are widely used in the
treatment of various human diseases, this complex interaction could have
general medical relevance too.”
Ignatowski TA, Spengler RN. 2004. Tumor
necrosis factor-alpha quantification and expression by insitu hybridization.
Methods Mol Biol 196:85-96.
Antidepressants may work as pain relievers by inhibiting production of the
inflammatory protein tumor necrosis factor in the brain.
Iguchi M., Katoh Y., Koike H. et al. 2002.
Randomized trial of trigger point injection for renal colic. Int J
Urol 9(9):475-479. “Trigger point injection, in our experience, is
an easy, safe and effective method for the amelioration of renal colic."
Ikeda H, Murase K. 2004. Glial nitric oxide-mediated long-term
presynaptic facilitation revealed by optical imaging in rat spinal
dorsal horn. J Neurosci. 24(44):9888-9896.
“Activity-dependent LTP of nociceptive afferent synaptic transmission
the spinal cord is believed to underlie central sensitization after
inflammation nerve injury. This glial NO-mediated control of presynaptic
excitation may contribute to the induction at least in part.”
Ilbuldu E, Cakmak A, Disci R et al. 2004. Comparison of laser, dry needling,
and placebo laser treatments in myofascial pain syndrome. Photomed
Laser Surg. 22(4):306-311. “Laser therapy could be useful as a
treatment modality in myofascial pain syndrome because of its
noninvasiveness, ease, and short-term application.”
Ilkjaer,
S., J. Dirks, J. Brennum, M. Wernberg and J. B. Dahl. 1997.
Effect of systemicN-methyl-D-aspartate receptor antagonist
(dextromethorphan) on primary and secondary hyperalgesia in humans.
Br J Anaesth
79(5):600-605.
Imamura M, Hsing WT, Kaziyama H et al. 2007.
Hyperalgesia of central origin in patients with severe
osteoarthritis of the knee. J Musculoskel Pain 15 (Supp
13):25 item 40. [Myopain 2007 Poster] “There is a
significant deficit in the PPT in all spinal levels studied. CS
(central sensitization) needs to be addressed as part of the treatment.”
[Central sensitization is often unacknowledged and untreated in
osteoarthritis, as are co-existing MTPs. Peripheral pain can cause
and maintain central sensitization, but the hypersensitive central
nervous system must be treated to enable the peripheral areas to better
respond to their treatment. DJS]
Imamura M, Kaziyama HHS, Hsing WT et al. 2007.
Efficacy of a segmental neuromyotherapy approach to improve pain pressure
threshold in patients with severe osteoarthritis of the knee. J
Musculoskel Pain 15 (Supp 13):25 item 39. [Myopain 2007 Poster]
“Segmental neuromyotherapy improved PPT immediately and after three months
of treatment.” [Sclerodermal hyperalgesia of the supraspinous ligaments in
addition to MTPs are often a vital yet unacknowledged and untreated
component of osteoarthritic pain. DJS]
Imamura, S.T., T.Y. Lin, M.J. Yriyrits,
S.S. Fischer, R.J. Azze, L. A. Rosgano and R. Mahar. 1997. The importance of
myofascial pain syndrome in reflex sympathetic dystrophy. Phys Med Rehab
Clinics of North Am 8:207-211.
Imbierowicz K., Egle U.T. 2003.
Childhood adversities in patients with fibromyalgia and somatoform pain
disorder. Eur J Pain 7(2):113-9. This study in primary
FM found that “The FM patients show the highest score of childhood
adversities. In addition to sexual and physical maltreatment, the FM
patients more frequently reported a poor emotional relationship with both
parents, a lack of physical affection, experiences of the parent’s physical
quarrels, as well as alcohol or other problems of addiction in the mother,
separation, and a poor financial situation before the age of 7.”
Inanici F, Yunus MB. 2004. History of
fibromyalgia: past to present. Curr Pain Headache Rep.
8(5):369-378. ”Fibromyalgia syndrome (FM) is now a recognized
clinical entity causing chronic and disabling pain.”
Ingber DE. 2008. Tensegrity and
mechanotransduction. J Bodywork Move Ther. 12(3):198-200.
This interesting article explains the malleability of the human body, and
how external forces such as massage and other intentional bodywork can
create ripple effects of movement on a cellular level, creating deep changes
in the tissues via the mechanotransduction process.
Ingber, R. S. 1989. Iliopsoas
myofascial dysfunction: a treatable cause of “failed” low back syndrome.
Arch Phys Med Rehabil 70(5):382-6.
Ingebrigtsen, T., B. Romner, K.
Waterloo and J. H. Trumpy. 1996. [Minor head injuries in sport. Occurrence,
management, sequelae and prevention.] Tidsskr Nor Laegeforen
116(30):3594-3597. [Norwegian].
Ingman T, Nieminen T, Hurmerinta K. 2004. Cephalometric comparison
of pharyngeal changes in subjects with upper airway resistance syndrome
or obstructive sleep apnoea in upright and supine positions.
Eur J Orthod 26(3):321-326. “The present results suggest that
OSA patients are prone to significant narrowing of their oropharyngeal,
but not of their naso- or hypopharyngeal, airways in the supine
position. Thus, treatment of OSA and UARS patients should mainly
be aimed at preventing further oropharyngeal airway narrowing as a
result of supine-dependent sleep.”
Innes KE, Selfe TK, Taylor AG. 2008. Menopause, the metabolic
syndrome, and mind-body therapies. Menopause. [Apr 17 Epub
ahead of print]. This paper explains the rise in the occurrence of
insulin resistance during menopause as well as the link between insulin
resistance and cardiovascular disease, mood dysfunction, and sleep
dysfunction.
Innes, K. E. and J. H. Wimsatt. 1999.
Pregnancy-induced hypertension and insulin resistance: evidence for a
connection. Acta Obstet Gynecol Scand 78(4):263-84.
Inoue K, Tsuda M, Koizumi S. 2004. Chronic pain and microglia: the
role of ATP. Novartis Found Symp. 261:55-64.
Inturrisi, C. E., W. A. Colburn, R. F.
Kaiko, R. W. Houde and K. M. Foley. 1987. Pharmacokinetics and
pharmacodynamics of methadone in patients with chronic pain. Clin
Pharmacol Ther 41(4):392-401.
Ionescu-Tirgoviste, C. 1998.
Proposal for a new classification of diabetes mellitus. Rom J Intern Med
36(1-2):121-34.
Irwin MR, Olmstead R, Oxman MN. 2007.
Augmenting immune responses to varicella zoster virus in older adults: a
randomized, controlled trial of tai chi. J Am Geriatr Soc.
55(4):511-517. “Tai Chi augments resting levels of VZV-specific CMI
and boosts VZV-CMI of the varicella vaccine.” Regular practice of t’ai
chi boosted cell-mediated immunity in immunized patients.
Irwin, M., J. McClintick, C. Costlow, M.
Fortner, J. White and J. C. Gillin. 1996. Partial night sleep deprivation
reduces natural killer and cellular immune responses in humans.
FASEB J10(5):643-653.
Irwin RS, Madison JM. 2000. Anatomical
diagnostic protocol in evaluating chronic cough with specific reference to
gastroesophageal reflux disease. Am J Med. 108 Suppl
4a:126S-130S. “Gastroesophageal reflux disease (GERD), along with
postnasal drip syndrome (PNDS) and asthma, is one of the three most common
causes of chronic cough in all age groups. When GERD is the cause of
chronic cough, there may be no gastrointestinal (GI) symptoms up to 75% of
the time, and, in these cases, the term ‘silent GERD’ is used.”
Irwin RW, Zuhosky JP, Sullivan WJ et al. 2007. Industrial medicine
and acute musculoskeletal rehabilitation. 4. Interventional
procedures for work-related cervical spine conditions. Arch
Phys Med Rehabil. 88(3 Suppl 1):S18-S21. An overview,
including myofascial pain.
Isomaa B. 2003. A major health
hazard: the metabolic syndrome. Life Sci 73(19):2395-2411.
“The metabolic syndrome seems to result from a collision between
susceptible ‘thrifty genes’ and a society characterized by an increased
prevalence of obesity and a sedentary lifestyle.” “The metabolic
syndrome constitutes a major challenge for public health…since more than
40 million U.S. adults seem
to be affected…. Lifestyle changes could have a profound influence
on the syndrome and its development.”
Israel HA, Ward JD. Horrell B, et al. 2003.
Oral and maxillofacial surgery in patients with chronic orofacial pain.
J Oral Maxillofac Surg 61(6):662-7.
“Misdiagnosis and multiple failed treatments were common in these
patients with chronic orofacial pain ..... surgical treatment was rarely
indicated as a treatment for pain relief ..... and it exacerbated and
perpetuated pain symptoms in some of them.”
Isomaa B. 2003. A major health hazard: the
metabolic syndrome. Life Sci 73(19):2395-2411. “The metabolic syndrome
seems to result from a collision between susceptible ‘thrifty genes’ and
a society characterized by an increased prevalence of obesity and a
sedentary lifestyle.” “The metabolic syndrome constitutes a major
challenge for public health…since more than 40 million U.S. adults seem
to be affected…. Lifestyle changes could have a profound influence on
the syndrome and its development.”
Itoh K, Hirota S, Katsumi Y et al. 2008.
Trigger point acupuncture for treatment of knee osteoarthritis – a
preliminary RCT for a pragmatic trial. Acupunct Med.
26(1):17-26. “These results suggest that trigger point acupuncture
therapy may be more effective for osteoarthritis of the knee in some
elderly patients than standard acupuncture therapy.” [This study
may indicate that treating the associated myofascial trigger points
results in more effective therapy of osteoarthritis of the knee. DJS]
Itoh K, Okada K. 2007. Influence of
ovariectomy on development of delayed onset muscle soreness in female
rates. J Musculoskel Pain 15 (Supp 13):26 item 42.
[Myopain 2007 Poster] “In the present study, the muscle pain
thresholds were influenced by the estrus cycle in the intact control
female rates. The delay of development of muscular hyperalgesia
was also detected in the OVX rats. These results suggest that the
change of estrogen content might be a possible influence on the
sensitivity of nociceptive process.” [This meshes well with other
research that suggests that changes in estrogen may be involved in pain
modulation. DJS]
Itoh K, Katsumi Y, Hirota S
et al. 2006. Effects of trigger point acupuncture on chronic low
back pain in elderly patients – a sham-controlled randomized trial.
Acupunct Med. 24(1):5-12. “These results suggest that
trigger point acupuncture may have greater short term effects on low
back pain in elderly patients than sham acupuncture.”
Itoh, Y, T Igarashi, N Tatsuma, T Imai, J
Yoshida, M Tsuchiya, M Murakami and Y Fukunaga. 1999. [Autoimmune
fatigue syndrome and fibromyalgia syndrome.] Nippon Ika Daigaku Zasshi
66(4):239-44.
Ivanichev GA, Kuznetsova EA. 2007. [Evoked
potentials in patients with myofascial pain syndrome in the late residual
period of natal cervical trauma.] Zh Nevrol Psikhiatr Im S S
Korsakova 107(4):49-53. [Russian] Specific audio testing indicates
that dysfunction in the somatosensory pathway of the brainstem is common in
patients with cervical spine birth trauma, “...being most significant in
patients with severe myofascial pain syndrome.”
Iverson L. 2004. GABA
pharmacology–what prospects for the future? Biochem Pharmacol
68(8):1537-1540. Gaboxadol (THIP) is one of the new
non-benzodiazepine hypnotics that acts on GABA A receptors. This
type of medication shows promise as a more specific type of sleep
medication.
Iwama H, Akama Y. 2000. The superiority of water-diluted 0.25% to
neat 1% lidocaine for trigger-point injections in myofascial pain
syndrome: a prospective, randomized, double-blinded trial.
Anesth Analg 91(2):408-409. “Trigger-point injection with a
mixture of commercially available 1% lidocaine in sterile distilled
water at a ratio of 1:3 compared with 1% lidocaine alone resulted in
better efficacy and less injection pain.” [Travell and Simons also
reported better effects with diluted local anesthetic. DJS]
Iwasaka, M., Ueno, S. 2003. Detection of
intracellular macromolecule behavior under strong magnetic fields by
linearly polarized light. Bioelectromagnetics
24(8):564-70. Strong static magnetic fields caused behavioral changes
in cell components that corresponded to changes in polarized light.
The intracellular macromolecular arrangement may be affected by these
fields.
Izquierdo-Alvarez S, Bocos-Terraz JP,
Bancalero-Flores JL et al. 2008. Is there an association between
fibromyalgia and below-normal levels of urinary cortisol? BMC
Res Notes. 1:134. “Our study confirms that women with FM have
significantly lower urinary cortisol levels than healthy women.”
Jackman
RP, Purvis JM, Mallett BS. 2008. Chronic nonmalignant pain in
primary care. Am Fam Physician. 78(10):1155-1162.
Jackson MJ. 2005. Use of microdialysis to study interstitial
nitric oxide and other reactive oxygen and nitrogen species in skeletal
muscle. Methods Enzymol. 396:514-525.
Jacob L, Jacob T, Jacob B. 2007.
Escitaloproan for fibromyalgia and multiple chemical sensitivity
syndrome: Tolerable efficacy. J Musculoskel Pain
15(Suppl 13):50. item 87. Escitalopran (Lexapro) seems
to help FM pain even if patients don't have MCS, and it appears
to be well tolerated and have few side-effects.
Jacobson BC, Somers SC, Fuchs CS et al.
2006. Body-mass index and symptoms of gastroesophageal
reflux in women. N Engl J Med. 354(22):2340-2348.
“BMI is associated with symptoms of gastroesophageal reflux
disease in both normal-weight and overweight women. Even
moderate weight gain among persons of normal weight may cause or
exacerbate symptoms of reflux.” [Obesity, or even
overweight, may be an important perpetuating factor for GERD,
which itself is an important perpetuating factor for sleep
apnea, fibromyalgia and some myofascial TrPs. DJS]
Jacobson PL, Mann JD. 2003. Evolving role of the neurologist in the
diagnosis and treatment of chronic noncancer pain. Mayo Clin Proc
78(1):80-84. “The neurologist has become increasingly involved in the
multidisciplinary treatment of patients with chronic noncancer pain.
Informed regulatory agencies and professional organizations such as the
American Academy of Neurology recognize the undertreatment of patients
with CNP and provide clear recommendations to help neurologists in the
ethical and effective treatment of patients with pain. Improved
education of neurologists, other health care professionals, patients,
and the media about evolving standards of pain care and therapy will
produce a more supportive environment for the compassionate and ethical
treatment of patients with CNP."
Jacobson PL, Mann JD. 2003. Evolving role of
the neurologist in the diagnosis and treatment of chronic noncancer
pain. Mayo Clin Proc. 78(1):80-84. “Informed
regulatory agencies and professional organizations such as the American
Academy of Neurology recognize the undertreatment of patients with CNP
and provide clear recommendations to help neurologists in the ethical
and effective treatment of patients with pain. Improved education
of neurologists, other health care professionals, patients, and the
media about evolving standards of pain care and therapy will produce a
more supportive environment for the compassionate and ethical treatment
of patients with CNP.”
Jacobsen,
S., I.S. Petersen and B. Danneskiold-Samsoe. 1993.Clinical features in
patients with chronic muscle pain-with special reference to fibromyalgia.
Scand J Rheumatol 22(2):69-76.
Jacobsen, S. and B. Danneskiold-Samsoe.
1992. Dynamic muscular endurance in primary fibromyalgia compared with
chronic myofascial pain syndrome.
Arch Phys Med Rehab 73(2):170-173.
Jacobsen, S., M. Hoyer-Madsen, B.
Danneskiold-Samsoe and A. Wiik. 1990. Screening for autoantibodies in
patients with primary fibromyalgia syndrome and a matched controlled group.
APMIS 98(7):655-8.
Jacobsen, S. 1998. Physical
biodynamics and performance capacities of muscle in patients with
fibromyalgia syndrome. Z Rheumatol Suppl 57 (2):43-6.
Jain AK, Carruthers BM, van de Sande MI, Barron SR,
Donaldson CCS, Dunne JV, Gingrich E, Heffez DS, Leung FYK, Malone DG,
Romano TJ, Russell IJ, Saul D, Seibel DG. 2003. Fibromyalgia
syndrome: Canadian clinical working case definition, diagnostic and
treatment protocols – a consensus document. J Musculoskel Pain
11(4):3-107.
James G., Butt A.M. 2002. P2Y and P2X
purinoceptor medicated Ca (2+) signaling in glial cell pathology in the
central nervous system. Eur J Pharmacol
447(2-3):247-60. This research suggests that ATP is a primary glial
cell signal molecule in response to central nervous system injury, and that
the named receptors are involved with this response.
Jamison, J. 1999. Stress: the
chiropractic patients’ self-perceptions. J Manipulative Physiol
Ther 22(6):395-8.
Jamison, R. N. 1996.
Comprehensive pretreatment and outcome assessment for chronic opioid therapy
in nonmalignant pain. J Pain Symptom Manage 11(4):231-241.
Jamison, R. N., K. O. Anderson and M. A.
Slater. 1995. Weather changes and pain: perceived influence of
local climate on pain complaint in chronic pain patients. Pain
61(2):309-315.
Jamison, R. N., K. O. Anderson, C.
Peeters-Asdourian and F. M. Ferrante. 1994. Survey of opioid use
in chronic nonmalignant pain patients. Reg Anesth
19(4):225-230.
Jan, J. E., M. B. Connolly, D. Hamilton, R.
D. Freeman and M. Laudon. 1999. Melatonin treatment of
non-epileptic myoclonus in children. Dev Med Child Neurol
41(4):255-9.
Janal MN, Ciccone DS, Natelson BH. 2006.
Sub-typing CFS patients on the basis of ‘minor’ symptoms. Biol
Psychol. [Feb 9 Epub ahead of print] “In 161 women meeting
1994 criteria for CFS, principal components analysis of the ten ‘minor’
symptoms of CFS produced three factors interpreted to indicate
musculoskeletal, infectious and neurological subtypes. Extreme scores
on one or more of these factors characterized about 2/3 of the sample.”
“Results suggest that subtypes of CFS may be identified from reports of the
minor diagnostic symptoms, and that these subtypes demonstrate construct
validity.”
Janig, W., H.
Blumberg, R. A. Boas et al. 1991. The reflex sympathetic dystrophy
syndrome: consensus statement and general recommendations for diagnosis and
clinical research. In Bond, M. R., J. E. Charleton and C. J. Woolf (eds):
Proceedings of the VI th World Congress on Pain. Elsevier,
Amsterdam, 1991, pp. 373-376.
Jankovic D, van Zundert A. 2006. The frozen
shoulder syndrome. Description of a new technique and five case
reports using the subscapular nerve block and subscapularis trigger point
infiltration. Acta Anaesthesiol Belg. 57(2):137-143.
Jansson C, Nordenstedt H, Wallander MA et
al. 2009. A population-based study showing an association between
gastroesophageal reflux disease and sleep problems. Clin
Gastroenterol Hepatol. [Mar 12 Epub ahead of print]. “A large,
population-based study indicates a link between sleep problems and
gastroesophageal reflux disease that might be bi-directional.” [This is a
very good example of interactive diagnoses. Also, both FM and TrPs can be
interactive with both sleep problems and GERD. Working on any one of these
conditions may help the others, and each of them may worsen the others. DJS]
Jaracz J, Rybakowski J. 2005. [Depression and
pain: novel clinical, neurobiological and psychopharmacological data]
Psychiatr Pol. 39(5):937-950. [Polish] “In the pathogenesis
of both depression and pain symptoms, an important role has been attributed
to disturbances of serotonergic and noradrenergic neurotransmission as well
as to neuropeptides such as opioids and substance P. In mood
regulation as well as in the perception and emotional dimension of pain
stimuli, such brain structures as the amygdala, anterior cingulate cortex
and prefrontal cortex are of main significance. The action of
antidepressant drugs results in a normalization of the activity of those
neurotransmitter systems an brain structures. It was found that dual
action antidepressants (i.e., influencing both serotonergic and
noradrenergic system) such as tricyclic antidepressants and new generation
drugs (venlafaxine, milnacipram, duloxetine, mirtazapine) exert a stronger
antidepressant effect and possess a broader therapeutic spectrum, including
also an effect on pain symptoms.”
Jarrell J. 2008. Gynecological pain and the viscero-somatic connection. J Musculoskel Pain
16(1-2):21-27. “Myofascial dysfunction is common
in the presence of endometriosis and visceral disease. There is an
interesting relationship of the number of reported laparoscopies and the
number of areas of myofascial dysfunction. This may reflect the
severity of the visceral disease being treated at laparoscopy but also
raises the possibility that laparoscopy may in some way exacerbate the viscero-somatic appreciation of pain physiology.”
Jarrell JF, Vilos GA,
Allaire C et al. 2005. Consensus guidelines for the management of
chronic pelvic pain. J Obstet Gynaecol Can. 27(8):781-826.
Myofascial pain must be taken into account when looking for possible causes
of chronic pelvic pain.
Jarrell J. 2004.
Myofascial dysfunction in the pelvis. Curr Pain Headache Rep
8:452-456. Between 25% and 40% of all laparoscopy for pelvic pain
finds no cause. Myofascial pain due to TrPs may be a significant and
unrecognized cause of much pelvic pain.
Jason LA, Taylor RR, Kennedy CL. 2000. Chronic fatigue syndrome,
fibromyalgia, and multiple chemical sensitivities in a community-based
sample of persons with chronic fatigue syndrome-like symptoms.
Psychosom Med. 62(5):655-663. “People with CFS, MCS or FM
endure significant disability in terms of physical, occupational and
social functioning, and those with more than one of these diagnoses also
report greater severity of physical and mental fatigue.”
Jaspers, J. P. 1998. Whiplash
and post-traumatic stress disorder. Disabil Rehabil
20(11):397-404.
Jaspersen D, Leodolter A. 2005. [Sleep
disorders associated with gastroesophageal reflux.] Dtsch Med
Wochenschr. 130(48):2779-2782. [German] “Individuals with clinical
sleep disorders have a greatly impaired quality of life. The causes
for sleeping disorders are complex, but evidence has recently come from
different trials supporting a causal relationship between gastroesophageal
reflux disease (GERD) and sleep disorders in some patients. The
majority of patients with GERD report reflux symptoms during the night.
It is well known that especially at night reflux is characterized by
prolonged esophageal acid exposure. Sleep disorders significantly
improve while on efficacious antisecretory treatment. In patients with
sleep disorders but no previously known GERD, the search for it is
recommended and should be followed by adequate antisecretory treatment.
In other severe diseases associated with sleep, like the obstructive sleep
apnoea syndrome (OSAS), an association with esophageal acid exposure has
been proven. The sleep apnea-associated reflux has probably a
multifactorial etiology: in cases with other predisposing conditions for
gastro-esophageal reflux, OSAS promotes the development of reflux."
Jeal, W. and P. Benfield. 1997.
Transdermal fentanyl. A review of its pharmacological properties and
therapeutic efficacy in pain control. Drugs 53(1):109-138.
Jennings, JR, Muldoon MF, Hall M et
al. 2007. Self-reported sleep quality is associated with the
metabolic syndrome. Sleep. 30(2):219-223.
Jennum, P., A. M. Drewes, A. Andreasen and
K. D. Nielsen. 1993. Sleep and other symptoms in primary fibromyalgia and in
healthy controls. J. Rheumatol 20(10):1756-1759.
Jensen B, Wittrup IH, Wiik A et al. 2004.
Antipolymer antibodies in Danish fibromyalgia patients.
Clin Exp Rheumatol 22(2):227-229.
Although FM patients in this study had
slightly higher APA levels than healthy people, the levels declined with
age.
Jensen B, Wittrup IH, Bliddal H et al.
2003. Bone mineral density in fibromyalgia patients – correlation to
disease activity. 32(3):146-150. “...the severity of FM might have a
negative impact on bone mass.”
Jensen, K. A., S. K. Christensen, E. M.
Nielsen, L. K. Bunemann, K. Therkelsen and F. Knudsen.1997. [Cerebral blood
flow and indomethacin. The effect of different doses administered as
continuous intravenous infusions or as suppositories in healthy adults].
Ugeskr Laeger 159(27):4257-4260 [Danish].
Jensen MP, Nielson WR, Turner JA et al. 2004.
Changes in readiness to self-manage pain are associated with improvement
in multidisciplinary pain treatment and pain coping. Pain
111(1-2):84-95.
Jespersen A, Dreyer L, Kendall S et al. 2007. Computerized cuff
pressure algometry: a new method to assess deep-tissue hypersensitivity
in fibromyalgia. Pain. [Jan 24 Epub ahead of print]
This is yet another study confirming Dr. J. B. Eisinger’s development of
FM diagnostic testing using tensiometry, or blood pressure cuff
tension. I believe that this article would have benefitted by
inclusion of Dr. Eisinger’s work. DJS]
Jevning, R., I. Wells, A. F. Wilson and S.
Guich. 1987. Plasma thyroid hormones, thyroid stimulating
hormone, and insulin during acute hypometabolic states in man.
Physiol Behav 40(5):603-6.
Jevning, R., A. F. Wilson and J. M.
Davidson. 1978. Adrenocortical activity during meditation.
Horm Behav 10(1):54-60.
Jevning, R., A. F. Wilson and W. R. Smith.
1978. The transcendental meditation technique, adrenocortical
activity, and implications for stress. Experientia 34(5):618-9.
Jevning, R., A. F. Wilson, H. Pirkle, J. P.
O’Halloran and R. N. Walsh. 1983. Metabolic control in a state
of decreased activation: modulation of red cell metabolism. Am J
Physiol 245(5 Pt 1):C457-61.
Jezova, D., Jurankova E., Mosnarova A., M.
Kriska and I Skultetyova. 1996. Neuroendocrine response during stress
with relation to gender differences. Acta Neurobiol Exp (Warsz)
56(3):779-985.
Johannesson U, de Boussard CN, Brodda Jansen G et
al. 2006. Evidence of diffuse noxious inhibitory controls (DNIC)
elicited by cold noxious stimulation in patients with provoked
vestibulodynia. Pain [Dec 12 Epub ahead of print]
Johansson, G., J. Risberg, U. Rosenhall, G.
Orndahl, L. Svennerholm and S. Nystrom. 1995. Cerebral dysfunction in
fibromyalgia; evidence from regional cerebral blood flow measurements,
otoneurological tests and cerebrospinal fluid analysis. Acta Psychiatr
Scand 91(2):86-94.
Johansson O, Gangi
S, Liang Y, Yoshimura K, Jing C, Liu PY. 2001. Cutaneous mast cells are
altered in normal healthy volunteers sitting in from of ordinary
TVs/PCsBresults from open-field provocation experiments. J Cutan Pathol
Nov;28(10):513-9. Normal cutaneous mast cells can be altered by exposure to
television or personal computer screens. The number of skin mast cells
increase in exposed skin in many patients after such an exposure.
After 24 hours, the number of mast cells returns to normal. [This may be
significant to FM patients with skin allergy symptoms. DJS]
Johnson EO, Babis GC, Soultanis KC et al.
2008. Functional neuroanatomy of proprioception. J Surg
Orthop Adv. 17(3):159-164. “Proprioception is the sense of
body position that is perceived both at the conscious and unconscious
levels. Typically, it refers to two kinds of sensations: that of
static limb position and of kinesthesia. Static position reflects
the recognition of the orientation of the different body parts, whereas
kinesthesia is the recognition of rates of movement.” This is a
very relevant and important review. When care providers who know
myofascial medicine think of TrPs, they often think only of pain.
Associated proprioceptive and autonomic dysfunctions are important as
well, as are muscle dysfunctions such as weakness caused by TrPs, but
this often goes unrecognized. DJS]
Johnson EO, Kostandi M, Moutsopoulos HM. 2006.
Hypothalamic-pituitary-adrenal axis function in Sjogren’s syndrome:
mechanisms of neuroendocrine and immune system homeostasis. Ann
N Y Acad Sci. 1088:41-51. “These findings suggest not only
adrenal axis hypoactivity in SS and FM patients, but also that varying
patterns of adrenal and thyroid axes dysfunction may exist in patients
with different rheumatic diseases.”
Johnson JD, O’Connor KA, Deak T et al.
2002. Prior stressor exposure primes the HPA axis.
Psychoneuroendocrinology 27(3):353-365.
Johnson JD,
O’Connor KA, Deak T et al. Psychoneuroendocrinology.
27(3):353-365. The stress response in rats is changed after an
initial HPA activation. Neural plasticity is affected by
stress, at least in rats.
Johnson KM, Bradley KA, Bush K et al.
2006. Frequency of mastalgia among women veterans.
Association with psychiatric conditions
and unexplained pain syndromes. J Gen Intern Med.
21 Suppl 3:S70-75. “Like other unexplained pain
syndromes, frequent mastalgia is strongly associated with
PTSD and other psychiatric conditions. Clinicians
seeing patients with frequent mastalgia should inquire about
anxiety, depression, alcohol misuse, and trauma history.”
[Unfortunately, these patients were not evaluated for
pectoral TrPs which may cause pain called mastalgia. DJS]
Jones AY, Dean E,
Scudds RJ. 2005. Effectiveness of a community-based Tai Chi
program and implications for public health initiatives. Arch
Phys Med Rehabil. 86(4):619-625. “A community-based Tai Chi
program produces beneficial effects comparable to those reported from
experimental laboratory trials of Tai Chi; therefore, it should be
considered as a public health strategy.” The regular practice of
t’ai chi improves handgrip strength, resting heart rate, and
flexibility.
Jones GT, Silman AJ, Macfarlane GJ. 2003.
Predicting the onset of widespread body pain among children.
Arthritis Rheum. 48(9):2402-2405. This English study indicates
that children who have behavioral problems or “common childhood somatic
symptoms” are at risk for developing widespread pain. [I would
love to see these children examined for developing FM, sleep
disturbances, and myofascial TrPs. DJS]
Jones KD, Horak FB, Winters-Stone K et
al. 2009. Fibromyalgia is associated with impaired balance and
falls. J Clin Rheumatol. 15(1):16-21. “FM is
associated with balance problems and increased fall frequency.
Patients were aware of their balance problems. These results
suggest that FM may affect peripheral and/or central mechanisms of
postural control. Further objective study is needed to
identify the relative contributions of various neural and
musculoskeletal and other impairments to postural stability in FM to
provide clinicians with methods to maximize postural stability and
help fall prevention.” [Since most FM patients have
considerable myofascial TrP involvement and specific TrPs can have a
profound affect on balance, it is unfortunate that these patients
were not assessed for co-existing TrPs. DJS]
Jones KD, Deodhar P, Lorentzen A et al. 2007.
Growth hormone perturbations in fibromyalgia: a review.
Semin Arthritis Rheum. [Jan 12 Epub ahead of print] This
study indicates normal pituitary function in FM patients, and that
dysfunction of the HP-GH-IGF-1 axis is most likely hypothalamic in
origin, but notes that more research is required.
Joranson DE, Gilson AM. 2001. Pharmacists’ knowledge of and
attitudes toward opioid pain medications in relation to federal and
state policies. J Am Pharm Assoc 41(2):213-220.
“Pharmacists play a pivotal role in ensuring patient access to
medications. Our findings suggest that the incorrect knowledge
and inappropriate attitudes of some pharmacists could contribute to
a failure to dispense valid prescriptions for opioid analgesics to
patients in pain.” [This is a very sad yet accurate commentary
on one more hurdle that some chronic pain patients must overcome to
gain access to adequate pain control.]
Joranson DE, Ryan KM, Gilson AM et al. 2000. Trends in medical use
and abuse of opioid analgesics. JAMA 283(13):1710-1714.
“The trend of increasing medical use of opioid analgesics to treat pain
does not appear to contribute to increases in the health consequences of
opioid analgesic abuse.”
Joranson, D. E. and A. M. Gilson.
1998. Regulatory barriers to pain management. Semin Oncol
Nurs 14(2):158-63.
Joranson, D. E. 1994. Are
health-care reimbursement policies a barrier to acute and cancer pain
management? J Pain Symptom Manage 9(4):244-53.
Joranson, D. E. 1990. Federal
and state regulation of opioids. J Pain Symptom Manage5(1
Suppl):S12-S23.
Joyce, E., S. Blumentahl and S. Wessely.
1996. Memory, attention and executive function in chronic fatigue
syndrome. J Neurol Neurosurg Psychiatry 60(5):459-503.
Joyce, P. and C. Clark. 1996.
The use of CranioSacral Therapy to treat gastroesophageal reflux in infants.
Inf Young Children 9(2):51-58.
Juhl GI, Jensen TS, Norholt SE et al. 2007.
Central sensitization phenomena after third molar surgery: a quantitative
sensory testing study. Eur J Pain. [Jun 4 Epub ahead of print]
“Even a minor orofacial surgical procedure may be sufficient to evoke signs
of both central and peripheral sensitization, which may play a role in the
transition from acute to chronic pain in susceptible individuals.”
Julien N, Goffaux P, Arsenault P et al. 2005.
Widespread pain in fibromyalgia is related to a deficit of endogenous
pain inhibition. Pain 114(1-2):295-302. “These data
support a deficit of endogenous pain inhibitory systems in fibromyalgia
but not in chronic low back pain. The treatments proposed to
fibromyalgia patients should aim at stimulating the activity of those
endogenous systems.” [This indicates that treatment of FM should
focus on central nervous system modulation. DJS]
Jung, A. C., T. Staiger and M. Sullivan.
1997. The efficacy of selective serotonin reuptake inhibitors for the
management of chronic pain. J Gen Intern Med 12(6):384-389.
Just MA, Keller TA, Cynkar J. 2008. A decrease
in brain activation associated with driving when listening to someone speak.
Brain Res 1205.:70-80. This study used functional MRI to show
that, even in healthy individuals, listening carefully to anyone speaking
can be dangerous. In this study, drivers had to listen carefully as
they needed to tell if statements were true or false. This produced
spatial processing associated parietal lobe activation, and resulted in
significant deterioration in driving ability, even though the drivers did
not have to hold or dial a phone. [This study has profound
ramifications for those of us with FM cognitive dysfunction. There may
be days that you don’t want to drive with that language tape going, days
when the talking book may be out of the question or days when even music is
too much to handle when driving. If FM flares or aggravating factors
are severe, driving may have to be suspended for a time until perpetuating
and aggravating factors are under control. This must be
individualized, and it is important that our traveling companions understand
this. DJS]
Juul-Kristensen B, Lund H, Hanses K et al. 2007.
Poorer elbow proprioception in patients with lateral epicondylitis than in
healthy controls: a cross-sectional study. J Shoulder Elbow Surg.
[Nov 22 Epub ahead of print]. “Proprioception seems...to be poorer in
elbows with lateral epicondylitis elbows than in the controls’ elbows.
This needs to be taken into consideration in the management of lateral
epicondylitis.” [This could be due to co-existing MTPs. DJS]
Kabongo,
M. L. and A. W. Bedell. 1987. Nail signs of systemic conditions.
AFP 36(4):109-116.
Kahan M, Srivastava A, Wilson L et al. 2006.
Opioids for managing chronic non-malignant pain: safe and effective
prescribing. Can Fam Physician. 52(9):1091-1096. When
pain control with other medications have failed, titration to find the
lowest dose opioids that might be effective is the next logical step.
“Most patients with chronic non-malignant pain can be managed with <300 mg/d
of morphine (or equivalent). Opioids are safe and effective for
managing chronic pain.” [Non-medicinal pain relief methods should be
part of any pain control program. DJS]
Kakojic, D., V. Demarin, M. Kadojic, I.
Mihaljevic and B. Barac. 1999. Influence of prolonged stress on
risk factors for cerebrovascular disease. Coll Antropol
23(1):213-9.
Kalichman L. 2009. Association
between fibromyalgia and sexual dysfunction in women. Clin
Rheumatol. [Jan 23 Epub ahead of print]. It would have been valuable to
assess these patients for co-existing TrPs, as their role in sexual
dysfunction in both women and men has been carefully documented. DJS]
Kallenberg LA, Hermens HJ. 2004. Motor unit
action potential rate and motor unit action potential shape properties
in subjects with work-related chronic pain. Eur J Appl Physiol.
[Epub ahead of print.] “...more high-threshold Mus contribute to
low-level computer work-related tasks in chronic pain cases.
Additionally, the results suggest that the input of the central nervous
system to the muscle is higher in the cases with chronic pain.”
Kalmer, J. M. and E. Cafarelli1999. Effects
of caffeine on neuromuscular function. A Appl Physiol 87(2):801-808.
Kamanli A, Kaya A, Ardicoglu O et al. 2004.
Comparison of lidocaine injection, botulinum toxin injection, and dry
needling to trigger points in myofascial pain syndrome.
Rheumatol Int. [Epub ahead of print.] Lidocaine injection
appears to offer the best results of the three according to this study,
as it causes less problems than the dry needling and is less expensive
than BTX-A. BTX-A may be the treatment of choice in patients with
resistant TrPs. [Perpetuating factors must always be identified
and brought under control. DJS.]
Kandt RS, Daniel FL. 1986.
Glossopharyngeal neuralgia in a child. A diagnostic and
therapeutic dilemma. Arch Neurol 43(3):301-302. Symptoms
were caused by TrPs in the right tonsil area.
Kang Y, Yi Y, Kim J. 2007. Pain drawings of
the phantom pain of the patients with amputation. J Musculoskel
Pain 15 (Supp 13):27 item 43. [Myopain 2007 Poster] “The
patterns of phantom pain were very similar to the referred pain patterns of
the MPS. A new assumption would be possible: that ‘phantom pain in
MPS’s clothing’ like ‘sheep in wolf’s clothing’.” [This finding agrees with
other research and observation that indicates phantom limb (and breast,
uterine and ovarian) pain may be due to MTPs or other tissue TrPs. DJS]
Kankaanpaa, M. S. Taimela, D. Laaksonen, O.
Hanninen and O. Airaksinen. 1998. Back and hip extensor
fatigability in chronic low back pain patients and controls. Arch
Phys Med Rehabil 79(4):412-7.
Kao MJ, Hsieh YL, Kuo FJ et al. 2006.
Electrophysiological assessment of acupuncture points. Am J
Phys Med Rehabil. 85(5):443-448. “Similar to the
distribution of EPN loci in an MTrP region, significantly more EPN
(end plate noise) loci can be identified in an AcP (acupuncture
point) region of Stomach-36 than in a nearby non-AcP site.
This study provides additional support to the hypothesis that some
AcPs are also myofascial trigger points.”
Kaplan, R. M., S. M. Schmidt and T. A.
Cronan. 2000. Quality of well being in patients with
fibromyalgia. J Rheumatol
27(3):785-9.
Kapreli E, Vourazanis E,
Strimpakos N. 2007. Neck pain causes respiratory dysfunction.
Med Hypotheses [Oct 22 Epub ahead of print]. “The patient with
neck pain presents a number of factors that could constitute a
predisposition of leading to a respiratory dysfunction: (a) the decreased
strength of deep neck flexors and extensors, (b) the hyperactivity and
increased fatigability of superficial neck flexors, (c) the limitation of
range of motion, (d) the decrease in proprioception and disturbances in
neuromuscular control, (e) the existence of pain and (f) the psychosocial
influence of dysfunction. The possible connection of neck pain and
respiratory function could have a great impact on various clinical aspects,
notably patient assessment, rehabilitation and pharmacological
prescription.”
Kaput J,
Perlina A, Hatipoglu B et al. 2007. Nutrigenomics: concepts and
applications to pharmacogenomics and clinical medicine.
Pharmacogenomics. 8(4):369-390. “The maintenance of health and the
prevention and treatment of chronic diseases
are influenced by naturally
occurring chemicals in foods. In addition to supplying the
substrates for producing energy, a large number of dietary chemicals are
bioactive -- that is, they alter the regulation of biological processes
and, either directly or indirectly, the expression of genetic
information. Nutrients and
bioactives may produce different
physiological phenotypes among individuals
because of genetic variability and
not only alter health, but also disease initiation,
progression and severity. The
study and application of gene-nutrient interactions is called
nutritional genomics or nutrigenomics. Nutrigenomic concepts,
research strategies and
clinical implementation are similar to and overlap those of
pharmacogenomics, and both are fundamental to the treatment of disease
and maintenance of optimal health.”
Kaput J,
Rodriguez RL. 2004. Nutritional genomics: the next frontier in the
post genomic era. Physiol Genomics. 16(2):166-177. “…dietary
intervention based on knowledge of nutritional requirement, nutritional
status, and genotype (i.e., ‘individualized nutrition’) can be used to
prevent, mitigate, or cure chronic disease.”
Kar, A., B. K. Choudhary and N. G.
Bandyopadhyay. 1999. Preliminary studies on the inorganic constituents of
some indigenous hypoglycaemic herbs on oral glucose tolerance test. J
Ethnopharmacol 64(2):179-84.
Karalis, K. P., E. Kontopoulos, L. J.
Muglia and J. A. Majzoub. 1999. Corticotropin-releasing hormone
deficiency unmask the proinflammatory effect of epinephrine. Proc
Natl Acad Sci U S A 96(12):7093-7.
Karim MR, Fann
AV, Gray RP et al. 2005. Enthesitis of biceps brachii short
head and coracobrachialis at the coracoid process: a generator of
shoulder and neck pain. Am J Phys Med Rehabil.
84(5):376-380. [This study used Marcaine and DepoMedrol for
anterior shoulder pain and MPS, with a diagnosis of enthesitis.
It would be interesting to know what would have happened if the
patients had been examined for attachment trigger points and
injected with procaine or lidocaine. A less toxic local
anesthetic may often be effective for enthesiopathy caused by
attachment trigger points. DJS]
Karmakar MK, Ho AM. 2004. Postthoracotomy
pain syndrome. Thorac Surg. Clin. 14(3):345-352.
About 30% of posthoracotomy patients experience chronic pain as a
result. The authors advocate aggressive pain control before
incision, but neglect to mention the possibility of TrPs.
Kashikar-Zuck S, Lynch AM, Slater S et al.
2008. Family factors, emotional functioning, and functional
impairment in juvenile fibromyalgia syndrome. Arthritis Rheum.
59(10):1392-1398. “Mothers of adolescents with JPFS (juvenile
primary fibromyalgia syndrome) reported twice as many pain conditions
and significantly greater depressive symptoms than mothers of comparison
peers. The JPFS group also had poorer overall family functioning
and more conflicted family relationships. In adolescents with
JPFS, maternal pain history was associated with significantly higher
functional impairment. Conclusion: Increased distress and chronic
pain are evident in families of adolescents with JPFS, and family
relationships are also impacted. Implications for child functional
impairment and the need for inclusion of caregivers in treatment are
discussed.”
Kashikar-Zuck S, Parkins IS, Graham TB et al. 2008. Anxiety, mood,
and behavioral disorders among pediatric patients with juvenile
fibromyalgia syndrome. Clin J Pain 24(7):620-626.
“There seems to be a high prevalence of anxiety disorders in patients
with JPFS, and presence of anxiety disorder is associated with poorer
physician-rated functioning.” [This is written by psychology
specialists, with an acknowledgment of potential co-existing myofascial
TrPs that might create symptoms that could be mistaken as psychological.
DJS]
Kashikar-Zuck S, Lynch AM, Graham TB et al. 2007. Social
functioning and peer relationships of adolescents with juvenile
fibromyalgia syndrome. Arthritis Rheum. 57(3):474-480.
“Adolescents with JPFS were perceived (by peer and self reports) as
being more isolated and withdrawn and less popular. Adolescents
with JPFS were less well liked, were selected less often as a best
friend, and had fewer reciprocated friendships.” “Given the
central role that peer relationships play in psychological development
of children, and because peer rejection and isolation have been
associated with subsequent adjustment problems, these findings are
concerning.” [This is a significant study and indicates a great
need for more attention to the support systems of adolescents with FM.
DJS]
Kashikar-Zuck
S, Vaught MH, Goldschneider KR et al. 2002. Depression, coping, and
functional disability in juvenile primary fibromyalgia syndrome. J
Pain 3(5):412-419. In this study, children with juvenile primary
fibromyalgia syndrome (JPFS) and nonmalignant chronic back pain (CBP) were
compared. “...both JPFS and CBP
groups reported significant disruption in functional abilities and school
attendance as a result of chronic pain.... The JPFS group had suffered
from pain for significantly longer than the CBP group before being referred
for specialty care... The JPFS group reported somewhat more school
absences.”
Kashima, K., O. I. Rahman, S. Sakoda and R.
Shiba. 1999. Increased pain sensitivity of the upper extremities
of TMD patients with myalgia to experimentally-evoked noxious stimulation:
possibility of worsened endogenous opioid systems. Cranio
17(4):241-6.
Kasikcioglu E, Dinler M, Berker E. 2006.
Reduced tolerance of exercise in fibromyalgia may be a consequence of
impaired microcirculation initiated by deficient action of nitric oxide.
Med. Hypotheses [Jan 9 Epub ahead of print].
Kassirer, J. P. 1997. Federal
foolishness and marijuana. N Engl J Med 366(5):336-7.
Kasteleijn-Nolst Trenite, D. G., A. M. da
Silva, S. Ricci, C. D. Binnie, G. Rubboli, C. A. Tassinari and J. P. Segers.
1999. Video-game epilepsy: a European study. Epilepsia 40
(Suppl 4):70-4.
Kato K, Sullivan PF, Evengard B et al. 2006.
Importance of genetic influences on chronic widespread pain.
Arthritis Rheum. 54(5):1682-1686. “Individual
differences in the likelihood of developing chronic widespread pain
reflect modest genetic influences. There are no significant
sex differences in the type or expression of the genes responsible
for chronic widespread pain or in the magnitude of the relative
importance of these influences on chronic widespread pain.”
Kato T, Rompre P, Montplaisir JY et al. 2001.
Sleep bruxism: an oromotor activity secondary to micro-arousal.
J Dent Res. 80(10):1940-1944. “A clear sequence of
cortical to autonomic-cardiac activation precedes jaw motor activity
in SB [sleep bruxism] patients. This suggests that SB is a
powerful oromotor manifestation secondary to micro-arousal.”
[This is contrary to the belief that jaw clenching and grinding is
primarily caused by stress. It indicates that care providers should
be checking sleep quality. DJS]
Kato T, Montplaisir JY, Guitard F et al.
2003. Evidence that experimentally induced sleep bruxism is a
consequence of transient arousal. J Dent Res.
82(4):284-288.
Katz J, McCartney CJ. 2002. Current status of
pre-emptive analgesia. Curr Opin Anaesthesiol. 15(4):435-441.
“The application of preventive perioperative analgesia (not necessarily
preincisional) is associated with a significant reduction in pain beyond the
clinical duration of action of the analgesic agent, in particular for the
N-methyl-D-aspartate antagonists.”
Katz J, Cohen L, Schmid R, et al. 2003.
Postoperative morphine use and hyperalgesia are reduced by preoperative but
not intraoperative epidural analgesia: implications for preemptive analgesia
and the prevention of central sensitization.
Anesthesiology 98(6):144-1460.
Katz, N. P. 2000. MorphiDex (MS:DM)
double-blind, multiple-dose studies in chronic pain patients. J
Pain Symptom Manage 19(1 Suppl):S37-41.
Katz RS, Heard AR, Mills M et al. 2004. The
prevalence and clinical impact of reported cognitive difficulties (fibrofog)
in patients with rheumatic disease with and without fibromyalgia. J
Clin Rheumatol. 10(2):53-58. “Memory decline and mental confusion
were coupled more often in patients with FM (50.9-8.8%). Patients
with FM with this combination of cognitive problems reported more pain
(76.0-45.4%), stiffness (79.7-43.7%), fatigue (79.6-52.6%) and disturbed
sleep (59.2-36.6%) compared with patients with FM with memory problems
alone. Patients with rheumatic disease substantially differ in
cognitive vulnerability, with patients with FM at considerably higher risk
for cognitive difficulty. More importantly, the prevalence of a
combined disturbance in memory and mental clarity is high and closely
associated with the perception of increased illness severity and diminished
mental health in FM. That this linkage has the possibility of having
a great deal to do with an important clinical variant of FM underscores the
need for greater clinical recognition of this underrecognized pattern and
for further research.”
Kaufmann, H. 1997. Neurally mediated
syncope and syncope due to autonomic failure: differences and similarities.
J Clin Neurophysiol
14(3):183-196.
Kaufmann I, Schelling G, Eisner C et al.
2008. Decrease in adhesion molecules on polymorphonuclear
leukocytes of patients with fibromyalgia. Rheumatol Int.
[Dec. 4 Epub ahead of print]. This is a study indicating yet
another physiological difference in FM patients. “These changes might
lower the rate of polymorphonuclear leukocyte migration to sites of
inflammation and thereby compromise defense against infection and pain
control.”
Kaufmann I, Schelling G, Eisner C et al. 2008. Anandamide and
neutrophil function in patients with fibromyalgia.
Psychoneuroendocrinology [Apr 4 Epub ahead of print]. The
endocannabinoid system is a critical pathway in pain perception in
mammals. It is activated during stressful situations, and can be
part of the immune system activation that, in turn, is associated with
the development of chronic pain. This study indicates that
“...patients with FM might benefit from pharmacologic manipulation of
the endocannabinoid signaling...” Controlled research is needed.
[This research may help us get over the prejudice concerning cannabinoid
use for chronic pain. DJS]
Kauppila, T., X. J. Xu, W. Yu and Z
Wiesenfeld-Hallin. 1998. Dextromethorphan potentiates the effect
of morphine in rats with peripheral neuropathy. Neuroreport
9(6):1071-1074.
Kavlock, R. J. 1999.
Overview of endocrine disruptor research activity in the United States.
Chemosphere 39(8):1227-36.
Kawakita K, Itoh K, Okada K. 2007.
Experimental model of trigger points using eccentric exercise. J
Musculoskel Pain 15 (Supp 13):4 item 4. [Myopain 2007 Poster]
“The tissue injuries and subsequent inflammation processes produced by the
REC play an important role in the development of TrP, and ischemic condition
could induce synaptic changes in the spinal cord. Sensitization of
peripheral sensory could induce synaptic changes in the spinal cord.
Sensitization of peripheral sensory receptors presumably polymodal receptors
of the fascia and central sensitization might be a possible underlying
mechanism of the TrP formation and referred pain phenomena.”
Kawakita K, Okada K. 2006. Mechanisms of action of acupuncture for
chronic pain relief – polymodal receptors are the key candidates.
Acupunct Med. 24 Suppl:S58-S66.
Kawamata, T., K. Omote, M. Kawamata and A.
Namiki. 1998. Premedication with oral dextromethorphan reduces
postoperative pain after tonsillectomy. Anesth Analg
86(3):594-597.
Kay, G.G. and A. G. Harris. 1999.
Loratadine [Note: Claritin]: a non-sedating antihistamine. Review of its
effects on cognition, psychomotor performance, mood and sedation.
Clin Exp Allergy 29(S3):147-150.
Kayyali HA, Weimer S, Frederick C et al.
2008. Remotely attended home monitoring of sleep disorders.
Telemed J E Health 14(4):371-374. “A new enabling home telehealth
technology for real-time sleep disorders monitoring was developed and tested
with encouraging preliminary results. The sample size is too small to
derive any clinical conclusions about the sleep quality of FM patients.
However, this study validates the underlying technology and demonstrates the
role of new wireless technologies in the future of sleep disorders
diagnosis.” [This is a potentially important development that may
allow polysomnography to be available to those who otherwise would not be
able to receive it. DJS]
Kazennikov OV, Wiesendanger M. 2005. Goal
synchronization of bimanual skills depends on proprioception.
Neurosci Lett. [Epub ahead of print Jul 20] Proprioceptive
feedback is necessary for the brain to monitor, correct and coordinate
bimanual movements. [Proprioceptive dysfunction associated with
myofascial TrPs may contribute to much more disability or dysfunction
than is recognized.]
Keel, P. 1999. Pain management
strategies and team approach. Baillieres Best Pract Res Clin
Rheumatol 13(3):493-506.
Keel, P.J., C. Bodoky, U. Gerhard and W.
Muller. 1998. Comparison of integrated group therapy and group relaxation
training for fibromyalgia. Clin J Pain 14(3):232-8.
Keitel, W. 1999. [Occupational therapy in
the diseases of the locomotor system]. Z Arztl Fortbild Qualitatssich
93(5):335-40 [German].
Keitel, W. 1999. [ No title available]
Fortschr Med
117(5):32-6. [German]
Kelly A, Khan K. 2008. Prevalence of
allergies in children with complex medical problems. Clin Pediatr.
47(8):809-816. “The authors report a higher than expected prevalence
of allergic and immune abnormalities in children with complex medical
problems.” [We must be attentive to the possibility of co-existing
conditions in children with FM or CMP. DJS]
Kelly G.S. 2000. Insulin resistance: lifestyle and
nutritional interventions. Altern Med Rev 5(2):109-32. Insulin
resistance seems to be common and contributes to several frequent health
problems including sleep apnea, obesity, and type 2 diabetes. Possible
perpetuating factors include diet, exercise, smoking and stress.
Kelly M, Gagne R, Newman JD et al. 2008.
Assessment of fibromyalgia and chronic fatigue syndrome: a new protocol
designed to determine work capability – chronic pain abilities determination
(CPAD). Ir Med J. 101(9):277-278. [There are some very
good aspects of this new protocol, but no protocol will be complete until it
takes into account assessment of specific musculoskeletal weakness,
dysfunction, proprioception and autonomic concomitants from myofascial TrPs.
When patients have multiple interactive diagnoses including chronic
myofascial pain, they must all be taken into account. DJS]
Kemeny, M. E. and T. L. Gruenewald.
1999. Psychoneuroimmunology update. Semin Gastrointest Dis
10(1):20-9.
Kemoun G, Carette P, Watelain E et al. 2008.
Thymocognitive input and postural regulation: a study on
obsessive-compulsive disorder patients. Neurophysiol Clin.
38(2):99-104. This review covers the recent research on nerve networks
that are common to both postural balance and psychological states.
“When interpreting symptoms, these interactions should be taken into
account.” [They should also be taken into account when designing
therapies. DJS]
Kempermann G, Neumann H. 2003.
Neuroscience. Microglia: the enemy within? Science
302(5651):1689-1690. Microglia "...may be central players in repairing
brain tissue and maintaining its integrity...and also...contribute to the
rearrangement of neural connections and hence to the plasticity of normal
brain tissue." [Microglia may be part of the cause and the cure of
central sensitization. DJS]
Kendall, SA, Henriksson, KG, Hurtig, I et
al. 2003. Differences in sensory thresholds in the skin of women with
fibromyalgia syndrome: a comparison between ketamine responders and ketamine
non-responders. J Muscoloskel Pain
11(2):3-9. This is another
study indicating that subsets of patients with FM have different pain
processing dysfunctions.
Kern, W., E. F. Stange, H. L. Fehm and H.
H. Klein. 1999. [No title available]. Z Gastroenterol
Suppl 1 (13):36-42 [German].
Kerns RD, Rosenberg R. 2000.
Predicting responses to self-management treatments for chronic pain:
application of the pain stages of change model. Pain
84(1):49-55. “These findings suggest that increased commitment to
a self-management approach to chronic pain may serve as a mediator or
moderator of successful treatment.”
Kerr CE, Shaw JR, Wasserman RH et al. 2008.
Tactile acuity in experienced Tai Chi practitioners: evidence for use
dependent plasticity as an effect of sensory-attentional training.
Exp Brain Res. 188(2):317-322. [Practitioners of t’ai chi had
greater spatial acuity than controls. T’ai chi may be valuable in
patients with proprioceptive dysfunction due to myofascial trigger points or
FM. DJS]
Kerr, S. J. , P. J. Armati and B. J. Brew.
1995. Neurocytotoxity of quinolinic acid in human brain cultures. J
Neurovirol
1(5-6):375-380.
Ketroser DB 2000. Whiplash, chronic
neck pain, and zygapophyseal joint disorders. A selective review. Minn
Med 83(2):51-4
Keverne, E. B. 1999. The
Vomeronasal Organ. Science 286(5440):716-720.
Khaki AM. 2006. Pain clinic experience in a teaching hospital in Western, Saudi Arabia.
Relationship of patient’s age and gender to various types of pain.
Saudi Med J. 27(12):1882-1886. “Various types of chronic
pain managed in the pain clinic (required) full understanding of pain
neurophysiology as well as familiarity with contributing factors to the
prevalence of pain.”
Khalsa PS.
2004. Biomechanics of musculoskeletal pain: dynamics of the neuromatrix.
J Electromyogr Kinesiol. 14(1):109-120. “Mammals
in general, and humans in particular, have evolved a highly sophisticated
system of pain perception, which is characterized in humans by complementary
but distinct neural processing of the intensity and location of a noxious
stimulus, and a motivational/emotional or affective response to the
stimulus. The peripheral and central neurons that comprise this
system, which has been called the 'neuromatrix', dynamically (temporally)
respond and adapt to noxious biomechanical stimuli. However,
phenotypic variability of the neuromatrix can be large, which can result in
a host of musculoskeletal conditions that are characterized by altered pain
perception, which can and often does alter the course of the condition.
This neural plasticity has been well recognized in the central nervous
system, but it has only more recently become known that peripheral
nociceptors also adapt to their altered extracellular matrix environment.
This work reviews the biomechanics of pain focusing on the relevant stimulus
that initiates responses by nociceptors to the cognitive perception of
pain.” [It is becoming increasingly evident that each of us is indeed
unique, including in response to medications and to just about everything
else. One size does not fit all, and, especially in complex medical
conditions, tailoring the medications and therapies to the individual is
vital to success. DJS]
Khan MA,
Lichtensteiger CA, Faroon O, Mumtaz M, Schaeffer DJ, Hansen LG. The
hypothalamo-pituitary-thyroid (HPT) axis: a target of nonpersistent ortho-substituted
PCB congeners.2002. Toxicol Sci
Jan;65(1):52-61.
Khasar SG, Burkham J, Dina OA et al. 2008.
Stress induces a switch of intracellular signaling in sensory neurons in a
model of generalized pain. J Neurosci. 28(22):5721:5730.
“Thus, an important mechanism in generalized pain syndromes may be
stress-induced coactivation of the hypothalamo-pituitary-adrenal and
sympathoadrenal axes, causing a long-lasting alteration in intracellular
signaling pathways, enabling normally innocuous levels of immune mediators
to produce chronic hyperalgesia.” Stress can be an important
contributor to the change from acute to chronic illness, and then can
maintain that chronicity.
Khasar SG, Green PG, Levine JD. 2005.
Repeated sound stress enhances inflammatory pain in the rat.
Pain 116(1-2):79-86. “Stress-induced enhancement of
inflammatory hyperalgesia is associated with a change in mechanism
by which bradykinin induces hyperalgesia, from being sympathetically
mediated to being sympathetically independent. This
sympathetic-independent enhancement of mechanical hyperalgesia is
mediated by the stress-induced release of epinephrine from the
adrenal medulla.”
Kharkevich, D. A. and V. V. Churukanov.
1999. Pharmacological regulation of descending cortical control of the
nociceptive processing. Eur J Pharmacol 375(1-3):121-31.
Kidd, P. M. 1999. A review of
nutrients and botanicals in the integrative management of cognitive
dysfunction. Altern Med Rev
4(3);144-61.
Kiecolt-Glaser JK, McGuire L, Robles TF, Glaser R.
Emotions, Morbidity, and Mortality: New Perspectives from
Psychoneuroimmunology. 2002. Annu Rev Psychol
53:83-107.
Kim, J. Y. L. A. Nolte, P. A. Hansen, D. H.
Hanm, K. Kawanaka and J. O. Holloszy. 1999. Insulin resistance of muscle
glucose transport in male and female rats fed a high-sucrose diet. Am J
Physiol 276(3 Pt 2): R665-R672.
Kim PS. 2002. Role
of injection therapy: review of indications for trigger point injections,
regional blocks, facet joint injections, and intra-articular injections.
Curr Opin Rheumatol
Jan;14(1):52-7. Multidiciplinary therapies for many chronic pain patients
may often include injection therapies as part of effective pain management.
Kim SH, Kim DH, Oh DH et al. 2008.
Characteristic electron microscopic findings in the skin of patients with
fibromyalgia-preliminary study. Clin Rheumatol. 27(3):407-411.
“The EM findings seen in the skin of FM patients show unusual patterns of
unmyelinated nerve fibers as well as associated Schwann cells.” [This
study may implicate a mechanism of hypersensitivity in a variety of tissues
in the FM patient. Larger studies are needed. DJS]
Kim SH. 2007. Skin biopsy findings:
implications for the pathophysiology of fibromyalgia. Med
Hypotheses [Jan 8 Epub ahead of print] Skin abnormalities in FM
patients may be significant.
Kim SH, Jang TJ, Moon IS. 2006. Increased
expression of N-Methyl-D-Aspartate Receptor Subunit 2D in the skin of
patients with fibromyalgia. J Rheumatol. 33(4):785-788.
“The increased expression of NMDAR found in FM skin could be indicative of a
more generalized increase in other peripheral nerves. This suggests
that NR2D-selective antagonists may have implications in the treatment of
allodynia in patients with FM.”
Kim SH, Won SJ, Mao XO et al. 2005. Molecular
mechanisms of cannabinoid protection from neuronal excitotoxicity.
Mol Pharmacol. [Nov 18 Epub ahead of print]. “Cannabinoids appear
to protect neurons against NMDA toxicity at least partly by activation of
CB1R and downstream inhibition of PKA signaling and NO generation.”
Kimmelberg H.K., Zhou M. 2002.
Hippocampal astrocytes show heterogeneity of swelling activated anion
currents. Glia (Suppl 1):S55 [Abstract].
King, D. E. and B. Bushwick. 1994.
Beliefs and attitudes of hospital inpatients about faith healing and prayer.
J Fam Pract
39(4):349-52.
Kipen, H. M., W. Hallman, H. Kang, N.
Fiedler and B. H. Natelson. 1999. Prevalence of chronic fatigue
and chemical sensitivities in Gulf Registry Veterans. Arch Environ
Health 54(5):313-8.
Kinsley, C. H.., L. Madonia, G. W. Gifford,
K. Tureski, G. R. Griffin, C. Lowry, J. Williams, J. Collins, H. McLearie
and K. G. Lambert. 1999. Motherhood improves learning and memory. Nature
402(6758):137-8.
Kiraly, S. J., R. J. Ancill and G.
Dimitrova. 1997. The relationship of endogenous cortisol to
psychiatric disorder: a review. Can J Psychiatry 42(4):415-420.
Kirchgessner ,A. L., and M. Liu. 1999.
Orexin synthesis and response in the gut. Neuron. 24(4):941-51
Kirchheiner J, Brockmoller J. 2005. Clinical
consequences of cytochrome P450 2C9 polymorphisms. Clin
Pharmacol Ther. 77(1):1-16. This is a good review of the
current knowledge of the effects of genetic variations on drug
metabolism. Phenotyping has potential use indicating both
potential drug effectiveness and potential toxicity, but the knowledge
needs to be developed.
Kischka, U. T. Ettlin, S. Heim and G.
Schmid. 1991. Cerebral symptoms following whiplash injury. Eur Neurol
31(3):136-140.
Kiser RS, Cohen HM, Freedenfeld RN et al. 2001.
Olanzapine for the treatment of fibromyalgia symptoms. J Pain
Symptom Manage 22(2):704-708. This is a potential medication
for FM with few serious side effects found thus far.
Kivimaki M, Leino-Arjas P, Kaila-Kangas L et
al. 2006. Increased sickness absence among employees with
fibromyalgia. Ann Rheum Dis June 22 [Epub ahead of
print]. “FM is associated with a substantially increased risk
of medically certified sickness absence...”
Klauenberg S, Maier C, Assion HJ et al.
2008. Depression and changed pain perception: Hints for a central
disinhibition mechanism. Pain. [Oct 14 Epub ahead of
print]. “The results contradict the former assumption of a general
insensitivity to experimental pain in depressive disorder. In the
mostly pain-free patients signs of an enhanced central hyperexcitability
are even more pronounced than usually found in chronic pain patients
(e.g. FM), indicating common mechanisms in depressive disorder and
chronic pain in accordance with the assumption of non-pain associated
mechanisms in depressive disorder for central hyperexcitability, e.g. by
inhibited serotonergic function. Furthermore, this trial
demonstrates the feasibility of QST (quantitative sensory testing) in
depressive patients.”
Klein, R., and P. A. Berg. 1995. High
incidence of antibodies 5-hydroxytryptamine, gangliosides, and phospholipids
in patients with chronic fatigue and fibromyalgia syndrome and their
relatives: evidence for a clinical entity of both disorders. Eur J Med
Res 1(1):21-6.
Klein, R. , M. Bansch and P. A. Berg. 1992.
Clinical relevance of antibodies against serotonin and gangliosides in
patients with primary fibromyalgia syndrome. Psychoneuroimmunology
17(6):593-8.
Klekner A, Felszeghy S, Tammi R et al. 2005.
Quantitative determination of hyaluronan content in cerebral aneurysms by
digital densitometry. Zentralbl Neurochir. 66(4):207-212.
“Results suggest that an elevated hyaluronan level in the extracellular
matrix may affect the cerebral arterial wall architecture. It is
reasonable to suppose that the increased hyaluronan content creates a
viscoelastic ECM which might improve the biomechanical resistance of the
thinned vessel wall.” [This seemingly unrelated piece of research may
provide clues to the higher viscosity of the extracellular matrix of a
subset of patients with both FM and CMP, especially in relation to the
geloid mass. DJS]
Klingmann PO, Kugler I, Steffke TS et al. 2008. Sex-specific
prenatal programming: a risk for fibromyalgia? Ann N Y Acad Sci.
1148:446-455.
Knardahl, S., M. Elam, B. Olausson and B.
G. Wallin. 1998. Sympathetic nerve activity after acupuncture in
humans. Pain
75(1):19-25.
Knobler, H. A. Schattner, T. Zhornicki, S.
D. Malnick, D. Keter, N. Sokolovskaya, Y. Lurie and D. D. Bass. 1999. Fatty
liver-and additional and treatable feature of the insulin resistance
syndrome. QMJ 9(2):73-9.
Knoll, R, Hoshijima, M, Chien, K. 2003.
Cardiac mechanotransduction and implications for heart disease. Oct 9
[Epub ahead of print.] This article concerns mechanotransduction,
which includes the translation of mechanoreception to proprioception.
The authors ask some interesting questions concerning conversion of stimuli
to electrochemical signaling and cover recent research in cardiac
cytoskeleton structure. Fascia is everywhere, and my heart tells me
that the authors should be aware of myofascial medicine and the possible
permutations that may be involved.
Koch, K. L. 1999. Illusory
self-motion and motion sickness: a model for brain-gut interactions and
nausea. Dig Dis Sci
44(8 Suppl):53S-57S.
Koelback Johnson, M., T. Graven Nielsen, A.
Schou Olesen and L. Arendt-Nielsen. 1999. Generalized muscular hyperalgesia
in chronic whiplash syndrome. Pain 83(2):229-234.
Koenig, H. G., J. C. Hays, D. B. Larson, L.
K. George, H. J. Cohen, M. E. McCullough, K. G. Meador and D. G. Blazer.
1999. Does religious attendance prolong survival? A six-year
follow-up study of 3,968 older adults. J Gerontol A Biol Sci Med
Sci 54(7):M370-6.
Koenig, H. G., L. K. George and B. L.
Peterson. 1998. Religiosity and remission of depression in
medically ill older patients.
Am J Psychiatry 155(4):536-542.
Koenig, H. G., H. J. Cohen, L. K. George,
J. C. Hays, D. B. Larson and D. G. Blazer. 1997. Attendance at
religious services, interleukin-6, and other biological parameters of immune
function in older adults. Int J Psychiatry Med 27(3):233-50.
Koenig M, Cathebras P, Guy C et al. 2005.
[Pentoxiphylline: a cheap substitute for anti-TNFalpha agents?] Rev
Med Interne. [Nov 8 Epub ahead of print] [French] [This
medication may be a useful agent for use in chronic pain states. DJS ]
Kohnen R, Farber L,
Spath M. 2004. The assessment of vegetative and functional symptoms in
fibromyalgia patients: the tropisetron experience. Scand J
Rheumatol Suppl. (119):67-71. Tropisetron, in general, helped
sleep dysfunction but worsened gastrointestinal function in these FM
patients.
Kohlmann T. 2003. [Musculoskeletal pain in the
population] [German] Schmerz. 17(6):405-411. This review
indicates that about 16% of the German population has severe musculoskeletal
pain.
Kolbinson, D. A. , J. B. Epstein, A.
Senthilselvan and J. A. Burgess. 1998. Effect of impact and injury
characteristics on post-motor vehicle accident temporomandibular disorders.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 85(6):665-73.
Komaroff, A. L. and D. S. Buchwald.
1998. Chronic fatigue syndrome: an update. Annu Rev Med
49:1-13.
Komiyama, O., M. Kawara, M. Arai, T. Asano
and K. Kobayashi. 1999. Posture correction as part of behavioral
therapy in treatment of myofascial pain with limited opening. J
Oral Rehabil26(5):428-35.
Koolstra JH, van Eijden TM. 2005. Combined
finite-element and rigid-body analysis of human jaw joint dynamics.
J Biomech 38(12):2431-2439. The (jaw) joint is subjected to
loading which causes tensions and deformations in its cartilaginous
structures. These are assumed to be a major determinant for
development, maintenance, and also degeneration of the joint...It was
demonstrated that joint loads increase with muscle activation, irrespective
of the external loads..”
Kop WJ, Lyden A, Berlin AA et al. 2005.
Ambulatory monitoring of physical activity and symptoms in
fibromyalgia and chronic fatigue syndrome.
Arthritis Rheum. 52(1):296-303. “Patients with FM
and/or CFS engaged in less high-intensity physical activities than
that recorded for sedentary control subjects. This reduced
peak activity was correlated with measures of poor physical
function. Activity levels appear to be contingent on, rather
than predictive of, symptoms.”
Kopf A, Janson W, Stein C. 2003. [Opioid
therapy in chronic non-malignant pain] [German] Anaesthesist.
52(2):103-114. Therapeutic recommendations from the DGSS consensus
conference include a validated indication for the use of opioids for
chronic nonmalignant pain.
Koppert W. 2005. [Opioid-induced
analgesia and hyperalgesia] Schmerz [Aug 12 Epub ahead
of print] [German] “Successful strategies that may decrease or
prevent opioid-induced hyperalgesia include the concomitant
administration of drugs such as NMDA antagonists, alpha(2)-agonists,
or nonsteroidal anti-inflammatory drugs (NSAID), opioid rotation, or
combinations of opioids with different receptor selectivity.”
Koppert W, Weigand M, Neumann F et al. 2004.
Perioperative intravenous lidocaine has preventive effects on postoperative
pain and morphine consumption after major abdominal surgery.
Anesth Analg 98(4):1050-1055.
Koppert, W., S. Zeck, R. Sittl, R. Likar,
R. Knoll and M. Schmelz. 1998. Low-dose lidocaine suppresses experimentally
induced hyperalgesia in humans. Anesthesiology 89(6):1345-53.
Koppert, W., P. W. Reeh and H. O.
Handwerker. 1993. Conditioning of history mind by bradykinen alters
responses of wrapped nociceptors and human itch sensation. Neurosci Lett
152(1-2):117-20.
Korneyev, A. Y. 1997. The role
of the hypothalamic-pituitary-adrenocortical axis in memory-related effects
of anxiolytics.
Neurobiol Learn Mem 67(1):1-13.
Kornick CA,
Santiago-Palma J, Moryl N et al. 2003. Benefit-risk assessment of
transdermal fentanyl for the treatment of chronic pain. Drug Saf
26(13):951-973. “Transdermal fentanyl is effective and well
tolerated for the treatment of chronic pain caused by malignancy and
non-malignant conditions when administered according to the manufacturer’s
recommendations. Compared with oral opioids, advantages of transdermal
fentanyl include a lower incidence and impact of adverse effects
(constipation, nausea and vomiting, and daytime drowsiness), higher degree
of patient satisfaction, improved quality of life, improved convenience and
compliance resulting from administration every 72 hours, and decreased use
of rescue medication.”
Kornstein, S. G. 1998. Gender differences
in depression: implications for treatment. J Clin Psychiatry 58 Suppl
15:12-8.
Korszun, A., L. Sackett-Lundeen, E.
Papadopoulos, C. Brucksch, L. Masterson, N. C. Engelberg, E. Haus, M. A.
Demitrack and L. Crofford. 1999. Melatonin levels in women with
fibromyalgia and chronic fatigue syndrome. J Rheumatol
26(12):2675-80.
Kosek, E., J. Ekholm and P. Hansson. 1996.
“Sensory dysfunction in fibromyalgia patients with implications for
pathogenic mechanisms.” Pain 68 (2-3): 375-383.
Kostopoulos D. 2008. Reduction of spontaneous
electrical activity and pain perception of trigger points in the upper trapezius muscle through trigger point compression and passive stretching.
J Musculoskel Pain 16(4):266-278. “Although each technique significantly reduced pain perception
and SEA (spontaneous electrical activity) the combination of Ic (ischemic
compression) and PS (passive stretching) was superior, apparently because of
the complementary nature of the therapeutic interventions.”
Kotarinos RK. 2003. Pelvic floor physical
therapy in urogynecologic disorders. Curr Womens Health Rep.
3(4):334-339.
Kotter I, Neuscheler D, Gunaydin I et al. 2007.
Is there a predisposition for the development of autoimmune diseases in
patients with fibromyalgia? Retrospective analysis with long term
follow-up. Rheumatol Int. [Jul 20 Epub ahead of print].
“The risk of CTD (connective tissue disease) is not increased in FM.
The detection of ANA (antinuclear antibodies) does not predict the
development of CTD.”
Kovacevic-Ristanovic, R., R. D. Cartwright
and S. Lloyd. 1991. Nonpharmacologic treatment of period leg
movements in sleep. Arch Phys Med Rehabil 72(6):385-9.
Kovacs, F. M., V. Abraira, F. Pozo, D. G.
Kleinbaum, J. Beltran, I. Mateo, C. Perez de Ayala, A. Pena, A. Zea, M.
Gonzalez-Lanza and L. Morillas. 1997. Local and remote sustained
trigger point therapy for exacerbations of chronic low back pain. A
randomized, double-blind, controlled, multicenter trial. Spine
22(7):786-797.
Kraegen EW, Cooney GJ, Ye J, et al. 2001. Triglycerides, fatty acids and
insulin resistance B hyperinsulinemia. Exp Clin Enocrinol Diabetes
109(4):S516-26. "A key issue for development of insulin resistance is
skeletal muscle. At least some of the lipid accumulation is inside the
muscle cell (myocyte). Unless there is significant weight loss, short
or medium term dietary manipulation does not alter insulin sensitivity.
Evidence is growing that excess muscle and liver lipid accumulation causes
or exacerbates insulin resistance."
Krag, N. J. , J. Norregaard, J. K. Larsen,
B. Danneskiold-Samsoe. 1994. A blinded, controlled evaluation of anxiety and
depressive symptoms in patients with fibromyalgia, as measured by
standardized psychometric interview scales. Acta Psychiatr Scand
89(6):370-5.
Kramis, R. C., W. J. Roberts and R. G.
Gillette. 1996. Non-nociceptive aspects of persistent musculoskeletal pain.
J Orthop Sports Phys Ther
24(4):255-267.
Kratz AL, Davis MC, Zautra AJ. 2007. Pain
acceptance moderates the relation between pain and negative affect in female
osteoarthritis and fibromyalgia patients. Ann Behav Med.
33(3):291-301. “These findings suggest that pain patients with greater
capacity to accept pain may be emotionally resilient in managing their
condition.”
Kraus, H. and A. A. Fischer. 1991.
Diagnosis and treatment of myofascial pain. Mt Sinai J Med58(3):235-9
Krause, K-H, J. Krause, I. Magyarosy, E.
Ernst and D. Pongratz. 1998. Fibromyalgia syndrome and attention deficit
hyperactivity disorder: is there a co morbidity and are their consequences
for the therapy of fibromyalgia syndrome. J Musculoskel Pain 6(4):
111-116.
Kravitz HM, Esty ML, Karz RS et al. 2006.
Treatment of fibromyalgia syndrome using low-intensity neurofeedback with
the Flexyx Neurotherapy System: A randomized controlled clinical trial.
J Neurother 10(2/3):41-46.
Kreczy, A., M. Kofler and A. Gschwendtner.
1999. Underestimated health hazard: proposal for an ergonomic
microscope workstation. Lancet
354:1701-1702.
Krishman SK, Benzon HT, Siddiqui T et al.
2000. Pain on intramuscular injection of bupivacaine, ropivacaine,
with and without dexamethasone. Reg Anesth Pain Med
25(6):615-619. “The pain on intramuscular injection of bupivacaine
is significantly more intense than with ropivacaine.” Yet another
study documenting that Marcaine is not acceptable for TrP injections.
Krishnaswamy G, Ajitawi O, Chi DS. 2005.
The human mast cell: an overview. Methods Mol Biol.
315:13-34. “Mast cells may be capable of regulating
inflammation, host defense, and innate immunity. After
activation, mast cells express histamine, leukotrienes, and
prostanoids, as well as proteases, and many cytokines and
chemokines. These mediators may be pivotal to the genesis of
an inflammatory response. By virtue of their location and
mediator expression, mast cells may play an active role in many
diseases. Recent data also suggest that mast cells play a
vital role in host defense against pathogens by elaboration of tumor
necrosis factor alpha. Mast cells also express the Toll-like
receptor, which may further accentuate their role in the
immune-inflammatory response.”
Kroboth, P. D., F. S. Salek, A. L.
Pittenger, T. J. Fabian and R. F. Frye. 1999. DHEA and DHEA-S: a
review. J Clin Pharmacol
39(4):327-48.
Kroese MD, Schulpen GJ, Bessems MC et al.
2008. Substitution of specialized rheumatology nurses for
rheumatologists in the diagnostic process of fibromyalgia: a randomized
controlled trial. Arthritis Rheum. 59(9):1299-1305.
“Substituting specialized nurses for rheumatologists in the diagnostic
process of FM is a trustworthy and successful approach that saves waiting
time, provides greater patients satisfaction, and is cost-effective.”
Kruger, L. R., W. J. Van Der Linden and P.
E. Cleaton-Jones. 1998. Transcutaneous electrical nerve
stimulation in the treatment or myofascial pain dysfunction. S Afr
J Surg
36(1):35-38.
Kuan LC, Li YT, Chen FM et al. 2006. Efficacy
of treating abdominal wall pain by local injection. Taiwan J Obstet
Gynecol. 45(3):239-243. “Local injection for selective abdominal
wall pain patients produces significant pain relief. The diagnosis of
abdominal wall pain is an important component in avoiding unnecessary
operations in patients with abdominal pain.”
Kuan TS, Hsieh YL, Chen SM et al. 2007. The
myofascial trigger point region: correlation between the degree of
irritability and the prevalence of endplate noise. Am J Phys Med
Rehabil. 86(3):183-189. “The irritability of an MTrP is highly
correlated with the prevalence of EPN in the MTrP region of the upper
trapezius muscle. The assessment of EPN prevalence in an MTrP region
may be applied to evaluate the irritability of that MTrP.”
Kuan TS, Chen JT, Chen SM, Chien CH, Hong CZ. 2002.
Effect of botulinum toxin on endplate noise in myofascial trigger spots of
rabbit skeletal muscle. Am J Phys Med Rehabil 81(7):512-20.
This study confirms the association of excess acetylcholine in the motor
endplates as part of the pathogenesis of myofascial trigger points.
Kuch, K., B. J. Cox and R. J. Evans. 1996.
Posttraumatic stress disorder and motor vehicle accidents: a
multidisciplinary overview. Can J Psychiatry 41(7):429-434.
Kuch, K., B. Cox, R. J. Evans, P. C.
Watson and C. Bubela. 1993. To what extent do anxiety and depression
interact with chronic pain? Can J Psychiatry 38(1):38(1):36-38.
Kuchinad A, Schweinhardt P, Seminowicz
DA et al. 2007. Accelerated brain gray matter loss in
fibromyalgia patients: premature aging of the brain? J
Neurosci. 27(15):4004-4007. “…fibromyalgia patients had
significantly less total gray matter volume and showed a 3.3 times
greater age-associated decrease in gray matter than healthy
controls. The longer the individuals had had fibromyalgia, the
greater the gray matter loss, with each year of fibromyalgia being
equivalent to 9.5 times the loss in normal aging. In addition,
fibromyalgia patients demonstrated significantly less gray matter
density than healthy controls in several brain regions, including
the cingulate, insular and medical frontal cortices, and
parahippocampal gyri.” “...fibromyalgia appears to be
associated with an acceleration of age-related changes in the very
substance of the brain. Moreover, the regions in which we
demonstrate objective changes may be functionally linked to core
features of the disorder including affective disturbances and
chronic widespread pain.”
Kudo, Y. 1997. [Ca2+dynamics in glial
cells]. Nippon Yakurigaku Zasshi 109(3):111-7.
Kuhajda, M. C., B. E. Thorn and M. R.
Klinger. 1998. The effect of pain on memory for affective words.
Ann Behav Med
20(1):31-5.
Kuiper, G. G., J. G. Lemmen, B. Carlsson,
J. C. Corton, S. H. Safe, P. T. van der Saag and B. van der Burg.
1998. Interaction of estrogenic chemicals and phytoestrogens with
estrogen receptor beta. Endocrinology
139(10):4252-63.
Kujala, U. M., S. Taimela and T. Viljanen.
1999. Leisure physical activity and various pain symptoms among
adolescents. Br J Sports Med 33(5):325-8.
Kumar S, Ferrari R, Narayan Y. 2004.
Cervical muscle response to posterolateral impacts — effect of head
rotation. Clin Biomech 19(9):899-905. “Head rotation
in a right posterolateral impact modifies the cervical response mainly
by generating an asymmetry in the paired sternocleidomastoid
electromyograms. This may asymmetrically affect the risk of injury
to the sternocleidomastoids “
Kumar S, Ferrari R, Narayan Y. 2004.
Electromyographic and kinematic exploration of whiplash-type rear
impacts: effect of left offset impact. Spine J.
4(6):656-665. “When a rear impact is offset to the subject’s left,
it results in not only increased electromyographic generation in both
sternocleidomastoids, but the splenius capitis contralateral to the
direction of impact offset also bears part of the force of the neck
perturbation. Expecting or being aware of imminent impact also
plays a role in reducing muscle responses in low-velocity offset rear
impacts.” [It is an interesting reflection that while some
researchers are working to understand the mechanisms of whiplash and
thus benefiting patients and care providers, and perhaps preventing
further injury, there are doctors (primarily under the pay and/or
influence of insurance companies) who still refuse to believe whiplash
exists. DJS]
Kumar S, Narayan Y, Amell T. 2002. An
electromyographic study of low-velocity rear-end impacts. Spine
27(10):1044-1055. “Muscle responses were greater with higher levels of
acceleration. Because the muscular component of the head-neck complex
plays a central role in the abatement of higher acceleration levels, it
may be a primary site of injury in the whiplash phenomenon.”
Kundermann B, Krieg JC, Schreiber W et al.
2004. The effect of sleep deprivation on pain. Pain Res
Manag. 9(1):25-32. “Chronic pain syndromes are associated with
alterations in sleep continuity and sleep architecture. One
perspective of this relationship, which has not received much attention
to date, is that disturbances of sleep affect pain. Sleep
deprivation produces hyperalgesic changes. Sleep deprivation can
counteract analgesic effects of pharmacological treatments involving
opioidergic and serotoninergic mechanisms of action.”
Kuo LE, Kitlinska JB, Tilan JU et al. 2007. Neuropeptide Y acts
directly in the periphery on fat tissue and mediates stress-induced
obesity and metabolic syndrome. Nat Med. 13(7):803-811.
Kung YY, Chen FP, Chaung HL et al. 2001.
Evaluation of acupuncture effect to chronic myofascial pain syndrome in
the cervical and upper back regions by the concept of Meridians.
Acupunct Electrother Res. 26(3):195-202. “Acupuncture is a
somewhat effective method for pain relief of patients with chronic MPS
in the cervical and upper back regions. The effect of acupuncture
with the concept of meridians on MPS is insidious and the duration of
the relief is not long enough.”
Kupers RC, Svensson P, Jensen TS. 2004.
Central representation of muscle pain and mechanical hyperesthesia in
the orofacial region: a positron emission tomography study.
Pain 108(3):284-293. s “Cerebral processing of jaw-muscle pain may
differ from the processing of cutaneous pain and that mechanical
hyperesthesia, which often is encountered in clinical cases, has a
unique representation in the brain.”
Kuramoto AM. 2006. Therapeutic benefits
of Tai Chi exercise: research review. WMJ 105(7):42-46.
Kurland JE, Coyle WJ, Winkler A et al. 2006.
Prevalence of irritable bowel syndrome and depression in fibromyalgia.
Dig Dis Sci. 51(3):454-460. “The prevalence of IBS and
depressive symptoms was higher in FM patients compared to the control
population.”
Kurosinski P, Gotz J. 2002. Glial
cells under physiologic and pathologic conditions. Arch Nerol
59(10):1524-8. Glial cell loss may contribute to cognitive deficits such as
memory impairment.
Kurtze, N., K. T. Gundersen and S. Svebak.
1999. Quality of life, functional disability and lifestyle among
subgroups of fibromyalgia patients: the significance of anxiety and
depression. Br J Med Psychol 72 (Pt 4):471-84.
Kurtze, N., K. T. Gundersen and S. Svebak.
1998. The role of anxiety and depression in fatigue and patterns of
pain among subgroups of fibromyalgia patients. Br J Med Psychol
71(Pt 2):185-194.
Kusano M, Kouzu T, Kawano T et al. 2008.
Nationwide epidemiological study on gastroesophageal reflux disease and
sleep disorders in the Japanese population. J Gastroenterol.
43(11):833-841. “In Japanese people, patients with heartburn had a
significantly higher prevalence of sleep disorders than those without
heartburn.” [Another good study verifying this link. Sleep
studies, which should be part of all FM workups, should include testing
for GERD. GERD may often be “silent,” lacking usual symptoms.
DJS]
Kvale A, Skouen JS, Ljunggren, AE. 2003.
Discriminative validity of the global physiotherapy examination-52 in
patients with long lasting musculoskeletal pain versus healthy persons.
J Musculoskel Pain 11(3):23-35. This study separated patients
into subgroups, comparing healthy patients, patients with long-standing
musculoskeletal pain, men and women. The physical therapy evaluations
were separated into 5 domains: Posture, Respiration, Movement, Muscle and
Skin. They found significant variations, especially in Movement and
Muscle groups, and also differences dependent on gender and pain
distribution.
Kwan CL, Diamant NE,
Pope G et al. 2005. Abnormal forebrain activity in functional bowel
disorder patients with chronic pain. Neurology
65(8):1268-1277. Abnormal brain responses in IBS may cause many
sensory symptoms including pain, dysfunction and dysfunctional processing of
visceromotor stimuli.
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