Current pain and headache reports
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Pathologies currently defined as temporomandibular disorders may be different in nature. Temporomandibular joint (TMJ) disorders and craniofacial and cervical myogenous pain (MP) are distinct pathologies but may be superimposed and share some etiologic factors. ⋯ Psychiatric comorbidity (depression and/or anxiety disorder) is less frequent in sheer TMJ disorders, compared with MP and TTH. A screening for the presence of an underlying psychiatric disorder should be part of the clinical evaluation in patients suffering from headache and facial pain.
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Chronic neck pain is a common patient complaint. Despite its frequency as a clinical problem, there are few evidence-based studies that document efficacy of therapies for neck pain. The treatment of this symptom is based primarily on clinical experience. ⋯ Local injections of anesthetics with or without soluble corticosteroid preparations offer additional pain relief. The purpose of these agents is to diminish pain to facilitate normal neck movement. Surgical therapy with cervical spine fusion is indicated for the rare patient with intractable neck pain resistant to all nonsurgical therapies.
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The association between tension-type headache and cognitive ability was assessed among 971 members of a longitudinal birth cohort study. Primary headache status was determined at age 32 years according to 2004 International Headache Society criteria, frequent childhood headaches were identified from parent report from ages 7 to 13 years, and data relating to cognitive and academic performance from ages 3 to 32 years were analyzed. ⋯ Instead, a consistent relation was found between childhood headache (regardless of headache diagnosis in adulthood) and lower scores on most cognitive measures from age 3 years through adolescence (verbal and performance IQ, receptive language, and reading scores). The data indicate that cognitive performance deficits in childhood headache sufferers can probably be attributed to factors stemming from utero or early childhood.
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After several decades of senescence, the twin fields of hyperuricemia and gout have again regained attention in both the scientific and clinical spheres, and this review highlights several recent advancements. Specifically, we review newly discovered mechanisms of uric acid-induced inflammation, uric acid's putative role as a "danger signal" in innate immunity, the possible link between hyperuricemia and cardiovascular disease, and evolutionary evidence suggesting that hyperuricemia conferred a survival advantage in primates (when the gene for uricase was lost) several million years ago. Finally, we provide an overview of the current approach to gout, as well as what treatments are on the horizon.
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During the past 2 years, a great deal of evaluation has been conducted on the cardiovascular (CV) effects of nonsteroidal anti-inflammatory drugs (NSAIDs) and selective cyclooxygenase (COX)-2 inhibitors. This review focuses on the effects of the NSAIDs and COX-2 inhibitors on blood pressure and CV events. Clinical trial databases for NSAIDs and COX-2 inhibitors have shown varying levels of destabilization of blood pressure control in treated hypertensive patients as well as variable incident rates of the development of arrhythmias, congestive heart failure, myocardial infarction, and stroke. Nonselective and COX-2 selective NSAIDs can be used carefully in arthritis patients with hypertension and stable CV disorders (excluding congestive heart failure and moderate to severe kidney dysfunction) when the individual clinical benefit of anti-inflammatory therapy outweighs the CV and gastrointestinal risk.