MS Contin [keywords]
- Diagnosis of Intraabdominal Fluid Extravasation After Hip Arthroscopy With Point-of-Care Ultrasonography Can Identify Patients at an Increased Risk for Postoperative Pain. [JOURNAL ARTICLE]
- Anesth Analg 2016 Aug 22.
Intraabdominal fluid extravasation (IAFE) after hip arthroscopy has historically been diagnosed in catastrophic circumstances with abdominal compartment syndrome requiring diuresis or surgical decompression. A previous retrospective study found the prevalence of symptomatic IAFE requiring diuresis or decompression to be 0.16%, with risk factors including surgical procedure and high pump pressures. IAFE can be diagnosed rapidly by using point-of-care ultrasound (POCUS) via the Focused Assessment With Sonography for Trauma (FAST) examination, which is a well-established means to detect free fluid with high specificity and sensitivity. In this study, we used POCUS to determine the incidence of IAFE in patients undergoing hip arthroscopy. We predicted a higher incidence and that patients with IAFE would have symptoms of peritoneal irritation such as pain and nausea.One hundred patients undergoing ambulatory hip arthroscopy were prospectively enrolled. A FAST examination was performed after induction by a trained anesthesiologist to exclude the preoperative presence of intraperitoneal fluid. Postoperatively, the same anesthesiologist repeated the FAST examination, and patients with new fluid in the abdominal or pelvic peritoneum were diagnosed with IAFE. Patients were followed up in the postanesthesia care unit (PACU) for 6 hours assessing pain, antiemetic and opioid use, and length of stay.Sixteen of 100 patients were found to have IAFE (16.0%; 99% confidence interval [CI], 8.4-28.1). These patients had, on average, a greater increase in pain score from their baseline assessment throughout their entire PACU stay (adjusted difference in means [99% CI]: 2.1 points [0.4-3.9]; P = .002). Patients with IAFE used more opioids, but this difference did not meet statistical significance (adjusted difference in means [99% CI]: 7.8 mg oral morphine equivalents [-2.8 to 18.3]; P = .053). There were no differences in postoperative nausea interventions or length of stay.Our incidence of IAFE was 16%, showing that IAFE occurs quite commonly in hip arthroscopy. Patients with IAFE had a greater increase in pain scores from baseline throughout the PACU stay. None of our patients required interventions. These findings suggest that even a small amount of new fluid in the peritoneum may be associated with a worse postoperative experience. This study brings awareness to a common yet potentially life-threatening complication of hip arthroscopy and highlights a unique and meaningful way that anesthesiologists in the perioperative setting can use POCUS to rapidly identify and guide management of these patients. Further studies with a larger sample size are needed to identify surgical and patient risk factors.
- The French Syrette of morphine for administration to combat casualties. [Journal Article]
- Br J Pain 2016 May; 10(2):66.
- Synergistic effects of social isolation and morphine addiction on reduced neurogenesis and BDNF levels and the resultant deficits in cognition and emotional state. [JOURNAL ARTICLE]
- Curr Mol Pharmacol 2016 Aug 22.
Addiction to drugs of abuse is a devastating condition which results in deterioration of brain functioning. On the other hand, social isolation also produces cognitive deficits such as learning and memory impairment. This study was designed to evaluate the potential negative synergistic effects of social isolation and morphine addiction on brain functions.One hundred and two Sprague-Dawley rats were randomly divided into four groups for assessing neurogenesis and behaviour: group-housed, isolated, morphine-treated group-housed and morphine-treated isolated groups. Morphine-treated animals received BrdU (50 mg/kg; i.p.) and Morphine (0.75 mg/rat; i.p.) for 14 consecutive days, whereas, control rats received BrdU (50 mg/kg; i.p.) only. At the end of the study, Morris water maze and elevated plus maze tasks were performed to assess spatial working memory and anxiety levels, respectively. Furthermore, neurogenesis and BDNF levels were studied.Reference and working memory was markedly impaired in isolated and morphine-treated isolated rats as compared to group-housed rats and morphine-treated group-housed rats, respectively. Neurogenesis and BDNF levels were reduced in isolated and morphine-treated isolated rats as compared to group-housed rats and morphine-treated group-housed rats, respectively. Furthermore, rats in both isolated groups demonstrated high anxiety levels when compared to group housed groups.Isolation during addiction imparts devastating effects on brain. Thus, socialization of addicts can minimize addiction - induced cognitive deficits and improve neurogenesis. CIntroduction: Addiction to drugs of abuse is a devastating condition which results in deterioration of brain functioning. On the other hand, social isolation also produces cognitive deficits such as learning and memory impairment. This study was designed to evaluate the potential negative synergistic effects of social isolation and morphine addiction on brain functions.One hundred and two Sprague-Dawley rats were randomly divided into four groups for assessing neurogenesis and behaviour: group-housed, isolated, morphine-treated group-housed and morphine-treated isolated groups. Morphine-treated animals received BrdU (50 mg/kg; i.p.) and Morphine (0.75 mg/rat; i.p.) for 14 consecutive days, whereas, control rats received BrdU (50 mg/kg; i.p.) only. At the end of the study, Morris water maze and elevated plus maze tasks were performed to assess spatial working memory and anxiety levels, respectively. Furthermore, neurogenesis and BDNF levels were studied.Reference and working memory was markedly impaired in isolated and morphine-treated isolated rats as compared to group-housed rats and morphine-treated group-housed rats, respectively. Neurogenesis and BDNF levels were reduced in isolated and morphine-treated isolated rats as compared to group-housed rats and morphine-treated group-housed rats, respectively. Furthermore, rats in both isolated groups demonstrated high anxiety levels when compared to group housed groups.Isolation during addiction imparts devastating effects on brain. Thus, socialization of addicts can minimize addiction - induced cognitive deficits and improve neurogenesis.
- Morphine treatment enhances glutamatergic input onto neurons of the nucleus accumbens via both disinhibitory and stimulating effect. [JOURNAL ARTICLE]
- Addict Biol 2016 Aug 22.
Drug addiction is a chronic brain disorder characterized by the compulsive repeated use of drugs. The reinforcing effect of repeated use of drugs on reward plays an important role in morphine-induced addictive behaviors. The nucleus accumbens (NAc) is an important site where morphine treatment produces its reinforcing effect on reward. However, how morphine treatment produces its reinforcing effect on reward in the NAc remains to be clarified. In the present study, we studied the influence of morphine treatment on the effects of DA and observed whether morphine treatment could directly change glutamatergic synaptic transmission in the NAc. We also explored the functional significance of morphine-induced potentiation of glutamatergic synaptic transmission in the NAc at behavioral level. Our results show that (1) morphine treatment removes the inhibitory effect of DA on glutamatergic input onto NAc neurons; (2) morphine treatment potentiates glutamatergic input onto NAc neurons, especially the one from the basolateral amygdala (BLA) to the NAc; (3) blockade of glutamatergic synaptic transmission in the NAc or ablation of projection neurons from BLA to NAc significantly decreases morphine treatment-induced increase in locomotor activity. These results suggest that morphine treatment enhances glutamatergic input onto neurons of the NAc via both disinhibitory and stimulating effect and therefore increases locomotor activity.
- Perception of the risk of adverse reactions to analgesics: differences between medical students and residents. [Journal Article]
- PeerJ 2016.:e2255.
Background.Medications are not exempt from adverse drug reactions (ADR) and how the physician perceives the risk of prescription drugs could influence their availability to report ADR and their prescription behavior. Methods. We assess the perception of risk and the perception of ADR associated with COX2-Inbitors, paracetamol, NSAIDs, and morphine in medical students and residents of northeast of Mexico.
Results.The analgesic with the highest risk perception in both group of students was morphine, while the drug with the least risk perceived was paracetamol. Addiction and gastrointestinal bleeding were the ADR with the highest score for morphine and NSAIDs respectively. Discussion. Our findings show that medical students give higher risk scores than residents toward risk due to analgesics. Continuing training and informing physicians about ADRs is necessary since the lack of training is known to induce inadequate use of drugs.
- Melatonin as a potential counter-effect of hyperalgesia induced by neonatal morphine exposure. [JOURNAL ARTICLE]
- Neurosci Lett 2016 Aug 18.
Morphine administration in the neonatal period can induce long-term effects in pain circuitry leading to hyperalgesia induced by the opioid in adult life. This study explored a new pharmacological approach for reversing this effect of morphine. We focused on melatonin owing its well-known antinociceptive and anti-inflammatory effects, and its ability to interact with the opioid system. We used the formalin test to assess the medium and long-term effects of melatonin administration on hyperalgesia induced by morphine in early life. Newborn rats were divided into two groups: the control group, which received saline, and the morphine group, which received morphine (5μg subcutaneously [s.c.]) in the mid-scapular area, once daily for 7 days, from P8 (postnatal day 8) until P14. At postnatal days 30 (P30) and 60 (P60), both groups were divided in two subgroups, which received melatonin or melatonin vehicle 30min before the formalin test. The nociceptive responses were assessed by analyzing the total time spent biting, flicking, and licking the formalin-injected hind paw; these responses were recorded during the first 5min (neurogenic/acute phase) and from 15-30min (inflammatory/tonic phase). Initially, animals in the morphine/vehicle group showed increased nociceptive behavior in phase II (inflammatory) of the formalin test at P30, and in the neurogenic and inflammatory phases at P60. These increased nociceptive responses were fully reversed by melatonin administration at either age. These findings show that melatonin administration is a potential means for countering hyperalgesia induced by neonatal morphine exposure in young and adult rats.
- Analysis of Morphine-Induced Changes in the Activity of Periaqueductal Gray Neurons in the Intact Rat. [JOURNAL ARTICLE]
- Neuroscience 2016 Aug 18.
Microinjection of morphine into the periaqueductal gray (PAG) produces antinociception. In vitro slice recordings indicate that all PAG neurons are sensitive to morphine either by direct inhibition or indirect disinhibition. We tested the hypothesis that all PAG neurons respond to opioids in vivo by examining the extracellular activity of PAG neurons recorded in lightly anesthetized and awake rats. Spontaneous activity was less than 1 Hz in most neurons. Noxious stimuli (heat, pinch) caused an increase in activity in 57% and 75% of the neurons recorded in anesthetized and awake rats, respectively. The same noxious stimuli caused a decrease in activity in only 17% and 6% of neurons recorded in anesthetized and awake rats. Systemic administration of morphine caused approximately equal numbers of neurons to increase, decrease, or show no change in activity in lightly anesthetized rats. In contrast, administration of morphine caused an increase in the activity of 22 of the 27 neurons recorded in awake rats. No change in activity was evident in the remaining five neurons. Changes in activity caused by morphine were surprisingly modest (a median increase from 0.7 to 1.3 Hz). The small inconsistent effects of morphine are in stark contrast to the large changes produced by morphine on the activity of RVM neurons or the widespread inhibition and excitation of PAG neurons treated with opioids in in vitro slice experiments. The relatively modest effects of morphine in the present study suggest that morphine produces antinociception by causing small changes in the activity of many PAG neurons.
- Sleep disturbance in patients taking opioid medication for chronic back pain. [JOURNAL ARTICLE]
- Anaesthesia 2016 Aug 22.
Poor sleep is an increasingly recognised problem with chronic pain and further increases the effect on daily function. To identify the relationship between chronic pain, opioid analgesia and sleep quality, this study investigated activity and sleep patterns in patients taking opioid and non-opioid analgesia for chronic back pain. Thirty-one participants (10 healthy controls, 21 patients with chronic pain: 6 on non-opioid medication; 15 on opioid medication) were assessed using actigraphy, polysomnography and questionnaires. Patients with chronic pain subjectively reported significant sleep and wake disturbances as shown by decreased overall sleep quality (Pittsburgh Sleep Quality Index, p < 0.001), increased symptoms of insomnia (Insomnia Severity Index, p < 0.001) and increased fatigue (Fatigue Severity Scale, p = 0.002). They also spent increased time in bed (p = 0.016), took longer to get to sleep (p = 0.005) and had high interindividual variability in other measures of activity but no overall irregular rest-activity pattern. Patients on high doses of opioids (> 100 mg morphine-equivalent/day) demonstrated distinctly abnormal brain activity during sleep suggesting that polysomnography is necessary to detect sleep disturbance in this population in the absence of irregular rest-activity behaviour. Night-time sleep disturbance is common in individuals suffering from chronic pain and may be further exacerbated by opioid treatment. Considerations must be made regarding the appropriate use of combined actigraphy and miniaturised polysomnography for future population-based studies.
- [Research progress on the impact of morphine on antiplatelet effects of P2Y12 receptor antagonists]. [Journal Article]
- Zhonghua Xin Xue Guan Bing Za Zhi 2016 Aug 24; 44(8):734-6.
- Influences of CCK-8 on Expressions of Apoptosis-related Genes in Prefrontal Cortex Neurons of Morphine-relapse Rats. [JOURNAL ARTICLE]
- Neurosci Lett 2016 Aug 17.
In order to elucidate the influences of CCK-8 on expressions of apoptosis-related genes, Bax, Bcl-2 and Caspase-3, of prefrontal cortex neurons in morphine-relapse rats, an effective, successful morphine-relapse-rat model using the conditioned place preference (CPP) under CCK-8 (0.01, 0.1 and 1.0μg, i.c.v) intervention was established. The prefrontal cortexes were made into slices with the cellular plasmas immunohistochemically stained. The expressions of Bax, Bcl-2, Caspase-3 of neurons were evaluated through their scores, and each corresponding ratio of Bax and Bcl-2 (Bax/Bcl-2) was also computed. The results showed that the expression of Bcl-2 was very weak and those of Bax and Caspase-3 were hardly seen in group normal saline; the expressions of Bax and Caspase-3 were strong and that of Bcl-2 was weak in group morphine and compared to group normal saline, there were significant differences(P<0.05); the expressions of Bax, Caspase-3 and the ratios of Bax/Bcl-2 have a gradually-decreased trend in the sequence of group 0.01μg, group 0.1μg and group 1.0μg, but the expression of Bcl-2 has an opposite trend in the same sequence, and compared to group morphine, there were significant differences (P<0.05) excluding group 0.01μg. So we draw a conclusion that CCK-8 (0.1 and 1.0μg, i.c.v) could protect neurons of prefrontal cortex through up-regulating the expression of Bcl-2, down-regulating those of Bax and Caspase-3 and reducing Bax/Bcl-2 ratio in the model of morphine-relapse rats.