What do you need to buy nexavar

page
to 1
 
ID price area
ID: 426449

Nexavar 200mg price in uk

Nexavar 200mg price in uk

View

i was reading this this drug benefit was "carved into" the Medicaid managed care benefit package. Before that date, people enrolled in a Medicaid managed care plan obtained all of their health care through the plan, but used their regular Medicaid card to access any drug available on the state formulary on a "fee for service" basis without needing to utilize a restricted pharmacy network or comply with managed care plan rules. COMING IN April 2021 - In the NYS Budget enacted in April 2020, the pharmacy benefit was "carved out" of "mainstream" Medicaid managed care plans. That means that members of managed care plans will access their drugs outside their plan, unlike the rest of their medical care, which what do you need to buy nexavar is accessed from in-network providers.

How Prescription Drugs are Obtained through Managed Care plans No - Until April 2020 HOW DO MANAGED CARE PLANS DEFINE THE PHARMACY BENEFIT FOR CONSUMERS?. The Medicaid pharmacy benefit includes all FDA approved prescription drugs, as well as some over-the-counter drugs and medical supplies. Under what do you need to buy nexavar Medicaid managed care. Plan formularies will be comparable to but not the same as the Medicaid formulary.

Managed care plans are required to have drug formularies that are “comparable” to the Medicaid fee for service formulary. Plan formularies do what do you need to buy nexavar not have to include all drugs covered listed on the fee for service formulary, but they must include generic or therapeutic equivalents of all Medicaid covered drugs. The Pharmacy Benefit will vary by plan. Each plan will have its own formulary and drug coverage policies like prior authorization and step therapy.

Pharmacy networks can also differ from plan what do you need to buy nexavar to plan. Prescriber Prevails applies in certain drug classes. Prescriber prevails applys to medically necessary precription drugs in the following classes. atypical antipsychotics, anti-depressants, anti-retrovirals, what do you need to buy nexavar anti-rejection, seizure, epilepsy, endocrine, hemotologic and immunologic therapeutics.

Prescribers will need to demonstrate reasonable profession judgment and supply plans witht requested information and/or clinical documentation. Pharmacy Benefit Information Website -- http://mmcdruginformation.nysdoh.suny.edu/-- This website provides very helpful information on a plan by plan basis regarding pharmacy networks and drug formularies. The Department of what do you need to buy nexavar Health plans to build capacity for interactive searches allowing for comparison of coverage across plans in the near future. Standardized Prior Autorization (PA) Form -- The Department of Health worked with managed care plans, provider organizations and other state agencies to develop a standard prior authorization form for the pharmacy benefit in Medicaid managed care.

The form will be posted on the Pharmacy Information Website in July of 2013. Mail Order Drugs what do you need to buy nexavar -- Medicaid managed care members can obtain mail order/specialty drugs at any retail network pharmacy, as long as that retail network pharmacy agrees to a price that is comparable to the mail order/specialty pharmacy price. CAN CONSUMERS SWITCH PLANS IN ORDER TO GAIN ACCESS TO DRUGS?. Changing plans is often an effective strategy for consumers eligible for both Medicaid and Medicare (dual eligibles) who receive their pharmacy service through Medicare Part D, because dual eligibles are allowed to switch plans at any time.

Medicaid consumers will have what do you need to buy nexavar this option only in the limited circumstances during the first year of enrollment in managed care. Medicaid managed care enrollees can only leave and join another plan within the first 90 days of joining a health plan. After the 90 days has expired, enrollees are “locked in” to the plan for the rest of the year. Consumers can switch plans during the “lock in” period only what do you need to buy nexavar for good cause.

The pharmacy benefit changes are not considered good cause. After the first 12 months of enrollment, Medicaid managed care enrollees can switch plans at any time. STEPS CONSUMERS CAN TAKE WHEN A MANAGED CARE PLAM DENIES ACCESS TO A NECESSARY DRUG As a first step, consumers should try to work with their providers to satisfy plan requirements for prior authorization or step therapy or any other utilization what do you need to buy nexavar control requirements. If the plan still denies access, consumers can pursue review processes specific to managed care while at the same time pursuing a fair hearing.

All plans are required to maintain an internal and external review process for complaints and appeals of service denials. Some plans may develop special procedures what do you need to buy nexavar for drug denials. Information on these procedures should be provided in member handbooks. Beginning April 1, 2018, Medicaid managed care enrollees whose plan denies prior approval of a prescription drug, or discontinues a drug that had been approved, will receive an Initial Adverse Determination notice from the plan - See Model Denial IAD Notice and IAD Notice to Reduce, Suspend or Stop Services The enrollee must first request an internal Plan Appeal and wait for the Plan's decision.

An adverse what do you need to buy nexavar decision is called a 'FInal Adverse Determination" or FAD. See model Denial FAD Notice and FAD Notice to Reduce, Suspend or Stop Services. The enroll has the right to request a fair hearing to appeal an FAD. The enrollee may only what do you need to buy nexavar request a fair hearing BEFORE receiving the FAD if the plan fails to send the FAD in the required time limit, which is 30 calendar days in standard appeals, and 72 hours in expedited appeals.

The plan may extend the time to decide both standard and expedited appeals by up to 14 days if more information is needed and it is in the enrollee's interest. AID CONTINUING -- If an enrollee requests a Plan Appeal and then a fair hearing because access to a drug has been reduced or terminated, the enrollee has the right to aid continuing (continued access to the drug in question) while waiting for the Plan Appeal and then the fair hearing. The enrollee must request the Plan Appeal and then the Fair Hearing before the effective date of the IAD and FAD notices, which is a very short time - only what do you need to buy nexavar 10 days including mailing time. See more about the changes in Managed Care appeals here.

Even though that article is focused on Managed Long Term Care, the new appeals requirements also apply to Mainstream Medicaid managed care. Enrollees who are in the first 90 days what do you need to buy nexavar of enrollment, or past the first 12 months of enrollment also have the option of switching plans to improve access to their medications. Consumers who experience problems with access to prescription drugs should always file a complaint with the State Department of Health’s Managed Care Hotline, number listed below. ACCESSING MEDICAID'S PHARMACY BENEFIT IN FEE FOR SERVICE MEDICAID For those Medicaid recipients who are not yet in a Medicaid Managed Care program, and who do not have Medicare Part D, the Medicaid Pharmacy program covers most of their prescription drugs and select non-prescription drugs and medical supplies for Family Health Plus enrollees.

Certain drugs/drug categories require the prescribers to obtain what do you need to buy nexavar prior authorization. These include brand name drugs that have a generic alternative under New York's mandatory generic drug program or prescribed drugs that are not on New York's preferred drug list. The full Medicaid formulary can be searched on the eMedNY website. Even in fee for service Medicaid, prescribers must obtain prior authorization before prescribing non-preferred drugs unless what do you need to buy nexavar otherwise indicated.

Prior authorization is required for original prescriptions, not refills. A prior authorization is effective for the original dispensing and up to five refills of that prescription within the next six months. Click here what do you need to buy nexavar for more information on NY's prior authorization process. The New York State Board of Pharmacy publishes an annual list of the 150 most frequently prescribed drugs, in the most common quantities.

The State Department of Health collects retail price information on these drugs from pharmacies that participate in the Medicaid program. Click here to search for a specific drug from the most frequently prescribed drug list and this site can also provide you with the locations of pharmacies that provide this drug what do you need to buy nexavar as well as their costs. Click here to view New York State Medicaid’s Pharmacy Provider Manual. WHO YOU CAN CALL FOR HELP Community Health Advocates Hotline.

1-888-614-5400 NY State Department what do you need to buy nexavar of Health's Managed Care Hotline. 1-800-206-8125 (Mon. - Fri. 8:30 am - 4:30 pm) NY State Department of Insurance what do you need to buy nexavar.

1-800-400-8882 NY State Attorney General's Health Care Bureau. 1-800-771-7755Haitian individuals and immigrants from some other countries who have applied for Temporary Protected Status (TPS) may be eligible for public health insurance in New York State. 2019 what do you need to buy nexavar updates - The Trump administration has taken steps to end TPS status. Two courts have temporarily enjoined the termination of TPS, one in New York State in April 2019 and one in California in October 2018.

The California case was argued in an appeals court on August 14, 2019, which the LA Times reported looked likely to uphold the federal action ending TPS. See what do you need to buy nexavar US Immigration Website on TPS - General TPS website with links to status in all countries, including HAITI. See also Pew Research March 2019 article. Courts Block Changes in Public charge rule- See updates on the Public Charge rule here, blocked by federal court injunctions in October 2019.

Read more about this change in public what do you need to buy nexavar charge rules here. What is Temporary Protected Status?. TPS is a temporary immigration status granted to eligible individuals of a certain country designated by the Department of Homeland Security because serious temporary conditions in that country, such as armed conflict or environmental disaster, prevents people from that country to return safely. On January 21, 2010 the United States determined that individuals from Haiti warranted TPS because of what do you need to buy nexavar the devastating earthquake that occurred there on January 12.

TPS gives undocumented Haitian residents, who were living in the U.S. On January 12, 2010, protection from forcible deportation and allows them to work legally. It is important what do you need to buy nexavar to note that the U.S. Grants TPS to individuals from other countries, as well, including individuals from El Salvador, Honduras, Nicaragua, Somalia and Sudan.

TPS and Public Health Insurance TPS applicants residing in New York are eligible for Medicaid and Family Health Plus as long as they also meet the income requirements for these programs. In New York, what do you need to buy nexavar applicants for TPS are considered PRUCOL immigrants (Permanently Residing Under Color of Law) for purposes of medical assistance eligibility and thus meet the immigration status requirements for Medicaid, Family Health Plus, and the Family Planning Benefit Program. Nearly all children in New York remain eligible for Child Health Plus including TPS applicants and children who lack immigration status. For more information on immigrant eligibility for public health insurance in New York see 08 GIS MA/009 and the attached chart.

Where to Apply What to BringIndividuals who have applied for TPS will need to bring several documents to what do you need to buy nexavar prove their eligibility for public health insurance. Individuals will need to bring. 1) Proof of identity. 2) Proof of residence in New what do you need to buy nexavar York.

3) Proof of income. 4) Proof of application for TPS. 5) Proof that what do you need to buy nexavar U.S. Citizenship and Immigration Services (USCIS) has received the application for TPS.

Free Communication Assistance All applicants for public health insurance, including Haitian Creole speakers, have a right to get help in a language they can understand. All Medicaid offices and enrollers are required to what do you need to buy nexavar offer free translation and interpretation services to anyone who cannot communicate effectively in English. A bilingual worker or an interpreter, whether in-person or over the telephone, must be provided in all interactions with the office. Important documents, such as Medicaid applications, should be translated either orally or in writing.

Interpreter services must be offered what do you need to buy nexavar free of charge, and applicants requiring interpreter services must not be made to wait unreasonably longer than English speaking applicants. An applicant must never be asked to bring their own interpreter. Related Resources on TPS and Public Health Insurance o The New York Immigration Coalition (NYIC) has compiled a list of agencies, law firms, and law schools responding to the tragedy in Haiti and the designation of Haiti for Temporary Protected Status. A copy of the list is posted at the NYIC’s website at http://www.thenyic.org.

o USCIS TPS website with links to status in all countries, including HAITI. O For information on eligibility for public health insurance programs call The Legal Aid Society’s Benefits Hotline 1-888-663-6880 Tuesdays, Wednesdays and Thursdays. 9:30 am - 12:30 pm FOR IMMIGRATION HELP. CONTACT THE New York State New Americans Hotline for a referral to an organization to advise you.

212-419-3737 Monday-Friday, from 9:00 a.m. To 8:00 p.m.Saturday-Sunday, from 9:00 a.m. To 5:00 p.m. Or call toll-free in New York State at 1-800-566-7636 Please see these fact sheets and web sites of national organizations for more information about the new PUBLIC CHARGE rules.

Nexavar 200mg price in uk

Nexavar
Arimidex
Nolvadex
Droxia
Buy with Bitcoin
Consultation
No
Consultation
Consultation
Long term side effects
No more than once a day
Once a day
No more than once a day
No more than once a day
Dosage
200mg 60 bottle $599.95
1mg 56 tablet $489.95
10mg 120 tablet $71.95
500mg 90 tablet $279.60
How fast does work
One pill
1mg
Ask your Doctor
Ask your Doctor
Best way to use
Yes
No
No
Yes

Scientists have created a mystery material that seems to conduct electricity without any resistance at temperatures of up to nexavar 200mg price in uk about 15 °C. That’s a new record for superconductivity, a phenomenon usually associated with very cold temperatures. The material itself is poorly understood, but nexavar 200mg price in uk it shows the potential of a class of superconductors discovered in 2015.

The superconductor has one serious limitation, however. It survives only under extremely high pressures, approaching those at the centre of Earth, meaning that it will not have any immediate practical applications. Still, physicists hope it could pave the way for the development of zero-resistance nexavar 200mg price in uk materials that can function at lower pressures.

Superconductors have a number of technological applications, from magnetic resonance imaging machines to mobile-phone towers, and researchers are beginning to experiment with them in high-performance generators for wind turbines. But their usefulness is still limited by the need for bulky cryogenics. Common superconductors work at atmospheric pressures, nexavar 200mg price in uk but only if they are kept very cold.

Even the most sophisticated ones—copper oxide-based ceramic materials—work only below 133 kelvin (−140 °C). Superconductors that work at room temperature could have a big technological impact, for example in electronics that run faster without overheating. The latest study, published in Nature on 14 October, seems to provide convincing evidence of high-temperature conductivity, says physicist Mikhail Eremets at the Max Planck Institute for Chemistry in Mainz, Germany—although he adds that nexavar 200mg price in uk he would like to see more “raw data” from the experiment.

He adds that it vindicates a line of work that he started in 2015, when his group reported the first high-pressure, high-temperature superconductor—a compound of hydrogen and sulfur that had zero resistance up to −70 °C. In 2018, a high-pressure compound of hydrogen and lanthanum was shown to be superconductive at −13 °C. But the latest result marks the first time this kind of superconductivity has nexavar 200mg price in uk been seen in a compound of three elements rather than two—the material is made of carbon, sulfur and hydrogen.

Adding a third element greatly broadens the combinations that can be included in future experiments searching for new superconductors, says study co-author Ashkan Salamat, a physicist at the University of Nevada, Las Vegas. €œWe’ve opened a whole new region” of exploration, he says. Materials that superconduct at nexavar 200mg price in uk high but not extreme pressures could already be put to use, says Maddury Somayazulu, a high-pressure-materials scientist at Argonne National Laboratory in Lemont, Illinois.

The study shows that by “judiciously choosing the third and fourth element” in a superconductor, he says, you could in principle bring down its operational pressure. The work also validates decades-old predictions by theoretical physicist Neil Ashcroft at Cornell University in Ithaca, nexavar 200mg price in uk New York, that hydrogen-rich materials might superconduct at temperatures much higher than was thought possible. €œI think there were very few people outside of the high-pressure community who took him seriously,” Somayazulu says.

Mystery material Physicist Ranga Dias at the University of Rochester in New York, along with Salamat and other collaborators, placed a mixture of carbon, hydrogen and sulfur in a microscopic niche they had carved between the tips of two diamonds. They then triggered chemical reactions in the sample with laser nexavar 200mg price in uk light, and watched as a crystal formed. As they lowered the experimental temperature, resistance to a current passed through the material dropped to zero, indicating that the sample had become superconductive.

Then they increased the pressure, and found that this transition occurred at higher and higher temperatures. Their best result was a transition temperature of 287.7 kelvin at 267 gigapascals—2.6 million times atmospheric pressure at sea level nexavar 200mg price in uk. The researchers also found some evidence that the crystal expelled its magnetic field at the transition temperature, a crucial test of superconductivity.

But much about the material remains unknown, researchers warn. €œThere are a lot of things to do,” nexavar 200mg price in uk says Eremets. Even the crystal’s exact structure and chemical formula are not yet understood.

€œAs you go to higher pressures, the sample size gets smaller,” says Salamat. €œThat’s what makes these types of measurements really challenging.” High-pressure superconductors made of hydrogen and one other nexavar 200mg price in uk element are well understood. And researchers have made computer simulations of high-pressure mixtures of carbon, hydrogen and sulfur, says Eva Zurek, a computational chemist at the State University of New York at Buffalo.

But she says those studies cannot explain the exceptionally high superconducting temperatures seen by Dias’s group. €œI am sure, after this manuscript is published, many theoretical and experimental groups will jump on this nexavar 200mg price in uk problem,” she says. This article is reproduced with permission and was first published on October 14 2020.Zeke Dunn of Brooklyn has worked at polling places in nearly every primary and general election since 2017.

The 39-year-old television producer says doing so nexavar 200mg price in uk provides a way for him to connect with his neighbors and fulfill his civic duty. But this past June he skipped working in New York State’s primary. His partner is pregnant, and he could not risk bringing the novel coronavirus home from a polling place.

As infection rates nexavar 200mg price in uk in New York City declined to low levels over the summer, Dunn decided to work the polls this November. But he worries about getting COVID-19. €œI’m not crazy about the risks,” he says.

€œIf it’s the same as it normally is, it’s exactly what they nexavar 200mg price in uk tell you not to do” to avoid COVID-19. Spending 12- to 14-hour shifts in close proximity to other poll workers, as well as interacting with hundreds of voters, in an old and poorly ventilated building. Dunn says he is determined to show up despite the risks—and this was not a decision he came to lightly.

€œI thought about how many older people nexavar 200mg price in uk work these jobs,” he says. €œIf my being willing to work in a high-contact role means they can be put in a job that has less contact with other people because I came to work that day, I’d be happy to make that concession.” He plans on bringing a face shield and several KN95 masks, which block 95 percent of particles larger than 0.3 micron, on Election Day.* In June the U.S. Centers for Disease Control and Prevention issued guidelines to help prevent the spread of COVID-19 at polling places.

The recommendations nexavar 200mg price in uk advise poll workers and voters to adopt many of the same measures public health experts have encouraged in other settings. Wearing masks, maintaining social distancing, and disinfecting surfaces and voting equipment. And people who feel unwell or have recently been exposed to someone with the virus should stay home.

€œIt’s incumbent upon all election officials at every level to advocate for the recommendations by the CDC for social distancing and mask wearing,” says nexavar 200mg price in uk C. Perry Brown, an epidemiologist at Florida A&M University’s Institute of Public Health. €œThe only way to cut down on transmission is to adhere to the recommendations.” Brown says he thinks officials should even go so nexavar 200mg price in uk far as to mandate wearing a mask in public.

(Some states already have such mandates, but others do not.) Brown recommends that voters look for a voting booth that is next to an empty one and bring disinfecting wipes to quickly clean the booth before touching anything in it. Voters should also pay attention to whether their polling place is following proper infection control protocols—and speak up if it is not—says Lenora Campbell, dean of the College of Health and Human Sciences at North Carolina Agricultural and Technical State University. She says nexavar 200mg price in uk poll workers should have a plan for how to deal with any voters who might refuse to wear a mask.

€œIt is everyone’s responsibility to ensure a safe voting experience,” Campbell says. Michael Kohanski, a rhinology fellow at the University of Pennsylvania’s Perelman School of Medicine, recommends that voters go to the polls at times that are less likely to be crowded and take advantage of early voting options if available. €œAlso, plan a backup time to vote in case you are not comfortable with the wait nexavar 200mg price in uk time at a polling location,” he says.

€œTake the time to know all the up- and down-ballot candidates and any referendum items that are on your ballot, so you can reduce your indoor time while voting.” The polling places themselves need to be prepared, too. In July Lidia Morawska, an aerosol scientist who directs the International Laboratory for Air Quality and Health at Queensland University of Technology in Australia, co-authored an open letter in Clinical Infectious Diseases urging public health agencies such as the World Health Organization to recognize the possibility of airborne transmission of coronavirus. That week nexavar 200mg price in uk the WHO updated its guidelines to acknowledge the risk of such transmission.

The CDC made a similar update on October 5. Morawska says election officials should maximize airflow at polling places by opening windows or running ventilation systems on high and without recirculation in order to bring in fresh outside air and reduce the risk of airborne spread. €œLocal building ventilation engineers nexavar 200mg price in uk should be consulted to identify the best measures,” Morawska says.

€œIf it is not possible to provide adequate ventilation, air purifiers may be installed—and everybody should be wearing masks, particularly the [polling] staff, as they may be potentially exposed in these environments for a long time.” President Donald Trump—who trails his opponent, former vice president Joe Biden, in national polls—has frequently distorted the facts about mail-in voting and has made unfounded claims about potential ballot fraud. Mail-in ballots are safe and secure, but Trump’s falsehoods may persuade some Americans to vote in person instead. Ben Hovland, chairman of the U.S nexavar 200mg price in uk.

Election Assistance Commission, says it is important for voters to know they have options. €œ[Voters should] think about how they’re going to engage and know what their options are,” he says. €œEvery state has an option to nexavar 200mg price in uk vote by mail or absentee ballot,” although a handful of states still require an excuse, such as age or disability.

People who either want or need to vote in person should go during off hours or take advantage of early voting wherever it is available. €œElection Day is the last day to vote,” nexavar 200mg price in uk Hovland says. €œAs we spread out the number of Americans participating over a broader election period, rather than just on Election Day, that helps reduce congestion and helps make a safer voting experience for all Americans.” Read more about the coronavirus outbreak from Scientific American here.

And read coverage from our international network of magazines here. *Editor’s Note (10/14/20) nexavar 200mg price in uk. This sentence has been edited after posting to correct the description of KN95 masks.Arts &.

Culture[embedded content]Four hundred years ago Galileo Galilei’s scientific findings were rejected because they didn’t fit the prevailing beliefs of the time. His story is disturbingly nexavar 200mg price in uk relevant today. Astrophysicist and author Mario Livio and Scientific American editor Clara Moskowitz to discusses lessons from Galileo’s life for dealing with science deniers now, plus a historical detective story about Galileo’s famous motto, “And yet it moves.”AdvertisementRelated VideoSupport Science JournalismDiscover world-changing science.

Explore our digital archive back to 1845, including articles by more than 150 Nobel Prize winners.Subscribe Now!. In late September, a New York nexavar 200mg price in uk Supreme Court judge ordered a judicial inquiry into the death of Eric Garner. In 2014, Garner's last words, "I can't breathe," caught on tape, became a national rally cry for criminal justice reform in the United States.

Those same words have been spoken by many Black men during their last moments of life while interacting with the police. It has been known for centuries that black men are more likely to die in police custody than men nexavar 200mg price in uk of other races. Could there be other factors aside from the color of their skin that puts these men at risk?.

Because “I can’t breathe” is so frequently uttered, one such factor could be asthma. Asthma, also known as nexavar 200mg price in uk bronchial asthma, is a chronic disease of the airway characterized by intermittent inflammation of the airways, which over time leads to irreversible changes. An estimated 339 million people globally had asthma in 2016.

Asthma is a nexavar 200mg price in uk common disease in both children and adults. People living with asthma frequently have difficulty breathing and wheezing brought on by stress, exertion, and irritants in the air. Most mortality from asthma occurs in low- and middle-income countries.

Usually, it has a low fatality rate compared to nexavar 200mg price in uk other chronic diseases. However, in 2014, African Americans were about three times more likely to die from asthma-related causes than the white population. Black children are over four times more likely to be admitted to hospital for asthma compared to white children.

African Americans nexavar 200mg price in uk do not only have a higher prevalence of asthma than whites. They are also plagued with higher rates of asthma-related morbidity and death. Multiple factors contribute to this disparity in prevalence rates including socioeconomic status, environmental factors and, plausibly, genetics.

While it is well established that genetic factors strongly affect susceptibility to asthma, it is uncertain the extent to which genetic variations contribute to the disparity in asthma prevalence, morbidity and mortality in different races nexavar 200mg price in uk. African Americans living in low-income areas have a higher prevalence of asthma and are at a greater risk of asthma-related death. Evidence suggests that both the African American race and lower socioeconomic status are independent risk factors for asthma prevalence, morbidity, and mortality affect the rate of asthma diagnosis in African Americans.

Patients who lack sufficient financial support or health insurance are nexavar 200mg price in uk at greater risk of asthma-related mortality. The quality of air breathed, which depends on the degree of environmental pollution, contributes to the asthma morbidity of urban residents in the United States like African Americans. Obesity, which is now pandemic, is another risk factor for bronchial asthma.

These are two issues that particularly plague the Black nexavar 200mg price in uk people of American inner cities. Unfortunately, the American health care system has many inequalities that negatively impact people of color. These inequalities lead to gaps in health insurance coverage, poor access to health care with higher mortalities, poor health maintenance behavior due to lack of nexavar 200mg price in uk follow up, and poor provider-patient communication.

The result is poorer outcomes for Black people living with asthma. Police brutality is inordinately a cause of mortality amongst the people of color. In the United States, African Americans disproportionately bear the brunt of these brutalities nexavar 200mg price in uk.

Many of them, unfortunately, MAY have some underlying or undiagnosed health challenges like asthma. Incidents of police brutality involving all races tend to be targeted at lower-income people who often do not have the financial resources to effectively publicize their complaints of police brutality or to seek redress. There are nexavar 200mg price in uk no large studies on the knowledge, attitudes and practices of police officers concerning asthma.

It is uncertain that police officers are aware of the symptoms, signs and immediate care that can be given to asthmatic patients in custody until help arrives. In 2014 there was a case of an asthmatic in police custody who kept saying he was asthmatic and could not breathe in Los Angeles. The police officers could not recognize nexavar 200mg price in uk the warning signs.

That inmate died. If the officers knew how to recognize the clinical tale-tell signs, he might have been alive today. The doctor who performed an autopsy on Eric Garner nexavar 200mg price in uk testified that a police officer choked him with enough force that it triggered a "lethal cascade" of events, ending in a fatal asthma attack.

How many more Black men have died in the hands of the police because of their asthma?. How many more must die before we make the needed changes?. There is nexavar 200mg price in uk a need to put an end to racism in the United States and the world at large.

Given that asthma is prevalent in communities of color, the police must embrace better tactics in apprehending, restraining and keeping custody of suspects. We must de-emphasize the use of force and firearms while we work to improve the health and health care of all communities..

Scientists have created a mystery material that seems to conduct electricity what do you need to buy nexavar without any resistance at nexavar uses temperatures of up to about 15 °C. That’s a new record for superconductivity, a phenomenon usually associated with very cold temperatures. The material itself is poorly understood, but it what do you need to buy nexavar shows the potential of a class of superconductors discovered in 2015. The superconductor has one serious limitation, however.

It survives only under extremely high pressures, approaching those at the centre of Earth, meaning that it will not have any immediate practical applications. Still, physicists hope it could pave the way for the development of what do you need to buy nexavar zero-resistance materials that can function at lower pressures. Superconductors have a number of technological applications, from magnetic resonance imaging machines to mobile-phone towers, and researchers are beginning to experiment with them in high-performance generators for wind turbines. But their usefulness is still limited by the need for bulky cryogenics.

Common superconductors work at atmospheric pressures, but only if they are kept very what do you need to buy nexavar cold. Even the most sophisticated ones—copper oxide-based ceramic materials—work only below 133 kelvin (−140 °C). Superconductors that work at room temperature could have a big technological impact, for example in electronics that run faster without overheating. The latest study, published in Nature on 14 October, seems to provide convincing evidence of high-temperature conductivity, says physicist Mikhail Eremets at the Max Planck Institute for Chemistry in Mainz, Germany—although he adds that he would like to see more “raw data” from the experiment what do you need to buy nexavar.

He adds that it vindicates a line of work that he started in 2015, when his group reported the first high-pressure, high-temperature superconductor—a compound of hydrogen and sulfur that had zero resistance up to −70 °C. In 2018, a high-pressure compound of hydrogen and lanthanum was shown to be superconductive at −13 °C. But the latest result marks the first time this kind of superconductivity has been seen in a compound of three elements rather than two—the material is made what do you need to buy nexavar of carbon, sulfur and hydrogen. Adding a third element greatly broadens the combinations that can be included in future experiments searching for new superconductors, says study co-author Ashkan Salamat, a physicist at the University of Nevada, Las Vegas.

€œWe’ve opened a whole new region” of exploration, he says. Materials that superconduct at high but not extreme pressures could already be what do you need to buy nexavar put to use, says Maddury Somayazulu, a high-pressure-materials scientist at Argonne National Laboratory in Lemont, Illinois. The study shows that by “judiciously choosing the third and fourth element” in a superconductor, he says, you could in principle bring down its operational pressure. The work also what do you need to buy nexavar validates decades-old predictions by theoretical physicist Neil Ashcroft at Cornell University in Ithaca, New York, that hydrogen-rich materials might superconduct at temperatures much higher than was thought possible.

€œI think there were very few people outside of the high-pressure community who took him seriously,” Somayazulu says. Mystery material Physicist Ranga Dias at the University of Rochester in New York, along with Salamat and other collaborators, placed a mixture of carbon, hydrogen and sulfur in a microscopic niche they had carved between the tips of two diamonds. They then triggered chemical reactions in the sample with laser light, and what do you need to buy nexavar watched as a crystal formed. As they lowered the experimental temperature, resistance to a current passed through the material dropped to zero, indicating that the sample had become superconductive.

Then they increased the pressure, and found that this transition occurred at higher and higher temperatures. Their best result what do you need to buy nexavar was a transition temperature of 287.7 kelvin at 267 gigapascals—2.6 million times atmospheric pressure at sea level. The researchers also found some evidence that the crystal expelled its magnetic field at the transition temperature, a crucial test of superconductivity. But much about the material remains unknown, researchers warn.

€œThere are a lot of things to do,” what do you need to buy nexavar says Eremets. Even the crystal’s exact structure and chemical formula are not yet understood. €œAs you go to higher pressures, the sample size gets smaller,” says Salamat. €œThat’s what makes these types of measurements really challenging.” High-pressure superconductors what do you need to buy nexavar made of hydrogen and one other element are well understood.

And researchers have made computer simulations of high-pressure mixtures of carbon, hydrogen and sulfur, says Eva Zurek, a computational chemist at the State University of New York at Buffalo. But she says those studies cannot explain the exceptionally high superconducting temperatures seen by Dias’s group. €œI am sure, what do you need to buy nexavar after this manuscript is published, many theoretical and experimental groups will jump on this problem,” she says. This article is reproduced with permission and was first published on October 14 2020.Zeke Dunn of Brooklyn has worked at polling places in nearly every primary and general election since 2017.

The 39-year-old television producer says doing so provides a way for him to connect with his neighbors and what do you need to buy nexavar fulfill his civic duty. But this past June he skipped working in New York State’s primary. His partner is pregnant, and he could not risk bringing the novel coronavirus home from a polling place. As infection rates in New York City declined to low levels over the summer, Dunn decided to work the polls this November what do you need to buy nexavar.

But he worries about getting COVID-19. €œI’m not crazy about the risks,” he says. €œIf it’s the same as it normally is, it’s exactly what they what do you need to buy nexavar tell you not to do” to avoid COVID-19. Spending 12- to 14-hour shifts in close proximity to other poll workers, as well as interacting with hundreds of voters, in an old and poorly ventilated building.

Dunn says he is determined to show up despite the risks—and this was not a decision he came to lightly. €œI thought about what do you need to buy nexavar how many older people work these jobs,” he says. €œIf my being willing to work in a high-contact role means they can be put in a job that has less contact with other people because I came to work that day, I’d be happy to make that concession.” He plans on bringing a face shield and several KN95 masks, which block 95 percent of particles larger than 0.3 micron, on Election Day.* In June the U.S. Centers for Disease Control and Prevention issued guidelines to help prevent the spread of COVID-19 at polling places.

The recommendations advise poll workers and voters to what do you need to buy nexavar adopt many of the same measures public health experts have encouraged in other settings. Wearing masks, maintaining social distancing, and disinfecting surfaces and voting equipment. And people who feel unwell or have recently been exposed to someone with the virus should stay home. €œIt’s incumbent upon all election officials at every level to advocate for the recommendations by what do you need to buy nexavar the CDC for social distancing and mask wearing,” says C.

Perry Brown, an epidemiologist at Florida A&M University’s Institute of Public Health. €œThe only way to cut down on transmission is to adhere to the recommendations.” Brown says he thinks officials should even go so far as to what do you need to buy nexavar mandate wearing a mask in public. (Some states already have such mandates, but others do not.) Brown recommends that voters look for a voting booth that is next to an empty one and bring disinfecting wipes to quickly clean the booth before touching anything in it. Voters should also pay attention to whether their polling place is following proper infection control protocols—and speak up if it is not—says Lenora Campbell, dean of the College of Health and Human Sciences at North Carolina Agricultural and Technical State University.

She says poll workers should what do you need to buy nexavar have a plan for how to deal with any voters who might refuse to wear a mask. €œIt is everyone’s responsibility to ensure a safe voting experience,” Campbell says. Michael Kohanski, a rhinology fellow at the University of Pennsylvania’s Perelman School of Medicine, recommends that voters go to the polls at times that are less likely to be crowded and take advantage of early voting options if available. €œAlso, plan a backup time to vote in case you are what do you need to buy nexavar not comfortable with the wait time at a polling location,” he says.

€œTake the time to know all the up- and down-ballot candidates and any referendum items that are on your ballot, so you can reduce your indoor time while voting.” The polling places themselves need to be prepared, too. In July Lidia Morawska, an aerosol scientist who directs the International Laboratory for Air Quality and Health at Queensland University of Technology in Australia, co-authored an open letter in Clinical Infectious Diseases urging public health agencies such as the World Health Organization to recognize the possibility of airborne transmission of coronavirus. That week the what do you need to buy nexavar WHO updated its guidelines to acknowledge the risk of such transmission. The CDC made a similar update on October 5.

Morawska says election officials should maximize airflow at polling places by opening windows or running ventilation systems on high and without recirculation in order to bring in fresh outside air and reduce the risk of airborne spread. €œLocal building ventilation what do you need to buy nexavar engineers should be consulted to identify the best measures,” Morawska says. €œIf it is not possible to provide adequate ventilation, air purifiers may be installed—and everybody should be wearing masks, particularly the [polling] staff, as they may be potentially exposed in these environments for a long time.” President Donald Trump—who trails his opponent, former vice president Joe Biden, in national polls—has frequently distorted the facts about mail-in voting and has made unfounded claims about potential ballot fraud. Mail-in ballots are safe and secure, but Trump’s falsehoods may persuade some Americans to vote in person instead.

Ben Hovland, chairman of the what do you need to buy nexavar U.S. Election Assistance Commission, says it is important for voters to know they have options. €œ[Voters should] think about how they’re going to engage and know what their options are,” he says. €œEvery state has what do you need to buy nexavar an option to vote by mail or absentee ballot,” although a handful of states still require an excuse, such as age or disability.

People who either want or need to vote in person should go during off hours or take advantage of early voting wherever it is available. €œElection Day what do you need to buy nexavar is the last day to vote,” Hovland says. €œAs we spread out the number of Americans participating over a broader election period, rather than just on Election Day, that helps reduce congestion and helps make a safer voting experience for all Americans.” Read more about the coronavirus outbreak from Scientific American here. And read coverage from our international network of magazines here.

*Editor’s Note what do you need to buy nexavar (10/14/20). This sentence has been edited after posting to correct the description of KN95 masks.Arts &. Culture[embedded content]Four hundred years ago Galileo Galilei’s scientific findings were rejected because they didn’t fit the prevailing beliefs of the time. His story is disturbingly relevant today what do you need to buy nexavar.

Astrophysicist and author Mario Livio and Scientific American editor Clara Moskowitz to discusses lessons from Galileo’s life for dealing with science deniers now, plus a historical detective story about Galileo’s famous motto, “And yet it moves.”AdvertisementRelated VideoSupport Science JournalismDiscover world-changing science. Explore our digital archive back to 1845, including articles by more than 150 Nobel Prize winners.Subscribe Now!. In late September, a New what do you need to buy nexavar York Supreme Court judge ordered a judicial inquiry into the death of Eric Garner. In 2014, Garner's last words, "I can't breathe," caught on tape, became a national rally cry for criminal justice reform in the United States.

Those same words have been spoken by many Black men during their last moments of life while interacting with the police. It has been known for centuries that what do you need to buy nexavar black men are more likely to die in police custody than men of other races. Could there be other factors aside from the color of their skin that puts these men at risk?. Because “I can’t breathe” is so frequently uttered, one such factor could be asthma.

Asthma, also known as bronchial asthma, is a chronic disease of the airway characterized by intermittent what do you need to buy nexavar inflammation of the airways, which over time leads to irreversible changes. An estimated 339 million people globally had asthma in 2016. Asthma is what do you need to buy nexavar a common disease in both children and adults. People living with asthma frequently have difficulty breathing and wheezing brought on by stress, exertion, and irritants in the air.

Most mortality from asthma occurs in low- and middle-income countries. Usually, it has a low fatality rate compared to other chronic diseases what do you need to buy nexavar. However, in 2014, African Americans were about three times more likely to die from asthma-related causes than the white population. Black children are over four times more likely to be admitted to hospital for asthma compared to white children.

African Americans do not only have a higher prevalence what do you need to buy nexavar of asthma than whites. They are also plagued with higher rates of asthma-related morbidity and death. Multiple factors contribute to this disparity in prevalence rates including socioeconomic status, environmental factors and, plausibly, genetics. While it is well established that genetic factors strongly affect susceptibility to asthma, what do you need to buy nexavar it is uncertain the extent to which genetic variations contribute to the disparity in asthma prevalence, morbidity and mortality in different races.

African Americans living in low-income areas have a higher prevalence of asthma and are at a greater risk of asthma-related death. Evidence suggests that both the African American race and lower socioeconomic status are independent risk factors for asthma prevalence, morbidity, and mortality affect the rate of asthma diagnosis in African Americans. Patients who what do you need to buy nexavar lack sufficient financial support or health insurance are at greater risk of asthma-related mortality. The quality of air breathed, which depends on the degree of environmental pollution, contributes to the asthma morbidity of urban residents in the United States like African Americans.

Obesity, which is now pandemic, is another risk factor for bronchial asthma. These are two issues that particularly what do you need to buy nexavar plague the Black people of American inner cities. Unfortunately, the American health care system has many inequalities that negatively impact people of color. These inequalities lead to gaps in health insurance coverage, poor access to health care with higher mortalities, poor health maintenance behavior due to lack of follow up, and poor provider-patient communication what do you need to buy nexavar.

The result is poorer outcomes for Black people living with asthma. Police brutality is inordinately a cause of mortality amongst the people of color. In the United States, African Americans disproportionately bear the brunt what do you need to buy nexavar of these brutalities. Many of them, unfortunately, MAY have some underlying or undiagnosed health challenges like asthma.

Incidents of police brutality involving all races tend to be targeted at lower-income people who often do not have the financial resources to effectively publicize their complaints of police brutality or to seek redress. There are no large studies on the knowledge, attitudes and practices of police officers what do you need to buy nexavar concerning asthma. It is uncertain that police officers are aware of the symptoms, signs and immediate care that can be given to asthmatic patients in custody until help arrives. In 2014 there was a case of an asthmatic in police custody who kept saying he was asthmatic and could not breathe in Los Angeles.

The police officers what do you need to buy nexavar could not recognize the warning signs. That inmate died. If the officers knew how to recognize the clinical tale-tell signs, he might have been alive today. The doctor who performed an autopsy on Eric Garner testified that a police officer choked him with enough force that it triggered a what do you need to buy nexavar "lethal cascade" of events, ending in a fatal asthma attack.

How many more Black men have died in the hands of the police because of their asthma?. How many more must die before we make the needed changes?. There is a need to put an end to racism in the United States and the world at large what do you need to buy nexavar. Given that asthma is prevalent in communities of color, the police must embrace better tactics in apprehending, restraining and keeping custody of suspects.

We must de-emphasize the use of force and firearms while we work to improve the health and health care of all communities..

What if I miss a dose?

Take the missed dose as soon as you remember, but at least 2 hours since your last meal. Skip the missed dose if it is almost time for your next scheduled dose. Do not take extra medicine to make up the missed dose.

Nexavar side effects liver cancer

How to nexavar side effects liver cancer cite this article:Singh nexavar uses O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly nexavar side effects liver cancer 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 nexavar side effects liver cancer 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 nexavar side effects liver cancer 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 nexavar side effects liver cancer 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 nexavar side effects liver cancer of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and illness and nexavar side effects liver cancer also his relationships and finances. Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him.

The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the nexavar side effects liver cancer 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 nexavar side effects liver cancer professionals were called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

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

Methods and principles of interaction with media should form a part of our training curriculum. Many professional nexavar side effects liver cancer 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 educate the public about nexavar side effects liver cancer mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr. O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource nexavar side effects liver cancer of Support. None, Conflict of Interest.

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

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

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

However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords. Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update.

Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al. In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies. The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time.

Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness. However, there are obvious ethical issues in designing human studies that are designed to answer this specific question. Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions.

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

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

In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today. The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain. The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes.

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

Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al. Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al.

That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies. In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al.

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

Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms. Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al. In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression.

It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus. The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe.

It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al. Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population. It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder.

The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al. In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered.

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

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

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

Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite. However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies. It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations.

The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis. Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

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

Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results. The ACC is another area which has been studied in some detail utilizing the MRSI technique. In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT.

This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al. In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al. Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity.

A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al. In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al.

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

This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT. However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development.

The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect. It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT. Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder.

The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration. However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory.

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

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

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

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

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

However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J. Electroconvulsive therapy. Part I.

A perspective on the evolution and current practice of ECT. J Psychiatr Pract 2009;15:346-68. 2.Lauber C, Nordt C, Falcato L, Rössler W. Can a seizure help?.

The public's attitude toward electroconvulsive therapy. Psychiatry Res 2005;134:205-9. 3.Stefanazzi M. Is electroconvulsive therapy (ECT) ever ethically justified?.

If so, under what circumstances. HEC Forum 2013;25:79-94. 4.Devanand DP, Dwork AJ, Hutchinson ER, Bolwig TG, Sackeim HA. Does ECT alter brain structure?.

Am J Psychiatry 1994;151:957-70. 5.Devanand DP. Does electroconvulsive therapy damage brain cells?. Semin Neurol 1995;15:351-7.

6.Pearsall J, Trumble B, editors. The Oxford English Reference Dictionary. 2nd ed. Oxford, England.

New York. Oxford University Press. 1996. 7.Collin PH.

Dictionary of Medical Terms. 4th ed. London. Bloomsbury.

2004. 8.Hajdu SI. Entries on laboratory medicine in the first illustrated medical dictionary. Ann Clin Lab Sci 2005;35:465-8.

9.Mander AJ, Whitfield A, Kean DM, Smith MA, Douglas RH, Kendell RE. Cerebral and brain stem changes after ECT revealed by nuclear magnetic resonance imaging. Br J Psychiatry 1987;151:69-71. 10.Coffey CE, Weiner RD, Djang WT, Figiel GS, Soady SA, Patterson LJ, et al.

Brain anatomic effects of electroconvulsive therapy. A prospective magnetic resonance imaging study. Arch Gen Psychiatry 1991;48:1013-21. 11.Scott AI, Douglas RH, Whitfield A, Kendell RE.

Time course of cerebral magnetic resonance changes after electroconvulsive therapy. Br J Psychiatry 1990;156:551-3. 12.Pande AC, Grunhaus LJ, Aisen AM, Haskett RF. A preliminary magnetic resonance imaging study of ECT-treated depressed patients.

Biol Psychiatry 1990;27:102-4. 13.Coffey CE, Figiel GS, Djang WT, Sullivan DC, Herfkens RJ, Weiner RD. Effects of ECT on brain structure. A pilot prospective magnetic resonance imaging study.

Am J Psychiatry 1988;145:701-6. 14.Qiu H, Li X, Zhao W, Du L, Huang P, Fu Y, et al. Electroconvulsive therapy-Induced brain structural and functional changes in major depressive disorders go. A longitudinal study.

Med Sci Monit 2016;22:4577-86. 15.Kunigiri G, Jayakumar PN, Janakiramaiah N, Gangadhar BN. MRI T2 relaxometry of brain regions and cognitive dysfunction following electroconvulsive therapy. Indian J Psychiatry 2007;49:195-9.

[PUBMED] [Full text] 16.Pirnia T, Joshi SH, Leaver AM, Vasavada M, Njau S, Woods RP, et al. Electroconvulsive therapy and structural neuroplasticity in neocortical, limbic and paralimbic cortex. Transl Psychiatry 2016;6:e832. 17.Szabo K, Hirsch JG, Krause M, Ende G, Henn FA, Sartorius A, et al.

Diffusion weighted MRI in the early phase after electroconvulsive therapy. Neurol Res 2007;29:256-9. 18.Nordanskog P, Dahlstrand U, Larsson MR, Larsson EM, Knutsson L, Johanson A. Increase in hippocampal volume after electroconvulsive therapy in patients with depression.

A volumetric magnetic resonance imaging study. J ECT 2010;26:62-7. 19.Nordanskog P, Larsson MR, Larsson EM, Johanson A. Hippocampal volume in relation to clinical and cognitive outcome after electroconvulsive therapy in depression.

Acta Psychiatr Scand 2014;129:303-11. 20.Tendolkar I, van Beek M, van Oostrom I, Mulder M, Janzing J, Voshaar RO, et al. Electroconvulsive therapy increases hippocampal and amygdala volume in therapy refractory depression. A longitudinal pilot study.

Psychiatry Res 2013;214:197-203. 21.Dukart J, Regen F, Kherif F, Colla M, Bajbouj M, Heuser I, et al. Electroconvulsive therapy-induced brain plasticity determines therapeutic outcome in mood disorders. Proc Natl Acad Sci U S A 2014;111:1156-61.

22.Abbott CC, Jones T, Lemke NT, Gallegos P, McClintock SM, Mayer AR, et al. Hippocampal structural and functional changes associated with electroconvulsive therapy response. Transl Psychiatry 2014;4:e483. 23.Lyden H, Espinoza RT, Pirnia T, Clark K, Joshi SH, Leaver AM, et al.

Electroconvulsive therapy mediates neuroplasticity of white matter microstructure in major depression. Transl Psychiatry 2014;4:e380. 24.Bouckaert F, De Winter FL, Emsell L, Dols A, Rhebergen D, Wampers M, et al. Grey matter volume increase following electroconvulsive therapy in patients with late life depression.

A longitudinal MRI study. J Psychiatry Neurosci 2016;41:105-14. 25.Ota M, Noda T, Sato N, Okazaki M, Ishikawa M, Hattori K, et al. Effect of electroconvulsive therapy on gray matter volume in major depressive disorder.

J Affect Disord 2015;186:186-91. 26.Zeng J, Luo Q, Du L, Liao W, Li Y, Liu H, et al. Reorganization of anatomical connectome following electroconvulsive therapy in major depressive disorder. Neural Plast 2015;2015:271674.

27.van Eijndhoven P, Mulders P, Kwekkeboom L, van Oostrom I, van Beek M, Janzing J, et al. Bilateral ECT induces bilateral increases in regional cortical thickness. Transl Psychiatry 2016;6:e874. 28.Bouckaert F, Dols A, Emsell L, De Winter FL, Vansteelandt K, Claes L, et al.

Relationship between hippocampal volume, serum BDNF, and depression severity following electroconvulsive therapy in late-life depression. Neuropsychopharmacology 2016;41:2741-8. 29.Depping MS, Nolte HM, Hirjak D, Palm E, Hofer S, Stieltjes B, et al. Cerebellar volume change in response to electroconvulsive therapy in patients with major depression.

Prog Neuropsychopharmacol Biol Psychiatry 2017;73:31-5. 30.Joshi SH, Espinoza RT, Pirnia T, Shi J, Wang Y, Ayers B, et al. Structural plasticity of the hippocampus and amygdala induced by electroconvulsive therapy in major depression. Biol Psychiatry 2016;79:282-92.

31.Wade BS, Joshi SH, Njau S, Leaver AM, Vasavada M, Woods RP, et al. Effect of electroconvulsive therapy on striatal morphometry in major depressive disorder. Neuropsychopharmacology 2016;41:2481-91. 32.Wolf RC, Nolte HM, Hirjak D, Hofer S, Seidl U, Depping MS, et al.

Structural network changes in patients with major depression and schizophrenia treated with electroconvulsive therapy. Eur Neuropsychopharmacol 2016;26:1465-74. 33.Ende G, Braus DF, Walter S, Weber-Fahr W, Henn FA. The hippocampus in patients treated with electroconvulsive therapy.

A proton magnetic resonance spectroscopic imaging study. Arch Gen Psychiatry 2000;57:937-43. 34.Michael N, Erfurth A, Ohrmann P, Arolt V, Heindel W, Pfleiderer B. Metabolic changes within the left dorsolateral prefrontal cortex occurring with electroconvulsive therapy in patients with treatment resistant unipolar depression.

Psychol Med 2003;33:1277-84. 35.Michael N, Erfurth A, Ohrmann P, Arolt V, Heindel W, Pfleiderer B. Neurotrophic effects of electroconvulsive therapy. A proton magnetic resonance study of the left amygdalar region in patients with treatment-resistant depression.

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

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

Regional brain volumes, diffusivity, and metabolite changes after electroconvulsive therapy for severe depression. Acta Psychiatr Scand 2016;133:154-64. 39.Njau S, Joshi SH, Espinoza R, Leaver AM, Vasavada M, Marquina A, et al. Neurochemical correlates of rapid treatment response to electroconvulsive therapy in patients with major depression.

J Psychiatry Neurosci 2017;42:6-16. 40.Cano M, Martínez-Zalacaín I, Bernabéu-Sanz Á, Contreras-Rodríguez O, Hernández-Ribas R, Via E, et al. Brain volumetric and metabolic correlates of electroconvulsive therapy for treatment-resistant depression. A longitudinal neuroimaging study.

Transl Psychiatry 2017;7:e1023. 41.Figiel GS, Krishnan KR, Doraiswamy PM. Subcortical structural changes in ECT-induced delirium. J Geriatr Psychiatry Neurol 1990;3:172-6.

42.Rotheneichner P, Lange S, O'Sullivan A, Marschallinger J, Zaunmair P, Geretsegger C, et al. Hippocampal neurogenesis and antidepressive therapy. Shocking relations. Neural Plast 2014;2014:723915.

43.Singh A, Kar SK. How electroconvulsive therapy works?. Understanding the neurobiological mechanisms. Clin Psychopharmacol Neurosci 2017;15:210-21.

44.Gbyl K, Videbech P. Electroconvulsive therapy increases brain volume in major depression. A systematic review and meta-analysis. Acta Psychiatr Scand 2018;138:180-95.

45.Oltedal L, Narr KL, Abbott C, Anand A, Argyelan M, Bartsch H, et al. Volume of the human hippocampus and clinical response following electroconvulsive therapy. Biol Psychiatry 2018;84:574-81. 46.Breggin PR.

Brain-Disabling Treatments in Psychiatry. Drugs, Electroshock, and the Role of the FDA. New York. Springer Pub.

Co.. 1997. 47.Posse S, Otazo R, Dager SR, Alger J. MR spectroscopic imaging.

Principles and recent advances. J Magn Reson Imaging 2013;37:1301-25. 48.Simmons ML, Frondoza CG, Coyle JT. Immunocytochemical localization of N-acetyl-aspartate with monoclonal antibodies.

Neuroscience 1991;45:37-45. 49.Obergriesser T, Ende G, Braus DF, Henn FA. Long-term follow-up of magnetic resonance-detectable choline signal changes in the hippocampus of patients treated with electroconvulsive therapy. J Clin Psychiatry 2003;64:775-80.

50.Bramham CR, Messaoudi E. BDNF function in adult synaptic plasticity. The synaptic consolidation hypothesis. Prog Neurobiol 2005;76:99-125.

51.Duman RS, Monteggia LM. A neurotrophic model for stress-related mood disorders. Biol Psychiatry 2006;59:1116-27. 52.Bocchio-Chiavetto L, Bagnardi V, Zanardini R, Molteni R, Nielsen MG, Placentino A, et al.

Serum and plasma BDNF levels in major depression. A replication study and meta-analyses. World J Biol Psychiatry 2010;11:763-73. 53.Brunoni AR, Lopes M, Fregni F.

A systematic review and meta-analysis of clinical studies on major depression and BDNF levels. Implications for the role of neuroplasticity in depression. Int J Neuropsychopharmacol 2008;11:1169-80. 54.Rocha RB, Dondossola ER, Grande AJ, Colonetti T, Ceretta LB, Passos IC, et al.

Increased BDNF levels after electroconvulsive therapy in patients with major depressive disorder. A meta-analysis study. J Psychiatr Res 2016;83:47-53. 55.UK ECT Review Group.

Efficacy and safety of electroconvulsive therapy in depressive disorders. A systematic review and meta-analysis. Lancet 2003;361:799-808. 56.57.Semkovska M, McLoughlin DM.

Objective cognitive performance associated with electroconvulsive therapy for depression. A systematic review and meta-analysis. Biol Psychiatry 2010;68:568-77. 58.Tulving E, Madigan SA.

Memory and verbal learning. Annu Rev Psychol 1970;21:437-84. 59.Rose D, Fleischmann P, Wykes T, Leese M, Bindman J. Patients' perspectives on electroconvulsive therapy.

Systematic review. BMJ 2003;326:1363. 60.Semkovska M, McLoughlin DM. Measuring retrograde autobiographical amnesia following electroconvulsive therapy.

Historical perspective and current issues. J ECT 2013;29:127-33. 61.Fraser LM, O'Carroll RE, Ebmeier KP. The effect of electroconvulsive therapy on autobiographical memory.

A systematic review. J ECT 2008;24:10-7. 62.Squire LR, Chace PM. Memory functions six to nine months after electroconvulsive therapy.

Arch Gen Psychiatry 1975;32:1557-64. 63.Squire LR, Slater PC. Electroconvulsive therapy and complaints of memory dysfunction. A prospective three-year follow-up study.

Br J Psychiatry 1983;142:1-8. 64.Squire LR, Slater PC, Miller PL. Retrograde amnesia and bilateral electroconvulsive therapy. Long-term follow-up.

Arch Gen Psychiatry 1981;38:89-95. 65.Squire LR, Wetzel CD, Slater PC. Memory complaint after electroconvulsive therapy. Assessment with a new self-rating instrument.

Biol Psychiatry 1979;14:791-801. 66.Calev A, Nigal D, Shapira B, Tubi N, Chazan S, Ben-Yehuda Y, et al. Early and long-term effects of electroconvulsive therapy and depression on memory and other cognitive functions. J Nerv Ment Dis 1991;179:526-33.

67.Sackeim HA, Prudic J, Devanand DP, Nobler MS, Lisanby SH, Peyser S, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral electroconvulsive therapy at different stimulus intensities. Arch Gen Psychiatry 2000;57:425-34. 68.Abrams R.

Does brief-pulse ECT cause persistent or permanent memory impairment?. J ECT 2002;18:71-3. 69.Peretti CS, Danion JM, Grangé D, Mobarek N. Bilateral ECT and autobiographical memory of subjective experiences related to melancholia.

A pilot study. J Affect Disord 1996;41:9-15. 70.Weiner RD, Rogers HJ, Davidson JR, Squire LR. Effects of stimulus parameters on cognitive side effects.

Ann N Y Acad Sci 1986;462:315-25. 71.Prudic J, Peyser S, Sackeim HA. Subjective memory complaints. A review of patient self-assessment of memory after electroconvulsive therapy.

J ECT 2000;16:121-32. 72.Sackeim HA, Prudic J, Devanand DP, Kiersky JE, Fitzsimons L, Moody BJ, et al. Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 1993;328:839-46.

73.Frith CD, Stevens M, Johnstone EC, Deakin JF, Lawler P, Crow TJ. Effects of ECT and depression on various aspects of memory. Br J Psychiatry 1983;142:610-7. 74.Ng C, Schweitzer I, Alexopoulos P, Celi E, Wong L, Tuckwell V, et al.

Efficacy and cognitive effects of right unilateral electroconvulsive therapy. J ECT 2000;16:370-9. 75.Coleman EA, Sackeim HA, Prudic J, Devanand DP, McElhiney MC, Moody BJ. Subjective memory complaints prior to and following electroconvulsive therapy.

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

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

Electroconvulsive therapy and risk of dementia in patients with affective disorders. A cohort study. Lancet Psychiatry 2018;5:348-56. Correspondence Address:Dr.

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

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

This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report what do you need to buy nexavar 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 what do you need to buy nexavar full of speculations about the person's mental condition and illness and also his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric what do you need to buy nexavar Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental health professionals were called by media what do you need to buy nexavar 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 what do you need to buy nexavar “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be what do you need to buy nexavar mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions. Methods and principles of interaction with media should form a part of our training curriculum.

Many professional societies have guidelines and what do you need to buy nexavar 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 what do you need to buy nexavar goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Part I. A perspective on the evolution and current practice of ECT. J Psychiatr Pract 2009;15:346-68. 2.Lauber C, Nordt C, Falcato L, Rössler W. Can a seizure help?.

The public's attitude toward electroconvulsive therapy. Psychiatry Res 2005;134:205-9. 3.Stefanazzi M. Is electroconvulsive therapy (ECT) ever ethically justified?. If so, under what circumstances.

HEC Forum 2013;25:79-94. 4.Devanand DP, Dwork AJ, Hutchinson ER, Bolwig TG, Sackeim HA. Does ECT alter brain structure?. Am J Psychiatry 1994;151:957-70. 5.Devanand DP.

Does electroconvulsive therapy damage brain cells?. Semin Neurol 1995;15:351-7. 6.Pearsall J, Trumble B, editors. The Oxford English Reference Dictionary. 2nd ed.

Oxford, England. New York. Oxford University Press. 1996. 7.Collin PH.

Dictionary of Medical Terms. 4th ed. London. Bloomsbury. 2004.

8.Hajdu SI. Entries on laboratory medicine in the first illustrated medical dictionary. Ann Clin Lab Sci 2005;35:465-8. 9.Mander AJ, Whitfield A, Kean DM, Smith MA, Douglas RH, Kendell RE. Cerebral and brain stem changes after ECT revealed by nuclear magnetic resonance imaging.

Br J Psychiatry 1987;151:69-71. 10.Coffey CE, Weiner RD, Djang WT, Figiel GS, Soady SA, Patterson LJ, et al. Brain anatomic effects of electroconvulsive therapy. A prospective magnetic resonance imaging study. Arch Gen Psychiatry 1991;48:1013-21.

11.Scott AI, Douglas RH, Whitfield A, Kendell RE. Time course of cerebral magnetic resonance changes after electroconvulsive therapy. Br J Psychiatry 1990;156:551-3. 12.Pande AC, Grunhaus LJ, Aisen AM, Haskett RF. A preliminary magnetic resonance imaging study of ECT-treated depressed patients.

Biol Psychiatry 1990;27:102-4. 13.Coffey CE, Figiel GS, Djang WT, Sullivan DC, Herfkens RJ, Weiner RD. Effects of ECT on brain structure. A pilot prospective magnetic resonance imaging study. Am J Psychiatry 1988;145:701-6.

14.Qiu H, Li X, Zhao W, Du L, Huang P, Fu Y, et al. Electroconvulsive therapy-Induced brain structural and functional changes in major depressive disorders. A longitudinal study. Med Sci Monit 2016;22:4577-86. 15.Kunigiri G, Jayakumar PN, Janakiramaiah N, Gangadhar BN.

MRI T2 relaxometry of brain regions and cognitive dysfunction following electroconvulsive therapy. Indian J Psychiatry 2007;49:195-9. [PUBMED] [Full text] 16.Pirnia T, Joshi SH, Leaver AM, Vasavada M, Njau S, Woods RP, et al. Electroconvulsive therapy and structural neuroplasticity in neocortical, limbic and paralimbic cortex. Transl Psychiatry 2016;6:e832.

17.Szabo K, Hirsch JG, Krause M, Ende G, Henn FA, Sartorius A, et al. Diffusion weighted MRI in the early phase after electroconvulsive therapy. Neurol Res 2007;29:256-9. 18.Nordanskog P, Dahlstrand U, Larsson MR, Larsson EM, Knutsson L, Johanson A. Increase in hippocampal volume after electroconvulsive therapy in patients with depression.

A volumetric magnetic resonance imaging study. J ECT 2010;26:62-7. 19.Nordanskog P, Larsson MR, Larsson EM, Johanson A. Hippocampal volume in relation to clinical and cognitive outcome after electroconvulsive therapy in depression. Acta Psychiatr Scand 2014;129:303-11.

20.Tendolkar I, van Beek M, van Oostrom I, Mulder M, Janzing J, Voshaar RO, et al. Electroconvulsive therapy increases hippocampal and amygdala volume in therapy refractory depression. A longitudinal pilot study. Psychiatry Res 2013;214:197-203. 21.Dukart J, Regen F, Kherif F, Colla M, Bajbouj M, Heuser I, et al.

Electroconvulsive therapy-induced brain plasticity determines therapeutic outcome in mood disorders. Proc Natl Acad Sci U S A 2014;111:1156-61. 22.Abbott CC, Jones T, Lemke NT, Gallegos P, McClintock SM, Mayer AR, et al. Hippocampal structural and functional changes associated with electroconvulsive therapy response. Transl Psychiatry 2014;4:e483.

23.Lyden H, Espinoza RT, Pirnia T, Clark K, Joshi SH, Leaver AM, et al. Electroconvulsive therapy mediates neuroplasticity of white matter microstructure in major depression. Transl Psychiatry 2014;4:e380. 24.Bouckaert F, De Winter FL, Emsell L, Dols A, Rhebergen D, Wampers M, et al. Grey matter volume increase following electroconvulsive therapy in patients with late life depression.

A longitudinal MRI study. J Psychiatry Neurosci 2016;41:105-14. 25.Ota M, Noda T, Sato N, Okazaki M, Ishikawa M, Hattori K, et al. Effect of electroconvulsive therapy on gray matter volume in major depressive disorder. J Affect Disord 2015;186:186-91.

26.Zeng J, Luo Q, Du L, Liao W, Li Y, Liu H, et al. Reorganization of anatomical connectome following electroconvulsive therapy in major depressive disorder. Neural Plast 2015;2015:271674. 27.van Eijndhoven P, Mulders P, Kwekkeboom L, van Oostrom I, van Beek M, Janzing J, et al. Bilateral ECT induces bilateral increases in regional cortical thickness.

Transl Psychiatry 2016;6:e874. 28.Bouckaert F, Dols A, Emsell L, De Winter FL, Vansteelandt K, Claes L, et al. Relationship between hippocampal volume, serum BDNF, and depression severity following electroconvulsive therapy in late-life depression. Neuropsychopharmacology 2016;41:2741-8. 29.Depping MS, Nolte HM, Hirjak D, Palm E, Hofer S, Stieltjes B, et al.

Cerebellar volume change in response to electroconvulsive therapy in patients with major depression. Prog Neuropsychopharmacol Biol Psychiatry 2017;73:31-5. 30.Joshi SH, Espinoza RT, Pirnia T, Shi J, Wang Y, Ayers B, et al. Structural plasticity of the hippocampus and amygdala induced by electroconvulsive therapy in major depression. Biol Psychiatry 2016;79:282-92.

31.Wade BS, Joshi SH, Njau S, Leaver AM, Vasavada M, Woods RP, et al. Effect of electroconvulsive therapy on striatal morphometry in major depressive disorder. Neuropsychopharmacology 2016;41:2481-91. 32.Wolf RC, Nolte HM, Hirjak D, Hofer S, Seidl U, Depping MS, et al. Structural network changes in patients with major depression and schizophrenia treated with electroconvulsive therapy.

Eur Neuropsychopharmacol 2016;26:1465-74. 33.Ende G, Braus DF, Walter S, Weber-Fahr W, Henn FA. The hippocampus in patients treated with electroconvulsive therapy. A proton magnetic resonance spectroscopic imaging study. Arch Gen Psychiatry 2000;57:937-43.

34.Michael N, Erfurth A, Ohrmann P, Arolt V, Heindel W, Pfleiderer B. Metabolic changes within the left dorsolateral prefrontal cortex occurring with electroconvulsive therapy in patients with treatment resistant unipolar depression. Psychol Med 2003;33:1277-84. 35.Michael N, Erfurth A, Ohrmann P, Arolt V, Heindel W, Pfleiderer B. Neurotrophic effects of electroconvulsive therapy.

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

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

Acta Psychiatr Scand 2016;133:154-64. 39.Njau S, Joshi SH, Espinoza R, Leaver AM, Vasavada M, Marquina A, et al. Neurochemical correlates of rapid treatment response to electroconvulsive therapy in patients with major depression. J Psychiatry Neurosci 2017;42:6-16. 40.Cano M, Martínez-Zalacaín I, Bernabéu-Sanz Á, Contreras-Rodríguez O, Hernández-Ribas R, Via E, et al.

Brain volumetric and metabolic correlates of electroconvulsive therapy for treatment-resistant depression. A longitudinal neuroimaging study. Transl Psychiatry 2017;7:e1023. 41.Figiel GS, Krishnan KR, Doraiswamy PM. Subcortical structural changes in ECT-induced delirium.

J Geriatr Psychiatry Neurol 1990;3:172-6. 42.Rotheneichner P, Lange S, O'Sullivan A, Marschallinger J, Zaunmair P, Geretsegger C, et al. Hippocampal neurogenesis and antidepressive therapy. Shocking relations. Neural Plast 2014;2014:723915.

43.Singh A, Kar SK. How electroconvulsive therapy works?. Understanding the neurobiological mechanisms. Clin Psychopharmacol Neurosci 2017;15:210-21. 44.Gbyl K, Videbech P.

Electroconvulsive therapy increases brain volume in major depression. A systematic review and meta-analysis. Acta Psychiatr Scand 2018;138:180-95. 45.Oltedal L, Narr KL, Abbott C, Anand A, Argyelan M, Bartsch H, et al. Volume of the human hippocampus and clinical response following electroconvulsive therapy.

Biol Psychiatry 2018;84:574-81. 46.Breggin PR. Brain-Disabling Treatments in Psychiatry. Drugs, Electroshock, and the Role of the FDA. New York.

Springer Pub. Co.. 1997. 47.Posse S, Otazo R, Dager SR, Alger J. MR spectroscopic imaging.

Principles and recent advances. J Magn Reson Imaging 2013;37:1301-25. 48.Simmons ML, Frondoza CG, Coyle JT. Immunocytochemical localization of N-acetyl-aspartate with monoclonal antibodies. Neuroscience 1991;45:37-45.

49.Obergriesser T, Ende G, Braus DF, Henn FA. Long-term follow-up of magnetic resonance-detectable choline signal changes in the hippocampus of patients treated with electroconvulsive therapy. J Clin Psychiatry 2003;64:775-80. 50.Bramham CR, Messaoudi E. BDNF function in adult synaptic plasticity.

The synaptic consolidation hypothesis. Prog Neurobiol 2005;76:99-125. 51.Duman RS, Monteggia LM. A neurotrophic model for stress-related mood disorders. Biol Psychiatry 2006;59:1116-27.

52.Bocchio-Chiavetto L, Bagnardi V, Zanardini R, Molteni R, Nielsen MG, Placentino A, et al. Serum and plasma BDNF levels in major depression. A replication study and meta-analyses. World J Biol Psychiatry 2010;11:763-73. 53.Brunoni AR, Lopes M, Fregni F.

A systematic review and meta-analysis of clinical studies on major depression and BDNF levels. Implications for the role of neuroplasticity in depression. Int J Neuropsychopharmacol 2008;11:1169-80. 54.Rocha RB, Dondossola ER, Grande AJ, Colonetti T, Ceretta LB, Passos IC, et al. Increased BDNF levels after electroconvulsive therapy in patients with major depressive disorder.

A meta-analysis study. J Psychiatr Res 2016;83:47-53. 55.UK ECT Review Group. Efficacy and safety of electroconvulsive therapy in depressive disorders. A systematic review and meta-analysis.

Lancet 2003;361:799-808. 56.57.Semkovska M, McLoughlin DM. Objective cognitive performance associated with electroconvulsive therapy for depression. A systematic review and meta-analysis. Biol Psychiatry 2010;68:568-77.

58.Tulving E, Madigan SA. Memory and verbal learning. Annu Rev Psychol 1970;21:437-84. 59.Rose D, Fleischmann P, Wykes T, Leese M, Bindman J. Patients' perspectives on electroconvulsive therapy.

Systematic review. BMJ 2003;326:1363. 60.Semkovska M, McLoughlin DM. Measuring retrograde autobiographical amnesia following electroconvulsive therapy. Historical perspective and current issues.

J ECT 2013;29:127-33. 61.Fraser LM, O'Carroll RE, Ebmeier KP. The effect of electroconvulsive therapy on autobiographical memory. A systematic review. J ECT 2008;24:10-7.

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

A prospective three-year follow-up study. Br J Psychiatry 1983;142:1-8. 64.Squire LR, Slater PC, Miller PL. Retrograde amnesia and bilateral electroconvulsive therapy. Long-term follow-up.

Arch Gen Psychiatry 1981;38:89-95. 65.Squire LR, Wetzel CD, Slater PC. Memory complaint after electroconvulsive therapy. Assessment with a new self-rating instrument. Biol Psychiatry 1979;14:791-801.

66.Calev A, Nigal D, Shapira B, Tubi N, Chazan S, Ben-Yehuda Y, et al. Early and long-term effects of electroconvulsive therapy and depression on memory and other cognitive functions. J Nerv Ment Dis 1991;179:526-33. 67.Sackeim HA, Prudic J, Devanand DP, Nobler MS, Lisanby SH, Peyser S, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral electroconvulsive therapy at different stimulus intensities.

Arch Gen Psychiatry 2000;57:425-34. 68.Abrams R. Does brief-pulse ECT cause persistent or permanent memory impairment?. J ECT 2002;18:71-3. 69.Peretti CS, Danion JM, Grangé D, Mobarek N.

Bilateral ECT and autobiographical memory of subjective experiences related to melancholia. A pilot study. J Affect Disord 1996;41:9-15. 70.Weiner RD, Rogers HJ, Davidson JR, Squire LR. Effects of stimulus parameters on cognitive side effects.

Ann N Y Acad Sci 1986;462:315-25. 71.Prudic J, Peyser S, Sackeim HA. Subjective memory complaints. A review of patient self-assessment of memory after electroconvulsive therapy. J ECT 2000;16:121-32.

72.Sackeim HA, Prudic J, Devanand DP, Kiersky JE, Fitzsimons L, Moody BJ, et al. Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 1993;328:839-46. 73.Frith CD, Stevens M, Johnstone EC, Deakin JF, Lawler P, Crow TJ. Effects of ECT and depression on various aspects of memory.

Br J Psychiatry 1983;142:610-7. 74.Ng C, Schweitzer I, Alexopoulos P, Celi E, Wong L, Tuckwell V, et al. Efficacy and cognitive effects of right unilateral electroconvulsive therapy. J ECT 2000;16:370-9. 75.Coleman EA, Sackeim HA, Prudic J, Devanand DP, McElhiney MC, Moody BJ.

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

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

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

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

Nexavar cost

After voters expanded Medicaid in conservative states like Missouri and Oklahoma, health care advocates are renewing a push for expansion in Mississippi and other Southern states where Republican leaders have long been opposed.They say the changing tide has followed rising income inequality, joblessness and pressure from hospitals in economic turmoil — issues exacerbated by the coronavirus pandemic."There have been, in the last two years, votes on Medicaid expansion in some of the most conservative, Republican-leaning states in the country, and Medicaid expansion has never lost," said Eliot Fishman, senior director of Health Policy at Families USA, a health care advocacy nexavar cost organization.Fishman spoke Thursday during an online forum about Medicaid expansion hosted by the Mississippi Health Advocacy Program and the Mississippi Center for Justice.Medicaid expansion is an option under the health care overhaul that then-President Barack Obama signed into law in 2010. Many Democratic-controlled states agreed to expansion, mainly for people whose jobs don't provide health insurance.However, since Republican Donald Trump became president in January 2017, voters in Idaho, Nebraska, Utah, Oklahoma, Maine and most recently nexavar cost Missouri have approved Medicaid expansion by ballot measures. In Virginia, legislators passed Medicaid expansion after Democrats gained power."This is clearly an issue which you can no longer shut down voter interest by just saying the word 'Obamacare,' " Fishman said. "That power has waned."There are now 12 states — including Mississippi, Georgia, Alabama, Texas, South Carolina, North Carolina, Tennessee and Florida — that have not expanded nexavar cost Medicaid.

A newly formed collaborative, "Southerners for Medicaid Expansion," is aiming to put pressure on the holdouts.Medicaid is a government health insurance program for the needy, aged, blind and disabled, and nexavar cost it is paid by state and federal money. Because Mississippi is poor, the federal government pays nearly 78% of the cost.Under expansion, the federal government pays 90% of the cost in any state.About 25% of Mississippi's nearly 3 million residents are already enrolled in Medicaid, and opponents have said they don't want more people taking part in a government program.Roy Mitchell, executive director of the Mississippi Health Advocacy Program, said hospitals are in desperate need of the dollars. Uncompensated care costs in Mississippi nexavar cost exceed $600 million annually, according to a 2019 statement from the Mississippi Hospital Association."Let's face it, providers are businessmen. Despite their marketing, they are inherently out to make a profit, and they are going to have to wake up in Mississippi," Mitchell said.

"I'm sure COVID nexavar cost did a good job of doing that."Addressing ailing hospitals has been controversial. Republican Gov nexavar cost. Tate Reeves and leaders in the Republican-controlled Mississippi Legislature have opposed Medicaid expansion. Reeves has said money should go instead to federally funded community health centers that help people in need.Reeves has said repeatedly that the pandemic has not nexavar cost changed his mind about expansion.

And Republican House Speaker Philip Gunn told reporters this month that he also remains opposed.The Mississippi Hospital Association in 2019 proposed "Mississippi Cares," which it called Medicaid reform but not expansion. It was modeled nexavar cost after an Indiana program enacted under then-Gov. Mike Pence nexavar cost. It would expand Medicaid eligibility while setting $20 monthly premium payments and copays.

The proposal gained no traction during this year's Mississippi legislative session.While advocates for Medicaid expansion say they are hopeful, they acknowledge difficulties.Out of the 12 nonexpansion states, Mississippi and Florida are the only two with a ballot initiative process.Mississippi law nexavar cost says that for an initiative to be placed on the ballot, at least 106,190 certified signatures must be gathered, and those must be evenly divided among the five congressional districts that Mississippi used 20 years ago. Even if signature-gathering is successful, the earliest a proposal is likely to be on the ballot is November 2022."For all the stars to align in a ballot initiative ... There's got to nexavar cost be a commitment on the part of providers in Mississippi, I think, and we have to also look realistically at the amount of resources that it takes to do a ballot initiative," Mitchell said. "But it is certainly not out of reach."Consultations nexavar cost via tablets, laptops and phones linked patients and doctors when society shut down in early spring.

Telehealth visits dropped with the reopening, but they're still far more common than before and now there's a push to make them widely available in the future.Permanently expanding access will involve striking a balance between costs and quality, dealing with privacy concerns and potential fraud, and figuring out how telehealth can reach marginalized patients, including people with mental health problems."I don't think it is ever going to replace in-person visits, because sometimes a doctor needs to put hands on a patient," said CMS Administrator Seema Verma, the Trump administration's leading advocate for telehealth.Caveats aside, "it's almost a modern-day house call," she added."It's fair to say that telemedicine was in its infancy prior to the pandemic, but it's come of age this year," said Murray Aitken of the data firm IQVIA, which tracks the impact.In the depths of the coronavirus shutdown, telehealth accounted for more than 40% of primary care visits for patients with traditional Medicare, up from a tiny 0.1% sliver before the public health emergency. As the government's flagship health care program, Medicare covers more than 60 million people, including those age 65 and older, nexavar cost and younger disabled people.A recent poll of older adults by the University of Michigan Institute for Healthcare Policy &. Innovation found that more than 7 in 10 are interested in using telehealth for follow-ups with their doctor, and nearly 2 out of 3 feel comfortable with nexavar cost video conferences.But privacy was an issue, especially for those who hadn't tried telehealth. The poll found 27% of older adults who had not had a telemedicine visit were concerned about privacy, compared with 17% of those who tried it.Those who tried telehealth weren't completely sold.

About 4 in 5 were concerned the doctor couldn't physically examine them, and 64% nexavar cost worried the quality wasn't as good."After the initial excitement, in the afterglow, patients realize 'I can't get my vaccine,' or 'You can't see this thing in the back of my throat over the computer,' " said Dr. Gary LeRoy of Dayton, Ohio, a primary care doctor and president of the American Academy of Family Physicians.For Medicare beneficiary Jean Grady of Westford, Vermont, telemedicine was a relief. She needed a checkup nexavar cost required by Medicare to continue receiving supplies for her wearable insulin pump. Being in a high risk group for COVID-19, Grady worried about potential exposure in a doctor's waiting room, and even more about losing her diabetes supplies if she missed Medicare's checkup deadline."I would have had to go back to taking insulin by syringe," she said.Grady prepared for nexavar cost the virtual visit by calling her clinician's tech department and downloading teleconference software.

She says she would do some future visits by video, but not all. For example, people with diabetes need nexavar cost periodic blood tests, and their feet must be checked for signs of circulatory problems.Still, quite a few follow-ups "could be done very efficiently and be just as useful to the physician and myself as going in and seeing them in person," Grady said.Many private insurance plans, including those in Medicare Advantage, offer some level of telemedicine coverage.But traditional Medicare has restricted it to rural residents, who generally had to travel to specially designated sites to connect.Under the coronavirus public health emergency, the administration temporarily waived Medicare's restrictions so enrollees anywhere could use telemedicine. Patients could connect from home. Making such changes nexavar cost permanent would require legislation from Congress, but there's bipartisan interest.Sen.

Lamar Alexander, chairman of the Senate Health, Education, Labor and Pensions Committee, says he'd like to see broader access, without breaking the bank."Our job should be to ensure that change is done with the goals of better outcomes and better patient experiences, at nexavar cost a lower cost," said Alexander, R-Tenn.That's a tall order.Payment will be a sticky obstacle. For now, Medicare is paying clinicians on par for virtual and in-person visits."Policymakers seems to be in a rush to pass legislation, but I think it is worth taking a little more time," said Juliette Cubanski, a Medicare expert with the nonpartisan Kaiser Family Foundation. "Fraud is one big area that policymakers need to be cognizant of."Fraud-busters agree.Telehealth is so new that "we don't have at this point a real sense nexavar cost of where the huge risks lie," said Andrew VanLandingham, a senior lawyer with the Health and Human Services inspector general's office. "We are sort of in an experimental phase."Despite the risks, advocates see opportunities.Expanded Medicare telehealth could:help move the nation closer to a long-sought goal of treating mental health the same as physical conditions.

Sen. Ron Wyden, D-Ore., wants to use telemedicine as a springboard to improve mental health care. IQVIA data shows 60% of psychiatric consults took place by telehealth during the shutdown.increase access for people living in remote communities, in low-income urban areas and even nursing homes. Medicare's research shows low-income beneficiaries have had similar patterns of using telehealth for primary care as program enrollees overall.improve coordination of care for people with chronic health conditions, a goal that requires patient and persistent monitoring.

Chronic care accounts for most program spending.University of Michigan health policy expert Mark Fendrick says Medicare should figure out what services add value for patients' health and taxpayers' wallets, and pay just for those.Telehealth "was an overnight sensation," said Fendrick. "Hopefully it's not a one-hit wonder."As the wind howled and the rain slammed down, a team of nurses, respiratory therapists and a doctor worked through the night to care for 19 tiny babies as Hurricane Laura slammed southwestern Louisiana.The babies, some on ventilators or eating through a feeding tube, seemed to weather the storm just fine, said Dr. Juan Bossano, the medical director of the neonatal intensive care unit at Lake Charles Memorial Hospital for Women. "They did very well.

They tolerated it very well. We had a very good day," he said.Laura made landfall early Thursday morning as a Category 4 storm, packing top winds of 150 mph (241 kph), and pushing a storm surge as high as 15 feet in some areas.Hours before it made landfall, officials had to move the babies from the women's hospital to the main hospital in the system after it became clear that storm surge could inundate the women's hospital, located on the southern end of Lake Charles. The hospital has its own generator and hospital administrator Alesha Alford said it was built to withstand hurricane force winds. But in the single story facility, there's no room to move up and storm surge in that area was expected to hit nine feet.

In a roughly two-hour operation the babies in the intensive care unit were transferred by ambulance to Lake Charles Memorial Hospital, a ten-story facility on the northern side of the city. Trucks carried needed equipment such as incubators.Alford said the storm hadn't yet hit but "the skies looked very ominous." She said everyone pitched in to get supplies moved to the other hospital."It went as smooth as could be because we had everyone helping," she said.Alford said three mothers who couldn't be discharged from the women's hospital were also transferred. Two of them had their newborns with them while the child of the third mom was in the intensive care unit. Parents of the other children in the neonatal intensive care unit couldn't stay with them during the storm because there wasn't enough room so Bossano said one nurse was tasked with calling parents to keep them informed of how their children were doing.

Bossano occasionally posted updates on Facebook.Once they got situated at the larger hospital and the winds picked up, Alford said the patients were moved into the hallways. To "protect our babies," mattresses were pushed up against the windows to prevent flying glass although none of the windows ended up breaking.She said as huge gusts of wind started coming in, they could feel the building vibrate. In addition to Bossano, the medical staff consisted of two neonatal nurse practitioners, 14 nurses and three respiratory therapists who worked on 12-hour shifts. Some of the staff slept on air mattresses in the hallway, Alford said.

After making it through the hurricane, the plan was to have the babies stay in Lake Charles. While electricity was out in the city, the hospital has its own generator. But Alford said the city's water system has been so heavily damaged that it ultimately forced them to transfer the babies as well as other patients to other hospitals around the state Friday.Both Alford and Bossano repeatedly praised the nursing staff for their work in caring for the babies that in some cases were born weighing only a pound or two. Some of the nursing staff lost their houses in the storm, and they were worried about their own families, but they put those concerns aside to care for their tiny patients."Really the nurses and the respiratory therapists are the heroes here," Bosanno said.

"They showed that very clearly the way they performed."There aren’t many hospital visitors amid the COVID-19 pandemic. But, if you were to walk through intensive-care units at one New York City hospital, you’d see internet-connected speakers—about the size of a stack of Post-it Notes—affixed to the bedrails of some patient beds.It’s part of a project by two Weill Cornell Medicine doctors to help family members speak with ICU patients, often intubated or otherwise not able to hold up a phone themselves, from afar.“The patients could be completely sedated, they could be in a coma,” but families still want to be there with them, said Dr. Marc Schiffman, an interventional radiologist and one of the doctors who spearheaded bringing the devices into ICUs.The speakers, now in 11 units at Weill Cornell, are part of a two-way communication system from company Relay, originally developed as a walkie-talkie system of sorts for children to stay in touch with their parents throughout the day. Users on one end record snippets of conversation using a mobile app, which are automatically played out loud through the small speaker.Users on the other end push a button on the device to record a response.“Whenever (families) have a story they want to recount, they can just talk into their phone,” Schiffman said.

€œIt gives the families a sense of autonomy (and) connection,” even when the patient can’t respond.The effort, dubbed the VoiceLove Project, began about four months ago, at the height of the COVID-19 pandemic in New York City.Families and other visitors were no longer allowed inside Weill Cornell, but still wanted a way to connect with patients who were sick with COVID-19. Initially, that involved a nurse standing in the ICU and holding up a phone or tablet so families could see the patient—a task that took time out of their already busy day, potentially exposed them to COVID-19 and often meant using scarce personal protective equipment.“It really wasn’t a practical solution,” said Dr. Tamatha Fenster, a minimally invasive gynecologic surgeon.So Fenster and Schiffman began brainstorming hands-free technologies they could install directly at the bedside. Schiffman drove to a local Target store and bought a few Relay walkie-talkie devices.

After testing it with families and patients in the ICU, the two decided it was a “grand slam,” Schiffman said.Since March, hospitals have been trying new ways to keep patients connected to families at home, said Bill Flatley, senior service delivery manager at consulting firm OST. He said he’s mainly seen hospitals repurpose technology usually used for telemedicine, like tablets and cameras mounted on telemedicine carts.It’s likely hospitals will have to continue to restrict visitors, at least as long as there’s uncertainty around COVID-19 treatment. So it’s integral for staff to figure out processes that make it easy for families to talk to patients—without putting an additional burden on clinicians or expecting them to serve as tech support.For Fenster and Schiffman, deploying walkie-talkies in the ICU for the first time took some leg work.To scale the walkie-talkie system, Schiffman reached out to Relay’s team via the company’s website, and the company agreed to donate roughly 130 devices and waived the per-user subscription fee. The doctors and Relay have continued to work together on best practices for using the devices in ICUs, a use case Relay is marketing and could sell to other hospitals, according to Jon Schniepp, Relay’s senior vice president of marketing.But Fenster and Schiffman couldn’t just bring walkie-talkies into the ICU.

In the hospital setting, there are additional quality and privacy concerns. To address those, the doctors created a disposable case, which made it easier to keep the device sterile and blocked passersby from accidentally pressing the button that would transmit sounds to a family’s Relay app.The two spent thousands of dollars out of their own pockets to devise the best case design, Fenster said, working with an industrial designer in New Jersey to 3D print different models. The final plastic case, customized with the phrase “VoiceLove” on the front, costs about $10 per case to print and ship. They’ve started reaching out to acute-care and post-acute facilities in California, Texas and other COVID hot spots to explain how the VoiceLove Project works, hoping to connect other groups with Relay and share the case design.

But the doctors say they’re still working out the logistics of getting the equipment to interested organizationsWhen Dr. George Wanna saw how devastated St. George Hospital University Medical Center was by an explosion that shook Beirut, he felt a need to help his hometown. The Aug.

4 blast in the city’s harbor ravaged St. George’s, so Wanna launched a GoFundMe page to help the hospital, where a good friend of his, Dr. Alexander Nehme, is chief medical officer.At deadline, more than $86,600 had been raised, with a goal of $100,000. €œThis is the first time in their 140-year history when St.

George’s Hospital was damaged so severely that it is unable to function,” said Wanna, chair of the otolaryngology department at New York Eye and Ear Infirmary of Mount Sinai and Mount Sinai Beth Israel in New York. €¨St. George Hospital even remained open during Lebanon’s 15-year civil war, a conflict that wracked Beirut and forced Wanna to spend much of his childhood in bomb shelters. Wanna is also working with Mount Sinai to send medical supplies.

€œSt. George Hospital is in need of everything needed to run a hospital—beds, ventilators, protective equipment.” The tragedy also affected Wanna’s family. His parents weren’t home when the blast struck and were unharmed. But “my parents’ home was severely damaged by the blast.

Sadly, we lost the lives of several of my dad’s relatives,” he said via email. Wanna, who spent his residency at Mount Sinai, is grateful to the system. €œThey have given me a chance to have the kind of life I could never have hoped for—they helped me build a home and a life in this great country.”.

After voters expanded Medicaid in conservative states like Missouri and Oklahoma, health care advocates are renewing a push for expansion in Mississippi and other Southern states where Republican leaders have long been opposed.They say the changing tide has followed rising income inequality, joblessness and pressure from hospitals in economic turmoil — issues exacerbated by the coronavirus pandemic."There have been, in what do you need to buy nexavar the last two years, votes on Medicaid expansion in some of the most conservative, Republican-leaning states in the country, and Medicaid expansion has never lost," said Eliot Fishman, senior director of Health Policy at Families USA, a health care advocacy organization.Fishman spoke Thursday during an online forum about Medicaid expansion hosted by the Mississippi Health Advocacy Program and the Mississippi Center for Justice.Medicaid expansion is an option under the health care overhaul that then-President Barack Obama signed into law in 2010. Many Democratic-controlled states agreed to expansion, mainly for people whose jobs don't provide health insurance.However, since Republican Donald Trump became president in January 2017, voters in Idaho, Nebraska, Utah, Oklahoma, what do you need to buy nexavar Maine and most recently Missouri have approved Medicaid expansion by ballot measures. In Virginia, legislators passed Medicaid expansion after Democrats gained power."This is clearly an issue which you can no longer shut down voter interest by just saying the word 'Obamacare,' " Fishman said. "That power has waned."There are now 12 states — including Mississippi, Georgia, Alabama, Texas, South Carolina, North Carolina, Tennessee and Florida — that have not expanded Medicaid what do you need to buy nexavar. A newly formed collaborative, "Southerners for Medicaid Expansion," is aiming to put what do you need to buy nexavar pressure on the holdouts.Medicaid is a government health insurance program for the needy, aged, blind and disabled, and it is paid by state and federal money.

Because Mississippi is poor, the federal government pays nearly 78% of the cost.Under expansion, the federal government pays 90% of the cost in any state.About 25% of Mississippi's nearly 3 million residents are already enrolled in Medicaid, and opponents have said they don't want more people taking part in a government program.Roy Mitchell, executive director of the Mississippi Health Advocacy Program, said hospitals are in desperate need of the dollars. Uncompensated care costs in Mississippi exceed $600 million annually, according to a 2019 statement from the Mississippi Hospital Association."Let's what do you need to buy nexavar face it, providers are businessmen. Despite their marketing, they are inherently out to make a profit, and they are going to have to wake up in Mississippi," Mitchell said. "I'm sure COVID did a good job of doing that."Addressing ailing hospitals what do you need to buy nexavar has been controversial. Republican Gov what do you need to buy nexavar.

Tate Reeves and leaders in the Republican-controlled Mississippi Legislature have opposed Medicaid expansion. Reeves has said money should go instead to federally funded community health centers that help people in need.Reeves has what do you need to buy nexavar said repeatedly that the pandemic has not changed his mind about expansion. And Republican House Speaker Philip Gunn told reporters this month that he also remains opposed.The Mississippi Hospital Association in 2019 proposed "Mississippi Cares," which it called Medicaid reform but not expansion. It was modeled what do you need to buy nexavar after an Indiana program enacted under then-Gov. Mike Pence what do you need to buy nexavar.

It would expand Medicaid eligibility while setting $20 monthly premium payments and copays. The proposal gained no traction during this year's Mississippi legislative session.While advocates for Medicaid expansion say they are hopeful, they acknowledge difficulties.Out of the 12 nonexpansion states, Mississippi and Florida are the only two with a ballot initiative process.Mississippi law says that for an initiative to be placed on the ballot, at least 106,190 certified signatures must be gathered, and those must be evenly divided among what do you need to buy nexavar the five congressional districts that Mississippi used 20 years ago. Even if signature-gathering is successful, the earliest a proposal is likely to be on the ballot is November 2022."For all the stars to align in a ballot initiative ... There's got to be a commitment on the part of providers in Mississippi, I think, and we have to also look realistically at the amount of what do you need to buy nexavar resources that it takes to do a ballot initiative," Mitchell said. "But it is certainly not out of reach."Consultations via tablets, laptops and what do you need to buy nexavar phones linked patients and doctors when society shut down in early spring.

Telehealth visits dropped with the reopening, but they're still far more common than before and now there's a push to make them widely available in the future.Permanently expanding access will involve striking a balance between costs and quality, dealing with privacy concerns and potential fraud, and figuring out how telehealth can reach marginalized patients, including people with mental health problems."I don't think it is ever going to replace in-person visits, because sometimes a doctor needs to put hands on a patient," said CMS Administrator Seema Verma, the Trump administration's leading advocate for telehealth.Caveats aside, "it's almost a modern-day house call," she added."It's fair to say that telemedicine was in its infancy prior to the pandemic, but it's come of age this year," said Murray Aitken of the data firm IQVIA, which tracks the impact.In the depths of the coronavirus shutdown, telehealth accounted for more than 40% of primary care visits for patients with traditional Medicare, up from a tiny 0.1% sliver before the public health emergency. As the government's flagship health care program, Medicare covers more than 60 million people, including those age 65 and older, and younger disabled people.A recent poll of older adults by the what do you need to buy nexavar University of Michigan Institute for Healthcare Policy &. Innovation found that more than 7 in 10 are interested in using telehealth for follow-ups with their doctor, and nearly 2 out of 3 feel comfortable with video conferences.But privacy was an issue, especially for those who what do you need to buy nexavar hadn't tried telehealth. The poll found 27% of older adults who had not had a telemedicine visit were concerned about privacy, compared with 17% of those who tried it.Those who tried telehealth weren't completely sold. About 4 in 5 were concerned the doctor couldn't physically examine them, and 64% worried what do you need to buy nexavar the quality wasn't as good."After the initial excitement, in the afterglow, patients realize 'I can't get my vaccine,' or 'You can't see this thing in the back of my throat over the computer,' " said Dr.

Gary LeRoy of Dayton, Ohio, a primary care doctor and president of the American Academy of Family Physicians.For Medicare beneficiary Jean Grady of Westford, Vermont, telemedicine was a relief. She needed a checkup required by Medicare to continue receiving what do you need to buy nexavar supplies for her wearable insulin pump. Being in a high risk group for COVID-19, Grady worried about potential what do you need to buy nexavar exposure in a doctor's waiting room, and even more about losing her diabetes supplies if she missed Medicare's checkup deadline."I would have had to go back to taking insulin by syringe," she said.Grady prepared for the virtual visit by calling her clinician's tech department and downloading teleconference software. She says she would do some future visits by video, but not all. For example, people with diabetes need periodic blood tests, and their feet must be checked for signs of circulatory problems.Still, quite a few follow-ups "could be done very efficiently and be just as useful to the physician and myself as going in and seeing them in person," Grady said.Many private insurance plans, including those in Medicare Advantage, offer some level what do you need to buy nexavar of telemedicine coverage.But traditional Medicare has restricted it to rural residents, who generally had to travel to specially designated sites to connect.Under the coronavirus public health emergency, the administration temporarily waived Medicare's restrictions so enrollees anywhere could use telemedicine.

Patients could connect from home. Making such changes permanent would require legislation from Congress, but there's bipartisan interest.Sen what do you need to buy nexavar. Lamar Alexander, chairman of the Senate Health, Education, Labor and Pensions Committee, what do you need to buy nexavar says he'd like to see broader access, without breaking the bank."Our job should be to ensure that change is done with the goals of better outcomes and better patient experiences, at a lower cost," said Alexander, R-Tenn.That's a tall order.Payment will be a sticky obstacle. For now, Medicare is paying clinicians on par for virtual and in-person visits."Policymakers seems to be in a rush to pass legislation, but I think it is worth taking a little more time," said Juliette Cubanski, a Medicare expert with the nonpartisan Kaiser Family Foundation. "Fraud is one big area that policymakers need to be cognizant of."Fraud-busters agree.Telehealth is so new that "we what do you need to buy nexavar don't have at this point a real sense of where the huge risks lie," said Andrew VanLandingham, a senior lawyer with the Health and Human Services inspector general's office.

"We are sort of in an experimental phase."Despite the risks, advocates see opportunities.Expanded Medicare telehealth could:help move the nation closer to a long-sought goal of treating mental health the same as physical conditions. Sen. Ron Wyden, D-Ore., wants to use telemedicine as a springboard to improve mental health care. IQVIA data shows 60% of psychiatric consults took place by telehealth during the shutdown.increase access for people living in remote communities, in low-income urban areas and even nursing homes. Medicare's research shows low-income beneficiaries have had similar patterns of using telehealth for primary care as program enrollees overall.improve coordination of care for people with chronic health conditions, a goal that requires patient and persistent monitoring.

Chronic care accounts for most program spending.University of Michigan health policy expert Mark Fendrick says Medicare should figure out what services add value for patients' health and taxpayers' wallets, and pay just for those.Telehealth "was an overnight sensation," said Fendrick. "Hopefully it's not a one-hit wonder."As the wind howled and the rain slammed down, a team of nurses, respiratory therapists and a doctor worked through the night to care for 19 tiny babies as Hurricane Laura slammed southwestern Louisiana.The babies, some on ventilators or eating through a feeding tube, seemed to weather the storm just fine, said Dr. Juan Bossano, the medical director of the neonatal intensive care unit at Lake Charles Memorial Hospital for Women. "They did very well. They tolerated it very well.

We had a very good day," he said.Laura made landfall early Thursday morning as a Category 4 storm, packing top winds of 150 mph (241 kph), and pushing a storm surge as high as 15 feet in some areas.Hours before it made landfall, officials had to move the babies from the women's hospital to the main hospital in the system after it became clear that storm surge could inundate the women's hospital, located on the southern end of Lake Charles. The hospital has its own generator and hospital administrator Alesha Alford said it was built to withstand hurricane force winds. But in the single story facility, there's no room to move up and storm surge in that area was expected to hit nine feet. In a roughly two-hour operation the babies in the intensive care unit were transferred by ambulance to Lake Charles Memorial Hospital, a ten-story facility on the northern side of the city. Trucks carried needed equipment such as incubators.Alford said the storm hadn't yet hit but "the skies looked very ominous." She said everyone pitched in to get supplies moved to the other hospital."It went as smooth as could be because we had everyone helping," she said.Alford said three mothers who couldn't be discharged from the women's hospital were also transferred.

Two of them had their newborns with them while the child of the third mom was in the intensive care unit. Parents of the other children in the neonatal intensive care unit couldn't stay with them during the storm because there wasn't enough room so Bossano said one nurse was tasked with calling parents to keep them informed of how their children were doing. Bossano occasionally posted updates on Facebook.Once they got situated at the larger hospital and the winds picked up, Alford said the patients were moved into the hallways. To "protect our babies," mattresses were pushed up against the windows to prevent flying glass although none of the windows ended up breaking.She said as huge gusts of wind started coming in, they could feel the building vibrate. In addition to Bossano, the medical staff consisted of two neonatal nurse practitioners, 14 nurses and three respiratory therapists who worked on 12-hour shifts.

Some of the staff slept on air mattresses in the hallway, Alford said. After making it through the hurricane, the plan was to have the babies stay in Lake Charles. While electricity was out in the city, the hospital has its own generator. But Alford said the city's water system has been so heavily damaged that it ultimately forced them to transfer the babies as well as other patients to other hospitals around the state Friday.Both Alford and Bossano repeatedly praised the nursing staff for their work in caring for the babies that in some cases were born weighing only a pound or two. Some of the nursing staff lost their houses in the storm, and they were worried about their own families, but they put those concerns aside to care for their tiny patients."Really the nurses and the respiratory therapists are the heroes here," Bosanno said.

"They showed that very clearly the way they performed."There aren’t many hospital visitors amid the COVID-19 pandemic. But, if you were to walk through intensive-care units at one New York City hospital, you’d see internet-connected speakers—about the size of a stack of Post-it Notes—affixed to the bedrails of some patient beds.It’s part of a project by two Weill Cornell Medicine doctors to help family members speak with ICU patients, often intubated or otherwise not able to hold up a phone themselves, from afar.“The patients could be completely sedated, they could be in a coma,” but families still want to be there with them, said Dr. Marc Schiffman, an interventional radiologist and one of the doctors who spearheaded bringing the devices into ICUs.The speakers, now in 11 units at Weill Cornell, are part of a two-way communication system from company Relay, originally developed as a walkie-talkie system of sorts for children to stay in touch with their parents throughout the day. Users on one end record snippets of conversation using a mobile app, which are automatically played out loud through the small speaker.Users on the other end push a button on the device to record a response.“Whenever (families) have a story they want to recount, they can just talk into their phone,” Schiffman said. €œIt gives the families a sense of autonomy (and) connection,” even when the patient can’t respond.The effort, dubbed the VoiceLove Project, began about four months ago, at the height of the COVID-19 pandemic in New York City.Families and other visitors were no longer allowed inside Weill Cornell, but still wanted a way to connect with patients who were sick with COVID-19.

Initially, that involved a nurse standing in the ICU and holding up a phone or tablet so families could see the patient—a task that took time out of their already busy day, potentially exposed them to COVID-19 and often meant using scarce personal protective equipment.“It really wasn’t a practical solution,” said Dr. Tamatha Fenster, a minimally invasive gynecologic surgeon.So Fenster and Schiffman began brainstorming hands-free technologies they could install directly at the bedside. Schiffman drove to a local Target store and bought a few Relay walkie-talkie devices. After testing it with families and patients in the ICU, the two decided it was a “grand slam,” Schiffman said.Since March, hospitals have been trying new ways to keep patients connected to families at home, said Bill Flatley, senior service delivery manager at consulting firm OST. He said he’s mainly seen hospitals repurpose technology usually used for telemedicine, like tablets and cameras mounted on telemedicine carts.It’s likely hospitals will have to continue to restrict visitors, at least as long as there’s uncertainty around COVID-19 treatment.

So it’s integral for staff to figure out processes that make it easy for families to talk to patients—without putting an additional burden on clinicians or expecting them to serve as tech support.For Fenster and Schiffman, deploying walkie-talkies in the ICU for the first time took some leg work.To scale the walkie-talkie system, Schiffman reached out to Relay’s team via the company’s website, and the company agreed to donate roughly 130 devices and waived the per-user subscription fee. The doctors and Relay have continued to work together on best practices for using the devices in ICUs, a use case Relay is marketing and could sell to other hospitals, according to Jon Schniepp, Relay’s senior vice president of marketing.But Fenster and Schiffman couldn’t just bring walkie-talkies into the ICU. In the hospital setting, there are additional quality and privacy concerns. To address those, the doctors created a disposable case, which made it easier to keep the device sterile and blocked passersby from accidentally pressing the button that would transmit sounds to a family’s Relay app.The two spent thousands of dollars out of their own pockets to devise the best case design, Fenster said, working with an industrial designer in New Jersey to 3D print different models. The final plastic case, customized with the phrase “VoiceLove” on the front, costs about $10 per case to print and ship.

They’ve started reaching out to acute-care and post-acute facilities in California, Texas and other COVID hot spots to explain how the VoiceLove Project works, hoping to connect other groups with Relay and share the case design. But the doctors say they’re still working out the logistics of getting the equipment to interested organizationsWhen Dr. George Wanna saw how devastated St. George Hospital University Medical Center was by an explosion that shook Beirut, he felt a need to help his hometown. The Aug.

4 blast in the city’s harbor ravaged St. George’s, so Wanna launched a GoFundMe page to help the hospital, where a good friend of his, Dr. Alexander Nehme, is chief medical officer.At deadline, more than $86,600 had been raised, with a goal of $100,000. €œThis is the first time in their 140-year history when St. George’s Hospital was damaged so severely that it is unable to function,” said Wanna, chair of the otolaryngology department at New York Eye and Ear Infirmary of Mount Sinai and Mount Sinai Beth Israel in New York.

€¨St. George Hospital even remained open during Lebanon’s 15-year civil war, a conflict that wracked Beirut and forced Wanna to spend much of his childhood in bomb shelters. Wanna is also working with Mount Sinai to send medical supplies. €œSt. George Hospital is in need of everything needed to run a hospital—beds, ventilators, protective equipment.” The tragedy also affected Wanna’s family.

His parents weren’t home when the blast struck and were unharmed. But “my parents’ home was severely damaged by the blast. Sadly, we lost the lives of several of my dad’s relatives,” he said via email. Wanna, who spent his residency at Mount Sinai, is grateful to the system. €œThey have given me a chance to have the kind of life I could never have hoped for—they helped me build a home and a life in this great country.”.

Can you buy nexavar over the counter usa

The Henry nexavar uses J can you buy nexavar over the counter usa. Kaiser Family can you buy nexavar over the counter usa Foundation Headquarters. 185 Berry St., Suite 2000, San Francisco, CA 94107 | Phone 650-854-9400 Washington Offices and Barbara Jordan Conference can you buy nexavar over the counter usa Center.

1330 G Street, NW, Washington, DC 20005 | Phone 202-347-5270 www.kff.org | Email Alerts. Kff.org/email | facebook.com/KaiserFamilyFoundation | twitter.com/kff Filling the need for trusted information on national health issues, the Kaiser Family Foundation is a nonprofit organization based in San Francisco, California.President Trump and Democratic nominee Joe Biden hold widely divergent views on health issues, with the president’s record and response to the coronavirus pandemic likely to play a central role in November’s elections.A new KFF side-by-side comparison examines President Trump’s record and former Vice President Biden’s positions across a wide range of key health issues, including the response to the pandemic, the Affordable Care Act marketplace, Medicaid, Medicare, drug prices, reproductive health, HIV, mental can you buy nexavar over the counter usa health and opioids, immigration and health coverage, and health costs.The resource provides a concise overview of the candidates’ positions on a range of health policy issues. While the Biden campaign has put forward many specific proposals, the Trump campaign has offered few new proposals for addressing health care can you buy nexavar over the counter usa in a second term and is instead running on his record in office.It is part of KFF’s ongoing efforts to provide useful information related to the health policy issues relevant for the 2020 elections, including policy analysis, polling, and journalism.

Find more on our Election 2020 resource page..

The Henry nexavar patient assistance program J what do you need to buy nexavar. Kaiser Family what do you need to buy nexavar Foundation Headquarters. 185 Berry St., Suite 2000, San Francisco, CA 94107 | what do you need to buy nexavar Phone 650-854-9400 Washington Offices and Barbara Jordan Conference Center.

1330 G Street, NW, Washington, DC 20005 | Phone 202-347-5270 www.kff.org | Email Alerts. Kff.org/email | facebook.com/KaiserFamilyFoundation | twitter.com/kff Filling the need for trusted information on national health issues, the Kaiser Family Foundation is a nonprofit organization based in San Francisco, California.President Trump and Democratic nominee Joe Biden hold widely divergent views on health issues, with the president’s record and response to the coronavirus pandemic likely to play a what do you need to buy nexavar central role in November’s elections.A new KFF side-by-side comparison examines President Trump’s record and former Vice President Biden’s positions across a wide range of key health issues, including the response to the pandemic, the Affordable Care Act marketplace, Medicaid, Medicare, drug prices, reproductive health, HIV, mental health and opioids, immigration and health coverage, and health costs.The resource provides a concise overview of the candidates’ positions on a range of health policy issues. While the Biden campaign has put forward many what do you need to buy nexavar specific proposals, the Trump campaign has offered few new proposals for addressing health care in a second term and is instead running on his record in office.It is part of KFF’s ongoing efforts to provide useful information related to the health policy issues relevant for the 2020 elections, including policy analysis, polling, and journalism.

Find more on our Election 2020 resource page..


ID: 424522

Nexavar 200mg price in uk

Nexavar 200mg price in uk

View

page
to 1
 
ID price area
Search

Nexavar 200mg price in uk

Offer property

Nexavar 200mg price in uk

Submit request

Nexavar 200mg price in uk

Register
City Real Estate recommends
Commercial premises for lease in Riga, Riga center

Commercial premises for lease in Riga, Riga center
Bruninieku street, 3th floor, 2 rooms, 40.11m2
200.00 EUR 4.99 EUR / m2

Commercial premises for lease in Riga, Riga center

Commercial premises for lease in Riga, Riga center
Elizabetes street, 1th floor, 2 rooms, 35.00m2
245.00 EUR 7 EUR / m2

Commercial premises for lease in Riga, Riga center

Commercial premises for lease in Riga, Riga center
Bruninieku street, 1th floor, 2 rooms, 60.00m2
220.00 EUR 3.67 EUR / m2

View all offers