Pub Date : 2013-04-01DOI: 10.1097/01.PSYPHR.0000429900.76636.70
M. McKean
{"title":"Psychiatric Care During Pregnancy and Postpartum: Part II Management of Anxiety, Psychosis, and Lactation","authors":"M. McKean","doi":"10.1097/01.PSYPHR.0000429900.76636.70","DOIUrl":"https://doi.org/10.1097/01.PSYPHR.0000429900.76636.70","url":null,"abstract":"","PeriodicalId":90307,"journal":{"name":"Psychopharm review : timely reports in psychopharmacology and device-based therapies","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.PSYPHR.0000429900.76636.70","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61610151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-03-01DOI: 10.1097/01.PSYPHR.0000428766.86387.F4
M. McKean
{"title":"Psychiatric Care During Pregnancy and Postpartum: Part I: Diagnosis and Management of Mood Disorders","authors":"M. McKean","doi":"10.1097/01.PSYPHR.0000428766.86387.F4","DOIUrl":"https://doi.org/10.1097/01.PSYPHR.0000428766.86387.F4","url":null,"abstract":"","PeriodicalId":90307,"journal":{"name":"Psychopharm review : timely reports in psychopharmacology and device-based therapies","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.PSYPHR.0000428766.86387.F4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61610107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-02-01DOI: 10.1097/01.PSYPHR.0000427461.48450.93
M. Dokucu, A. Denunzio, E. Esen
Lippincott Continuing Medical Education Institute, Inc. is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. Lippincott Continuing Medical Education Institute, Inc., designates this enduring material for a maximum of 1 AMA PRA Category 1 CreditTM. Physicians should only claim credit commensurate with the extent of their participation in the activity. To earn CME credit, you must read the CME article(s) and complete the quiz and evaluation assessment survey on the enclosed form, answering at least 80% of the quiz questions correctly. This activity expires on January 31, 2014. Anxiety disorders are more common than depression in the United States, with an overall lifetime prevalence of 29%, and a 12-month prevalence of 18%. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR), lists (from most to least prevalent): specific phobia (lifetime 12.5%, 12-month 8.7%); social anxiety disorder (SAD) (12.1%, 6.8%); posttraumatic stress disorder (PTSD) (6.8%, 3.5%); generalized anxiety disorder (GAD) (5.7%, 3.1%); panic disorder (PD) (4.7%, 2.7%); and obsessive-compulsive disorder (OCD) (1.6%, 1.0%). The DSM-V revisions proposed for these disorders involve minor changes in criteria while maintaining the current subclassification. The level of functional impairment for most people with anxiety disorders is significant, and related estiAfter participating in this CME activity, the psychiatrist should be better able to:
{"title":"Transcranial Magnetic Stimulation in the Treatment Of Anxiety Disorders","authors":"M. Dokucu, A. Denunzio, E. Esen","doi":"10.1097/01.PSYPHR.0000427461.48450.93","DOIUrl":"https://doi.org/10.1097/01.PSYPHR.0000427461.48450.93","url":null,"abstract":"Lippincott Continuing Medical Education Institute, Inc. is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. Lippincott Continuing Medical Education Institute, Inc., designates this enduring material for a maximum of 1 AMA PRA Category 1 CreditTM. Physicians should only claim credit commensurate with the extent of their participation in the activity. To earn CME credit, you must read the CME article(s) and complete the quiz and evaluation assessment survey on the enclosed form, answering at least 80% of the quiz questions correctly. This activity expires on January 31, 2014. Anxiety disorders are more common than depression in the United States, with an overall lifetime prevalence of 29%, and a 12-month prevalence of 18%. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR), lists (from most to least prevalent): specific phobia (lifetime 12.5%, 12-month 8.7%); social anxiety disorder (SAD) (12.1%, 6.8%); posttraumatic stress disorder (PTSD) (6.8%, 3.5%); generalized anxiety disorder (GAD) (5.7%, 3.1%); panic disorder (PD) (4.7%, 2.7%); and obsessive-compulsive disorder (OCD) (1.6%, 1.0%). The DSM-V revisions proposed for these disorders involve minor changes in criteria while maintaining the current subclassification. The level of functional impairment for most people with anxiety disorders is significant, and related estiAfter participating in this CME activity, the psychiatrist should be better able to:","PeriodicalId":90307,"journal":{"name":"Psychopharm review : timely reports in psychopharmacology and device-based therapies","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.PSYPHR.0000427461.48450.93","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61610093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01DOI: 10.1097/01.PSYPHR.0000425505.76789.f1
Alyson K. Myers, M. Trivedi
{"title":"The Effect of Antidepressant Therapy on Blood Pressure and Heart Rate Variability: A Review","authors":"Alyson K. Myers, M. Trivedi","doi":"10.1097/01.PSYPHR.0000425505.76789.f1","DOIUrl":"https://doi.org/10.1097/01.PSYPHR.0000425505.76789.f1","url":null,"abstract":"","PeriodicalId":90307,"journal":{"name":"Psychopharm review : timely reports in psychopharmacology and device-based therapies","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.PSYPHR.0000425505.76789.f1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61610029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2012-12-01DOI: 10.1097/01.PSYPHR.0000423006.73274.e7
Ma Commodore
States was estimated to be 9%. Major depression can lead to deleterious effects on the medical, social, and vocational lives of sufferers in addition to costing the economy more than $50 billion per year as a result of treatment costs and lost productivity. Despite a steady increase in the size of the antidepressant armamentarium, no randomized clinical trial has demonstrated at least a 50% response for major depression (much less for the more significant endpoint of remission). Furthermore, all available antidepressants trace their mechanisms of action back to the biogenic amine hypothesis, raising the question of whether other avenues might produce more effective treatments. To that end, we examine the data for the efficacy, safety, and comparative effectiveness of agomelatine, a novel antidepressant. Disruptions of the sleep-wake cycle are key features of mood disorders, and residual symptoms, including sleep disturbances, are well-known risk factors for relapse. Furthermore, various manipulations of circadian rhythm (eg, rapid eye movement [REM] sleep deprivation, phase advancement) may produce antidepressant activity. Thus, influencing circadian rhythm patterns could be a potential antidepressant strategy. The core biological clock is located in the suprachiasmatic nucleus (SCN) in the anterior hypothalamus. The rhythms generated by the SCN are continuously synchronized by photic and nonphotic signals (Figure 1). The primary nonphotic inputs to the SCN originate in the median raphe nucleus, a major site of serotonergic neurons. The SCN projects to the pineal gland, stimulating the synthesis of melatonin, which provides negative feedback onto the pineal gland. Although it is neither a pacemaker nor does it function independently as an antidepressant, its main function is to set the endogenous clock’s sensitivity to light. Melatonin also acts to set the onset and duration of darkness by producing phase shifts in the signal patterns of the SCN. Data from rodent and primate studies indicate that the serotonergic projections onto the SCN serve to modulate After participating in this CME activity, the psychiatrist should be better able to: • Evaluate the pharmacologic profile of agomelatine and its potential mechanism of action. • Interpret the trial data supporting the efficacy of agomelatine in the treatment of major depression. • Compare the adverse-effect profile of agomelatine with that of other commonly used antidepressants.
{"title":"Agomelatine: A Novel Antidepressant Therapy","authors":"Ma Commodore","doi":"10.1097/01.PSYPHR.0000423006.73274.e7","DOIUrl":"https://doi.org/10.1097/01.PSYPHR.0000423006.73274.e7","url":null,"abstract":"States was estimated to be 9%. Major depression can lead to deleterious effects on the medical, social, and vocational lives of sufferers in addition to costing the economy more than $50 billion per year as a result of treatment costs and lost productivity. Despite a steady increase in the size of the antidepressant armamentarium, no randomized clinical trial has demonstrated at least a 50% response for major depression (much less for the more significant endpoint of remission). Furthermore, all available antidepressants trace their mechanisms of action back to the biogenic amine hypothesis, raising the question of whether other avenues might produce more effective treatments. To that end, we examine the data for the efficacy, safety, and comparative effectiveness of agomelatine, a novel antidepressant. Disruptions of the sleep-wake cycle are key features of mood disorders, and residual symptoms, including sleep disturbances, are well-known risk factors for relapse. Furthermore, various manipulations of circadian rhythm (eg, rapid eye movement [REM] sleep deprivation, phase advancement) may produce antidepressant activity. Thus, influencing circadian rhythm patterns could be a potential antidepressant strategy. The core biological clock is located in the suprachiasmatic nucleus (SCN) in the anterior hypothalamus. The rhythms generated by the SCN are continuously synchronized by photic and nonphotic signals (Figure 1). The primary nonphotic inputs to the SCN originate in the median raphe nucleus, a major site of serotonergic neurons. The SCN projects to the pineal gland, stimulating the synthesis of melatonin, which provides negative feedback onto the pineal gland. Although it is neither a pacemaker nor does it function independently as an antidepressant, its main function is to set the endogenous clock’s sensitivity to light. Melatonin also acts to set the onset and duration of darkness by producing phase shifts in the signal patterns of the SCN. Data from rodent and primate studies indicate that the serotonergic projections onto the SCN serve to modulate After participating in this CME activity, the psychiatrist should be better able to: • Evaluate the pharmacologic profile of agomelatine and its potential mechanism of action. • Interpret the trial data supporting the efficacy of agomelatine in the treatment of major depression. • Compare the adverse-effect profile of agomelatine with that of other commonly used antidepressants.","PeriodicalId":90307,"journal":{"name":"Psychopharm review : timely reports in psychopharmacology and device-based therapies","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2012-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.PSYPHR.0000423006.73274.e7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61610014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2012-11-01DOI: 10.1097/01.psyphr.0000422135.23603.07
Maria J. Julios Costa, M. Moyer, J. O'reardon
{"title":"Monoamine Oxidase Inhibitors: An Important but Underutilized Treatment Part II: Safety and Tolerability","authors":"Maria J. Julios Costa, M. Moyer, J. O'reardon","doi":"10.1097/01.psyphr.0000422135.23603.07","DOIUrl":"https://doi.org/10.1097/01.psyphr.0000422135.23603.07","url":null,"abstract":"","PeriodicalId":90307,"journal":{"name":"Psychopharm review : timely reports in psychopharmacology and device-based therapies","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2012-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.psyphr.0000422135.23603.07","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61609947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2012-10-01DOI: 10.1097/01.PSYPHR.0000421537.96374.a0
Maria J. Julios Costa, M. Moyer, J. O'reardon
HISTORY AND BACKGROUND Monoamine oxidase (MAO) is an enzyme that converts biogenic amines to their corresponding aldehydes. In the brain, its primary substrates are epinephrine (EPI), norepinephrine (NE), dopamine (DA), and serotonin (5-HT). Tyramine is also catabolized by MAO after being absorbed from the gastrointestinal tract or after being generated by bacterial metabolic transformations. Johnston first demonstrated the existence of 2 forms of MAO in the brain, type A (MAO-A) and type B (MAO-B), which differ in their substrate affinities and inhibitor sensitivities. During the late 1940s, isoniazid and related compounds were used to treat tuberculosis but also produced unanticipated mood elevation. Later, it was determined that these drugs shared an ability to inhibit the MAO enzyme and increase the levels of 5-HT, NE, and DA in the brain. Hence, (MAOIs were the first class of antidepressant drugs to be identified and have long been recognized as efficacious for the treatment of depression. However, because of reports of acute hypertension after the ingestion of dietary tyramine After participating in this CME activity, the psychiatrist should be better able to:
{"title":"Monoamine Oxidase Inhibitors: An Important but Underutilized Treatment Part I Efficacy","authors":"Maria J. Julios Costa, M. Moyer, J. O'reardon","doi":"10.1097/01.PSYPHR.0000421537.96374.a0","DOIUrl":"https://doi.org/10.1097/01.PSYPHR.0000421537.96374.a0","url":null,"abstract":"HISTORY AND BACKGROUND Monoamine oxidase (MAO) is an enzyme that converts biogenic amines to their corresponding aldehydes. In the brain, its primary substrates are epinephrine (EPI), norepinephrine (NE), dopamine (DA), and serotonin (5-HT). Tyramine is also catabolized by MAO after being absorbed from the gastrointestinal tract or after being generated by bacterial metabolic transformations. Johnston first demonstrated the existence of 2 forms of MAO in the brain, type A (MAO-A) and type B (MAO-B), which differ in their substrate affinities and inhibitor sensitivities. During the late 1940s, isoniazid and related compounds were used to treat tuberculosis but also produced unanticipated mood elevation. Later, it was determined that these drugs shared an ability to inhibit the MAO enzyme and increase the levels of 5-HT, NE, and DA in the brain. Hence, (MAOIs were the first class of antidepressant drugs to be identified and have long been recognized as efficacious for the treatment of depression. However, because of reports of acute hypertension after the ingestion of dietary tyramine After participating in this CME activity, the psychiatrist should be better able to:","PeriodicalId":90307,"journal":{"name":"Psychopharm review : timely reports in psychopharmacology and device-based therapies","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2012-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.PSYPHR.0000421537.96374.a0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61609934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2012-09-01DOI: 10.1097/01.PSYPHR.0000419187.87926.2d
C. M. Gould
{"title":"Psychopharmacologic Treatment of Acute Agitation: Part II","authors":"C. M. Gould","doi":"10.1097/01.PSYPHR.0000419187.87926.2d","DOIUrl":"https://doi.org/10.1097/01.PSYPHR.0000419187.87926.2d","url":null,"abstract":"","PeriodicalId":90307,"journal":{"name":"Psychopharm review : timely reports in psychopharmacology and device-based therapies","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2012-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.PSYPHR.0000419187.87926.2d","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61610420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2012-07-01DOI: 10.1097/01.PSYPHR.0000415883.88497.AC
C. M. Gould
{"title":"Psychopharmacologic Treatment of Acute Agitation: Part I","authors":"C. M. Gould","doi":"10.1097/01.PSYPHR.0000415883.88497.AC","DOIUrl":"https://doi.org/10.1097/01.PSYPHR.0000415883.88497.AC","url":null,"abstract":"","PeriodicalId":90307,"journal":{"name":"Psychopharm review : timely reports in psychopharmacology and device-based therapies","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2012-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.PSYPHR.0000415883.88497.AC","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61610392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：