The journal of pain : official journal of the American Pain Society
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Comment Letter Case Reports
Complex regional pain syndrome-a multifaceted disorder requiring multidimensional care: case study.
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Herpes zoster causes substantial morbidity, especially among older adults. Although the acute cutaneous manifestations can be painful and troublesome, the most important consequence of herpes zoster (shingles) is the chronic pain syndrome known as postherpetic neuralgia (PHN). Previous studies have suggested that declining varicella-zoster virus (VZV)-specific cell-mediated immune (CMI) responses account for the increased frequency of herpes zoster seen in older adults. This led to the idea that immunization designed to boost VZV-specific CMI responses might reduce the risk of herpes zoster. This hypothesis was tested in a large, randomized, placebo-controlled clinical trial called the Shingles Prevention Study (SPS). Compared with the placebo group, herpes zoster vaccine recipients had a 61.1% reduction in zoster "burden of illness" (an index incorporating incidence and severity of herpes zoster); a 66.5% reduction in the incidence of postherpetic neuralgia; and a 51.3% reduction in the incidence of herpes zoster. The incidence of serious adverse events was not different between the overall vaccine and placebo populations. The most frequently encountered adverse event among vaccine recipients was local reactogenicity, with self-limited and generally mild tenderness, warmth, or erythema occurring at the injection site in about one-half of vaccine recipients. The zoster vaccine was approved by the US Food and Drug Administration in 2006 and is indicated for prevention of herpes zoster in immunocompetent persons aged 60 years and older. ⋯ The herpes zoster vaccine provides physicians with an effective means for reducing a patient's risk for developing shingles and its attendant complications. No significant safety concerns regarding the vaccine have been identified. Indications for use of the attenuated-virus vaccine in special subpopulations continue to evolve.
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Randomized Controlled Trial Comparative Study
Lumiracoxib 400 mg compared with celecoxib 400 mg and placebo for treating pain following dental surgery: a randomized, controlled trial.
This randomized, double-blinded, double-dummy, parallel-group, single-center study compared a single dose of the novel selective COX-2 inhibitor lumiracoxib (400 mg), with celecoxib (400 mg) or placebo in dental pain. Patients > or =17 years with moderate-to-severe dental pain were recruited after surgical extraction of 2 or more partially or fully bony impacted molars. Pain intensity was measured using the categorical scale and the primary efficacy variable was the summed pain intensity difference over 8 hours after dosing (SPID-8). Patient disposition and demographics were comparable between lumiracoxib 400 mg (n = 156), celecoxib 400 mg (n = 156), and placebo (n = 52) groups. Lumiracoxib was statistically superior (P < .001) to both celecoxib and placebo in reducing pain intensity (SPID-8; least-squares means: 8.31, lumiracoxib; 4.26, celecoxib; -1.87, placebo). Significantly more patients treated with lumiracoxib (58.9%) considered treatment to be good or excellent compared with celecoxib and placebo (42.3% and 5.7%, respectively; P = .001). Lumiracoxib was superior to celecoxib and placebo for all other secondary efficacy variables. All treatments were well-tolerated. In conclusion, 400 mg lumiracoxib was well-tolerated and provided significantly superior analgesia to 400 mg celecoxib or placebo in patients with moderate-to-severe pain after dental surgery. ⋯ In a randomized, double-blinded, double-dummy, parallel-group, single-center study, a single dose of the novel selective COX-2 inhibitor lumiracoxib (400 mg) was well-tolerated and provided significantly superior analgesia to 400 mg celecoxib or placebo in patients with moderate-to-severe dental pain after surgical extraction of impacted molars.
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Like other types of neuropathic pain, postherpetic neuralgia (PHN) can be resistant to many types of pharmacologic and interventional therapies. Although many analgesic agents have been used for the treatment of other types of neuropathic pain, tricyclic antidepressants, antiepileptic drugs, opioids, and lidocaine patch appear to demonstrate relative analgesic efficacy for the treatment of pain from PHN. There are fewer studies on the use of interventional options for the treatment of pain from PHN. The majority of interventional therapies show equivocal analgesic efficacy although some data indicate that intrathecal methylprednisolone may be effective. Further randomized, controlled trials will be needed to confirm the analgesic efficacy of analgesic and interventional therapies to determine their role in the overall treatment of patients with PHN. ⋯ This article reviews the analgesic options for the treatment of PHN and suggests that tricyclic antidepressants, membrane stabilizers, opioids, and lidocaine patch may demonstrate analgesic efficacy in this group of patients. These data may potentially help clinicians who attempt to provide analgesia in patients with PHN.
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Comparative Study
Neuromodulation of thoracic intraspinal visceroreceptive transmission by electrical stimulation of spinal dorsal column and somatic afferents in rats.
Clinical studies have shown that neuromodulation therapies, such as spinal cord stimulation (SCS) and transcutaneous electrical nerve stimulation (TENS), reduce symptoms of chronic neuropathic and visceral pain. The neural mechanisms underlying SCS and TENS therapy are poorly understood. The present study was designed to compare the effects of SCS and TENS on spinal neuronal responses to noxious stimuli applied to the heart and esophagus. Direct stimulation of an intercostal nerve (ICNS) was used to simulate the effects of TENS. Extracellular potentials of left thoracic (T3) spinal neurons were recorded in pentobarbital anesthetized, paralyzed, and ventilated male rats. SCS (50 Hz, 0.2 ms, 3-5 minutes) at a clinical relevant intensity (90% of motor threshold) was applied on the C1-C2 or C8-T1 ipsilateral spinal segments. Intercostal nerve stimulation (ICNS) at T3 spinal level was performed using the same parameters as SCS. Intrapericardial injection of bradykinin (IB, 10 microg/mL, 0.2 mL, 1 minute) was used as the noxious cardiac stimulus. Noxious thoracic esophageal distension (ED, 0.4 mL, 20 seconds) was produced by water inflation of a latex balloon. C1-C2 SCS suppressed excitatory responses of 16/22 T3 spinal neurons to IB and 25/30 neurons to ED. C8-T1 SCS suppressed excitatory responses of 10/15 spinal neurons to IB and 17/23 neurons to ED. ICNS suppressed excitatory responses of 9/12 spinal neurons to IB and 17/22 neurons to ED. These data showed that SCS and ICNS modulated excitatory responses of T3 spinal neurons to noxious stimulation of the heart and esophagus. ⋯ Neuromodulation of noxious cardiac and esophageal inputs onto thoracic spinal neurons by spinal cord and intercostal nerves stimulation observed in the present study may help account for therapeutic effects on thoracic visceral pain by activating the spinal dorsal column or somatic afferents.