PURPOSE: To describe a technique for percutaneous vertebroplasty of osteoporotic vertebral body compression fractures and to report early results of its use. METHODS: The technique was used over a 3-year period in 29 patients with 47 painful vertebral fractures. The technique involves percutaneous puncture of the involved vertebra(e) via a transpedicular approach followed by injection of polymethylmethacrylate (PMMA) into the vertebral body. RESULTS: The procedure was technically successful in all patients, with an average injection amount of 7.1 mL PMMA per vertebral body. Two patients sustained single, nondisplaced rib fractures during the procedure; otherwise, no clinically significant complications were noted. Twenty-six patients (90%) reported significant pain relief immediately after treatment. CONCLUSION: Vertebroplasty is a valuable tool in the treatment of painful osteoporotic vertebral fractures, providing acute pain relief and early mobilization in appropriate patients.

http://www.ajnr.org/content/ajnr/18/10/1897.full.pdf

Percutaneous polymethylmethacrylate vertebroplasty in the treatment of osteoporotic vertebral body compression fractures: Technical aspects

The purpose of this review was to identify and analyze the controlled clinical trial data for peripheral neuropathic pain (PNP) and complex regional pain syndromes (CRPS). A total of 72 articles were found, which included 92 controlled drug trials using 48 different treatments. The methods of these studies were critically reviewed and the results summarized and compared. The PNP trial literature gave consistent support (two or more trials) for the analgesic effectiveness of tricyclic antidepressants, intravenous and topical lidocaine, intravenous ketamine, carbamazepine and topical aspirin. There was limited support (one trial) for the analgesic effectiveness of oral, topical and epidural clonidine and for subcutaneous ketamine. The trial data were contradictory for mexiletine, phenytoin, topical capsaicin, oral non-steroidal anti-inflammatory medication, and intravenous morphine. Analysis of the trial methods indicated that mexiletine and intravenous morphine were probably effective analgesics for PNP, while non-steroidals were probably ineffective. Codeine, magnesium chloride, propranolol, lorazepam, and intravenous phentolamine all failed to provide analgesia in single trials. There were no long-term data supporting the analgesic effectiveness of any drug and the etiology of the neuropathy did not predict treatment outcome. Review of the controlled trial literature for CRPS identified several potential problems with current clinical practices. The trial data only gave consistent support for analgesia with corticosteroids, which had long-term effectiveness. There was limited support for the analgesic effectiveness of topical dimethylsulfoxyde (DMSO), epidural clonidine and intravenous regional blocks (IVRBs) with bretylium and ketanserin. The trial data were contradictory for intranasal calcitonin and intravenous phentolamine and analysis of the trial methods indicated that both treatments were probably ineffective for most patients. There were consistent trial data indicating that guanethidine and reserpine IVRBs were ineffective, and limited trial data indicating that droperidol and atropine IVRBs were ineffective. No placebo controlled data were available to evaluated sympathetic ganglion blocks (SGBs) with local anesthetics, surgical sympathectomy, or physical therapy. Only the capsaicin trials presented data which allowed for meta-analysis. This meta-analysis demonstrated a significant capsaicin effect with a pooled odds ratio of 2.35 (95% confidence intervals 1.48, 3.22). The methods scores were higher (P<0.01) for the PNP trials (66.2±1.5, n=66) than the CRPS trials (57.6±2.9, n=26). The CRPS trials tended to use less subjects and were less likely to use placebo controls, double-blinding, or perform statistical tests for differences in outcome measures between groups. There was almost no overlap in the controlled trial literature between treatments for PNP and CRPS, and treatments used in both conditions (intravenous phentolamine and epidural clonidine) had similar results.

A critical review of controlled clinical trials for peripheral neuropathic pain and complex regional pain syndromes.

Local Anesthetics and the Inflammatory Response: A New Therapeutic Indication? Markus Hollmann;Marcel Durieux; Anesthesiology

Local anesthetics and the inflammatory response: a new therapeutic indication?

Four cases of cauda equina syndrome occurring after continuous spinal anesthesia are reported. In all four cases, there was evidence of a focal sensory block and, to achieve adequate analgesia, a dose of local anesthetic was given that was greater than that usually administered with a single-injection technique. We postulate that the combination of maldistribution and a relatively high dose of local anesthetic resulted in neurotoxic injury. Suggestions that may reduce the potential for neurotoxicity are discussed. Use of a lower concentration and a "ceiling" or maximum dose of local anesthetic to establish the block should be considered. If maldistribution of local anesthetic is suspected (as indicated by a focal sensory block), the use of maneuvers to increase the spread of local anesthetic is recommended. If such maneuvers prove unsuccessful, the technique should be abandoned.

Cauda equina syndrome after continuous spinal anesthesia.

Alcohol dependence belongs to the globally leading health risk factors Therapeutic success of psychosocial programs for relapse prevention is moderate and could be increased by an adjuvant treatment with the opioid antagonists naltrexone and nalmefene
 
The objective of this review is to determine the effectiveness and tolerability of opioid antagonists in the treatment of alcohol dependence

Opioid antagonists for alcohol dependence

To compare the respiratory depressant and analgesic effects of nalbuphine and morphine, six healthy male subjects were given the drugs as single 0.15-mg/kg doses, and as four successive doses of 0.15 mg/kg. Respiratory depression was monitored by ventilatory and mouth occlusion pressure responses du

Analgesic and respiratory depressant activity of nalbuphine: a comparison with morphine.

One hundred forty-eight adult patients having epidural anesthesia for cesarean section, postpartum tubal ligation, lower extremity orthopedic procedures, or lithotriptic therapy were assigned to five groups. Group 1 patients were given a commercially prepared 1.5% lidocaine solution with 1:200,000 epinephrine plus 1 ml of normal saline per 10 ml of lidocaine; the solution pH was 4.6. Group 2 patients were given commercially prepared 1.5% lidocaine solution plus 1:200,000 epinephrine, with 1 mEq (1 ml) NaHCO3 per 10 ml of lidocaine; the solution pH was 7.15. Group 3 patients received the commercial solution of 1.5% lidocaine with 1:200,000 epinephrine; the solution pH was 4.55. Group 4 patients were given a mixture of 18 ml of 2% lidocaine with 30 ml of 1.5% lidocaine, both commercially packaged with 1:200,000 epinephrine, plus 1 mEq (1 ml) of NaHCO3 added per 10 ml of solution; the solution pH was 7.2. Group 5 patients received 1.5% plain lidocaine to which epinephrine was added to a final concentration of 1:200,000; the solution pH was 6.35. Times of onset of analgesia (time between the completion of the anesthetic injection and loss of scratch sensation at the right hip (L-2 dermatome)) and of surgical anesthesia (time between completion of injection and loss of discomfort following tetanic stimulation produced by a nerve stimulator applied to skin on the right hip) were significantly more rapid in the groups that received the pH-adjusted solutions (groups 4 and 2). Group 4 had the fastest mean onset time, 1.92 ± 0.17 min, followed by group 2, 3.31 ± 0.23 min. Onset times were progressively longer in group 5 at 4.27 ± 0.51 min, group 3 at 4.73 ± 0.37 min, and group 1 at 7.11 ± 0.82 min. The spread of sensory blockade was also significantly more rapid in the pH-adjusted groups 5, 10, and 15 min after epidural injection. In patients having cesarean sections in groups 1 and 2, plasma lidocaine levels in the maternal peripheral venous and in umbilical cord blood and Apgar scores were similar in both groups.

Comparison of pH-adjusted lidocaine solutions for epidural anesthesia.

The effects of various plasma concentrations of lidocaine on nitrous oxide anesthesia in man and halothane requirements in the dog were studied The response to incision of the skin was observed in 20 patients who were anesthetized with nitrous oxide, 70% inspired, and oxygen, 30%, plus various plasma levels of lidocaine In addition, changes in the MAC of halothane in dogs were observed at various levels of lidocaine In both circumstances lidocaine concentrations of 3 to 6 microgram/ml decreased anesthetic requirements approximately 10 to 28% At clinically common concentrations of lidocaine, significant decreases in anesthetic requirements should be anticipated

Effects of Lidocaine on the Anesthetic Requirements for Nitrous Oxide and Halothane

The microvascular effects of varying concentrations of lidocaine were evaluated with the use of videomicroscopy in an in vivo rat cremaster muscle preparation. Animals were anesthetized with chloralose and urethane and breathed room air spontaneously. Mean arterial pressure and heart rate were measured via a carotid artery cannula. The cremaster muscle was suffused with a balanced electrolyte solution and pH, temperature, PO2, PCO2, and osmolarity were controlled. Internal diameters of fourth-order arterioles in the cremaster muscle were measured with an electronic vernier system. In one group of animals (n = 7), arteriolar diameters were measured every 30 s during a 10-min control period, a 10-min period of topical application of lidocaine hydrochloride, and a 10-min recovery period. Lidocaine hydrochloride, 10(0), 10(1), 10(2), 10(3), or 10(4) micrograms X ml-1, produced changes in arteriolar diameters to 88.9 +/- 0.9, 79.0 +/- 1.3, 67.5 +/- 2.4, 60.1 +/- 3.4, and 127.1 +/- 7.2 per cent of control, respectively (P less than 0.001). In a second group of animals (n = 4), fourth-order arteriolar diameters were measured during administration of intravenous lidocaine, 1.2 mg X kg-1 bolus plus 0.3 mg X kg-1 X min-1. Vasoconstriction to 91.3 +/- 0.9% of control was observed (P less than 0.001). These results demonstrate a biphasic dose-dependent response to lidocaine. At lesser concentrations, including those that occur in the plasma of patients during intravenous infusion or nerve blocks, dose-related vasoconstriction occurred. Lidocaine, 10(4) micrograms X ml-1, a concentration similar to that which occurs at the site of injection during infiltration, nerve block, or epidural anesthesia, produced vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Lidocaine constricts or dilates rat arterioles in a dose-dependent manner.

Nitric oxide is a newly recognized cell messenger for the activation of soluble guanylate cyclase and is produced from L-arginine by the enzyme nitric oxide synthase in a wide variety of tissues, including vascular endothelium and brain. Inhalational anesthetics inhibit nitric oxide production from vascular endothelium and also decrease resting cyclic guanosine monophosphate content in multiple brain regions. Halothane has been shown to depress neurotransmission by L-glutamate and N-methyl-D-aspartate. These amino acid neurotransmitters are known to increase neuronal cyclic guanosine monophosphate content by stimulation of nitric oxide production. To investigate the possible involvement of the L-arginine-to-nitric oxide pathway in the anesthetic state, the effect of a specific nitric oxide synthase inhibitor, nitroG-L-arginine methyl ester, on the minimum alveolar concentration (MAC) for halothane anesthesia was determined in Sprague-Dawley rats. Bolus injection of nitroG-L-arginine methyl ester at 0, 1, 5, 10, 20, and 30 mg/kg resulted in a dose-dependent reduction in MAC for halothane of 0 ± 0, 2.3 ± 0.4, 21.5 ± 3.9, 30.5 ± 2.4, 51.0 ± 7.8, and 26.0 ± 2.8%, respectively. NitroG-L-arginine methyl ester had no effect on MAC for halothane. Bolus infusion of L-arginine 300 mg/kg after MAC reduction by nitroG-L-arginine methyl ester 10 mg/kg resulted in an immediate and complete reversal of the MAC reduction. No reversal was observed after infusion of D-arginine 300 mg/kg. MAC reduction by nitroG-L-arginine methyl ester 1, 5, 10, 20 and 30 mg/kg was accompanied by an increase in systolic blood pressure (1 ± 3, 29 ± 6, 27 ± 3, 45 ± 3, and 27 ± 5% respectively) and diastolic blood pressure (1 ± 6, 30 ± 6, 29 ± 7, 53 ± 2, and 29 ± 7% respectively), and a small decrease in heart rate (−2 ± 3, −8 ± 4, −11 ± 2, −5 ± 8, and −15 ± 3%, respectively). This dose-dependent and reversible decrease in MAC by nitroG-L-arginine methyl ester suggests that inhibition of the nitric oxide pathway decreases the level of consciousness and augments anesthesia, analgesia, or sedation.

Nitric oxide synthase inhibitor dose-dependently and reversibly reduces the threshold for halothane anesthesia. A role for nitric oxide in mediating consciousness?

Cosmo A. DiFazio

Papers

Analgesic and respiratory depressant activity of nalbuphine: a comparison with morphine.

Comparison of pH-adjusted lidocaine solutions for epidural anesthesia.

Effects of Lidocaine on the Anesthetic Requirements for Nitrous Oxide and Halothane

Lidocaine constricts or dilates rat arterioles in a dose-dependent manner.

Nitric oxide synthase inhibitor dose-dependently and reversibly reduces the threshold for halothane anesthesia. A role for nitric oxide in mediating consciousness?