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19 in school) buy flagyl no prescription 138% FPL*** 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 $884 (up from $875 in 2020) $1300 (up from $1,284 in 2020) $1,482 $2,004 $2,526 $2,146 $2,903 Resources $15,900 (up from $15,750 in 2020) $23,400 (up from $23,100 in 2020) NO LIMIT** NO LIMIT 2020 levels are in GIS 19 MA/12 â 2020 Medicaid Levels and Other Updates and attachments here * MAGI and ESSENTIAL plan levels are based on Federal Poverty Levels, which are not released until later in 2021.

2020 levels buy flagyl no prescription are used until then. NEED TO KNOW PAST MEDICAID INCOME AND RESOURCE LEVELS?. WHAT IS THE HOUSEHOLD SIZE?.

See buy flagyl no prescription rules here. HOW TO READ 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 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 buy flagyl no prescription 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 C.F.R buy flagyl no prescription. Â§ 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 - 19 buy flagyl no prescription. 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 buy flagyl no prescription 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.

GOOD buy flagyl no prescription. Veteran's benefits, Workers compensation, and gifts from family or others no longer count as income. BAD.

There is no more "spousal" or parental buy flagyl no prescription 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 HOW TO DETERMINE SIZE OF HOUSEHOLD TO IDENTIFY WHICH INCOME LIMIT APPLIES 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, buy flagyl no prescription 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 are the 2 basic categories and the rules for calculating their household size.

People who are Disabled, Aged 65+ buy flagyl no prescription 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 buy flagyl no prescription 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.

See buy flagyl no prescription 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 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 buy flagyl no prescription 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 Medicaid buy flagyl no prescription 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 buy flagyl no prescription 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 "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 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 Medicaid will subsidize their purchase of Qualified Health Plans on the Exchange.

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Beethoven Visit. The Museum of Smells Experience. The Sounds of Quarantine AdvertisementContinue reading the main storySupported byContinue reading the main storyYes, Many of Us Are Stress-Eating and Gaining Weight in the flagylA global study confirms that during the flagyl, many of us ate more junk food, exercised less, were more anxious and got less sleep.Credit...Lorenzo GrittiBy Dec.

4, 2020Not long ago, Stephen Loy had a lot of healthy habits. He went to exercise classes three or four times a week, cooked nutritious dinners for his family, and snacked on healthy foods like hummus and bell peppers.But that all changed when the flagyl struck. During the lockdowns, when he was stuck at home, his anxiety levels went up.

He stopped exercising and started stress eating. Gone were the hummus and vegetables. Instead, he snacked on cookies, sweets and Layâs potato chips.

He ate more fried foods and ordered takeout from local restaurants.âWe were feeding the soul more than feeding the stomach,â said Mr. Loy, 49, who lives in Baton Rouge and is the executive director of a tech incubator. ÂWe were making sure to eat things that made us feel better â not just nutritional items.âNow a global survey conducted earlier this year confirms what Mr.

Loy and many others experienced firsthand. The antibiotics flagyl and resulting lockdowns led to dramatic changes in health behaviors, prompting people around the world to cut back on physical activity and eat more junk foods. It drove anxiety levels higher and disrupted sleep.

And those who are obese, who already face increased health risks, may have fared the worst, the researchers found. While they tended to experience improvements in some aspects of their diets, such as cooking at home more and eating out less, they were also the most likely to report struggling with their weight and mental health.The findings, published in the journal Obesity, offer a cautionary lesson for many of us as antibiotics cases continue to surge and renewed calls for lockdowns and other restrictions again take hold. With months to go before a treatment becomes widely available and we can safely resume our pre-flagyl routines, now might be a good time to assess the healthy habits we may have let slip and to find new ways to be proactive about our physical and mental health.The study, carried out by researchers at the Pennington Biomedical Research Center in Louisiana, surveyed almost 8,000 adults across the globe, including people from 50 different countries and every state in America.

The researchers found that the decline in healthy behaviors during the flagyl and widespread lockdowns was fairly common regardless of geography.âIndividuals with obesity were impacted the most â and thatâs what we were afraid of,â said Emily Flanagan, an author of the study and postdoctoral fellow at the Pennington Biomedical Research Center.

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The Museum of Smells Experience. The Sounds of Quarantine AdvertisementContinue reading the main storySupported byContinue reading the main storyYes, Many of Us Are Stress-Eating and Gaining Weight in the flagylA global study confirms that during the flagyl, many of us ate more junk food, exercised less, were more anxious and got less sleep.Credit...Lorenzo GrittiBy Dec. 4, 2020Not long ago, Stephen Loy had a lot of healthy habits.

He went to exercise classes three or four times a week, cooked nutritious dinners for his family, and snacked on healthy foods like hummus and bell peppers.But that all changed when the flagyl struck. During the lockdowns, when he was stuck at home, his anxiety levels went up. He stopped exercising and started stress eating.

Gone were the hummus and vegetables. Instead, he snacked on cookies, sweets and Layâs potato chips. He ate more fried foods and ordered takeout from local restaurants.âWe were feeding the soul more than feeding the stomach,â said Mr.

Loy, 49, who lives in Baton Rouge and is the executive director of a tech incubator. ÂWe were making sure to eat things that made us feel better â not just nutritional items.âNow a global survey conducted earlier this year confirms what Mr. Loy and many others experienced firsthand.

The antibiotics flagyl and resulting lockdowns led to dramatic changes in health behaviors, prompting people around the world to cut back on physical activity and eat more junk foods. It drove anxiety levels higher and disrupted sleep. And those who are obese, who already face increased health risks, may have fared the worst, the researchers found.

While they tended to experience improvements in some aspects of their diets, such as cooking at home more and eating out less, they were also the most likely to report struggling with their weight and mental health.The findings, published in the journal Obesity, offer a cautionary lesson for many of us as antibiotics cases continue to surge and renewed calls for lockdowns and other restrictions again take hold. With months to go before a treatment becomes widely available and we can safely resume our pre-flagyl routines, now might be a good time to assess the healthy habits we may have let slip and to find new ways to be proactive about our physical and mental health.The study, carried out by researchers at the Pennington Biomedical Research Center in Louisiana, surveyed almost 8,000 adults across the globe, including people from 50 different countries and every state in America. The researchers found that the decline in healthy behaviors during the flagyl and widespread lockdowns was fairly common regardless of geography.âIndividuals with obesity were impacted the most â and thatâs what we were afraid of,â said Emily Flanagan, an author of the study and postdoctoral fellow at the Pennington Biomedical Research Center.

ÂThey not only started off with higher anxiety levels before the flagyl, but they also had the largest increase in anxiety levels throughout the flagyl.âThe findings shed light on exactly how people altered their routines and behaviors in response to the lockdowns that were implemented in countries around the world this year to slow the spread of the flagyl. The flagyl disrupted everyday life, isolated people from friends and family, and spawned an economic crisis, with tens of millions of people losing jobs or finding their incomes sharply reduced.Dr. Flanagan and her colleagues assumed many people were experiencing enormous levels of stress.

But they were not sure how the flagyl and stay-at-home orders were impacting how people slept, how much they exercised and what they ate.

What side effects may I notice from Flagyl?

Side effects that you should report to your doctor or health care professional as soon as possible:

allergic reactions like skin rash or hives, swelling of the face, lips, or tongue
confusion, clumsiness
dark or white patches in the mouth
fever,
numbness, tingling, pain or weakness in the hands or feet
pain when passing urine
seizures
unusually weak or tired
vaginal irritation or discharge

Side effects that usually do not require medical attention (report to your doctor or health care professional if they continue or are bothersome):

diarrhea
headache
metallic taste
nausea
stomach pain or cramps

This list may not describe all possible side effects.

Does flagyl make you sleepy

antibiotics or Click This Link the Flu does flagyl make you sleepy. Is There a Difference Between Symptoms?. |A potentially dicey phase of does flagyl make you sleepy the flagyl is almost here.

Flu season. The yearly influx of s will soon coincide with antibiotics in the Northern Hemisphere. Normally, healthcare practitioners that see patients with flu-like symptoms in late fall, does flagyl make you sleepy winter and early spring assume the individual has influenza and treat them accordingly.

This year is different. “Going into respiratory flagyl season, we’re going to have a much harder time knowing what is the cause of a person’s symptoms,” says Lisa Maragakis, the senior director of prevention at the Johns Hopkins Health System.Even with the potential for uncertainty, there are still some practices that physicians recommend everyone follows as the double-whammy draws near — especially if you start to develop symptoms.Take PrecautionsFor starters, get your flu shot, says Maragakis. These treatments aren’t perfect — according to the CDC, each yearly flu treatment bounces does flagyl make you sleepy between about 20 and 60 percent efficacy.

Even though the injections don’t guarantee protection for everyone, they will work for some and can help rule out the possibility that any sniffles or body aches you develop stem from the flu.Speaking of those all-too-familiar aches and pains. If you develop any respiratory symptoms, a fever, does flagyl make you sleepy headaches or gastrointestinal issues that are out of the ordinary, isolate yourself. Stay home from work, skip social gatherings, and if there are any high-risk people in your home — individuals with diabetes, for example — keep to yourself if possible, says Sankar Swaminathan, chief of the infectious diseases division at University of Utah Health.“It would be hard for me, with most people, to get at whether they have the flu or buy antibiotics because the symptoms overlap to such a degree,” he adds.

For the most part, only a test can parse whether or not you have the flu, a cold or buy antibiotics. So until you’re able to talk to a medical professional or get results back from the lab, it’s best to take precautions and behave as if you have a buy antibiotics diagnosis does flagyl make you sleepy. Remember that symptoms that look like a cold might actually be buy antibiotics related.

Recent surveys suggest that about 63 does flagyl make you sleepy percent of people tested wait longer than one to two days for results, even though that is the ideal turnaround window for contact tracing. The shortfall may stem from national coordination issues. "As far as I have seen, it's not a lack of willingness to provide more tests — it comes down to ability," says Maragakis.

Faltering supply chains mean the essential tools needed does flagyl make you sleepy to test and test fast are in short supply. "In my opinion, we need a much more coordinated national response to testing in order to solve those problems." What A Test Can Doantibiotics tests do more than deliver peace of mind if, say, you feel congested and learn that it’s a regular cold. The results inform public health officials about the spread and containment of buy antibiotics and help determine what kind of care you get.For example, many people getting a antibiotics test will also get an influenza test (possibly with a new two-in-one technology).

If someone has the regular flu, there are approved medications to fight off does flagyl make you sleepy the they can take. In past flu seasons, healthcare practitioners administered influenza tests but often treated the individual as if they had the before getting results, Swaminathan says. The odds of their illness being the flu are high enough to make that a reasonable choice does flagyl make you sleepy.

With much more uncertainty this year about what someone might have and what treatments could help them, the prescribe-before-results habit will likely be much less common. The prospects of not knowing what kind of illness you might have, or waiting a long time for official lab results, might sound gloomy. But there is a bright does flagyl make you sleepy side.

To keep influenza and buy antibiotics cases low — and to keep you from playing the symptomatic guessing game with yourself — stick with those preventative health measures for the foreseeable future. "It’s not going to last forever," says Swaminathan, "but we have to be patient and we have to be vigilant.".

antibiotics or buy flagyl no prescription Amoxil online the Flu. Is There a Difference Between Symptoms?. |A potentially dicey phase of the flagyl is almost buy flagyl no prescription here. Flu season. The yearly influx of s will soon coincide with antibiotics in the Northern Hemisphere.

Normally, healthcare practitioners that see patients with flu-like symptoms in late fall, winter and early spring assume buy flagyl no prescription the individual has influenza and treat them accordingly. This year is different. “Going into respiratory flagyl season, we’re going to have a much harder time knowing what is the cause of a person’s symptoms,” says Lisa Maragakis, the senior director of prevention at the Johns Hopkins Health System.Even with the potential for uncertainty, there are still some practices that physicians recommend everyone follows as the double-whammy draws near — especially if you start to develop symptoms.Take PrecautionsFor starters, get your flu shot, says Maragakis. These treatments aren’t perfect — according to the CDC, each yearly flu treatment bounces between about 20 and 60 percent buy flagyl no prescription efficacy. Even though the injections don’t guarantee protection for everyone, they will work for some and can help rule out the possibility that any sniffles or body aches you develop stem from the flu.Speaking of those all-too-familiar aches and pains.

If you develop any respiratory buy flagyl no prescription symptoms, a fever, headaches or gastrointestinal issues that are out of the ordinary, isolate yourself. Stay home from work, skip social gatherings, and if there are any high-risk people in your home — individuals with diabetes, for example — keep to yourself if possible, says Sankar Swaminathan, chief of the infectious diseases division at University of Utah Health.“It would be hard for me, with most people, to get at whether they have the flu or buy antibiotics because the symptoms overlap to such a degree,” he adds. For the most part, only a test can parse whether or not you have the flu, a cold or buy antibiotics. So until you’re able to talk to a medical professional or get results back from the lab, it’s best buy flagyl no prescription to take precautions and behave as if you have a buy antibiotics diagnosis. Remember that symptoms that look like a cold might actually be buy antibiotics related.

Colds will still be circulating among people during the fall and winter, and already Maragakis has heard from patients who chalked their runny nose and sore throat up as a typical cold. To combat those kinds of assumptions, “we’re asking people to have a high index of suspicion,” she says.Since the best way to diagnose someone is to examine which (if any) buy flagyl no prescription flagyl is living in their body, antibiotics testing needs to be widespread, accessible and fast. Right now, however, a majority of states fall short of daily testing goals. Recent surveys suggest buy flagyl no prescription that about 63 percent of people tested wait longer than one to two days for results, even though that is the ideal turnaround window for contact tracing. The shortfall may stem from national coordination issues.

"As far as I have seen, it's not a lack of willingness to provide more tests — it comes down to ability," says Maragakis. Faltering supply buy flagyl no prescription chains mean the essential tools needed to test and test fast are in short supply. "In my opinion, we need a much more coordinated national response to testing in order to solve those problems." What A Test Can Doantibiotics tests do more than deliver peace of mind if, say, you feel congested and learn that it’s a regular cold. The results inform public health officials about the spread and containment of buy antibiotics and help determine what kind of care you get.For example, many people getting a antibiotics test will also get an influenza test (possibly with a new two-in-one technology). If someone has the regular flu, there are approved medications to fight off buy flagyl no prescription the they can take.

In past flu seasons, healthcare practitioners administered influenza tests but often treated the individual as if they had the before getting results, Swaminathan says. The odds of their illness being the flu are high enough to make that a buy flagyl no prescription reasonable choice. With much more uncertainty this year about what someone might have and what treatments could help them, the prescribe-before-results habit will likely be much less common. The prospects of not knowing what kind of illness you might have, or waiting a long time for official lab results, might sound gloomy. But there is a bright side buy flagyl no prescription.

It's possible that our buy antibiotics mitigation tactics, like wearing masks, social distancing and avoiding large gatherings, could reduce influenza spread as well. This scenario likely played out in the Southern Hemisphere earlier this year. That half of the buy flagyl no prescription globe sees an influenza season during the Northern Hemisphere's spring and summer, and many countries reported very low non-buy antibiotics diagnoses. To keep influenza and buy antibiotics cases low — and to keep you from playing the symptomatic guessing game with yourself — stick with those preventative health measures for the foreseeable future. "It’s not going to last forever," says Swaminathan, "but we have to be patient and we have to be vigilant.".

Flagyl toxicity

How to review cite this flagyl toxicity article:Singh O P. Aftermath of celebrity suicide â Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized events in flagyl toxicity our country.

Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went into a frenzy as newspapers, news channels, and social media were full of stories providing minute details flagyl toxicity of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor.

All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private and personal details flagyl toxicity 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 flagyl toxicity from their patients in despair with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his flagyl toxicity consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide.

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 flagyl toxicity 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 flagyl toxicity comment on the episode. Many psychiatrists were quoted, or âmisquoted,â or âquoted out of context,â commenting on the life of a person whom they had never examined and had no âprofessional authorityâ 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 âmisleading flagyl toxicity conceptsâ about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of âThe Goldwater Ruleâ by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential flagyl toxicity candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but âstatements to the mediaâ can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and resource books for interacting with media, and flagyl toxicity 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 flagyl toxicity âoff the recordâ 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 â professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, flagyl toxicity 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.

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 â 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 bloodâbrain 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 amygdalaâhippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies.

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 â amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study â Nordanskog et al., 2014 â has followed study patients for a long term â 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 â 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 â focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder.

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 doseâresponse 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 â 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 â 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 â 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 â 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 â 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 â 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 â Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 â have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] â 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.

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 â 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 â 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 â 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 1â2 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 â 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 â 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 â 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 â due to the transient inflammation â and the long-term improvement in mood â 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, MartÃnez-ZalacaÃn I, BernabÃ©u-Sanz Ã, Contreras-RodrÃguez O, HernÃ¡ndez-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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44.Gbyl K, Videbech P. Electroconvulsive therapy increases brain volume in major depression. A systematic review and meta-analysis.

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54.Rocha RB, Dondossola ER, Grande AJ, Colonetti T, Ceretta LB, Passos IC, et al. Increased BDNF levels after electroconvulsive therapy in patients with major depressive disorder. A meta-analysis study.

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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 Low price kamagra this article:Singh O buy flagyl no prescription P. Aftermath of celebrity suicide â Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized events in buy flagyl no prescription our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide.

As expected, the media went into a frenzy as newspapers, news channels, and social media buy flagyl no prescription were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and buy flagyl no prescription discussed on electronic, print, and social media.

We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress calls from buy flagyl no prescription 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 buy flagyl no prescription 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 buy flagyl no prescription and finances. Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him.

The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even buy flagyl no prescription 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 buy flagyl no prescription and mental health professionals were called by media houses to comment on the episode. Many psychiatrists were quoted, or âmisquoted,â or âquoted out of context,â commenting on the life of a person whom they had never examined and had no âprofessional authorityâ 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 âmisleading conceptsâ about buy flagyl no prescription psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the buy flagyl no prescription formulation of âThe Goldwater Ruleâ 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 âstatements to the mediaâ can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and resource books for buy flagyl no prescription 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 âoff the recordâ as the media person is most likely recording the interview, buy flagyl no prescription and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made â professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr. O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, buy flagyl no prescription 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.

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.

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 bloodâbrain 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 amygdalaâhippocampal 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 â amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study â Nordanskog et al., 2014 â has followed study patients for a long term â 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.

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 â 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 â 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 doseâresponse 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 â 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 â 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 â 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.

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.

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.

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 â Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 â have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] â 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 â 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 â 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 â 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 1â2 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.

And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence â 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 â 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.

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

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

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

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

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

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

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

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

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

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

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

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

Flagyl hair loss

Start Preamble Centers flagyl hair loss for Medicare &. Medicaid Services (CMS), HHS. Final rule flagyl hair loss. Correction. In the August 4, 2020 issue of the Federal Register, we published a final rule entitled âFY 2021 Inpatient Psychiatric Facilities Prospective Payment System (IPF PPS) and Special Requirements for Psychiatric Hospitals for Fiscal Year Beginning October 1, 2020 (FY 2021)â.

The August 4, 2020 final rule updates the flagyl hair loss prospective payment rates, the outlier threshold, and the wage index for Medicare inpatient hospital services provided by Inpatient Psychiatric Facilities (IPF), which include psychiatric hospitals and excluded psychiatric units of an Inpatient Prospective Payment System (IPPS) hospital or critical access hospital. In addition, we adopted more recent Office of Management and Budget (OMB) statistical area delineations, and applied a 2-year transition for all providers negatively impacted by wage index changes. This correction document corrects the flagyl hair loss statement of economic significance in the August 4, 2020 final rule. This correction is effective October 1, 2020. Start Further Info The IPF Payment Policy mailbox at IPFPaymentPolicy@cms.hhs.gov for general information.

Nicolas Brock, (410) flagyl hair loss 786-5148, for information regarding the statement of economic significance. End Further Info End Preamble Start Supplemental Information I. Background In flagyl hair loss FR Doc. 2020-16990 (85 FR 47042), the final rule entitled âFY 2021 Inpatient Psychiatric Facilities Prospective Payment System (IPF PPS) and Special Requirements for Psychiatric Hospitals for Fiscal Year Beginning October 1, 2020 (FY 2021)â (hereinafter referred to as the FY 2021 IPF PPS final rule) there was an error in the statement of economic significance and status as major under the Congressional Review Act (5 U.S.C. 801 et seq.).

Based on an estimated flagyl hair loss total impact of $95 million in increased transfers from the federal government to IPF providers, we previously stated that the final rule was not economically significant under Executive Order (E.O.) 12866, and that the rule was not a major rule under the Congressional Review Act. However, the Office of Management and Budget designated this rule as economically significant under E.O. 12866 and flagyl hair loss major under the Congressional Review Act. We are correcting our previous statement in the August 4, 2020 final rule accordingly. This correction is effective October 1, 2020.

II. Summary of Errors On page 47064, in the third column, the third full paragraph under B. Overall Impact should be replaced entirely. The entire paragraph stating. ÂWe estimate that this rulemaking is not economically significant as measured by the $100 million threshold, and hence not a major rule under the Congressional Review Act.

Accordingly, we have prepared a Regulatory Impact Analysis that to the best of our ability presents the costs and benefits of the rulemaking.â should be replaced with. ÂWe estimate that the total impact of this final rule is close to the $100 million threshold. The Office of Management and Budget has designated this rule as economically significant under E.O. 12866 and a major rule under the Congressional Review Act (5 U.S.C. 801 et seq.).

Accordingly, we have prepared a Regulatory Impact Analysis that to the best of our ability presents the costs and benefits of the rulemaking.â III. Waiver of Proposed Rulemaking and Delay in Effective Date We ordinarily publish a notice of proposed rulemaking in the Federal Register to provide a period for public comment before the provisions of a rule take effect in accordance with section 553(b) of the Administrative Procedure Act (APA) (5 U.S.C. 553(b)). However, we can waive this notice and comment procedure if the Secretary of the Department of Human Services finds, for good cause, that the notice and comment process is impracticable, unnecessary, or contrary to the public interest, and incorporates a statement of the finding and the reasons therefore in the notice. This correction document does not constitute a rulemaking that would be subject to these requirements because it corrects only the statement of economic significance included in the FY 2021 IPF PPS final rule.

The corrections contained in this document are consistent with, and do not make substantive changes to, the policies and payment methodologies that were adopted and subjected to notice and comment procedures in the FY 2021 IPF PPS final rule. Rather, the corrections made through this correction document are intended to ensure that the FY 2021 IPF PPS final rule accurately reflects OMB's determination about its economic significance and major status under the Congressional Review Act (CRA). Executive Order 12866 and CRA determinations are functions of the Office of Management and Budget, not the Department of Health and Human Services, and are not rules as defined by the Administrative Procedure Act (5 U.S. Code 551(4)). We ordinarily provide a 60-day delay in the effective date of final rules after the date they are issued, in accordance with the CRA (5 U.S.C.

801(a)(3)). However, section 808(2) of the CRA provides that, if an agency finds good cause that notice and public procedure are impracticable, unnecessary, or contrary to the public interest, the rule shall take effect at such time as the agency determines. Even if this were a rulemaking to which the delayed effective date requirement applied, we found, in the FY 2021 IPF PPS Final Rule (85 FR 47043), good cause to waive the 60-day delay in the effective date of the IPF PPS final rule. In the final rule, we explained that, due to CMS prioritizing efforts in support of containing and combatting the buy antibiotics-Start Printed Page 5292419 public health emergency by devoting significant resources to that end, the work needed on the IPF PPS final rule was not completed in accordance with our usual rulemaking schedule. We noted that it is critical, however, to ensure that the IPF PPS payment policies are effective on the first day of the fiscal year to which they are intended to apply and therefore, it would be contrary to the public interest to not waive the 60-day delay in the effective date.

Undertaking further notice and comment procedures to incorporate the corrections in this document into the FY 2021 IPF PPS final rule or delaying the effective date would be contrary to the public interest because it is in the public's interest to ensure that the policies finalized in the FY 2021 IPF PPS are effective as of the first day of the fiscal year to ensure providers and suppliers receive timely and appropriate payments. Further, such procedures would be unnecessary, because we are not altering the payment methodologies or policies. Rather, the correction we are making is only to indicate that the FY 2021 IPF PPS final rule is economically significant and a major rule under the CRA. For these reasons, we find we have good cause to waive the notice and comment and effective date requirements. IV.

Correction of Errors in the Preamble In FR Doc. 2020-16990, appearing on page 47042 in the Federal Register of Tuesday, August 4, 2020, the following correction is made. 1. On page 47064, in the 3rd column, under B. Overall Impact, correct the third full paragraph to read as follows.

We estimate that the total impact of this final rule is very close to the $100 million threshold. The Office of Management and Budget has designated this rule as economically significant under E.O. 12866 and a major rule under the Congressional Review Act (5 U.S.C. 801 et seq.). Accordingly, we have prepared a Regulatory Impact Analysis that to the best of our ability presents the costs and benefits of the rulemaking.

Start Signature Dated. August 24, 2020. Wilma M. Robinson, Deputy Executive Secretary to the Department, Department of Health and Human Services. End Signature End Supplemental Information [FR Doc.

2020-18902 Filed 8-26-20. 8:45 am]BILLING CODE 4120-01-PBy Cyndie Shearing @CyndieShearing Americans from all walks of life are struggling to cope with an array of issues related to the buy antibiotics flagyl. Fear and anxiety about this new disease and what could happen is sometimes overwhelming and can cause strong emotions in adults and children. But long before the flagyl hit the U.S., farmers and ranchers were struggling. Years of falling commodity prices, natural disasters, declining farm income and trade disputes with China hit rural America hard, and not just financially.

Farmersâ mental health is at risk, too. Long before the flagyl hit the U.S., farmers and ranchers were struggling. Fortunately, Americaâs food producers have proven to be a resilient bunch. Across the country, they continue to adopt new ways to manage stress and cope with the difficult situations theyâre facing. A few examples are below.

In Oklahoma, Bryan Vincent and Gary Williams are part of an informal group that meets on a regular basis to share their burdens. âItâs way past farming,â said Vincent, a local crop consultant. ÂItâs a chance to meet with like-minded people. Itâs a chance for us to let some things out. We laugh, we may cry together, we may be disgusted together.

We share our emotions, whether good, bad.â Gathering with trusted friends has given them the chance to talk about whatâs happening in their lives, both good and bad. ÂI would encourage anybody â any group of farmers, friends, whatever â to form a groupâ to meet regularly, said Williams, a farmer. ÂNot just in bad times. I think you should do that regardless, even in good times. Share your victories and triumphs with one another, support one another.â James Young Credit.

Nocole Zema/Virginia Farm Bureau In Michigan, dairy farmer Ashley Messing Kennedy battled postpartum depression and anxiety while also grieving over a close friend and farm employee who died by suicide. At first she coped by staying busy, fixing farm problems on her own and rarely asking for help. But six months later, she knew something wasnât right. Finding a meaningful activity to do away from the farm was a positive step forward. ÂRunningâs been a game-changer for me,â Kennedy said.

ÂItâs so important to interact with people, face-to-face, that you donât normally engage with. Whatever that is for you, do it â take time to get off the farm and walk away for a while. It will be there tomorrow.â Rich Baker also farms in Michigan and has found talking with others to be his stress management tactic of choice. ÂYou canât just bottle things up,â Baker said. ÂIf you donât have a built-in network of farmers, go talk to a professional.

In some cases that may be even more beneficial because their opinions may be more impartial.â James Young, a beef cattle farmer in Virginia, has found that mental health issues are less stigmatized as a whole today compared to the recent past. But there are farmers âwho would throw you under the bus pretty fastâ if they found out someone was seeking professional mental health, he said. ÂItâs still stigmatized here.â RFD-TV Special on Farm Stress and Farmer Mental HealthAs part of the American Farm Bureau Federationâs ongoing effort to raise awareness, reduce stigma and share resources related to mental health, the organization partnered with RFD-TV to produce a one-hour episode of âRural America Liveâ on farm stress and farmer mental health. The episode features AFBF President Zippy Duvall, Farm Credit Council President Todd Van Hoose and National Farmers Union President Rob Larew, as well as two university Extension specialists, a rural pastor and the author of âStress-Free You!. Â The program aired Thursday, Aug.

27, and will be re-broadcast on Saturday, Aug. 29, at 6 a.m. Eastern/5 a.m. Central. Cyndie Shearing is director of communications at the American Farm Bureau Federation.

Quotes in this column originally appeared in state Farm Bureau publications and are reprinted with permission. Vincent, Williams (Oklahoma). Kennedy, Baker (Michigan) and Young (Virginia)..

Start Preamble buy flagyl no prescription Centers for Learn More Medicare &. Medicaid Services (CMS), HHS. Final rule buy flagyl no prescription. Correction.

In the August 4, 2020 issue of the Federal Register, we published a final rule entitled âFY 2021 Inpatient Psychiatric Facilities Prospective Payment System (IPF PPS) and Special Requirements for Psychiatric Hospitals for Fiscal Year Beginning October 1, 2020 (FY 2021)â. The August 4, 2020 final rule updates the prospective payment rates, the outlier threshold, and the wage index for Medicare inpatient hospital services provided by Inpatient Psychiatric Facilities (IPF), which include buy flagyl no prescription psychiatric hospitals and excluded psychiatric units of an Inpatient Prospective Payment System (IPPS) hospital or critical access hospital. In addition, we adopted more recent Office of Management and Budget (OMB) statistical area delineations, and applied a 2-year transition for all providers negatively impacted by wage index changes. This correction document corrects the statement of buy flagyl no prescription economic significance in the August 4, 2020 final rule.

This correction is effective October 1, 2020. Start Further Info The IPF Payment Policy mailbox at IPFPaymentPolicy@cms.hhs.gov for general information. Nicolas Brock, (410) 786-5148, for information regarding the statement buy flagyl no prescription of economic significance. End Further Info End Preamble Start Supplemental Information I.

Background In buy flagyl no prescription FR Doc. 2020-16990 (85 FR 47042), the final rule entitled âFY 2021 Inpatient Psychiatric Facilities Prospective Payment System (IPF PPS) and Special Requirements for Psychiatric Hospitals for Fiscal Year Beginning October 1, 2020 (FY 2021)â (hereinafter referred to as the FY 2021 IPF PPS final rule) there was an error in the statement of economic significance and status as major under the Congressional Review Act (5 U.S.C. 801 et seq.). Based on an estimated total impact of $95 million in increased transfers from the federal government to IPF buy flagyl no prescription providers, we previously stated that the final rule was not economically significant under Executive Order (E.O.) 12866, and that the rule was not a major rule under the Congressional Review Act.

However, the Office of Management and Budget designated this rule as economically significant under E.O. 12866 and major under the buy flagyl no prescription Congressional Review Act. We are correcting our previous statement in the August 4, 2020 final rule accordingly. This correction is effective October 1, 2020.

II. Summary of Errors On page 47064, in the third column, the third full paragraph under B. Overall Impact should be replaced entirely. The entire paragraph stating.

ÂWe estimate that this rulemaking is not economically significant as measured by the $100 million threshold, and hence not a major rule under the Congressional Review Act. Accordingly, we have prepared a Regulatory Impact Analysis that to the best of our ability presents the costs and benefits of the rulemaking.â should be replaced with. ÂWe estimate that the total impact of this final rule is close to the $100 million threshold. The Office of Management and Budget has designated this rule as economically significant under E.O.

12866 and a major rule under the Congressional Review Act (5 U.S.C. 801 et seq.). Accordingly, we have prepared a Regulatory Impact Analysis that to the best of our ability presents the costs and benefits of the rulemaking.â III. Waiver of Proposed Rulemaking and Delay in Effective Date We ordinarily publish a notice of proposed rulemaking in the Federal Register to provide a period for public comment before the provisions of a rule take effect in accordance with section 553(b) of the Administrative Procedure Act (APA) (5 U.S.C.

553(b)). However, we can waive this notice and comment procedure if the Secretary of the Department of Human Services finds, for good cause, that the notice and comment process is impracticable, unnecessary, or contrary to the public interest, and incorporates a statement of the finding and the reasons therefore in the notice. This correction document does not constitute a rulemaking that would be subject to these requirements because it corrects only the statement of economic significance included in the FY 2021 IPF PPS final rule. The corrections contained in this document are consistent with, and do not make substantive changes to, the policies and payment methodologies that were adopted and subjected to notice and comment procedures in the FY 2021 IPF PPS final rule.

Rather, the corrections made through this correction document are intended to ensure that the FY 2021 IPF PPS final rule accurately reflects OMB's determination about its economic significance and major status under the Congressional Review Act (CRA). Executive Order 12866 and CRA determinations are functions of the Office of Management and Budget, not the Department of Health and Human Services, and are not rules as defined by the Administrative Procedure Act (5 U.S. Code 551(4)). We ordinarily provide a 60-day delay in the effective date of final rules after the date they are issued, in accordance with the CRA (5 U.S.C.

We noted that it is critical, however, to ensure that the IPF PPS payment policies are effective on the first day of the fiscal year to which they are intended to apply and therefore, it would be contrary to the public interest to not waive the 60-day delay in the effective date. Undertaking further notice and comment procedures to incorporate the corrections in this document into the FY 2021 IPF PPS final rule or delaying the effective date would be contrary to the public interest because it is in the public's interest to ensure that the policies finalized in the FY 2021 IPF PPS are effective as of the first day of the fiscal year to ensure providers and suppliers receive timely and appropriate payments. Further, such procedures would be unnecessary, because we are not altering the payment methodologies or policies. Rather, the correction we are making is only to indicate that the FY 2021 IPF PPS final rule is economically significant and a major rule under the CRA.

For these reasons, we find we have good cause to waive the notice and comment and effective date requirements. IV. Correction of Errors in the Preamble In FR Doc. 2020-16990, appearing on page 47042 in the Federal Register of Tuesday, August 4, 2020, the following correction is made.

1. On page 47064, in the 3rd column, under B. Overall Impact, correct the third full paragraph to read as follows. We estimate that the total impact of this final rule is very close to the $100 million threshold.

The Office of Management and Budget has designated this rule as economically significant under E.O. 12866 and a major rule under the Congressional Review Act (5 U.S.C. 801 et seq.). Accordingly, we have prepared a Regulatory Impact Analysis that to the best of our ability presents the costs and benefits of the rulemaking.

Start Signature Dated. August 24, 2020. Wilma M. Robinson, Deputy Executive Secretary to the Department, Department of Health and Human Services.

End Signature End Supplemental Information [FR Doc. 2020-18902 Filed 8-26-20. 8:45 am]BILLING CODE 4120-01-PBy Cyndie Shearing @CyndieShearing Americans from all walks of life are struggling to cope with an array of issues related to the buy antibiotics flagyl. Fear and anxiety about this new disease and what could happen is sometimes overwhelming and can cause strong emotions in adults and children.

But long before the flagyl hit the U.S., farmers and ranchers were struggling. Years of falling commodity prices, natural disasters, declining farm income and trade disputes with China hit rural America hard, and not just financially. Farmersâ mental health is at risk, too. Long before the flagyl hit the U.S., farmers and ranchers were struggling.

Fortunately, Americaâs food producers have proven to be a resilient bunch. Across the country, they continue to adopt new ways to manage stress and cope with the difficult situations theyâre facing. A few examples are below. In Oklahoma, Bryan Vincent and Gary Williams are part of an informal group that meets on a regular basis to share their burdens.

âItâs way past farming,â said Vincent, a local crop consultant. ÂItâs a chance to meet with like-minded people. Itâs a chance for us to let some things out. We laugh, we may cry together, we may be disgusted together.

Share your victories and triumphs with one another, support one another.â James Young Credit. Nocole Zema/Virginia Farm Bureau In Michigan, dairy farmer Ashley Messing Kennedy battled postpartum depression and anxiety while also grieving over a close friend and farm employee who died by suicide. At first she coped by staying busy, fixing farm problems on her own and rarely asking for help. But six months later, she knew something wasnât right.

Finding a meaningful activity to do away from the farm was a positive step forward. ÂRunningâs been a game-changer for me,â Kennedy said. ÂItâs so important to interact with people, face-to-face, that you donât normally engage with. Whatever that is for you, do it â take time to get off the farm and walk away for a while.

It will be there tomorrow.â Rich Baker also farms in Michigan and has found talking with others to be his stress management tactic of choice. ÂYou canât just bottle things up,â Baker said. ÂIf you donât have a built-in network of farmers, go talk to a professional. In some cases that may be even more beneficial because their opinions may be more impartial.â James Young, a beef cattle farmer in Virginia, has found that mental health issues are less stigmatized as a whole today compared to the recent past.

But there are farmers âwho would throw you under the bus pretty fastâ if they found out someone was seeking professional mental health, he said. ÂItâs still stigmatized here.â RFD-TV Special on Farm Stress and Farmer Mental HealthAs part of the American Farm Bureau Federationâs ongoing effort to raise awareness, reduce stigma and share resources related to mental health, the organization partnered with RFD-TV to produce a one-hour episode of âRural America Liveâ on farm stress and farmer mental health. The episode features AFBF President Zippy Duvall, Farm Credit Council President Todd Van Hoose and National Farmers Union President Rob Larew, as well as two university Extension specialists, a rural pastor and the author of âStress-Free You!. Â The program aired Thursday, Aug.

27, and will be re-broadcast on Saturday, Aug. 29, at 6 a.m. Eastern/5 a.m. Central.

Cyndie Shearing is director of communications at the American Farm Bureau Federation. Quotes in this column originally appeared in state Farm Bureau publications and are reprinted with permission. Vincent, Williams (Oklahoma). Kennedy, Baker (Michigan) and Young (Virginia)..

Flagyl antibiootti

This notice announces an extension of the timeline for publication of a Medicare final rule in accordance with the Social Security Act, which allows us to extend the timeline for publication of the flagyl antibiootti final rule. As of August 26, 2020, the timeline for publication of the final rule to finalize the provisions of the October 17, 2019 proposed rule (84 FR 55766) is extended until August 31, 2021. Start Further Info Lisa O. Wilson, (410) flagyl antibiootti 786-8852. End Further Info End Preamble Start Supplemental Information In the October 17, 2019 Federal Register (84 FR 55766), we published a proposed rule that addressed undue regulatory impact and burden of the physician self-referral law.

The proposed rule was issued in conjunction with the Centers for Medicare &. Medicaid Services' (CMS) Patients over Paperwork initiative and the Department of flagyl antibiootti Health and Human Services' (the Department or HHS) Regulatory Sprint to Coordinated Care. In the proposed rule, we proposed exceptions to the physician self-referral law for certain value-based compensation arrangements between or among physicians, providers, and suppliers. A new exception for certain arrangements under which a physician receives limited remuneration for items or services actually provided by the physician. A new exception for donations of cybersecurity technology and related flagyl antibiootti services.

And amendments to the existing exception for electronic health records (EHR) items and services. The proposed rule also provides critically necessary guidance for physicians and health care providers and suppliers whose financial relationships are governed by the physician self-referral statute and regulations. This notice announces an extension of the timeline for publication of the final rule and the continuation of effectiveness flagyl antibiootti of the proposed rule. Section 1871(a)(3)(A) of the Social Security Act (the Act) requires us to establish and publish a regular timeline for the publication of final regulations based on the previous publication of a proposed regulation. In accordance with section 1871(a)(3)(B) of the Act, the timeline may vary among different regulations based on differences in the complexity of the regulation, the number and scope of comments received, and other relevant factors, but may not be longer than 3 years except under exceptional circumstances.

In addition, flagyl antibiootti in accordance with section 1871(a)(3)(B) of the Act, the Secretary may extend the initial targeted publication date of the final regulation if the Secretary, no later than the regulation's previously established proposed publication date, publishes a notice with the new target date, and such notice includes a brief explanation of the justification for the variation. We announced in the Spring 2020 Unified Agenda (June 30, 2020, www.reginfo.gov) that we would issue the final rule in August 2020. However, we are still working through the Start Printed Page 52941complexity of the issues raised by comments received on the proposed rule and therefore we are not able to meet the announced publication target date. This notice extends flagyl antibiootti the timeline for publication of the final rule until August 31, 2021. Start Signature Dated.

August 24, 2020. Wilma M flagyl antibiootti. Robinson, Deputy Executive Secretary to the Department, Department of Health and Human Services. End Signature End Supplemental Information [FR Doc. 2020-18867 Filed flagyl antibiootti 8-26-20.

8:45 am]BILLING CODE 4120-01-PThe Centers for Medicare &. Medicaid Services (CMS) today announced efforts underway to support Louisiana and Texas in response to Hurricane Laura. On August 26, 2020, Department of Health and Human Services (HHS) Secretary Alex Azar declared public health emergencies (PHEs) in these states, retroactive to August 22, 2020 flagyl antibiootti for the state of Louisiana and to August 23, 2020 for the state of Texas. CMS is working to ensure hospitals and other facilities can continue operations and provide access to care despite the effects of Hurricane Laura. CMS provided numerous waivers to health care providers during the current antibiotics disease 2019 (buy antibiotics) flagyl to meet the needs of beneficiaries and providers.

The waivers already in place flagyl antibiootti will be available to health care providers to use during the duration of the buy antibiotics PHE determination timeframe and for the Hurricane Laura PHE. CMS may waive certain additional Medicare, Medicaid, and Childrenâs Health Insurance Program (CHIP) requirements, create special enrollment opportunities for individuals to access healthcare quickly, and take steps to ensure dialysis patients obtain critical life-saving services. âOur thoughts are with everyone who is in the path of this powerful and dangerous hurricane and CMS is doing everything within its authority to provide assistance and relief to all who are affected,â said CMS Administrator Seema Verma. ÂWe will partner and coordinate with state, federal, and local officials to flagyl antibiootti make sure that in the midst of all of the uncertainty a natural disaster can bring, our beneficiaries will not have to worry about access to healthcare and other crucial life-saving and sustaining services they may need.â Below are key administrative actions CMS will be taking in response to the PHEs declared in Louisiana and Texas. Waivers and Flexibilities for Hospitals and Other Healthcare Facilities.

CMS has already waived many Medicare, Medicaid, and CHIP requirements for facilities. The CMS Dallas Survey flagyl antibiootti &. Enforcement Division, under the Survey Operations Group, will grant other provider-specific requests for specific types of hospitals and other facilities in Louisiana and Texas. These waivers, once issued, will help provide continued access to care for beneficiaries. For more information flagyl antibiootti on the waivers CMS has granted, visit.

Www.cms.gov/emergency. Special Enrollment Opportunities for Hurricane Victims. CMS will make available special enrollment periods for certain Medicare beneficiaries and certain individuals seeking health plans offered through the Federal Health Insurance Exchange. This gives people impacted by the hurricane the opportunity to change their Medicare health and prescription drug plans and gain access to health coverage on the Exchange if eligible for the special enrollment period flagyl antibiootti. For more information, please visit.

Disaster Preparedness Toolkit for State Medicaid Agencies. CMS developed an inventory of Medicaid and CHIP flagyl antibiootti flexibilities and authorities available to states in the event of a disaster. For more information and to access the toolkit, visit. Https://www.medicaid.gov/state-resource-center/disaster-response-toolkit/index.html. Dialysis Care flagyl antibiootti.

CMS is helping patients obtain access to critical life-saving services. The Kidney Community Emergency Response (KCER) program has been activated and is working with the End Stage Renal Disease (ESRD) Network, Network 13 â Louisiana, and Network 14 - Texas, to assess the status of dialysis facilities in the potentially impacted areas related to generators, alternate water supplies, education and materials for patients and more. The KCER is also assisting flagyl antibiootti patients who evacuated ahead of the storm to receive dialysis services in the location to which they evacuated. Patients have been educated to have an emergency supply kit on hand including important personal, medical and insurance information. Contact information for their facility, the ESRD Network hotline number, and contact information of those with whom they may stay or for out-of-state contacts in a waterproof bag.

They have also been instructed to have flagyl antibiootti supplies on hand to follow a three-day emergency diet. The ESRD Network 8 â Mississippi hotline is 1-800-638-8299, Network 13 â Louisiana hotline is 800-472-7139, the ESRD Network 14 - Texas hotline is 877-886-4435, and the KCER hotline is 866-901-3773. Additional information is available on the KCER website www.kcercoalition.com. During the 2017 and 2018 hurricane seasons, CMS approved special purpose renal dialysis facilities in several states to furnish dialysis on a short-term basis at designated locations to serve ESRD patients under emergency circumstances in which there were limited dialysis resources or flagyl antibiootti access-to-care problems due to the emergency circumstances. Medical equipment and supplies replacements.

Under the COVD-19 waivers, CMS suspended certain requirements necessary for Medicare beneficiaries who have lost or realized damage to their durable medical equipment, prosthetics, orthotics and supplies as a result of the PHE. This will help to make sure that beneficiaries flagyl antibiootti can continue to access the needed medical equipment and supplies they rely on each day. Medicare beneficiaries can contact 1-800-MEDICARE (1-800-633-4227) for assistance. Ensuring Access to Care in Medicare Advantage and Part D. During a public health emergency, Medicare Advantage Organizations and Part D Plan sponsors flagyl antibiootti must take steps to maintain access to covered benefits for beneficiaries in affected areas.

These steps include allowing Part A/B and supplemental Part C plan benefits to be furnished at specified non-contracted facilities and waiving, in full, requirements for gatekeeper referrals where applicable. Emergency Preparedness Requirements. Providers and suppliers are expected to have emergency flagyl antibiootti preparedness programs based on an all-hazards approach. To assist in the understanding of the emergency preparedness requirements, CMS Central Office and the Regional Offices hosted two webinars in 2018 regarding Emergency Preparedness requirements and provider expectations. One was an all provider training on June 19, 2018 with more than 3,000 provider participants and the other an all-surveyor training on August 8, 2018.

Both presentations covered flagyl antibiootti the emergency preparedness final rule which included emergency power supply. 1135 waiver process. Best practices and lessons learned from past disasters. And helpful flagyl antibiootti resources and more. Both webinars are available at https://qsep.cms.gov/welcome.aspx.

CMS also compiled a list of Frequently Asked Questions (FAQs) and useful national emergency preparedness resources to assist state Survey Agencies (SAs), their state, tribal, regional, local emergency management partners and health care providers to develop effective and robust emergency plans and tool kits to assure compliance with the emergency preparedness rules. The tools can be flagyl antibiootti located at. CMS Regional Offices have provided specific emergency preparedness information to Medicare providers and suppliers through meetings, dialogue and presentations. The regional offices also provide regular technical assistance in emergency preparedness to state agencies and staff, who, since November 2017, have been regularly surveying providers and suppliers for compliance with emergency preparedness regulations. Additional information on the emergency preparedness requirements can be found here.

Https://www.cms.gov/Regulations-and-Guidance/Guidance/Manuals/downloads/som107ap_z_emergprep.pdf CMS will continue to work with all geographic areas impacted by Hurricane Laura. We encourage beneficiaries and providers of healthcare services that have been impacted to seek help by visiting CMSâ emergency webpage (www.cms.gov/emergency). For more information about the HHS PHE, please visit.

Extension of timeline for publication of buy flagyl no prescription final rule. This notice announces an extension of the timeline for publication of a Medicare final rule in accordance with the Social Security Act, which allows us to extend the timeline for publication of the final rule. As of August 26, 2020, the timeline for publication of the final rule to finalize the provisions of the October 17, 2019 proposed rule (84 FR 55766) is extended until August 31, 2021. Start Further buy flagyl no prescription Info Lisa O. Wilson, (410) 786-8852.

End Further Info End Preamble Start Supplemental Information In the October 17, 2019 Federal Register (84 FR 55766), we published a proposed rule that addressed undue regulatory impact and burden of the physician self-referral law. The proposed rule was issued in conjunction with the Centers buy flagyl no prescription for Medicare &. Medicaid Services' (CMS) Patients over Paperwork initiative and the Department of Health and Human Services' (the Department or HHS) Regulatory Sprint to Coordinated Care. In the proposed rule, we proposed exceptions to the physician self-referral law for certain value-based compensation arrangements between or among physicians, providers, and suppliers. A new exception for certain arrangements under which a physician receives limited remuneration for items buy flagyl no prescription or services actually provided by the physician.

A new exception for donations of cybersecurity technology and related services. And amendments to the existing exception for electronic health records (EHR) items and services. The proposed rule also provides critically necessary guidance for physicians and health care buy flagyl no prescription providers and suppliers whose financial relationships are governed by the physician self-referral statute and regulations. This notice announces an extension of the timeline for publication of the final rule and the continuation of effectiveness of the proposed rule. Section 1871(a)(3)(A) of the Social Security Act (the Act) requires us to establish and publish a regular timeline for the publication of final regulations based on the previous publication of a proposed regulation.

In accordance with section 1871(a)(3)(B) of the Act, the timeline may vary among different regulations based on differences in the complexity of the regulation, the number and scope of comments received, and other relevant factors, but may not be longer than 3 years except under exceptional buy flagyl no prescription circumstances. In addition, in accordance with section 1871(a)(3)(B) of the Act, the Secretary may extend the initial targeted publication date of the final regulation if the Secretary, no later than the regulation's previously established proposed publication date, publishes a notice with the new target date, and such notice includes a brief explanation of the justification for the variation. We announced in the Spring 2020 Unified Agenda (June 30, 2020, www.reginfo.gov) that we would issue the final rule in August 2020. However, we are still working through the Start Printed Page 52941complexity of the issues raised by comments buy flagyl no prescription received on the proposed rule and therefore we are not able to meet the announced publication target date. This notice extends the timeline for publication of the final rule until August 31, 2021.

Start Signature Dated. August 24, 2020 buy flagyl no prescription. Wilma M. Robinson, Deputy Executive Secretary to the Department, Department of Health and Human Services. End Signature End Supplemental Information [FR Doc buy flagyl no prescription.

2020-18867 Filed 8-26-20. 8:45 am]BILLING CODE 4120-01-PThe Centers for Medicare &. Medicaid Services (CMS) today announced efforts underway to support Louisiana and Texas buy flagyl no prescription in response to Hurricane Laura. On August 26, 2020, Department of Health and Human Services (HHS) Secretary Alex Azar declared public health emergencies (PHEs) in these states, retroactive to August 22, 2020 for the state of Louisiana and to August 23, 2020 for the state of Texas. CMS is working to ensure hospitals and other facilities can continue operations and provide access to care despite the effects of Hurricane Laura.

CMS provided numerous waivers to health care providers during the current antibiotics disease 2019 buy flagyl no prescription (buy antibiotics) flagyl to meet the needs of beneficiaries and providers. The waivers already in place will be available to health care providers to use during the duration of the buy antibiotics PHE determination timeframe and for the Hurricane Laura PHE. CMS may waive certain additional Medicare, Medicaid, and Childrenâs Health Insurance Program (CHIP) requirements, create special enrollment opportunities for individuals to access healthcare quickly, and take steps to ensure dialysis patients obtain critical life-saving services. âOur thoughts are with everyone who is in the path of this powerful and dangerous buy flagyl no prescription hurricane and CMS is doing everything within its authority to provide assistance and relief to all who are affected,â said CMS Administrator Seema Verma. ÂWe will partner and coordinate with state, federal, and local officials to make sure that in the midst of all of the uncertainty a natural disaster can bring, our beneficiaries will not have to worry about access to healthcare and other crucial life-saving and sustaining services they may need.â Below are key administrative actions CMS will be taking in response to the PHEs declared in Louisiana and Texas.

Waivers and Flexibilities for Hospitals and Other Healthcare Facilities. CMS has already waived many Medicare, Medicaid, and CHIP requirements for facilities buy flagyl no prescription. The CMS Dallas Survey &. Enforcement Division, under the Survey Operations Group, will grant other provider-specific requests for specific types of hospitals and other facilities in Louisiana and Texas. These waivers, once issued, will help provide buy flagyl no prescription continued access to care for beneficiaries.

For more information on the waivers CMS has granted, visit. Www.cms.gov/emergency. Special Enrollment Opportunities for Hurricane Victims. CMS will make available special enrollment periods for certain Medicare beneficiaries and certain individuals seeking health plans buy flagyl no prescription offered through the Federal Health Insurance Exchange. This gives people impacted by the hurricane the opportunity to change their Medicare health and prescription drug plans and gain access to health coverage on the Exchange if eligible for the special enrollment period.

For more information, please visit. Disaster Preparedness Toolkit for buy flagyl no prescription State Medicaid Agencies. CMS developed an inventory of Medicaid and CHIP flexibilities and authorities available to states in the event of a disaster. For more information and to access the toolkit, visit. Https://www.medicaid.gov/state-resource-center/disaster-response-toolkit/index.html.

Dialysis Care. CMS is helping patients obtain access to critical life-saving services. The Kidney Community Emergency Response (KCER) program has been activated and is working with the End Stage Renal Disease (ESRD) Network, Network 13 â Louisiana, and Network 14 - Texas, to assess the status of dialysis facilities in the potentially impacted areas related to generators, alternate water supplies, education and materials for patients and more. The KCER is also assisting patients who evacuated ahead of the storm to receive dialysis services in the location to which they evacuated. Patients have been educated to have an emergency supply kit on hand including important personal, medical and insurance information.

Contact information for their facility, the ESRD Network hotline number, and contact information of those with whom they may stay or for out-of-state contacts in a waterproof bag. They have also been instructed to have supplies on hand to follow a three-day emergency diet. The ESRD Network 8 â Mississippi hotline is 1-800-638-8299, Network 13 â Louisiana hotline is 800-472-7139, the ESRD Network 14 - Texas hotline is 877-886-4435, and the KCER hotline is 866-901-3773. Additional information is available on the KCER website www.kcercoalition.com. During the 2017 and 2018 hurricane seasons, CMS approved special purpose renal dialysis facilities in several states to furnish dialysis on a short-term basis at designated locations to serve ESRD patients under emergency circumstances in which there were limited dialysis resources or access-to-care problems due to the emergency circumstances.

Medical equipment and supplies replacements. Under the COVD-19 waivers, CMS suspended certain requirements necessary for Medicare beneficiaries who have lost or realized damage to their durable medical equipment, prosthetics, orthotics and supplies as a result of the PHE. This will help to make sure that beneficiaries can continue to access the needed medical equipment and supplies they rely on each day. Medicare beneficiaries can contact 1-800-MEDICARE (1-800-633-4227) for assistance. Ensuring Access to Care in Medicare Advantage and Part D.

During a public health emergency, Medicare Advantage Organizations and Part D Plan sponsors must take steps to maintain access to covered benefits for beneficiaries in affected areas. These steps include allowing Part A/B and supplemental Part C plan benefits to be furnished at specified non-contracted facilities and waiving, in full, requirements for gatekeeper referrals where applicable. Emergency Preparedness Requirements. Providers and suppliers are expected to have emergency preparedness programs based on an all-hazards approach. To assist in the understanding of the emergency preparedness requirements, CMS Central Office and the Regional Offices hosted two webinars in 2018 regarding Emergency Preparedness requirements and provider expectations.

One was an all provider training on June 19, 2018 with more than 3,000 provider participants and the other an all-surveyor training on August 8, 2018. Both presentations covered the emergency preparedness final rule which included emergency power supply. 1135 waiver process. Best practices and lessons learned from past disasters. And helpful resources and more.

Both webinars are available at https://qsep.cms.gov/welcome.aspx. CMS also compiled a list of Frequently Asked Questions (FAQs) and useful national emergency preparedness resources to assist state Survey Agencies (SAs), their state, tribal, regional, local emergency management partners and health care providers to develop effective and robust emergency plans and tool kits to assure compliance with the emergency preparedness rules. The tools can be located at. CMS Regional Offices have provided specific emergency preparedness information to Medicare providers and suppliers through meetings, dialogue and presentations. The regional offices also provide regular technical assistance in emergency preparedness to state agencies and staff, who, since November 2017, have been regularly surveying providers and suppliers for compliance with emergency preparedness regulations.

Additional information on the emergency preparedness requirements can be found here. Https://www.cms.gov/Regulations-and-Guidance/Guidance/Manuals/downloads/som107ap_z_emergprep.pdf CMS will continue to work with all geographic areas impacted by Hurricane Laura. We encourage beneficiaries and providers of healthcare services that have been impacted to seek help by visiting CMSâ emergency webpage (www.cms.gov/emergency).