Anesth Analg 2002 Mar;94(3):694-700
Department of Anesthesia and Pain Therapy, Klinikum Krefeld, Krefeld, Germany.
[Medline record in process]
We studied the effects of spinal cord stimulation (SCS) on postherpetic neuralgia (PHN). Data of 28 patients were prospectively investigated over a median period of 29 (quartiles 9--39) mo. In addition, four patients with acute herpes zoster (HZ) pain were studied simultaneously. After intractable pain for more than 2 yr, long-term pain relief was achieved in 23 (82%) PHN patients (median, 70 yr) during SCS treatment confirmed by a median decrease from 9 to 1 on the visual analog scale (P < 0.001). In five cases with serious comorbidity, the initial pain alleviation could not be stabilized. Spontaneous improvement was always confirmed or excluded by SCS inactivation tests at quarterly intervals. Eight patients discontinued SCS permanently because of complete pain relief after stimulation periods of 3--66 mo, whereas 2 reestablished SCS because of recrudescence after 2 and 6 mo. Considerable impairments in everyday life, objectified by the pain disability index, were also significantly improved (P < 0.001). In 4 patients with acute HZ pain, SCS was promptly effective and after periods of 2.5 (quartiles 2--3) months the pain had subsided. SCS seems to offer a therapeutic option for pharmacological nonresponders. IMPLICATIONS: In many patients with postherpetic neuralgia and acute herpes zoster pain is not satisfactorily alleviated with pharmacological approaches. We report on 23 of 28 patients with postherpetic neuralgia and 4 of 4 with acute herpes zoster whose chronic pain was improved by electrical spinal cord stimulation.
PMID: 11867400, UI: 21855815
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Anesth Analg 2002 Mar;94(3):577-85
Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas.
PMID: 11867379, UI: 21855794
Anesth Analg 2002 Mar;94(3):523-8
Department of Anesthesia, Groote Schuur Hospital, Cape Town, South Africa.
We compared continuous IV tramadol as an alternative to neuraxial or systemic opioids for the management of postthoracotomy pain in a prospective, randomized, double-blinded, controlled study. General anesthesia was supplemented by thoracic epidural analgesia with 0.25% bupivacaine. At rib approximation, patients received one of the following: IV tramadol (150-mg bolus followed by infusion, total 450 mg/24 h, n = 29), epidural morphine (2 mg, then 0.2 mg/h, n = 30), or patient-controlled analgesia (PCA) morphine only (n = 30). All patients received PCA morphine and rescue morphine as necessary postoperatively. For the first 24 h, pain and sedation scores and respiratory, cardiovascular, and side effect measures were monitored. There was no significant difference in pain scores and PCA morphine use between tramadol and epidural morphine. Pain scores at rest and on coughing were lower in the Tramadol and Epidural Morphine groups than in the PCA Morphine group at various time points over the first 12 h. The Tramadol and Epidural Morphine groups used significantly less hourly PCA morphine than the PCA Morphine group at specific time points in the first 10 h. Vital capacities in the Tramadol group were significantly closer to baseline values at the 20-h point than in the PCA Morphine group. We conclude that an intraoperative bolus of tramadol followed by an infusion was as effective as epidural morphine and avoided the necessity of placing a thoracic epidural catheter. IMPLICATIONS: A prospective, randomized, double-blinded, placebo-controlled study of postthoracotomy pain relief showed that IV tramadol in the form of a bolus followed by continuous infusion was as effective as epidural morphine. The use of tramadol avoids the necessity of placing a thoracic epidural catheter.
PMID: 11867369, UI: 21855784
Anesthesiology 2002 Mar;96(3):725-41
Department of Anesthesiology, Herlev University Hospital, Herlev, Denmark, and the Department of Surgical Gastroenterology, Hvidovre University Hospital, Hvidovre, Denmark.
PMID: 11873051, UI: 21861195
Anesthesiology 2002 Mar;96(3):627-32
EMI INSERM/UdA 9904-Pharmacologie Fondamentale et Clinique de la Douleur, Laboratoire de Pharmacologie Medicale, Faculte de Medecine, Clermont-Ferrand, France.
BACKGROUND: An excess of excitatory pathway activation via N-methyl-d-aspartate (NMDA) receptors has been described in neuropathic pain that responds poorly to morphine. However, in this situation, several published data sets show that coadministration of NMDA receptor antagonists restores the efficacy of opioids. Considering that magnesium behaves like an NMDA receptor antagonist, we investigated the effect of the combination of magnesium and morphine in experimental models of chronic and tonic pain. METHODS: Mechanical hyperalgesia was assessed with the paw-pressure test in mononeuropathic (chronic constrictive injury model) and diabetic rats. Behavioral reactions were scored in a model of inflammation induced by formalin. The animals were assigned to one of three groups according to the intraperitoneal pretreatment: magnesium (30 mg/kg x 3), magnesium (30 mg/kg), and saline. Before testing, morphine was injected intravenously in mononeuropathic (0.3 mg/kg) and diabetic rats (1 mg/kg) and by the subcutaneous route in rats with the formalin test (1.5 mg/kg). RESULTS: Magnesium alone induced a significant antihyperalgesic effect in mononeuropathic and diabetic rats after a cumulative dose of 90 mg/kg. Furthermore, it significantly increased morphine analgesia, regardless of the loading dose used (30 or 90 mg/kg) in the two models of neuropathic pain. In the formalin test, magnesium alone did not have a significant effect. However, in combination with morphine, it revealed the analgesic effect of this opiate. CONCLUSIONS: These data show that magnesium amplifies the analgesic effect of low-dose morphine in conditions of sustained pain. Considering the good tolerability of magnesium, these findings may have clinical applications in neuropathic and persistent pain.
PMID: 11873038, UI: 21861182
Anesthesiology 2002 Mar;96(3):528-35
IWK Health Centre, Halifax, Nova Scotia, Canada.
BACKGROUND: This study evaluated the psychometric properties of the Non-communicating Children's Pain Checklist-Postoperative Version (NCCPC-PV) when used with children with severe intellectual disabilities. METHODS: The caregivers of 24 children with severe intellectual disabilities (aged 3-19 yr) took part. Each child was observed by one of their caregivers and one of the researchers for 10 min before and after surgery. They independently completed the NCCPC-PV and made a visual analog scale rating of the child's pain intensity for those times. A nurse also completed a visual analog scale for the same observations. RESULTS: The NCCPC-PV was internally reliable (Cronbach alpha = 0.91) and showed good interrater reliability. A repeated-measures analysis of variance indicated NCCPC-PV total and subscale scores were significantly higher after surgery and did not differ by observer. Postoperative NCCPC-PV scores correlated with visual analog scale ratings provided by caregivers and researchers, but not with those of nurses. A score of 11 on the NCCPC-PV, by caregivers, provided 0.88 sensitivity and 0.81 specificity for classifying children with moderate to severe pain. CONCLUSIONS: The NCCPC-PV displayed good psychometric properties when used for the postoperative pain of children with severe intellectual disabilities and has the potential to be useful in a clinical setting. The results suggest familiarity with an individual child with intellectual disabilities is not necessary for pain assessment.
PMID: 11873023, UI: 21861167
Anesthesiology 2002 Mar;96(3):523-6
PMID: 11873021, UI: 21861165
J Pain Symptom Manage 2002 Jan;23(1):58-9
Center for Bioethics, Clinical Research Institute of Montreal, 110 Pine Avenue West, Montreal, P.Q. H2W 1R7 Canada.
Publication Types:
PMID: 11811155, UI: 21669444
J Pain Symptom Manage 2002 Jan;23(1):57-8
Hospice of the North Shore, 2821 Central St., Evanston, IL 60201, USA.
PMID: 11811154, UI: 21669443
J Pain Symptom Manage 2002 Jan;23(1):54-7
Division of Medical Ethics, Department of Public Health, Weill Medical College of Cornell University, 525 East 68th Street, F-173, New York, NY 10021, USA.
PMID: 11779669, UI: 21638571
J Pain Symptom Manage 2002 Jan;23(1):48-53
Division of Chronic Pain Management, Department of Anesthesia, St. Joseph Medical Center, 120 Sister Pierre Drive, Suite 303, Baltimore, MD 21204, USA.
The most common side effect of opioid therapy is constipation. It is often difficult to treat and is believed to be primarily a peripheral effect. Single large doses of oral naloxone have been shown to be efficacious in reversing opioid-induced constipation. However, they often cause the unwanted side effect of analgesia reversal. This study evaluated the effects on constipation and analgesia of low doses of oral naloxone given three times daily. Patients taking stable doses of opioids with complaints of constipation were recruited for this double-blind, randomized, placebo-controlled study. Patients were given 4 mg or 2 mg of oral naloxone, or placebo, three times daily. Stool frequency and symptoms related to constipation were recorded daily. Patients also recorded the daily amount of analgesics required to maintain pain control. Nine patients were recruited for the study. All the patients who received oral naloxone had some improvement in their bowel frequency. Three of the patients also experienced reversal of analgesia, including one who had complete reversal of analgesia. This study demonstrates that reversal of analgesia still occurred despite dividing the oral naloxone into very low doses relative to the total dose of opioid used. Patients using high doses of opioids appear to be the most vulnerable to the analgesic effect of oral naloxone.
PMID: 11779668, UI: 21638570
J Pain Symptom Manage 2002 Jan;23(1):5-7
PMID: 11779661, UI: 21638563
Lancet 2002 Jan 26;359(9303):355
PMID: 11830233, UI: 21819226
Lancet 2002 Jan 26;359(9303):354-5
PMID: 11830230, UI: 21819223
Lancet 2002 Jan 26;359(9303):354; discussion 354-5
PMID: 11830229, UI: 21819222
Lancet 2002 Jan 26;359(9303):294-302
BACKGROUND: To obtain more reliable and precise estimates of the effect of direct thrombin inhibitors in the management of acute coronary syndromes, including patients undergoing percutaneous coronary intervention, we undertook a meta-analysis based on individual patients' data from randomised trials comparing a direct thrombin inhibitor (hirudin, bivalirudin, argatroban, efegatran, or inogatran) with heparin. METHODS: We included trials that involved at least 200 patients. The primary efficacy outcome was death or myocardial infarction, and the primary safety outcome was major bleeding. Data from individual trials were combined by use of a modified Mantel-Haenszel method. FINDINGS: In 11 randomised trials, 35,970 patients were assigned up to 7 days' treatment with a direct thrombin inhibitor or heparin and followed up for at least 30 days. Compared with heparin, direct thrombin inhibitors were associated with a lower risk of death or myocardial infarction at the end of treatment (4.3% vs 5.1%; odds ratio 0.85 [95% CI 0.77-0.94]; p=0.001) and at 30 days (7.4% vs 8.2%; 0.91 [0.84-0.99]; p=0.02). This was due primarily to a reduction in myocardial infarctions (2.8% vs 3.5%; 0.80 [0.71-0.90]; p<0.001) with no apparent effect on deaths (1.9% vs 2.0%; 0.97 [0.83-1.13]; p=0.69). Subgroup analyses suggested a benefit of direct thrombin inhibitors on death or myocardial infarction in trials of both acute coronary syndromes and percutaneous coronary interventions. A reduction in death or myocardial infarction was seen with hirudin and bivalirudin but not with univalent agents. Compared with heparin, there was an increased risk of major bleeding with hirudin, but a reduction with bivalirudin. There was no excess in intracranial haemorrhage with direct thrombin inhibitors. INTERPRETATION: Direct thrombin inhibitors are superior to heparin for the prevention of death or myocardial infarction in patients with acute coronary syndromes. This information should prompt further clinical development of direct thrombin inhibitors for the management of arterial thrombosis.
PMID: 11830196, UI: 21819189
Neurology 2002 Feb 26;58(4):554-563
Centre d'Evaluation et de Traitement de la Douleur et Departement d'Anesthesiologie (Drs. Attal, Guirimand, Brasseur, Chauvin, Bouhassira, and V. Gaude), and Hopital Ambroise Pare, Boulogne, INSERM U-161 (Drs. Attal, Guirimand, Brasseur, Chauvin, and Bouhassira), Paris, France.
[Record supplied by publisher]
OBJECTIVE: To investigate the effects of IV morphine on central pain syndromes through quantitative sensory testing and to assess the long-term benefit of oral morphine. METHODS: After an initial open titration phase aiming to determine the maximal tolerated dosage of IV morphine, the efficacy of morphine infusion (9--30 mg; mean dosage, 16 mg) was assessed in a double-blind, placebo-controlled and crossover fashion in 15 patients with poststroke- (6 patients) or spinal cord injury- (9 patients) related pain. All of the patients subsequently received sustained oral morphine. RESULTS: Morphine significantly reduced the intensity of brush-induced allodynia but had no effect on other evoked pains (i.e., static mechanical and thermal allodynia/hyperalgesia). The effects of morphine on ongoing pain were not significantly different from those of the placebo, but 7 patients (46%) responded to morphine. There was a correlation between the effects of morphine on spontaneous pain and the decrease of the responses to suprathreshold thermal stimuli on the nonpainful contralateral side, suggesting that these effects were related to the general antinociceptive activity of the drug. The effects of IV morphine were correlated with those of oral morphine at 1 month, but only 3 patients (20%) were still taking morphine after 1 year. CONCLUSIONS: IV morphine induces analgesic effects on some components of central neuropathic pain syndromes, but only a minority of patients may benefit from long-term opioid treatment.
PMID: 11865132
Neurology 2002 Feb 26;58(4):517-8
Departments of Neurology (Dr. Jensen), Aarhus University Hospital, Aarhus.
PMID: 11865125, UI: 21853810
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