Ventolin nebules for saleventolin and atrovent together

Concerned but not giving up, President Joe Biden is anxiously pushing ahead to prod people to get asthma treatment shots after the Supreme Court put a halt to the administration's sweeping vaccinate-or-test plan for large employers.At a time ventolin nebules for saleventolin and atrovent together when hospitals are being overrun and record why not look here numbers of people are getting infected with the omicron variant, the administration hopes states and companies will order their own vaccinate-or-test requirements. And if the presidential "bully pulpit" still counts for persuasion, Biden intends to use it.While some in the ventolin nebules for saleventolin and atrovent together business community cheered the defeat of the mandate, Biden insisted the administration effort has not been for naught. The high court's ruling on Thursday "does not stop me from using my voice as president to advocate for employers to do the right thing to protect Americans' health and economy," he said.The court's conservative majority all-but-struck down the Occupational Safety and Health Administration's requirement that employers with 100 or more employees require their workers to be vaccinated against the asthma or tested weekly. However, it did leave in place a vaccination requirement for healthcare workers.Meanwhile, the White House announced Friday that the federal ventolin nebules for saleventolin and atrovent together website where Americans can request their own free asthma treatment tests will begin accepting orders next Wednesday. Those tests could provide motivation for some people to seek vaccination, and the administration is looking to address nationwide shortages.

Supplies will be limited to just ventolin nebules for saleventolin and atrovent together four free tests per home.Website to order free asthma treatment tests from federal government launches next weekOn Thursday, the Supreme Court ruled that OSHA appeared to overstep its congressional authority to implement occupational standards, saying, "Although asthma treatment–19 is a risk that occurs in many workplaces, it is not an occupational hazard in most."The mandate was announced last September, accompanied by biting criticism from Biden for the roughly 80 million American adults who hadn't yet gotten shots."We've been patient. But our patience is wearing thin, and your refusal has cost all of us," he said. The unvaccinated minority, he said, "can cause a lot of damage, and they are."In a statement after the Supreme Court ruling, Biden expressed disappointment with the outcome but said the mandates have already had their desired effect on reducing the number of unvaccinated adults."Today, that number is down to under 35 ventolin nebules for saleventolin and atrovent together million," he said of the unvaccinated. "Had my administration not put vaccination requirements in place, we would be now experiencing a higher death toll from asthma treatment and even more hospitalizations."While the court left open the possibility for the U.S. To pursue more targeted mandates, White House officials said there were no immediate plans to seek a redo of the regulation."It's now up to the states and individual employers to put in place vaccination ventolin nebules for saleventolin and atrovent together requirements," said White House press secretary Jen Psaki on Friday.The United States is already "languishing,'' with a 60% vaccination rate, near the bottom of peer nations, said Lawrence Gostin, a public health law expert at Georgetown University."The OSHA rule was truly the president's last best shot at significantly boosting the vaccination rate,'' Gostin said.

But the court, "in a very highly partisan way, intentionally tried to handcuff the president in doing what he needs to do.''Many large businesses that had already put in place vaccination-or-testing requirements indicated they had no plans to reverse course. But smaller companies said they were breathing a sigh of relief, fearing ventolin nebules for saleventolin and atrovent together worker shortages if the OSHA rule had been allowed to go into force.The Supreme Court decision has "taken a little bit of a burden of worry off of our shoulders," said Kyle Caraway, marketing director at Doolittle Trailer Manufacturing, which joined a lawsuit by the Missouri attorney general challenging Biden's policy. About 90% of the 175 employees at the Holts Summit, Missouri-based company had indicated they would refuse to comply with a vaccination requirement, he said."It became apparent to us that our team was going to shrink greatly overnight if that treatment mandate went into place," said Caraway, who counted himself among those opposing Biden's policy. Halting production could have forced the company "to consider shuttering our doors," he said.The Service Employees International Union, which represents more than 2 million workers, said the court decision was a relief for healthcare workers but leaves others without critical protections."In blocking the treatment-or-test rule for large employers, the court has placed millions of other essential workers further at risk, ventolin nebules for saleventolin and atrovent together caving to corporations that are trying to rig the rules against workers permanently," the union said.Not a Modern Healthcare subscriber?. Sign up today.The union called on Congress and ventolin nebules for saleventolin and atrovent together states to pass laws requiring vaccinations, masks and paid sick leave.

Workers also need better access to testing and protective equipment, the union said.The renewed debate over vaccination mandates comes as a record number of Americans are hospitalized with asthma treatment, the country is averaging nearly 800,000 new cases and 1,700 deaths a day and resistance to treatments remains a problem, most notably in deeply conservative states like Mississippi, Alabama, Wyoming and Idaho where less than half the population is fully vaccinated.Hospitals nationwide are suffering chronic staffing shortages and being bombarded with people showing up at emergency rooms in need of ventolin tests. National Guard troops have been activated in dozens of states to help out at medical centers, nursing homes and testing sites.A hospital on the edge of the Kansas City area had to borrow ventilators from the state of Missouri's stockpile and hunt for more high-flow oxygen machines, and the largest county in Kansas said Friday ventolin nebules for saleventolin and atrovent together that it's running out of morgue space — again.Gostin predicted the court's action would have grave influence on other federal agencies' efforts to protect public health, by ruling that OSHA can't regulate something that would have a huge economic impact without explicit authorization from Congress. And he said states won't be able to make up for the ruling's impact."If asthma treatment has taught us anything, it's taught us that states can't deal with big, bold problems, can't prevent a pathogen from going from Florida to New York," he said. "These are ventolin nebules for saleventolin and atrovent together national problems requiring federal solutions.''Psaki said the White House would work with businesses to promote the benefits of vaccination-or-testing requirements and that Biden would highlight successful programs."The Court has ruled that my administration cannot use the authority granted to it by Congress to require this measure," Biden said. So "I call on business leaders to immediately join those who have already stepped up – including one third of Fortune 100 companies – and institute vaccination requirements to protect their workers, customers, and communities."Healthcare workers in the 24 states that are newly subject to the Centers for Medicare and Medicaid Services' asthma treatment mandate will need to get their first shot by Feb.

14 and final shot by March 15, according to new guidance released by ventolin nebules for saleventolin and atrovent together CMS Friday. Facilities in the 24 states subject to the new guidance will also need to demonstrate that they've developed policies and procedures to make sure all facility staff are vaccinated against asthma treatment by Feb. 14.The guidance specifically applies to Alabama, Alaska, Arizona, Arkansas, Georgia, Idaho, Indiana, Iowa, Kansas, Kentucky, Louisiana, Mississippi, Missouri, Montana, Nebraska, New Hampshire, North Dakota, Ohio, Oklahoma, South Carolina, South Dakota, Utah, West Virginia ventolin nebules for saleventolin and atrovent together and Wyoming. The guidance does not apply to Texas, since the state is part of a separate lawsuit that wasn't before the Supreme Court. The mandate is still ventolin nebules for saleventolin and atrovent together stayed in the state.

The Supreme Court ruled Thursday that CMS' requirement that employees at Medicare and Medicaid-certified facilities get vaccinated against asthma treatment could go into effect pending appeals in lower courts. The mandate was previously stayed in about half the ventolin nebules for saleventolin and atrovent together country after states brought lawsuits against the policy. Thursday's decision does not affect compliance dates for providers in states where the mandate was already in effect, CMS says. Health workers ventolin nebules for saleventolin and atrovent together in those 25 states, plus the District of Columbia and the territories, must get their first dose by Jan. 27 and ventolin nebules for saleventolin and atrovent together by fully vaccinated or exempt from the requirement by Feb.

28.Some hospitals have had to cancel surgeries and redirect emergency care as the national blood supply drops.Only about half of hospitals' blood orders are being filled, according to the group purchasing organization Vizient. Some rural facilities have been forced to triage care by ventolin nebules for saleventolin and atrovent together prioritizing who gets treatment and who doesn't."Some of my colleagues in rural areas are doing that on a daily basis," said Dr. Claudia Cohn, medical director of the M Health Fairview University of Minnesota Medical Center's blood bank. M Health, 15-hospital system based in Minneapolis, had to slightly reduce its standard inventory ventolin nebules for saleventolin and atrovent together levels and avoided delaying or canceling care."Lowering your standard inventory in rural areas is a much scarier thing. If there's a car crash or someone has a gastrointestinal bleed in the middle of the night, that can be a life-or-death situation," Cohn said.More than a third of community blood centers report having a one-day supply or less, according to America's Blood Centers' daily update from 59 banks.

Centers with three or more days have worth enough supply to meet normal operating demands, but more than two-thirds have two days of blood or less on hand.One hospital in Raleigh, North Carolina, recently went through 10 units of Type O blood after a multiple-patient trauma event, said Akiva Faerber, Vizient's senior principal of laboratory and blood consulting ventolin nebules for saleventolin and atrovent together. The hospitals supply of O blood, typically at 20 units, fell to seven, he said."Many of our Vizient members have called me over the last three weeks in desperation to try to get additional product," said Faerber, who described the present shortfall as the worst during his 47 years in the industry. "Many hospitals ventolin nebules for saleventolin and atrovent together are asking for Os, but the Red Cross is metering out regularly scheduled orders. Some have been cut back as much as 60%," he said.Harbor-UCLA Medical Center, which is owned and operated by Los Angeles County, temporarily closed its trauma center to new patients for hours this week."It's already having a profoundly negative impact on patient care, ranging from the cancellation of elective procedures in an attempt to preserve scarce resources, to [emergency departments] on diversion," said Christopher Godfrey, CEO of Bloodbuy, which sells software to facilitate blood distribution. "We're currently in the midst of an unprecedented blood supply crisis that has been building for several months, as a result of asthma treatment and the negative impact it's ventolin nebules for saleventolin and atrovent together had on blood donation nationwide.

It's truly a public health crisis and all indications are that it is likely to get worse before it gets better."The asthma treatment ventolin has depressed blood donations for several reasons. Among them is that vacant ventolin nebules for saleventolin and atrovent together offices and schools mean fewer donation drives. Blood suppliers, like the rest of the healthcare industry, are also having staffing issues.Blood donation has declined 10% since March 2020, Red Cross data show. There's been a 62% drop in college and high school blood drives ventolin nebules for saleventolin and atrovent together due to the ventolin, illness, weather and staffing, according to the organization.Many hospitals have had to postpone non-urgent surgeries once again as they struggle to keep up with the latest asthma treatment surge. That has helped conserve blood, but many facilities have adjusted or are considering adjusting their blood allocation protocols."It's the worst blood shortage in over a decade, posing a concerning risk to patient care," the Red Cross website says ventolin nebules for saleventolin and atrovent together.

"Doctors have been forced to make difficult decisions about who receives blood transfusions and who will need to wait until more products become available. Blood and platelet donations are critically needed to help prevent further delays in vital medical treatments."Traditionally, clinicians default ventolin nebules for saleventolin and atrovent together to blood transfusions when patient's hemoglobin counts are below 10 grams per deciliter. But many patients with levels between 7 and 10 grams per deciliter may not need blood transfusions according to recent research that suggests one unit of blood rather than two may be safer.Now, hospitals are telling patients to eat more leafy greens, nuts and other food to boost their iron levels and giving them intravenous iron or red cell stimulators before surgery to reduce blood loss. Some are ventolin nebules for saleventolin and atrovent together using cell-saver devices, which recycle blood during surgery."Those measures are really important and need to be a part of hospitals' pre-surgery assessments," Cohn said.Clinicians are taking more time than previously to determine whether patients are stable enough or if they need transfusions, and they're developing alternatives, Faerber said. "We are still behind the times in evaluating our blood use more carefully," he said.In the meantime, larger health systems have fared better because they can transfer blood between hospitals, which is the case at Roseville, California-based Adventist Health and its West Coast facilities, a spokesperson said.University of Utah Health of Salt Lake City has maintained adequate blood supplies and has not had to delay care, similar to Memorial Hermann Health System in Houston and Froedtert Health of Milwaukee, according to the companies.Edward-Elmhurst Health of Naperville, Illinois, has expanded its blood supplier network and has received shipments from Florida and New York, said Guy Diehl, blood bank supervisor at Edward Hospital."It's a testament to how hard the system is working," Diehl said.

"We would love it if folks could donate."The Medicare Payment Advisory Commission thinks a new model with different risk tracks and administratively-set savings benchmarks could be the way forward for population-based alternative ventolin nebules for saleventolin and atrovent together payment models, though commission members noted during a Friday meeting that there are still many details to work out. MedPAC should recommend that Congress have timeliness and simplicity in mind, Commissioner Brian DeBusk, CEO of medical equipment manufacturer DeRoyal Industries, said during Friday's meeting. As Medicare Advantage grows each year, population-based alternative payment models like accountable care organizations are left with a shrinking pool of beneficiaries, he added ventolin nebules for saleventolin and atrovent together. In October, MedPAC commissioners discussed developing a single multi-track, population-based payment model to guide CMS' alternative payment model strategy. CMS set a goal that same month to have ventolin nebules for saleventolin and atrovent together all Medicare beneficiaries in a value-based payment arrangement by 2030.

MedPAC followed with a November discussion about developing administratively-set benchmarks for ACOs, which can share in Medicare savings if their beneficiaries' expenditures come in below an assigned benchmark level. The benchmark ventolin nebules for saleventolin and atrovent together is determined based on spending for beneficiaries who would've been eligible for the ACO in the baseline years, along with the growth in an ACO's spending between the baseline and performance years.Because ACO benchmarks are reset each performance period based on the ACO's past performance, an ACO that improves the amount of savings it generates each year will have to deal with benchmarks that are increasingly harder to exceed, which puts long-term ACO participation at risk. MedPAC staff ventolin nebules for saleventolin and atrovent together Friday provided commissioners with a blueprint for a hypothetical new three-track alternative payment model. The model would divide providers into three separate categories. Independent physician practices, small safety net providers or rural providers, could be in a track that involves no financial risk ventolin nebules for saleventolin and atrovent together.

Providers could keep up to 50% of savings generated relative to their benchmark after a minimum savings rate is met. Mid-sized organizations ventolin nebules for saleventolin and atrovent together like multi-specialty physician practices or small community hospitals could keep up to 75% of savings generated or repay 75% of losses. Large health systems would use a 100% shared savings or loss rate. Commissioner Dr ventolin nebules for saleventolin and atrovent together. Jonathan Jaffery, who leads the University of Wisconsin Health ACO, questioned whether an organization's size should determine its risk readiness.

Large organizations could have trouble earning shared savings when the cost of the care they deliver is low, and smaller organizations are sometimes more nimble than larger ones, ventolin nebules for saleventolin and atrovent together he said. Also up for debate is how quickly providers should be pushed to accept financial risk. Small providers could be allowed to stay in the no-risk track indefinitely, or eventually be encouraged to move to ventolin nebules for saleventolin and atrovent together another track. Commissioner David Grabowski, a professor at Harvard Medical School, said downside risk shouldn't be forced onto providers, while Commissioner Dana Gelb Safran, president and CEO of the National Quality Forum, said two-sided risk can make providers serious about generating savings. Getting providers ventolin nebules for saleventolin and atrovent together to participate in such models in the first place is another hurdle MedPAC wants to clear.

Incentives for providers to participate in APMs are already written into statute. By 2040, payment rates will be 8% higher for physicians in advanced APMs than those who choose not to participate, MedPAC staff ventolin nebules for saleventolin and atrovent together said. But to encourage even ventolin nebules for saleventolin and atrovent together more participation, officials could simply make the model mandatory for certain providers to receive Medicare funds. Other options include paying lower rates to clinicians not enrolled in the model, waiving certain Medicare requirements for participants and offering participants more technical assistance. Setting future dates for mandatory participation for at least mid-sized and larger organizations ventolin nebules for saleventolin and atrovent together might help generate participation in the short-run, said Commissioner Dr.

Lawrence Casalino, a professor at Weill Cornell Graduate School of Medical Sciences."One of the things that I heard a lot when when payment reform was my job was how important it was for there to be a clear signal of where things are going," Safran said in agreement. "That would certainly be a very clear signal."The hypothetical model would ventolin nebules for saleventolin and atrovent together also administratively set ACO benchmarks using external factors to work around the ratcheting effect. Most commissioners applauded this idea. "Eliminating the ventolin nebules for saleventolin and atrovent together ratchet effect is absolutely critical. The ACO program can't work as long as the ratchet is a problem," Casalino said.

But Commissioner Lynn Barr, leader of Caravan Health, which guides providers through value-based care, expressed concern about changing the system in a way that would cause providers ventolin nebules for saleventolin and atrovent together to generate less savings and end up having to pay the government back. MedPAC should assume legislation will be needed to make the alternative payment model reforms the commission is looking towards, according to Vice Chair Paul Ginsburg, a senior fellow at the USC-Brookings Schaeffer Initiative for Health Policy."We don't want to lock ourselves into the 2010 statutes, where there was much less experience with these approaches to payments," he said.Humana named Dr. Andrew Agwunobi president of its growing home solutions business on Friday, ventolin nebules for saleventolin and atrovent together with the veteran health insurer and provider executive slated to start Feb. 21. Agwunobi comes to the insurer from the University of Connecticut, where he currently serves as interim ventolin nebules for saleventolin and atrovent together president of the university and CEO of the UConn Health System.

He previously served as chief operating officer of St. Joseph Health System, a 14-hospital network headquartered in Irvine, California, and also led ventolin nebules for saleventolin and atrovent together Renton, Washington-based Providence Health Care System as CEO. Agqunobi additionally oversaw the Florida Agency for Health Care ventolin nebules for saleventolin and atrovent together Administration and its $16 billion budget. In his new role at Humana, Agwunobi will report directly to CEO Bruce Broussard and serve as a member of the management team. He fills an opening left by Susan Diamond, who moved from president of the home care business division to Humana's chief financial ventolin nebules for saleventolin and atrovent together officer last June.

Broussard pointed to Agwunobi's medical and professional experience leading a home healthcare organization as a benefit to the insurer. Agwunobi is ventolin nebules for saleventolin and atrovent together a pediatrician who earned his medical degree from the University of Jos in Nigeria and master's in business administration from Stanford University. "He's a doctor—he understands the value of care in the home, why seniors want more of it, and our vision a Humana for making it much easier for people to get the care they need at home," Broussard said in a news release. Humana, the second-largest Medicare Advantage carrier in the nation with 4.3 million members, ventolin nebules for saleventolin and atrovent together has been investing in its home care services. UnitedHealthcare is the nation's largest Medicare Advantage insurer with 6.4 million enrollees.

Last August, Humana paid $5.7 billion to buy the remaining shares of Kindred at Home, bringing the insurer's total investment in the nation's largest home care and hospice provider to ventolin nebules for saleventolin and atrovent together $8.1 billion. Humana eventually plans to integrate the home health side of Kindred into Agwunobi's Home Solutions division, with the aim of providing care to those insured under different carriers. Integrating the two businesses will continue through 2023, the company ventolin nebules for saleventolin and atrovent together said. In June, the insurer also paid an undisclosed sum to acquire One Home Healthcare, which does business as onehome, to build on its growing value-based home health segment. In 2021, Humana also partnered with in-home service provider DispatchHealth to offer in-home emergency and acute care to its traditional Medicare and Medicare Advantage ventolin nebules for saleventolin and atrovent together members.

"As the ongoing asthma treatment ventolin has accelerated interest in and shifts to in-home care and home health models, I'm highly confident that we will be able to help the people we serve achieve better health outcomes," Agwunobi said in a news release..

How many puffs of ventolin can a child have

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Female dosage	Canadian pharmacy only	In online pharmacy	Canadian pharmacy only	Register first	100mcg	In online pharmacy
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The asthma Disease 2019 (asthma treatment) treatment FAQ sheet on the American Society of Transplantation (AST) website relays information on the current state of knowledge to transplant professionals and the community regarding the asthma treatment.1 Last updated on August 13, 2021, from this source this document includes the acknowledgment that “data on clinical efficacy of mRNA treatments in solid organ transplant (SOT) recipients are incomplete.” In phase III clinical trials, severe acute respiratory syndrome asthma 2 (asthma) how many puffs of ventolin can a child have treatments generated robust titers of anti-spike1 protein (S1) IgGs that conferred >94% protection against severe asthma treatment. Very shortly after their use was authorized, however, it became clear that the standard vaccination schedule is insufficient to elicit a protective response in over half of kidney transplant recipients on maintenance immunosuppression (IS), a population that was excluded from the initial clinical trials. Underlying this failure is the impaired generation of treatment-specific helper T cells, plasmablasts, and memory B cells because of IS.2,3 Such patients remain susceptible to severe asthma treatment despite vaccination and are in urgent need of an effective how many puffs of ventolin can a child have vaccination strategy.The Food and Drug Administration authorized the administration of a third dose of asthma mRNA treatment to immunocompromised patients in August 2021, based on multiple small reports of efficacy.

In this issue of JASN, Schrezenmeier et al. Report their analysis of serological responses and treatment-specific B- and T-cell immunity in 25 kidney transplant recipients without humoral response after two doses of BNT162b2 how many puffs of ventolin can a child have (BioNTech) treatment who then received a third dose of either heterologous ChAdOx1 (AstraZeneca) or homologous BNT162b2 treatment.4 Maintenance IS in this cohort is typical of the long-term kidney transplant population, with 84% being on a calcineurin inhibitor and all except one patient on mycophenolate mofetil (MMF). Thirty-six percent of the patients demonstrated positive anti-S1 IgG by day 27 after the third vaccination and this paralleled the neutralization capacity of their sera.

Only three responders (12%) developed high anti-S1 IgG titers how many puffs of ventolin can a child have and one of them was the patient not on MMF. Those with a humoral response had significantly higher frequencies of viral spike protein receptor-binding domain specific B cells as well as spike-reactive CD4+ T helper cells compared with nonresponders.An important finding of this study, similar to that of other recent reports5, is that while a third dose can boost the immune response in some kidney transplant recipients on IS, it is by no means a universal panacea, effecting a response in only one-third of recipients without a previous response. Indeed, one patient even in this small cohort developed severe asthma treatment 10 days after the third how many puffs of ventolin can a child have dose, starkly illustrating the continuing threat to this population.

The single patient in this study who was not on MMF and who developed high titer anti-S1 IgG after the third dose provides a glimmer of direction. Other groups have shown that how many puffs of ventolin can a child have MMF therapy significantly curtails the odds of a response to the treatment and that the correlation is dose-dependent.6 Modulation of the IS regimen may be necessary to increase the probability as well as the magnitude of response to vaccination, at least in a subset of patients. Interruption of MMF treatment improved the antibody response to vaccination in patients with autoimmune disease7.

The safety and efficacy of such an approach in transplant recipients is now being formally addressed in a prospective National Institutes of Health trial (NCT05077254).In the general population, the durability of the humoral response and the effectiveness of subsequent vaccination is strikingly superior in those with previous compared with uninfected persons.8 Somewhat surprisingly, titers of how many puffs of ventolin can a child have neutralizing antibodies post in kidney transplant recipients9 and the subsequent vaccination-induced boost in these antibody titers are comparable to those in nontransplant patients,10 showing that it is indeed possible to generate a strong protective response even in this group. Strategies to improve treatment immunogenicity therefore remain critical to the effort to protect transplant patients from asthma treatment. Schrezenmeier et how many puffs of ventolin can a child have al.

Did not find a statistically significant difference in the success of boosting with BNT162b2 (n=14) or ChAdOx1 (n=11) treatment, although the latter group had a numerically visit the site higher response (45% versus 28%). A recent study of two-dose homologous or heterologous treatment regimens in SOT recipients and healthy controls found that IgG and neutralizing activity were more pronounced after mRNA priming, whereas CD4 and CD8 T cell levels were higher after vector priming.11 Interestingly, SOT recipients showed the strongest induction of antibodies and CD4 T cells with heterologous vaccination, in contrast to immunocompetent patients how many puffs of ventolin can a child have who had similar responses with either approach. This finding may explain the comparatively higher success rate (60%) seen after a dose of mRNA-1273 in a small cohort of nonresponders to BNT162b2.12In line with previous reports, Schrezenmeier et al.

Observed a high degree of correlation between spike IgG antibody and how many puffs of ventolin can a child have neutralizing antibody titers. Measurement of anti-S1 IgG in transplant recipients may become a useful clinical aid to identify and counsel patients who remain serologically unresponsive after booster doses. It should be noted, however, how many puffs of ventolin can a child have that time since receipt of the treatment dose, and possibly other factors, can modulate the relationship between anti-S1 IgG and neutralizing antibody levels, and routine use of anti-S1 IgG is not currently recommended by the AST.

Finally, Schrezenmeier et al. Demonstrated a strong correlation between treatment-specific T cell frequencies and antibody titers after how many puffs of ventolin can a child have vaccination. The relative importance of humoral versus cellular immunity in treatment-derived protection and the degree of concordance between the two in transplant recipients remains an area of active investigation.

Ultimately, optimization of treatment efficacy in this population will require a multipronged strategy that incorporates emerging information on host factors how many puffs of ventolin can a child have correlating with the strength and durability of protection after vaccination, as well as data from trials of new regimens of treatment delivery. In the interim, the less than optimal immune response to a third dose of asthma mRNA in post-transplant patients should provide the impetus for intensifying efforts to complete asthma treatment vaccination prior to transplant. Transplant centers need to combat treatment hesitancy with how many puffs of ventolin can a child have education and ultimately treatment mandates for waitlisted patients awaiting transplantation.DisclosuresS.

Chandran reports consultancy agreements with Everest Clinical Research and Bride Bio Gene Therapy. And research funding from Bristol-Myers Squibb and how many puffs of ventolin can a child have Genentech-Roche. The remaining author has nothing to disclose.FundingNone.FootnotesPublished online ahead of print.

Publication date available at www.jasn.org.See related rapid communication, “B and T Cell Responses after a Third Dose of asthma treatment in Kidney Transplant Recipients,” on pages 3027–3033.Copyright © 2021 by the American Society of Nephrology.

The asthma Disease 2019 (asthma treatment) treatment FAQ sheet on the American Society of Transplantation (AST) website relays information on the current state of knowledge to transplant professionals and the ventolin nebules for saleventolin and atrovent together community regarding the asthma treatment.1 Last updated on August 13, 2021, this document includes the acknowledgment that “data on clinical efficacy of mRNA treatments in solid organ transplant (SOT) recipients are incomplete.” In phase III clinical trials, severe acute respiratory syndrome asthma 2 (asthma) treatments generated robust titers of anti-spike1 protein (S1) IgGs that conferred >94% protection against severe asthma treatment. Very shortly after their use was authorized, however, it became clear that the standard vaccination schedule is insufficient to elicit a protective response in over half of kidney transplant recipients on maintenance immunosuppression (IS), a population that was excluded from the initial clinical trials. Underlying this failure is the impaired generation of treatment-specific helper T cells, plasmablasts, and memory B cells because of IS.2,3 Such patients remain susceptible to severe asthma treatment despite vaccination and are in urgent need of an effective vaccination strategy.The Food and Drug Administration authorized the administration of a third dose of ventolin nebules for saleventolin and atrovent together asthma mRNA treatment to immunocompromised patients in August 2021, based on multiple small reports of efficacy.

In this issue of JASN, Schrezenmeier et al. Report their analysis of serological responses and treatment-specific B- and T-cell immunity in 25 kidney transplant recipients without humoral response after two doses of BNT162b2 (BioNTech) treatment who then received a third dose of either heterologous ChAdOx1 (AstraZeneca) or homologous BNT162b2 treatment.4 Maintenance IS in this cohort is typical of the long-term kidney transplant population, with 84% being on a calcineurin inhibitor ventolin nebules for saleventolin and atrovent together and all except one patient on mycophenolate mofetil (MMF). Thirty-six percent of the patients demonstrated positive anti-S1 IgG by day 27 after the third vaccination and this paralleled the neutralization capacity of their sera.

Only three responders (12%) developed high anti-S1 IgG titers and one of them was the patient not ventolin nebules for saleventolin and atrovent together on MMF. Those with a humoral response had significantly higher frequencies of viral spike protein receptor-binding domain specific B cells as well as spike-reactive CD4+ T helper cells compared with nonresponders.An important finding of this study, similar to that of other recent reports5, is that while a third dose can boost the immune response in some kidney transplant recipients on IS, it is by no means a universal panacea, effecting a response in only one-third of recipients without a previous response. Indeed, one patient even in this small cohort developed ventolin nebules for saleventolin and atrovent together severe asthma treatment 10 days after the third dose, starkly illustrating the continuing threat to this population.

The single patient in this study who was not on MMF and who developed high titer anti-S1 IgG after the third dose provides a glimmer of direction. Other groups have shown that MMF therapy significantly curtails the ventolin nebules for saleventolin and atrovent together odds of a response to the treatment and that the correlation is dose-dependent.6 Modulation of the IS regimen may be necessary to increase the probability as well as the magnitude of response to vaccination, at least in a subset of patients. Interruption of MMF treatment improved the antibody response to vaccination in patients with autoimmune disease7.

The safety and efficacy of such an approach in transplant recipients is ventolin nebules for saleventolin and atrovent together now being formally addressed in a prospective National Institutes of Health trial (NCT05077254).In the general population, the durability of the humoral response and the effectiveness of subsequent vaccination is strikingly superior in those with previous compared with uninfected persons.8 Somewhat surprisingly, titers of neutralizing antibodies post in kidney transplant recipients9 and the subsequent vaccination-induced boost in these antibody titers are comparable to those in nontransplant patients,10 showing that it is indeed possible to generate a strong protective response even in this group. Strategies to improve treatment immunogenicity therefore remain critical to the effort to protect transplant patients from asthma treatment. Schrezenmeier et ventolin nebules for saleventolin and atrovent together al.

Did not find a statistically significant difference in the success of boosting with BNT162b2 (n=14) or ChAdOx1 (n=11) treatment, although the latter group had a numerically higher response (45% versus 28%). A recent study of two-dose homologous or heterologous treatment regimens in SOT recipients and healthy controls found that IgG and neutralizing activity were more pronounced after mRNA priming, whereas CD4 and CD8 T cell levels were ventolin nebules for saleventolin and atrovent together higher after vector priming.11 Interestingly, SOT recipients showed the strongest induction of antibodies and CD4 T cells with heterologous vaccination, in contrast to immunocompetent patients who had similar responses with either approach. This finding may explain the comparatively higher success rate (60%) seen after a dose of mRNA-1273 in a small cohort of nonresponders to BNT162b2.12In line with previous reports, Schrezenmeier et al.

Observed a high degree ventolin nebules for saleventolin and atrovent together of correlation between spike IgG antibody and neutralizing antibody titers. Measurement of anti-S1 IgG in transplant recipients may become a useful clinical aid to identify and counsel patients who remain serologically unresponsive after booster doses. It should be noted, however, that time since receipt of the treatment dose, and possibly other ventolin nebules for saleventolin and atrovent together factors, can modulate the relationship between anti-S1 IgG and neutralizing antibody levels, and routine use of anti-S1 IgG is not currently recommended by the AST.

Finally, Schrezenmeier et al. Demonstrated a ventolin nebules for saleventolin and atrovent together strong correlation between treatment-specific T cell frequencies and antibody titers after vaccination. The relative importance of humoral versus cellular immunity in treatment-derived protection and the degree of concordance between the two in transplant recipients remains an area of active investigation.

Ultimately, optimization of treatment efficacy in this population will require a multipronged strategy that incorporates emerging information on host factors correlating with the strength and durability of protection after vaccination, as well as data from trials ventolin nebules for saleventolin and atrovent together of new regimens of treatment delivery. In the interim, the less than optimal immune response to a third dose of asthma mRNA in post-transplant patients should provide the impetus for intensifying efforts to complete asthma treatment vaccination prior to transplant. Transplant centers need to combat treatment hesitancy with education and ultimately treatment mandates for waitlisted patients ventolin nebules for saleventolin and atrovent together awaiting transplantation.DisclosuresS.

Chandran reports consultancy agreements with Everest Clinical Research and Bride Bio Gene Therapy. And research funding from ventolin nebules for saleventolin and atrovent together Bristol-Myers Squibb and Genentech-Roche. The remaining author has nothing to disclose.FundingNone.FootnotesPublished online ahead of print.

Publication date available at www.jasn.org.See related rapid communication, “B and T Cell Responses after a Third Dose of asthma treatment in Kidney Transplant Recipients,” on pages 3027–3033.Copyright © 2021 by the American Society of Nephrology.

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ALBUTEROL (also known as salbutamol) is a bronchodilator. It helps open up the airways in your lungs to make it easier to breathe. Ventolin is used to treat and to prevent bronchospasm.

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How to cite how much does ventolin cost this article:Singh albuterol ventolin produces which actions O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity albuterol ventolin produces which actions suicide is one of the highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went albuterol ventolin produces which actions 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 albuterol ventolin produces which actions 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 started getting distress calls from their patients in despair with albuterol ventolin produces which actions 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 albuterol ventolin produces which actions 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 and illness and also his relationships albuterol ventolin produces which actions and finances.

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

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our albuterol ventolin produces which actions 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 albuterol ventolin produces which actions 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 albuterol ventolin produces which actions societies have guidelines and resource books for interacting with media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to albuterol ventolin produces which actions 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, albuterol ventolin produces which actions Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

How to ventolin nebules for saleventolin and atrovent together 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 ventolin nebules for saleventolin and atrovent together one of the highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went into a frenzy ventolin nebules for saleventolin and atrovent together 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 ventolin nebules for saleventolin and atrovent together 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 ventolin nebules for saleventolin and atrovent together 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 ventolin nebules for saleventolin and atrovent together 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 and ventolin nebules for saleventolin and atrovent together 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 ventolin nebules for saleventolin and atrovent together reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental health professionals were ventolin nebules for saleventolin and atrovent together 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 and are detrimental to the ventolin nebules for saleventolin and atrovent together 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 ventolin nebules for saleventolin and atrovent together 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 ventolin nebules for saleventolin and atrovent together interacting with media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments ventolin nebules for saleventolin and atrovent together are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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