Pub Date : 2022-04-29DOI: 10.1176/appi.ajp-rj.2022.170305
M. Yau
{"title":"A Tribute to the Mind","authors":"M. Yau","doi":"10.1176/appi.ajp-rj.2022.170305","DOIUrl":"https://doi.org/10.1176/appi.ajp-rj.2022.170305","url":null,"abstract":"","PeriodicalId":74938,"journal":{"name":"The American journal of psychiatry residents' journal","volume":"64 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86873608","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 : 2022-04-29DOI: 10.1176/appi.ajp-rj.2022.170302
Nicolas R. Genovese, Christopher W Racine, Lee A Wolfrum
{"title":"Intravenous Ketamine as a Treatment Option for Patients Presenting to the ED With Suicidal Ideation","authors":"Nicolas R. Genovese, Christopher W Racine, Lee A Wolfrum","doi":"10.1176/appi.ajp-rj.2022.170302","DOIUrl":"https://doi.org/10.1176/appi.ajp-rj.2022.170302","url":null,"abstract":"","PeriodicalId":74938,"journal":{"name":"The American journal of psychiatry residents' journal","volume":"19 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77467624","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 : 2022-04-29DOI: 10.1176/appi.ajp-rj.2022.170301
Jiansan Gu, Maria Amir
{"title":"Following a Family Legacy: A Personal Journey","authors":"Jiansan Gu, Maria Amir","doi":"10.1176/appi.ajp-rj.2022.170301","DOIUrl":"https://doi.org/10.1176/appi.ajp-rj.2022.170301","url":null,"abstract":"","PeriodicalId":74938,"journal":{"name":"The American journal of psychiatry residents' journal","volume":"159 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85316230","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 : 2022-04-29DOI: 10.1176/appi.ajp-rj.2022.170303
Alison Mause, Samuel Warn
{"title":"Suicidal Ideation on Day of Discharge","authors":"Alison Mause, Samuel Warn","doi":"10.1176/appi.ajp-rj.2022.170303","DOIUrl":"https://doi.org/10.1176/appi.ajp-rj.2022.170303","url":null,"abstract":"","PeriodicalId":74938,"journal":{"name":"The American journal of psychiatry residents' journal","volume":"30 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89373215","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 : 2022-04-12DOI: 10.1176/appi.ajp.21020125
R. Keefe, Elena Cañadas, Deborah Farlow, A. Etkin
OBJECTIVE The authors evaluated AKL-T03, an investigational digital intervention delivered through a video game-based interface, designed to target the fronto-parietal network to enhance functional domains for attentional control. AKL-T03 was tested in adult patients with major depressive disorder and a demonstrated cognitive impairment at baseline. METHODS Adults ages 25-55 years on a stable antidepressant medication regimen with residual mild to moderate depression and an objective impairment in cognition (as measured using the symbol coding test) were enrolled in a double-blind randomized controlled study. Participants were randomized either to AKL-T03 or to an expectation-matched digital control intervention. Participants were assessed at baseline and after completion of their 6-week at-home intervention. The primary outcome measure was improvement in sustained attention, as measured by the Test of Variables of Attention (TOVA). RESULTS AKL-T03 (N=37) showed a statistically significant medium-effect-size improvement in sustained attention compared with the control intervention on the TOVA primary outcome (N=37) (partial eta-squared=0.11). Additionally, a composite score derived from all cognitive measures demonstrated significant improvement with AKL-T03 over the control intervention. Individual secondary and exploratory endpoints did not demonstrate statistically significant between-group differences. No serious adverse events were reported, and two patients (5.5%) in the AKL-T03 group reported an intervention-related adverse event (headache). CONCLUSIONS Treatment with AKL-T03 resulted in significant improvement in sustained attention, as well as in cognitive functioning as a whole, compared with a control intervention. AKL-T03 is a safe digital intervention that is effective in the treatment of cognitive impairment associated with major depression. Further research will be needed to understand the clinical consequences of this treatment-induced change.
{"title":"Digital Intervention for Cognitive Deficits in Major Depression: A Randomized Controlled Trial to Assess Efficacy and Safety in Adults.","authors":"R. Keefe, Elena Cañadas, Deborah Farlow, A. Etkin","doi":"10.1176/appi.ajp.21020125","DOIUrl":"https://doi.org/10.1176/appi.ajp.21020125","url":null,"abstract":"OBJECTIVE\u0000The authors evaluated AKL-T03, an investigational digital intervention delivered through a video game-based interface, designed to target the fronto-parietal network to enhance functional domains for attentional control. AKL-T03 was tested in adult patients with major depressive disorder and a demonstrated cognitive impairment at baseline.\u0000\u0000\u0000METHODS\u0000Adults ages 25-55 years on a stable antidepressant medication regimen with residual mild to moderate depression and an objective impairment in cognition (as measured using the symbol coding test) were enrolled in a double-blind randomized controlled study. Participants were randomized either to AKL-T03 or to an expectation-matched digital control intervention. Participants were assessed at baseline and after completion of their 6-week at-home intervention. The primary outcome measure was improvement in sustained attention, as measured by the Test of Variables of Attention (TOVA).\u0000\u0000\u0000RESULTS\u0000AKL-T03 (N=37) showed a statistically significant medium-effect-size improvement in sustained attention compared with the control intervention on the TOVA primary outcome (N=37) (partial eta-squared=0.11). Additionally, a composite score derived from all cognitive measures demonstrated significant improvement with AKL-T03 over the control intervention. Individual secondary and exploratory endpoints did not demonstrate statistically significant between-group differences. No serious adverse events were reported, and two patients (5.5%) in the AKL-T03 group reported an intervention-related adverse event (headache).\u0000\u0000\u0000CONCLUSIONS\u0000Treatment with AKL-T03 resulted in significant improvement in sustained attention, as well as in cognitive functioning as a whole, compared with a control intervention. AKL-T03 is a safe digital intervention that is effective in the treatment of cognitive impairment associated with major depression. Further research will be needed to understand the clinical consequences of this treatment-induced change.","PeriodicalId":74938,"journal":{"name":"The American journal of psychiatry residents' journal","volume":"22 1","pages":"appiajp21020125"},"PeriodicalIF":0.0,"publicationDate":"2022-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74912945","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 : 2022-04-01DOI: 10.1176/appi.ajp.2021.21070700
B. Watts, D. Gottlieb, N. Riblet, Jiang Gui, B. Shiner
OBJECTIVE Understanding the effectiveness of medication treatment for opioid use disorder to decrease the risk of suicide mortality may inform clinical and policy decisions. The authors sought to describe the effect of medications for opioid use disorder (MOUD) on risk of suicide mortality. METHODS This was a retrospective cohort study in Department of Veterans Affairs (VA) patients from 2003 to 2017. The authors linked three data sources: the VA Corporate Data Warehouse, Centers for Medicare and Medicaid Services Claims Data, and the VA-Department of Defense Mortality Data Repository. The exposure of interest was MOUD, including starting periods (first 14 days on treatment), stopping periods (first 14 days off treatment), stable time on treatment, and stable time off treatment (reference category). The main outcome measures included suicide mortality, external-cause mortality, and all-cause mortality in the 5 years following initiation of MOUD. RESULTS Over 60,000 VA patients received MOUD. Patients were typically male (92.8%) and their mean age was 46.5 years (SD=13.1). After adjusting for demographic characteristics, mental health and physical health conditions, and health care utilization, the adjusted hazard ratio during stable MOUD was 0.45 (95% CI=0.32, 0.63) for suicide mortality, 0.35 (95% CI=0.31, 0.40) for external-cause mortality, and 0.34 (95% CI=0.31, 0.37) for all-cause mortality. MOUD starting periods were associated with an adjusted hazard ratio for suicide mortality of 0.55 (95% CI=0.25, 1.21), and MOUD stopping periods were associated with an adjusted hazard ratio for suicide mortality of 1.38 (95% CI=0.82, 2.34). CONCLUSIONS Treatment with MOUD was associated with a substantial reduction in suicide mortality as well external causes of mortality and all-cause mortality.
{"title":"Association of Medication Treatment for Opioid Use Disorder With Suicide Mortality.","authors":"B. Watts, D. Gottlieb, N. Riblet, Jiang Gui, B. Shiner","doi":"10.1176/appi.ajp.2021.21070700","DOIUrl":"https://doi.org/10.1176/appi.ajp.2021.21070700","url":null,"abstract":"OBJECTIVE\u0000Understanding the effectiveness of medication treatment for opioid use disorder to decrease the risk of suicide mortality may inform clinical and policy decisions. The authors sought to describe the effect of medications for opioid use disorder (MOUD) on risk of suicide mortality.\u0000\u0000\u0000METHODS\u0000This was a retrospective cohort study in Department of Veterans Affairs (VA) patients from 2003 to 2017. The authors linked three data sources: the VA Corporate Data Warehouse, Centers for Medicare and Medicaid Services Claims Data, and the VA-Department of Defense Mortality Data Repository. The exposure of interest was MOUD, including starting periods (first 14 days on treatment), stopping periods (first 14 days off treatment), stable time on treatment, and stable time off treatment (reference category). The main outcome measures included suicide mortality, external-cause mortality, and all-cause mortality in the 5 years following initiation of MOUD.\u0000\u0000\u0000RESULTS\u0000Over 60,000 VA patients received MOUD. Patients were typically male (92.8%) and their mean age was 46.5 years (SD=13.1). After adjusting for demographic characteristics, mental health and physical health conditions, and health care utilization, the adjusted hazard ratio during stable MOUD was 0.45 (95% CI=0.32, 0.63) for suicide mortality, 0.35 (95% CI=0.31, 0.40) for external-cause mortality, and 0.34 (95% CI=0.31, 0.37) for all-cause mortality. MOUD starting periods were associated with an adjusted hazard ratio for suicide mortality of 0.55 (95% CI=0.25, 1.21), and MOUD stopping periods were associated with an adjusted hazard ratio for suicide mortality of 1.38 (95% CI=0.82, 2.34).\u0000\u0000\u0000CONCLUSIONS\u0000Treatment with MOUD was associated with a substantial reduction in suicide mortality as well external causes of mortality and all-cause mortality.","PeriodicalId":74938,"journal":{"name":"The American journal of psychiatry residents' journal","volume":"234 1","pages":"298-304"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73489902","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 : 2022-04-01DOI: 10.1176/appi.ajp.20220173
Larissa J. Mooney
{"title":"Medication Treatment for Opioid Use Disorder Reduces Suicide Risk.","authors":"Larissa J. Mooney","doi":"10.1176/appi.ajp.20220173","DOIUrl":"https://doi.org/10.1176/appi.ajp.20220173","url":null,"abstract":"","PeriodicalId":74938,"journal":{"name":"The American journal of psychiatry residents' journal","volume":"22 1","pages":"262-263"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88266499","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 : 2022-04-01DOI: 10.1176/appi.ajp.20220151
N. Kalin
{"title":"Integrating Clinical and Basic Research: Opioid Use Disorder, Psychotic Illnesses, and Prefrontal Microcircuits Relevant to Schizophrenia.","authors":"N. Kalin","doi":"10.1176/appi.ajp.20220151","DOIUrl":"https://doi.org/10.1176/appi.ajp.20220151","url":null,"abstract":"","PeriodicalId":74938,"journal":{"name":"The American journal of psychiatry residents' journal","volume":"56 1","pages":"255-258"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83013230","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 : 2022-04-01DOI: 10.1176/appi.ajp.20220182
M. Teesson
{"title":"Opioid Prescribing and the Very Human Toll of Drug Harms.","authors":"M. Teesson","doi":"10.1176/appi.ajp.20220182","DOIUrl":"https://doi.org/10.1176/appi.ajp.20220182","url":null,"abstract":"","PeriodicalId":74938,"journal":{"name":"The American journal of psychiatry residents' journal","volume":"78 1","pages":"264-266"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88378911","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 : 2022-04-01DOI: 10.1176/appi.ajp.20220147
V. Sohal
The major cause of disability in schizophrenia is cognitive impairment, which remains largely refractory to existing treatments. This reflects the fact that antipsychotics and other therapies have not been designed to address specific brain abnormalities that cause cognitive impairment. This overview proposes that understanding how specific cellular and synaptic loci within cortical microcircuits contribute to cortical gamma oscillations may reveal treatments for cognitive impairment. Gamma oscillations are rhythmic patterns of high frequency (∼30-100 Hz) neuronal activity that are synchronized within and across brain regions, generated by a class of inhibitory interneurons that express parvalbumin, and recruited during a variety of cognitive tasks. In schizophrenia, both parvalbumin interneuron function and task-evoked gamma oscillations are deficient. While it has long been controversial whether gamma oscillations are merely a biomarker of circuit function or actually contribute to information processing by neuronal networks, recent neurobiological studies in mice have shown that disrupting or enhancing synchronized gamma oscillations can reproduce or ameliorate cognitive deficits resembling those seen in schizophrenia. In fact, transiently enhancing the synchrony of parvalbumin interneuron-generated gamma oscillations can lead to long-lasting improvements in cognition in mice that model aspects of schizophrenia. Gamma oscillations emerge from specific patterns of connections between a variety of cell types within cortical microcircuits. Thus, a critical next step is to understand how specific cell types and synapses generate gamma oscillations, mediate the effects of gamma oscillations on information processing, and/or undergo plasticity following the induction of gamma oscillations. Modulating these circuit loci, potentially in combination with other approaches such as cognitive training and brain stimulation, may yield potent and selective interventions for enhancing cognition in schizophrenia.
{"title":"Transforming Discoveries About Cortical Microcircuits and Gamma Oscillations Into New Treatments for Cognitive Deficits in Schizophrenia.","authors":"V. Sohal","doi":"10.1176/appi.ajp.20220147","DOIUrl":"https://doi.org/10.1176/appi.ajp.20220147","url":null,"abstract":"The major cause of disability in schizophrenia is cognitive impairment, which remains largely refractory to existing treatments. This reflects the fact that antipsychotics and other therapies have not been designed to address specific brain abnormalities that cause cognitive impairment. This overview proposes that understanding how specific cellular and synaptic loci within cortical microcircuits contribute to cortical gamma oscillations may reveal treatments for cognitive impairment. Gamma oscillations are rhythmic patterns of high frequency (∼30-100 Hz) neuronal activity that are synchronized within and across brain regions, generated by a class of inhibitory interneurons that express parvalbumin, and recruited during a variety of cognitive tasks. In schizophrenia, both parvalbumin interneuron function and task-evoked gamma oscillations are deficient. While it has long been controversial whether gamma oscillations are merely a biomarker of circuit function or actually contribute to information processing by neuronal networks, recent neurobiological studies in mice have shown that disrupting or enhancing synchronized gamma oscillations can reproduce or ameliorate cognitive deficits resembling those seen in schizophrenia. In fact, transiently enhancing the synchrony of parvalbumin interneuron-generated gamma oscillations can lead to long-lasting improvements in cognition in mice that model aspects of schizophrenia. Gamma oscillations emerge from specific patterns of connections between a variety of cell types within cortical microcircuits. Thus, a critical next step is to understand how specific cell types and synapses generate gamma oscillations, mediate the effects of gamma oscillations on information processing, and/or undergo plasticity following the induction of gamma oscillations. Modulating these circuit loci, potentially in combination with other approaches such as cognitive training and brain stimulation, may yield potent and selective interventions for enhancing cognition in schizophrenia.","PeriodicalId":74938,"journal":{"name":"The American journal of psychiatry residents' journal","volume":"32 1","pages":"267-276"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89307431","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}
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