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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pain properties of 50 fibromyalgia patients were examined and compared with pain properties of 50 rheumatoid arthritis patients. In both fibromyalgia and rheumatoid arthritis, pain was bilateral, involved multiple sites, and was of equal intensity (60.8 versus 58.7, respectively, on a scale of 100). Fibromyalgia pain, however, was less localized to the joints and suggested greater spatial diffusion. It involved more kinds of pain experiences (radiating, steady, spreading, spasms, gnawing, unlocalized, pricking, crushing, shooting, pressing, splitting, cramping, nagging, and pins and needles), and was dispersed over larger areas of the body. The anatomic sites best for discrimination between patients with fibromyalgia and patients with rheumatoid arthritis were the lower back, thigh, abdomen, head, and hips for fibromyalgia, and wrist, foot, and fingers for rheumatoid arthritis. The traditional clinical description of aching and stiffness does not appear to accurately describe the complexity of the fibromyalgia pain syndrome.
Arthritis Rheum 1986 Jun
PMID:Comparison of pain properties in fibromyalgia patients and rheumatoid arthritis patients. 348 24

Carpal tunnel syndrome, although rare, is known to occur in children mainly because of genetic or metabolic disorders. The clinical findings are variable and include symptoms of burning pain, tingling, numbness, and weakness or atrophy in the hands of the patients. It is usually diagnosed by demonstration of prolonged distal latency times during the electrodiagnostic studies. Reported here is a patient with juvenile chronic arthritis and a diagnosis of severe bilateral carpal tunnel syndrome, the first patient reported in the literature, to the best of the authors' knowledge.
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PMID:Severe bilateral carpal tunnel syndrome in juvenile chronic arthritis. 1464

Heel pain is a common condition in adults that may cause significant discomfort and disability. A variety of soft tissue, osseous, and systemic disorders can cause heel pain. Narrowing the differential diagnosis begins with a history and physical examination of the lower extremity to pinpoint the anatomic origin of the heel pain. The most common cause of heel pain in adults is plantar fasciitis. Patients with plantar fasciitis report increased heel pain with their first steps in the morning or when they stand up after prolonged sitting. Tenderness at the calcaneal tuberosity usually is apparent on examination and is increased with passive dorsiflexion of the toes. Tendonitis also may cause heel pain. Achilles tendonitis is associated with posterior heel pain. Bursae adjacent to the Achilles tendon insertion may become inflamed and cause pain. Calcaneal stress fractures are more likely to occur in athletes who participate in sports that require running and jumping. Patients with plantar heel pain accompanied by tingling, burning, or numbness may have tarsal tunnel syndrome. Heel pad atrophy may present with diffuse plantar heel pain, especially in patients who are older and obese. Less common causes of heel pain, which should be considered when symptoms are prolonged or unexplained, include osteomyelitis, bony abnormalities (such as calcaneal stress fracture), or tumor. Heel pain rarely is a presenting symptom in patients with systemic illnesses, but the latter may be a factor in persons with bilateral heel pain, pain in other joints, or known inflammatory arthritis conditions.
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PMID:Diagnosing heel pain in adults. 1529 Oct 91

Every pain syndrome has an inflammatory profile consisting of the inflammatory mediators that are present in the pain syndrome. The inflammatory profile may have variations from one person to another and may have variations in the same person at different times. The key to treatment of Pain Syndromes is an understanding of their inflammatory profile. Pain syndromes may be treated medically or surgically. The goal should be inhibition or suppression of production of the inflammatory mediators and inhibition, suppression or modulation of neuronal afferent and efferent (motor) transmission. A successful outcome is one that results in less inflammation and thus less pain. We hereby briefly describe the inflammatory profile for several pain syndromes including arthritis, back pain, neck pain, fibromyalgia, interstitial cystitis, migraine, neuropathic pain, complex regional pain syndrome/reflex sympathetic dystrophy (CRPS/RSD), bursitis, shoulder pain and vulvodynia. These profiles are derived from basic science and clinical research performed in the past by numerous investigators and serve as a foundation to be built upon by other researchers and will be updated in the future by new technologies such as magnetic resonance spectroscopy. Our unifying theory or law of pain states: the origin of all pain is inflammation and the inflammatory response. The biochemical mediators of inflammation include cytokines, neuropeptides, growth factors and neurotransmitters. Irrespective of the type of pain whether it is acute or chronic pain, peripheral or central pain, nociceptive or neuropathic pain, the underlying origin is inflammation and the inflammatory response. Activation of pain receptors, transmission and modulation of pain signals, neuro plasticity and central sensitization are all one continuum of inflammation and the inflammatory response. Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arise from inflammation and the inflammatory response. We are proposing a re-classification and treatment of pain syndromes based upon their inflammatory profile.
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PMID:The biochemical origin of pain: the origin of all pain is inflammation and the inflammatory response. Part 2 of 3 - inflammatory profile of pain syndromes. 1772 71

A patient was admitted reporting tingling pain and numbness in the right hand. Neurological examination--including nerve conduction studies--diagnosed carpal tunnel syndrome. Operative carpal tunnel release was performed without complications. Four months postoperatively the otherwise healthy patient presented again due to persistent complaints, although preoperative symptoms had improved. On this occasion, the patient reported loss of strength accompanied by rigidity in the wrist. Clinical examination showed some swelling adjacent to the operation wound. A postoperative ganglion cyst was suspected and a conservative treatment option--splinting the wrist--was chosen. Four weeks later the patient presented again with further swelling and increasing rigidity of the wrist. Surgical intervention was planned. Preoperative plain radiographs of the wrist revealed chronic palmar dislocation of the lunate to be the cause of the symptoms in our patient. Radiological signs of scapholunate advanced collapse arthritis (SLAC wrist) were also observed.
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PMID:Initially unrecognised lunate dislocation as a cause of carpal tunnel syndrome. 2351 27