OBJECTIVE: A clinically relevant approach to patient care grounded in neurobiological constructs and evidence based practice which emphasizes a relevant psychopharmacology is needed to optimally train psychiatry residents. METHODS: We implemented a biological psychiatry course that now incorporates neurobiology, psychopharmacology, and evidence-based practice in conjunction with a Research Domain Criteria (RDoC) perspective. A survey launched prior to course implementation and following each class session, served as the outcome metric of residents' attitudes toward the new curriculum and followed a baseline attitudinal survey designed to evaluate the program. RESULTS: Greater than 90% of the psychiatry residents at Duke University who took the attitudinal survey agreed or strongly agreed with needing a course that helped them develop an understanding of neurobiology, psychopharmacology, and evidence-based practice concepts. Most residents also indicated a less than adequate understanding of the neurobiology and psychopharmacology of psychiatric disorders prior to sessions. CONCLUSION: Our biological psychiatry curriculum was associated with enthusiasm among residents regarding the incorporation of neurobiology, psychopharmacology, and evidence-based practice into course topics and discussions. A biological psychiatry curriculum with integrated neurobiology and psychopharmacology built on an evidence base approach is possible, well-received, and needed in training of future psychiatrists.
Biological Psychiatry* ; Curriculum* ; Evidence-Based Practice* ; Learning* ; Neurobiology* ; Patient Care ; Problem-Based Learning ; Psychiatry ; Psychopharmacology* ; Teaching

Objective: Although evidence implicates striatal cholinergic impairment as a mechanism underlying tardive dyskinesia, trials of nonspecific cholinergic agents have been inconclusive. As a partial agonist at specific nicotinic receptor subtypes, varenicline reduces drug-induced dyskinesias in animal models suggesting promise as a treatment for tardive dyskinesia. Methods: Three schizophrenia patients with tardive dyskinesia who were smokers underwent an open trial of varenicline. After a 2-week baseline, subjects received varenicline 1 mg twice daily. Changes from baseline on the Abnormal Involuntary Movement Scale were measured after a 4-week varenicline stabilization period, and 6 weeks after the smoking quit date in one patient. Results: Varenicline had no effect on mean Abnormal Involuntary Movement Scale scores after 4 weeks. Although smoking decreased after 4 weeks on varenicline and diminished further in one patient after 10 weeks, this also appeared to have no effect on ratings of tardive dyskinesia. Conclusion In contrast to animal models, no significant change in tardive dyskinesia occurred in response to varenicline replacement in three schizophrenia patients. Further investigations of cholinergic mechanisms in tardive dyskinesia are worthwhile as agents for specific cholinergic targets become available for treatment. In addition, treatment trials of tardive dyskinesia should control for smoking status, while patients on antipsychotics receiving nicotine replacement therapies for smoking should be studied further for changes in movement.

Objective: Although evidence implicates striatal cholinergic impairment as a mechanism underlying tardive dyskinesia, trials of nonspecific cholinergic agents have been inconclusive. As a partial agonist at specific nicotinic receptor subtypes, varenicline reduces drug-induced dyskinesias in animal models suggesting promise as a treatment for tardive dyskinesia. Methods: Three schizophrenia patients with tardive dyskinesia who were smokers underwent an open trial of varenicline. After a 2-week baseline, subjects received varenicline 1 mg twice daily. Changes from baseline on the Abnormal Involuntary Movement Scale were measured after a 4-week varenicline stabilization period, and 6 weeks after the smoking quit date in one patient. Results: Varenicline had no effect on mean Abnormal Involuntary Movement Scale scores after 4 weeks. Although smoking decreased after 4 weeks on varenicline and diminished further in one patient after 10 weeks, this also appeared to have no effect on ratings of tardive dyskinesia. Conclusion In contrast to animal models, no significant change in tardive dyskinesia occurred in response to varenicline replacement in three schizophrenia patients. Further investigations of cholinergic mechanisms in tardive dyskinesia are worthwhile as agents for specific cholinergic targets become available for treatment. In addition, treatment trials of tardive dyskinesia should control for smoking status, while patients on antipsychotics receiving nicotine replacement therapies for smoking should be studied further for changes in movement.

BACKGROUND:This prospective, randomized trial was undertaken to evaluate the utility of adding end-tidal capnometry (ETC) to pulse oximetry (PO) in patients undergoing procedural sedation and analgesia (PSA) in the emergency department (ED). METHODS:The patients were randomized to monitoring with or without ETC in addition to the current standard of care. Primary endpoints included respiratory adverse events, with secondary endpoints of level of sedation, hypotension, other PSA-related adverse events and patient satisfaction. RESULTS:Of 986 patients, 501 were randomized to usual care and 485 to additional ETC monitoring. In this series, 48％ of the patients were female, with a mean age of 46 years. Orthopedic manipulations (71％), cardioversion (12％) and abscess incision and drainage (12％) were the most common procedures, and propofol and fentanyl were the sedative/analgesic combination used for most patients. There was no difference in patients experiencing de-saturation (SaO2<90％) between the two groups; however, patients in the ETC group were more likely to require airway repositioning (12.9％ vs. 9.3％,P=0.003). Hypotension (SBP<100 mmHg or <85 mmHg if baseline <100 mmHg) was observed in 16 (3.3％) patients in the ETC group and 7 (1.4％) in the control group (P=0.048). CONCLUSIONS:The addition of ETC does not appear to change any clinically significant outcomes. We found an increased incidence of the use of airway repositioning maneuvers and hypotension in cases where ETC was used. We do not believe that ETC should be recommended as a standard of care for the monitoring of patients undergoing PSA.

Parenteral nutrition-associated liver disease (PNALD) is a liver dysfunction caused by various risk factors presented in patients receiving total parenteral nutrition (TPN). Omega-6 rich Intralipid® and omega-3 rich Omegaven® are two intravenous lipid emulsions used in TPN. TPN could affect the hepatic expression of genes in anti-oxidative stress, but it's unknown whether TPN affects genes in drug metabolism. In this study, either Intralipid®- or Omegaven®-based TPN was administered to mice and the expression of a cohort of genes involved in anti-oxidative stress or drug metabolism was analyzed, glutathione (GSH) levels were measured, and protein levels for two key drug metabolism genes were determined. Overall, the expression of most genes was downregulated by Intralipid®-based TPN ( and ). Omegaven® showed similar results as Intralipid® except for preserving the expression of and and increasing . Total GSH levels were decreased by Intralipid®, but increased by Omegaven®. CYP3A11 protein levels were increased by Omegaven®. In conclusion, TPN reduced the expression of many genes involved in anti-oxidative stress and drug metabolism in mice. However, Omegaven® preserved expression of , suggesting another beneficial effect of Omegaven® in protecting liver functions.