Online doctor ventolin

Date published online doctor ventolin check my source. May 7, 2021On this page Purpose and backgroundHealth Canada regulates the sale and import of medical devices, including commercial testing devices related to asthma treatment.As noted elsewhere, Health Canada has made it a priority to review applications for asthma treatment devices that meet an urgent public health need in Canada. These devices are needed immediately to protect or improve the health of Canadians, whether at the individual or community level.The purpose online doctor ventolin of this notice is to communicate the types of testing technologies that Health Canada considers are a priority for review.Only commercial testing devices that we have authorized can be advertised, imported or sold in Canada. Unauthorized tests may not produce accurate results, leading to potential misdiagnosis. Authorized asthma treatment tests are well supported by evidence that shows they will provide accurate and reliable results.Technologies that are a priorityWorking with our public health partners, we have identified the following testing technologies as being online doctor ventolin of the highest priority for evaluation at this time.

Self-testing devices point-of-care antigen or molecular testing devices that use nasal swab or saliva samples for use in symptomatic and asymptomatic populations administered by trained operators (rather than health care professionals) asymptomatic populations are people who do not display asthma treatment symptoms at the time of testing (see the guide on asthma treatment signs, symptoms and severity of disease) to add to clinical trial populations, asymptomatic people may include those who have recently had contact with someone diagnosed with asthma treatment (applicants are encouraged to contact us before designing a clinical trial to ensure appropriate populations are included and adequately characterized) We welcome new applications for these types of tests, as well as applications to amend authorized tests to include these new features.Applicants should provide direct evidence or scientific justification if appropriate. Scientific justification could include scientific articles on the performance of an applicant's device or highly similar device by trained operators, or in sample asymptomatic populations.Applicants are invited to consider strategies to strengthen the performance of their device for its claimed indications. Strategies may online doctor ventolin include. Serial testing strategies paired testing strategies clarification of how the intended purpose of the testing device meets specific public health goalsThese strategies could likewise be supported by direct evidence or scientific justification, if appropriate.Other technologies that are a priority include. Point-of-care antigen tests that do not use only nasopharyngeal (NP) swab samples, or may be used in asymptomatic people or may be administered by trained operators point-of-care molecular tests that do not use only NP swab samples, or may be used in asymptomatic people or may be administered by trained operators tests designed to address emerging variants tests that offer new or unique advantages compared to other tests of the same type novel diagnostic technologies that may use alternative samples, such as breath, or a different analytical approachWe may review the types of applications or tests that we are prioritizing at any time to ensure our focus continues to reflects Canadian public health priorities.Technologies that are not prioritized for reviewTo ensure that the number and types of authorized testing technologies is aligned with the public health need, Health Canada has been online doctor ventolin prioritizing certain tests.

Given the number of tests already authorized, as well as current public health needs, the following testing technologies are now considered to be of less priority. Lab-based molecular tests that do not use saliva samples or otherwise offer new or unique advantages point-of-care online doctor ventolin antigen or molecular tests that use only NP swab samples lab-based and point-of-care serology testsThis means that these files will be advanced as quickly as can be enabled once the priority tests have been addressed. Identifying a file as being of lower priority may occur at any point after we receive an application. Often, when we "deprioritize" a file, it means that we will address such applications while we wait for information from an applicant for a priority test. Thus, it will take online doctor ventolin us longer to process applications for deprioritized tests than for priority tests.Access to testing devices for asthma treatmentEarly diagnosis is critical to slowing and reducing the spread of asthma treatment in Canada.

As part of the government's broad response to the ventolin, Health Canada introduced a number of agile regulatory measures to expedite the regulatory review of asthma treatment health products. These measures do not compromise Canada's safety, online doctor ventolin efficacy and quality standards. We are committed to getting Canadians access to the tools they need to fight the spread of asthma treatment in Canada.We have authorized a number of asthma treatment tests and continue to expedite the review of testing device submissions. For more information on the authorization process for asthma treatment testing devices, please consult testing devices for asthma treatment..

How to use ventolin respirator solution

#masthead-section-label, #masthead-bar-one how to use ventolin respirator solution Zithromax cost walmart { display. None }asthma treatmentstreatment QuestionsWhich States are Increasing AccessRollout by StateHow 9 treatments WorkAdvertisementContinue reading the main storySupported byContinue reading the main storyAsk WellWhat You Can Do to Avoid the New asthma Variant Right NowIt’s more contagious than the original how to use ventolin respirator solution and spreading quickly. Upgrade your mask and double down on precautions to protect yourself.Credit...Getty ImagesJan. 19, 2021Leer en españolNew variants how to use ventolin respirator solution of the asthma continue to emerge.

But one in particular has caused concern in the United States because it’s so contagious and spreading fast. To avoid it, you’ll need to double down on the same ventolin precautions that have how to use ventolin respirator solution kept you safe so far.The variant known as B.1.1.7., which was first identified in Britain, doesn’t appear to cause more severe disease, but it has the potential to infect an estimated 50 percent more people. The Centers for Disease Control and Prevention has predicted that this variant could become the dominant source of in the United States by March. Variants with how to use ventolin respirator solution the same mutation have been reported in Brazil and South Africa, and now scientists are studying whether a variant with a different mutation, and first found in Denmark, along with one identified in California, have caused a surge of cases in California.The new variant spreading in the United States appears to latch onto our cells more efficiently.

(You can find a detailed look inside the variant here.) The change suggests it could take less ventolin and less time in the same room with an infected person for someone to become ill. People infected with the variant may also shed larger quantities of ventolin, how to use ventolin respirator solution which increases the risk to people around them.“The exact mechanism in which it’s more transmissible isn’t entirely known,” said Nathan D. Grubaugh, assistant professor and epidemiologist at the Yale School of Public Health. €œIt might just be that when you’re infected, you’re exhaling more infectious how to use ventolin respirator solution ventolin.”So how do you avoid a more contagious version of the asthma?.

I spoke with some of the leading ventolin and infectious disease experts about what makes the new variant so worrisome and what we can do about it. Here’s what they had to say.How can how to use ventolin respirator solution I protect myself from the new asthma variant?. The variant spreads the same way the asthma has always spread. You’re most likely to contract the ventolin if you spend time in an enclosed space breathing the air of how to use ventolin respirator solution an infected person.

The same things that have protected you from the original strain should help protect you from the variant, although you may need to be more rigorous. Wear a two- or how to use ventolin respirator solution three-layer mask. Don’t spend time indoors with people not from your household. Avoid crowds, how to use ventolin respirator solution and keep your distance.

Wash your hands often, and avoid touching your face.“The first thing I say to people is that it’s not a different ventolin. All the things we have learned how to use ventolin respirator solution about this ventolin still apply,” said Dr. Ashish K. Jha, dean of the how to use ventolin respirator solution Brown University School of Public Health.

€œIt’s not like this variant is somehow magically spreading through other means. Anything risky under how to use ventolin respirator solution the normal strain just becomes riskier with the variant.”And let’s face it, after months of ventolin living, many of us have become lax about our asthma treatment safety precautions. Maybe you’ve let down your guard, and you’re spending time indoors and unmasked with trusted friends. Or perhaps you’ve been dining in restaurants or making more trips to how to use ventolin respirator solution the grocery store each week than you did at the start of lockdowns.

The arrival of the variant means you should try to cut back on potential exposures where you can and double down on basic precautions for the next few months until you and the people around you get vaccinated.“The more I hear about the new variants, the more concerned I am,” said Linsey Marr, professor of civil and environmental engineering at Virginia Tech and one of the world’s leading aerosol scientists. €œI think there how to use ventolin respirator solution is no room for error or sloppiness in following precautions, whereas before, we might have been able to get away with letting one slide.”Should I upgrade my mask?. You should be wearing a high-quality mask when you run errands, go shopping or find yourself in a situation where you’re spending time indoors with people who don’t live with you, Dr. Marr said how to use ventolin respirator solution.

€œI am how to use ventolin respirator solution now wearing my best mask when I go to the grocery store,” she said. €œThe last thing I want to do is get asthma treatment in the month before I get vaccinated.”Dr. Marr’s lab recently tested 11 mask materials and found that the right cloth mask, properly fitted, does a good job of filtering viral how to use ventolin respirator solution particles of the size most likely to cause . The best mask has three layers — two cloth layers with a filter sandwiched in between.

Masks should be how to use ventolin respirator solution fitted around the bridge of the nose and made of flexible material to reduce gaps. Head ties create a better fit than ear loops..css-c7gg1r{font-family:nyt-franklin,helvetica,arial,sans-serif;font-weight:700;font-size:0.875rem;line-height:0.875rem;margin-bottom:15px;color:#121212 !. Important;}@media (min-width:740px){.css-c7gg1r{font-size:0.9375rem;line-height:0.9375rem;}}.css-1sjr751{-webkit-text-decoration:none;text-decoration:none;}.css-1sjr751 a:hover{border-bottom:1px solid #dcdcdc;}.css-yoay6m{margin:0 auto 5px;font-family:nyt-franklin,helvetica,arial,sans-serif;font-weight:700;font-size:1.125rem;line-height:1.3125rem;color:#121212;}@media (min-width:740px){.css-yoay6m{font-size:1.25rem;line-height:1.4375rem;}}.css-1dg6kl4{margin-top:5px;margin-bottom:15px;}.css-k59gj9{display:-webkit-box;display:-webkit-flex;display:-ms-flexbox;display:flex;-webkit-flex-direction:column;-ms-flex-direction:column;flex-direction:column;width:100%;}.css-1e2usoh{font-family:inherit;display:-webkit-box;display:-webkit-flex;display:-ms-flexbox;display:flex;-webkit-box-pack:justify;-webkit-justify-content:space-between;-ms-flex-pack:justify;justify-content:space-between;border-top:1px solid #ccc;padding:10px 0px 10px 0px;background-color:#fff;}.css-1jz6h6z{font-family:inherit;font-weight:bold;font-size:1rem;line-height:1.5rem;text-align:left;}.css-1t412wb{box-sizing:border-box;margin:8px 15px 0px 15px;cursor:pointer;}.css-hhzar2{-webkit-transition:-webkit-transform ease 0.5s;-webkit-transition:transform ease 0.5s;transition:transform ease 0.5s;}.css-t54hv4{-webkit-transform:rotate(180deg);-ms-transform:rotate(180deg);transform:rotate(180deg);}.css-1r2j9qz{-webkit-transform:rotate(0deg);-ms-transform:rotate(0deg);transform:rotate(0deg);}.css-e1ipqs{font-size:1rem;line-height:1.5rem;padding:0px 30px 0px 0px;}.css-e1ipqs a{color:#326891;-webkit-text-decoration:underline;text-decoration:underline;}.css-e1ipqs a:hover{-webkit-text-decoration:none;text-decoration:none;}.css-1o76pdf{visibility:show;height:100%;padding-bottom:20px;}.css-1sw9s96{visibility:hidden;height:0px;}#masthead-bar-one{display:none;}#masthead-bar-one{display:none;}.css-1prex18{background-color:white;border:1px solid #e2e2e2;width:calc(100% - 40px);max-width:600px;margin:1.5rem auto 1.9rem;padding:15px;font-family:'nyt-franklin',arial,helvetica,sans-serif;text-align:left;}@media (min-width:740px){.css-1prex18{padding:20px;}}.css-1prex18:focus{outline:1px how to use ventolin respirator solution solid #e2e2e2;}asthma treatments ›Answers to Your treatment QuestionsWhile the exact order of treatment recipients may vary by state, most will likely put medical workers and residents of long-term care facilities first. If you want to understand how this decision is getting made, this article will help.Life will return to normal only when society as a whole gains enough protection against the asthma.

Once countries how to use ventolin respirator solution authorize a treatment, they’ll only be able to vaccinate a few percent of their citizens at most in the first couple months. The unvaccinated majority will still remain vulnerable to getting infected. A growing number of asthma treatments are showing how to use ventolin respirator solution robust protection against becoming sick. But it’s also possible for people to spread the ventolin without even knowing they’re infected because they experience only mild symptoms or none at all.

Scientists don’t yet know if the how to use ventolin respirator solution treatments also block the transmission of the asthma. So for the time being, even vaccinated people will need to wear masks, avoid indoor crowds, and so on. Once enough people get vaccinated, it will become very difficult for the asthma to how to use ventolin respirator solution find vulnerable people to infect. Depending on how quickly we as a society achieve that goal, life might start approaching something like normal by the fall 2021.Yes, but not forever.

The two treatments that will potentially get authorized this month clearly protect people from getting how to use ventolin respirator solution sick with asthma treatment. But the clinical trials that delivered these results were not designed to determine whether vaccinated people could still spread the asthma without developing symptoms. That remains a possibility how to use ventolin respirator solution. We know that people who are naturally infected by the asthma can spread it while they’re not experiencing any cough or other symptoms.

Researchers will be intensely studying how to use ventolin respirator solution this question as the treatments roll out. In the meantime, even vaccinated people will need to think of themselves as possible spreaders.The Pfizer and BioNTech treatment is delivered as a shot in the arm, like other typical treatments. The injection won’t be any different from ones you’ve gotten how to use ventolin respirator solution before. Tens of thousands of people have already received the treatments, and none of them have reported any serious health problems.

But some of them have felt short-lived discomfort, including aches how to use ventolin respirator solution and flu-like symptoms that typically last a day. It’s possible that people may need to plan to take a day off work or school after the second shot. While these experiences how to use ventolin respirator solution aren’t pleasant, they are a good sign. They are the result of your own immune system encountering the treatment and mounting a potent response that will provide long-lasting immunity.No.

The treatments from Moderna and Pfizer use a genetic molecule to prime the how to use ventolin respirator solution immune system. That molecule, known as mRNA, is eventually destroyed by the body. The mRNA is packaged in an oily bubble that can fuse how to use ventolin respirator solution to a cell, allowing the molecule to slip in. The cell uses the mRNA to how to use ventolin respirator solution make proteins from the asthma, which can stimulate the immune system.

At any moment, each of our cells may contain hundreds of thousands of mRNA molecules, which they produce in order to make proteins of their own. Once those proteins are made, our how to use ventolin respirator solution cells then shred the mRNA with special enzymes. The mRNA molecules our cells make can only survive a matter of minutes. The mRNA in treatments is engineered to how to use ventolin respirator solution withstand the cell's enzymes a bit longer, so that the cells can make extra ventolin proteins and prompt a stronger immune response.

But the mRNA can only last for a few days at most before they are destroyed.If you don’t want to buy a new mask, a simple solution is to wear an additional mask when you find yourself in closer proximity to strangers. I wear a single mask when I how to use ventolin respirator solution walk my dog or exercise outdoors. But if I’m going to a store, taking a taxi or getting in the subway, I double mask by using a disposable surgical mask and covering it with my cloth mask.Do I need an N95 medical mask?. While medical workers who come into close contact with sick patients rely on the gold-standard N95 masks, you don’t need that level of protection if you’re avoiding group gatherings, limiting shopping trips and keeping your distance from others.“N95s are hard to get,” said how to use ventolin respirator solution Dr.

Jha. €œI don’t how to use ventolin respirator solution think people should think that’s what they need. Certainly there are a lot of masks out in the marketplace that are pretty good.”If you’re working in an office or grocery store, or find yourself in a situation where you want added mask protection, you can get an alternative to the N95. Dr.

Jha suggested using a KF94 mask, a type of mask made in South Korea that can be purchased easily online. It resembles an N95, with some differences. It’s made of a similar nonwoven material that blocks 94 percent of the hardest-to-trap viral particles. But the KF94 has ear loops, instead of elastic head bands, so it won’t fit as snugly as an N95.The KF94 is also disposable — you can buy a pack of 20 for about $40 on Amazon.

While you can let a KF94 mask air dry and reuse it a few times, it can’t be laundered and won’t last as long as a cloth mask. One solution is to save your KF94 mask for higher-risk situations — like riding a subway, spending time in a store or going to a doctor’s appointment. Use your cloth mask for outdoor errands, exercise or walking the dog.Are there additional ways to reduce my risk?. Getting the treatment is the ultimate way to reduce risk.

But until then, take a look at your activities and try reducing the time and number of exposures to other people.For instance, if you now go to the store two or three times a week, cut back to just once a week. If you’ve been spending 30 to 45 minutes in the grocery store, cut your time down to 15 or 20 minutes. If the store is crowded, come back later. If you’re waiting in line, be mindful of staying at least six feet apart from the people ahead of you and behind you.

Try delivery or curbside pickup, if that’s an option for you.If you’ve been spending time indoors with other people who aren’t from your household, consider skipping those events until you and your friends get vaccinated. If you must spend time with others, wear your best mask, make sure the space is well ventilated (open windows and doors) and keep the visit as short as possible. It’s still safest to take your social plans outdoors. And if you are thinking about air travel, it’s a good idea to reschedule given the high number of cases around the country and the emergence of the more contagious variant.“The new variants are making me think twice about my plan to teach in-person, which would have been with masks and with good ventilation anyway,” Dr.

Marr said. €œThey’re making me think twice about getting on an airplane.”Will the current asthma treatments work against the new variants?. Experts are cautiously optimistic that the current generation of treatments will be mostly effective against the emerging asthma variants. Earlier this month, Pfizer and BioNTech announced that their asthma treatment works against one of the key mutations present in some of the variants.

That’s good news, but the variants have other potentially risky mutations that haven’t been studied yet.Some data also suggest that variants with certain mutations may be more resistant to the treatments, but far more study is needed and those variants haven’t yet been detected in the United States. While the data are concerning, experts said the current treatments generate extremely high levels of antibodies, and they are likely to at least prevent serious illness in people who are immunized and get infected.“The reason why I’m cautiously optimistic is that from what we know about how treatments work, it’s not just one antibody that provides all the protection,” said Dr. Adam Lauring, associate professor of infectious disease at the University of Michigan. €œWhen you get vaccinated you generate antibodies all over the spike protein.

That makes it less likely that one mutation here or there is going to leave you completely unprotected. That’s what gives me reason for optimism that this is going to be OK in terms of the treatment, but there’s more work to be done.”If I catch asthma treatment, will I know if I have the new variant?. Probably not. If you test positive for the asthma, the standard PCR test can’t definitively determine if you have the variant or the original strain.

While some PCR test results can signal if a person is likely to be infected with a variant, that information probably won’t be shared with patients. The only way to know for sure which variant is circulating is to use gene sequencing technology, but that technology is not used to alert individuals of their status. While some public health and university laboratories are using genomic surveillance to track the prevalence of variants in a community, the United States doesn’t yet have a large-scale, nationwide system for checking asthma genomes for new mutations.Treatment for asthma treatment is the same whether you have the original strain or the variant. You can read more about what to do if you get infected here.Are children more at risk from the new variant?.

Children appear to get infected with the variant at about the same rate as the original strain. A large study by health officials in Britain found that young children are only about half as likely as adults to transmit the variant to others. While that’s good news, the highly contagious nature of the variant means more children will get the ventolin, even if they are still proportionately less contagious and less prone to getting infected than adults. You can learn more here.If I’ve already had asthma treatment, am I likely to have the same level of immunity to the new strain?.

Most experts agree that once you’ve had asthma treatment, your body has some level of natural immunity to help fight off a second — although it’s not known how long the protection lasts. The variants circulating in Brazil and South Africa appear to have mutations that allow the ventolin to evade natural antibodies and reinfect someone who has already had the ventolin. The concern is based on lab tests using antibodies of people with a previous , so whether that translates to more res in the real world isn’t known. The effect of the treatment against these variants isn’t known yet either.

While all of this sounds frightening, scientists are hopeful that even if the treatments don’t fully protect against new variations of the ventolin, the antibodies generated by the treatment still will protect people from more serious illness.AdvertisementContinue reading the main storyAdvertisementContinue reading the main storySupported byContinue reading the main storyThe Toll of Fried Foods on Heart HealthEating fried foods increased the risk of heart disease, stroke, heart failure and premature death.Credit...Max Whittaker for The New York TimesJan. 22, 2021Most of us know that a diet rich in fried foods is bad for us. A review of studies quantifies just how bad it can be.In a meta-analysis of 19 studies that included diet and health data on more than 1.2 million men and women from around the world, Chinese researchers calculated the effect of eating French fries, fried fish, fried snacks and other fried foods on cardiovascular health.Comparing the groups with the highest intake of fried food with people who ate the least over an average period of nine years, they found that high consumption of fried foods increased the relative risk for coronary heart disease by 22 percent. For stroke by 37 percent.

For heart failure by 37 percent. For death from cardiovascular disease by 2 percent. And for death from any cause by 3 percent.The analysis, in the journal Heart, found no evidence that one kind of fried food was any better than another. Using the combined data, the researchers calculated that each additional weekly 114-gram (about 4-ounce) serving of fried food increases the risk for heart failure by 12 percent and for a major cardiovascular event by 3 percent.The Dietary Guidelines for Americans discourages fried food consumption, but it offers no specific limits on amounts in a healthy diet.The senior author, Dr.

Fulan Hu of the Shenzhen University Health Science Center in Shenzhen, China, offered this advice. €œReduce restaurant meals. Reduce fast-food intake. Use healthier boiling, steaming, baking or grilling cooking methods instead of frying for home-cooked food.”AdvertisementContinue reading the main story.

#masthead-section-label, #masthead-bar-one Zithromax cost walmart { display online doctor ventolin. None }asthma treatmentstreatment online doctor ventolin QuestionsWhich States are Increasing AccessRollout by StateHow 9 treatments WorkAdvertisementContinue reading the main storySupported byContinue reading the main storyAsk WellWhat You Can Do to Avoid the New asthma Variant Right NowIt’s more contagious than the original and spreading quickly. Upgrade your mask and double down on precautions to protect yourself.Credit...Getty ImagesJan. 19, 2021Leer online doctor ventolin en españolNew variants of the asthma continue to emerge. But one in particular has caused concern in the United States because it’s so contagious and spreading fast.

To avoid it, you’ll need to double down on the same ventolin precautions that have kept online doctor ventolin you safe so far.The variant known as B.1.1.7., which was first identified in Britain, doesn’t appear to cause more severe disease, but it has the potential to infect an estimated 50 percent more people. The Centers for Disease Control and Prevention has predicted that this variant could become the dominant source of in the United States by March. Variants with the same mutation have been reported in Brazil and South Africa, and now scientists are studying whether a variant with a different mutation, and first found in online doctor ventolin Denmark, along with one identified in California, have caused a surge of cases in California.The new variant spreading in the United States appears to latch onto our cells more efficiently. (You can find a detailed look inside the variant here.) The change suggests it could take less ventolin and less time in the same room with an infected person for someone to become ill. People infected with the variant may also shed larger quantities of ventolin, which increases the risk to people around them.“The exact mechanism in which it’s online doctor ventolin more transmissible isn’t entirely known,” said Nathan D.

Grubaugh, assistant professor and epidemiologist at the Yale School of Public Health. €œIt might just be that when you’re online doctor ventolin infected, you’re exhaling more infectious ventolin.”So how do you avoid a more contagious version of the asthma?. I spoke with some of the leading ventolin and infectious disease experts about what makes the new variant so worrisome and what we can do about it. Here’s what they had to say.How can I online doctor ventolin protect myself from the new asthma variant?. The variant spreads the same way the asthma has always spread.

You’re most likely to contract the ventolin if you spend time in an enclosed space breathing the air of online doctor ventolin an infected person. The same things that have protected you from the original strain should help protect you from the variant, although you may need to be more rigorous. Wear a two- or three-layer online doctor ventolin mask. Don’t spend time indoors with people not from your household. Avoid crowds, and keep your online doctor ventolin distance.

Wash your hands often, and avoid touching your face.“The first thing I say to people is that it’s not a different ventolin. All the things we have learned about this ventolin online doctor ventolin still apply,” said Dr. Ashish K. Jha, dean of online doctor ventolin the Brown University School of Public Health. €œIt’s not like this variant is somehow magically spreading through other means.

Anything risky under the normal strain just becomes riskier with the variant.”And let’s face it, after months of ventolin living, many of online doctor ventolin us have become lax about our asthma treatment safety precautions. Maybe you’ve let down your guard, and you’re spending time indoors and unmasked with trusted friends. Or perhaps you’ve been dining in restaurants online doctor ventolin or making more trips to the grocery store each week than you did at the start of lockdowns. The arrival of the variant means you should try to cut back on potential exposures where you can and double down on basic precautions for the next few months until you and the people around you get vaccinated.“The more I hear about the new variants, the more concerned I am,” said Linsey Marr, professor of civil and environmental engineering at Virginia Tech and one of the world’s leading aerosol scientists. €œI think there is no room for error online doctor ventolin or sloppiness in following precautions, whereas before, we might have been able to get away with letting one slide.”Should I upgrade my mask?.

You should be wearing a high-quality mask when you run errands, go shopping or find yourself in a situation where you’re spending time indoors with people who don’t live with you, Dr. Marr said online doctor ventolin. €œI am now wearing my best online doctor ventolin mask when I go to the grocery store,” she said. €œThe last thing I want to do is get asthma treatment in the month before I get vaccinated.”Dr. Marr’s lab recently tested 11 mask materials and found that the right cloth mask, properly fitted, does a good job of filtering online doctor ventolin viral particles of the size most likely to cause .

The best mask has three layers — two cloth layers with a filter sandwiched in between. Masks should be fitted around the bridge of the nose and made of flexible material to reduce online doctor ventolin gaps. Head ties create a better fit than ear loops..css-c7gg1r{font-family:nyt-franklin,helvetica,arial,sans-serif;font-weight:700;font-size:0.875rem;line-height:0.875rem;margin-bottom:15px;color:#121212 !. Important;}@media (min-width:740px){.css-c7gg1r{font-size:0.9375rem;line-height:0.9375rem;}}.css-1sjr751{-webkit-text-decoration:none;text-decoration:none;}.css-1sjr751 a:hover{border-bottom:1px solid #dcdcdc;}.css-yoay6m{margin:0 auto 5px;font-family:nyt-franklin,helvetica,arial,sans-serif;font-weight:700;font-size:1.125rem;line-height:1.3125rem;color:#121212;}@media (min-width:740px){.css-yoay6m{font-size:1.25rem;line-height:1.4375rem;}}.css-1dg6kl4{margin-top:5px;margin-bottom:15px;}.css-k59gj9{display:-webkit-box;display:-webkit-flex;display:-ms-flexbox;display:flex;-webkit-flex-direction:column;-ms-flex-direction:column;flex-direction:column;width:100%;}.css-1e2usoh{font-family:inherit;display:-webkit-box;display:-webkit-flex;display:-ms-flexbox;display:flex;-webkit-box-pack:justify;-webkit-justify-content:space-between;-ms-flex-pack:justify;justify-content:space-between;border-top:1px solid #ccc;padding:10px 0px 10px 0px;background-color:#fff;}.css-1jz6h6z{font-family:inherit;font-weight:bold;font-size:1rem;line-height:1.5rem;text-align:left;}.css-1t412wb{box-sizing:border-box;margin:8px 15px 0px 15px;cursor:pointer;}.css-hhzar2{-webkit-transition:-webkit-transform ease 0.5s;-webkit-transition:transform ease 0.5s;transition:transform ease 0.5s;}.css-t54hv4{-webkit-transform:rotate(180deg);-ms-transform:rotate(180deg);transform:rotate(180deg);}.css-1r2j9qz{-webkit-transform:rotate(0deg);-ms-transform:rotate(0deg);transform:rotate(0deg);}.css-e1ipqs{font-size:1rem;line-height:1.5rem;padding:0px 30px 0px 0px;}.css-e1ipqs a{color:#326891;-webkit-text-decoration:underline;text-decoration:underline;}.css-e1ipqs a:hover{-webkit-text-decoration:none;text-decoration:none;}.css-1o76pdf{visibility:show;height:100%;padding-bottom:20px;}.css-1sw9s96{visibility:hidden;height:0px;}#masthead-bar-one{display:none;}#masthead-bar-one{display:none;}.css-1prex18{background-color:white;border:1px solid #e2e2e2;width:calc(100% - 40px);max-width:600px;margin:1.5rem auto 1.9rem;padding:15px;font-family:'nyt-franklin',arial,helvetica,sans-serif;text-align:left;}@media (min-width:740px){.css-1prex18{padding:20px;}}.css-1prex18:focus{outline:1px solid #e2e2e2;}asthma treatments ›Answers online doctor ventolin to Your treatment QuestionsWhile the exact order of treatment recipients may vary by state, most will likely put medical workers and residents of long-term care facilities first. If you want to understand how this decision is getting made, this article will help.Life will return to normal only when society as a whole gains enough protection against the asthma.

Once countries authorize a treatment, they’ll only be able to online doctor ventolin vaccinate a few percent of their citizens at most in the first couple months. The unvaccinated majority will still remain vulnerable to getting infected. A growing online doctor ventolin number of asthma treatments are showing robust protection against becoming sick. But it’s also possible for people to spread the ventolin without even knowing they’re infected because they experience only mild symptoms or none at all. Scientists don’t yet know if the treatments also block the transmission of online doctor ventolin the asthma.

So for the time being, even vaccinated people will need to wear masks, avoid indoor crowds, and so on. Once enough people get vaccinated, it will become online doctor ventolin very difficult for the asthma to find vulnerable people to infect. Depending on how quickly we as a society achieve that goal, life might start approaching something like normal by the fall 2021.Yes, but not forever. The two treatments that will potentially get authorized this month clearly protect online doctor ventolin people from getting sick with asthma treatment. But the clinical trials that delivered these results were not designed to determine whether vaccinated people could still spread the asthma without developing symptoms.

That remains online doctor ventolin a possibility. We know that people who are naturally infected by the asthma can spread it while they’re not experiencing any cough or other symptoms. Researchers will be online doctor ventolin intensely studying this question as the treatments roll out. In the meantime, even vaccinated people will need to think of themselves as possible spreaders.The Pfizer and BioNTech treatment is delivered as a shot in the arm, like other typical treatments. The injection won’t be any different from online doctor ventolin ones you’ve gotten before.

Tens of thousands of people have already received the treatments, and none of them have reported any serious health problems. But some online doctor ventolin of them have felt short-lived discomfort, including aches and flu-like symptoms that typically last a day. It’s possible that people may need to plan to take a day off work or school after the second shot. While these experiences aren’t pleasant, online doctor ventolin they are a good sign. They are the result of your own immune system encountering the treatment and mounting a potent response that will provide long-lasting immunity.No.

The treatments from Moderna online doctor ventolin and Pfizer use a genetic molecule to prime the immune system. That molecule, known as mRNA, is eventually destroyed by the body. The mRNA is packaged in an oily bubble that can fuse to a cell, allowing the molecule to slip in online doctor ventolin. The cell online doctor ventolin uses the mRNA to make proteins from the asthma, which can stimulate the immune system. At any moment, each of our cells may contain hundreds of thousands of mRNA molecules, which they produce in order to make proteins of their own.

Once those proteins are made, our cells then shred online doctor ventolin the mRNA with special enzymes. The mRNA molecules our cells make can only survive a matter of minutes. The mRNA in treatments is engineered to withstand the cell's enzymes a bit longer, so that the cells can make extra ventolin proteins online doctor ventolin and prompt a stronger immune response. But the mRNA can only last for a few days at most before they are destroyed.If you don’t want to buy a new mask, a simple solution is to wear an additional mask when you find yourself in closer proximity to strangers. I wear online doctor ventolin a single mask when I walk my dog or exercise outdoors.

But if I’m going to a store, taking a taxi or getting in the subway, I double mask by using a disposable surgical mask and covering it with my cloth mask.Do I need an N95 medical mask?. While medical workers who come into close contact with sick patients rely online doctor ventolin on the gold-standard N95 masks, you don’t need that level of protection if you’re avoiding group gatherings, limiting shopping trips and keeping your distance from others.“N95s are hard to get,” said Dr. Jha. €œI don’t online doctor ventolin think people should think that’s what they need. Certainly there are a lot of masks out in the marketplace that are pretty good.”If you’re working in an office or grocery store, or find yourself in a situation where you want added mask protection, you can get an alternative to the N95.

Dr. Jha suggested using a KF94 mask, a type of mask made in South Korea that can be purchased easily online. It resembles an N95, with some differences. It’s made of a similar nonwoven material that blocks 94 percent of the hardest-to-trap viral particles. But the KF94 has ear loops, instead of elastic head bands, so it won’t fit as snugly as an N95.The KF94 is also disposable — you can buy a pack of 20 for about $40 on Amazon.

While you can let a KF94 mask air dry and reuse it a few times, it can’t be laundered and won’t last as long as a cloth mask. One solution is to save your KF94 mask for higher-risk situations — like riding a subway, spending time in a store or going to a doctor’s appointment. Use your cloth mask for outdoor errands, exercise or walking the dog.Are there additional ways to reduce my risk?. Getting the treatment is the ultimate way to reduce risk. But until then, take a look at your activities and try reducing the time and number of exposures to other people.For instance, if you now go to the store two or three times a week, cut back to just once a week.

If you’ve been spending 30 to 45 minutes in the grocery store, cut your time down to 15 or 20 minutes. If the store is crowded, come back later. If you’re waiting in line, be mindful of staying at least six feet apart from the people ahead of you and behind you. Try delivery or curbside pickup, if that’s an option for you.If you’ve been spending time indoors with other people who aren’t from your household, consider skipping those events until you and your friends get vaccinated. If you must spend time with others, wear your best mask, make sure the space is well ventilated (open windows and doors) and keep the visit as short as possible.

It’s still safest to take your social plans outdoors. And if you are thinking about air travel, it’s a good idea to reschedule given the high number of cases around the country and the emergence of the more contagious variant.“The new variants are making me think twice about my plan to teach in-person, which would have been with masks and with good ventilation anyway,” Dr. Marr said. €œThey’re making me think twice about getting on an airplane.”Will the current asthma treatments work against the new variants?. Experts are cautiously optimistic that the current generation of treatments will be mostly effective against the emerging asthma variants.

Earlier this month, Pfizer and BioNTech announced that their asthma treatment works against one of the key mutations present in some of the variants. That’s good news, but the variants have other potentially risky mutations that haven’t been studied yet.Some data also suggest that variants with certain mutations may be more resistant to the treatments, but far more study is needed and those variants haven’t yet been detected in the United States. While the data are concerning, experts said the current treatments generate extremely high levels of antibodies, and they are likely to at least prevent serious illness in people who are immunized and get infected.“The reason why I’m cautiously optimistic is that from what we know about how treatments work, it’s not just one antibody that provides all the protection,” said Dr. Adam Lauring, associate professor of infectious disease at the University of Michigan. €œWhen you get vaccinated you generate antibodies all over the spike protein.

That makes it less likely that one mutation here or there is going to leave you completely unprotected. That’s what gives me reason for optimism that this is going to be OK in terms of the treatment, but there’s more work to be done.”If I catch asthma treatment, will I know if I have the new variant?. Probably not. If you test positive for the asthma, the standard PCR test can’t definitively determine if you have the variant or the original strain. While some PCR test results can signal if a person is likely to be infected with a variant, that information probably won’t be shared with patients.

The only way to know for sure which variant is circulating is to use gene sequencing technology, but that technology is not used to alert individuals of their status. While some public health and university laboratories are using genomic surveillance to track the prevalence of variants in a community, the United States doesn’t yet have a large-scale, nationwide system for checking asthma genomes for new mutations.Treatment for asthma treatment is the same whether you have the original strain or the variant. You can read more about what to do if you get infected here.Are children more at risk from the new variant?. Children appear to get infected with the variant at about the same rate as the original strain. A large study by health officials in Britain found that young children are only about half as likely as adults to transmit the variant to others.

While that’s good news, the highly contagious nature of the variant means more children will get the ventolin, even if they are still proportionately less contagious and less prone to getting infected than adults. You can learn more here.If I’ve already had asthma treatment, am I likely to have the same level of immunity to the new strain?. Most experts agree that once you’ve had asthma treatment, your body has some level of natural immunity to help fight off a second — although it’s not known how long the protection lasts. The variants circulating in Brazil and South Africa appear to have mutations that allow the ventolin to evade natural antibodies and reinfect someone who has already had the ventolin. The concern is based on lab tests using antibodies of people with a previous , so whether that translates to more res in the real world isn’t known.

The effect of the treatment against these variants isn’t known yet either. While all of this sounds frightening, scientists are hopeful that even if the treatments don’t fully protect against new variations of the ventolin, the antibodies generated by the treatment still will protect people from more serious illness.AdvertisementContinue reading the main storyAdvertisementContinue reading the main storySupported byContinue reading the main storyThe Toll of Fried Foods on Heart HealthEating fried foods increased the risk of heart disease, stroke, heart failure and premature death.Credit...Max Whittaker for The New York TimesJan. 22, 2021Most of us know that a diet rich in fried foods is bad for us. A review of studies quantifies just how bad it can be.In a meta-analysis of 19 studies that included diet and health data on more than 1.2 million men and women from around the world, Chinese researchers calculated the effect of eating French fries, fried fish, fried snacks and other fried foods on cardiovascular health.Comparing the groups with the highest intake of fried food with people who ate the least over an average period of nine years, they found that high consumption of fried foods increased the relative risk for coronary heart disease by 22 percent. For stroke by 37 percent.

For heart failure by 37 percent. For death from cardiovascular disease by 2 percent. And for death from any cause by 3 percent.The analysis, in the journal Heart, found no evidence that one kind of fried food was any better than another. Using the combined data, the researchers calculated that each additional weekly 114-gram (about 4-ounce) serving of fried food increases the risk for heart failure by 12 percent and for a major cardiovascular event by 3 percent.The Dietary Guidelines for Americans discourages fried food consumption, but it offers no specific limits on amounts in a healthy diet.The senior author, Dr. Fulan Hu of the Shenzhen University Health Science Center in Shenzhen, China, offered this advice.

€œReduce restaurant meals. Reduce fast-food intake. Use healthier boiling, steaming, baking or grilling cooking methods instead of frying for home-cooked food.”AdvertisementContinue reading the main story.

What if I miss a dose?

If you miss a dose, take it as soon as you can. If it is almost time for your next dose, take only that dose. Do not take double or extra doses.

Atrovent vs ventolin

How to atrovent vs ventolin buy ventolin online canada cite this article:Singh O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one atrovent vs ventolin 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 atrovent vs ventolin 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 atrovent vs ventolin 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, 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 atrovent vs ventolin 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 atrovent vs ventolin 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 atrovent vs ventolin 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 atrovent vs ventolin 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 atrovent vs ventolin professionals were called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry atrovent vs ventolin and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of atrovent vs ventolin 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” 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 atrovent vs ventolin 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 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 atrovent vs ventolin 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, atrovent vs ventolin 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.

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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 online doctor ventolin cite ventolin cost australia this article:Singh O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly online doctor ventolin 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 online doctor ventolin went into a frenzy as newspapers, news channels, and social media were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed online doctor ventolin on electronic, print, and social media.

We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress online doctor ventolin 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 online doctor ventolin 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 condition online doctor ventolin 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 online doctor ventolin 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 online doctor ventolin media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to online doctor ventolin the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time 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 online doctor ventolin 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 online doctor ventolin 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 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 online doctor ventolin 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 online doctor ventolin SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, 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. Part I.

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Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

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