Marshall and Rotterdam Computed Tomography scores in predicting early deaths after brain trauma

Trauma is one of the most important issues of most healthcare systems accompanying with head trauma in the most cases. We sought to determine the scoring system and initial Computed Tomography (CT) findings predicting the death at hospital discharge (early death) in patients with traumatic brain injury based on Marshall and Rotterdam CT scores. This is a cross sectional study on traumatic neurosurgical patients with mild-to-severe traumatic brain injury admitted to the emergency department of Emam Reza Hospital, Birjand University of Medical Sciences. Patients≥18 years old with TBI during last 24 hours with GCS≤13 were included and exclusion criteria were multiple trauma, penetrating injuries, previous history of anticoagulant therapy, pregnancy, not willingness for participation. Their initial CT and status at hospital discharge, one and three months (dead or alive) were reviewed, and both CT scores were calculated. We examined whether each score is related to death using SPSS11 by The Mann–Whitney U at the level of p≤0.05. Overall, 98 patients were included. Mean age was 43.52±21.29. Most patients were male (63.3%). Mean Marshall and Rotterdam CT scores were 3.2±1.3 and 2.5±1. The mortality at two weeks, one moth and three months were 19.4%, 20.4%, and 20.4%. Rotterdam CT score was significantly different based on type of hematoma. Median GCS score in alive and dead patients on 2 weeks were 10 and 4 (p=0.0001), at one month were 10 and 4 (p=0.0001), and at three months were 10 and 4 (p=0.0001). The median Marshall CT score on 2 weeks were 2 and 4 (p=0.0001), at one month were 2 and 4 (p=0.0001), and at three months were 2 and 4 (p=0.0001). The median Rotterdam CT score on 2 weeks were 2 and 4 (p=0.0001), at one month were 2 and 3 (p=0.001), and at three months were 2 and 3 (p=0.001). The Rotterdam CT score was significantly correlated with mortality at two weeks, one month and three months (p=0.004, p=0.001, and p=0.001, respectively). The Marshall CT score was not significantly correlated with mortality at any time. The Rotterdam CT score was more accurate for prediction of mortality on 2 weeks (ROC80.9), at one month (ROC80.7), and at three months were (ROC80.7) than The Rotterdam CT score (ROC 76, 74.1, and 74.1, respectively). This study concluded that The Marshall CT score was more accurate for prediction of mortality on 2 weeks, at one month, and at three months were than The Marshall CT score with higher ROC. The correlation of the Rotterdam CT score with mortality was significant

Microinjection of WIN55,212-2 as a Cannabinoid Agonist into the Basolateral Amygdala Induces Sensitization to Morphine in Rats

Introduction: Previous studies have shown that the basolateral amygdale (BLA) is rich of CB1 cannabinoid receptors and involved in cannabinoid-induced antinociception. Also, it seems that there are functional interactions between the cannabinoid CB1 and opioid receptors in the process of sensitization to opiates. In the present study, we tried to examine the role of intra-BLA cannabinoid receptors on development of sensitization to morphine.  Methods: In this study, seventy two adult male albino Wistar rats weighting 230-280 g were included. Antinociception response of subcutaneous (sc), administration of saline (1 ml/kg), and morphine (1 and 10 mg/kg) were measured by the tail-flick test in animals that were received subcutaneous administration of morphine (5 mg/kg) or saline (1 ml/kg) once a day for three days (sensitization period), followed by five days free of drug. The dose of 1 mg/kg of morphine was selected as the appropriate (ineffective) dose in the next stages of experiment for measuring analgesia in the tail-flick test in sensitive animals which previously received bilateral intra-BLA CB1 receptor agonist, WIN55,212-2 (0.5, 1, 2 and 4 mM/0.3 μl/side), DMSO, or saline (0.3 μl/side) during sensitization period.  Results: Bilateral intra-BLA administration of WIN55, 212-2, increased morphine-induced antinociception in ineffective dose, while this effect was not observed in the groups that received DMSO or saline. Our findings indicated that CB1 receptors within the BLA are involved in the sensitization to morphine.  Discussion: It seems that glutamatergic projections from the BLA to the nucleus accumbens are involved in the development of morphine sensitization induced by cannabinoids