Weight gain is an important issue in the use of atypical antipsychotics, including olanzapine. A retrospective analysis of patterns of weight gain and possible covariates was performed for 1191 patients diagnosed with schizophrenia or schizoaffective disorder who were treated with olanzapine for up to 52 weeks. Patients were dichotomized into 2 main groups according to the percentage of body weight gained during the first 6 weeks of treatment with olanzapine: (1) patients who gained > or =7% of their body weight (Rapid Weight Gain Group [RWG]), and (2) patients who lost weight, gained no weight, or gained <7% of their body weight (Nonrapid Weight Gain Group [NRWG]). Results demonstrated that approximately 15% of the patient population showed rapid increases in weight (RWG group), whereas 85% of patients gained weight more slowly or not at all (NRWG group). Patients in the RWG group gained an average of 4% of their body weight (approximately 4-7 lb) within the first 2 weeks of treatment with olanzapine. Furthermore, patients in the RWG group were younger, had a lower baseline body mass index, were more likely to report an increase in appetite, and showed a more robust clinical response compared with patients in the NRWG group. Over the course of 52 weeks, patients in the RWG group gained significantly more weight and reached a higher plateau for mean weight increase at 38 weeks compared with the mean increase observed for patients in the NRWG group. By measuring the weight of patients during the first few weeks of olanzapine treatment and by assessing changes in appetite, clinicians may be able to identify those patients at risk for substantial weight gain.

In this study, venlafaxine ER was effective and well tolerated in short-term and continuation treatment of patients with posttraumatic stress disorder.

Background: Obstructive sleep apnea (OSA) is associated with obesity, metabolic syndrome, and dyslipidemia, which may be related to decrease androgen levels found in OSA patients. Dyslipidemia may contribute to atherosclerosis leading to increasing risk of heart disease. Methods: Systematic review was conducted using PubMed and Cochrane library by utilizing different combinations of key words; sleep apnea, obstructive sleep apnea, serum lipids, dyslipidemia, cholesterol, total cholesterol, low density lipoprotein (LDL), high density lipoprotein (HDL), and triglyceride (TG). Inclusion criteria were: English articles, and studies with adult population in 2 groups of patients (patients with OSA and without OSA). A total 96 studies were reviewed for inclusion, with 25 studies pooled for analysis. Results: Sixty-four studies were pooled for analysis; since some studies have more than one dataset, there were 107 datasets with 18,116 patients pooled for meta-analysis. All studies measured serum lipids. Total cholesterol pooled standardized difference in means was 0.267 (p = 0.001). LDL cholesterol pooled standardized difference in means was 0.296 (p = 0.001). HDL cholesterol pooled standardized difference in means was -0.433 (p = 0.001). Triglyceride pooled standardized difference in means was 0.603 (p = 0.001). Meta-regression for age, BMI, and AHI showed that age has signifi cant effect for TC, LDL, and HDL. BMI had signifi cant effect for LDL and HDL, while AHI had signifi cant effect for LDL and TG. S C I E N T I F I C I N V E S T I G A T I O N SO bstructive sleep apnea (OSA) is a common disorder affecting about 4% of middle-aged males and 2% of middle-aged women in the developed world and is a significant source of morbidity and mortality. 1,2 OSA is characterized by recurrent episodes of upper airway collapses during sleep. These recurrent episodes of upper airway collapse usually are accompanied by oxyhemoglobin desaturation and terminated by brief arousals which result in marked sleep fragmentation and chronic excessive daytime sleepiness (EDS). 1,2 OSA has been increasingly linked to cardiovascular and cerebrovascular disease, and many studies have shown that OSA is associated with increased cardiovascular and cerebrovascular morbidity. 3-9 OSA is associated with obesity and metabolic syndrome. 10 Multiple studies addressing this interesting and complex issue are available where lipid profi le was measured in subjects with OSA. We performed metaanalysis (MA) and meta-regression (MR) to specifi cally detect if OSA adversely affects degree of dyslipidemia; elevation of total cholesterol (TC), low density lipoprotein cholesterol (LDL), triglyceride (TG), and reduces level of high density lipoprotein cholesterol (HDL). Effect of Obstructive Sleep Apnea Hypopnea Syndrome on METHODS Data Source and Study SelectionStudies for review were found searching the PubMed, Cochrane, and EMBASE databases from January 01, 196801, , to November 30th, 2013. Unpublished data from scientifi c meetings were not searched, since...

Background and Objectives Buprenorphine's high‐binding affinity as a partial µ‐opioid agonist displaces preexisting full agonists causing precipitated withdrawal, which requires most individuals starting buprenorphine to endure moderate withdrawal prior to induction to avoid precipitated withdrawal. A novel approach called microinduction has emerged to remove this prerequisite. Our aim is to review the literature on these alternative approaches. Methods Using keywords including buprenorphine, buprenorphine/naloxone, transdermal buprenorphine, suboxone, microinduction, microdosing, rapid induction, buprenorphine‐dosing protocol, the authors searched PubMed/Medline, EMBASE, PsycINFO, PsychARTICLES, and Scopus databases from the date of inception through April 30, 2020, which yielded 1726 results, which, in turn, after manual exclusion for irrelevant content and publication in languages other than English, generated a total of 18 papers. Results On the basis of 18 papers included in this review, 63 patients were successfully transitioned to buprenorphine using different microdosing techniques, primarily in the inpatient setting. From the available data, patients were transitioned from a variety of opioids over a range of dosing without significant withdrawal, and initial doses ranged most frequently from 0.2 to 0.5 mg. While the timeframe for the various schedules ranged from 3 to 112 days, most transitioned over a period of 4 to 8 days, and most participants completed the cross titration at 8 to 16 mg. Discussion and Conclusions The growing literature demonstrates some initial promise for alternative induction models, specifically targeting patients averse to withdrawal, patients prescribed opioids for chronic pain, patients on high‐dose methadone, and patients using illicit or pharmaceutical fentanyl. Scientific Significance This manuscript provides a review of the existing literature to help clinicians better understand the approaches to microdosing of buprenorphine in various clinical settings and populations. (Am J Addict 2020;00:00–00)

The family of 5 muscarinic acetylcholine receptors belongs to the superfamily of G protein coupled neurotransmitter receptors that serve in part as regulators of synaptic function. Muscarinic receptors are anatomically positioned in cortical and subcortical areas and modulate dopaminergic and glutamatergic neurotransmission thought to be dysfunctional in schizophrenia. Neurochemical studies have shown that dopamine and muscarinic receptors reciprocally modulate one another. For example, the muscarinic agonist xanomeline increases extracellular levels of dopamine and Fos expression in cortical areas greater than subcortical areas, similar to effects of atypical antipsychotics. In electrophysiological studies, xanomeline with acute and chronic administration decreased firing of the mesocorticolimbic dopamine A10 tract, but not the motoric dopamine A9 tract. Behavioral investigations have shown that muscarinic agonists, like dopamine antagonists, inhibit conditioned-avoidance responding and dopamine-agonist-induced behaviors including hyperactivity, climbing behavior and disruption of prepulse inhibition, models for positive symptoms of schizophrenia. Transgenic knockout mice lacking M(4) receptors are hyperactive and hyper-responsive to dopamine D(1) agonists, suggesting a dynamic balance between the dopamine and M(4) receptors. Muscarinic agonists had activity in animal models of negative symptoms, cognitive dysfunction and affective disorders, symptoms that are prominent in schizophrenic patients. Consistent with effects in animal models, preliminary clinical investigation indicates that muscarinic agonists like xanomeline may be effective in the pharmacotherapy of schizophrenia. Thus, we hypothesize that a combined M(1) agonist to promote cognition and a M(4) agonist for antipsychotic-like effects would treat the symptom domains of schizophrenia without parasympathomimetic side effects.

Traumatic brain injury (TBI) occurs when a blow or jolt to the head or a penetrating injury results in damage to the brain. It is the most frequent cause of hospitalization in young people with a higher prevalence in men. TBI is the leading cause of disability and mortality between the ages 1 and 45. TBI can be caused either by the direct result of trauma or due to a complication of the primary injury. The most common etiological factors for TBI are falls, road traffic accidents, violent physical assaults, and injuries associated with athletic activities. Following TBI, significant neurologic complications may occur which include seizures, dementia, Alzheimer's disease, and cranial nerve injuries. In addition, people may suffer from various psychiatric complications such as depression, posttraumatic stress disorder, generalized anxiety disorder, obsessive-compulsive disorder, and other cognitive and behavioral sequel that might significantly increase the comorbidity of the victims. Considering all of the above complications, TBI is one of the significant public health burdens. Literature has shown that only about 25% of people achieve long-term functional independence following TBI. In this paper, we focused not only on the epidemiology but also the etiology, complications following TBI and understanding their underlying pathogenesis. Further, we focused on analyzing the options to improve the treatment and rehabilitation following TBI in future.

Borderline personality disorder (BPD) patients, when in crisis, are frequent visitors of emergency departments (EDs). When these patients exhibit symptoms such as aggressiveness, impulsivity, intense anxiety, severe depression, self-harm, and suicidal attempts or gestures, diagnosis, and treatment of the BPD becomes challenging for ED doctors. This review will, therefore, outline advice to physicians and health-care providers who face this challenging patient population in the EDs. Crisis intervention should be the first objective of clinicians when dealing with BPD in the emergency. For the patients with agitation, symptom-specific pharmacotherapy is usually recommended, while for non-agitated patients, short but intensive psychotherapy especially dialectical behavior therapy (DBT) has a positive effect. Although various psychotherapies, either alone or integrated, are preferred modes of treatment for this group of patients, the effects of psychotherapies on BPD outcomes are small to medium. Proper risk management along with developing a positive attitude and empathy toward these patients will help them in normalizing in an emergency setting after which treatment course can be decided.

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