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Explore full-page map The number of new erectile dysfunction treatment s dropped for the third consecutive week, but the rural http://tvandfilmtoys.com/cheap-40mg-levitra/ rate remains significantly higher than the buy levitra canada online metropolitan rate. The gap between the rural and metropolitan death rates is even more pronounced, according to a Daily Yonder analysis. New s fell by about 12% in rural counties last week, compared to a buy levitra canada online 11% drop in metropolitan counties. erectile dysfunction treatment-related deaths in rural counties fell by about 14%, while the death rate fell about 13% in metropolitan counties. For the week ending Saturday, October 9, the rural rate was about two thirds higher than the metropolitan rate.

The rural death rate was 89% higher than the metropolitan death rate buy levitra canada online. Like this story?. Sign up for our newsletter. New cases are buy levitra canada online trending downward nationally, but 12 states had higher rural rates last week than they did two weeks ago. Nevada saw the biggest jump in rural s, with an increase of 84% last week compared to two weeks ago.

Nevada is part of erectile dysfunction treatment hot-spots covering parts of the northern Great Plains, Rocky Mountains, and interior West. Other states buy levitra canada online that saw double-digit percentage increases in rural rates were New Hampshire, Colorado, Pennsylvania, Massachusetts, Connecticut, North Dakota, and Montana. States that reduced their rural rates by more than 30% were Nebraska, Alaska, Texas, Alabama, Georgia, Florida, West Virginia, and Maine. Despite the decreases, nearly 90% of the nation’s 1,976 rural counties were in the red zone, meaning they had rates of more than 100 new cases per buy levitra canada online 100,000 residents in a single week. The White House has advised localities that exceed this threshold to take additional steps to contain the levitra.

The number of rural red-zone counties fell by 85 last week, to 1,734. Three hundred of these counties had very high rates – over 500 new cases per buy levitra canada online 100,000 for the week. Texas and Georgia moved the most rural counties out of red zone last week. Texas had a net loss of 29 rural red-zone counties, and Georgia had a net loss of 22. This week’s Daily Yonder erectile dysfunction treatment analysis covers Sunday, October 3, through Saturday, October 9 buy levitra canada online.

Data is from USA Facts and the Centers for Disease Control and Prevention. You Might Also LikeStart Preamble Office of the Assistant Secretary for Health, Office of the Secretary, Department of Health and Human Services. Notice of meeting buy levitra canada online. As required by the Federal Advisory Committee Act, the U.S. Department of Health and Human Services buy levitra canada online (HHS) is hereby giving notice that the erectile dysfunction treatment Health Equity Task Force (Task Force) will hold a virtual meeting on October 28, 2021.

The purpose of this meeting is to present and vote on the Task Force Final Report with recommended Implementation Plan and Accountability Plan for mitigating inequities caused or exacerbated by the erectile dysfunction treatment levitra and for preventing such inequities in the future. This meeting is open to the public and will be live-streamed at www.hhs.gov/​live. Information about the meeting will be posted on the HHS Office buy levitra canada online of Minority Health website. Www.minorityhealth.hhs.gov/​healthequitytaskforce/​ prior to the meeting. The Task Force meeting will be held on Thursday, October 28, 2021, from 1 p.m.

To approximately buy levitra canada online 4 p.m. ET (date and time are tentative and subject to change). The confirmed time and agenda will be posted on the erectile dysfunction treatment Health Equity Task Force web page. Www.minorityhealth.hhs.gov/​healthequitytaskforce/​ when buy levitra canada online this information becomes available. Start Further Info Samuel Wu, Designated Federal Officer for the Task Force.

Office of Minority Health, Department of Health and Human Services, Tower Building, 1101 Wootton Parkway, Suite 100, Rockville, Maryland 20852. Phone. 240-453-6173. Email. erectile dysfunction treatment19HETF@hhs.gov.

End Further Info End Preamble Start Supplemental Information   Background. The erectile dysfunction treatment Health Equity Task Force (Task Force) was established by Executive Order 13995, dated January 21, 2021. The Task Force is tasked with providing specific recommendations to the President, through the Coordinator of the erectile dysfunction treatment Response and Counselor to the President (erectile dysfunction treatment Response Coordinator), for mitigating the health inequities caused or exacerbated by the erectile dysfunction treatment levitra and for preventing such inequities in the future. The Task Force shall submit a final report to the erectile dysfunction treatment Response Coordinator addressing any ongoing health inequities faced by erectile dysfunction treatment survivors that may merit a public health response, describing the factors that contributed to disparities in erectile dysfunction treatment outcomes, and recommending actions to combat such disparities in future levitra responses. The meeting is open to the public and will be live-streamed at www.hhs.gov/​live.

No registration is required. A public comment session will be held during the meeting. Pre-registration is required to provide public comment during the meeting. To pre-register, please send an email to erectile dysfunction treatment19HETF@hhs.gov and include your name, title, and organization by close of business on Friday, October 22, 2021. Comments will be limited to no more than three minutes per speaker and should be pertinent to the meeting discussion.

Individuals are encouraged to provide a written statement of any public comment(s) for accurate minute-taking purposes. If you decide you would like to provide public comment but do not pre-register, you may submit your written statement by emailing erectile dysfunction treatment19HETF@hhs.gov no later than close of business on Thursday, November 4, 2021. Individuals who plan to attend and need special assistance, such as sign language interpretation or other reasonable accommodations, should contact. erectile dysfunction treatment19HETF@hhs.gov and reference this meeting. Requests for special accommodations should be made at least 10 business days prior to the meeting.

Start Signature Dated. October 7, 2021. Samuel Wu, Designated Federal Officer, erectile dysfunction treatment Health Equity Task Force. End Signature End Supplemental Information [FR Doc. 2021-22330 Filed 10-13-21.

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View more levitra price in canada Jul 9, 2021 Every buy levitra online cheap day you're using skills to help end substance use disorders (SUD) within your community. The Health Resources and Services Administration (HRSA) is here to help you with the new Substance Use Disorder Treatment and Recovery Loan Repayment Program (STAR LRP). Apply for this program buy levitra online cheap through Thursday, July 22, 2021 at 7:30 p.m. Eastern. Pay off your school loans with up to $250,000 from the STAR LRP in exchange for six years of full-time service at an approved facility.

Behavioral health clinicians, paraprofessionals, clinical support staff and many others trained in buy levitra online cheap substance use disorder treatment are encouraged to apply. Visit the STAR LRP website for a full list of eligible disciplines. For help with your application, join one of HRSA's upcoming STAR LRP Q&A Sessions. Source. Health Resources and Services AdministrationWALDEN, Colo.

€” The building that once housed the last drugstore in this town of fewer than 600 is now a barbecue restaurant, where pit boss Larry Holtman dishes out smoked brisket and pulled pork across the same counter where pharmacists dispensed vital medications more than 30 years ago. It’s an hourlong drive over treacherous mountain passes to Laramie, Wyoming, or Granby or Steamboat Springs, Colorado — and the nearest pharmacies. The routes out of the valley in which Walden lies are regularly closed by heavy winter snows, keeping residents in and medications out. Walden has suffered the fate of many small towns across the United States, as the economics of the pharmacy business have made it difficult for community drugstores to survive. With large pharmacy chains buying up independent drugstores and increasingly controlling the supply chain, towns such as Walden have too few residents to attract a chain drugstore and no great appeal for pharmacists willing to strike out on their own.

With no local access to prescription drugs, the town of mainly cattle ranchers and hay farmers has crowdsourced a delivery system, taking advantage of anyone’s trip to those bigger cities to pick up medications for the rest of the town. €œReally, it’s a network of community and people reaching out and knowing that others have needs,” said Tina Maddux, who runs a nonprofit that provides food and other assistance in Walden. €œWe’re a community that pulls together for the wellness of everyone.” The system is just one of the creative ways that rural communities deal with a lack of health care. In Walden, the senior center runs a regular shuttle to the bigger locales so older residents don’t have to drive to pick up groceries, visit doctors or refill their meds. In October, a pharmacy in Steamboat Springs began delivering medications to Walden once a week.

Mail-order pharmacies can help with medications for chronic conditions, but not for acute needs. Yet these solutions can’t replace a bricks-and-mortar pharmacy, as pharmacists do much more than count pills. They can give flu or erectile dysfunction treatment shots and, in some states, such as Colorado, even prescribe contraceptives. Some run diabetes management or smoking cessation programs. Medications can be complicated, and without a live person to talk to, patients can struggle to take them correctly.

In Walden, Colorado — a town of fewer than 600 residents that no longer has a drugstore — residents are crowdsourcing ways of getting prescription medicines delivered to those who can’t travel the long distances to the closest big community with a pharmacist.(Kyle Spradley / for KHN) All Smoked Up BBQ in downtown Walden used to be a pharmacy — the last drugstore in the town. Smoked brisket and pulled pork now move across the same counter where pharmacists dispensed vital medications more than 30 years ago. (Kyle Spradley / for KHN) In Walden, locals are one snowstorm, one mishap, from being cut off from their meds. That uncertainty leaves Whitney Milek with constant anxiety. Her younger son, 8-year-old Wade, relies on medications to control his seizures.

She usually picks up his medicines in Laramie, where the family does its big grocery runs. But when she needs to refill in between trips, she turns to her neighbors for help. The informal system runs primarily through a Facebook group created in 2013 as a sort of online garage sale. For years, people have been posting to ask if anybody is headed toward a pharmacy and can bring back a prescription. Neighbors deliver to neighbors, even during the levitra, and no money is exchanged.

€œThere are times when nobody is going and you end up having to have them mailed, which is a whole other thing, especially with seizure meds,” Milek said. €œSome are controlled substances and they can’t mail them.” Two winters ago, Milek called in one of her son’s prescriptions to a Steamboat Springs pharmacy. But when she arrived, the medication was out of stock. With road conditions rapidly worsening, she asked if the pharmacy would mail the medication but was told she lived too close for mail delivery. She turned to a pharmacy in Laramie, which eventually agreed to mail it to her — but also didn’t have it in stock.

€œSo, he ended up going five days without,” Milek said. €œIt’s not a big deal if you miss a dose here or there. But when you miss that many over click this link now a period of time, your tolerance level goes down.” That medication must be carefully managed to build up gradually in Wade’s blood to avoid a severe allergic reaction. It took three weeks to scale up to his daily dose when he started taking the drug two years ago. €œWhen he went five days without it, he had to basically start all over again.

It was over Christmas break, so he wasn’t in school. I brought him to work with me because I didn’t feel comfortable leaving him with anybody else,” said Milek, a bookkeeper. €œI didn’t know what was going to happen.” Whitney Milek’s younger son, Wade, relies on medications to control his seizures. The family, photographed in March 2020 before the erectile dysfunction treatment levitra took hold, lives in Walden, Colorado, an hour’s drive over treacherous mountain passes to Laramie, Wyoming. That’s where they get groceries — and often pick up Wade’s prescriptions.

But sometimes they need refills before they can make those trips and rely on help from neighbors.(Kyle Spradley / for KHN) Wade was fortunate to avoid complications that time. But having a local pharmacy mail medications comes with added costs — $26, in their case, for a prescription last month — an extra tax on those who cannot get to a pharmacy. Mail-order pharmacies typically don’t charge for shipping yet can run into snags, too. Last year, some of Wade’s mailed medications got stuck in a Denver processing facility for three weeks. The Mileks had to pay $1,600 out-of-pocket to get replacements.

Walden has no hospital, only a small clinic where Dr. Lynnette Telck and a nurse practitioner care for residents. The clinic stocks some basic medications to handle routine acute needs — antibiotics for strep throat, inhalers for asthma — and they can mix up liquid suspensions for those who can’t swallow pills. €œIt’s a small town, so we all wear many hats,” Telck said. Studies show that, without a drugstore nearby, patients aren’t as likely to keep up with their medications and their chronic conditions can worsen.

Without readily available medications, Telck said, patients can end up taking an ambulance to an emergency room. €œIt’s just so darn expensive to the system,” she said. Walden touts itself as the moose-viewing capital of Colorado and is a recreation mecca for hunting, fishing and snowmobiling. But Telck said it could be hard to attract a pharmacist because the town lacks amenities like movie theaters and shopping malls. €œIt’s pristine and wonderful in its own quirky way and we love it,” she said.

€œBut not a lot of people want to come to rural areas. The wages aren’t as high as in the big cities.” Middle Park Health, the Granby-based hospital system that operates the Walden clinic, had looked at putting a more complete pharmacy in the clinic but couldn’t find a technician to staff it. €œThe days of that being a profitable, desirable business?. It’s a lot tougher than it was a decade or two ago,” said Gina Moore, an associate dean at the University of Colorado’s School of Pharmacy. €œYou come out of eight years of college — four years of undergraduate and four years of pharmacy school — with pretty significant student loan debt.

It’s very hard to go to a rural community where you don’t make any money.” In towns without an ER or a clinic open late, pharmacists often become the health provider of last resort. They tell patients whether they need to make the long trek to a hospital late at night or can wait until morning. €œA patient will often come to the pharmacy as the first point of access for health care,” Moore said. €œOur pharmacists are taught to understand and to be able to advise people on what can be self-treated with over-the-counter medications versus when you need to see a higher-level provider or an urgent care.” Researchers from the Rural Policy Research Institute at the University of Iowa have documented how the deck is increasingly stacked against community pharmacies. €œIt’s just not a really attractive business model anymore,” said Keith Mueller, the institute’s director.

In 2013, they found that new Medicare Part D drug plans resulted in low and late reimbursements, replacing direct out-of-pocket payments from customers. That left many pharmacies unable to turn a profit. By 2018, surveys showed pharmacies were struggling more with the narrowing margin between what they paid for the drugs and what they were being reimbursed by health plans. Towns of more than 10,000 people are often served by at least a Walmart or a supermarket pharmacy, Mueller said. €œBut you get out into smaller communities, the predominant modality had been the corner drugstore,” he said.

€œWe’re not seeing that replacement of the closed independents by a CVS, Rite Aid or Walgreens.” The Mileks have talked about whether they should move near her family in Wyoming to be closer to a hospital and pharmacy. €œWhen you can’t get to a pharmacy, it’s scary, because things can happen so fast,” Milek said. €œPeople just have no concept of what it’s like out here.” The Milek family, photographed in March 2020 before the erectile dysfunction treatment levitra took hold, has talked about whether they need to leave rural Walden, Colorado, to move near family in Wyoming to be closer to a hospital and pharmacy. Their younger son, Wade, relies on medications to control his seizures and Walden does not have a pharmacy, making it challenging to get his medications.(Kyle Spradley / for KHN) Markian Hawryluk. MarkianH@kff.org, @MarkianHawryluk Related Topics Contact Us Submit a Story Tip.

View more Jul 9, 2021 buy levitra canada online Every day you're using skills http://www.ec-jacqueline-strasbourg.ac-strasbourg.fr/ecole/?p=1508 to help end substance use disorders (SUD) within your community. The Health Resources and Services Administration (HRSA) is here to help you with the new Substance Use Disorder Treatment and Recovery Loan Repayment Program (STAR LRP). Apply for this program buy levitra canada online through Thursday, July 22, 2021 at 7:30 p.m.

Eastern. Pay off your school loans with up to $250,000 from the STAR LRP in exchange for six years of full-time service at an approved facility. Behavioral health clinicians, paraprofessionals, clinical support staff and many others buy levitra canada online trained in substance use disorder treatment are encouraged to apply.

Visit the STAR LRP website for a full list of eligible disciplines. For help with your application, join one of HRSA's upcoming STAR LRP Q&A Sessions. Source.

Health Resources and Services AdministrationWALDEN, Colo. €” The building that once housed the last drugstore in this town of fewer than 600 is now a barbecue restaurant, where pit boss Larry Holtman dishes out smoked brisket and pulled pork across the same counter where pharmacists dispensed vital medications more than 30 years ago. It’s an hourlong drive over treacherous mountain passes to Laramie, Wyoming, or Granby or Steamboat Springs, Colorado — and the nearest pharmacies.

The routes out of the valley in which Walden lies are regularly closed by heavy winter snows, keeping residents in and medications out. Walden has suffered the fate of many small towns across the United States, as the economics of the pharmacy business have made it difficult for community drugstores to survive. With large pharmacy chains buying up independent drugstores and increasingly controlling the supply chain, towns such as Walden have too few residents to attract a chain drugstore and no great appeal for pharmacists willing to strike out on their own.

With no local access to prescription drugs, the town of mainly cattle ranchers and hay farmers has crowdsourced a delivery system, taking advantage of anyone’s trip to those bigger cities to pick up medications for the rest of the town. €œReally, it’s a network of community and people reaching out and knowing that others have needs,” said Tina Maddux, who runs a nonprofit that provides food and other assistance in Walden. €œWe’re a community that pulls together for the wellness of everyone.” The system is just one of the creative ways that rural communities deal with a lack of health care.

In Walden, the senior center runs a regular shuttle to the bigger locales so older residents don’t have to drive to pick up groceries, visit doctors or refill their meds. In October, a pharmacy in Steamboat Springs began delivering medications to Walden once a week. Mail-order pharmacies can help with medications for chronic conditions, but not for acute needs.

Yet these solutions can’t replace a bricks-and-mortar pharmacy, as pharmacists do much more than count pills. They can give flu or erectile dysfunction treatment shots and, in some states, such as Colorado, even prescribe contraceptives. Some run diabetes management or smoking cessation programs.

Medications can be complicated, and without a live person to talk to, patients can struggle to take them correctly. In Walden, Colorado — a town of fewer than 600 residents that no longer has a drugstore — residents are crowdsourcing ways of getting prescription medicines delivered to those who can’t travel the long distances to the closest big community with a pharmacist.(Kyle Spradley / for KHN) All Smoked Up BBQ in downtown Walden used to be a pharmacy — the last drugstore in the town. Smoked brisket and pulled pork now move across the same counter where pharmacists dispensed vital medications more than 30 years ago.

(Kyle Spradley / for KHN) In Walden, locals are one snowstorm, one mishap, from being cut off from their meds. That uncertainty leaves Whitney Milek with constant anxiety. Her younger son, 8-year-old Wade, relies on medications to control his seizures.

She usually picks up his medicines in Laramie, where the family does its big grocery runs. But when she needs to refill in between trips, she turns to her neighbors for help. The informal system runs primarily through a Facebook group created in 2013 as a sort of online garage sale.

For years, people have been posting to ask if anybody is headed toward a pharmacy and can bring back a prescription. Neighbors deliver to neighbors, even during the levitra, and no money is exchanged. €œThere are times when nobody is going and you end up having to have them mailed, which is a whole other thing, especially with seizure meds,” Milek said.

€œSome are controlled substances and they can’t mail them.” Two winters ago, Milek called in one of her son’s prescriptions to a Steamboat Springs pharmacy. But when she arrived, the medication was out of stock. With road conditions rapidly worsening, she asked if the pharmacy would mail the medication but was told she lived too close for mail delivery.

She turned to a pharmacy in Laramie, which eventually agreed to mail it to her — but also didn’t have it in stock. €œSo, he ended up going five days without,” Milek said. €œIt’s not a big deal if you miss a dose here or there.

But when you miss that many over a period of time, your tolerance level goes down.” That medication must be carefully managed check my reference to build up gradually in Wade’s blood to avoid a severe allergic reaction. It took three weeks to scale up to his daily dose when he started taking the drug two years ago. €œWhen he went five days without it, he had to basically start all over again.

It was over Christmas break, so he wasn’t in school. I brought him to work with me because I didn’t feel comfortable leaving him with anybody else,” said Milek, a bookkeeper. €œI didn’t know what was going to happen.” Whitney Milek’s younger son, Wade, relies on medications to control his seizures.

The family, photographed in March 2020 before the erectile dysfunction treatment levitra took hold, lives in Walden, Colorado, an hour’s drive over treacherous mountain passes to Laramie, Wyoming. That’s where they get groceries — and often pick up Wade’s prescriptions. But sometimes they need refills before they can make those trips and rely on help from neighbors.(Kyle Spradley / for KHN) Wade was fortunate to avoid complications that time.

But having a local pharmacy mail medications comes with added costs — $26, in their case, for a prescription last month — an extra tax on those who cannot get to a pharmacy. Mail-order pharmacies typically don’t charge for shipping yet can run into snags, too. Last year, some of Wade’s mailed medications got stuck in a Denver processing facility for three weeks.

The Mileks had to pay $1,600 out-of-pocket to get replacements. Walden has no hospital, only a small clinic where Dr. Lynnette Telck and a nurse practitioner care for residents.

The clinic stocks some basic medications to handle routine acute needs — antibiotics for strep throat, inhalers for asthma — and they can mix up liquid suspensions for those who can’t swallow pills. €œIt’s a small town, so we all wear many hats,” Telck said. Studies show that, without a drugstore nearby, patients aren’t as likely to keep up with their medications and their chronic conditions can worsen.

Without readily available medications, Telck said, patients can end up taking an ambulance to an emergency room. €œIt’s just so darn expensive to the system,” she said. Walden touts itself as the moose-viewing capital of Colorado and is a recreation mecca for hunting, fishing and snowmobiling.

But Telck said it could be hard to attract a pharmacist because the town lacks amenities like movie theaters and shopping malls. €œIt’s pristine and wonderful in its own quirky way and we love it,” she said. €œBut not a lot of people want to come to rural areas.

The wages aren’t as high as in the big cities.” Middle Park Health, the Granby-based hospital system that operates the Walden clinic, had looked at putting a more complete pharmacy in the clinic but couldn’t find a technician to staff it. €œThe days of that being a profitable, desirable business?. It’s a lot tougher than it was a decade or two ago,” said Gina Moore, an associate dean at the University of Colorado’s School of Pharmacy.

€œYou come out of eight years of college — four years of undergraduate and four years of pharmacy school — with pretty significant student loan debt. It’s very hard to go to a rural community where you don’t make any money.” In towns without an ER or a clinic open late, pharmacists often become the health provider of last resort. They tell patients whether they need to make the long trek to a hospital late at night or can wait until morning.

€œA patient will often come to the pharmacy as the first point of access for health care,” Moore said. €œOur pharmacists are taught to understand and to be able to advise people on what can be self-treated with over-the-counter medications versus when you need to see a higher-level provider or an urgent care.” Researchers from the Rural Policy Research Institute at the University of Iowa have documented how the deck is increasingly stacked against community pharmacies. €œIt’s just not a really attractive business model anymore,” said Keith Mueller, the institute’s director.

In 2013, they found that new Medicare Part D drug plans resulted in low and late reimbursements, replacing direct out-of-pocket payments from customers. That left many pharmacies unable to turn a profit. By 2018, surveys showed pharmacies were struggling more with the narrowing margin between what they paid for the drugs and what they were being reimbursed by health plans.

Towns of more than 10,000 people are often served by at least a Walmart or a supermarket pharmacy, Mueller said. €œBut you get out into smaller communities, the predominant modality had been the corner drugstore,” he said. €œWe’re not seeing that replacement of the closed independents by a CVS, Rite Aid or Walgreens.” The Mileks have talked about whether they should move near her family in Wyoming to be closer to a hospital and pharmacy.

€œWhen you can’t get to a pharmacy, it’s scary, because things can happen so fast,” Milek said. €œPeople just have no concept of what it’s like out here.” The Milek family, photographed in March 2020 before the erectile dysfunction treatment levitra took hold, has talked about whether they need to leave rural Walden, Colorado, to move near family in Wyoming to be closer to a hospital and pharmacy. Their younger son, Wade, relies on medications to control his seizures and Walden does not have a pharmacy, making it challenging to get his medications.(Kyle Spradley / for KHN) Markian Hawryluk.

MarkianH@kff.org, @MarkianHawryluk Related Topics Contact Us Submit a Story Tip.

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Keep out of the reach of children. Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F). Throw away any unused medicine after the expiration date.

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Shutterstock buy levitra usa The U.S. Department of Justice recently awarded the Wisconsin Department of Safety and Professional Services (DSPS) a $1.9 million grant for its Wisconsin Enhanced Prescription Drug Monitoring Program (ePDMP).ePDMP is a clinical decision support tool used more than buy levitra usa 650,000 times monthly by more than 55,000 licensed health care professionals. Funding will be used to upgrade the user experience for those accessing through the use of an electronic health record system, improve patient matching accuracy, assist providers in making decisions regarding prescribing and dispensing controlled substances, and further customize analytics for health care professionals.Rep. Mike Gallagher buy levitra usa (R-WI) wrote the department and urged it to fulfill the grant application.“For far too many Wisconsinites, the opioid epidemic hits close to home,” Gallagher said.

€œOur state relies on the Wisconsin buy levitra usa Enhanced Prescription Drug Monitoring Program to combat prescription drug abuse, and this announcement will help ensure that DSPS has the resources it needs to improve this tool. I’m proud to have advocated on the program’s behalf and am confident that these funds will help make the system more effective, user-friendly, and sustainable.”“Our award-winning program is an invaluable tool that has transformed prescribing culture and curbed prescription opioid use in Wisconsin,” Dawn Crim, DSPS secretary-designee, said.Shutterstock The U.S. Department of Health and Human Services (HHS) recently awarded two North Dakota programs $1.9 million.“This funding from HHS will benefit two North buy levitra usa Dakota entities as they prepare children for school, work to keep them engaged and protect them from the dangers of substance abuse, supporting the students’ long-term success” Sen. John Hoeven (R-ND), a member of the Senate Appropriations Committee, said.The Administration for Children and Families for Head Start and Early Head Start services in Dickinson awarded the Community Action Partnership $1.2 million.The partnership is a private, nonprofit membership organization representing the seven community action agencies and providing buy levitra usa services statewide.

The partnership has three programs. Sportsmen Against Hunger distributes donated venison buy levitra usa to food pantries. Supportive Services for Veteran Families provides support and services to low-income veterans and their families living in, or transitioning to, permanent housing. And the Weatherization Assistance Program provides energy conservation services to low-income households to make their homes more energy efficient, including insulation and caulking.The Centers for Disease Control and Prevention’s Drug Free Communities Support Program for Project .03 in Bismarck also awarded the city $125,000 to reduce alcohol and marijuana use among middle and high school students..

Shutterstock buy levitra canada online The U.S. Department of Justice recently awarded the Wisconsin Department of Safety and buy levitra canada online Professional Services (DSPS) a $1.9 million grant for its Wisconsin Enhanced Prescription Drug Monitoring Program (ePDMP).ePDMP is a clinical decision support tool used more than 650,000 times monthly by more than 55,000 licensed health care professionals. Funding will be used to upgrade the user experience for those accessing through the use of an electronic health record system, improve patient matching accuracy, assist providers in making decisions regarding prescribing and dispensing controlled substances, and further customize analytics for health care professionals.Rep. Mike Gallagher (R-WI) wrote the department and buy levitra canada online urged it to fulfill the grant application.“For far too many Wisconsinites, the opioid epidemic hits close to home,” Gallagher said. €œOur state relies on the Wisconsin Enhanced Prescription Drug Monitoring Program to combat prescription drug abuse, and this announcement will help ensure that DSPS has the buy levitra canada online resources it needs to improve this tool.

I’m proud to have advocated on the program’s behalf and am confident that these funds will help make the system more effective, user-friendly, and sustainable.”“Our award-winning program is an invaluable tool that has transformed prescribing culture and curbed prescription opioid use in Wisconsin,” Dawn Crim, DSPS secretary-designee, said.Shutterstock The U.S. Department of Health and buy levitra canada online Human Services (HHS) recently awarded two North Dakota programs $1.9 million.“This funding from HHS will benefit two North Dakota entities as they prepare children for school, work to keep them engaged and protect them from the dangers of substance abuse, supporting the students’ long-term success” Sen. John Hoeven (R-ND), a member of the Senate Appropriations Committee, said.The Administration for Children and Families for Head Start and Early buy levitra canada online Head Start services in Dickinson awarded the Community Action Partnership $1.2 million.The partnership is a private, nonprofit membership organization representing the seven community action agencies and providing services statewide. The partnership has three programs. Sportsmen Against Hunger distributes donated venison to food pantries buy levitra canada online.

Supportive Services for Veteran Families provides support and services to low-income veterans and their families living in, or transitioning to, permanent housing. And the Weatherization Assistance Program provides energy conservation services to low-income households to make their homes more energy efficient, including insulation and caulking.The Centers for Disease Control and Prevention’s Drug Free Communities Support Program for Project .03 in Bismarck also awarded the city $125,000 to reduce alcohol and marijuana use among middle and high school students..

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Grief management can levitra be taken daily http://baselaunch.biocom.de/online-levitra/ in erectile dysfunction treatment. Indian context. Indian J Psychiatry 2021;63:211Grief is a normal response to loss and bereavement. Human beings are aware of the concept of death and permanence of loss leading can levitra be taken daily to grief and bereavement. It may be seen in some other species also.

While there has been a neurobiological mechanism explaining grief, it primarily remains a sociocultural phenomenon affecting the brain and the body. The perception of can levitra be taken daily death followed by the gradual “sinking in” of its consequences leads to psychobiological reaction. Grief which is unmanaged can lead to serious health reactions like increased cardiovascular mortality (broken heart) and psychiatric disorders like depression and suicide.erectile dysfunction treatment as an epidemic has brought grief and bereavement to the doorstep of each and every person. Constantly hearing, seeing about death, and losing friends and family has brought enormous strain to people's lives. Death rituals have a can levitra be taken daily therapeutic function wherein they allow a family and a group to mourn in a ritualistic way.

This allows people to share grief and keep the deceased as focus of attention for a fixed time and then to move on with life. Sometimes, this process is hampered by what Kenneth Doka called “disenfranchised grief” in 1989 and defined it “as a process in which loss is felt as not being openly acknowledged, socially validated or publicly mourned.”[1] Externally imposed disenfranchised grief leads to grief remaining unresolved and unaddressed, and the person feels that his right to grieve has been denied.erectile dysfunction treatment has unexpectedly disturbed the process of death rituals as it leads to:Unexpected or sudden lossDepletion of emotional and coping resourcesLimitation in visiting and end of care supportNot able to perform last ritualsLack of social support due to erectile dysfunction treatment restrictions.[2]The mechanical and impersonal process has led to severe psychological trauma in the survivors, particularly in the early phase of the disease when the knowledge was less and health-care workers were burdened and under cover of personal protective equipment, communication was difficult. Realizing this, the Indian Council of Medical Research has come out with guidelines for health-care workers to deal with death and guide family members can levitra be taken daily. However, persistence of grief reaction remains a problem, and due to lack of social support due to erectile dysfunction treatment, people are increasingly relying on professionals to take care of their grief reactions.In India, the sharing of grief is very important. People try to reach the grieving family.

So, what can levitra be taken daily should be the model of care for these people?. We should try to increase the sharing of grief and the handling of the person should be allowed to take placeThe physical support and the economical support have to be arranged, particularly where both parents have diedThere are some common modes like “condolence meetings” or “smaran sabha” which should be attended by both family members and colleagues.erectile dysfunction treatment has brought an unprecedented amount of grief, and it is our duty to manage grief with innovative solutions to prevent the emergence of prolonged grief reaction, depression, and suicide. References 1.Doka KJ, editor. Disenfranchised Grief can levitra be taken daily. New Directions, Challenges, and Strategies for Practice.

Champaign, IL. Research Press can levitra be taken daily. 2002. 2.Albuquerque S, Teixeira AM, Rocha JC. erectile dysfunction treatment and can levitra be taken daily Disenfranchised Grief.

Front Psychiatry 2021;12:638874. Correspondence Address:Om Prakash SinghDepartment of Psychiatry, WBMES, Kolkata, West Bengal. AMRI Hospitals, Kolkata, West can levitra be taken daily Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI.

10.4103/indianjpsychiatry.indianjpsychiatry_489_21How to cite this article:Parthasarathy R, Channaveerachari NK, Manjunatha N, Sadh K, Kalaivanan RC, Gowda GS, Basvaraju V, Harihara SN, Rao GN, Math can levitra be taken daily SB, Thirthalli J. Mental health care in Karnataka. Moving beyond the Bellary model of District Mental Health Program. Indian J Psychiatry 2021;63:212-4How can levitra be taken daily to cite this URL:Parthasarathy R, Channaveerachari NK, Manjunatha N, Sadh K, Kalaivanan RC, Gowda GS, Basvaraju V, Harihara SN, Rao GN, Math SB, Thirthalli J. Mental health care in Karnataka.

Moving beyond the Bellary model of District Mental Health Program. Indian J Psychiatry [serial online] can levitra be taken daily 2021 [cited 2021 Jul 27];63:212-4. Available from. Https://www.indianjpsychiatry.org/text.asp?. 2021/63/3/212/318719Karnataka state has taken many strides forward can levitra be taken daily with regard to the District Mental Health Program (DMHP) and is one of the few states to have dedicated DMHP psychiatrists as team leaders in all the districts.

Moreover, some of the recent developments have moved beyond the Bellary model and augur well for the nation. This article attempts to provide a summary of such developments in the state and discusses the future directions. Core Services DMHP in Karnataka offers (a) clinical services, including the outreach services (on a rotation can levitra be taken daily basis), covering the primary health centers (PHCs), community health centers, and taluk hospitals. (b) training of all the medical officers and other health professionals such as nurses and pharmacists of the district. (c) information, education, and communication (IEC) activities – posters, wall paintings in PHCs, IEC activities for schools, colleges, police personnel, judicial departments, elected representatives, faith healers, bus branding, radio talks, etc., In addition, sensitization of Anganwadi workers, accredited social health activists, auxiliary nurse midwives, police/prison staff, agriculture department/horticulture department/primary land development bank staff, village rehabilitation workers, staff of noncommunicable disease/revised National Tuberculosis Control Program, etc..

And (d) targeted interventions are being focused on life skills education and counseling in schools, college counseling services, workplace stress management, can levitra be taken daily and suicide prevention services. These initiatives have led to a phenomenal increase in patient footfalls to clinics [Figure 1] and >100,000 stakeholders are trained in various aspects of mental health (in the past 3 years).Figure 1. Chart showing the phenomenal increase in the number of footfalls covered over the past 3 yearsClick here to view Seamless Medication Availability The procurement has been streamlined. The state-level purchase is done by the Karnataka Drugs and Logistics Society, based can levitra be taken daily on the indents collated from each of the districts, and then, sent to their respective district warehouses. Individual indenters (taluk hospitals, community health centers, and primary health centers) then need to procure them from the district warehouses.

The amount spent for the purpose has gone up drastically to INR 3 crores (30 million rupees) in the past financial year (2017–2018). However, further streamlining is possible in can levitra be taken daily the sense that the delays can be further curtailed. The Collaboration with the Karnataka State Wakf Board The WAKF board of Karnataka runs a “Darga” in south interior Karnataka. Thousands of persons with mental illnesses do come over here for religious cure. On a day of every week, the attendance crosses 10,000 footfalls.

Recently, the authorities have agreed can levitra be taken daily to come up with an allopathic PHC inside the campus of the Darga. The idea is to have integrated and comprehensive care for patients without hurting their religious sentiments. Although such collaborative initiatives are spread across the country, this one is occurring at a larger scale with involvement of governmental agencies [Table 1].Table 1. Details of the key developments and innovations in mental health care in IndiaClick here to view Research Initiatives Although excellent evidence-based studies have come out in community settings, actual involvement of government machinery in these can levitra be taken daily kinds of initiatives is few and far. Their involvement is imperative for the evidence to become pragmatic and generalizable.

Of course, by doing so, the methodological rigor compromises a bit. NIMHANS and Government of Karnataka have been collaborating for such can levitra be taken daily service-driven research initiatives for over a decade and a half. Community-based interventions are going on in three taluks – Thirthahalli, Turuvekere, and Jagaluru, wherein cohorts of severe mental disorders are being cared for. In addition, several research questions (of public health significance) are being answered.[6],[7] Exciting new initiatives are also underway. Examining the magnitude of reduction of treatment gap by these community interventions, impact of care at doorsteps (CAD) can levitra be taken daily services from the DMHP machinery, impact of technology-based mentoring program for DMHP staff, evaluation of the impact of tele-OCT, etc.

Discussion and Future Directions All the above-mentioned activities in Karnataka take it beyond the Bellary model of DMHP. For example, the Memorandum of understanding (MOU) between NIMHANS and the state gives the flexibility and easy maneuverability for active collaboration. Odisha is another state which can levitra be taken daily has taken this path of MOU. This collaborative activity can be expanded pan India as there are several Centers of Excellence spread throughout India. Another aspect of the Karnataka story is collaborative research activity.

As described above, many activities going on across the state have the can levitra be taken daily potential to inform public health policies. Karnataka has also been able to counter long-standing and well-known criticisms of DMHP/NMHP. For example, issues related to human resources, availability of medications, funding, mentoring and monitoring, and sustenance, etc., at least to an extent. Of course, the state needs to can levitra be taken daily do much more for mental health care. For example, compliance with Mental Health Care Act-2017.

Handling unequal distribution of mental health human resources. Rigorous involvement of local administration to tackle micro-level can levitra be taken daily issues. Refining DMHP to suit special populations such as geriatric, children, and adolescents. And perinatal and upscaling urban DMHP, in areas such as Bengaluru Metropolitan City. Another area for improvement is that the DMHP evaluation strategies should move beyond head counting can levitra be taken daily and consider meaningful patient-related outcomes, including cost-effective analysis.

Digital technology should further be exploited. The upcoming Karnataka Mental Healthcare Management System is a step in the right direction.[8] Finally, the DMHP should involve health and wellness centers to cater to the mental health needs, particularly for follow-up services, case detection, providing basic counseling, stress management, advocating lifestyle changes, relapse prevention strategies, and other preventive and promotive strategies. References 1.Manjunatha N, Kumar CN, Chander KR, can levitra be taken daily Sadh K, Gowda GS, Vinay B, et al. Taluk Mental Health Program. The new kid on the block?.

Indian J can levitra be taken daily Psychiatry 2019;61:635-9. [PUBMED] [Full text] 2.Manjunatha N, Kumar CN, Math SB, Thirthalli J. Designing and implementing an innovative digitally driven primary care psychiatry program in India. Indian J can levitra be taken daily Psychiatry 2018;60:236-44. [PUBMED] [Full text] 3.Pahuja E, Santhosh KT, Fareeduzzafar, Manjunatha N, Kumar CK, Gupta R, et al.

An impact of digitally-driven Primary Care Psychiatry Pr. Indian J Psychiatry can levitra be taken daily 2020;62 Suppl 1:S17. 4.Manjunatha N, Singh G. Manochaitanya. Integrating mental can levitra be taken daily health into primary health care.

Lancet 2016;387:647-8. 5.Manjunatha N, Singh G, Chaturvedi SK. Manochaitanya programme for can levitra be taken daily better utilization of primary health centres. Indian J Med Res 2017;145:163-5. [PUBMED] [Full text] 6.Agarwal PP, Manjunatha N, Parthasarathy R, Kumar CN, Kelkar R, Math SB, et al.

A performance audit of first 30 months of Manochaitanya programme at secondary care level of can levitra be taken daily Karnataka, India. Indian J Community Med 2019;44:222-4. [PUBMED] [Full text] 7.Kumar CN, Thirthalli J, Suresha KK, Arunachala U, Gangadhar BN. Alcohol use disorders in patients with can levitra be taken daily schizophrenia. Comparative study with general population controls.

Addict Behav 2015;45:22-5. 8. Correspondence Address:Naveen Kumar ChannaveerachariDepartment of Psychiatry, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka IndiaSource of Support. None, Conflict of Interest. NoneDOI.

Om Prakash buy levitra canada online SinghProfessor of Psychiatry, WBMES. Consultant Psychiatrist, AMRI Hospitals, Kolkata, West Bengal, IndiaClick here for correspondence address and email Date of Submission11-Jun-2021Date of Decision11-Jun-2021Date of Acceptance11-Jun-2021Date of Web Publication17-Jun-2021 How to cite this article:Singh OP. Grief management in erectile dysfunction treatment.

Indian context buy levitra canada online. Indian J Psychiatry 2021;63:211Grief is a normal response to loss and bereavement. Human beings are aware of the concept of death and permanence of loss leading to grief and bereavement.

It may be seen buy levitra canada online in some other species also. While there has been a neurobiological mechanism explaining grief, it primarily remains a sociocultural phenomenon affecting the brain and the body. The perception of death followed by the gradual “sinking in” of its consequences leads to psychobiological reaction.

Grief which is unmanaged can lead to serious health reactions like increased cardiovascular mortality (broken heart) and psychiatric disorders like depression and suicide.erectile dysfunction treatment as an epidemic has brought grief buy levitra canada online and bereavement to the doorstep of each and every person. Constantly hearing, seeing about death, and losing friends and family has brought enormous strain to people's lives. Death rituals have a therapeutic function wherein they allow a family and a group to mourn in a ritualistic way.

This allows people to share grief and keep the buy levitra canada online deceased as focus of attention for a fixed time and then to move on with life. Sometimes, this process is hampered by what Kenneth Doka called “disenfranchised grief” in 1989 and defined it “as a process in which loss is felt as not being openly acknowledged, socially validated or publicly mourned.”[1] Externally imposed disenfranchised grief leads to grief remaining unresolved and unaddressed, and the person feels that his right to grieve has been denied.erectile dysfunction treatment has unexpectedly disturbed the process of death rituals as it leads to:Unexpected or sudden lossDepletion of emotional and coping resourcesLimitation in visiting and end of care supportNot able to perform last ritualsLack of social support due to erectile dysfunction treatment restrictions.[2]The mechanical and impersonal process has led to severe psychological trauma in the survivors, particularly in the early phase of the disease when the knowledge was less and health-care workers were burdened and under cover of personal protective equipment, communication was difficult. Realizing this, the Indian Council of Medical Research has come out with guidelines for health-care workers to deal with death and guide family members.

However, persistence of grief reaction remains a problem, and due to lack of social support due to erectile dysfunction treatment, people are increasingly relying on professionals to take care of their grief reactions.In India, the sharing of buy levitra canada online grief is very important. People try to reach the grieving family. So, what should be the model of care for these people?.

We should try to increase the sharing of grief and the handling of the person should be allowed to take placeThe buy levitra canada online physical support and the economical support have to be arranged, particularly where both parents have diedThere are some common modes like “condolence meetings” or “smaran sabha” which should be attended by both family members and colleagues.erectile dysfunction treatment has brought an unprecedented amount of grief, and it is our duty to manage grief with innovative solutions to prevent the emergence of prolonged grief reaction, depression, and suicide. References 1.Doka KJ, editor. Disenfranchised Grief.

New Directions, buy levitra canada online Challenges, and Strategies for Practice. Champaign, IL. Research Press.

2002. 2.Albuquerque S, Teixeira AM, Rocha JC. erectile dysfunction treatment and Disenfranchised Grief.

Front Psychiatry 2021;12:638874. Correspondence Address:Om Prakash SinghDepartment of Psychiatry, WBMES, Kolkata, West Bengal. AMRI Hospitals, Kolkata, West Bengal IndiaSource of Support.

None, Conflict of Interest. NoneDOI. 10.4103/indianjpsychiatry.indianjpsychiatry_489_21How to cite this article:Parthasarathy R, Channaveerachari NK, Manjunatha N, Sadh K, Kalaivanan RC, Gowda GS, Basvaraju V, Harihara SN, Rao GN, Math SB, Thirthalli J.

Mental health care in Karnataka. Moving beyond the Bellary model of District Mental Health Program. Indian J Psychiatry 2021;63:212-4How to cite this URL:Parthasarathy R, Channaveerachari NK, Manjunatha N, Sadh K, Kalaivanan RC, Gowda GS, Basvaraju V, Harihara SN, Rao GN, Math SB, Thirthalli J.

Mental health care in Karnataka. Moving beyond the Bellary model of District Mental Health Program. Indian J Psychiatry [serial online] 2021 [cited 2021 Jul 27];63:212-4.

Available from. Https://www.indianjpsychiatry.org/text.asp?. 2021/63/3/212/318719Karnataka state has taken many strides forward with regard to the District Mental Health Program (DMHP) and is one of the few states to have dedicated DMHP psychiatrists as team leaders in all the districts.

Moreover, some of the recent developments have moved beyond the Bellary model and augur well for the nation. This article attempts to provide a summary of such developments in the state and discusses the future directions. Core Services DMHP in Karnataka offers (a) clinical services, including the outreach services (on a rotation basis), covering the primary health centers (PHCs), community health centers, and taluk hospitals.

(b) training of all the medical officers and other health professionals such as nurses and pharmacists of the district. (c) information, education, and communication (IEC) activities – posters, wall paintings in PHCs, IEC activities for schools, colleges, police personnel, judicial departments, elected representatives, faith healers, bus branding, radio talks, etc., In addition, sensitization of Anganwadi workers, accredited social health activists, auxiliary nurse midwives, police/prison staff, agriculture department/horticulture department/primary land development bank staff, village rehabilitation workers, staff of noncommunicable disease/revised National Tuberculosis Control Program, etc.. And (d) targeted interventions are being focused on life skills education and counseling in schools, college counseling services, workplace stress management, and suicide prevention services.

These initiatives have led to a phenomenal increase in patient footfalls to clinics [Figure 1] and >100,000 stakeholders are trained in various aspects of mental health (in the past 3 years).Figure 1. Chart showing the phenomenal increase in the number of footfalls covered over the past 3 yearsClick here to view Seamless Medication Availability The procurement has been streamlined. The state-level purchase is done by the Karnataka Drugs and Logistics Society, based on the indents collated from each of the districts, and then, sent to their respective district warehouses.

Individual indenters (taluk hospitals, community health centers, and primary health centers) then need to procure them from the district warehouses. The amount spent for the purpose has gone up drastically to INR 3 crores (30 million rupees) in the past financial year (2017–2018). However, further streamlining is possible in the sense that the delays can be further curtailed.

The Collaboration with the Karnataka State Wakf Board The WAKF board of Karnataka runs a “Darga” in south interior Karnataka. Thousands of persons with mental illnesses do come over here for religious cure. On a day of every week, the attendance crosses 10,000 footfalls.

Recently, the authorities have agreed to come up with an allopathic PHC inside the campus of the Darga. The idea is to have integrated and comprehensive care for patients without hurting their religious sentiments. Although such collaborative initiatives are spread across the country, this one is occurring at a larger scale with involvement of governmental agencies [Table 1].Table 1.

Details of the key developments and innovations in mental health care in IndiaClick here to view Research Initiatives Although excellent evidence-based studies have come out in community settings, actual involvement of government machinery in these kinds of initiatives is few and far. Their involvement is imperative for the evidence to become pragmatic and generalizable. Of course, by doing so, the methodological rigor compromises a bit.

NIMHANS and Government of Karnataka have been collaborating for such service-driven research initiatives for over a decade and a half. Community-based interventions are going on in three taluks – Thirthahalli, Turuvekere, and Jagaluru, wherein cohorts of severe mental disorders are being cared for. In addition, several research questions (of public health significance) are being answered.[6],[7] Exciting new initiatives are also underway.

Examining the magnitude of reduction of treatment gap by these community interventions, impact of care at doorsteps (CAD) services from the DMHP machinery, impact of technology-based mentoring program for DMHP staff, evaluation of the impact of tele-OCT, etc. Discussion and Future Directions All the above-mentioned activities in Karnataka take it beyond the Bellary model of DMHP. For example, the Memorandum of understanding (MOU) between NIMHANS and the state gives the flexibility and easy maneuverability for active collaboration.

Odisha is another state which has taken this path of MOU. This collaborative activity can be expanded pan India as there are several Centers of Excellence spread throughout India. Another aspect of the Karnataka story is collaborative research activity.

As described above, many activities going on across the state have the potential to inform public health policies. Karnataka has also been able to counter long-standing and well-known criticisms of DMHP/NMHP. For example, issues related to human resources, availability of medications, funding, mentoring and monitoring, and sustenance, etc., at least to an extent.

Of course, the state needs to do much more for mental health care. For example, compliance with Mental Health Care Act-2017. Handling unequal distribution of mental health human resources.

Rigorous involvement of local administration to tackle micro-level issues. Refining DMHP to suit special populations such as geriatric, children, and adolescents. And perinatal and upscaling urban DMHP, in areas such as Bengaluru Metropolitan City.

Another area for improvement is that the DMHP evaluation strategies should move beyond head counting and consider meaningful patient-related outcomes, including cost-effective analysis. Digital technology should further be exploited. The upcoming Karnataka Mental Healthcare Management System is a step in the right direction.[8] Finally, the DMHP should involve health and wellness centers to cater to the mental health needs, particularly for follow-up services, case detection, providing basic counseling, stress management, advocating lifestyle changes, relapse prevention strategies, and other preventive and promotive strategies.

References 1.Manjunatha N, Kumar CN, Chander KR, Sadh K, Gowda GS, Vinay B, et al. Taluk Mental Health Program. The new kid on the block?.

Indian J Psychiatry 2019;61:635-9. [PUBMED] [Full text] 2.Manjunatha N, Kumar CN, Math SB, Thirthalli J. Designing and implementing an innovative digitally driven primary care psychiatry program in India.

Indian J Psychiatry 2018;60:236-44. [PUBMED] [Full text] 3.Pahuja E, Santhosh KT, Fareeduzzafar, Manjunatha N, Kumar CK, Gupta R, et al. An impact of digitally-driven Primary Care Psychiatry Pr.

Indian J Psychiatry 2020;62 Suppl 1:S17. 4.Manjunatha N, Singh G. Manochaitanya.

Integrating mental health into primary health care. Lancet 2016;387:647-8. 5.Manjunatha N, Singh G, Chaturvedi SK.

Manochaitanya programme for better utilization of primary health centres. Indian J Med Res 2017;145:163-5. [PUBMED] [Full text] 6.Agarwal PP, Manjunatha N, Parthasarathy R, Kumar CN, Kelkar R, Math SB, et al.

A performance audit of first 30 months of Manochaitanya programme at secondary care level of Karnataka, India. Indian J Community Med 2019;44:222-4. [PUBMED] [Full text] 7.Kumar CN, Thirthalli J, Suresha KK, Arunachala U, Gangadhar BN.

Alcohol use disorders in patients with schizophrenia. Comparative study with general population controls. Addict Behav 2015;45:22-5.

8. Correspondence Address:Naveen Kumar ChannaveerachariDepartment of Psychiatry, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka IndiaSource of Support.

Buy cheap levitra uk

How to cite buy cheap levitra uk this article:Singh O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity buy cheap levitra uk 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 as newspapers, news channels, and social media were full of stories providing minute details of the buy cheap levitra uk 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 actor were besmirched and their private and personal details were freely and blatantly broadcast and buy cheap levitra uk 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 buy cheap levitra uk started getting distress calls from 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 Suicide buy cheap levitra uk.

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 buy cheap levitra uk of 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 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 buy cheap levitra uk 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 houses buy cheap levitra uk 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 buy cheap levitra uk 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 buy cheap levitra uk the time 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 buy cheap levitra uk societies have guidelines and resource books for interacting with media, and psychiatrists should familiarize 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 be assumed that no statement goes “off the record” as the media person is most likely recording buy cheap levitra uk 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, Kolkata - 700 094, West buy cheap levitra uk 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.

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Neuropsychopharmacology 2003;28:720-5. 36.Pfleiderer B, Michael N, Erfurth A, Ohrmann P, Hohmann U, Wolgast M, et al. Effective electroconvulsive therapy reverses glutamate/glutamine deficit in the left anterior cingulum of unipolar depressed patients. Psychiatry Res 2003;122:185-92.

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Biol Psychiatry 1996;39:346-56. 76.Berggren Š, Gustafson L, Höglund P, Johanson A. A long-term longitudinal follow-up of depressed patients treated with ECT with special focus on development of dementia. J Affect Disord 2016;200:15-24.

77.Brodaty H, Hickie I, Mason C, Prenter L. A prospective follow-up study of ECT outcome in older depressed patients. J Affect Disord 2000;60:101-11. 78.Osler M, Rozing MP, Christensen GT, Andersen PK, Jørgensen MB.

Electroconvulsive therapy and risk of dementia in patients with affective disorders. 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 buy levitra canada online cite this http://abelvettes.com/?page_id=2 article:Singh O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide buy levitra canada online 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 buy levitra canada online 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 actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, buy levitra canada online 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 their patients in buy levitra canada online 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 buy levitra canada online 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 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 buy levitra canada online 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 levitra canada online 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 houses to buy levitra canada online 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 addition to doing harm and injustice to buy levitra canada online 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 should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” buy levitra canada online 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 buy levitra canada online familiarize 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 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 buy levitra canada online 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, buy levitra canada online Patuli Township, 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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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].