Neuroprotective effects of dexmedetomidine are reported in preclinical and clinical studies but evidence regarding the postoperative neurocognitive function is not as clear. This study performed a meta-analysis on outcomes of studies which examined neurocognitive performance by using valid assessment tools before and after perioperative dexmedetomidine treatment. Literature was searched in several electronic databases and studies were selected by following précised inclusion criteria. Meta-analyses of mean differences in percent changes from baseline in neurocognitive assessment scores were carried out and subgroup analyses were performed. Eighteen studies were included. Initial dose of dexmedetomidine (mean ± SD) was 1.28 ± 0.97 μg/kg and maintenance dose was 0.41 ± 0.11 μg/kg per hour. In healthy volunteers, there was no significant difference in the neurocognitive performance between dexmedetomidine and controls/comparators (mean difference (95% confidence interval (CI)): -12.72 (-50.25, 24.80) %; P = 0.51). Perioperative dexmedetomidine treatment was associated with significantly better neurocognitive performance in comparison with saline (mean difference (95% CI): 9.10 (3.03, 15.16) %; P = 0.003) as well as with comparator anaesthetics (mean difference: 5.50 (0.15, 10.86) %; P = 0.04) treated patients. In the submeta-analyses of studies which utilized neurocognitive assessment tools other than Mini-Mental State Examination (mean difference: 6.66 (-3.42, 16.74); P = 0.20) or studies with patients under 60 years of age (mean difference: 7.48 (-3.00, 17.96); P = 0.16), the differences were not significant between dexmedetomidine- and saline-/comparator-treated patients. Perioperative dexmedetomidine treatment is associated with significantly better neurocognitive function postoperatively in comparison with both saline controls and comparator anaesthetics (predominantly midazolam).
Common chemotherapeutic agents such as oxaliplatin often cause neuropathic pain during cancer treatment in patients. Such neuropathic pain is difficult to treat and responds poorly to common analgesics, which represents a challenging clinical issue. Corydalis yanhusuo is an old traditional Chinese medicine with demonstrated analgesic efficacy in humans. However, the potential analgesic effect of its active component, levo-tetrahydropalmatine (l-THP), has not been reported in conditions of neuropathic pain. This study found that l-THP (1–4 mg/kg, i.p.) produced a dose-dependent anti-hyperalgesic effect in a mouse model of chemotherapeutic agent oxaliplatin-induced neuropathic pain. In addition, we found that the anti-hyperalgesic effect of l-THP was significantly blocked by a dopamine D1 receptor antagonist SCH23390 (0.02 mg/kg), suggesting a dopamine D1 receptor mechanism. In contrast, l-THP did not significantly alter the general locomotor activity in mice at the dose that produced significant anti-hyperalgesic action. In summary, this study reported that l-THP possesses robust analgesic efficacy in mice with neuropathic pain and may be a useful analgesic in the management of neuropathic pain.
Background Dexmedetomidine, an α2-receptor agonist, provides potent sedation, analgesia, and anxiolysis without respiratory depression and is used in a variety of surgical and procedural situations. Aim of the review The aim of this study was to estimate the incidence of bradycardia in pediatric patients who received dexmedetomidine as a sole agent for any procedural, intensive care or surgical sedation. Method Literature was searched in electronic databases and studies were selected by following pre-determined eligibility criteria. Meta-analyses were carried out by pooling the percent incidence of bradycardia to attain a weighted overall effect size. Age-wise subgroup analyses and meta-regression analyses for the identification of factors affecting the incidence were also performed. Results Data of 2835 patients from 21 studies were included. The mean age was 62.21 ± 35.68 months. Initial, maintenance and total doses of dexmedetomidine (mean ± standard deviation) were 1.63 ± 0.33 μg/kg body weight, 0.86 ± 0.68 μg/kg/h, and 26.7 ± 20.8 μg/kg. The overall incidence of bradycardia (95% confidence interval) was 3.067 (2.863, 3.270)%; P < 0.0001. However, range was wider (0-22%) with 9 studies observed 0% incidence. The mean change in the heart rate was -17.26 (-21.60, -12.92); P < 0.00001. In the meta-regression analyses, age, body weight and dexmedetomidine dose were not significantly associated with the incidence of bradycardia. The minimum heart rate observed during the dexmedetomidine treatment period was positively associated with baseline heart rate. Conclusion Incidence of bradycardia in dexmedetomidine treated pediatric patients is 3%.
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