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When John Cush, MD, started treating people with rheumatoid arthritis (RA) in the acyclovir online purchase 1980s, doctors considered the disease to be caught early if they diagnosed it up to https://www.voiture-et-handicap.fr/acyclovir-online-purchase/ 8 years after patients first noticed their symptoms. €œEight years!. € says Cush, a rheumatologist at UT Southwestern Medical Center in acyclovir online purchase Dallas.

€œThat's an atrocious definition today.” By a decade ago, the average time to diagnosis had fallen to less than 3 years. Now, thanks to better research and education for both doctors and patients, that window has shrunk to just 6 months. Yet that’s still too acyclovir online purchase slow.

€œIt's a heck of a heck of a lot better than 10 years ago,” Cush says. But even today, “the average person is not getting diagnosed early enough.” Research shows that in some cases, RA may lead to joint damage in as little as 12 to 16 weeks. That’s why it’s so important to get to a specialist who can diagnose acyclovir online purchase your RA and start you on the right treatment plan.

But baffling symptoms, lack of definitive diagnostic tests, long waits for specialists, and other hurdles can sometimes get in the way. Tricky Diagnosis The three hallmarks of a joint with RA sound deceptively simple. Painful, tender, acyclovir online purchase and swollen.

But without an RA specialist, says Stanford Shoor, MD, clinical professor of medicine and rheumatology at Stanford University, the path to a correct diagnosis can be anything but straightforward. For example, RA can look like osteoarthritis, a far more widespread acyclovir online purchase condition that stems from mechanical wear and tear instead of the faulty immune response that causes RA. Or it could mirror the symptoms of carpal tunnel syndrome, which is usually triggered by repetitive motion, or of lupus, another autoimmune condition.

Recent injuries or viral illnesses, like a cold or flu, can cause RA-like pain and swelling in the short term. That’s why, in order to acyclovir online purchase rule out these causes, the American College of Rheumatology requires 6 weeks of symptoms to make an RA diagnosis. And even if many of your lingering symptoms point to RA, “It doesn't mean you have it,” Shoor says.

€œIt just means you should see a rheumatologist.” Continued On the flip side, any nagging joint pain could turn out to be RA, even if it’s not in a common spot. Cush, of UT Southwestern, once saw a patient with long-term pain in the thumb at the joint closest to the thumbnail, which for acyclovir online purchase RA is highly unusual. €œShe evolved over a year into someone who had six or more swollen joints and ultimately had very severe rheumatoid arthritis that required surgeries.” Earlier diagnosis and treatment, Cush says, may have spared her severe damage.

Primary care doctors, often the first stop for patients, also may delay a diagnosis, especially if they don’t see a lot of RA. That could waste valuable acyclovir online purchase weeks. And by the time your doctor finally sends you to a specialist, you’re likely in for another long wait.

A nationwide survey found that it takes an average of almost 45 days to get a first appointment with a rheumatologist. That was far longer than any other specialty and 2.5 times the wait to acyclovir online purchase see a cardiologist. Another problem is that some people simply don’t seek help early enough, Cush says.

They may put off acyclovir online purchase visiting a doctor, self-treat with over-the-counter pain relievers, or dismiss their symptoms as normal aging. That delay could be costly, Cush says. In 40% of cases, RA causes work disability of some type within 10 years of diagnosis.

And research shows acyclovir online purchase the ideal “treatment window” for RA seems to be within the first 3 months. €œPatients who are treated earlier are less likely to have joint surgery. They're less likely to have disability,” Cush says.

€œThey're less likely to be hospitalized later on in their disease.” Symptoms to Watch For Certain benchmarks can help you and your doctor figure out acyclovir online purchase if you have RA, says Shoor of Stanford. The first is simple. Do you have pain in one or more joints?.

The second is tenderness acyclovir online purchase. That means pain when you move or push on a joint. €œYou can test acyclovir online purchase this yourself,” Cush says.

€œPress on the finger joint with the other hand and see whether it's tender. Normally it shouldn't be.” For bigger joints, like the knee, move it in the normal range of motion to see if it hurts more. Continued The location of the joints acyclovir online purchase also matters.

The three most common ones for RA are the wrist, the elbow, and the knuckle where each finger meets your hand (metacarpophalangeal, or MCP, joint). That doesn’t mean you can’t get RA in other joints. But problems in those acyclovir online purchase joints, along with in your ankle, are more likely to suggest RA, in part because they’re rarely affected by osteoarthritis.

In contrast, Shoor says, symptoms in the knee, shoulder, or middle joint of your finger (proximal interphalangeal) could point equally to osteoarthritis or RA. The number of joints involved is another clue. RA usually acyclovir online purchase hits more than four.

And its symptoms tend to be symmetrical. That means if your right index finger is swollen, tender, and painful, you likely will have similar symptoms on the fingers or wrist on the opposite side. But the most telling symptom acyclovir online purchase may be any unexplained joint pain that persists for weeks.

If you notice that, it’s likely time to talk to a doctor, ideally a rheumatologist. In fact, acyclovir online purchase Shoor says, talking to your doctor may be the most beneficial thing you can do for RA, even after your diagnosis. Research shows that successful long-term RA treatment has little to do with fancy imaging or biomarkers or blood tests.

The key factor is something far simpler. Good communication acyclovir online purchase. These studies show that visiting your doctor more often and constantly adjusting your medication is pivotal for managing RA.

Lab testing, no matter how cutting-edge, has surprisingly little effect, both Cush and Shoor say. This research has led to new treatment guidelines that doctors call “treat to target,” or T2T, where you acyclovir online purchase set a treatment goal based on pain levels with your rheumatologist and then work closely together to make it happen. This is now the standard approach for many rheumatologists.

In fact, Shoor says, one of the most powerful weapons against RA may just be yourself. Sources John Cush, MD, rheumatologist, UT Southwestern acyclovir online purchase Medical Center, Dallas. Stanford Shoor, MD, clinical professor of medicine and rheumatology, Stanford University.

Internal Medicine Journal. "Treatment delays for patients with new‐onset rheumatoid arthritis presenting to an Australian early arthritis clinic." University acyclovir online purchase of Wisconsin Medicine. "Comparing Rheumatoid Arthritis and Osteoarthritis." Rheumatology.

"Symptoms associated acyclovir online purchase with inflammatory arthritis are common in the primary care population. Results from the joint symptoms survey." UpToDate. €œEpidemiology of, risk factors for, and possible causes of rheumatoid arthritis.” Athenahealth.

"The doctor acyclovir online purchase will see you ... Sometime." © 2020 WebMD, LLC. All rights reserved.By Serena Gordon HealthDay Reporter WEDNESDAY, Oct.

14, 2020 (HealthDay News) -- Older adults who aren't interested or enthusiastic about their acyclovir online purchase usual activities may have a higher risk of developing dementia, new research suggests. The nine-year study of more than 2,000 older adults -- average age 74 -- found that people with severe apathy (a lack of interest or concern) were 80% more likely to develop dementia during the study period than those with low apathy. "Apathy is not subtle.

It's something that families can pick up on acyclovir online purchase. More research is needed, but this is another potential red flag symptom of the prodromal (early) phase of dementia," said the study's lead author, Dr. Meredith Bock.

She's a clinical fellow in neurology at the acyclovir online purchase University of California, San Francisco Institute for Neurosciences. The prevalence of dementia (including Alzheimer's disease) is on the rise, and researchers are trying to find new ways to identify who's at risk of the disease. Mood and behavior symptoms, such as depression or irritability, are examples acyclovir online purchase of changes that may be clues to an impending dementia diagnosis.

Previous studies have also linked mild cognitive impairment (a potential precursor to dementia) and apathy, but the researchers wanted to look at a group of people who had no known memory or thinking issues yet. The current study included people aged 70 to 79. None had dementia acyclovir online purchase at the start.

The researchers also had medical records, including medication use, hospitalizations and cognitive testing. To evaluate apathy levels, the study participants answered questions, such as. In the past four weeks, how often have you been interested in leaving your home acyclovir online purchase and going out?.

In the past four weeks, how often have you been interested in doing your usual activities?. After nine years, the researchers found that 381 people had developed dementia. In the low apathy group, 14% acyclovir online purchase developed dementia.

For those with moderate apathy levels, that number was 19%. But one in four -- 25% -- in the severe apathy group had dementia by the end of acyclovir online purchase the study. When the researchers controlled the data for age, education, heart and blood vessel disease, depression and genetic risk of Alzheimer's disease, they reported that people with severe apathy at the start of the study had 80% higher odds of having dementia later in life.

Continued Bock said by asking about apathy, doctors might be able to learn which patients have a higher risk of dementia. The information could be particularly helpful in research trials, she added acyclovir online purchase. Rebecca Edelmayer, director of scientific engagement at the Alzheimer's Association, said, "This type of research is critical to help us identify who is at risk.

We are driving towards being able to identify people with a higher risk as soon as possible as we strive for treatments that will be transformational for patients and their families. But it's too soon to say if only looking at apathy can identify who is at risk of dementia." Edelmayer explained that acyclovir online purchase it can be difficult to tease out apathy from other changes that may be happening, such as depression or isolation. She said if you have concerns about your own or a loved one's memory or behavior, you should speak with your doctor or call the Alzheimer's Association's 24/7 helpline at 1-800-272-3900.

The study findings were published online Oct. 14 in acyclovir online purchase Neurology. WebMD News from HealthDay Copyright © 2013-2020 HealthDay.

All rights reserved.By Alan Mozes HealthDay Reporter THURSDAY, Oct. 15, 2020 (HealthDay News) -- Offering fresh insight into the deep-seated roots of dementia, new research finds that diminished blood flow to the brain is tied to buildup a protein long associated with Alzheimer's acyclovir online purchase disease. Called "tau," high levels of the protein are "one of the hallmark pathologies that define Alzheimer's disease in the brain," explained study author Judy Pa.

She is an associate acyclovir online purchase professor of neurology with the Mark and Mary Stevens Neuroimaging and Informatics Institute and the Alzheimer's Disease Research Center at the University of Southern California. "Tau tangles very closely track Alzheimer's disease progression, such that when the number of tau tangles in the brain increases, problems in memory and thinking will also increase," Pa noted. And the new investigation indicates that "decreased blood flow [is] associated with increased tau in brain areas important for Alzheimer's disease," Pa added.

According to acyclovir online purchase the U.S. National Institute on Aging, the brain's billions of neurons work tirelessly to ensure proper nervous system communication and healthy body function. But that mission is seriously undermined when abnormal tangles of tau protein take up shop inside neurons.

Yet, NIA experts and acyclovir online purchase Pa both point out that poor vascular function --which often manifests as decreased cerebral blood flow-- has also long been linked to Alzheimer's risk. "It is known that some risk factors for Alzheimer's disease are associated with vascular health," Pa noted, with risk going up among patients with high blood pressure and among those who smoke or are physically inactive. But do tau tangles and poor blood flow in the brain go hand-in-hand?.

Pa's team acyclovir online purchase set out to find out. Between 2016 and 2019, brain scans were conducted among a group of 68 men and women between the ages of 46 and 80. The group included patients who ran the gamut, from being mentally healthy to having mild cognitive impairment.

The scans revealed that brain areas with increased tau tangles were also subject to a drop in blood flow acyclovir online purchase. This was particularly true in an area of the brain -- known as the "inferior temporal gyrus"-- that is believed to be among the first brain regions where tau buildup is seen in Alzheimer's patients, even before obvious signs of thinking impairment become evident. Continued The team then poured over brain acyclovir online purchase scan data collected between 2017 and 2019 concerning a separate group of 138 patients who had been enrolled in the "Alzheimer's Disease Neuroimaging Initiative." Patients included men and women with diagnoses ranging from mild cognitive impairment to full-blown Alzheimer's dementia.

Again, the team found that a drop in cerebral blood flow overlapped with an increase in brain tangles. "We then found that this association was stronger in those with poorer cognition and in those with higher amyloid pathology levels [plaques]," said Pa. That suggests that acyclovir online purchase the "relationship between blood flow and tau is important and meaningful," and that "maintaining vascular health is very important as one ages." The findings were published Oct.

12 in the Journal of Neuroscience. "At the end of the day, we want to prevent Alzheimer's disease before it happens," said Pa. "And current research suggests that managing risk factors, including those that are vascular in acyclovir online purchase nature, could aid in preventing or lowering Alzheimer's risk." As a practical matter, that would mean trying to get those risk factors that are modifiable under better control, said Rebecca Edelmayer, director of scientific engagement with the Alzheimer's Association.

"Age is clearly the biggest risk factor for Alzheimer's," she noted. "And genetics and family history also drive risk. But we're doing a lot of research these days into different ways we can influence modifiable risk factors in order to support our cardiovascular health, because doing so may end up supporting not only our heart health but the vasculature of the brain." That, said Edelmayer, could mean eating better and exercising more, or reining in high blood pressure through a combination of medications and lifestyle changes acyclovir online purchase.

But which comes first. Poor vascular acyclovir online purchase health or tau buildup?. Edelmayer cautioned that the answer "remains unclear." "This research is exciting," Edelmayer said.

"But until we're better able to understand the sequence of events that leads to Alzheimer's, we can't truly say that we know the causal factors." That, she said, will require more research "that leaves no stone unturned." WebMD News from HealthDay Copyright © 2013-2020 HealthDay. All rights reserved.By Robert Preidt acyclovir online purchase HealthDay Reporter THURSDAY, Oct. 15, 2020 (HealthDay News) -- Masks or no masks?.

Social distancing or not?. New research suggests that acyclovir online purchase the media Americans consume matters when these decisions are made. The study found that folks drawn to conservative-leaning TV news were much less likely to follow COVID prevention guidelines.

Researchers analyzed data from more than 4,800 U.S. Adults who took part in acyclovir online purchase a nationwide online survey between April 1 and June 9. Participants were asked about their COVID-19 preventive behaviors over the past week, including hand-washing and use of face coverings.

They were also asked about risky behaviors, such as going to bars or clubs, attending gatherings of more than 10 people, and visiting other people's homes. In addition, they were asked how much they trusted 18 professional media sources for COVID-19 information, including CNN acyclovir online purchase and Fox News, the two largest news outlets in the United States. On average, respondents had used three professional sources and about six others (including social media, friends, family, colleagues and the White House) to learn about the coronavirus in the preceding week.

About 29% said they trusted CNN more than acyclovir online purchase Fox News. 20% said they trusted Fox News more than CNN. More than half (52%) said they had no preference.

People who acyclovir online purchase trusted CNN were more likely to follow preventive measures and less likely to report risky behaviors than those who trusted Fox News, according to findings published recently in the online journal BMJ Global Health. On average, CNN fans practiced an average of 3.85 preventive behaviors and 0.94 risky behaviors, compared with 3.41 and 1.25, respectively, for those who preferred Fox News. Overall, seniors, women, those of non-Hispanic Asian ethnic backgrounds, and those with the most education were more likely to follow preventive guidelines.

Those who had a job but weren't able acyclovir online purchase to work from home were least likely to do so. The study only observed associations, and did not determine cause and effect. "This study has many policy implications for the future progression of COVID-19 and health messaging in general.

In a highly partisan environment, false information can be easily disseminated," said the authors led by Erfei Zhao, from the University of Southern California's Leonard Davis School of Gerontology. Compared to CNN, Fox News "consistently downplayed the danger of the virus for the sake of political interest," the researchers said in a journal news release. "Health messaging, despite being one of the few effective ways to slow down the spread of the virus in the absence of a vaccine, is doomed to fail if the media prioritize political interests over population health," they concluded..

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WASHINGTON, DC – https://www.voiture-et-handicap.fr/acyclovir-online-purchase/ The U.S how to get acyclovir online. Department of Labor’s Wage and Hour Division (WHD) today posted revisions to regulations that implemented the paid sick leave and expanded family and medical leave provisions of the Families First Coronavirus Response Act (FFCRA). The revisions made by the new rule clarify workers’ rights and employers’ responsibilities under the FFCRA’s how to get acyclovir online paid leave provisions, in light of the U.S. District Court for the Southern District of New York in an Aug.

3, 2020, decision that found portions of the regulations invalid. The revisions do the following how to get acyclovir online. Reaffirm and provide additional explanation for the requirement that employees may take FFCRA leave only if work would otherwise be available to them. Reaffirm and how to get acyclovir online provide additional explanation for the requirement that an employee have employer approval to take FFCRA leave intermittently.

Revise the definition of “healthcare provider” to include only employees who meet the definition of that term under the Family and Medical Leave Act regulations or who are employed to provide diagnostic services, preventative services, treatment services or other services that are integrated with and necessary to the provision of patient care which, if not provided, would adversely impact patient care. Clarify that employees must provide required documentation supporting their need for FFCRA leave to their employers as soon as practicable. Correct an inconsistency regarding when employees may be required to provide notice of a need to take expanded family and medical leave to their employers.“As the economy continues to rebound, more businesses how to get acyclovir online return to full capacity, and schools reopen, the need for clarity regarding the Families First Coronavirus Response Act paid leave provisions may be greater than ever,” said Wage and Hour Administrator Cheryl Stanton. €œToday’s updates respond to this evolving situation and address some of the challenges the American workforce faces.

Our continuing robust response to this pandemic balances support for workers and employers alike, and remains our priority.” The Department issued its initial temporary rule implementing provisions under the FFCRA on April how to get acyclovir online 1, 2020. Read the revisions to that temporary rule, which will become effective Sept. 16, 2020 in the Federal Register. The FFCRA helps how to get acyclovir online the U.S.

Combat and defeat the workplace effects of the coronavirus by giving tax credits to American businesses with fewer than 500 employees to provide employees with paid leave for certain reasons related to the coronavirus. Please visit how to get acyclovir online WHD’s “Quick Benefits Tips” for information about how much leave workers may qualify to use, and the wages employers must pay. The law enables employers to provide paid leave reimbursed by tax credits, while at the same time ensuring that workers are not forced to choose between their paychecks and the public health measures needed to combat the virus. WHD continues to provide updated information on its website and through extensive outreach efforts to ensure that workers and employers have the information they need about the benefits and protections of the FFCRA.

The agency also provides additional information on common issues employers and employees face when responding to the coronavirus and its how to get acyclovir online effects on wages and hours worked under the Fair Labor Standards Act and on job-protected leave under the Family and Medical Leave Act at https://www.dol.gov/agencies/whd/pandemic. WHD’s mission is to promote and achieve compliance with labor standards to protect and enhance the welfare of the nation’s workforce. WHD enforces federal minimum wage, overtime pay, recordkeeping, and child labor requirements of the how to get acyclovir online FLSA. WHD also enforces the paid sick leave and expanded family and medical leave requirements of the Families First Coronavirus Response Act, the Migrant and Seasonal Agricultural Worker Protection Act, the Employee Polygraph Protection Act, the Family and Medical Leave Act, wage garnishment provisions of the Consumer Credit Protection Act, and a number of employment standards and worker protections as provided in several immigration related statutes.

Additionally, WHD administers and enforces the prevailing wage requirements of the Davis Bacon Act and the Service Contract Act and other statutes applicable to Federal contracts for construction and for the provision of goods and services. The mission of the Department of Labor is to foster, promote and develop the welfare of the wage earners, job seekers and how to get acyclovir online retirees of the United States. Improve working conditions. Advance opportunities for profitable how to get acyclovir online employment.

And assure work-related benefits and rights.PARAMUS, NJ – The U.S. Department of Labor’s Occupational Safety and Health Administration (OSHA) has cited CarePlus Bergen Inc., doing business as Bergen New Bridge Medical Center, for violating respiratory protection standards at its Paramus, New Jersey, location. OSHA cited the hospital for two serious violations, with proposed penalties of $9,639.Based on a coronavirus-related inspection, OSHA cited the Bergen New Bridge Medical Center for failing to fit test tight-fitting face piece respirators on employees who were how to get acyclovir online required to use them. The hospital also failed to train employees on proper respirator use and ensure employees understood when to wear a respirator.

“Employers must take action to protect their employees how to get acyclovir online during the pandemic, including implementing effective respiratory protection programs,” said OSHA Hasbrouck Heights Area Office Director Lisa Levy. €œOSHA standards require healthcare workers to be fit-tested to ensure the respirators they use provide adequate protection.” Employers with questions on compliance with OSHA standards should contact their local OSHA office for guidance and assistance at 800-321-OSHA (6742). OSHA’s COVID-19 response webpage offers extensive resources for addressing safety and health hazards during the evolving coronavirus pandemic. The company has 15 business days from receipt of the citations and penalties to comply, request an informal conference with OSHA’s area director or contest the findings before the independent Occupational Safety and how to get acyclovir online Health Review Commission.

Under the Occupational Safety and Health Act of 1970, employers are responsible for providing safe and healthful workplaces for their employees. OSHA’s role is to help ensure these conditions for America’s working men and women by setting and enforcing standards, and providing training, how to get acyclovir online education and assistance. For more information, visit http://www.osha.gov. The mission of the Department of Labor is to foster, promote and develop the welfare of the wage earners, job seekers and retirees of the United States.

Improve working conditions. Advance opportunities for profitable employment. And assure work-related benefits and rights..

WASHINGTON, DC acyclovir online purchase – The U.S. Department of Labor’s Wage and Hour Division (WHD) today posted revisions to regulations that implemented the paid sick leave and expanded family and medical leave provisions of the Families First Coronavirus Response Act (FFCRA). The revisions acyclovir online purchase made by the new rule clarify workers’ rights and employers’ responsibilities under the FFCRA’s paid leave provisions, in light of the U.S. District Court for the Southern District of New York in an Aug. 3, 2020, decision that found portions of the regulations invalid.

The revisions do acyclovir online purchase the following. Reaffirm and provide additional explanation for the requirement that employees may take FFCRA leave only if work would otherwise be available to them. Reaffirm and provide additional explanation for the requirement that an employee acyclovir online purchase have employer approval to take FFCRA leave intermittently. Revise the definition of “healthcare provider” to include only employees who meet the definition of that term under the Family and Medical Leave Act regulations or who are employed to provide diagnostic services, preventative services, treatment services or other services that are integrated with and necessary to the provision of patient care which, if not provided, would adversely impact patient care. Clarify that employees must provide required documentation supporting their need for FFCRA leave to their employers as soon as practicable.

Correct an inconsistency regarding when employees may be required to provide notice of a need to take expanded family and medical leave to their employers.“As the economy continues acyclovir online purchase to rebound, more businesses return to full capacity, and schools reopen, the need for clarity regarding the Families First Coronavirus Response Act paid leave provisions may be greater than ever,” said Wage and Hour Administrator Cheryl Stanton. €œToday’s updates respond to this evolving situation and address some of the challenges the American workforce faces. Our continuing robust response to this pandemic balances support for workers and employers alike, and remains our priority.” The Department issued its initial temporary rule implementing provisions under acyclovir online purchase the FFCRA on April 1, 2020. Read the revisions to that temporary rule, which will become effective Sept. 16, 2020 in the Federal Register.

The acyclovir online purchase FFCRA helps the U.S. Combat and defeat the workplace effects of the coronavirus by giving tax credits to American businesses with fewer than 500 employees to provide employees with paid leave for certain reasons related to the coronavirus. Please visit WHD’s “Quick Benefits Tips” acyclovir online purchase for information about how much leave workers may qualify to use, and the wages employers must pay. The law enables employers to provide paid leave reimbursed by tax credits, while at the same time ensuring that workers are not forced to choose between their paychecks and the public health measures needed to combat the virus. WHD continues to provide updated information on its website and through extensive outreach efforts to ensure that workers and employers have the information they need about the benefits and protections of the FFCRA.

The agency also provides additional information on common issues employers and employees face when responding to the coronavirus and its effects on wages and hours worked under the Fair Labor Standards Act and on job-protected leave under the acyclovir online purchase Family and Medical Leave Act at https://www.dol.gov/agencies/whd/pandemic. WHD’s mission is to promote and achieve compliance with labor standards to protect and enhance the welfare of the nation’s workforce. WHD enforces federal minimum wage, overtime acyclovir online purchase pay, recordkeeping, and child labor requirements of the FLSA. WHD also enforces the paid sick leave and expanded family and medical leave requirements of the Families First Coronavirus Response Act, the Migrant and Seasonal Agricultural Worker Protection Act, the Employee Polygraph Protection Act, the Family and Medical Leave Act, wage garnishment provisions of the Consumer Credit Protection Act, and a number of employment standards and worker protections as provided in several immigration related statutes. Additionally, WHD administers and enforces the prevailing wage requirements of the Davis Bacon Act and the Service Contract Act and other statutes applicable to Federal contracts for construction and for the provision of goods and services.

The mission of the Department of Labor is to foster, promote acyclovir online purchase and develop the welfare of the wage earners, job seekers and retirees of the United States. Improve working conditions. Advance opportunities for profitable employment acyclovir online purchase. And assure work-related benefits and rights.PARAMUS, NJ – The U.S. Department of Labor’s Occupational Safety and Health Administration (OSHA) has cited CarePlus Bergen Inc., doing business as Bergen New Bridge Medical Center, for violating respiratory protection standards at its Paramus, New Jersey, location.

OSHA cited the hospital for two serious violations, with proposed penalties of $9,639.Based on a coronavirus-related inspection, OSHA cited acyclovir online purchase the Bergen New Bridge Medical Center for failing to fit test tight-fitting face piece respirators on employees who were required to use them. The hospital also failed to train employees on proper respirator use and ensure employees understood when to wear a respirator. “Employers must take action to acyclovir online purchase protect their employees during the pandemic, including implementing effective respiratory protection programs,” said OSHA Hasbrouck Heights Area Office Director Lisa Levy. €œOSHA standards require healthcare workers to be fit-tested to ensure the respirators they use provide adequate protection.” Employers with questions on compliance with OSHA standards should contact their local OSHA office for guidance and assistance at 800-321-OSHA (6742). OSHA’s COVID-19 response webpage offers extensive resources for addressing safety and health hazards during the evolving coronavirus pandemic.

The company has 15 business days from receipt of the citations and penalties to comply, request an informal conference with OSHA’s area director or contest the findings before the independent Occupational Safety and acyclovir online purchase Health Review Commission. Under the Occupational Safety and Health Act of 1970, employers are responsible for providing safe and healthful workplaces for their employees. OSHA’s role is to help acyclovir online purchase ensure these conditions for America’s working men and women by setting and enforcing standards, and providing training, education and assistance. For more information, visit http://www.osha.gov. The mission of the Department of Labor is to foster, promote and develop the welfare of the wage earners, job seekers and retirees of the United States.

Improve working conditions. Advance opportunities for profitable employment. And assure work-related benefits and rights..

Acyclovir vs valacyclovir for genital herpes

On this page BackgroundIn the summer of 2018, several medications containing the active ingredient Valsartan were recalled in acyclovir vs valacyclovir for genital herpes Canada and elsewhere in the world. This was because the nitrosamine impurity, N-nitrosodimethylamine (NDMA), was found in the active pharmaceutical ingredient (API). APIs are the substances in pharmaceutical medications that are responsible for the beneficial health effects experienced by patients or consumers. Since then, acyclovir vs valacyclovir for genital herpes some other medications made by different manufacturers have been found to contain NDMA or other similar nitrosamine impurities, such as.

N-nitrosodiethylamine (NDEA) N-nitrosodiisopropylamine (NDIPA) N-nitrosomethyl-n-butylamine (NMBA)About nitrosamine impuritiesBased primarily on animal studies, nitrosamine impurities are probable human carcinogens. This means that long-term exposure to a level above what is considered safe may increase the risk of cancer. There is no immediate health risk associated with the use of medications containing low levels of a nitrosamine impurity acyclovir vs valacyclovir for genital herpes. Foods such as meats, dairy products and vegetables as well as drinking water may also contain low levels of nitrosamines.

We don’t expect that a nitrosamine impurity will cause harm when exposure is at or below the acceptable level. For example, no increase in the risk of cancer is expected if exposure to the nitrosamine impurity below the acceptable level occurs every day for 70 years acyclovir vs valacyclovir for genital herpes. The actual health risk varies from person to person. The risk depends on several factors, such as.

The daily dose of the medication how long the medication is taken the level of the nitrosamine impurity in the finished productPatients should always talk to their health care provider before stopping a acyclovir vs valacyclovir for genital herpes prescribed medication. Not treating a condition may pose a greater health risk than the potential exposure to a nitrosamine impurity. What we're doing Health Canada recognizes that the nitrosamine impurity issue may cause concern for Canadians. Your health and safety is our top priority and we will continue to take action to address risks acyclovir vs valacyclovir for genital herpes and inform you of new safety information.

We have created a list of all medications currently known to contain nitrosamine impurities. We will continue to update it, as needed, as more information becomes available. As we continue acyclovir vs valacyclovir for genital herpes to hold companies accountable for determining the root causes, we’re learning more about how nitrosamine impurities may have formed or be present in medications. In the meantime, we will continue to take action to address and prevent the presence of unacceptable levels of these impurities.

These actions may include. Assess the manufacturing processes of companies determine the risk to Canadians and the impact on the Canadian market test samples of drug products on the market or soon to be released to the market for NDMA and other nitrosamine impurities ask companies to stop distribution as an interim precautionary measure while we gather more information make information available to health care professionals and to patients to enable informed decisions acyclovir vs valacyclovir for genital herpes regarding the medications that we takeAs the federal regulator of health products in Canada, we also. Request, confirm and monitor the effectiveness of recalls by companies as necessary conduct our own laboratory tests, where necessary, and assess if the results present a health risk to humans conduct inspections of domestic and foreign sites and restrict certain products from being on the market when problems are identifiedWe share information on potential root causes of nitrosamines identified to date in medications with Canadian drug companies. We also ask the companies to.

Review their manufacturing acyclovir vs valacyclovir for genital herpes processes and controls take action to avoid nitrosamine impurities in all medications, as necessary test any products that could potentially contain nitrosamine impurities report their findings to Health Canada To better understand this global issue, we are collaborating and sharing information with international regulators, such as. U.S. Food and Drug Administration European Medicines Agency Australia’s Therapeutic Goods Administration Japan’s Ministry of Health, Labour and Welfare and Pharmaceuticals and Medical Devices Agency Switzerland’s Swissmedic Singapore’s Health Sciences AuthorityWe continue to work with companies and our international regulatory partners to. Determine the root causes of the issue verify that appropriate actions acyclovir vs valacyclovir for genital herpes are taken to minimize or avoid the presence of nitrosamine impurities We regularly communicate information on health risks, test results, recalls and other actions taken.

Some of these key actions and communications include. Letter to all manufacturers (October 2, 2019). Health Canada issued a key communication to all companies marketing acyclovir vs valacyclovir for genital herpes human prescription and non-prescription medications requesting them to conduct detailed evaluations of their manufacturing procedures and controls for the potential presence of nitrosamines. The letter outlined examples of potential root causes for the presence of nitrosamines and included a request for a stepwise approach to conduct these risk assessments and expectations for any necessary subsequent actions.

Nitrosamines Questions and Answers (Q&A) document (November 26, 2019). Health Canada issued a Q&A document on acyclovir vs valacyclovir for genital herpes issues relating to the control of nitrosamines in medicines. This Q&A document will be updated periodically as new information becomes available. Webinar on Nitrosamines (January 31, 2020).

The purpose of this session was to provide an opportunity for a discussion of this issue with Health Canada and acyclovir vs valacyclovir for genital herpes stakeholders. Health Canada provided overviews of the situation relating to nitrosamine impurities in pharmaceuticals and stakeholders had the opportunity to share their experiences, successes and challenges in addressing the issue of nitrosamine contamination. The on-line webinar was well intended by approximately 500 participants from over 18 countries and provided valuable information to respond to this global issue.We will continue to update Canadians if a product is being recalled. Related linksOn this page Overview One of Health Canada’s roles is to regulate and authorize health products acyclovir vs valacyclovir for genital herpes that improve and maintain the health and well-being of Canadians.

The COVID-19 pandemic has created an unprecedented demand on Canada’s health care system and has led to an urgent need for access to health products. As part of the government's broad response to the pandemic, Health Canada introduced innovative and agile regulatory measures. These measures expedite the regulatory review of COVID-19 health products without compromising safety, efficacy and quality standards. These measures are helping to make acyclovir vs valacyclovir for genital herpes health products and medical supplies needed for COVID-19 available to Canadians and health care workers.

Products include. testing devices, such as test kits and swabs personal protective equipment (PPE) for medical purposes, such as medical masks, N95 respirators, gowns and gloves disinfectants and hand sanitizers investigational drugs and vaccines We support the safe and timely access to these critical products through. temporary legislative, regulatory and policy measures partnerships and networks with companies, provinces and territories, other government departments, international regulatory bodies and health care professionals easily accessed and available guidance and other priority information We have also taken immediate steps to protect consumers acyclovir vs valacyclovir for genital herpes from unauthorized health products and illegal, false or misleading product advertisements that claim to mitigate, prevent, treat, diagnose or cure COVID-19. Medical devices Medical devices play an important role in diagnosing, treating, mitigating or preventing COVID-19.

We are expediting access to medical devices through an interim order for importing and selling medical devices. This interim acyclovir vs valacyclovir for genital herpes order, which was introduced on March 18, 2020, covers medical devices such as. Since the release of the interim order, we have authorized hundreds of medical devices for use against COVID-19. We have also expedited the review and issuance of thousands of Medical Device Establishment Licences (MDELs).

These have been issued for companies asking to manufacture (Class I), import or distribute acyclovir vs valacyclovir for genital herpes medical devices in relation to COVID-19. Testing devices Early diagnosis is critical to slowing and reducing the spread of COVID-19 in Canada. Our initial focus during the pandemic has been the scientific review and authorization of testing devices. We made it a priority acyclovir vs valacyclovir for genital herpes to review diagnostic tests using nucleic acid technology.

This helped to increase the number of testing devices available in Canada to diagnose active and early-stage infections of COVID-19. We are also reviewing and authorizing serological tests that detect previous exposure to COVID-19. In May 2020, we authorized the first serological testing device to acyclovir vs valacyclovir for genital herpes help improve our understanding of the immune status of people infected. We also provided guidance on serological tests.

We continue to collaborate with the Public Health Agency of Canada’s National Microbiology Laboratory (NML) and with provincial public health and laboratory partners as they. review and engage in their own studies of acyclovir vs valacyclovir for genital herpes serological technologies develop tests assess commercial tests The NML is known around the world for its scientific evidence. It works with public health partners to prevent the spread of infectious diseases. When making regulatory decisions, we consider the data provided by the NML and provincial public health and laboratory partners.

This work will facilitate access to acyclovir vs valacyclovir for genital herpes devices that will improve our testing capacity. It will also support research into understanding immunity against COVID-19 and the possibility of re-infection. Personal protective equipment Personal protective equipment (PPE) is key to protecting health care workers, patients and Canadians through infection prevention and control. We play an important role in providing guidance to acyclovir vs valacyclovir for genital herpes companies and manufacturers in Canada that want to supply PPE.

We are increasing the range of products available without compromising safety and effectiveness. For example, we are. We have authorized acyclovir vs valacyclovir for genital herpes hundreds of new PPE products and other devices, all while ensuring the safety and quality of PPE. Hand sanitizers, disinfectants, cleaners and soaps The COVID-19 pandemic created an urgent need for disinfectants, hand sanitizers, cleaners and soaps.

To increase supply and ensure Canadians have access to these products, we. We will continue our efforts acyclovir vs valacyclovir for genital herpes to support supply and access to these essential products. Drugs and vaccines We are closely tracking all potential drugs and vaccines in development in Canada and abroad. We are working with companies, academic research centres and investigators to help expedite the development and availability of drugs and vaccines to prevent and treat COVID-19.

Clinical trials On May 23, 2020, the acyclovir vs valacyclovir for genital herpes Minister of Health signed a clinical trials interim order. This temporary measure is designed to meet the urgent need to diagnose, treat, reduce or prevent COVID-19. The interim order facilitates clinical trials in Canada to investigate and offer greater patient access to potential COVID-19 drugs and medical devices, while upholding strong patient safety requirements. As well, to encourage the rapid development of drugs and vaccines, we are.

prioritizing COVID-19 clinical trial applications providing regulatory agility and guidance on how clinical trials are to be conducted this encourages and supports the launch of new trials and the continuation of existing ones, as well as broader patient participation across the country working with companies outside of Canada to bring clinical trials to our country working with researchers around the world to add Canadian sites to their research efforts On May 15, 2020, we authorized Canada’s first vaccine clinical trial. Addressing critical product shortages We have taken steps to address critical product shortages caused by the COVID-19 pandemic. One of these steps was an interim order to prevent or ease shortages of drugs, medical devices and foods for a special dietary purpose.

The https://www.voiture-et-handicap.fr/acyclovir-online-purchase/ actual health risk acyclovir online purchase varies from person to person. The risk depends on several factors, such as. The daily dose of the medication how long the medication is taken the level of the nitrosamine impurity in the finished productPatients should always talk to their health care provider before stopping a prescribed medication. Not treating a condition may pose a acyclovir online purchase greater health risk than the potential exposure to a nitrosamine impurity.

What we're doing Health Canada recognizes that the nitrosamine impurity issue may cause concern for Canadians. Your health and safety is our top priority and we will continue to take action to address risks and inform you of new safety information. We have created acyclovir online purchase a list of all medications currently known to contain nitrosamine impurities. We will continue to update it, as needed, as more information becomes available.

As we continue to hold companies accountable for determining the root causes, we’re learning more about how nitrosamine impurities may have formed or be present in medications. In the meantime, we will continue to take action to address and prevent the presence of unacceptable levels of acyclovir online purchase these impurities. These actions may include. Assess the manufacturing processes of companies determine the risk to Canadians and the impact on the Canadian market test samples of drug products on the market or soon to be released to the market for NDMA and other nitrosamine impurities ask companies to stop distribution as an interim precautionary measure while we gather more information make information available to health care professionals and to patients to enable informed decisions regarding the medications that we takeAs the federal regulator of health products in Canada, we also.

Request, confirm and monitor the effectiveness of recalls by companies as necessary conduct our own laboratory tests, where necessary, and assess if the results present a health risk to humans conduct inspections of domestic and foreign sites and restrict certain products from being on the market when problems are identifiedWe share information on potential root causes of nitrosamines identified to date in medications with Canadian drug companies acyclovir online purchase. We also ask the companies to. Review their manufacturing processes and controls take action to avoid nitrosamine impurities in all medications, as necessary test any products that could potentially contain nitrosamine impurities report their findings to Health Canada To better understand this global issue, we are collaborating and sharing information with international regulators, such as. U.S acyclovir online purchase.

Food and Drug Administration European Medicines Agency Australia’s Therapeutic Goods Administration Japan’s Ministry of Health, Labour and Welfare and Pharmaceuticals and Medical Devices Agency Switzerland’s Swissmedic Singapore’s Health Sciences AuthorityWe continue to work with companies and our international regulatory partners to. Determine the root causes of the issue verify that appropriate actions are taken to minimize or avoid the presence of nitrosamine impurities We regularly communicate information on health risks, test results, recalls and other actions taken. Some of these key actions and communications include acyclovir online purchase. Letter to all manufacturers (October 2, 2019).

Health Canada issued a key communication to all companies marketing human prescription and non-prescription medications requesting them to conduct detailed evaluations of their manufacturing procedures and controls for the potential presence of nitrosamines. The letter outlined examples of potential root causes for the presence of nitrosamines and included a request for a stepwise acyclovir online purchase approach to conduct these risk assessments and expectations for any necessary subsequent actions. Nitrosamines Questions and Answers (Q&A) document (November 26, 2019). Health Canada issued a Q&A document on issues relating to the control of nitrosamines in medicines.

This Q&A document will be acyclovir online purchase updated periodically as new information becomes available. Webinar on Nitrosamines (January 31, 2020). The purpose of this session was to provide an opportunity for a discussion of this issue with Health Canada and stakeholders. Health Canada provided overviews of the situation relating to nitrosamine impurities in pharmaceuticals and stakeholders had the opportunity to share their acyclovir online purchase experiences, successes and challenges in addressing the issue of nitrosamine contamination.

The on-line webinar was well intended by approximately 500 participants from over 18 countries and provided valuable information to respond to this global issue.We will continue to update Canadians if a product is being recalled. Related linksOn this page Overview One of Health Canada’s roles is to regulate and authorize health products that improve and maintain the health and well-being of Canadians. The COVID-19 pandemic has created an unprecedented demand on Canada’s health care system and acyclovir online purchase has led to an urgent need for access to health products. As part of the government's broad response to the pandemic, Health Canada introduced innovative and agile regulatory measures.

These measures expedite the regulatory review of COVID-19 health products without compromising safety, efficacy and quality standards. These measures are helping to make health products and medical supplies acyclovir online purchase needed for COVID-19 available to Canadians and health care workers. Products include. testing devices, such as test kits and swabs personal protective equipment (PPE) for medical purposes, such as medical masks, N95 respirators, gowns and gloves disinfectants and hand sanitizers investigational drugs and vaccines We support the safe and timely access to these critical products through.

temporary legislative, regulatory and acyclovir online purchase policy measures partnerships and networks with companies, provinces and territories, other government departments, international regulatory bodies and health care professionals easily accessed and available guidance and other priority information We have also taken immediate steps to protect consumers from unauthorized health products and illegal, false or misleading product advertisements that claim to mitigate, prevent, treat, diagnose or cure COVID-19. Medical devices Medical devices play an important role in diagnosing, treating, mitigating or preventing COVID-19. We are expediting access to medical devices through an interim order for importing and selling medical devices. This interim order, which was introduced on acyclovir online purchase March 18, 2020, covers medical devices such as.

Since the release of the interim order, we have authorized hundreds of medical devices for use against COVID-19. We https://www.voiture-et-handicap.fr/acyclovir-online-purchase/ have also expedited the review and issuance of thousands of Medical Device Establishment Licences (MDELs). These have been issued for companies asking to manufacture (Class I), import or distribute medical devices in relation to COVID-19. Testing acyclovir online purchase devices Early diagnosis is critical to slowing and reducing the spread of COVID-19 in Canada.

Our initial focus during the pandemic has been the scientific review and authorization of testing devices. We made it a priority to review diagnostic tests using nucleic acid technology. This helped acyclovir online purchase to increase the number of testing devices available in Canada to diagnose active and early-stage infections of COVID-19. We are also reviewing and authorizing serological tests that detect previous exposure to COVID-19.

In May 2020, we authorized the first serological testing device to help improve our understanding of the immune status of people infected. We also provided guidance on serological tests acyclovir online purchase. We continue to collaborate with the Public Health Agency of Canada’s National Microbiology Laboratory (NML) and with provincial public health and laboratory partners as they. review and engage in their own studies of serological technologies develop tests assess commercial tests The NML is known around the world for its scientific evidence.

It works acyclovir online purchase with public health partners to prevent the spread of infectious diseases. When making regulatory decisions, we consider the data provided by the NML and provincial public health and laboratory partners. This work will facilitate access to devices that will improve our testing capacity. It will also support research into understanding immunity against COVID-19 and the possibility of acyclovir online purchase re-infection.

Personal protective equipment Personal protective equipment (PPE) is key to protecting health care workers, patients and Canadians through infection prevention and control. We play an important role in providing guidance to companies and manufacturers in Canada that want to supply PPE. We are increasing the range acyclovir online purchase of products available without compromising safety and effectiveness. For example, we are.

We have authorized hundreds of new PPE products and other devices, all while ensuring the safety and quality of PPE. Hand sanitizers, disinfectants, cleaners and acyclovir online purchase soaps The COVID-19 pandemic created an urgent need for disinfectants, hand sanitizers, cleaners and soaps. To increase supply and ensure Canadians have access to these products, we. We will continue our efforts to support supply and access to these essential products.

Drugs and acyclovir online purchase vaccines We are closely tracking all potential drugs and vaccines in development in Canada and abroad. We are working with companies, academic research centres and investigators to help expedite the development and availability of drugs and vaccines to prevent and treat COVID-19. Clinical trials On May 23, 2020, the Minister of Health signed a clinical trials interim order. This temporary acyclovir online purchase measure is designed to meet the urgent need to diagnose, treat, reduce or prevent COVID-19.

The interim order facilitates clinical trials in Canada to investigate and offer greater patient access to potential COVID-19 drugs and medical devices, while upholding strong patient safety requirements. As well, to encourage the rapid development of drugs and vaccines, we are. prioritizing COVID-19 clinical trial applications providing regulatory agility and guidance acyclovir online purchase on how clinical trials are to be conducted this encourages and supports the launch of new trials and the continuation of existing ones, as well as broader patient participation across the country working with companies outside of Canada to bring clinical trials to our country working with researchers around the world to add Canadian sites to their research efforts On May 15, 2020, we authorized Canada’s first vaccine clinical trial. Addressing critical product shortages We have taken steps to address critical product shortages caused by the COVID-19 pandemic.

One of these steps was an interim order to prevent or ease shortages of drugs, medical devices and foods for a special dietary purpose. Introduced on March 30, 2020, this interim order temporarily. allows companies with an MDEL to import foreign devices that meet similar high quality and manufacturing standards as Canadian-approved devices makes it mandatory to report shortages of medical devices that are considered critical during the pandemic allows companies with Drug Establishment Licences to import foreign drugs that meet similar high quality and manufacturing standards as Canadian-approved drugs We also work with provinces and territories, companies and manufacturers, health care providers and patient groups to strengthen the drug supply chain. To identify, prevent and ease shortages for Canadians, we.

stepped up monitoring and surveillance activities to identify potential shortages early on have introduced temporary regulatory agility so manufacturers can ramp up production for example, increased the batch sizes regularly engaged stakeholders to share information and look at how we can prevent tier 3 drug shortages, which have the greatest impact on Canada’s drug supply and health care system helped to access extra supplies of. Drugs, including muscle relaxants, inhalers and sedatives medical devices, such as PPE (medical masks and gowns) and ventilators Post-market surveillance activities We actively monitor the post-market safety and effectiveness of health products related to COVID-19. For example, we work with industry members and health care workers to. monitor safety issues take the necessary steps to protect Canadians from the effects of harmful products To ensure the ongoing safety of marketed health products, we.

take proactive steps to identify COVID-19-related adverse events from drugs and medical devices being used in Canada for COVID-19 proactively monitor major online retailers to identify authorized/unauthorized products making false and misleading COVID-19 claims manage risk communications for COVID-19 public advisories, information updates, health care professional communications and shortages take a proactive approach to identifying false and misleading ads for health products related to COVID-19 take part in international discussions on the real-world safety and effectiveness of COVID-19 treatments Engaging with partners and stakeholders To support access to health products for COVID-19, we collaborate with a range of organizations and stakeholders. These include other government departments, including the Public Health Agency of Canada, as well as provinces and territories, international partners, companies and health care professionals. Engaging with stakeholders We take a whole-of-government approach to address stakeholder issues by.

Acyclovir dosage for shingles treatment

A dormitory-wide https://www.voiture-et-handicap.fr/acyclovir-online-purchase/ quarantine in Marist College's Champagnat Hall, its largest housing unit, has been lifted after students' COVID tests came acyclovir dosage for shingles treatment back negative. The quarantine was put in place after an off-campus student tested positive for the virus, according to a letter that the college sent to students, and that student "came into contact with several Marist students, including residents of Champagnat Hall, at an off-campus acyclovir dosage for shingles treatment party." According to the college's Executive Vice President Geoff Brackett, only test results from students that were quarantined in the dorm have been received. Other students who attended the party whose results have yet to be produced are reportedly quarantining off-campus, and prohibited from college grounds until they complete a 14-day quarantine.According to Julia Fishman, the college's director of media relations, this most recent party was a separate incident from another off-campus party that flouted social distancing guidelines and led to the suspension of 15 students.Marist will now launch a surveillance testing program, according to college Executive Vice President Geoff Brackett, and has "robust testing protocols" in place with MidHudson Regional Hospital for future incidents. "While our local health officials recognized the College for its 'swift and impressive response' to this incident," wrote Brackett in a letter to students, "it should serve as a reminder to all members of the Marist community acyclovir dosage for shingles treatment that we must uphold our shared responsibility to protect our community by wearing masks, washing hands, and maintaining social distance."Attending parties or large gatherings is prohibited. Individuals who do not follow these guidelines acyclovir dosage for shingles treatment will face disciplinary action." Click here to sign up for Daily Voice's free daily emails and news alerts.A man has been accused of recording his sexual abuse of a child, state police said.On Friday, Aug.

28, State Police from the Poughkeepsie barracks responded to an address in can you take acyclovir with alcohol the town of Stanford for a report of sexual assault. An investigation acyclovir dosage for shingles treatment revealed Santiago A. Andujar, 41, of Stanford, recorded his sexual assault of a child Andujar was familiar with, state police said.Andujar was arrested acyclovir dosage for shingles treatment and charged with:use of a child in a sexual performance, a Class C felony, promoting the sexual performance of a child, a Class D felony, and rape in the third degree, a Class E felony.Andujar was arraigned before the town of Stanford Court and remanded to the Dutchess County Jail without bail. He is next scheduled to appear before the court on Wednesday, Sept. 2.

Click here to sign up for Daily Voice's free daily emails and news alerts..

A dormitory-wide quarantine in Marist College's Champagnat Hall, its largest housing acyclovir online purchase unit, has been lifted after students' COVID tests came acyclovir dosage during outbreak back negative. The quarantine was put in place after an off-campus student tested positive acyclovir online purchase for the virus, according to a letter that the college sent to students, and that student "came into contact with several Marist students, including residents of Champagnat Hall, at an off-campus party." According to the college's Executive Vice President Geoff Brackett, only test results from students that were quarantined in the dorm have been received. Other students who attended the party whose results have yet to be produced are reportedly quarantining off-campus, and prohibited from college grounds until they complete a 14-day quarantine.According to Julia Fishman, the college's director of media relations, this most recent party was a separate incident from another off-campus party that flouted social distancing guidelines and led to the suspension of 15 students.Marist will now launch a surveillance testing program, according to college Executive Vice President Geoff Brackett, and has "robust testing protocols" in place with MidHudson Regional Hospital for future incidents. "While our local health officials recognized the College acyclovir online purchase for its 'swift and impressive response' to this incident," wrote Brackett in a letter to students, "it should serve as a reminder to all members of the Marist community that we must uphold our shared responsibility to protect our community by wearing masks, washing hands, and maintaining social distance."Attending parties or large gatherings is prohibited.

Individuals who do not follow these guidelines will face disciplinary action." Click here to sign up for Daily Voice's free daily emails and news alerts.A man has been accused of recording his sexual abuse of a child, acyclovir online purchase state police said.On Friday, Aug. 28, State Police from the Poughkeepsie barracks responded to an address in the town of Stanford useful content for a report of sexual assault. An investigation acyclovir online purchase revealed Santiago A. Andujar, 41, of Stanford, recorded his sexual assault of a child Andujar was familiar with, state police said.Andujar was arrested and charged with:use of a child acyclovir online purchase in a sexual performance, a Class C felony, promoting the sexual performance of a child, a Class D felony, and rape in the third degree, a Class E felony.Andujar was arraigned before the town of Stanford Court and remanded to the Dutchess County Jail without bail.

He is next scheduled to appear before the court on Wednesday, Sept. 2. Click here to sign up for Daily Voice's free daily emails and news alerts..

How effective is acyclovir in treating herpes

The number of reported Covid-19 cases across the globe has surpassed 25 million, with the U.S., Brazil and India leading the grim how effective is acyclovir in treating herpes count, according to data https://www.voiture-et-handicap.fr/acyclovir-online-purchase/ from Johns Hopkins University. The coronavirus has killed more than 843,000 people worldwide since it emerged from Wuhan, China, late last year, with the Americas reporting the bulk of fatalities. The U.S., Mexico and Brazil represent more than 40% of how effective is acyclovir in treating herpes the global death toll, according to Johns Hopkins.

Reported Covid-19 cases first surpassed 10 million in late June, then reached 20 million just over six weeks later on Aug. 10, according to Johns how effective is acyclovir in treating herpes Hopkins data. "This virus is going to be with us for a while.

Without a vaccine, it's going to be with us for years," Carissa Etienne, director of Pan American Health Organization and the World Health Organization's regional director for the how effective is acyclovir in treating herpes Americas, said during a news briefing Tuesday. "Reopening does not mean that the fight is over."Some European countries have started to report a recent resurgence in cases. France Prime Minister Jean Castex said the virus how effective is acyclovir in treating herpes has spread rapidly among young people, forcing the government to intervene.

Castex said France "must do everything to avoid a new confinement," the Associated Press reported on Thursday. Infections in Spain, which has the highest case count among European countries, have climbed to how effective is acyclovir in treating herpes nearly 440,000 cases since the country lifted its lockdown in late June, according to Hopkins. The U.S.

Continues to struggle with the world's worst outbreak and how effective is acyclovir in treating herpes largest reported case count, though the growth in new cases appears to be leveling off after a summer of surging outbreaks.The U.S. Reported an average of 42,000 new infections a day over the last week, a decline of more than 3.0% compared with the prior week, according to a CNBC analysis of Hopkins' data. New cases in how effective is acyclovir in treating herpes the U.S.

Peaked at 67,317 daily cases on July 22, based on a seven-day average, after a resurgence of coronavirus cases ripped through the Sun Belt states in June and July."The current plan — wearing a mask, watching your distance, washing your hands, supplemented by smart testing, according to the state plans, surge testing and extreme technical assistance by CDC as well as our craft teams — continues to yield results," Assistant Secretary for Health Adm. Brett Giroir told reporters on a conference call last week.However, health officials are concerned that the coronavirus may spread to America's heartland. As of Sunday, cases were growing by 19% or more in how effective is acyclovir in treating herpes Indiana, Iowa, Kansas, Nebraska, Michigan, Minnesota, North Dakota and South Dakota, according to a CNBC analysis of Hopkins' data.

Centers for Disease Control and Prevention Director Robert Redfield recently told Dr. Howard Bauchner of the Journal of the American Medical Association how effective is acyclovir in treating herpes that there are worrying signs in the middle of the country where cases appear to be plateauing but not falling. Redfield said the area "is getting stuck," which is a concern as seasonal influenza threatens to overwhelm hospitals and cause preventable deaths.

"We don't need to have a third wave in the heartland right now," he how effective is acyclovir in treating herpes said. "We need to prevent that particularly as we're coming to the fall."The U.S. Is gearing up to distribute a vaccine, which is expected sometime early next year, as part of the how effective is acyclovir in treating herpes Trump administration's Operation Warp Speed.

Health officials have said there's no returning to "normal" until a vaccine is distributed. On Wednesday, the CDC proposed guidelines for who would receive the first doses once a vaccine candidate is approve, prioritizing health-care workers, essential personnel and vulnerable Americans, such as the elderly how effective is acyclovir in treating herpes and those with underlying health conditions. White House coronavirus advisor Dr.

Anthony Fauci has said the initial supply of vaccine doses is expected to be limited and won't be widely available to Americans until "several months" into how effective is acyclovir in treating herpes 2021. The federal government has spent billions in vaccine development, locking in a minimum of 800 million doses as soon as the immunizations are cleared later this year or early next year. Russia registered how effective is acyclovir in treating herpes a vaccine, called "Sputnik V," on Aug.

11, though scientists warn that its candidate has only gone through phase one and phase two clinical trials and not large human trials to prove the vaccine's efficacy. Russia said it would begin phase how effective is acyclovir in treating herpes three trials in August. €” CNBC's Will Feuer, Berkeley Lovelace Jr.

And Holly Ellyatt contributed to this report..

The number of reported https://www.voiture-et-handicap.fr/acyclovir-online-purchase/ Covid-19 cases across the globe has surpassed 25 million, with acyclovir online purchase the U.S., Brazil and India leading the grim count, according to data from Johns Hopkins University. The coronavirus has killed more than 843,000 people worldwide since it emerged from Wuhan, China, late last year, with the Americas reporting the bulk of fatalities. The U.S., Mexico and Brazil represent more than 40% of the global death toll, according acyclovir online purchase to Johns Hopkins.

Reported Covid-19 cases first surpassed 10 million in late June, then reached 20 million just over six weeks later on Aug. 10, according to Johns acyclovir online purchase Hopkins data. "This virus is going to be with us for a while.

Without a vaccine, it's going to be with us for years," Carissa Etienne, director of Pan American Health Organization and the World Health Organization's regional director for the Americas, said during a news briefing acyclovir online purchase Tuesday. "Reopening does not mean that the fight is over."Some European countries have started to report a recent resurgence in cases. France Prime Minister Jean Castex acyclovir online purchase said the virus has spread rapidly among young people, forcing the government to intervene.

Castex said France "must do everything to avoid a new confinement," the Associated Press reported on Thursday. Infections in Spain, which has the highest case count among European countries, have climbed to acyclovir online purchase nearly 440,000 cases since the country lifted its lockdown in late June, according to Hopkins. The U.S.

Continues to acyclovir online purchase struggle with the world's worst outbreak and largest reported case count, though the growth in new cases appears to be leveling off after a summer of surging outbreaks.The U.S. Reported an average of 42,000 new infections a day over the last week, a decline of more than 3.0% compared with the prior week, according to a CNBC analysis of Hopkins' data. New cases in acyclovir online purchase the U.S.

Peaked at 67,317 daily cases on July 22, based on a seven-day average, after a resurgence of coronavirus cases ripped through the Sun Belt states in June and July."The current plan — wearing a mask, watching your distance, washing your hands, supplemented by smart testing, according to the state plans, surge testing and extreme technical assistance by CDC as well as our craft teams — continues to yield results," Assistant Secretary for Health Adm. Brett Giroir told reporters on a conference call last week.However, health officials are concerned that the coronavirus may spread to America's heartland. As of Sunday, cases were growing by 19% or more in Indiana, Iowa, Kansas, acyclovir online purchase Nebraska, Michigan, Minnesota, North Dakota and South Dakota, according to a CNBC analysis of Hopkins' data.

Centers for Disease Control and Prevention Director Robert Redfield recently told Dr. Howard Bauchner of the Journal of the American Medical Association that there are worrying signs acyclovir online purchase in the middle of the country where cases appear to be plateauing but not falling. Redfield said the area "is getting stuck," which is a concern as seasonal influenza threatens to overwhelm hospitals and cause preventable deaths.

"We don't need to have a third acyclovir online purchase wave in the heartland right now," he said. "We need to prevent that particularly as we're coming to the fall."The U.S. Is gearing up to distribute a vaccine, which is expected sometime early next year, as part of the Trump administration's Operation Warp acyclovir online purchase Speed.

Health officials have said there's no returning to "normal" until a vaccine is distributed. On Wednesday, the CDC proposed guidelines for who would receive the first doses once a vaccine candidate is approve, prioritizing health-care workers, essential personnel acyclovir online purchase and vulnerable Americans, such as the elderly and those with underlying health conditions. White House coronavirus advisor Dr.

Anthony Fauci has said the initial supply of vaccine acyclovir online purchase doses is expected to be limited and won't be widely available to Americans until "several months" into 2021. The federal government has spent billions in vaccine development, locking in a minimum of 800 million doses as soon as the immunizations are cleared later this year or early next year. Russia registered acyclovir online purchase a vaccine, called "Sputnik V," on Aug.

11, though scientists warn that its candidate has only gone through phase one and phase two clinical trials and not large human trials to prove the vaccine's efficacy. Russia said it would begin acyclovir online purchase phase three trials in August. €” CNBC's Will Feuer, Berkeley Lovelace Jr.

And Holly Ellyatt contributed to this report..

Acyclovir pharmacology

How to cite this article:Singh O why not try here P acyclovir pharmacology. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly acyclovir pharmacology 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 acyclovir pharmacology went into a frenzy as newspapers, news channels, and social media were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor.

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

Psychiatrists suddenly acyclovir pharmacology started getting distress calls from their patients in despair with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill acyclovir pharmacology 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 acyclovir pharmacology speculations about the person's mental condition and illness and also his relationships and finances.

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

Many psychiatrists and mental health professionals were called by media houses to comment acyclovir pharmacology 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, acyclovir pharmacology and “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 acyclovir pharmacology respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies acyclovir pharmacology 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 acyclovir pharmacology 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 acyclovir pharmacology Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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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.

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

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

How to cite can you take acyclovir with alcohol this article:Singh O acyclovir online purchase P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of acyclovir online purchase the highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide.

As expected, the media went acyclovir online purchase into a frenzy as newspapers, news channels, and social media were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were acyclovir online purchase besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media.

We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress calls acyclovir online purchase 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, acyclovir online purchase forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide.

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

The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there acyclovir online purchase is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental health professionals were called by media houses acyclovir online purchase to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients acyclovir online purchase. 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 acyclovir online purchase 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 acyclovir online purchase 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 acyclovir online purchase has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr. O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West acyclovir online purchase Bengal IndiaSource of Support. None, Conflict of Interest.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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NYS announced the 2020 Income and Resource levels in GIS 19 MA/12 – 2020 Medicaid Levels and Other Updates ) and levels based on the Federal Poverty Level are in GIS 20 MA/02 – 2020 Federal Poverty Levels Here is the 2020 HRA Income and Resources Level Chart Non-MAGI - zovirax acyclovir cream 5 2020 Disabled, 65+ or Blind ("DAB" or SSI-Related) and have Medicare MAGI (2020) (<. 65, Does not have Medicare)(OR has Medicare and has dependent child <. 18 or <. 19 in school) 138% FPL*** zovirax acyclovir cream 5 Children <.

5 and pregnant women have HIGHER LIMITS than shown ESSENTIAL PLAN For MAGI-eligible people over MAGI income limit up to 200% FPL No long term care. See info here 1 2 1 2 3 1 2 Income $875 (up from $859 in 201) $1284 (up from $1,267 in 2019) $1,468 $1,983 $2,498 $2,127 $2,873 Resources $15,750 (up from $15,450 in 2019) $23,100 (up from $22,800 in 2019) NO LIMIT** NO LIMIT SOURCE for 2019 figures is GIS 18 MA/015 - 2019 Medicaid Levels and Other Updates (PDF). All of the attachments with zovirax acyclovir cream 5 the various levels are posted here. NEED TO KNOW PAST MEDICAID INCOME AND RESOURCE LEVELS?.

Which household size applies?. The rules are complicated zovirax acyclovir cream 5. See rules here. On the HRA Medicaid Levels chart - Boxes 1 and 2 are NON-MAGI Income and Resource levels -- Age 65+, Blind or Disabled and other adults who need to use "spend-down" because they are over the MAGI income levels.

Box 10 on page 3 are the MAGI income levels -- The Affordable Care Act changed the rules for Medicaid zovirax acyclovir cream 5 income eligibility for many BUT NOT ALL New Yorkers. People in the "MAGI" category - those NOT on Medicare -- have expanded eligibility up to 138% of the Federal Poverty Line, so may now qualify for Medicaid even if they were not eligible before, or may now be eligible for Medicaid without a "spend-down." They have NO resource limit. Box 3 on page 1 is Spousal Impoverishment levels for Managed Long Term Care &. Nursing Homes and Box 8 has the Transfer Penalty rates for nursing home eligibility Box 4 has Medicaid Buy-In for Working People with Disabilities Under Age 65 (still 2017 levels til April 2018) zovirax acyclovir cream 5 Box 6 are Medicare Savings Program levels (will be updated in April 2018) MAGI INCOME LEVEL of 138% FPL applies to most adults who are not disabled and who do not have Medicare, AND can also apply to adults with Medicare if they have a dependent child/relative under age 18 or under 19 if in school.

42 C.F.R. § 435.4. Certain populations have an even higher income limit - 224% FPL for zovirax acyclovir cream 5 pregnant women and babies <. Age 1, 154% FPL for children age 1 - 19.

CAUTION. What is counted as income may not be what you zovirax acyclovir cream 5 think. For the NON-MAGI Disabled/Aged 65+/Blind, income will still be determined by the same rules as before, explained in this outline and these charts on income disregards. However, for the MAGI population - which is virtually everyone under age 65 who is not on Medicare - their income will now be determined under new rules, based on federal income tax concepts - called "Modifed Adjusted Gross Income" (MAGI).

There are good changes and bad changes zovirax acyclovir cream 5. GOOD. Veteran's benefits, Workers compensation, and gifts from family or others no longer count as income. BAD zovirax acyclovir cream 5.

There is no more "spousal" or parental refusal for this population (but there still is for the Disabled/Aged/Blind.) and some other rules. For all of the rules see. ALSO SEE 2018 Manual on Lump Sums and Impact on Public Benefits - with resource rules The income limits zovirax acyclovir cream 5 increase with the "household size." In other words, the income limit for a family of 5 may be higher than the income limit for a single person. HOWEVER, Medicaid rules about how to calculate the household size are not intuitive or even logical.

There are different rules depending on the "category" of the person seeking Medicaid. Here zovirax acyclovir cream 5 are the 2 basic categories and the rules for calculating their household size. People who are Disabled, Aged 65+ or Blind - "DAB" or "SSI-Related" Category -- NON-MAGI - See this chart for their household size. These same rules apply to the Medicare Savings Program, with some exceptions explained in this article.

Everyone else -- MAGI - zovirax acyclovir cream 5 All children and adults under age 65, including people with disabilities who are not yet on Medicare -- this is the new "MAGI" population. Their household size will be determined using federal income tax rules, which are very complicated. New rule is explained in State's directive 13 ADM-03 - Medicaid Eligibility Changes under the Affordable Care Act (ACA) of 2010 (PDF) pp. 8-10 of the PDF, This PowerPoint by NYLAG on MAGI Budgeting attempts to explain the new MAGI budgeting, including how to determine the Household Size zovirax acyclovir cream 5.

See slides 28-49. Also seeLegal Aid Society and Empire Justice Center materials OLD RULE used until end of 2013 -- Count the person(s) applying for Medicaid who live together, plus any of their legally responsible relatives who do not receive SNA, ADC, or SSI and reside with an applicant/recipient. Spouses or legally responsible for one another, and parents are legally responsible for zovirax acyclovir cream 5 their children under age 21 (though if the child is disabled, use the rule in the 1st "DAB" category. Under this rule, a child may be excluded from the household if that child's income causes other family members to lose Medicaid eligibility.

See 18 NYCRR 360-4.2, MRG p. 573, NYS GIS 2000 zovirax acyclovir cream 5 MA-007 CAUTION. Different people in the same household may be in different "categories" and hence have different household sizes AND Medicaid income and resource limits. If a man is age 67 and has Medicare and his wife is age 62 and not disabled or blind, the husband's household size for Medicaid is determined under Category 1/ Non-MAGI above and his wife's is under Category 2/MAGI.

The following programs were available prior to 2014, but are now discontinued because they are zovirax acyclovir cream 5 folded into MAGI Medicaid. Prenatal Care Assistance Program (PCAP) was Medicaid for pregnant women and children under age 19, with higher income limits for pregnant woman and infants under one year (200% FPL for pregnant women receiving perinatal coverage only not full Medicaid) than for children ages 1-18 (133% FPL). Medicaid for adults between ages 21-65 who are not disabled and without children under 21 in the household. It was sometimes known as zovirax acyclovir cream 5 "S/CC" category for Singles and Childless Couples.

This category had lower income limits than DAB/ADC-related, but had no asset limits. It did not allow "spend down" of excess income. This category has zovirax acyclovir cream 5 now been subsumed under the new MAGI adult group whose limit is now raised to 138% FPL. Family Health Plus - this was an expansion of Medicaid to families with income up to 150% FPL and for childless adults up to 100% FPL.

This has now been folded into the new MAGI adult group whose limit is 138% FPL. For applicants between 138%-150% FPL, they will be eligible for a new program where zovirax acyclovir cream 5 Medicaid will subsidize their purchase of Qualified Health Plans on the Exchange. PAST INCOME &. RESOURCE LEVELS -- Past Medicaid income and resource levels in NYS are shown on these oldNYC HRA charts for 2001 through 2019, in chronological order.

These include Medicaid levels for MAGI and non-MAGI populations, Child Health Plus, MBI-WPD, Medicare Savings Programs and zovirax acyclovir cream 5 other public health programs in NYS. This article was authored by the Evelyn Frank Legal Resources Program of New York Legal Assistance Group.A huge barrier to people returning to the community from nursing homes is the high cost of housing. One way New York State is trying to address that barrier is with the Special Housing Disregard that allows certain members of Managed Long Term Care or FIDA plans to keep more of their income to pay for rent or other shelter costs, rather than having to "spend down" their "excess income" or spend-down on the cost of Medicaid home care. The special income standard for housing expenses helps pay for zovirax acyclovir cream 5 housing expenses to help certain nursing home or adult home residents to safely transition back to the community with MLTC.

Originally it was just for former nursing home residents but in 2014 it was expanded to include people who lived in adult homes. GIS 14/MA-017 Since you are allowed to keep more of your income, you may no longer need to use a pooled trust. KNOW YOUR RIGHTS - zovirax acyclovir cream 5 FACT SHEET on THREE ways to Reduce Spend-down, including this Special Income Standard. September 2018 NEWS -- Those already enrolled in MLTC plans before they are admitted to a nursing home or adult home may obtain this budgeting upon discharge, if they meet the other criteria below.

"How nursing home administrators, adult home operators and MLTC plans should identify individuals who are eligible for the special income standard" and explains their duties to identify eligible individuals, and the MLTC plan must notify the local DSS that the individual may qualify. "Nursing home administrators, nursing home discharge planning staff, adult home operators zovirax acyclovir cream 5 and MLTC health plans are encouraged to identify individuals who may qualify for the special income standard, if they can be safely discharged back to the community from a nursing home and enroll in, or remain enrolled in, an MLTC plan. Once an individual has been accepted into an MLTC plan, the MLTC plan must notify the individual's local district of social services that the transition has occurred and that the individual may qualify for the special income standard. The special income standard will be effective upon enrollment into the MLTC plan, or, for nursing home residents already enrolled in an MLTC plan, the month of discharge to the community.

Questions regarding the special income standard may be directed to DOH at 518-474-8887 zovirax acyclovir cream 5. Who is eligible for this special income standard?. must be age 18+, must have been in a nursing home or an adult home for 30 days or more, must have had Medicaid pay toward the nursing home care, and must enroll in or REMAIN ENROLLED IN a Managed Long Term Care (MLTC) plan or FIDA plan upon leaving the nursing home or adult home must have a housing expense if married, spouse may not receive a "spousal impoverishment" allowance once the individual is enrolled in MLTC. How much is the allowance?.

The rates vary by region and change yearly. Region Counties Deduction (2020) Central Broome, Cayuga, Chenango, Cortland, Herkimer, Jefferson, Lewis, Madison, Oneida, Onondaga, Oswego, St. Lawrence, Tioga, Tompkins $436 Long Island Nassau, Suffolk $1,361 NYC Bronx, Kings, Manhattan, Queens, Richmond $1,451 (up from 1,300 in 2019) Northeastern Albany, Clinton, Columbia, Delaware, Essex, Franklin, Fulton, Greene, Hamilton, Montgomery, Otsego, Rensselaer, Saratoga, Schenectady, Schoharie, Warren, Washington $483 North Metropolitan Dutchess, Orange, Putnam, Rockland, Sullivan, Ulster, Westchester $930 Rochester Chemung, Livingston, Monroe, Ontario, Schuyler, Seneca, Steuben, Wayne, Yates $444 Western Allegany, Cattaraugus, Chautauqua, Erie, Genesee, Niagara, Orleans, Wyoming $386 Past rates published as follows, available on DOH website 2020 rates published in Attachment I to GIS 19 MA/12 – 2020 Medicaid Levels and Other Updates 2019 rates published in Attachment 1 to GIS 18/MA015 - 2019 Medicaid Levels and Other Updates 2018 rates published in GIS 17 MA/020 - 2018 Medicaid Levels and Other Updates. The guidance on how the standardized amount of the disregard is calculated is found in NYS DOH 12- ADM-05.

2017 rate -- GIS 16 MA/018 - 2016 Medicaid Only Income and Resource Levels and Spousal Impoverishment Standards Attachment 12016 rate -- GIS 15-MA/0212015 rate -- Were not posted by DOH but were updated in WMS. 2015 Central $382 Long Island $1,147 NYC $1,001 Northeastern $440 N. Metropolitan $791 Rochester $388 Western $336 2014 rate -- GIS-14-MA/017 HOW DOES IT WORK?. Here is a sample budget for a single person in NYC with Social Security income of $2,386/month paying a Medigap premium of $261/mo.

Gross monthly income $2,575.50 DEDUCT Health insurance premiums (Medicare Part B) - 135.50 (Medigap) - 261.00 DEDUCT Unearned income disregard - 20 DEDUCT Shelter deduction (NYC—2019) - 1,300 DEDUCT Income limit for single (2019) - 859 Excess income or Spend-down $0 WITH NO SPEND-DOWN, May NOT NEED POOLED TRUST!. HOW TO OBTAIN THE HOUSING DISREGARD. When you are ready to leave the nursing home or adult home, or soon after you leave, you or your MLTC plan must request that your local Medicaid program change your Medicaid budget to give you the Housing Disregard. See September 2018 NYS DOH Medicaid Update that requires MLTC plan to help you ask for it.

The procedures in NYC are explained in this Troubleshooting guide. NYC Medicaid program prefers that your MLTC plan file the request, using Form MAP-3057E - Special income housing Expenses NH-MLTC.pdf and Form MAP-3047B - MLTC/NHED Cover Sheet Form MAP-259f (revised 7-31-18)(page 7 of PDF)(DIscharge Notice) - NH must file with HRA upon discharge, certifying resident was informed of availability of this disregard. GOVERNMENT DIRECTIVES (beginning with oldest). NYS DOH 12- ADM-05 - Special Income Standard for Housing Expenses for Individuals Discharged from a Nursing Facility who Enroll into the Managed Long Term Care (MLTC) Program Attachment II - OHIP-0057 - Notice of Intent to Change Medicaid Coverage, (Recipient Discharged from a Skilled Nursing Facility and Enrolled in a Managed Long Term Care Plan) Attachment III - Attachment III – OHIP-0058 - Notice of Intent to Change Medicaid Coverage, (Recipient Disenrolled from a Managed Long Term Care Plan, No Special Income Standard) MLTC Policy 13.02.

MLTC Housing Disregard NYC HRA Medicaid Alert Special Income Standard for housing expenses NH-MLTC 2-9-2013.pdf 2018-07-28 HRA MICSA ALERT Special Income Standard for Housing Expenses for Individuals Discharged from a Nursing Facility and who Enroll into the MLTC Program - update on previous policy. References Form MAP-259f (revised 7-31-18)(page 7 of PDF)(Discharge Notice) - NH must file with HRA upon discharge, certifying resident was informed of availability of this disregard.

5 and pregnant women have HIGHER LIMITS than shown ESSENTIAL PLAN For MAGI-eligible people over MAGI income limit up to 200% acyclovir online purchase https://www.voiture-et-handicap.fr/acyclovir-online-purchase/ FPL No long term care. See info here 1 2 1 2 3 1 2 Income $875 (up from $859 in 201) $1284 (up from $1,267 in 2019) $1,468 $1,983 $2,498 $2,127 $2,873 Resources $15,750 (up from $15,450 in 2019) $23,100 (up from $22,800 in 2019) NO LIMIT** NO LIMIT SOURCE for 2019 figures is GIS 18 MA/015 - 2019 Medicaid Levels and Other Updates (PDF). All of the attachments with the various levels are posted here.

NEED TO KNOW PAST MEDICAID acyclovir online purchase INCOME AND RESOURCE LEVELS?. Which household size applies?. The rules are complicated.

See acyclovir online purchase rules here. On the HRA Medicaid Levels chart - Boxes 1 and 2 are NON-MAGI Income and Resource levels -- Age 65+, Blind or Disabled and other adults who need to use "spend-down" because they are over the MAGI income levels. Box 10 on page 3 are the MAGI income levels -- The Affordable Care Act changed the rules for Medicaid income eligibility for many BUT NOT ALL New Yorkers.

People acyclovir online purchase in the "MAGI" category - those NOT on Medicare -- have expanded eligibility up to 138% of the Federal Poverty Line, so may now qualify for Medicaid even if they were not eligible before, or may now be eligible for Medicaid without a "spend-down." They have NO resource limit. Box 3 on page 1 is Spousal Impoverishment levels for Managed Long Term Care &. Nursing Homes and Box 8 has the Transfer Penalty rates for nursing home eligibility Box 4 has Medicaid Buy-In for Working People with Disabilities Under Age 65 (still 2017 levels til April 2018) Box 6 are Medicare Savings Program levels (will be updated in April 2018) MAGI INCOME LEVEL of 138% FPL applies to most adults who are not disabled and who do not have Medicare, AND can also apply to adults with Medicare if they have a dependent child/relative under age 18 or under 19 if in school.

42 acyclovir online purchase C.F.R. § 435.4. Certain populations have an even higher income limit - 224% FPL for pregnant women and babies <.

Age 1, 154% FPL for children age 1 - acyclovir online purchase 19. CAUTION. What is counted as income may not be what you think.

For the NON-MAGI Disabled/Aged 65+/Blind, income will still be determined by the same rules as before, explained in this outline and these charts on income disregards acyclovir online purchase. However, for the MAGI population - which is virtually everyone under age 65 who is not on Medicare - their income will now be determined under new rules, based on federal income tax concepts - called "Modifed Adjusted Gross Income" (MAGI). There are good changes and bad changes.

GOOD acyclovir online purchase. Veteran's benefits, Workers compensation, and gifts from family or others no longer count as income. BAD.

There is no more "spousal" or parental refusal for this population (but there still is for the Disabled/Aged/Blind.) and some other acyclovir online purchase rules. For all of the rules see. ALSO SEE 2018 Manual on Lump Sums and Impact on Public Benefits - with resource rules The income limits increase with the "household size." In other words, the income limit for a family of 5 may be higher than the income limit for a single person.

HOWEVER, Medicaid rules about how to calculate acyclovir online purchase the household size are not intuitive or even logical. There are different rules depending on the "category" of the person seeking Medicaid. Here are the 2 basic categories and the rules for calculating their household size.

People who are Disabled, acyclovir online purchase Aged 65+ or Blind - "DAB" or "SSI-Related" Category -- NON-MAGI - See this chart for their household size. These same rules apply to the Medicare Savings Program, with some exceptions explained in this article. Everyone else -- MAGI - All children and adults under age 65, including people with disabilities who are not yet on Medicare -- this is the new "MAGI" population.

Their household size will be determined using federal income tax rules, which are very acyclovir online purchase complicated. New rule is explained in State's directive 13 ADM-03 - Medicaid Eligibility Changes under the Affordable Care Act (ACA) of 2010 (PDF) pp. 8-10 of the PDF, This PowerPoint by NYLAG on MAGI Budgeting attempts to explain the new MAGI budgeting, including how to determine the Household Size.

See slides 28-49 acyclovir online purchase. Also seeLegal Aid Society and Empire Justice Center materials OLD RULE used until end of 2013 -- Count the person(s) applying for Medicaid who live together, plus any of their legally responsible relatives who do not receive SNA, ADC, or SSI and reside with an applicant/recipient. Spouses or legally responsible for one another, and parents are legally responsible for their children under age 21 (though if the child is disabled, use the rule in the 1st "DAB" category.

Under this rule, a child may be excluded from the household if that child's acyclovir online purchase income causes other family members to lose Medicaid eligibility. See 18 NYCRR 360-4.2, MRG p. 573, NYS GIS 2000 MA-007 CAUTION.

Different people in the same household may be in different "categories" and hence have different household sizes AND acyclovir online purchase Medicaid income and resource limits. If a man is age 67 and has Medicare and his wife is age 62 and not disabled or blind, the husband's household size for Medicaid is determined under Category 1/ Non-MAGI above and his wife's is under Category 2/MAGI. The following programs were available prior to 2014, but are now discontinued because they are folded into MAGI Medicaid.

Prenatal Care Assistance Program (PCAP) was Medicaid for pregnant women and children under age 19, with higher income limits for pregnant woman and infants under one year (200% FPL for pregnant women receiving perinatal coverage only not full Medicaid) than for children ages 1-18 (133% FPL) acyclovir online purchase. Medicaid for adults between ages 21-65 who are not disabled and without children under 21 in the household. It was sometimes known as "S/CC" category for Singles and Childless Couples.

This category had lower income limits acyclovir online purchase than DAB/ADC-related, but had no asset limits. It did not allow "spend down" of excess income. This category has now been subsumed under the new MAGI adult group whose limit is now raised to 138% FPL.

Family Health Plus acyclovir online purchase - this was an expansion of Medicaid to families with income up to 150% FPL and for childless adults up to 100% FPL. This has now been folded into the new MAGI adult group whose limit is 138% FPL. For applicants between 138%-150% FPL, they will be eligible for a new program where Medicaid will subsidize their purchase of Qualified Health Plans on the Exchange.

PAST acyclovir online purchase INCOME &. RESOURCE LEVELS -- Past Medicaid income and resource levels in NYS are shown on these oldNYC HRA charts for 2001 through 2019, in chronological order. These include Medicaid levels for MAGI and non-MAGI populations, Child Health Plus, MBI-WPD, Medicare Savings Programs and other public health programs in NYS.

This article was authored by the Evelyn Frank Legal Resources Program of New York Legal Assistance Group.A huge barrier to people returning to the community from nursing homes is the high cost of housing acyclovir online purchase. One way New York State is trying to address that barrier is with the Special Housing Disregard that allows certain members of Managed Long Term Care or FIDA plans to keep more of their income to pay for rent or other shelter costs, rather than having to "spend down" their "excess income" or spend-down on the cost of Medicaid home care. The special income standard for housing expenses helps pay for housing expenses to help certain nursing home or adult home residents to safely transition back to the community with MLTC.

Originally it was just for acyclovir online purchase former nursing home residents but in 2014 it was expanded to include people who lived in adult homes. GIS 14/MA-017 Since you are allowed to keep more of your income, you may no longer need to use a pooled trust. KNOW YOUR RIGHTS - FACT SHEET on THREE ways to Reduce Spend-down, including this Special Income Standard.

September 2018 NEWS -- Those already enrolled in MLTC plans before they are admitted to a nursing home or adult home may obtain this budgeting upon discharge, acyclovir online purchase if they meet the other criteria below. "How nursing home administrators, adult home operators and MLTC plans should identify individuals who are eligible for the special income standard" and explains their duties to identify eligible individuals, and the MLTC plan must notify the local DSS that the individual may qualify. "Nursing home administrators, nursing home discharge planning staff, adult home operators and MLTC health plans are encouraged to identify individuals who may qualify for the special income standard, if they can be safely discharged back to the community from a nursing home and enroll in, or remain enrolled in, an MLTC plan.

Once an individual has acyclovir online purchase been accepted into an MLTC plan, the MLTC plan must notify the individual's local district of social services that the transition has occurred and that the individual may qualify for the special income standard. The special income standard will be effective upon enrollment into the MLTC plan, or, for nursing home residents already enrolled in an MLTC plan, the month of discharge to the community. Questions regarding the special income standard may be directed to DOH at 518-474-8887.

Who is eligible for this acyclovir online purchase special income standard?. must be age 18+, must have been in a nursing home or an adult home for 30 days or more, must have had Medicaid pay toward the nursing home care, and must enroll in or REMAIN ENROLLED IN a Managed Long Term Care (MLTC) plan or FIDA plan upon leaving the nursing home or adult home must have a housing expense if married, spouse may not receive a "spousal impoverishment" allowance once the individual is enrolled in MLTC. How much is the allowance?.

The rates vary by region and change acyclovir online purchase yearly. Region Counties Deduction (2020) Central Broome, Cayuga, Chenango, Cortland, Herkimer, Jefferson, Lewis, Madison, Oneida, Onondaga, Oswego, St. Lawrence, Tioga, Tompkins $436 Long Island Nassau, Suffolk $1,361 NYC Bronx, Kings, Manhattan, Queens, Richmond $1,451 (up from 1,300 in 2019) Northeastern Albany, Clinton, Columbia, Delaware, Essex, Franklin, Fulton, Greene, Hamilton, Montgomery, Otsego, Rensselaer, Saratoga, Schenectady, Schoharie, Warren, Washington $483 North Metropolitan Dutchess, Orange, Putnam, Rockland, Sullivan, Ulster, Westchester $930 Rochester Chemung, Livingston, Monroe, Ontario, Schuyler, Seneca, Steuben, Wayne, Yates $444 Western Allegany, Cattaraugus, Chautauqua, Erie, Genesee, Niagara, Orleans, Wyoming $386 Past rates published as follows, available on DOH website 2020 rates published in Attachment I to GIS 19 MA/12 – 2020 Medicaid Levels and Other Updates 2019 rates published in Attachment 1 to GIS 18/MA015 - 2019 Medicaid Levels and Other Updates 2018 rates published in GIS 17 MA/020 - 2018 Medicaid Levels and Other Updates.

The guidance on how the standardized amount acyclovir online purchase of the disregard is calculated is found in NYS DOH 12- ADM-05. 2017 rate -- GIS 16 MA/018 - 2016 Medicaid Only Income and Resource Levels and Spousal Impoverishment Standards Attachment 12016 rate -- GIS 15-MA/0212015 rate -- Were not posted by DOH but were updated in WMS. 2015 Central $382 Long Island $1,147 NYC $1,001 Northeastern $440 N.

Metropolitan $791 Rochester $388 acyclovir online purchase Western $336 2014 rate -- GIS-14-MA/017 HOW DOES IT WORK?. Here is a sample budget for a single person in NYC with Social Security income of $2,386/month paying a Medigap premium of $261/mo. Gross monthly income $2,575.50 DEDUCT Health insurance premiums (Medicare Part B) - 135.50 (Medigap) - 261.00 DEDUCT Unearned income disregard - 20 DEDUCT Shelter deduction (NYC—2019) - 1,300 DEDUCT Income limit for single (2019) - 859 Excess income or Spend-down $0 WITH NO SPEND-DOWN, May NOT NEED POOLED TRUST!.

HOW TO OBTAIN THE HOUSING DISREGARD. When you are ready to leave the nursing home or adult home, or soon after you leave, you or your MLTC plan must request that your local Medicaid program change your Medicaid budget to give you the Housing Disregard. See September 2018 NYS DOH Medicaid Update that requires MLTC plan to help you ask for it.

The procedures in NYC are explained in this Troubleshooting guide. NYC Medicaid program prefers that your MLTC plan file the request, using Form MAP-3057E - Special income housing Expenses NH-MLTC.pdf and Form MAP-3047B - MLTC/NHED Cover Sheet Form MAP-259f (revised 7-31-18)(page 7 of PDF)(DIscharge Notice) - NH must file with HRA upon discharge, certifying resident was informed of availability of this disregard. GOVERNMENT DIRECTIVES (beginning with oldest).

NYS DOH 12- ADM-05 - Special Income Standard for Housing Expenses for Individuals Discharged from a Nursing Facility who Enroll into the Managed Long Term Care (MLTC) Program Attachment II - OHIP-0057 - Notice of Intent to Change Medicaid Coverage, (Recipient Discharged from a Skilled Nursing Facility and Enrolled in a Managed Long Term Care Plan) Attachment III - Attachment III – OHIP-0058 - Notice of Intent to Change Medicaid Coverage, (Recipient Disenrolled from a Managed Long Term Care Plan, No Special Income Standard) MLTC Policy 13.02. MLTC Housing Disregard NYC HRA Medicaid Alert Special Income Standard for housing expenses NH-MLTC 2-9-2013.pdf 2018-07-28 HRA MICSA ALERT Special Income Standard for Housing Expenses for Individuals Discharged from a Nursing Facility and who Enroll into the MLTC Program - update on previous policy. References Form MAP-259f (revised 7-31-18)(page 7 of PDF)(Discharge Notice) - NH must file with HRA upon discharge, certifying resident was informed of availability of this disregard.

GIS 18 MA/012 - Special Income Standard for Housing Expenses for Certain Managed Long-Term Care Enrollees Who are Discharged from a Nursing Home issued Sept. 28, 2018 - this finally implements the most recent Special Terms &. Conditions of the CMS 1115 Waiver that governs the MLTC program, dated Jan.

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