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August 18, 2020 (TORONTO) — antabuse prices walmart Canada Health Infoway (Infoway) and Loblaw Companies Limited (Loblaw) are pleased to announce that they have reached an agreement to advance e-prescribing in Canada. Under the agreement, Shoppers Drug Mart, Loblaw retail pharmacies and QHR Technologies’ AccuroEMR®, Canada’s largest single electronic medical record platform, will work towards connecting with PrescribeIT®, Infoway’s national e-prescribing service.As a first step in the initiative, Shoppers Drug Mart and Loblaw will begin to roll out PrescribeIT® in pharmacies already using software that is integrated with PrescribeIT®. “This agreement will accelerate the adoption of e-prescribing in Canada, bringing significant benefits to patients, prescribers antabuse prices walmart and health care systems across the country,” said Ashesh Desai, Executive Vice President Pharmacy and Healthcare Businesses at Shoppers Drug Mart.“PrescribeIT® has shown tremendous momentum since it launched,” said Michael Green, President and CEO of Infoway. €œThis is an important expansion for PrescribeIT® and will help extend the benefits of the service more broadly.”Loblaw will continue to operate FreedomRx, the e-prescribing and messaging platform that is currently available predominantly to Loblaw and Shoppers Drug Mart pharmacies and physicians using AccuroEMR® as their electronic medical records system.About Canada Health InfowayInfoway helps to improve the health of Canadians by working with partners to accelerate the development, adoption and effective use of digital health across Canada.

Through our investments, we help deliver better quality and access to care and more efficient delivery of health antabuse prices walmart services for patients and clinicians. Infoway is an independent, not-for-profit organization funded by the federal government. Visit www.infoway-inforoute.ca.About PrescribeIT®Canada Health Infoway is working with Health Canada, the provinces and territories, and industry stakeholders to develop, operate and maintain the national e-prescribing service known as PrescribeIT® antabuse prices walmart. PrescribeIT® will serve all Canadians, pharmacies and prescribers and provide safer and more effective medication management by enabling prescribers to transmit a prescription electronically between a prescriber’s electronic medical record (EMR) and the pharmacy management system (PMS) of a patient’s pharmacy of choice.

PrescribeIT® will protect Canadians’ personal health information antabuse prices walmart from being sold or used for commercial activities. Visit www.PrescribeIT.ca.About Loblaw Companies LimitedLoblaw is Canada's food and pharmacy leader, and the nation's largest retailer. Loblaw provides Canadians with grocery, antabuse prices walmart pharmacy, health and beauty, apparel, general merchandise, financial services and wireless mobile products and services. With more than 2,400 corporate, franchised and Associate-owned locations, Loblaw, its franchisees and associate-owners employ approximately 200,000 full- and part-time employees, making it one of Canada's largest private sector employers.Loblaw's purpose – Live Life Well® – puts first the needs and well-being of Canadians who make one billion transactions annually in the company's stores.

Loblaw is positioned antabuse prices walmart to meet and exceed those needs in many ways. Convenient locations. More than 1,050 antabuse prices walmart grocery stores that span the value spectrum from discount to specialty. Full-service pharmacies at nearly 1,400 Shoppers Drug Mart® and Pharmaprix® locations and close to 500 Loblaw locations.

PC Financial® antabuse prices walmart services. Affordable Joe Fresh® fashion and family apparel. And three of Canada's top-consumer brands in Life Brand, antabuse prices walmart no name® and President's Choice. For more information, visit Loblaw's website at www.loblaw.ca.-30-Media InquiriesCatherine ThomasSenior Director, External CommunicationLoblaw Companies Limited This email address is being protected from spambots.

You need antabuse prices walmart JavaScript enabled to view it.Inquiries about PrescribeIT®July 22, 2020 (Toronto) – Rexall Pharmacy Group Ltd. (Rexall) and Canada Health Infoway (Infoway) are pleased to announce that PrescribeIT®, Infoway’s national e-prescribing service, will soon become available in more than 250 Rexall pharmacies across Canada. PrescribeIT® enables prescribers and pharmacists to electronically create, receive, renew and cancel prescriptions, while improving overall patient care through secure clinician messaging.“Rexall antabuse prices walmart is an important addition to the PrescribeIT® roster of partners and we are very pleased to have them on board,” noted Jamie Bruce, Executive Vice President, Canada Health Infoway. €œTogether we can help improve patient care through more effective medication management.”“At Rexall, we strive to build partnerships aimed at providing our pharmacists with innovative solutions to help improve overall patient care,” said Nicolas Caprio, President, Rexall.

€œPrescribeIT® is a great opportunity for us to continue strengthening our digital offering, allowing pharmacists and physicians antabuse prices walmart to increase their communication and ultimately positively impact patient health.”In anticipation of the agreement, Rexall has already introduced the service in key locations in Ontario, Alberta and New Brunswick. Additional sites will start to offer PrescribeIT® starting in the next several weeks.About Canada Health InfowayInfoway helps to improve the health of Canadians by working with partners to accelerate the development, adoption and effective use of digital health across Canada. Through our investments, we help deliver better quality and access antabuse prices walmart to care and more efficient delivery of health services for patients and clinicians. Infoway is an independent, not-for-profit organization funded by the federal government.

Visit www.infoway.ca.About PrescribeIT®Canada Health Infoway is working antabuse prices walmart with Health Canada, the provinces and territories, and industry stakeholders to develop, operate and maintain the national e-prescribing service known as PrescribeIT®. PrescribeIT® will serve all Canadians, pharmacies and prescribers and provide safer and more effective medication management by enabling prescribers to transmit a prescription electronically between a prescriber’s electronic medical record (EMR) and the pharmacy management system (PMS) of a patient’s pharmacy of choice. PrescribeIT® will protect Canadians’ personal antabuse prices walmart health information from being sold or used for commercial activities. Visit www.prescribeit.ca.About Rexall Pharmacy Group Ltd.With a heritage dating back over a century, Rexall is a leading drugstore operator with a dynamic history of innovation and growth, dedicated to caring for Canadians’ health…one person at a time.

Operating over 400 pharmacies across Canada, Rexall’s 8,500 employees provide antabuse prices walmart exceptional patient care and customer service. Rexall is part of the Rexall Pharmacy Group Ltd. And a proud member of the antabuse prices walmart global McKesson Corporation family. For more information, visit rexall.ca.

Follow us antabuse prices walmart on Twitter. @RexallDrugstore, on Instagram at @RexallDrugstoreOfficial and on Facebook at @RexallDrugstore.-30-Media InquiriesInquiries about PrescribeIT®Inquiries about McKesson CanadaAndrew ForgioneDirector, Media Relations and Public AffairsMcKesson Canada(905) 671-4586.

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Evidence and antabuse uk buy mass casualty natural antabuse events“I sat among the dead, dying and those fighting for life, I observed the pain and suffering and endured my own. I need to hear the truth to be able to move forward and I have to be there for those who didn't make it, they do not have a say in this, so I must speak up for them and for my own mental well-being, I cannot rest until the truth is told and evidence is shown to me…”I would urge all readers this month to consider carefully these words from an innocent victim of the 2017 Manchester Arena bombing. Among these natural antabuse harrowing words, we should be mindful of the use of the word “evidence,” as we consider the theme of several of our papers in this addition of Mass Casualty Events.

The first of these papers, our Editor’s choice from Dark and colleagues, considers evidence from a national trauma registry patient case series and hospital performance data from the Manchester bombing itself. In this important work, Dark presents routinely collected injury, management and outcome data from natural antabuse 153 patients who attended hospital after this incident. While this powerful data provides an objective evaluation of a system wide response and offers important learnings for systems moving forward, we should be mindful that the interpretation of what is evidence may be different for us as readers and most importantly the victims of such incidents.

Objective numbers natural antabuse can never describe pain and suffering. We discuss the ethical implications of the data presented within this manuscript, together with the outstanding community engagement work undertaken by Dark’s team within our accompanying editorial.Skryabina and colleagues, provide an alternative form of evidence in their mixed methods study involving interviews with healthcare staff who took part in responses to three terrorist attacks in the UK. It is pleasing to see patient and public involvement from victims again here, in informing interview design.

With this work we can identify themes that will be helpful to systems in planning for such events such as effective team working, communication natural antabuse and robust Major Incident Plans. Although one interview quote stands out. €œWe underestimate natural antabuse the post-trauma of it and that’s the one thing I definitely took away from this event is we are not prepared for the stress and trauma it caused.” As the authors highlight, the need for psychosocial support after such events is clearly underestimated.

A Short Report, by Mawhinney et al, demonstrates through a survey of nearly 200 doctors working in hospitals across the UK, that having a Major Incident Plan in place does not necessarily translate to preparedness and knowledge in the handling of mass casualty events. There is certainly work to do in terms of education natural antabuse here.Our final Mass Casualty Event themed paper this month takes an entirely different approach to evidence. By reviewing extensive written, photographic and video evidence from the Hillsborough Disaster (a crowd crush at a football stadium in the UK in 1989), Jerry Nolan and expert colleagues provide a unique clinical insight into compression asphyxia in their Practice Review.

Again, it is impressive to see engagement with the Hillsborough natural antabuse Families who gave permission for publication of this potentially emotive manuscript.Safety and service organisationCurrent daily clinical work in Emergency Departments (ED) across the world continues to be pressured. Lynsey Flowerdew identifies some familiar risks in our practice, in survey work covering over 1000 UK clinicians. Risks posed by interruptions, negative effects of targets, deficient mental healthcare and ED crowding are identified but an encouraging safety culture is also revealed.

Our Reader’s natural antabuse Choice also explores risks at a more granular level, in a prospective observational study of risk events during intrahospital transport from Australia. While risk events occur in almost 40% of patient journeys, with many resulting in harm, prior preparation would appear to prevent poor performance.One initiative to mitigate risk in EDs that are facing unprecedented demands, continues to be the integration of primary care/general practitioners within an ED setting (GPED). It is therefore a pleasure to see preliminary work mapping GPED published in the EMJ, natural antabuse led by my colleagues from the University of West of England, Bristol, UK.

While the majority of UK ED’s have adopted a GPED model, there appears heterogeneity in the type of model used and the relative effectiveness of these models remains unknown. There is more to come from this excellent project, that should provide answers natural antabuse. In a similar vein, Lasserson and colleagues identify significant heterogeneity in referral rates (between 1%–21% of patients seen) from out of hours primary care to the ED using operations research methods.

There is natural antabuse clearly still much work to be done to reduce variations in practice and maximise efficiency in this area.alcoholism treatmentAs we continue to see high volumes of patients with alcoholism treatment attending EDs across the world, work by Douillet et al highlights limitations in current structural design of departments in France to facilitate robust organisational responses. They showed that clinical guidelines are designed to fit an “ideal” rather than being more pragmatic for use in existing environments. Finally, an interesting Short Report from Davies and colleagues in Scotland explores the utility of exercise induced hypoxia in evaluating patients with alcoholism treatment and offers a standardised approach to this using a 1 min sit-to-stand test.

Readers may want to put this into perspective by looking at the secondary analysis from natural antabuse the PRIEST study, published in the EMJ earlier this year, which found post exertional oxygen saturations to be only a modest prognostic variable. Perhaps a standardised approach is key here." data-icon-position data-hide-link-title="0">Ethics statementsPatient consent for publicationNot required.There are certain events that resonate with all emergency clinicians, events that many of us hope we will never bear witness to and events that, unfortunately, some of us have. Mass casualty events are thankfully rare, with estimates in the USA of around 0.15% of all emergency service calls.1 However, in 2017 the NHS in the natural antabuse UK was faced with an unprecedented number of such events, including the Manchester Arena bombing.

Each event poses new challenges in terms of environment, threats posed to staff and casualties and the injuries sustained.2 It is therefore important for ‘lessons learnt’ from mass casualty events to continue to be written up and published in a robust and scientific manner.3 However, at the centre of every mass casualty event are the patients themselves, those who may not survive, those who survive with life-changing injuries and those who are lucky to escape without physical injury but who suffer long-term psychological trauma as a result of events they witness. Authors of reports around mass natural antabuse casualty events therefore have a unique challenge when presenting events in a way that is scientific yet considers ethical publishing in terms of patient consent, potentially identifiable data, considerations of impact of publishing on communities and inevitable media reporting. Editors and journals too have a similar responsibility to patients who are involved in such events.

It is therefore a great opportunity for the Emergency Medicine Journal (EMJ) not only to publish Dark et ….

Evidence and mass antabuse prices walmart casualty events“I sat among the dead, dying http://iconographymag.com/nyfw-custo-barcelona-fall-2011-collection/ and those fighting for life, I observed the pain and suffering and endured my own. I need to hear the truth to be able to move forward and I have to be there for those who didn't make it, they do not have a say in this, so I must speak up for them and for my own mental well-being, I cannot rest until the truth is told and evidence is shown to me…”I would urge all readers this month to consider carefully these words from an innocent victim of the 2017 Manchester Arena bombing. Among these harrowing words, we should be mindful of the use of the word “evidence,” as we consider the theme of several of our papers in this addition of Mass Casualty antabuse prices walmart Events. The first of these papers, our Editor’s choice from Dark and colleagues, considers evidence from a national trauma registry patient case series and hospital performance data from the Manchester bombing itself.

In this important work, Dark presents routinely collected injury, management and outcome data from antabuse prices walmart 153 patients who attended hospital after this incident. While this powerful data provides an objective evaluation of a system wide response and offers important learnings for systems moving forward, we should be mindful that the interpretation of what is evidence may be different for us as readers and most importantly the victims of such incidents. Objective numbers can never describe pain antabuse prices walmart and suffering. We discuss the ethical implications of the data presented within this manuscript, together with the outstanding community engagement work undertaken by Dark’s team within our accompanying editorial.Skryabina and colleagues, provide an alternative form of evidence in their mixed methods study involving interviews with healthcare staff who took part in responses to three terrorist attacks in the UK.

It is pleasing to see patient and public involvement from victims again here, in informing interview design. With this work we can identify themes that will be helpful to systems in planning for such events such as effective antabuse prices walmart team working, communication and robust Major Incident Plans. Although one interview quote stands out. €œWe underestimate the post-trauma of it and that’s the one thing I definitely took away from this event is we are not prepared for the stress and trauma it caused.” As the authors highlight, the need for psychosocial antabuse prices walmart support after such events is clearly underestimated.

A Short Report, by Mawhinney et al, demonstrates through a survey of nearly 200 doctors working in hospitals across the UK, that having a Major Incident Plan in place does not necessarily translate to preparedness and knowledge in the handling of mass casualty events. There is certainly work to do in terms of education here.Our final Mass Casualty Event antabuse prices walmart themed paper this month takes an entirely different approach to evidence. By reviewing extensive written, photographic and video evidence from the Hillsborough Disaster (a crowd crush at a football stadium in the UK in 1989), Jerry Nolan and expert colleagues provide a unique clinical insight into compression asphyxia in their Practice Review. Again, it is impressive to see engagement antabuse prices walmart with the Hillsborough Families who gave permission for publication of this potentially emotive manuscript.Safety and service organisationCurrent daily clinical work in Emergency Departments (ED) across the world continues to be pressured.

Lynsey Flowerdew identifies some familiar risks in our practice, in survey work covering over 1000 UK clinicians. Risks posed by interruptions, negative effects of targets, deficient mental healthcare and ED crowding are identified but an encouraging safety culture is also revealed. Our Reader’s Choice also explores risks at a more granular level, in a prospective observational study of antabuse prices walmart risk events during intrahospital transport from Australia. While risk events occur in almost 40% of patient journeys, with many resulting in harm, prior preparation would appear to prevent poor performance.One initiative to mitigate risk in EDs that are facing unprecedented demands, continues to be the integration of primary care/general practitioners within an ED setting (GPED).

It is therefore a pleasure to see preliminary work mapping GPED antabuse prices walmart published in the EMJ, led by my colleagues from the University of West of England, Bristol, UK. While the majority of UK ED’s have adopted a GPED model, there appears heterogeneity in the type of model used and the relative effectiveness of these models remains unknown. There is more to come from this excellent project, antabuse prices walmart that should provide answers. In a similar vein, Lasserson and colleagues identify significant heterogeneity in referral rates (between 1%–21% of patients seen) from out of hours primary care to the ED using operations research methods.

There is clearly still much work to be done to reduce variations in practice and maximise efficiency in this area.alcoholism treatmentAs we continue to see high volumes of patients with alcoholism treatment attending EDs across the world, work by Douillet et al highlights limitations antabuse prices walmart in current structural design of departments in France to facilitate robust organisational responses. They showed that clinical guidelines are designed to fit an “ideal” rather than being more pragmatic for use in existing environments. Finally, an interesting Short Report from Davies and colleagues in Scotland explores the utility of exercise induced hypoxia in evaluating patients with alcoholism treatment and offers a standardised approach to this using a 1 min sit-to-stand test. Readers may want to put this into perspective by looking at the secondary analysis from the PRIEST study, published in the EMJ earlier this year, which found post antabuse prices walmart exertional oxygen saturations to be only a modest prognostic variable.

Perhaps a standardised approach is key here." data-icon-position data-hide-link-title="0">Ethics statementsPatient consent for publicationNot required.There are certain events that resonate with all emergency clinicians, events that many of us hope we will never bear witness to and events that, unfortunately, some of us have. Mass casualty antabuse prices walmart events are thankfully rare, with estimates in the USA of around 0.15% of all emergency service calls.1 However, in 2017 the NHS in the UK was faced with an unprecedented number of such events, including the Manchester Arena bombing. Each event poses new challenges in terms of environment, threats posed to staff and casualties and the injuries sustained.2 It is therefore important for ‘lessons learnt’ from mass casualty events to continue to be written up and published in a robust and scientific manner.3 However, at the centre of every mass casualty event are the patients themselves, those who may not survive, those who survive with life-changing injuries and those who are lucky to escape without physical injury but who suffer long-term psychological trauma as a result of events they witness. Authors of antabuse prices walmart reports around mass casualty events therefore have a unique challenge when presenting events in a way that is scientific yet considers ethical publishing in terms of patient consent, potentially identifiable data, considerations of impact of publishing on communities and inevitable media reporting.

Editors and journals too have a similar responsibility to patients who are involved in such events. It is therefore a great opportunity for the Emergency Medicine Journal (EMJ) not only to publish Dark et ….

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DISULFIRAM can help patients with an alcohol abuse problem not to drink alcohol. When taken with alcohol, Antabuse produces unpleasant effects. Antabuse is part of a recovery program that includes medical supervision and counseling. It is not a cure.

Antabuse side effects with alcohol

The Arc Madison how much antabuse cost Cortland in Oneida, New York, knows that there is a lack of antabuse side effects with alcohol providers that specialize in the intellectual/developmental disability field. Making the problem antabuse side effects with alcohol worse, not so many that understand dual diagnosis.THE PROBLEMWith alcoholism treatment minimizing the ability for individuals to receive face-to-face services with their providers, many patients are resorting to emergency department visits.Additionally, The Arc is in a rural area requiring travel to see a provider, and there is a lack of providers in the field. The population itself is underserved, with a lack of transportation to get to appointments. Without the ability to institute telemedicine as a solution antabuse side effects with alcohol to these problems, the population supported by The Arc would have seen a lengthy (permanent?.

) pause for needed medical services.PROPOSALThe Arc this year received funding from the FCC to help provide telehealth services.“With this funding we can further treat patients, reduce crisis and allow for social distancing, which is imperative to our vulnerable population,” said Jackie Fahey, director of clinic services at antabuse side effects with alcohol The Arc Madison Cortland. €œWe could provide ongoing services to the individuals we serve to ensure there are no unnecessary emergency department visits. This places less of a strain antabuse side effects with alcohol on our local emergency departments and unneeded additional costs.”With the purchase of tablets and headsets and telehealth services from vendor Doxy.me, The Arc was able to still provide medical care to its population of people with an I/DD. Additionally, eliminating emergency department visits also eliminates their exposure to alcoholism treatment and eases the burden of the ED providers who are overburdened right now.MARKETPLACEThere are many vendors of telemedicine technology and services on the health antabuse side effects with alcohol IT market today.

Healthcare IT News recently compiled a comprehensive list of these vendors with detailed descriptions. To read this special report, click here.MEETING THE CHALLENGE“When all of our locations were closed abruptly in the middle of March due to the alcoholism treatment antabuse, we needed to determine a way to quickly and easily implement a telehealth solution so that we were able to still support the individuals that we serve during the crisis, especially when many were under strict quarantine protocols for a variety of reasons,” Fahey explained.“We signed up immediately for the Doxy.me telehealth platform as antabuse side effects with alcohol it was a user-friendly platform that is HIPAA-compliant. The feature we liked about Doxy.me was that it is web-based, so nothing had to be downloaded and antabuse side effects with alcohol it could easily be used on a laptop, tablet or smartphone.”The Arc rolled out the technology initially with its mental health providers, who offer psychiatry/medication monitoring services, social work counseling and mental health counseling. More than half the organization’s enrollment is enrolled in one or all of these three services, so it was able to continue providing services to a large number of enrolled individuals.“We then began to roll the telehealth services out to nutrition, speech therapy, physical therapy and occupational therapy caseloads if individuals were appropriate to receive the service through telehealth,” Fahey said.RESULTSThe first success metric The Arc has been able to achieve with the technology is maintaining its utilization for mental health services.

When everything was running normal prior to alcoholism treatment, The Arc’s mental health services made up about 25% of the services it provided on antabuse side effects with alcohol a monthly basis. With the implementation of telehealth services during the alcoholism treatment antabuse, the organization was antabuse side effects with alcohol able to achieve 20% of the services provided on a monthly basis.This has shown to staff that they have been able to still serve and respond to the needs of their psychiatry, social work and mental health counseling patients with minimal issues by implementing the telehealth technology.“The second success metric we have been able to achieve with the technology is we have been able to continue to receive referrals for our services and enroll new individuals into the services they need if the services are able to be completed via telehealth,” she said. €œBetween April, May and June, we have enrolled 16 new individuals into ongoing clinic services, which is right on par for our normal enrollment average per month.”USING FCC AWARD FUNDSThe Arc Madison Cortland was awarded $49,455 by the FCC earlier this year for laptop computers and headsets to provide remote consultations and treatment during the alcoholism treatment antabuse for psychological services, counseling, and occupational and physical therapy for people with developmental and other disabilities.“With the funds, we purchased headsets and tablets to allow the people we support to have access to medical appointments, along with physical therapy, occupational therapy and psychology appointments remotely,” Fahey explained. €œThe technology enables us to continue to provide these services at a time when the people we support are unable to leave for traditional in-person appointments.“Because these are antabuse side effects with alcohol such uncertain times, and a time frame for when we may return to ‘normalcy’ is unknown, the technology allows us to continue delivering medical support without the concern of a pause in those services.”Twitter.

@SiwickiHealthITEmail the antabuse side effects with alcohol writer. Bill.siwicki@himss.orgHealthcare IT News is a HIMSS Media publication..

The Arc Madison Cortland in Oneida, New York, knows that there is a lack of providers that specialize in the intellectual/developmental disability antabuse prices walmart field. Making the problem worse, not so many that understand dual diagnosis.THE PROBLEMWith alcoholism treatment minimizing the ability for individuals to receive face-to-face services with their providers, many patients are resorting to emergency department visits.Additionally, The Arc is in a rural area requiring travel to see a provider, and there is a lack of providers in the antabuse prices walmart field. The population itself is underserved, with a lack of transportation to get to appointments. Without the ability to institute telemedicine as a solution to these problems, the population supported by The Arc would have seen a lengthy (permanent? antabuse prices walmart. ) pause for needed medical services.PROPOSALThe Arc this year received funding from the FCC to help provide telehealth services.“With this antabuse prices walmart funding we can further treat patients, reduce crisis and allow for social distancing, which is imperative to our vulnerable population,” said Jackie Fahey, director of clinic services at The Arc Madison Cortland.

€œWe could provide ongoing services to the individuals we serve to ensure there are no unnecessary emergency department visits. This places less of antabuse prices walmart a strain on our local emergency departments and unneeded additional costs.”With the purchase of tablets and headsets and telehealth services from vendor Doxy.me, The Arc was able to still provide medical care to its population of people with an I/DD. Additionally, eliminating emergency department visits also eliminates their exposure to alcoholism treatment and eases the burden of the ED providers who are overburdened right now.MARKETPLACEThere are many vendors of telemedicine technology and services antabuse prices walmart on the health IT market today. Healthcare IT News recently compiled a comprehensive list of these vendors with detailed descriptions. To read this special report, click here.MEETING THE CHALLENGE“When all of our locations were antabuse prices walmart closed abruptly in the middle of March due to the alcoholism treatment antabuse, we needed to determine a way to quickly and easily implement a telehealth solution so that we were able to still support the individuals that we serve during the crisis, especially when many were under strict quarantine protocols for a variety of reasons,” Fahey explained.“We signed up immediately for the Doxy.me telehealth platform as it was a user-friendly platform that is HIPAA-compliant.

The feature we liked about antabuse prices walmart Doxy.me was that it is web-based, so nothing had to be downloaded and it could easily be used on a laptop, tablet or smartphone.”The Arc rolled out the technology initially with its mental health providers, who offer psychiatry/medication monitoring services, social work counseling and mental health counseling. More than half the organization’s enrollment is enrolled in one or all of these three services, so it was able to continue providing services to a large number of enrolled individuals.“We then began to roll the telehealth services out to nutrition, speech therapy, physical therapy and occupational therapy caseloads if individuals were appropriate to receive the service through telehealth,” Fahey said.RESULTSThe first success metric The Arc has been able to achieve with the technology is maintaining its utilization for mental health services. When everything was running normal prior to alcoholism treatment, The Arc’s mental health services made up about 25% of the services it provided on a antabuse prices walmart monthly basis. With the implementation of telehealth services during the alcoholism treatment antabuse, the organization was able to achieve 20% of the services provided on a monthly basis.This has shown to staff that they have been able to still serve and respond to antabuse prices walmart the needs of their psychiatry, social work and mental health counseling patients with minimal issues by implementing the telehealth technology.“The second success metric we have been able to achieve with the technology is we have been able to continue to receive referrals for our services and enroll new individuals into the services they need if the services are able to be completed via telehealth,” she said. €œBetween April, May and June, we have enrolled 16 new individuals into ongoing clinic services, which is right on par for our normal enrollment average per month.”USING FCC AWARD FUNDSThe Arc Madison Cortland was awarded $49,455 by the FCC earlier this year for laptop computers and headsets to provide remote consultations and treatment during the alcoholism treatment antabuse for psychological services, counseling, and occupational and physical therapy for people with developmental and other disabilities.“With the funds, we purchased headsets and tablets to allow the people we support to have access to medical appointments, along with physical therapy, occupational therapy and psychology appointments remotely,” Fahey explained.

€œThe technology enables us to continue to provide these services at a time when the people we support are unable to leave for traditional in-person appointments.“Because these are antabuse prices walmart such uncertain times, and a time frame for when we may return to ‘normalcy’ is unknown, the technology allows us to continue delivering medical support without the concern of a pause in those services.”Twitter. @SiwickiHealthITEmail the antabuse prices walmart writer. Bill.siwicki@himss.orgHealthcare IT News is a HIMSS Media publication..

Drinking 48 hours after antabuse

When we took how to get antabuse without a doctor the editorship of Evidence-Based Mental Health (EBMH) at the end of 2013, we set two main objectives drinking 48 hours after antabuse. To promote and embed an evidence-based medicine (EBM) drinking 48 hours after antabuse approach into daily mental health clinical practice, and to get an impact factor (IF) for EBMH. Both aims have been big challenges and we have learnt a lot.EBM has been around for about 30 years now, drinking 48 hours after antabuse shaping and changing the way we practice medicine. When Guyatt and colleagues published their seminal paper in 1992,1 EBM was described as the combination of three intersecting domains. The best available evidence, the clinical state and circumstances, and patient’s drinking 48 hours after antabuse preferences and values.

EBM and EBMH have since continuously evolved to deepen our understanding of these three domains.The best available evidenceWe keep complaining about the poor quality of studies in drinking 48 hours after antabuse mental health. To properly assess the effects of interventions and devices before and after regulatory approval, we all know that randomised controlled trials are the best study design.2 3 However, real-world data are crucial to shed light on key clinical questions,4 especially when adverse events5 or prognostic factors6 are investigated. It necessarily …IntroductionQuality-adjusted life years (QALYs) have been drinking 48 hours after antabuse increasingly used in general medicine and in psychiatry to evaluate the impact of a disease on both the quantity and quality of life.1 One QALY is equal to 1 year in perfect health, can range down to zero (death) or may take negative values (worse than death). QALYs can be used to compare the burdens of various diseases, to appreciate the impact of their interventions, to help set priorities in resource allocations across different diseases and interventions and to inform personal decisions.The representative method to evaluate QALYs is the generic, preference-based measure of health including the Euro-Qol five dimensions (EQ-5D)2 3 and the SF-6D based on Short Form Survey-36 (SF-36).4 5 Of these, the EQ-5D is the most frequently used and is the preferred instrument by the National Institute of Health and Care drinking 48 hours after antabuse Excellence in the UK. While the responsiveness of such generic measures to various mental conditions, especially severe mental illnesses, has been questioned,6 its validity and responsiveness to common mental disorders including depression drinking 48 hours after antabuse and anxiety have been generally established.7 8However, the traditional focus of measurements in mental health has centred mainly on symptoms.

Many trials have, therefore, not administered the generic health-related quality of life measures. This has hindered comparison of impacts of mental disorders vis-à-vis other medical conditions on the one hand and also evaluation of values of their interventions on the other.9 10We have been collecting individual participant-level data from randomised controlled trials of internet cognitive-behavioural therapies (iCBT) for depression,11 drinking 48 hours after antabuse several of which administered both symptomatologic scales and generic health status scales simultaneously. This study, therefore, attempts to link the depression-specific measure drinking 48 hours after antabuse onto the generic measure of health in order to enable estimation of QALYs for depressive states and their changes. Such cross-walking should facilitate assessment of burden of depression at its various severity and of the impacts of its various treatments.MethodsDatabaseWe have been accumulating a data set of individual participant data of randomised controlled trials of iCBT among adults with depressive symptoms, as established by specified cut-offs on self-report scales or by diagnostic interviews.11 For this study, we have selected studies that have administered the EQ-5D and depression severity scales at baseline and at end of treatment. We excluded patients if they had drinking 48 hours after antabuse missing data in either of the two scales at baseline or at endpoint.

We excluded studies that focused on patients with general medical disorders (eg, diabetes, glioma) and depressive symptoms.MeasuresEQ-5D-3LThe EQ-5D-3L comprises five dimensions of mobility, self-care, usual activities, pain/discomfort drinking 48 hours after antabuse and anxiety/depression, each rated on three levels corresponding with 1=no problems, 2=some/moderate problems or 3=extreme problems/unable to do. This produces 3ˆ5=243 different drinking 48 hours after antabuse health states, ranging from no problem at all in any dimension (11111) to severe problems on all dimensions (33333). Each of these 243 states is provided with a preference-based score, as determined through the time trade-off (TTO) technique in a sample of the general population. In TTO, respondents are asked to give the relative length of time in full health that they would be willing to sacrifice for the drinking 48 hours after antabuse poor health states as represented by each of the 243 combinations above. The EQ-5D scores range between 1=full health and 0=death drinking 48 hours after antabuse to minus values=worse than death bounded by −1.

The scoring algorithm for the UK is based on TTO responses of a random sample (n=2997) of noninstitutionalised adults. Over the years, value sets for EQ-5D-3L have been produced for many countries/regions.2 3 7Depression severity scalesWe included any validated drinking 48 hours after antabuse depression severity measures. The scale scores were converted into the most frequently used scale, namely, the Patient Health Questionnaire-9 (PHQ-9),12 using the established conversion algorithms13 14 for the Beck Depression Inventory, second edition (BDI-II)15 or the Centre for Epidemiologic Studies Depression Scale (CES-D).16The PHQ-9 consists of the nine drinking 48 hours after antabuse diagnostic criteria items of major depression from the DSM-IV, each rated on a scale between 0 and 3, making the total score range 0–27. The instrument has demonstrated excellent reliability, validity and responsiveness. The cut-offs have been proposed as 0–4, 5–9, 10–14, 15–19 and 20- for no, mild, moderate, moderately severe and severe depression, respectively.12Statistical analysesWe first calculated Spearman correlation coefficients drinking 48 hours after antabuse between PHQ-9 and EQ-5D total scores at baseline, at end of treatment and their changes, to establish if the linking is justified.

Correlations were considered weak if scores were <0.3, moderate if scores were ≥0.3 and<0.7 and strong drinking 48 hours after antabuse if scores were ≥0.7.17 Correlations ≥0.3 have been recommended to establish linking.18 We then applied the equipercentile linking procedure,19 which identified scores on PHQ-9 and EQ-5D or their changes with the same percentile ranks and allows for a nominal translation from PHQ-9 to EQ-5D by using their percentile values. This approach has been used successfully for scales in depression, schizophrenia or Alzheimer’s disease.14 20–22 We analysed all trials collectively rather than by trial to maximise the sample size, ensure variability in the included populations and attain robust estimates.We conducted a sensitivity analysis by excluding studies that require the conversion of various depression severity scores into PHQ-9.All the drinking 48 hours after antabuse analyses were conducted in R V.4.0.2, with the package equate V.2.0.7.23Ethics statementThe authors assert that all procedures contributing to this work comply with the ethical standards of the relevant national and institutional committees on human experimentation and with the Helsinki Declaration of 1975, as revised in 2008. Ethical approval was not required for this study as it used only deidentified patient data.FindingsIncluded studiesWe identified seven RCTs of iCBT (total n=2457), which administered validated depression scales and EQ-5D both at baseline and at endpoint (online supplemental eTable 1). Three studies included only patients with major depressive disorder (MDD), one only patients with subthreshold depression and the remaining three included drinking 48 hours after antabuse both. All the drinking 48 hours after antabuse studies administered EQ-5D-3L.

PHQ-9 scores were converted from the BDI-II in three studies24–26 and from the CES-D in one study.27 The mean age of the participants was 41.8 (SD=12.3) years, 66.0% (1622/2457) were women and they scored 14.0 (5.4) on PHQ-9 and 0.74 (0.20) on EQ-5D at baseline and 9.1 (6.0) and 0.79 (0.21), respectively, at endpoint. When using the standard cut-offs of the PHQ-9,12 2.4% (60/2449) suffered from drinking 48 hours after antabuse no depression (PHQ-9 scores <5), 20.2% (492/2449) from subthreshold depression (5≤PHQ-9 scores <10), 33.5% (820/2449) from mild depression (10≤PHQ-9 scores <15), 26.5% (649/2449) from moderate depression (15≤PHQ-9 scores <20) and 17.3% (424/2449) from severe depression (20≤PHQ-9 scores) at baseline.Supplemental materialEquipercentile linkingSpearman’s correlation coefficient between the PHQ-9 and the EQ-5D scores was r=−0.29 at baseline, increased to r=−0.50 after intervention and was r=−0.38 for change scores.Figure 1 shows the equipercentile linking between PHQ-9 and EQ-5D total scores at baseline and at endpoint. Figure 2 shows the same between drinking 48 hours after antabuse their change scores. Table 1 summarises the correspondences drinking 48 hours after antabuse between the two scales.PHQ-9 and EQ-5D total scores at baseline and endpoint. EQ-5D,Euro-Qol Five Dimensions.

PHQ-9, PatientHealth Questionnaire-9." data-icon-position data-hide-link-title="0">Figure 1 PHQ-9 and EQ-5D total scores at baseline and drinking 48 hours after antabuse endpoint. EQ-5D,Euro-Qol Five Dimensions drinking 48 hours after antabuse. PHQ-9, PatientHealth Questionnaire-9.PHQ-9 change scores and EQ-5D change scores. EQ-5D, Euro-Qol drinking 48 hours after antabuse Five Dimensions. PHQ-9, Patient Health drinking 48 hours after antabuse Questionnaire-9." data-icon-position data-hide-link-title="0">Figure 2 PHQ-9 change scores and EQ-5D change scores.

EQ-5D,Euro-Qol Five drinking 48 hours after antabuse Dimensions. PHQ-9, PatientHealth Questionnaire-9.View this table:Table 1 Conversion table from PHQ-9 to EQ-5D total and change scoresSensitivity analysisWhen we limited the samples to the three studies28–30 that administered PHQ-9 (total n=1375), the linking results were replicated (online supplemental eFigure 1).DiscussionThis is the first study to link a depression severity measure with the EQ-5D-3L both for total and change scores. To summarise, subthreshold depression corresponded with EQ-5D-3L index values of 0.9–0.8, mild major depression with 0.8–0.7, moderate depression with 0.7–0.5 and severe depression with 0.6–0.0 drinking 48 hours after antabuse. A five-point improvement in PHQ-9 corresponded approximately with an increase in EQ-5D-3L index values by drinking 48 hours after antabuse 0.03, and a ten-point improvement can lead to an increase by approximately 0.25.A systematic review of utility values for depression31 found that the pooled mean (SD) utilities based on studies using the standard gamble as a direct valuation method were 0.69 (0.14) for mild, 0.52 (0.28) for moderate and 0.27 (0.26) for severe major depression. The estimates based on studies using EQ-5D as an indirect valuation method were 0.56 (0.16) for mild, 0.52 (0.28) for moderate get antabuse and 0.25 (0.15) for severe depression.

One recent study regressed PHQ-9 on SF-6D scores among 394 patients in theimproving Access to Psychological Therapies (IAPT) cohort7 32 and estimated none/mild depression on PHQ-9 to drinking 48 hours after antabuse be worth 0.73 SF-6D scores, moderate depression 0.65 and severe depression 0.56. Our results are largely in line with these aforementioned studies.There was a consistent drinking 48 hours after antabuse difference of about 0.07 EQ-5D scores for the same PHQ-9 score if it represented the baseline or endpoint measurements (figure 1). This is understandable because a patient would rate their health status less satisfactory if they stayed equally symptomatic as before after the treatment and also because it means that they continued to suffer from depression for longer. It is, therefore, drinking 48 hours after antabuse reasonable to use the conversion table at baseline for relatively new cases of depression and that at end of treatment for more chronic cases (table 1).An effect size to be typically expected after 2 months of antidepressant pharmacotherapy33 or psychotherapy27 34 over the pill placebo condition is 0.3. Given that the average SD of PHQ-9 in the studies was about 6, an effect size of 0.3 corresponds to a difference by drinking 48 hours after antabuse two points on PHQ-9.

The differences drinking 48 hours after antabuse in EQ-5D scores corresponding with the end-of-treatment PHQ-9 scores of x versus x+2, where x is between 5 and 15 (table 1), ranges between 0.08 and 0.13, producing an approximate average of 0.1 EQ-5D scores. If we assume that the same difference would continue for the ensuing 10 months, the gain in QALY per year would be equal to 0.09 QALY. If we assume that the difference would eventually wear out over the course of the year due to naturalistic improvements to be expected in drinking 48 hours after antabuse the control group, the gain in QALY per year would be equal to 0.05 QALY. (See figure 3 drinking 48 hours after antabuse for a schematic drawing to help understand the calculation of QALYs based on changing EQ-5D scores. In reality, the changes will be more smoothly curvilinear but the calculation will be similar.) Since one QALY is typically valuated at US$50 000 or 3000 Stirling pounds,35 such therapies would be cost-effective if they cost US$2500 to US$4500 (150 to 270 pounds) or less.

If a 1 day fill of generic selective serotonergic reuptake inhibitor antidepressants costs 1–3 dollars and a 1-year prescription costs drinking 48 hours after antabuse US$400–1200 dollars, or if 8–16 sessions of psychotherapy cost US$1600–3200 dollars, both therapies would be deemed largely cost-effective. An individual’s decision, by contrast, drinking 48 hours after antabuse will and should be more variable and no one can categorically reject nor require such treatments for all patients.A schematic graph showing gains in QALY due to typical pharmacotherapies or psychotherapies. A patient may start with PHQ-9 of 20, corresponding with EQ-5D drinking 48 hours after antabuse index value of 0.5. Then they may improve after 2 months of antidepressant therapy to EQ-5D score of 0.9 (solid line), while they may improve to EQ-5D score of 0.8 even if on placebo (dashed line). If we assume that the same difference would continue for the ensuing 10 drinking 48 hours after antabuse months while showing slow gradual improvement in both cases, the gain in QALY per year would be equal to 0.09 QALY.

If we drinking 48 hours after antabuse assume that the difference would eventually wear out over the course of the year due to naturalistic improvements to be expected in the control group, the gain in QALY per year would be equal to 0.05 QALY. Please note that this is a schematic drawing for illustrative purposes. In reality, the changes will be more smoothly curvilinear but the calculation will be similar drinking 48 hours after antabuse. EQ-5D, Euro-Qol drinking 48 hours after antabuse Five Dimensions. PHQ-9, Patient drinking 48 hours after antabuse Health Questionnaire-9.

QALY, quality-adjusted life years." data-icon-position data-hide-link-title="0">Figure 3 A schematic graph showing gains in QALY due to typical pharmacotherapies or psychotherapies. A patient may start with PHQ-9 of drinking 48 hours after antabuse 20, corresponding with EQ-5D index value of 0.5. Then they may improve after 2 months of antidepressant therapy to EQ-5D score of 0.9 (solid line), while they drinking 48 hours after antabuse may improve to EQ-5D score of 0.8 even if on placebo (dashed line). If we assume that the same difference would continue for the ensuing 10 months while showing slow gradual improvement in both cases, the gain in QALY per year would be equal to 0.09 QALY. If we assume that the difference would eventually wear out over the course of the drinking 48 hours after antabuse year due to naturalistic improvements to be expected in the control group, the gain in QALY per year would be equal to 0.05 QALY.

Please note drinking 48 hours after antabuse that this is a schematic drawing for illustrative purposes. In reality, the changes will be more smoothly curvilinear but the calculation will be similar. EQ-5D,Euro-Qol Five drinking 48 hours after antabuse Dimensions. PHQ-9, PatientHealth drinking 48 hours after antabuse Questionnaire-9. QALY, quality-adjustedlife drinking 48 hours after antabuse years.Several caveats should be considered when interpreting the results.

First, our sample was limited to participants of trials of iCBT. It may drinking 48 hours after antabuse be argued that the results, therefore, would not apply to patients with depression undergoing other therapies or in other settings. Second, the correlations between PHQ-9 and EQ-5D were strong enough for total scores at endpoint and for change scores to justify linking but were somewhat weaker at baseline, probably due to limited variability in PHQ-9 scores at drinking 48 hours after antabuse baseline because some studies required minimum depression scores. However, the overall correspondence between PHQ-9 scores and EQ-5D had the same shape between baseline and endpoint, which will increase credibility of the linking at baseline as well. Third, we drinking 48 hours after antabuse were able to compare PHQ-9 to EQ-5D-3L only.

The EQ-5D-5L, which measures health in five levels instead of three, has been developed to be more sensitive to change and to milder conditions.36 When data become available, we will need to link PHQ-9 and EQ-5D-5L to examine if we can obtain similar conversion drinking 48 hours after antabuse values.Our study also has several important strengths. First, our sample included patients with subthreshold depression and major depression and from the community or workplace and the drinking 48 hours after antabuse primary care. Furthermore, they encompassed mild through severe major depression in approximately equal proportions. Second, all the patients drinking 48 hours after antabuse in our sample received iCBT or control interventions including care as usual. Potential side effects of different antidepressants, repetitive brain stimulation, electroconvulsive therapy and other more aggressive therapies must of course be taken into consideration when evaluating their impacts, but our estimates, arguably independent of major side effects, can better inform drinking 48 hours after antabuse such considerations.

Finaly, unlike any prior studies, we were able to link specific PHQ-9 scores and their changes scores to EQ-5D-3L index values.Conclusion and clinical implicationsIn conclusion, we constructed a conversion table linking the EQ-5D, the representative generic preference-based measure of health status, and the PHQ-9, one of the most popular depression severity rating scale, for both its total scores and change scores. The table will enable fine-grained assessment of burden of depression at its various levels of severity and of impacts of its various treatments which may bring various degrees of improvement at the expense of some potential side effects.Data availability drinking 48 hours after antabuse statementData are available upon reasonable request. The overall database used for this IPD is restricted due drinking 48 hours after antabuse to data sharing agreements with the research institutes where the studies were conducted. IPD from individual studies are available from the individual study authors.Ethics statementsPatient consent for publicationNot required..

When we took antabuse prices walmart the editorship of Evidence-Based Mental Health (EBMH) at the end of 2013, we set two main objectives. To promote and antabuse prices walmart embed an evidence-based medicine (EBM) approach into daily mental health clinical practice, and to get an impact factor (IF) for EBMH. Both aims have been big challenges and we have learnt a lot.EBM has been around for about 30 years now, antabuse prices walmart shaping and changing the way we practice medicine.

When Guyatt and colleagues published their seminal paper in 1992,1 EBM was described as the combination of three intersecting domains. The best antabuse prices walmart available evidence, the clinical state and circumstances, and patient’s preferences and values. EBM and EBMH have since continuously evolved to deepen our antabuse prices walmart understanding of these three domains.The best available evidenceWe keep complaining about the poor quality of studies in mental health.

To properly assess the effects of interventions and devices before and after regulatory approval, we all know that randomised controlled trials are the best study design.2 3 However, real-world data are crucial to shed light on key clinical questions,4 especially when adverse events5 or prognostic factors6 are investigated. It necessarily …IntroductionQuality-adjusted life years (QALYs) antabuse prices walmart have been increasingly used in general medicine and in psychiatry to evaluate the impact of a disease on both the quantity and quality of life.1 One QALY is equal to 1 year in perfect health, can range down to zero (death) or may take negative values (worse than death). QALYs can be used to compare the burdens of various diseases, to appreciate the impact of their interventions, to help set priorities in resource allocations across different diseases and interventions and to antabuse prices walmart inform personal decisions.The representative method to evaluate QALYs is the generic, preference-based measure of health including the Euro-Qol five dimensions (EQ-5D)2 3 and the SF-6D based on Short Form Survey-36 (SF-36).4 5 Of these, the EQ-5D is the most frequently used and is the preferred instrument by the National Institute of Health and Care Excellence in the UK.

While the responsiveness of such generic measures to various mental conditions, especially severe mental illnesses, has been questioned,6 its validity and responsiveness to common mental disorders including depression and antabuse prices walmart anxiety have been generally established.7 8However, the traditional focus of measurements in mental health has centred mainly on symptoms. Many trials have, therefore, not administered the generic health-related quality of life measures. This has hindered comparison of impacts of mental disorders vis-à-vis other medical conditions on the one hand and also evaluation of values of their interventions on the other.9 10We have been collecting individual participant-level data from randomised controlled trials of internet cognitive-behavioural therapies (iCBT) for depression,11 several of which administered both symptomatologic scales and generic health status scales simultaneously antabuse prices walmart.

This study, therefore, attempts to link the depression-specific measure onto the generic measure of health in order to enable estimation of QALYs for depressive states and antabuse prices walmart their changes. Such cross-walking should facilitate assessment of burden of depression at its various severity and of the impacts of its various treatments.MethodsDatabaseWe have been accumulating a data set of individual participant data of randomised controlled trials of iCBT among adults with depressive symptoms, as established by specified cut-offs on self-report scales or by diagnostic interviews.11 For this study, we have selected studies that have administered the EQ-5D and depression severity scales at baseline and at end of treatment. We excluded patients if they had missing data in either of the two antabuse prices walmart scales at baseline or at endpoint.

We excluded studies that focused on patients with general medical disorders (eg, diabetes, glioma) and depressive symptoms.MeasuresEQ-5D-3LThe EQ-5D-3L comprises antabuse prices walmart five dimensions of mobility, self-care, usual activities, pain/discomfort and anxiety/depression, each rated on three levels corresponding with 1=no problems, 2=some/moderate problems or 3=extreme problems/unable to do. This produces 3ˆ5=243 different health states, ranging from no problem at all in any dimension (11111) to antabuse prices walmart severe problems on all dimensions (33333). Each of these 243 states is provided with a preference-based score, as determined through the time trade-off (TTO) technique in a sample of the general population.

In TTO, respondents are asked to antabuse prices walmart give the relative length of time in full health that they would be willing to sacrifice for the poor health states as represented by each of the 243 combinations above. The EQ-5D scores antabuse prices walmart range between 1=full health and 0=death to minus values=worse than death bounded by −1. The scoring algorithm for the UK is based on TTO responses of a random sample (n=2997) of noninstitutionalised adults.

Over the years, value sets for EQ-5D-3L have been produced for many countries/regions.2 3 antabuse prices walmart 7Depression severity scalesWe included any validated depression severity measures. The scale scores were converted into the most frequently used scale, antabuse prices walmart namely, the Patient Health Questionnaire-9 (PHQ-9),12 using the established conversion algorithms13 14 for the Beck Depression Inventory, second edition (BDI-II)15 or the Centre for Epidemiologic Studies Depression Scale (CES-D).16The PHQ-9 consists of the nine diagnostic criteria items of major depression from the DSM-IV, each rated on a scale between 0 and 3, making the total score range 0–27. The instrument has demonstrated excellent reliability, validity and responsiveness.

The cut-offs have been proposed as 0–4, 5–9, 10–14, 15–19 and 20- for no, mild, moderate, moderately severe and severe depression, respectively.12Statistical analysesWe first calculated Spearman correlation coefficients between PHQ-9 and EQ-5D total antabuse prices walmart scores at baseline, at end of treatment and their changes, to establish if the linking is justified. Correlations were considered weak antabuse prices walmart if scores were <0.3, moderate if scores were ≥0.3 and<0.7 and strong if scores were ≥0.7.17 Correlations ≥0.3 have been recommended to establish linking.18 We then applied the equipercentile linking procedure,19 which identified scores on PHQ-9 and EQ-5D or their changes with the same percentile ranks and allows for a nominal translation from PHQ-9 to EQ-5D by using their percentile values. This approach has been used successfully for scales in depression, schizophrenia or Alzheimer’s disease.14 20–22 We analysed all trials collectively rather than antabuse prices walmart by trial to maximise the sample size, ensure variability in the included populations and attain robust estimates.We conducted a sensitivity analysis by excluding studies that require the conversion of various depression severity scores into PHQ-9.All the analyses were conducted in R V.4.0.2, with the package equate V.2.0.7.23Ethics statementThe authors assert that all procedures contributing to this work comply with the ethical standards of the relevant national and institutional committees on human experimentation and with the Helsinki Declaration of 1975, as revised in 2008.

Ethical approval was not required for this study as it used only deidentified patient data.FindingsIncluded studiesWe identified seven RCTs of iCBT (total n=2457), which administered validated depression scales and EQ-5D both at baseline and at endpoint (online supplemental eTable 1). Three studies included only patients with major depressive disorder (MDD), one only patients with subthreshold depression and the antabuse prices walmart remaining three included both. All the antabuse prices walmart studies administered EQ-5D-3L.

PHQ-9 scores were converted from the BDI-II in three studies24–26 and from the CES-D in one study.27 The mean age of the participants was 41.8 (SD=12.3) years, 66.0% (1622/2457) were women and they scored 14.0 (5.4) on PHQ-9 and 0.74 (0.20) on EQ-5D at baseline and 9.1 (6.0) and 0.79 (0.21), respectively, at endpoint. When using the standard cut-offs of the PHQ-9,12 2.4% (60/2449) suffered from no depression (PHQ-9 scores <5), 20.2% (492/2449) from subthreshold depression (5≤PHQ-9 scores <10), 33.5% (820/2449) from mild depression (10≤PHQ-9 scores antabuse prices walmart <15), 26.5% (649/2449) from moderate depression (15≤PHQ-9 scores <20) and 17.3% (424/2449) from severe depression (20≤PHQ-9 scores) at baseline.Supplemental materialEquipercentile linkingSpearman’s correlation coefficient between the PHQ-9 and the EQ-5D scores was r=−0.29 at baseline, increased to r=−0.50 after intervention and was r=−0.38 for change scores.Figure 1 shows the equipercentile linking between PHQ-9 and EQ-5D total scores at baseline and at endpoint. Figure 2 shows the same antabuse prices walmart between their change scores.

Table 1 summarises the correspondences between the two antabuse prices walmart scales.PHQ-9 and EQ-5D total scores at baseline and endpoint. EQ-5D,Euro-Qol Five Dimensions. PHQ-9, PatientHealth Questionnaire-9." data-icon-position data-hide-link-title="0">Figure 1 PHQ-9 and EQ-5D total scores antabuse prices walmart at baseline and endpoint.

EQ-5D,Euro-Qol Five antabuse prices walmart Dimensions. PHQ-9, PatientHealth Questionnaire-9.PHQ-9 change scores and EQ-5D change scores. EQ-5D, Euro-Qol Five antabuse prices walmart Dimensions.

PHQ-9, Patient Health Questionnaire-9." data-icon-position antabuse prices walmart data-hide-link-title="0">Figure 2 PHQ-9 change scores and EQ-5D change scores. EQ-5D,Euro-Qol Five antabuse prices walmart Dimensions. PHQ-9, PatientHealth Questionnaire-9.View this table:Table 1 Conversion table from PHQ-9 to EQ-5D total and change scoresSensitivity analysisWhen we limited the samples to the three studies28–30 that administered PHQ-9 (total n=1375), the linking results were replicated (online supplemental eFigure 1).DiscussionThis is the first study to link a depression severity measure with the EQ-5D-3L both for total and change scores.

To summarise, subthreshold depression antabuse prices walmart corresponded with EQ-5D-3L index values of 0.9–0.8, mild major depression with 0.8–0.7, moderate depression with 0.7–0.5 and severe depression with 0.6–0.0. A five-point improvement in PHQ-9 corresponded approximately with an increase in EQ-5D-3L index values by 0.03, and a ten-point improvement antabuse prices walmart can lead to an increase by approximately 0.25.A systematic review of utility values for depression31 found that the pooled mean (SD) utilities based on studies using the standard gamble as a direct valuation method were 0.69 (0.14) for mild, 0.52 (0.28) for moderate and 0.27 (0.26) for severe major depression. The estimates based on studies using EQ-5D as an indirect valuation method were 0.56 (0.16) for mild, 0.52 (0.28) for moderate and 0.25 (0.15) for severe depression.

One recent study regressed PHQ-9 on SF-6D scores among 394 patients in theimproving Access to Psychological Therapies (IAPT) cohort7 antabuse prices walmart 32 and estimated none/mild depression on PHQ-9 to be worth 0.73 SF-6D scores, moderate depression 0.65 and severe depression 0.56. Our results are largely in line with these aforementioned studies.There was antabuse prices walmart a consistent difference of about 0.07 EQ-5D scores for the same PHQ-9 score if it represented the baseline or endpoint measurements (figure 1). This is understandable because a patient would rate their health status less satisfactory if they stayed equally symptomatic as before after the treatment and also because it means that they continued to suffer from depression for longer.

It is, antabuse prices walmart therefore, reasonable to use the conversion table at baseline for relatively new cases of depression and that at end of treatment for more chronic cases (table 1).An effect size to be typically expected after 2 months of antidepressant pharmacotherapy33 or psychotherapy27 34 over the pill placebo condition is 0.3. Given that the antabuse prices walmart average SD of PHQ-9 in the studies was about 6, an effect size of 0.3 corresponds to a difference by two points on PHQ-9. The differences in EQ-5D scores corresponding with the end-of-treatment PHQ-9 scores of x versus x+2, where x is between 5 and 15 (table 1), ranges between 0.08 and antabuse prices walmart 0.13, producing an approximate average of 0.1 EQ-5D scores.

If we assume that the same difference would continue for the ensuing 10 months, the gain in QALY per year would be equal to 0.09 QALY. If we assume antabuse prices walmart that the difference would eventually wear out over the course of the year due to naturalistic improvements to be expected in the control group, the gain in QALY per year would be equal to 0.05 QALY. (See figure 3 for a schematic drawing to help understand the calculation antabuse prices walmart of QALYs based on changing EQ-5D scores.

In reality, the changes will be more smoothly curvilinear but the calculation will be similar.) Since one QALY is typically valuated at US$50 000 or 3000 Stirling pounds,35 such therapies would be cost-effective if they cost US$2500 to US$4500 (150 to 270 pounds) or less. If a 1 day fill of generic selective serotonergic reuptake inhibitor antidepressants costs 1–3 dollars and a 1-year antabuse prices walmart prescription costs US$400–1200 dollars, or if 8–16 sessions of psychotherapy cost US$1600–3200 dollars, both therapies would be deemed largely cost-effective. An individual’s decision, by contrast, will and should antabuse prices walmart be more variable and no one can categorically reject nor require such treatments for all patients.A schematic graph showing gains in QALY due to typical pharmacotherapies or psychotherapies.

A patient antabuse prices walmart may start with PHQ-9 of 20, corresponding with EQ-5D index value of 0.5. Then they may improve after 2 months of antidepressant therapy to EQ-5D score of 0.9 (solid line), while they may improve to EQ-5D score of 0.8 even if on placebo (dashed line). If we assume that the same difference would continue for the ensuing antabuse prices walmart 10 months while showing slow gradual improvement in both cases, the gain in QALY per year would be equal to 0.09 QALY.

If we assume that the difference would eventually wear out over the course of the antabuse prices walmart year due to naturalistic improvements to be expected in the control group, the gain in QALY per year would be equal to 0.05 QALY. Please note that this is a schematic drawing for illustrative purposes. In reality, the changes will be more smoothly curvilinear but antabuse prices walmart the calculation will be similar.

EQ-5D, Euro-Qol antabuse prices walmart Five Dimensions. PHQ-9, Patient antabuse prices walmart Health Questionnaire-9. QALY, quality-adjusted life years." data-icon-position data-hide-link-title="0">Figure 3 A schematic graph showing gains in QALY due to typical pharmacotherapies or psychotherapies.

A patient may start with PHQ-9 of 20, corresponding with EQ-5D index antabuse prices walmart value of 0.5. Then they may improve after 2 months of antidepressant therapy to EQ-5D score of 0.9 (solid line), while they may improve to EQ-5D score of 0.8 even if on placebo (dashed antabuse prices walmart line). If we assume that the same difference would continue for the ensuing 10 months while showing slow gradual improvement in both cases, the gain in QALY per year would be equal to 0.09 QALY.

If we assume that the difference would eventually wear out over the course of the year antabuse prices walmart due to naturalistic improvements to be expected in the control group, the gain in QALY per year would be equal to 0.05 QALY. Please note that this is a schematic drawing for illustrative purposes antabuse prices walmart. In reality, the changes will be more smoothly curvilinear but the calculation will be similar.

EQ-5D,Euro-Qol Five Dimensions antabuse prices walmart. PHQ-9, PatientHealth Questionnaire-9 antabuse prices walmart. QALY, quality-adjustedlife years.Several caveats antabuse prices walmart should be considered when interpreting the results.

First, our sample was limited to participants of trials of iCBT. It may be argued that antabuse prices walmart the results, therefore, would not apply to patients with depression undergoing other therapies or in other settings. Second, the correlations between PHQ-9 and EQ-5D were strong enough for antabuse prices walmart total scores at endpoint and for change scores to justify linking but were somewhat weaker at baseline, probably due to limited variability in PHQ-9 scores at baseline because some studies required minimum depression scores.

However, the overall correspondence between PHQ-9 scores and EQ-5D had the same shape between baseline and endpoint, which will increase credibility of the linking at baseline as well. Third, we antabuse prices walmart were able to compare PHQ-9 to EQ-5D-3L only. The EQ-5D-5L, which measures health in five levels instead of three, has been developed to be more sensitive to change and to milder conditions.36 When data become available, we will antabuse prices walmart need to link PHQ-9 and EQ-5D-5L to examine if we can obtain similar conversion values.Our study also has several important strengths.

First, our sample included patients with subthreshold depression and major depression and from the community or workplace and the primary antabuse prices walmart care. Furthermore, they encompassed mild through severe major depression in approximately equal proportions. Second, all the patients in our antabuse prices walmart sample received iCBT or control interventions including care as usual.

Potential side effects of different antidepressants, antabuse prices walmart repetitive brain stimulation, electroconvulsive therapy and other more aggressive therapies must of course be taken into consideration when evaluating their impacts, but our estimates, arguably independent of major side effects, can better inform such considerations. Finaly, unlike any prior studies, we were able to link specific PHQ-9 scores and their changes scores to EQ-5D-3L index values.Conclusion and clinical implicationsIn conclusion, we constructed a conversion table linking the EQ-5D, the representative generic preference-based measure of health status, and the PHQ-9, one of the most popular depression severity rating scale, for both its total scores and change scores. The table will enable antabuse prices walmart fine-grained assessment of burden of depression at its various levels of severity and of impacts of its various treatments which may bring various degrees of improvement at the expense of some potential side effects.Data availability statementData are available upon reasonable request.

The overall database used for this IPD is restricted due to data sharing agreements with antabuse prices walmart the research institutes where the studies were conducted. IPD from individual studies are available from the individual study authors.Ethics statementsPatient consent for publicationNot required..

Buy antabuse uk

How to Antabuse where to buy cite buy antabuse uk this article:Singh O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly buy antabuse uk publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, buy antabuse uk the media went into a frenzy as newspapers, news channels, and social media were full of stories providing minute details of the suicidal act.

Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the buy antabuse uk actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress calls from buy antabuse uk their patients in despair with increased suicidal ideation.

This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on buy antabuse uk Preventing Suicide. A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of buy antabuse uk speculations about the person's mental condition and illness and also his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian buy antabuse uk Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental health professionals were called by media buy antabuse uk houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in buy antabuse uk addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists buy antabuse uk should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions. Methods and principles of interaction with media should form a part of our training curriculum.

Many professional societies have guidelines and resource books for interacting with media, and psychiatrists should familiarize themselves buy antabuse uk with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is buy antabuse uk desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, buy antabuse uk Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment.

The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage. This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically. Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods.

These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies. And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain. However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords.

Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update. Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al.

In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies. The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time. Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness. However, there are obvious ethical issues in designing human studies that are designed to answer this specific question.

Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions. These studies have employed the following methods:Structural neuroimaging studiesFunctional neuroimaging studiesMetabolic neuroimaging studiesBody fluid biochemical marker studiesCognitive impairment studies.While the early studies tended to focus more on establishing the safety of ECT and finding out whether ECT causes gross microscopic brain damage, the later studies especially since the advent of advanced neuroimaging techniques have been focusing more on a mechanistic understanding of ECT. Hence, the primary objective of the later neuroimaging studies has been to look for structural and functional brain changes which might explain how ECT acts rather than evidence of gross structural damage per se. However, put together, all these studies would enable us to answer our titular question to some satisfaction. [Table 1] and [Table 2] provide an overview of the evidence base in this area.

Structural and Functional Neuroimaging Studies Devanand et al. Reviewed 16 structural neuroimaging studies on the effect of ECT on the brain.[4] Of these, two were pneumoencephalography studies, nine were computed tomography (CT) scan studies, and five were magnetic resonance imaging (MRI) studies. However, most of these studies were retrospective in design, with neuroimaging being done in patients who had received ECT in the past. In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT. In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today.

The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain. The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes. A single study by Coffey et al. Followed up the patients for a duration of 6 months and repeated neuroimaging again at 6 months in order to capture any long-term changes following ECT.[10]The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities.[4] The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h.

This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue.[11] The last significant observation by Coffey et al. In 1991 was that there was no significant temporal changes in the total volumes of the frontal lobes, temporal lobes, or amygdala–hippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies. Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al.

Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al. That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies. In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al.

In a follow-up study showed that though there was a significant increase in the volume of the hippocampus 1 week after a course of ECT, the hippocampal volume returned to the baseline after 6 months.[19] Two other studies in 2013 showed that in addition to the hippocampus, the amygdala also showed significant volume increase following ECT.[20],[21] A series of structural neuroimaging studies after that have expanded on these findings and as of now, gray matter volume increase following ECT has been demonstrated in the hippocampus, amygdala, anterior temporal pole, subgenual cortex,[21] right caudate nucleus, and the whole of the medial temporal lobe (MTL) consisting of the hippocampus, amygdala, insula, and the posterosuperior temporal cortex,[24] para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus,[25] left cerebellar area VIIa crus I,[29] putamen, caudate nucleus, and nucleus acumbens [31] and clusters of increased cortical thickness involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex.[27] However, the most consistently reported and replicated finding has been the bilateral increase in the volume of the hippocampus and amygdala. In light of these findings, it has been tentatively suggested that ECT acts by inducing neuronal regeneration in the hippocampus – amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study – Nordanskog et al., 2014 – has followed study patients for a long term – 6 months in their case. And significantly, the authors found out that after increasing immediately following ECT, the hippocampal volume returns back to baseline by 6 months.[19] This, however, was not associated with the relapse of depressive symptoms. Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms.

Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al. In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression. It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus.

The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe. It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al. Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population.

It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder. The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al. In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered.

Furthermore, bilateral (B/L) ECT was associated with an equal increase in volume in both right and left hippocampus, whereas right unilateral ECT was associated with greater volume increase in the right hippocampus. Finally, contrary to expectation, clinical improvement was found to be negatively correlated with hippocampal volume.Thus, a review of the current evidence amply demonstrates that from looking for ECT-related brain damage – and finding none, we have now moved ahead to looking for a mechanistic understanding of the effect of ECT. In this regard, it has been found that ECT does induce structural changes in the brain – a fact which has been seized upon by some to claim that ECT causes brain damage.[46] Such statements should, however, be weighed against the definition of damage as understood by the scientific medical community and patient population. Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage. Metabolic Neuroimaging Studies.

Magnetic Resonance Spectroscopic Imaging Magnetic resonance spectroscopic imaging (MRSI) uses a phase-encoding procedure to map the spatial distribution of magnetic resonance (MR) signals of different molecules. The crucial difference, however, is that while MRI maps the MR signals of water molecules, MRSI maps the MR signals generated by different metabolites – such as N-acetyl aspartate (NAA) and choline-containing compounds. However, the concentration of these metabolites is at least 10,000 times lower than water molecules and hence the signal strength generated would also be correspondingly lower. However, MRSI offers us the unique advantage of studying in vivo the change in the concentration of brain metabolites, which has been of great significance in fields such as psychiatry, neurology, and basic neuroscience research.[47]MRSI studies on ECT in patients with depression have focused largely on four metabolites in the human brain – NAA, choline-containing compounds (Cho) which include majorly cell membrane compounds such as glycerophosphocholine, phosphocholine and a miniscule contribution from acetylcholine, creatinine (Cr) and glutamine and glutamate together (Glx). NAA is located exclusively in the neurons, and is suggested to be a marker of neuronal viability and functionality.[48] Choline-containing compounds (Cho) mainly include the membrane compounds, and an increase in Cho would be suggestive of increased membrane turnover.

Cr serves as a marker of cellular energy metabolism, and its levels are usually expected to remain stable. The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT. Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite. However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies.

It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations. The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis. Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

More significantly, the authors also showed a significant increase in Glx levels in the hippocampus following ECT, which was also associated with an increase in hippocampal volume.[40] To explain these three findings, the authors proposed that ECT produces a neuroinflammatory response in the hippocampus – likely mediated by Glx, which has been known to cause inflammation at higher concentrations, thereby accounting for the increase in hippocampal volume with a reduction in NAA concentration. The cause for the volume increase remains unclear – with the authors speculating that it might be due to neuronal swelling or due to angiogenesis. However, the same study and multiple other past studies [21],[25],[30] have demonstrated that hippocampal volume increase was correlated with clinical improvement following ECT. Thus, we are led to the hypothesis that the same mechanism which drives clinical improvement with ECT is also responsible for the cognitive impairment following ECT. Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results.

The ACC is another area which has been studied in some detail utilizing the MRSI technique. In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT. This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al. In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al.

Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity. A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al.

In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al. In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied. In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus.

This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT. However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development. The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect.

It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT. Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder. The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration.

However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory. Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests. Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information.[58] As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT.[57] However, one of the major limitations of this meta-analysis was the lack of evidence on retrograde amnesia following ECT. This is particularly unfortunate considering that it is memory impairment – particularly retrograde amnesia which has received the most attention.[59] In addition, reports of catastrophic retrograde amnesia have been repeatedly held up as sensational evidence of the lasting brain damage produced by ECT.[59] Admittedly, studies on retrograde amnesia are fewer and less conclusive than on anterograde amnesia.[60],[61] At present, the results are conflicting, with some studies finding some impairment in retrograde memory – particularly autobiographical retrograde memory up to 6 months after ECT.[62],[63],[64],[65] However, more recent studies have failed to support this finding.[66],[67] While they do demonstrate an impairment in retrograde memory immediately after ECT, it was seen that this deficit returned to pre-ECT levels within a span of 1–2 months and improved beyond baseline performance at 6 months post ECT.[66] Adding to the confusion are numerous factors which confound the assessment of retrograde amnesia.

It has been shown that depressive symptoms can produce significant impairment of retrograde memory.[68],[69] It has also been demonstrated that sine-wave ECT produces significantly more impairment of retrograde memory as compared to brief-pulse ECT.[70] However, from the 1990s onward, sine-wave ECT has been completely replaced by brief-pulse ECT, and it is unclear as to the implications of cognitive impairment from the sine-wave era in contemporary ECT practice.Another area of concern are reports of subjective memory impairment following ECT. One of the pioneers of research into subjective memory impairment were Squire and Chace who published a series of studies in the 1970s demonstrating the adverse effect of bilateral ECT on subjective assessment of memory.[62],[63],[64],[65] However, most of the studies conducted post 1980 – from when sine-wave ECT was replaced by brief-pulse ECT report a general improvement in subjective memory assessments following ECT.[71] In addition, most of the recent studies have failed to find a significant association between measures of subjective and objective memory.[63],[66],[70],[72],[73],[74] It has also been shown that subjective memory impairment is strongly associated with the severity of depressive symptoms.[75] In light of these facts, the validity and value of measures of subjective memory impairment as a marker of cognitive impairment and brain damage following ECT have been questioned. However, concerns regarding subjective memory impairment and catastrophic retrograde amnesia continue to persist, with significant dissonance between the findings of different research groups and patient self-reports in various media.[57]Some studies reported the possibility of ECT being associated with the development of subsequent dementia.[76],[77] However, a recent large, well-controlled prospective Danish study found that the use of ECT was not associated with elevated incidence of dementia.[78] Conclusion Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function. This issue was last addressed by Devanand et al. In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail.

And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence – structural neuroimaging studies, functional neuroimaging studies, neurochemical and metabolic studies, and serum BDNF studies all point toward this. These neuromodulatory changes have been localized to the hippocampus, amygdala, and certain other parts of the limbic system. How exactly these changes mediate the improvement of depressive symptoms is a question that remains unanswered. However, there is little by way of evidence from neuroimaging studies which indicates that ECT causes destruction or degeneration of neurons.

Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks. Perhaps, the single-most important unaddressed concern is retrograde amnesia, which has been shown to persist for up to 2 months post ECT. In this regard, the recent neurometabolic studies have offered a tentative mechanism of action of ECT, producing a transient inflammation in the limbic cortex, which, in turn, drives neurogenesis, thereby exerting a neuromodulatory effect. This hypothesis would explain both the cognitive adverse effects of ECT – due to the transient inflammation – and the long-term improvement in mood – neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT.

However, these cannot be construed as brain damage as is usually understood. Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question. However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J. Electroconvulsive therapy.

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37.Merkl A, Schubert F, Quante A, Luborzewski A, Brakemeier EL, Grimm S, et al. Abnormal cingulate and prefrontal cortical neurochemistry in major depression after electroconvulsive therapy. Biol Psychiatry 2011;69:772-9. 38.Jorgensen A, Magnusson P, Hanson LG, Kirkegaard T, Benveniste H, Lee H, et al. Regional brain volumes, diffusivity, and metabolite changes after electroconvulsive therapy for severe depression.

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62.Squire LR, Chace PM. Memory functions six to nine months after electroconvulsive therapy. Arch Gen Psychiatry 1975;32:1557-64. 63.Squire LR, Slater PC. Electroconvulsive therapy and complaints of memory dysfunction.

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A cohort study. Lancet Psychiatry 2018;5:348-56. Correspondence Address:Dr. Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

How to http://wilcolquhoun.com/antabuse-where-to-buy/ cite antabuse prices walmart this article:Singh O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity antabuse prices walmart suicide is one of the highly publicized events in our country.

Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went into a frenzy antabuse prices walmart as newspapers, news channels, and social media were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor.

All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with antabuse prices walmart the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident.

Psychiatrists suddenly started getting distress calls from antabuse prices walmart their patients in despair with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing antabuse prices walmart Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and illness and also his relationships and finances antabuse prices walmart.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide antabuse prices walmart reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident.

Many psychiatrists antabuse prices walmart and mental health professionals were called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so. There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist.

These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry antabuse prices walmart and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time antabuse prices walmart of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and resource books for interacting with media, and psychiatrists should familiarize antabuse prices walmart themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion.

It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should antabuse prices walmart be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, antabuse prices walmart Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI.

10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment. The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage.

This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically.

Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods. These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies.

And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain. However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords.

Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update.

Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al. In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies.

The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time. Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness.

However, there are obvious ethical issues in designing human studies that are designed to answer this specific question. Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions. These studies have employed the following methods:Structural neuroimaging studiesFunctional neuroimaging studiesMetabolic neuroimaging studiesBody fluid biochemical marker studiesCognitive impairment studies.While the early studies tended to focus more on establishing the safety of ECT and finding out whether ECT causes gross microscopic brain damage, the later studies especially since the advent of advanced neuroimaging techniques have been focusing more on a mechanistic understanding of ECT.

Hence, the primary objective of the later neuroimaging studies has been to look for structural and functional brain changes which might explain how ECT acts rather than evidence of gross structural damage per se. However, put together, all these studies would enable us to answer our titular question to some satisfaction. [Table 1] and [Table 2] provide an overview of the evidence base in this area.

Structural and Functional Neuroimaging Studies Devanand et al. Reviewed 16 structural neuroimaging studies on the effect of ECT on the brain.[4] Of these, two were pneumoencephalography studies, nine were computed tomography (CT) scan studies, and five were magnetic resonance imaging (MRI) studies. However, most of these studies were retrospective in design, with neuroimaging being done in patients who had received ECT in the past.

In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT. In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today. The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain.

The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes. A single study by Coffey et al.

Followed up the patients for a duration of 6 months and repeated neuroimaging again at 6 months in order to capture any long-term changes following ECT.[10]The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities.[4] The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h. This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue.[11] The last significant observation by Coffey et al. In 1991 was that there was no significant temporal changes in the total volumes of the frontal lobes, temporal lobes, or amygdala–hippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies.

Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al.

Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al. That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies.

In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al. In a follow-up study showed that though there was a significant increase in the volume of the hippocampus 1 week after a course of ECT, the hippocampal volume returned to the baseline after 6 months.[19] Two other studies in 2013 showed that in addition to the hippocampus, the amygdala also showed significant volume increase following ECT.[20],[21] A series of structural neuroimaging studies after that have expanded on these findings and as of now, gray matter volume increase following ECT has been demonstrated in the hippocampus, amygdala, anterior temporal pole, subgenual cortex,[21] right caudate nucleus, and the whole of the medial temporal lobe (MTL) consisting of the hippocampus, amygdala, insula, and the posterosuperior temporal cortex,[24] para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus,[25] left cerebellar area VIIa crus I,[29] putamen, caudate nucleus, and nucleus acumbens [31] and clusters of increased cortical thickness involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex.[27] However, the most consistently reported and replicated finding has been the bilateral increase in the volume of the hippocampus and amygdala.

In light of these findings, it has been tentatively suggested that ECT acts by inducing neuronal regeneration in the hippocampus – amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study – Nordanskog et al., 2014 – has followed study patients for a long term – 6 months in their case. And significantly, the authors found out that after increasing immediately following ECT, the hippocampal volume returns back to baseline by 6 months.[19] This, however, was not associated with the relapse of depressive symptoms.

Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms. Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al.

In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression. It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus.

The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe. It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al.

Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population. It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder.

The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al.

In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered. Furthermore, bilateral (B/L) ECT was associated with an equal increase in volume in both right and left hippocampus, whereas right unilateral ECT was associated with greater volume increase in the right hippocampus. Finally, contrary to expectation, clinical improvement was found to be negatively correlated with hippocampal volume.Thus, a review of the current evidence amply demonstrates that from looking for ECT-related brain damage – and finding none, we have now moved ahead to looking for a mechanistic understanding of the effect of ECT.

In this regard, it has been found that ECT does induce structural changes in the brain – a fact which has been seized upon by some to claim that ECT causes brain damage.[46] Such statements should, however, be weighed against the definition of damage as understood by the scientific medical community and patient population. Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage. Metabolic Neuroimaging Studies.

Magnetic Resonance Spectroscopic Imaging Magnetic resonance spectroscopic imaging (MRSI) uses a phase-encoding procedure to map the spatial distribution of magnetic resonance (MR) signals of different molecules. The crucial difference, however, is that while MRI maps the MR signals of water molecules, MRSI maps the MR signals generated by different metabolites – such as N-acetyl aspartate (NAA) and choline-containing compounds. However, the concentration of these metabolites is at least 10,000 times lower than water molecules and hence the signal strength generated would also be correspondingly lower.

However, MRSI offers us the unique advantage of studying in vivo the change in the concentration of brain metabolites, which has been of great significance in fields such as psychiatry, neurology, and basic neuroscience research.[47]MRSI studies on ECT in patients with depression have focused largely on four metabolites in the human brain – NAA, choline-containing compounds (Cho) which include majorly cell membrane compounds such as glycerophosphocholine, phosphocholine and a miniscule contribution from acetylcholine, creatinine (Cr) and glutamine and glutamate together (Glx). NAA is located exclusively in the neurons, and is suggested to be a marker of neuronal viability and functionality.[48] Choline-containing compounds (Cho) mainly include the membrane compounds, and an increase in Cho would be suggestive of increased membrane turnover. Cr serves as a marker of cellular energy metabolism, and its levels are usually expected to remain stable.

The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT. Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite.

However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies. It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations. The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis.

Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

More significantly, the authors also showed a significant increase in Glx levels in the hippocampus following ECT, which was also associated with an increase in hippocampal volume.[40] To explain these three findings, the authors proposed that ECT produces a neuroinflammatory response in the hippocampus – likely mediated by Glx, which has been known to cause inflammation at higher concentrations, thereby accounting for the increase in hippocampal volume with a reduction in NAA concentration. The cause for the volume increase remains unclear – with the authors speculating that it might be due to neuronal swelling or due to angiogenesis. However, the same study and multiple other past studies [21],[25],[30] have demonstrated that hippocampal volume increase was correlated with clinical improvement following ECT.

Thus, we are led to the hypothesis that the same mechanism which drives clinical improvement with ECT is also responsible for the cognitive impairment following ECT. Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results. The ACC is another area which has been studied in some detail utilizing the MRSI technique.

In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT. This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al.

In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al. Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity.

A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al.

In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al. In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied.

In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus. This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT.

However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development.

The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect. It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT.

Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder. The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration.

However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory. Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests.

Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information.[58] As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT.[57] However, one of the major limitations of this meta-analysis was the lack of evidence on retrograde amnesia following ECT. This is particularly unfortunate considering that it is memory impairment – particularly retrograde amnesia which has received the most attention.[59] In addition, reports of catastrophic retrograde amnesia have been repeatedly held up as sensational evidence of the lasting brain damage produced by ECT.[59] Admittedly, studies on retrograde amnesia are fewer and less conclusive than on anterograde amnesia.[60],[61] At present, the results are conflicting, with some studies finding some impairment in retrograde memory – particularly autobiographical retrograde memory up to 6 months after ECT.[62],[63],[64],[65] However, more recent studies have failed to support this finding.[66],[67] While they do demonstrate an impairment in retrograde memory immediately after ECT, it was seen that this deficit returned to pre-ECT levels within a span of 1–2 months and improved beyond baseline performance at 6 months post ECT.[66] Adding to the confusion are numerous factors which confound the assessment of retrograde amnesia. It has been shown that depressive symptoms can produce significant impairment of retrograde memory.[68],[69] It has also been demonstrated that sine-wave ECT produces significantly more impairment of retrograde memory as compared to brief-pulse ECT.[70] However, from the 1990s onward, sine-wave ECT has been completely replaced by brief-pulse ECT, and it is unclear as to the implications of cognitive impairment from the sine-wave era in contemporary ECT practice.Another area of concern are reports of subjective memory impairment following ECT.

One of the pioneers of research into subjective memory impairment were Squire and Chace who published a series of studies in the 1970s demonstrating the adverse effect of bilateral ECT on subjective assessment of memory.[62],[63],[64],[65] However, most of the studies conducted post 1980 – from when sine-wave ECT was replaced by brief-pulse ECT report a general improvement in subjective memory assessments following ECT.[71] In addition, most of the recent studies have failed to find a significant association between measures of subjective and objective memory.[63],[66],[70],[72],[73],[74] It has also been shown that subjective memory impairment is strongly associated with the severity of depressive symptoms.[75] In light of these facts, the validity and value of measures of subjective memory impairment as a marker of cognitive impairment and brain damage following ECT have been questioned. However, concerns regarding subjective memory impairment and catastrophic retrograde amnesia continue to persist, with significant dissonance between the findings of different research groups and patient self-reports in various media.[57]Some studies reported the possibility of ECT being associated with the development of subsequent dementia.[76],[77] However, a recent large, well-controlled prospective Danish study found that the use of ECT was not associated with elevated incidence of dementia.[78] Conclusion Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function. This issue was last addressed by Devanand et al.

In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail. And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence – structural neuroimaging studies, functional neuroimaging studies, neurochemical and metabolic studies, and serum BDNF studies all point toward this.

These neuromodulatory changes have been localized to the hippocampus, amygdala, and certain other parts of the limbic system. How exactly these changes mediate the improvement of depressive symptoms is a question that remains unanswered. However, there is little by way of evidence from neuroimaging studies which indicates that ECT causes destruction or degeneration of neurons.

Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks. Perhaps, the single-most important unaddressed concern is retrograde amnesia, which has been shown to persist for up to 2 months post ECT. In this regard, the recent neurometabolic studies have offered a tentative mechanism of action of ECT, producing a transient inflammation in the limbic cortex, which, in turn, drives neurogenesis, thereby exerting a neuromodulatory effect.

This hypothesis would explain both the cognitive adverse effects of ECT – due to the transient inflammation – and the long-term improvement in mood – neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT. However, these cannot be construed as brain damage as is usually understood.

Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question. However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J.

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Correspondence Address:Dr. Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

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