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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because of other diseases mimicking the symptoms of temporomandibular dysfunction (TMD), differential diagnosis is of the utmost importance. Diagnostic subgroups of TMD (osteoarthrosis, anterior disc displacement with/without reduction, TMD-myo) can be distinguished by a combination of active movements, passive opening and palpation. Active movement appeared to be the most powerful test for distinguishing the subgroups of TMD, e.g. myogenous, arthrogenous, myogenous and arthrogenous. It is advised to have an open mind in the clinical examination and to be aware of the many mimicking disorders before reaching a diagnosis. An anamnestic questionnaire addressing the pain history, signs and symptoms of TMD, functional impairments, correlates of TMD, psychosocial evaluation and general health status is mandatory. Headache and neck pain often accompany TMD. In appropriate situations it is advised to refer to the proper specialist, before starting treatment for TMD. Orthopedic tests of the cervical spine are of minor importance in discriminating between patients with TMD and patients with cervical spine disorders (CSD). It is therefore advised to evaluate the function of the stomatognathic system in patients with neck complaints to rule out a possible involvement of this system.
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PMID:[Diagnosis and classification of temporomandibular dysfunction by the general dental practitioner]. 1192 96

Noxious stimuli and painful disorders interfere with sleep, but disturbances in sleep also contribute to the experience of pain.Chronic paroxysmal hemicrania and possibly cluster headaches are related to REM sleep. Whereas headache is associated with snoring and sleep apnea, morning headaches are not specific for any primary sleep disorder. Nevertheless, the management of the sleep disorder ameliorates both morning headache and migraine.Noxious stimuli administered into muscles during slow-wave sleep (SWS) result in decreases in delta and sigma but an increase in alpha and beta EEG frequencies during sleep. Noise stimuli that disrupt SWS result in unrefreshing sleep, diffuse musculoskeletal pain, tenderness, and fatigue in normal healthy subjects. Such symptoms accompany alpha EEG sleep patterns that often occur in patients with fibromyalgia. The alpha EEG patterns include phasic and tonic alpha EEG sleep as well as periodic K alpha EEG sleep or frequent periodic cyclical alternating pattern. Moreover, alpha EEG sleep, as well as sleep-related breathing disorder and periodic limb movement disorder, occur in some patients with fibromyalgia, rheumatoid arthritis and osteoarthritis. Depression and not alpha EEG sleep are features of somatoform pain disorder. Disturbances in sleep, pain behaviour and psychological distress influence return to work in workers who have suffered a soft tissue injury, e.g. low back pain. Patients with irritable bowel disorder have disturbed sleep and have increased REM sleep. In conclusion, there is a reciprocal relationship between sleep quality and pain. The recognition of disturbed or unrefreshing sleep influences the management of painful medical disorders.
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PMID:Sleep and pain. 1253 Oct 4

Pain produced by musculoskeletal disorders commonly misconceived as having mechanical etiology often is caused by inflammatory mechanisms. Simple analgesics (ie, those that lack anti-inflammatory action) often are used to treat musculoskeletal pain when an anti-inflammatory analgesic may be more effective for the painful condition. This review addresses the anti-inflammatory agents available for the symptomatic management of common inflammatory musculoskeletal conditions including osteoarthritis, rheumatoid arthritis, and low back pain.
Curr Pain Headache Rep 2004 Jun
PMID:Anti-inflammatory agents for the treatment of musculoskeletal pain and arthritis. 1511 34

Nabumetone is a nonsteroidal anti-inflammatory prodrug, which exerts its pharmacological effects via the metabolite 6-methoxy-2-naphthylacetic acid (6-MNA). Nabumetone itself is non-acidic and, following absorption, it undergoes extensive first-pass metabolism to form the main circulating active metabolite (6-MNA) which is a much more potent inhibitor of preferentially cyclo-oxygenase (COX)-2. The three major metabolic pathways of nabumetone are O-demethylation, reduction of the ketone to an alcohol, and an oxidative cleavage of the side-chain occurs to yield acetic acid derivatives. Essentially no unchanged nabumetone and < 1% of the major 6-MNA metabolite are excreted unchanged in the urine from which 80% of the dose can be recovered and another 10% in faeces. Nabumetone is clinically used mainly for the management of patients with osteoarthritis (OA) or rheumatoid arthritis (RA) to reduce pain and inflammation. The clinical efficacy of nabumetone has also been evaluated in patients with ankylosing spondylitis, soft tissue injuries and juvenile RA. The optimum oral dosage of nabumetone for OA patients is 1 g once daily, which is well tolerated. The therapeutic response is superior to placebo and similar to nonselective COX inhibitors. In RA patients, nabumetone 1 g at bedtime is optimal, but an additional 0.5-1 g can be administered in the morning for patients with persistent symptoms. In RA, nabumetone has shown a comparable clinical efficacy to aspirin (acetylsalicylic acid), diclofenac, piroxicam, ibuprofen and naproxen. Clinical trials and a decade of worldwide safety data and long-term postmarketing surveillance studies show that nabumetone is generally well tolerated. The most frequent adverse effects are those commonly seen with COX inhibitors, which include diarrhoea, dyspepsia, headache, abdominal pain and nausea. In common with other COX inhibitors, nabumetone may increase the risk of GI perforations, ulcerations and bleedings (PUBs). However, several studies show a low incidence of PUBs, and on a par with the numbers reported from studies with COX-2 selective inhibitors and considerably lower than for nonselective COX inhibitors. This has been attributed mainly to the non-acidic chemical properties of nabumetone but also to its COX-1/COX-2 inhibitor profile. Through its metabolite 6-MNA, nabumetone has a dose-related effect on platelet aggregation, but no effect on bleeding time in clinical studies. Furthermore, several short-term studies have shown little to no effect on renal function. Compared with COX-2 selective inhibitors, nabumetone exhibits similar anti-inflammatory and analgesic properties in patients with arthritis and there is no evidence of excess GI or other forms of complications to date.
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PMID:Nabumetone: therapeutic use and safety profile in the management of osteoarthritis and rheumatoid arthritis. 1545 29

Lumiracoxib is a highly selective and potent cyclo-oxygenase (COX)-2 inhibitor, with a novel structure that conveys weakly acidic properties and a unique pharmacological profile. It is rapidly absorbed, with a relatively short plasma half-life. In well designed clinical trials of 1-52 weeks' duration in patients with osteoarthritis (OA) or rheumatoid arthritis, the efficacy of oral lumiracoxib 100-400 mg/day in decreasing pain intensity and improving functional status was greater than that with placebo and similar to those with nonselective NSAIDs or celecoxib 200mg once daily. In single- and multiple-dose well designed trials in patients with acute pain associated with primary dysmenorrhoea, dental or orthopaedic surgery or tension-type headache, lumiracoxib 100-800 mg once daily was more effective in relieving acute pain than placebo or controlled-release oxycodone 20 mg, and was at least as effective as selective COX-2 inhibitors or nonselective NSAIDs. Lumiracoxib was generally well tolerated in clinical trials, with a similar overall tolerability profile to those of placebo and other COX-2-selective inhibitors. In a large 52-week safety trial in patients with OA, lumiracoxib 400mg once daily had a rate of gastrointestinal ulcer complications that was approximately one-third to one-quarter of that of ibuprofen 800 mg three times daily or naproxen 500 mg twice daily. Lumiracoxib was not associated with an increase in cardiovascular events.
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PMID:Lumiracoxib. 1545 39

Glucosamine products have been used extensively for the management of pain in osteoarthritis. This paper reviews the most recent clinical and experimental studies regarding its efficacy and safety. Although clinical trials include methodologic flaws and publication bias, glucosamine is likely an effective therapy for the symptomatic management of osteoarthritis. In turn, definite proof for chondromodulating effect requires well-conducted clinical trials. In North America, glucosamine is an over-the-counter dietary supplement and preparations made by different manufacturers may vary. There is also a need to standardize this therapy and allow practitioners to give patients suitable advice. An ongoing long-term clinical trial in the US will possibly permit to investigate the clinical relevance of these results and give appropriate recommendations.
Curr Pain Headache Rep 2004 Dec
PMID:The use of glucosamine therapy in osteoarthritis. 1550 66

The lumbar spine is a common location for osteoarthritis. The axial skeleton demonstrates the same classic alterations of cartilage loss, joint instability, and osteophytosis characteristic of symptomatic disease in the appendages. Despite these similarities, questions remain regarding the lumbar spine facet joints as a source of chronic back pain. The facet joints undergo a progression of degeneration that may result in pain. The facet joints have sensory input from two spinal levels that makes localization of pain difficult. Radiographic studies describe intervertebral disc abnormalities in asymptomatic individuals that are associated with, but not synonymous for, osteoarthritis. Patients who do not have osteoarthritis of the facet joints on magnetic resonance scan do not have back pain. Single photon emission computed tomography scans of the axial skeleton are able to identify painful facet joints with increased activity that may be helped by local anesthetic injections. Low back pain is responsive to therapies that are effective for osteoarthritis in other locations. Osteoarthritis of the lumbar spine does cause low back pain.
Curr Pain Headache Rep 2004 Dec
PMID:Does osteoarthritis of the lumbar spine cause chronic low back pain? 1550 67

Although menopause is a normal developmental milestone through which all women pass, the transition has been long associated with chronic pain conditions that may be more accurately viewed as secondary to aging. Clinicians need to understand management of pain problems women may experience. This article examines pain syndromes including headache, back pain, osteoarthritis, pelvic pain, vulvo-vaginal pain, and burning mouth syndrome.
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PMID:Pain at midlife. 1554 82

Non-steroidal anti-inflammatory drugs (NSAIDs) are indicated for treatment of rheumatoid arthritis and osteoarthritis, but often induce gastric adverse experiences (AE), including gastric ulcers and complications. Inhibitors of proton pump and H(2) antagonists are very effective for duodenal ulcer; meanwhile, cytoprotective drugs are more effective for gastric ulcer. D-002 is a mixture of higher aliphatic alcohols obtained from beeswax, wherein triacontanol is the most abundant. D-002 induces anti-ulcer effects through a cytoprotective mechanism, being more effective in protecting against ethanol- and NSAID-induced ulcers. The present double-blind, placebo-controlled clinical study was undertaken to investigate the effects of D-002 on gastric symptoms associated to piroxicam use on patients suffering osteoarthritis. Fifty-nine patients, all taking piroxicam, 20 mg/day, were randomized to placebo or D-002 (40 or 100 mg/day) for 14 days. The primary efficacy variable was the reduction on the frequency of patients with gastric AE compared with placebo. Pain evolution was investigated to discard any influence on D-002 on the analgesic effect of piroxicam. The frequency of patients treated with D-002, 40 and 100 mg/day, reporting acidity [0 of 18 (0%) and 1 of 21 (4.8%), respectively] was lower (P < .05) than in placebo [6 of 20 (30%)]. Also, the frequency of patients treated with 100 mg/day reporting some gastric AE [5 of 21 (23.8%)] was lower (P < .05) than in placebo [13 of 20 (65.0%)]. The analgesic effect of piroxicam was unaffected with D-002. Treatment was well tolerated. Two patients discontinued from the study because of gastrointestinal AE: one in the placebo group and the other treated with D-002, 40 mg/day. Other three patients discontinued because of other AE: mildly uncontrolled hypertension (one in the placebo group, one treated with D-002, 40 mg/day) and headache (one treated with D-200, 100 mg/day). It is concluded that D-002 could be useful for controlling gastric AE of patients treated with NSAIDs, although further studies with a larger sample size and longer follow-up are needed for definitive conclusions.
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PMID:Effects of D-002, a product isolated from beeswax, on gastric symptoms of patients with osteoarthritis treated with piroxicam: a pilot study. 1585 12

The most frequent symptom of craniomandibular dysfunction is pain in the preauricular area or in the temporo-mandibular joint, usually localized at the level of the masticatory musculature. Patients sometimes also complain of reflect otalgia, headaches and facial pain. Osteoarthrosis is a frequent degenerative debilitating chronic disorder that can affect the temporomandibular joint. It causes pain and articular rigidity, a reduction in mobility, and radiological alterations are visible in stratigraphy. The aim of this study was to compare the efficacy of a topically applied non-steroid anti-inflammatory drug that has recently become commercially available (diclofenac sodium in a patented carrier containing dimethyl sulfoxide, that favours transcutaneous absorption) which is commonly used to alleviate pain in knee or elbow joints, versus oral diclofenac, in the treatment of symptoms of temporomandibular joint dysfunction. Dysfunction of the temporomandibular joint was diagnosed in 36 adult patients. The patients were randomized in two age- and gender -matched groups. Group A (18 patients) received oral diclofenac sodium administered after a meal in 50-mg tablets twice a day for 14 days. Group B (18 patients) received 16 mg/ml topical diclofenac (diclofenac topical solution, 10 drops 4 times a day for 14 days). All patients completed a questionnaire at the start and end of therapy. Patients were asked to quantify on a graded visual analogue scale and to reply to questions about the pain and tenderness of the temporomandibular joint and the functional limitation of mouth opening. Patients were also requested to report side-effects of the treatment. All patients showed relief from pain after treatment: the difference between the two groups was not significant (p > 0.05). Post-treatment, 16 patients of group A had epigastralgic symptoms. Three patients treated with topical diclofenac showed a modest irritation of the temporomandibular joint region, and disappeared spontaneously. Our results demonstrate that topically applied diclofenac and oral diclofenac are equally effective in the treatment of temporomandibular joint dysfunction symptoms. Topical diclofenac has the advantage that it does not have adverse systemic effects, whereas oral diclofenac had untoward effects on the gastric apparatus. The efficacy of diclofenac topically applied on the temporomandibular joint region observed in group B is explained by the association of diclofenac with dimethyl-sulfoxide, which enables a rapid effective penetration into the joint tissues. It is noteworthy that dimethyl-sulfoxide favours transuctaneous absorption when used in a multi-dose regime as in our study with 4 doses a day. Thus, single, "as required", applications should be avoided because this practice results in scarce absorption of diclofenac.
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PMID:Topical versus systemic diclofenac in the treatment of temporo-mandibular joint dysfunction symptoms. 1587 9


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