Animal models are indispensible tools for advancing understanding of the cause of any given disease and developing new treatments. Developing animal models for schizophrenia presents formidable challenges owing to the distinctively human nature of the symptoms that define it and the thus-far-obscured underlying biological mechanisms. Nevertheless, progress has been and continues to be made in this important field of endeavor. This article discusses the challenges facing investigators who seek to develop and use animal models for translational research in schizophrenia and the responses that have emerged to those challenges, as well as the likely pathways that will lead to future progress.

The objective of this study was to investigate the safety of repeated parenteral ketamine for depression. An electronic survey inquiring about the frequency of adverse events was distributed to providers of parenteral ketamine for depression. In addition, the investigators conducted a search of published studies describing six or more repeated parenteral ketamine treatments administered to individuals for depression, and extracted reported adverse events. The survey was sent to 69 providers, of which 36 responded (52% response rate); after eliminating those that were incomplete, 27 were included in the analysis. The providers in the analysis collectively reported treating 6630 patients with parenteral ketamine for depression, one-third of whom received more than 10 treatments. Only 0.7% of patients experienced an adverse effect that required discontinuation of ketamine. Psychological distress during the treatment was the most frequent cause. Other adverse events were extremely rare (such as bladder dysfunction (0.1%), cognitive decline (0.03%) and psychotic symptoms (0.03%)). Among the 20 published reports of repeated parenteral ketamine treatments, rates of significant adverse events resulting in discontinuation were low (1.2%). The rate of adverse effects reported in the survey and the published literature is low, and suggests that long-term treatment of depression with ketamine is reasonably safe.

Pharmacist-psychiatrist collaborative clinic models in specialty mental health clinics are limited, and there has been only 1 report of a clinic focused on adult attention-deficit hyperactivity disorder (ADHD). In this article, we describe the successful implementation of a pharmacist-psychiatrist collaborative practice agreement in an adult ADHD clinic at an academic medical center. Adult patients diagnosed with ADHD after a comprehensive assessment, including a full neuropsychological evaluation, were enrolled in the collaborative treatment clinic. The collaboration was a partnership between a psychiatry department and a school of pharmacy at a public university. We report the details of 58 patients and 774 patient encounters at the collaborative pharmacist-psychiatrist practice from March 2015 through June 2018. The visits were billed using traditional medical billing codes for follow-up visits. Pharmacist practice opportunities included psychiatric evaluation, medication management, counseling, and referral to auxiliary services. Challenges to the clinic's success included limited pharmacist time, prescriptive authority, and reimbursement for services from payors. A collaborative practice model targeted at adult ADHD patients may be a unique clinic setting for psychiatric pharmacists.

Severe and enduring eating disorders (EDs) have the highest mortality rate of all psychiatric illnesses (Arch Gen Psychiatry, 2011, 68, 724), especially when comorbid with treatment-resistant depression (TRD) (Psychiatr Res, 2016, 244, 45). We report on four patients with enduring EDs and TRD treated with repeat ketamine over 12 + months, showing improvement in depression with only modest changes in ED symptoms.

Dysregulation of the Mirror Neuron System (MNS) in schizophrenia (SCZ) may underlie the cognitive and behavioral manifestations of social dysfunction associated with that disorder. In healthy subjects intranasal (IN) oxytocin (OT) improves neural processing in the MNS and is associated with improved social cognition. OT's brain effects can be measured through its modulation of the MNS by suppressing EEG mu-band electrical activity (8-13Hz) in response to motion perception. Although IN OT's effects on social cognition have been tested in SCZ, OT's impact on the MNS has not been evaluated to date. Therefore, we designed a study to investigate the effects of two different OT doses on biological motion-induced mu suppression in SCZ and healthy subjects. EEG recordings were taken after each subject received a single IN administration of placebo, OT-24IU and OT-48IU in randomized order in a double-blind crossover design. The results provide support for OT's regulation of the MNS in both healthy and SCZ subjects, with the optimal dose dependent on diagnostic group and sex of subject. A statistically significant response was seen in SCZ males only, indicating a heightened sensitivity to those effects, although sex hormone related effects cannot be ruled out. In general, OT appears to have positive effects on neural circuitry that supports social cognition and socially adaptive behaviors.

ภาวะกายใจไม่สงบ(agitation)พบบ่อยทั้งในภาวะฉุกเฉินทางอายุรกรรมและจิตเวช การรักษาพยาบาลได้อย่าง เหมาะสมในกรณีดังกล่าวถือเป็นสมรรถนะหลักอย่างหนึ่งของแพทย์เวชศาสตร์ฉุกเฉิน ในบทความนี้ผู้นิพนธ์ ได้รวบรวมการใช้ยารักษาโรคจิตในกลุ่ม first-generation second-generation และยา benzodiazepines เพื่อใช้ ในการรักษาภาวะกายใจไม่สงบ(agitation)ชนิดเฉียบพลัน รวมทั้งนำ�เสนอแนวทางจำ�เพาะในการรักษาภาวะกาย ใจไม่สงบ(agitation)ที่สัมพันธ์กับภาวะต่างๆได้แก่ การได้รับสารพิษ ภาวะจิตเภท อาการเพ้อ(delirium) รวมทั้ง เกิดขึ้นโดยไม่ทราบสาเหตุ การใช้ยาเพื่อรักษาภาวะกายใจไม่สงบควรพิจารณาตามสาเหตุก่อโรคที่เป็นไปได้มาก ที่สุด ถ้าภาวะกายใจไม่สงบเกิดจากอาการเพ้อ(delirium)หรือโรคทางกายอื่นๆ แพทย์ควรทำ�การรักษาสาเหตุก่อ โรคเป็นลำ�ดับแรกแทนที่จะให้เพียงแค่ยารักษาโรคจิตหรือยา benzodiazepines เท่านั้น [West J Emerg Med. 2012;13(1):26–34.]