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Query: UMLS:C0184567 (acute pain)
 3,962 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A unifying model of herpes zoster pain presents considerable analytical challenges due to the requirement for prospective data collection and the varying rates of pain resolution reported by individual patients. Demographic, clinical, and quality-of-life measures were collected on 166 human immunodeficiency virus (HIV)-infected patients enrolled in a randomized, controlled trial of antiviral therapy of herpes zoster comparing acyclovir with sorivudine. A "mixed model" was used to assess factors predictive of pain severity, activity impairment, and sleep interruption. The average rate of change in acute pain was -0.04 unit pain per day for the first month. Chronic pain decreased -0.12 per month for months 1-12. Acute pain severity was positively correlated with number of new skin vesicles, analgesic use, and baseline pain, and negatively related to percentage of lesion healing and crusting. Postherpetic neuralgia was correlated with baseline pain, pain at 1 month, and duration of lesions. Treatment group, gender, race, and CD4 count were not related to change in pain severity. These analyses verify the significance of baseline pain as a significant predictor of pain resolution and average pain severity as a predictor of return to normal daily activities and sleep. The severity of acute pain at presentation and at 1 month are significant predictors of chronic pain.
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PMID:A mixed model for factors predictive of pain in AIDS patients with herpes zoster. 1038 46

Some 250 million cases of sexually transmitted disease (STD) occur each year, and in some countries 1 or even 2 women in every 10 are infected with an STD. STDs are likely to reach an advanced stage before women notice them. The consequences of STDs are devastating, according to a report by the Population Information Program of the Johns Hopkins School of Public Health, and they include stillbirths, blinding eye infections in the newborn, chronic female abdominal pain, ectopic pregnancy, and infertility. There are social consequences for women such as divorce, and husbands may abandon infertile wives. Gonorrhea and chlamydia can cause both severe inflammation of the pelvis with acute pain and possible infertility. Pelvic inflammatory disease can permanently scar the fallopian tubes, increasing the risk of ectopic pregnancy, which can be fatal when the fallopian tube ruptures. Babies born to mothers with gonorrhea and chlamydia are likely to develop eye infections that may make them blind. Chlamydia infection in pregnant women may also cause premature rupture of the membranes, sepsis, and the death of premature neonate. Infection may spread to the lungs of newborns, leading to chlamydial pneumonia. Syphilis can cause spontaneous abortion, stillbirth, neonatal death, or congenital syphilis in the infant. Trichomoniasis and herpes can also be transmitted from mother to fetus. And infection with an STD increases the risk of infection with the human immunodeficiency virus (HIV). The World Health Organization (WHO) recommends that prenatal care should always include checks for STDs. A WHO Technical Working Group on Care of Mother and Baby has stressed the importance of detecting and treating STDs in pregnant women. The working group urged training of health workers to distinguish between STDs and other infections. The group, which met July 5-9, 1993, outlined health center strategies for prevention and treatment.
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PMID:STDs infect 250 million a year. 1234

Neuropathic pain (NP), caused by a primary lesion or dysfunction in the nervous system, affects approximately 4 million people in the United States each year. It is associated with many diseases, including diabetic peripheral neuropathy, postherpetic neuralgia, human immunodeficiency virus-related disorders, and chronic radiculopathy. Major pathophysiological mechanisms include peripheral sensitization, sympathetic activation, disinhibition, and central sensitization. Unlike most acute pain conditions, NP is extremely difficult to treat successfully with conventional analgesics. This article introduces a contemporary management approach, that is, one that incorporates nonpharmacological, pharmacological, and interventional strategies. Some nonpharmacological management strategies include patient education, physical rehabilitation, psychological techniques, and complementary medicine. Pharmacological strategies include the use of first-line agents that have been supported by randomized controlled trials. Finally, referral to a pain specialist may be indicated for additional assessment, interventional techniques, and rehabilitation. Integrating a comprehensive approach to NP gives the primary care physician and patient the greatest chance for success.
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PMID:Contemporary management of neuropathic pain for the primary care physician. 1559 38

Activation of glial cells and neuro-glial interactions are emerging as key mechanisms underlying chronic pain. Accumulating evidence has implicated 3 types of glial cells in the development and maintenance of chronic pain: microglia and astrocytes of the central nervous system (CNS), and satellite glial cells of the dorsal root and trigeminal ganglia. Painful syndromes are associated with different glial activation states: (1) glial reaction (ie, upregulation of glial markers such as IBA1 and glial fibrillary acidic protein (GFAP) and/or morphological changes, including hypertrophy, proliferation, and modifications of glial networks); (2) phosphorylation of mitogen-activated protein kinase signaling pathways; (3) upregulation of adenosine triphosphate and chemokine receptors and hemichannels and downregulation of glutamate transporters; and (4) synthesis and release of glial mediators (eg, cytokines, chemokines, growth factors, and proteases) to the extracellular space. Although widely detected in chronic pain resulting from nerve trauma, inflammation, cancer, and chemotherapy in rodents, and more recently, human immunodeficiency virus-associated neuropathy in human beings, glial reaction (activation state 1) is not thought to mediate pain sensitivity directly. Instead, activation states 2 to 4 have been demonstrated to enhance pain sensitivity via a number of synergistic neuro-glial interactions. Glial mediators have been shown to powerfully modulate excitatory and inhibitory synaptic transmission at presynaptic, postsynaptic, and extrasynaptic sites. Glial activation also occurs in acute pain conditions, and acute opioid treatment activates peripheral glia to mask opioid analgesia. Thus, chronic pain could be a result of "gliopathy," that is, dysregulation of glial functions in the central and peripheral nervous system. In this review, we provide an update on recent advances and discuss remaining questions.
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PMID:Glia and pain: is chronic pain a gliopathy? 2379 84

Capsaicin 8% patch (Qutenza) is mainly used to treat postherpetic neuralgia and human immunodeficiency virus-associated neuropathy. However, evidence of the efficacy of Qutenza in other forms of neuropathic pain is lacking. A 24-year old Libyan man, with no previous medical history, sustained multiple wounds in the right side of the chest and back after a bomb explosion. The patient experienced pain, which persisted in a wide location around the surgical intervention for a long time, beyond the usual course of natural healing of an acute pain and was different from that suffered preoperatively. The characteristics of the pain included burning, electric shock-like sensation, tingling, and numbness, and it was paroxysmal. The pain was associated with hyperalgesia and intense allodynia in a wide area, approximately of 1,100 cm2. Our initial treatment strategy included pregabalin, tramadol, and duloxetine. However, our patient's pain responded to treatment with capsaicin 8% patch when the initial treatments showed only minimal effectiveness regarding the intensity of pain. Interestingly, the most important finding was that capsaicin 8% patch showed a more than 80% reduction of the area of allodynia associated with the pain, when other treatments failed. Moreover, although recent data showed that in patients who respond to Qutenza, analgesia starts within a few days of treatment and lasts on average 5 months, our patient showed an initial response within 7 days of treatment but a longer duration of more than 18 months. Although further controlled studies are needed to explore the efficacy of the capsaicin 8% patch in patients who experience posttraumatic neuropathic pain, we encourage clinicians to try the capsaicin 8% patch when alternative treatments fail.
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PMID:Posttraumatic and postsurgical neuropathic pain responsive to treatment with capsaicin 8% topical patch. 2465 88

Pathological pain is a common and debilitating condition that is often poorly managed. Central sensitization is an important mechanism underlying pathological pain. However, candidate molecules involved in central sensitization remain unclear. Store-operated calcium channels (SOCs) mediate important calcium signals in nonexcitable and excitable cells. SOCs have been implicated in a wide variety of human pathophysiological conditions, including immunodeficiency, occlusive vascular diseases, and cancer. However, the role of SOCs in CNS disorders has been relatively unexplored. Orai1, a key component of SOCs, is expressed in the human and rodent spinal cord dorsal horn, but its functional significance in dorsal horn neurons is poorly understood. Here we sought to explore a potential role of Orai1 in the modulation of neuronal excitability and A-type potassium channels involved in pain plasticity. Using both male and female Orai1 knock-out mice, we found that activation of Orai1 increased neuronal excitability and reduced A-type potassium channels via the protein kinase C-extracellular signal-regulated protein kinase (PKC-ERK) pathway in dorsal horn neurons. Orai1 deficiency significantly decreased acute pain induced by noxious stimuli, nearly eliminated the second phase of formalin-induced nociceptive response, markedly attenuated carrageenan-induced ipsilateral pain hypersensitivity and abolished carrageenan-induced contralateral mechanical allodynia. Consistently, carrageenan-induced increase in neuronal excitability was abolished in the dorsal horn from Orai1 mutant mice. These findings uncover a novel signaling pathway involved in the pain process and central sensitization. Our study also reveals a novel link among Orai1, ERK, A-type potassium channels, and neuronal excitability.SIGNIFICANCE STATEMENT Orai1 is a key component of store-operated calcium channels (SOCs) in many cell types. It has been implicated in such pathological conditions as immunodeficiency, autoimmunity, and cancer. However, the role of Orai1 in CNS disorders remains poorly understood. The functional significance of Orai1 in neurons is elusive. Here we demonstrate that activation of Orai1 modulates neuronal excitability and Kv4-containing A-type potassium channels via the protein kinase C-extracellular signal-regulated protein kinase (PKC-ERK) pathway. Genetic knock-out of Orai1 nearly eliminates the second phase of formalin-induced pain and markedly attenuates carrageenan-induced pain hypersensitivity and neuronal excitability. These findings reveal a novel link between Orai1 and neuronal excitability and advance our understanding of central sensitization.
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PMID:Orai1 Plays a Crucial Role in Central Sensitization by Modulating Neuronal Excitability. 2922 3