Effect of transcutaneous electrical nerve stimulation on pain, edema, and trismus after surgical removal of impacted third molars: a split-mouth randomized clinical trial.

BACKGROUND: The transcutaneous electrical nerve stimulation (TENS) stimulus inhibits the activity of nociceptive neurons of the central nervous system. Pain relief is achieved by increasing the pulse amplitude of TENS to induce a non-painful paranesthesia beneath the electrodes. This study aimed to assess the effect of TENS on acute pain, edema, and trismus after surgical removal of impacted third molars. MATERIAL AND METHODS: This randomized, double blind, split-mouth clinical trial was conducted on 37 patients with bilaterally impacted mandibular third molars. The angle and body of mandible at the site of surgery in one randomly selected quadrant underwent TENS immediately after surgery (50 Hz, 100-µs short pulse, 15 minutes for 6 days). The TENS stimulator device was used in off mode for the placebo quadrant. The pain score (primary outcome) was measured for 7 days postoperatively, and edema and trismus (secondary outcomes) were assessed at 2, 4 and 7 days, postoperatively. The results were analyzed by repeated measures ANOVA using R software (alpha=0.05). RESULTS: The overall mean pain score was significantly lower in the TENS than the placebo group (P<0.05). The number of taken analgesics in the first 3 days was significantly lower in the TENS group (P<0.001). Postoperative edema in the TENS group was lower than the placebo group but only the difference was not statistically significant (P>.05). The inter-incisal distance, as an index to assess trismus, was not significantly different between the two group at day 2, but it was significantly higher in the TENS group after the second day (P<0.001). CONCLUSIONS: TENS effectively decreased pain and trismus following impacted third molar surgery, and may be recommended as a non-pharmaceutical method to relieve postoperative symptoms.

Silymarin pretreatment protects against ethanol-induced memory impairment: Biochemical and histopathological evidence.

BACKGROUND: Ethanol (Eth.) abuse induces memory impairment. Oxidative damage and apoptosis are considered the likely causes of memory impairment. Silymarin (Sil.) is a flavonoid isolated from the plant Silymarin marianum (milk thistle). While studies have reported the neuroprotective effect of Sil. against neurodegenerative processes, the precise mechanism of action of Sil. in Eth.-induced memory impairment remains unclear. METHODS: Twenty-eight rats were equally divided into four groups: Control (saline 1 ml/rat); Sil. (200 mg/kg for 30 days); Eth. (2 g/kg/day for 30 days); and Sil. + Eth. Behavioral tests including inhibitory avoidance and open field were used to investigate memory and locomotion. Brain antioxidant parameters, including catalase, superoxide dismutase, total antioxidant capacity and total thiol group, plus oxidative parameters, including malondialdehyde and total oxidant status, followed by hippocampal apoptosis (Bax/Bcl2, cleaved caspase) and histopathological changes were evaluated in the groups. RESULTS: While the administration of Eth. impaired memory, Sil. significantly reversed Eth-induced memory deficits. Eth. administration also augmented brain oxidative and hippocampal apoptosis parameters. In contrast, a marked reduction in brain antioxidant and anti-apoptotic parameters was observed in the Eth. group. At the tissue level, hippocampal sections from Eth.-treated animals revealed severe neuronal damage. The administration of Sil. to Eth.-treated rats remarkably alleviated all the said Eth.-induced biochemical and histopathological effects. On the contrary, Sil. alone did not change the behavior and biochemical/molecular parameters. CONCLUSION: The memory-enhancing effect of Sil. in Eth.-induced demented rats may be partly mediated by the augmented antioxidant effects and amelioration of apoptotic and histopathological changes.

Evaluation of rFVIIa (NovoSeven) in Glanzmann patients with thromboelastogram.

Glanzmann thrombasthenia (GT) is a rare platelet function disorder characterized by a defect in fibrinogen binding to platelet membrane glycoprotein (GP) IIb/IIIa. Recombinant FVIIa (rFVIIa) is a haemostatic agent approved for the treatment of haemophilia patients with inhibitors, patients with acquired haemophilia and in EU also for treatment of factor VII (FVII)-deficient patients and GT patients with antibodies to GPIIb-IIIa. The present study was conducted to evaluate the use of the whole blood test system, rotational thrombelastometry (ROTEM), in measuring the overall haemostasis potential of rFVIIa in 28 GT patients treated with rFVIIa. The correlation of administered rFVIIa and time to start fibrin formation and clot dynamic/stability was assessed and correlation to the clinical response was elucidated. Assessments were performed on predose blood samples spiked with four different concentrations of rFVIIa and whole blood samples taken at 10 and 120 min following dosing. ROTEM parameters clotting time (CT), clot formation time (CFT) and maximum clot firmness (MCF) were measured. Both ex vivo and in vivo data showed beneficial effects on CT in the presence of rFVIIa, but no effect of added rFVIIa was seen on CFT and MCF. In conclusion, the use of thrombelastography at least in the modified form of ROTEM seems to be of limited use in predicting an adequate dose of rFVIIa in GT patients. A good clinical haemostatic response was recorded in spite of the limited changes in the ROTEM pattern supporting the conclusion that ROTEM should not be the method of choice for monitoring rFVIIa therapy in Glanzmann patients.