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Comfort and pain management have always been paramount in the child-centered approach to care where to buy cheap cipro at UC cipro joint pain Davis Children’s Hospital. A new hospital initiative called Comfort Commitment launched where to buy cheap cipro this month, which provides a standardized approach to help pediatric patients better cope with distressing procedures and decrease pain and anxiety. Child life specialist Emily McDaniel and nurse Carter Todd discuss comfort planning with a patient.It involves four steps to managing a patient’s comfort:Ask the child and caregiver what they know and understand about the procedureShare more about the procedure in simple terms using honest, age-appropriate languagePlan for the procedure, considering medicine and numbing options, refocusing techniques (toys, electronics, music), comfort positions (chest-to-chest for small children with their caregiver, swaddle for infants and young toddlers) and a calming environment (with lights, noises and words)Follow the agreed-upon plan and ensure the child feels heard and modify comfort measures to meet the patient’s needs“Our ultimate goal is to establish an environment where hospital experiences can be growth-promoting for children and families,” said child life specialist Emily McDaniel. €œThrough individualizing procedural comfort plans with this collaborative four-step process, we are consistently able to provide coping support and empower the child to customize a plan that uniquely meets their specific needs.”The initiative was where to buy cheap cipro funded by a Children's Miracle Network at UC Davis grant. For more information, visit https://ucdavis.health/comfort.A cipro is probably not the best time to refer to someone’s personality as ‘infectious.’ Shalaine Reddic has always believed she could do more than people thought she could.But you don’t have to talk with Shalaine Reddic for long, even on the phone, to feel the positive energy and can-do spirit of this UC Davis Medical Center nurse.Reddic’s desire to help patients blends perfectly with her strong drive to succeed, academic muscle and never-say-die attitude – all wrapped up in what she calls her fashion-forward style.A single mother of three, Reddic has never stopped moving up the career ladder.

She started where to buy cheap cipro out doing clerical work on the Davis campus years ago. Today, Reddic is where to buy cheap cipro on the verge of becoming a licensed nurse practitioner.“I always like to stay busy,” said Reddic.That’s an understatement. She was deftly juggling the phone conversation after a long work week while providing cooking instruction to her 16-year-old son. €œAnd I’ve always believed that I could do more than people thought I could,” she said.When she first started working, the Rancho Cordova where to buy cheap cipro resident didn’t consider the patient side of health care. She didn’t enjoy the thought of seeing blood or being in the clinic environment.

But after becoming a clinical quality improvement coordinator at UC Davis Health, she started working with nurses and quickly gained an appreciation for the profession.Reddic spent nearly 10 years slowly but steadily taking classes and moving from one nursing degree to the next – from an associate of art’s degree at a community college to a bachelor’s degree (cum laude, of course) from Sacramento State – all while working and almost single-handedly raising her children.“I have seen her push through personal issues on numerous occasions,” said Darrell Desmond, nurse manager of Reddic’s where to buy cheap cipro hospital unit. €œBut she just keeps moving forward with an always positive attitude despite where to buy cheap cipro life’s many challenges.”It was while volunteering at a community clinic for underserved women in Sacramento that Reddic had what she calls an epiphany. It was a moment of intense clarity for someone who already had a rewarding nursing career.“I saw nurse practitioners working with patients, diagnosing health problems, prescribing medications,” Reddic said. €œThey were providers where to buy cheap cipro. They had the autonomy to make patient-care decisions.

For me, that was where to buy cheap cipro it. I was in tears because I knew then and there that was what I really wanted to do.”So, Reddic decided to add another academic achievement to her three nursing degrees and an AA degree in business administration. A graduate degree as a family nurse where to buy cheap cipro practitioner.Always on the move, Reddic never stops seeking new goals and achievements.Three years and many commute miles later, she recently completed her master’s from Sonoma State and is now studying for her boards. While working full time, of course.Reddic where to buy cheap cipro admits to being overwhelmed at times over the years. But she said strong faith and prayer helped her put things in perspective when she felt defeated and exhausted.“It’s been a journey and a learning process,” Reddic said.

€œI’ve got a few bruises, but I’m still where to buy cheap cipro here and excited about each day. When I face adversity, I always step it up a notch.”As if it wasn’t enough to become a nurse practitioner, Reddic is considering going back to school for a certificate in psychiatry and, perhaps, a doctorate at some point.She’s also dreaming about plans for starting two independent clinics. One would where to buy cheap cipro be dedicated to serving underprivileged communities. The other where to buy cheap cipro would be an IV hydration bar, a trending intravenous therapy program for wellness, beauty and health.“Shalaine has organized her life for success,” said Joleen Lonigan, an executive director of Patient Care Services at UC Davis Medical Center. €œShe’s turned her motivation into achievements and her pathway into inspiration that can benefit others.”Her story is undoubtedly motivational for anyone who knows Reddic.

Colleagues say her determination is impressive where to buy cheap cipro. Her attitude always stays positive, undoubtedly enhanced by that fashion-forward sensibility that can be seen, despite the required nursing apparel, in some colorful shoe choices and unique earrings. And those academic and clinical accomplishments? where to buy cheap cipro. They’re likely just steppingstones leading toward further personal and professional goals.In short, Shalaine Reddic and the spirit with which she approaches life seem – even in a cipro age – wonderfully contagious..

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Read the latest buy antibiotics information.​​Given the growing number of infectious cases in the community and unlinked cases of community transmission, buy antibiotics restrictions will be tightened across Greater Sydney including the Central Coast, Blue Mountains, Wollongong and Shellharbour.From 5pm today (Friday, 9 July) the following additional restrictions will be in placeOutdoor public gatherings limited to two people (excluding members of the same household)People must stay in their Local Government Area or within 10kms of home for exercise and outdoor recreation, with no carpooling between non-household membersBrowsing in shops is prohibited, plus only one person per household, per day may leave the home for shoppingFunerals limited to ten people in total (this will take effect from Sunday, 11 July).The four reasons to leave your home remain in placeShopping for food or other essential goods and services (one person only)Medical care or compassionate needs (only one visitor can enter another residence to fulfil carers' responsibilities or provide care or assistance, or for cipro side effects long term compassionate reasons)Exercise with no more than 2 (unless members of the same household)Essential work, or education, where you cannot work or study from home.Restrictions in regional NSW will remain unchanged.These tightened restrictions are based on health advice http://junksanfrancisco.com/2013/12/post-from-site-test/ from the Chief Health Officer Dr Kerry Chant.They are necessary due to the increasing number of unlinked cases in the community. We understand this is a difficult time cipro side effects long term for the community and businesses. We thank them for their understanding and patience. High testing numbers are key to finding unrecognised chains of transmission in the community, so please continue to cipro side effects long term come forward for a buy antibiotics test, even if you have the mildest of symptoms. Check the latest buy antibiotics information..

Given the ongoing number of infectious cases in the community, the current lockdown will be extended for at least another two weeks until 11:59pm where to buy cheap cipro on Friday, 30 July. We are constantly reviewing the health advice and will continue to update the community if any where to buy cheap cipro changes are required. This means the restrictions currently in place across Greater Sydney including the Central Coast, Blue Mountains, Wollongong and Shellharbour will remain in place until this time.In these areas, online learning for students will also continue for an additional two weeks.We understand this is a difficult time for the community and appreciate their ongoing patience. It is vital people continue to come forward for testing to help us find any buy antibiotics where to buy cheap cipro cases in the community. Restrictions in regional NSW remain unchanged.

Read the latest buy antibiotics information.​​Given the growing number of infectious cases in the community and unlinked cases of community transmission, buy antibiotics restrictions will be tightened across Greater Sydney including the Central Coast, Blue Mountains, Wollongong and Shellharbour.From 5pm today (Friday, 9 July) the following additional restrictions will be in placeOutdoor public gatherings limited to two people (excluding members of the same where to buy cheap cipro household)People must stay in their Local Government Area or within 10kms of home for exercise and outdoor recreation, with no carpooling between non-household membersBrowsing in shops is prohibited, plus only one person per household, per day may leave the home for shoppingFunerals limited to ten people in total (this will take effect from Sunday, 11 July).The four reasons to leave your home remain in placeShopping for food or other essential goods and services (one person only)Medical care or compassionate needs (only one visitor can enter another residence to fulfil carers' responsibilities or provide care or assistance, or for compassionate reasons)Exercise with no more than 2 (unless members of the same household)Essential work, or education, where you cannot work or study from home.Restrictions in regional NSW will remain unchanged.These tightened restrictions are based on health advice from the Chief Health Officer Dr Kerry Chant.They are necessary due to the increasing number of unlinked cases in the community. We understand this is a where to buy cheap cipro difficult time for the community and businesses. We thank them for their understanding and patience. High testing numbers are key to finding unrecognised chains of transmission in where to buy cheap cipro the community, so please continue to come forward for a buy antibiotics test, even if you have the mildest of symptoms. Check the latest buy antibiotics information..

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Start Preamble Office of the Assistant Secretary for Health, Office of how can i buy cipro the Secretary, Department of Health and Human Services cipro and yeast . Notice of a virtual meeting. As stipulated by the cipro and yeast Federal Advisory Committee Act, the U.S.

Department of Health and Human Service is hereby giving notice that the Presidential Advisory Council on HIV/AIDS (PACHA or the Council) will be holding the 71st full Council meeting utilizing virtual technology on Tuesday, August 3-Wednesday, August 4, 2021 from 1:00-5:00 p.m. (ET) on both cipro and yeast days. The meeting will be open to the public.

A public comment session will be held during the meeting. Pre-registration is required to provide cipro and yeast public comment during the meeting. To pre-register to attend or to provide public comment, please send an email to PACHA@hhs.gov and include your name, organization, and title by close of business Monday, July 26, 2021.

If you decide you would like to provide cipro and yeast public comment but do not pre-register, you may submit your written statement by emailing PACHA@hhs.gov by close of business Wednesday, August 11, 2021. The meeting agenda will be posted on the PACHA page on HIV.gov at https://www.hiv.gov/​federal-response/​pacha/​about-pacha prior to the meeting. The meeting will be held on Tuesday, August 3-Wednesday, August 4, 2021 from 1:00-5:00 p.m.

(ET) on both cipro and yeast days. This meeting will be conducted utilizing virtual technology. Instructions on attending this meeting virtually will be posted one week prior to cipro and yeast the meeting at.

Https://www.hiv.gov/​federal-response/​pacha/​about-pacha. Start Further Info Ms. Caroline Talev, MPA, Public Health Analyst, Presidential Advisory Council on cipro and yeast HIV/AIDS, 330 C Street SW, Room L609A, Washington, DC 20024.

(202) 795-7622 or PACHA@hhs.gov. Additional information cipro and yeast can be obtained by accessing the Council's page on the HIV.gov site at www.hiv.gov/​pacha. End Further Info End Preamble Start Supplemental Information PACHA was established by Executive Order 12963, dated June 14, 1995, as amended by Executive Order 13009, dated June 14, 1996 and is currently operating under the authority given in Executive Order 13889, dated September 27, 2019.

The Council was established to provide advice, information, and recommendations to the Secretary regarding programs and policies intended to promote effective prevention and care of HIV and AIDS. The functions of the Council are solely advisory in nature cipro and yeast . The Council consists of not more than 25 members.

Council members are selected from prominent community leaders with particular expertise in, or knowledge of, matters concerning HIV and AIDS, public health, global health, philanthropy, marketing or business, cipro and yeast as well as other national leaders held in high esteem from other sectors of society. Council members are appointed by the Secretary or designee, in consultation with the White House. Start Signature cipro and yeast Dated.

June 9, 2021. Caroline Talev, Management Analyst, Office of Infectious Disease and HIV/AIDS Policy, Alternate Designated Federal Officer, Presidential Advisory Council on HIV/AIDS, Office of the Assistant Secretary for Health, Department of Health and Human Services. End Signature End Supplemental cipro and yeast Information [FR Doc.

2021-14496 Filed 7-7-21. 8:45 am]BILLING CODE cipro and yeast 4150-43-PFull-page version of the map. Rural counties added jobs at about the same pace as the rest of the nation in May, but a Daily Yonder analysis of Bureau of Labor Statistics data shows that the size of the rural workforce has yet to rebound from the cipro.

Rural counties added 1.3 million jobs from May 2020 to May 2021. In May, rural employment was 2.2% lower than it was in May 2019, long before the start of the buy antibiotics cipro and yeast cipro. After adding about 13 million jobs from May 2020 to May 2021, metropolitan counties also had 2.2% fewer employees than they did in May 2019, before the start of the cipro.

(Our analysis uses data from May 2021, which BLS released last week cipro and yeast . To factor out seasonal variation in employment, we are comparing May data to the same month in 2020 and 2019.) Where rural and metropolitan counties differ is in how the size of the workforce responded to the cipro. Workforce includes all the people on the labor market – both people who have a job and those who don’t have a job but are seeking one.

The metropolitan labor cipro and yeast market shrank more than the nonmetropolitan labor market in the first months of the cipro. But the metropolitan labor market has bounced back more than the nonmetropolitan labor market this year. Labor force cipro and yeast includes people who have a job and people who are unemployed but looking for work.

(Daily Yonder graphic based on Bureau of Labor Statistics data) Like this story?. Sign up for cipro and yeast our newsletter. In metropolitan counties, the size of the labor force bounced back from May 2020 to May 2021 and is now only 0.9% lower than it was in May 2019, before the cipro.

In rural counties, however, the size of the labor force took a similar nosedive in May 2020 but barely grew in the subsequent year. The May cipro and yeast 2021 rural labor force was down 2.1% compared to the pre-cipro level. That’s more than twice the rate of decline in the metropolitan labor force.

Here is the total labor market for cipro and yeast rural counties for May of the last three years. May 2019. 21.2 million.May 2020.

20.7 million (down 482,000 from cipro and yeast 2019).May 2021. 20.8 million (down 454,000 from 2019). The good part of a smaller labor force is that it generally means a lower cipro and yeast unemployment rate because fewer people are seeking work.

The bad part is that it means a smaller labor market for potential employers, and it may signal the continuation of longer-term declines in the rural economy and consequently the size of the rural population. Regional Variance in Employment National figures disguise significant regional differences. The map cipro and yeast above reports how close each county was in May of this year to having the same number of jobs as in May of 2019, before anyone had heard of buy antibiotics.

(The darker the color on the map, the higher the percentage of jobs today compared to May 2019. To get your local cipro and yeast data, click on the map and then scroll over your county.) You can see that there are dozens of rural Texas counties that are well below the national average in job recovery. We suspect that is because of the falloff in oil and gas exploration and production.

Look at western North Dakota, where there was a boom in shale development until the onset of the cipro. The center of that activity was Williams County. This May, Williams had only 80% of the jobs that were there two years earlier.

The Mountain West and the Deep South are getting back to their 2019 numbers. The East Coast and the Midwest, however, are lagging. You Might Also Like.

Start Preamble Office of the cipro antibiotic price Assistant Secretary for Health, Office of the Secretary, Department where to buy cheap cipro of Health and Human Services. Notice of a virtual meeting. As stipulated by the Federal Advisory Committee Act, where to buy cheap cipro the U.S.

Department of Health and Human Service is hereby giving notice that the Presidential Advisory Council on HIV/AIDS (PACHA or the Council) will be holding the 71st full Council meeting utilizing virtual technology on Tuesday, August 3-Wednesday, August 4, 2021 from 1:00-5:00 p.m. (ET) on both where to buy cheap cipro days. The meeting will be open to the public.

A public comment session will be held during the meeting. Pre-registration is required to provide where to buy cheap cipro public comment during the meeting. To pre-register to attend or to provide public comment, please send an email to PACHA@hhs.gov and include your name, organization, and title by close of business Monday, July 26, 2021.

If you decide you would like to provide public comment but do not pre-register, you may submit your written statement by emailing PACHA@hhs.gov by close of business Wednesday, August where to buy cheap cipro 11, 2021. The meeting agenda will be posted on the PACHA page on HIV.gov at https://www.hiv.gov/​federal-response/​pacha/​about-pacha prior to the meeting. The meeting will be held on Tuesday, August 3-Wednesday, August 4, 2021 from 1:00-5:00 p.m.

(ET) on where to buy cheap cipro both days. This meeting will be conducted utilizing virtual technology. Instructions on attending this meeting virtually will be posted one where to buy cheap cipro week prior to the meeting at.

Https://www.hiv.gov/​federal-response/​pacha/​about-pacha. Start Further Info Ms. Caroline Talev, MPA, Public Health Analyst, Presidential Advisory Council where to buy cheap cipro on HIV/AIDS, 330 C Street SW, Room L609A, Washington, DC 20024.

(202) 795-7622 or PACHA@hhs.gov. Additional information can be obtained by accessing where to buy cheap cipro the Council's page on the HIV.gov site at www.hiv.gov/​pacha. End Further Info End Preamble Start Supplemental Information PACHA was established by Executive Order 12963, dated June 14, 1995, as amended by Executive Order 13009, dated June 14, 1996 and is currently operating under the authority given in Executive Order 13889, dated September 27, 2019.

The Council was established to provide advice, information, and recommendations to the Secretary regarding programs and policies intended to promote effective prevention and care of HIV and AIDS. The functions of where to buy cheap cipro the Council are solely advisory in nature. The Council consists of not more than 25 members.

Council members are selected from prominent community leaders with particular expertise in, or knowledge of, matters concerning HIV and AIDS, public health, global health, philanthropy, marketing or business, as well as other where to buy cheap cipro national leaders held in high esteem from other sectors of society. Council members are appointed by the Secretary or designee, in consultation with the White House. Start Signature where to buy cheap cipro Dated.

June 9, 2021. Caroline Talev, Management Analyst, Office of Infectious Disease and HIV/AIDS Policy, Alternate Designated Federal Officer, Presidential Advisory Council on HIV/AIDS, Office of the Assistant Secretary for Health, Department of Health and Human Services. End Signature End where to buy cheap cipro Supplemental Information [FR Doc.

2021-14496 Filed 7-7-21. 8:45 am]BILLING CODE where to buy cheap cipro 4150-43-PFull-page version of the map. Rural counties added jobs at about the same pace as the rest of the nation in May, but a Daily Yonder analysis of Bureau of Labor Statistics data shows that the size of the rural workforce has yet to rebound from the cipro.

Rural counties cipro online canada added 1.3 million jobs from May 2020 to May 2021. In May, rural employment was 2.2% lower where to buy cheap cipro than it was in May 2019, long before the start of the buy antibiotics cipro. After adding about 13 million jobs from May 2020 to May 2021, metropolitan counties also had 2.2% fewer employees than they did in May 2019, before the start of the cipro.

(Our analysis where to buy cheap cipro uses data from May 2021, which BLS released last week. To factor out seasonal variation in employment, we are comparing May data to the same month in 2020 and 2019.) Where rural and metropolitan counties differ is in how the size of the workforce responded to the cipro. Workforce includes all the people on the labor market – both people who have a job and those who don’t have a job but are seeking one.

The metropolitan labor market shrank more than where to buy cheap cipro the nonmetropolitan labor market in the first months of the cipro. But the metropolitan labor market has bounced back more than the nonmetropolitan labor market this year. Labor force includes people who have a job where to buy cheap cipro and people who are unemployed but looking for work.

(Daily Yonder graphic based on Bureau of Labor Statistics data) Like this story?. Sign up for our newsletter where to buy cheap cipro. In metropolitan counties, the size of the labor force bounced back from May 2020 to May 2021 and is now only 0.9% lower than it was in May 2019, before the cipro.

In rural counties, however, the size of the labor force took a similar nosedive in May 2020 but barely grew in the subsequent year. The May 2021 rural labor where to buy cheap cipro force was down 2.1% compared to the pre-cipro level. That’s more than twice the rate of decline in the metropolitan labor force.

Here is the total labor market for rural counties for May of the where to buy cheap cipro last three years. May 2019. 21.2 million.May 2020.

20.7 million (down 482,000 from 2019).May where to buy cheap cipro 2021. 20.8 million (down 454,000 from 2019). The good part of a smaller labor force is that it generally means a lower unemployment rate because fewer people are where to buy cheap cipro seeking work.

The bad part is that it means a smaller labor market for potential employers, and it may signal the continuation of longer-term declines in the rural economy and consequently the size of the rural population. Regional Variance in Employment National figures disguise significant regional differences. The map above reports how close each county was in May of this year to having the same number of jobs as in where to buy cheap cipro May of 2019, before anyone had heard of buy antibiotics.

(The darker the color on the map, the higher the percentage of jobs today compared to May 2019. To get your local data, click on the map and then scroll over your county.) You can see where to buy cheap cipro that there are dozens of rural Texas counties that are well below the national average in job recovery. We suspect that is because of the falloff in oil and gas exploration and production.

Look at western North Dakota, where there was a boom in shale development until the onset of the cipro. The center of that activity was where to buy cheap cipro Williams County. This May, Williams had only 80% of the jobs that were there two years earlier.

The Mountain West and where to buy cheap cipro the Deep South are getting back to their 2019 numbers. The East Coast and the Midwest, however, are lagging. You Might Also Like.

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Quick! navigate to this website ramas de cipres. Everybody into the conference room. Today, we’re going to ramas de cipres discuss what science has to say about some of the most memorable scenes from the enduring hit TV series, The Office.The Office ended in 2013, but the show continues to delight old fans and attract new ones on streaming services.

The success of the Office Ladies podcast, hosted by Jenna Fischer (Pam) and Angela Kinsey (Angela), further affirms the show’s abiding popularity. It’s apparent that people won’t stop appreciating the endearing employees at the Dunder Mifflin Paper Company anytime soon.The outlandish scenes still make for ramas de cipres interesting water cooler banter, and you might be wondering if there’s any truth to them. Let’s take a coffee break and have an educational look at five classic moments from the show.Angela’s Beet Juice CleanseIn S6:E23, Dwight and Angela meet with a lawyer to discuss their childbearing contract.

Item five, point “B” states that Angela must complete a “beet juice cleanse.” When Dwight asks for a stool sample to verify she is doing the cleanse, Angela flashes her ramas de cipres red-stained teeth as proof instead.Juice cleansing is a controversial dietary trend. During the cleanse period, which is performed for 3–10 days to reportedly detox and lose weight, participants usually consume nothing but juices extracted from fruits and vegetables. Beets are a root vegetable and a good source of some ramas de cipres nutrients such as folate, magnesium and vitamin C.

Betalain pigments, which give beets the deep red color that stained Angela’s teeth, are antioxidants that also have anti-inflammatory effects. Additionally, beets contain nitrates that widen blood vessels, which can reduce blood pressure and increase blood flow to the brain. One drawback to juicing is the loss of fiber, a key nutrient ramas de cipres in this vegetable.Due to the sharp drop in caloric intake, people on a juice cleanse often lose a little weight.

Unfortunately, it is typically gained back as soon as a normal diet resumes. Additionally, many juicers are likely to experience low blood sugar and ramas de cipres depleted energy levels. Restricting the juice diet to a single fruit or vegetable will also deprive the individual of other vital nutrients, including protein.On occasion, especially in people with pre-existing conditions, juicing can lead to excess oxalate in the body, causing acute kidney stones or damage.

Given the deprivation of calories, the limited nutrients and the potential adverse effects, a juice cleanse would not be advisable during pregnancy or while trying to conceive.Incidentally, Dwight ramas de cipres was not entirely off-base for requesting a stool sample to verify Angela’s compliance with the beet cleanse. In some people, the betalains can cause stools to darken and urine to redden (a side effect known as beeturia).Dwight’s “Hygiene Hypothesis”In S7:E7, Pam leads a discussion about how to minimize germs from being spread around the office. In response to hand sanitizers being set up in the workplace, Dwight protests, “The ramas de cipres worst thing you can do for your immune system is to coddle it.

€¦ If Sabre really cared about our well-being, they would set up hand desanitizing stations. A simple bowl at every juncture filled with dirt, vomit, fecal matter.”Dwight appears to be ramas de cipres referring to the so-called “hygiene hypothesis,” which suggests that our modern germaphobic tendencies are detrimental to our immune system. The idea is particularly applicable during childhood when the immune system is in its earliest stages of development.

Failing to appropriately train the immune system during this critical period may cause it to malfunction. Without germs to fight, some think that the immune system might resort to attacking harmless things or the body, leading to allergies and autoimmune disorders, respectively.Supporting the idea are studies that have ramas de cipres correlated the presence of microbes during childhood with decreased allergies. For example, some studies report a reduced incidence of hay fever in people who grew up on a farm as opposed to in a city.

In some studies, this effect ramas de cipres can be linked to animal exposure. Even in a city environment, pets, particularly dogs, can have a protective effect from the development of allergies.It is doubtful that the hygiene hypothesis applies in adults, as the developmental window on the immune system has largely closed after 3 – 4 years of age. So, Dwight’s ramas de cipres idea to dirty up the office is not only gross, but also scientifically unsound.

Furthermore, the hygiene hypothesis is far from proven, and many confounding variables such as genes, diet and the prevalence of antibiotics and pollutants likely conspire to shape a person’s immune system.Since it was first proposed in 1989, the hygiene hypothesis has been controversial. Some scientists have ramas de cipres argued that use of the word hygiene is an unfortunate misnomer that discourages people from being sanitary. Returning to an era of filth would only increase rates and detract from finding the real explanation behind the rise of asthma and allergy in developed societies.

A more recent version of the idea known as the “old friends” hypothesis distinguishes between good and bad microbes. It asserts that we should certainly protect ourselves ramas de cipres and children from dangerous pathogens, such as those lurking in fecal matter, vomit or unclean food, but not be overly concerned about beneficial or harmless microbes that are routinely encountered. These are already present in and around our bodies and may be important for appropriately training the immune system.Rabies Awareness Fun RunIn S4:E1, Michael hits Meredith with his car, sending her to the hospital with a cracked pelvis.

At the hospital, Meredith reveals she was also recently bitten by a bat, ramas de cipres racoon and rat, on separate occasions. This prompts the doctors to begin treatment for rabies. And it inspires Michael to organize the "Michael Scott's Dunder Mifflin Scranton Meredith Palmer ramas de cipres Memorial Celebrity Rabies Awareness Pro-Am Fun Run Race for the Cure."But how big of a threat is rabies in reality?.

Rabies is common enough in wildlife, but is rarely seen these days in domesticated animals and people living in developed nations. From 2009 to 2018, only 25 cases of human ramas de cipres rabies were reported in the U.S.. That’s just one to three cases per year.

Any mammal can be infected with rabies, but it is most frequently transmitted to humans by raccoons, skunks, bats and foxes.Rabies is a bullet-shaped cipro that slowly creeps through the nerves until it finds the brain, where it causes a terrifying transformation that blurs the line between ramas de cipres human and beast. Rabid animals foam at the mouth and become ferociously aggressive. The sickness can turn a lamb into a lion.

Also, as Michael Scott points out, people suffering from rabies develop an intense aversion to water known as hydrophobia.The rabies cipro concentrates ramas de cipres in saliva and can be transmitted through biting. You might think that a cipro capable of such wizardry would be highly complex, but it contains only five genes. One of ramas de cipres these genes makes a protein that appears to interfere with communication between cells in the brain, which likely contributes to the behavioral changes caused by rabies.

Fun fact. The hangover remedy known as “hair of the dog” has its origins in a supposed rabies treatment devised by the ramas de cipres Roman naturalist Pliny the Elder. Pliny suggested rabies victims should “insert in the wound ashes of hairs from the tail of the dog that inflicted the bite.” Don’t try this.

It does not work.As for Michael’s efforts, his Rabies Fun Run would have been more relevant prior to ramas de cipres the 1880s, before Louis Pasteur developed the first rabies treatment. Or, in other parts of the world that face more cases of rabies. Globally, rabies kills nearly 60,000 people each year, largely due to lack of resources and access to medical care.Lice Bug BombPediculus humanus capitis was the featured guest on S9:E10, causing an infestation across cubicles at 1725 Slough Avenue.

While everyone assumed the head lice came from ramas de cipres Meredith, the source was actually Pam, who contracted them from her daughter Cece.Lice are tiny insect parasites that take up residence on the scalp. These so-called skull vampires suck blood for nourishment and glue their eggs (nits) tightly to the hair. The insects can’t jump or fly, but can be passed between people who share hairbrushes, clips, ramas de cipres bedding, towels, clothing or hats.

The most common source of transmission is through direct contact with an infested person’s hair. While head lice are an annoyance, they do not carry any known disease.Our friends on The Office put their heads together (not literally, thankfully) ramas de cipres and offered several different solutions. Following Erin's advice, infected co-workers applied generous globs of mayonnaise to each other's hair to try to suffocate the lice.

Meredith took a more radical approach ramas de cipres and shaved her head. True to form, Dwight overreacts and attempts to rid the office of lice with a bug bomb grenade. Naturally, it explodes before he leaves the room, ramas de cipres and the toxic fumes cause him to hallucinate and faint.Of all the solutions attempted, Meredith’s is most certain to work.

Depriving the lice of hair deprives them of a place to lay eggs, and the adults are easily washed away. But many people are not willing to sacrifice their locks. While it’s a popular home remedy, Erin’s idea to suffocate the lice with mayonnaise (petroleum jelly is also common) rarely works, according to (the aptly named) ramas de cipres Mayo Clinic.

And, as this episode illustrates, bug bombs are far more trouble than they are worth. Lice cannot survive without a host for more than a day, so there is no ramas de cipres need to fumigate and risk exposure to dangerous chemicals. More than 3,200 cases of bug bomb-related illnesses, including four human deaths, were reported in the U.S.

Between 2007 and 2015.One effective way to treat lice is to use a shampoo containing an ramas de cipres insecticide like permethrin. Permethrin is an insect neurotoxin that causes paralysis in the louse by disrupting sodium transport across its cellular membranes. Nit combs can ramas de cipres be used in conjunction with the shampoo treatment to physically remove eggs unaffected by the insecticide.

Multiple treatments are advised to ensure all of the lice have been eradicated.Kevin’s Stinky FeetJim and Pam’s wedding in S6:E4 was filled with unforgettable moments, including the revelation that Kevin has a serious foot odor issue. Kevin left his shoes outside his hotel door to be cleaned, only to find that they had disappeared during the night. The hotel ramas de cipres manager told him.

€œMr. Malone, your ramas de cipres shoes are gone. €¦ When the bag was opened by our shoeshine, the smell overcame him.

I, too, smelled them and http://www.ec-schluthfeld-strasbourg.ac-strasbourg.fr/wp/?p=2305 made ramas de cipres the choice that they must be thrown away. Incinerated, actually.”Scientists have sniffed out the cause of bromodosis (foot odor), and it can be traced to a bacterium called Brevibacterium linens. Our bodies are home to trillions of bacteria, likely more than 10,000 different species, ramas de cipres that live on or inside us.

B. Linens are harmless denizens of our skin, where they ramas de cipres consume dead cells. As they digest the dead skin cells, they release smelly sulfur-containing compounds called S-methyl thioesters as waste products.Sweaty feet create a moist and salty environment that allows this species of bacteria to thrive, generating pungent odors as they excrete more and more S-methyl thioesters.

Incidentally, these are the same bacteria used to produce the rind of smelly cheeses like Limburger.Kevin could have reduced his foot odor by depriving the bacteria of the sweat they need to grow. He could have achieved this by wearing open-toed shoes whenever possible, using powder or carrying an extra pair of dry, ramas de cipres fresh socks. There may also be additional hope on the horizon for folks like Kevin, cursed with industrial strength foot odor.

Scientists recently found that socks coated in zinc oxide nanoparticles, which have potent antibacterial activity, are effective at preventing foot odor.Armed with that knowledge, you can ramas de cipres now comfortably prop up your feet and marathon through all nine seasons of The Office. Or, at least track down these standout episodes — with an eye toward science.For some people, the idea of going to the store without a mask right now is so shocking, they’re having stress dreams about it. But once the need to wear a face-covering every time we go shopping is over, our instinct to ramas de cipres reach for our masks might not disappear entirely in the U.S.

Living through the worst epidemic Americans have seen in a century might shift attitudes about long-term mask use, in part because what many people experienced during the cipro is uniquely traumatic, says Isaac Fung, an epidemiologist at Georgia Southern University. €œIt’s probably a once-in-a-lifetime experience, even though there have been, and will be, antibioticses that create an epidemic.” Who changes behaviors and how frequently they reach for their face coverings, however, could ramas de cipres depend on a few factors.Lasting Effects of TraumaPart of why it’s possible that masks could become a more long-term fixture in the U.S. Is because elsewhere in the world, previous cipros had the same effect.

In 2003, the SARS outbreaks in parts of Asia, including China, Taiwan and South Korea, required mask-wearing. The shock of the SARS outbreaks and a cultural memory of what helped control them could partially ramas de cipres explain why the transition to consistent mask use in some of these nations during buy antibiotics was seamless compared to the U.S., Fung says. €œThey have both the fortunate and misfortune of the impact of SARS in 2003.” In between the cipros, consistent mask-wearing in parts of Asia evolved into an occasional polite choice someone might make if they had a cold or cough and were out in public.

Masks, along with other buy antibiotics protocols like hand ramas de cipres washing and social distancing, can reduce the odds of someone spreading other illnesses like the seasonal flu. In the U.S., a similar scenario — a population scarred by a cipro comes to realize how useful the masks are for other illnesses — might play out. Granted, mask use has become political in the ramas de cipres U.S.

In a way it hasn’t in many other places, Fung points out. But throughout the cipro, Pew Research Center surveys have shown that the partisan divide on masking behaviors lessened over time.Christos Lynteris, a social anthropologist at the University of St Andrews in Scotland, thinks ramas de cipres future consistent mask use might stand a chance in part because the cipro won’t end with one theatrical, celebratory announcement. If the health crisis was suddenly “over” one day, some people might reject masks completely from there on out.

€œThrowing your mask away [could be] like ramas de cipres you're unshackling yourself from the epidemic, which is over,” Lynteris says. But it’s more likely the cipro could see seasonal resurgences like the flu and draw out for a while. In that case, the longer battle with antibiotics could help individuals see masks as a more consistent part of life that comes with other health benefits.

Too Close for ComfortThe realization of the perpetual benefits of masks might take hold in cities best, particularly ramas de cipres if many residents rely on public transit, Fung says. When people don’t own cars and need to get around via packed buses or train cars, they spend a lot more time in close contact with other people. It’s hard to be in ramas de cipres that environment daily and not see the value of a face covering, Fung says.

In large swathes of the U.S. Where people commute in their own cars or rely on relatively-empty public transportation, the appeal of wearing masks ramas de cipres might not be as strong.Future mask use could also depend on how well people transform the face-covering into an effective but appealing — maybe even fashionable — accessory. If public health departments had wanted to make mask-wearing a more consistent part of long-term healthy behaviors, the institutions could have been more intentional about encouraging this transition, Lynteris says.

€œYou need to allow people ramas de cipres to adopt the mask as their own thing,” he says. Meeting with different communities and encouraging people to make masks look the way they want them to could make them more appealing. In parts of Asia, people pulled off this exact transition with masks over the years.

People sell and purchase masks that coordinate with outfits, and when it is part of the wardrobe, ramas de cipres the face-covering becomes even more likely to be worn, Fung says. If covering faces in public persists for years to come, the well-meaning action would be more likely to be effective if people had a better idea of how to handle the masks. In fact, this is ramas de cipres a part of mask education that Fung thinks could be improved right now during the cipro.

€œThis part of health education I do not see happening in the U.S.,” he says. €œWe are only focusing on wearing it, not how to properly take it off or wash it.” Handling masks correctly ramas de cipres can reduce the likelihood that any cipro on the material doesn’t make its way into your nose or mouth. And while the CDC has guidelines on appropriate behavior, simply having online information available for those who search for it isn’t quite enough, Lynteris notes.

Appropriate mask protocols are another ramas de cipres topic public health officials should discuss with communities. A chance to ask questions — about when masks should be cleaned or how to dispose of them, for example — or even hear from others about the mistakes they’ve made can familiarize people with what they need to do themselves. €œIf you don’t use the mask correctly but think it's protecting you, you may be engaging in behavior where you put yourself and others at risk,” ramas de cipres Lynteris says.

€œIt’s an important conversation we’re not having.”Alcohol consumption in the U.S. Surged in 2020. Booze delivery services gained popularity while market reports relayed information about higher sales ramas de cipres volumes.

Even academic surveys found people were drinking more — one sample representing roughly 1,500 American adults found that on average, three of every four individuals were pouring themselves a drink an extra day every month.Of course, having a beer one extra day of the month doesn’t necessarily mean someone is drinking too much. But when it comes ramas de cipres to self-assessing booze habits, people tend to define the problem in a way that somehow leaves their own habits in good standing, says Patricia E. Molina, the director of the Alcohol and Drug Abuse Center of Excellence at LSU Health Sciences Center New Orleans.

€œWhat the lay public tends to do is pay attention or focus on one aspect that is convenient ramas de cipres for their definition." Beyond Binge DrinkingTypically, people use the term binge drinking as a benchmark of whether or not they’ve had one too many. The term refers to booze consumption that brings someone’s blood alcohol content (BAC) to .08g/dl or above — the legal limit for driving in the U.S. Most men reach that value ramas de cipres after having five drinks in two hours, while women typically reach it after having four drinks in the same time span.

Binge drinking is the most common and deadly form of excessive drinking in the U.S., according to the CDC, as it’s associated with a wide range of health consequences. Some stem from the impact alcohol has on the body, such as alcohol poisoning, while others are due to the way alcohol disrupts our ability to function, like injuries from car accidents. But even ramas de cipres when people haven't reached excessive BAC levels, it doesn’t exempt them, or others, from harm.

€œOne could make the argument that, okay, if I don't drink that much in two hours, but over a longer period of time, is that okay?. € Molina ramas de cipres says. €œWell, not completely.” Besides binge drinking, the CDC also labels heavy drinking as a risky, harmful behavior, and is a concept Molina thinks should be a larger part of alcohol education campaigns.

Classified as eight or more drinks a week for women and 15 or more a week for men, ramas de cipres heavy drinking is less likely to cause short-term issues, like car accidents. But over time, the habit can lead to a range of cancers, liver disease and heart problems, as well as depression and anxiety. So while someone might be able to drive their car after tailgating all Saturday, they may still have put away several drinks over the entire afternoon, Molina says, pushing the limit of what qualifies as a week of heavy drinking ramas de cipres.

Ultimately, the fewer drinks someone has, the better. To keep the health consequences of alcohol low, the official USDA dietary guidelines for 2020 to 2025 cap moderate drinking at two drinks a day for men ramas de cipres and one drink a day for women. However, the scientific advisory group that helps craft these guidelines has recommended that the cap be one drink a day for everyone.

No Sense of StandardEven if someone was keeping track of their beer habit and trying to stick to these quantities, a lot of people don’t know or can’t estimate what qualifies as a single drink, Molina says. In the U.S., a standard drink contains 14 grams of alcohol. Since different kinds of drinks have a range of alcohol content, that serving size pans out to be 12 ounces of a 5 percent alcohol beer, five ounces of wine and one and a half ounces of liquor.

These volumes don’t always match what someone might perceive as a single serving, like an oversized can of beer or a restaurant pour of wine, which is often closer to eight ounces, Molina says. Studies have shown that people tend to overestimate what qualifies as a standard drink anyways, and when asked to pour out a single serving, are too generous. If people drink more than they think they do, then their threshold for what it takes to feel buzzed is likely higher than they thought, too.

How people develop alcohol tolerance — where a given number of drinks has less of an effect on their ability to function over time — isn’t well understood by researchers, though there are likely genetic and social influences at work. But increasing tolerance is often associated with alcohol use disorder or alcohol dependence. The more someone drinks, Molina says, the more they need to achieve the relaxation or buzz they’re seeking through alcohol.

At the same time, “you increase the risk of falling into a pattern of drinking to avoid negative feelings,” she says.For anyone curious about the best ways to recalibrate their drinking patterns, Molina recommends Rethinking Drinking, a National Institute of Health resource that spells out serving sizes, how those compare to what standard drink containers hold, and what different drinking habits look like..

Quick!. Everybody into the conference room. Today, we’re going to discuss what science has to say about some of the most memorable scenes from the enduring hit TV series, The Office.The Office ended in 2013, but the show continues to delight old fans and attract new ones on streaming services. The success of the Office Ladies podcast, hosted by Jenna Fischer (Pam) and Angela Kinsey (Angela), further affirms the show’s abiding popularity.

It’s apparent that people won’t stop appreciating the endearing employees at the Dunder Mifflin Paper Company anytime soon.The outlandish scenes still make for interesting water cooler banter, and you might be wondering if there’s any truth to them. Let’s take a coffee break and have an educational look at five classic moments from the show.Angela’s Beet Juice CleanseIn S6:E23, Dwight and Angela meet with a lawyer to discuss their childbearing contract. Item five, point “B” states that Angela must complete a “beet juice cleanse.” When Dwight asks for a stool sample to verify she is doing the cleanse, Angela flashes her red-stained teeth as proof instead.Juice cleansing is a controversial dietary trend. During the cleanse period, which is performed for 3–10 days to reportedly detox and lose weight, participants usually consume nothing but juices extracted from fruits and vegetables.

Beets are a root vegetable and a good source of some nutrients such as folate, magnesium and vitamin C. Betalain pigments, which give beets the deep red color that stained Angela’s teeth, are antioxidants that also have anti-inflammatory effects. Additionally, beets contain nitrates that widen blood vessels, which can reduce blood pressure and increase blood flow to the brain. One drawback to juicing is the loss of fiber, a key nutrient in this vegetable.Due to the sharp drop in caloric intake, people on a juice cleanse often lose a little weight.

Unfortunately, it is typically gained back as soon as a normal diet resumes. Additionally, many juicers are likely to experience low blood sugar and depleted energy levels. Restricting the juice diet to a single fruit or vegetable will also deprive the individual of other vital nutrients, including protein.On occasion, especially in people with pre-existing conditions, juicing can lead to excess oxalate in the body, causing acute kidney stones or damage. Given the deprivation of calories, the limited nutrients and the potential adverse effects, a juice cleanse would not be advisable during pregnancy or while trying to conceive.Incidentally, Dwight was not entirely off-base for requesting a stool sample to verify Angela’s compliance with the beet cleanse.

In some people, the betalains can cause stools to darken and urine to redden (a side effect known as beeturia).Dwight’s “Hygiene Hypothesis”In S7:E7, Pam leads a discussion about how to minimize germs from being spread around the office. In response to hand sanitizers being set up in the workplace, Dwight protests, “The worst thing you can do for your immune system is to coddle it. €¦ If Sabre really cared about our well-being, they would set up hand desanitizing stations. A simple bowl at every juncture filled with dirt, vomit, fecal matter.”Dwight appears to be referring to the so-called “hygiene hypothesis,” which suggests that our modern germaphobic tendencies are detrimental to our immune system.

The idea is particularly applicable during childhood when the immune system is in its earliest stages of development. Failing to appropriately train the immune system during this critical period may cause it to malfunction. Without germs to fight, some think that the immune system might resort to attacking harmless things or the body, leading to allergies and autoimmune disorders, respectively.Supporting the idea are studies that have correlated the presence of microbes during childhood with decreased allergies. For example, some studies report a reduced incidence of hay fever in people who grew up on a farm as opposed to in a city.

In some studies, this effect can be linked to animal exposure. Even in a city environment, pets, particularly dogs, can have a protective effect from the development of allergies.It is doubtful that the hygiene hypothesis applies in adults, as the developmental window on the immune system has largely closed after 3 – 4 years of age. So, Dwight’s idea to dirty up the office is not only gross, but also scientifically unsound. Furthermore, the hygiene hypothesis is far from proven, and many confounding variables such as genes, diet and the prevalence of antibiotics and pollutants likely conspire to shape a person’s immune system.Since it was first proposed in 1989, the hygiene hypothesis has been controversial.

Some scientists have argued that use of the word hygiene is an unfortunate misnomer that discourages people from being sanitary. Returning to an era of filth would only increase rates and detract from finding the real explanation behind the rise of asthma and allergy in developed societies. A more recent version of the idea known as the “old friends” hypothesis distinguishes between good and bad microbes. It asserts that we should certainly protect ourselves and children from dangerous pathogens, such as those lurking in fecal matter, vomit or unclean food, but not be overly concerned about beneficial or harmless microbes that are routinely encountered.

These are already present in and around our bodies and may be important for appropriately training the immune system.Rabies Awareness Fun RunIn S4:E1, Michael hits Meredith with his car, sending her to the hospital with a cracked pelvis. At the hospital, Meredith reveals she was also recently bitten by a bat, racoon and rat, on separate occasions. This prompts the doctors to begin treatment for rabies. And it inspires Michael to organize the "Michael Scott's Dunder Mifflin Scranton Meredith Palmer Memorial Celebrity Rabies Awareness Pro-Am Fun Run Race for the Cure."But how big of a threat is rabies in reality?.

Rabies is common enough in wildlife, but is rarely seen these days in domesticated animals and people living in developed nations. From 2009 to 2018, only 25 cases of human rabies were reported in the U.S.. That’s just one to three cases per year. Any mammal can be infected with rabies, but it is most frequently transmitted to humans by raccoons, skunks, bats and foxes.Rabies is a bullet-shaped cipro that slowly creeps through the nerves until it finds the brain, where it causes a terrifying transformation that blurs the line between human and beast.

Rabid animals foam at the mouth and become ferociously aggressive. The sickness can turn a lamb into a lion. Also, as Michael Scott points out, people suffering from rabies develop an intense aversion to water known as hydrophobia.The rabies cipro concentrates in saliva and can be transmitted through biting. You might think that a cipro capable of such wizardry would be highly complex, but it contains only five genes.

One of these genes makes a protein that appears to interfere with communication between cells in the brain, which likely contributes to the behavioral changes caused by rabies. Fun fact. The hangover remedy known as “hair of the dog” has its origins in a supposed rabies treatment devised by the Roman naturalist Pliny the Elder. Pliny suggested rabies victims should “insert in the wound ashes of hairs from the tail of the dog that inflicted the bite.” Don’t try this.

It does not work.As for Michael’s efforts, his Rabies Fun Run would have been more relevant prior to the 1880s, before Louis Pasteur developed the first rabies treatment. Or, in other parts of the world that face more cases of rabies. Globally, rabies kills nearly 60,000 people each year, largely due to lack of resources and access to medical care.Lice Bug BombPediculus humanus capitis was the featured guest on S9:E10, causing an infestation across cubicles at 1725 Slough Avenue. While everyone assumed the head lice came from Meredith, the source was actually Pam, who contracted them from her daughter Cece.Lice are tiny insect parasites that take up residence on the scalp.

These so-called skull vampires suck blood for nourishment and glue their eggs (nits) tightly to the hair. The insects can’t jump or fly, but can be passed between people who share hairbrushes, clips, bedding, towels, clothing or hats. The most common source of transmission is through direct contact with an infested person’s hair. While head lice are an annoyance, they do not carry any known disease.Our friends on The Office put their heads together (not literally, thankfully) and offered several different solutions.

Following Erin's advice, infected co-workers applied generous globs of mayonnaise to each other's hair to try to suffocate the lice. Meredith took a more radical approach and shaved her head. True to form, Dwight overreacts and attempts to rid the office of lice with a bug bomb grenade. Naturally, it explodes before he leaves the room, and the toxic fumes cause him to hallucinate and faint.Of all the solutions attempted, Meredith’s is most certain to work.

Depriving the lice of hair deprives them of a place to lay eggs, and the adults are easily washed away. But many people are not willing to sacrifice their locks. While it’s a popular home remedy, Erin’s idea to suffocate the lice with mayonnaise (petroleum jelly is also common) rarely works, according to (the aptly named) Mayo Clinic. And, as this episode illustrates, bug bombs are far more trouble than they are worth.

Lice cannot survive without a host for more than a day, so there is no need to fumigate and risk exposure to dangerous chemicals. More than 3,200 cases of bug bomb-related illnesses, including four human deaths, were reported in the U.S. Between 2007 and 2015.One effective way to treat lice is to use a shampoo containing an insecticide like permethrin. Permethrin is an insect neurotoxin that causes paralysis in the louse by disrupting sodium transport across its cellular membranes.

Nit combs can be used in conjunction with the shampoo treatment to physically remove eggs unaffected by the insecticide. Multiple treatments are advised to ensure all of the lice have been eradicated.Kevin’s Stinky FeetJim and Pam’s wedding in S6:E4 was filled with unforgettable moments, including the revelation that Kevin has a serious foot odor issue. Kevin left his shoes outside his hotel door to be cleaned, only to find that they had disappeared during the night. The hotel manager told him.

€œMr. Malone, your shoes are gone. €¦ When the bag was opened by our shoeshine, the smell overcame him. I, too, smelled them and made the choice that they must be thrown away.

Incinerated, actually.”Scientists have sniffed out the cause of bromodosis (foot odor), and it can be traced to a bacterium called Brevibacterium linens. Our bodies are home to trillions of bacteria, likely more than 10,000 different species, that live on or inside us. B. Linens are harmless denizens of our skin, where they consume dead cells.

As they digest the dead skin cells, they release smelly sulfur-containing compounds called S-methyl thioesters as waste products.Sweaty feet create a moist and salty environment that allows this species of bacteria to thrive, generating pungent odors as they excrete more and more S-methyl thioesters. Incidentally, these are the same bacteria used to produce the rind of smelly cheeses like Limburger.Kevin could have reduced his foot odor by depriving the bacteria of the sweat they need to grow. He could have achieved this by wearing open-toed shoes whenever possible, using powder or carrying an extra pair of dry, fresh socks. There may also be additional hope on the horizon for folks like Kevin, cursed with industrial strength foot odor.

Scientists recently found that socks coated in zinc oxide nanoparticles, which have potent antibacterial activity, are effective at preventing foot odor.Armed with that knowledge, you can now comfortably prop up your feet and marathon through all nine seasons of The Office. Or, at least track down these standout episodes — with an eye toward science.For some people, the idea of going to the store without a mask right now is so shocking, they’re having stress dreams about it. But once the need to wear a face-covering every time we go shopping is over, our instinct to reach for our masks might not disappear entirely in the U.S. Living through the worst epidemic Americans have seen in a century might shift attitudes about long-term mask use, in part because what many people experienced during the cipro is uniquely traumatic, says Isaac Fung, an epidemiologist at Georgia Southern University.

€œIt’s probably a once-in-a-lifetime experience, even though there have been, and will be, antibioticses that create an epidemic.” Who changes behaviors and how frequently they reach for their face coverings, however, could depend on a few factors.Lasting Effects of TraumaPart of why it’s possible that masks could become a more long-term fixture in the U.S. Is because elsewhere in the world, previous cipros had the same effect. In 2003, the SARS outbreaks in parts of Asia, including China, Taiwan and South Korea, required mask-wearing. The shock of the SARS outbreaks and a cultural memory of what helped control them could partially explain why the transition to consistent mask use in some of these nations during buy antibiotics was seamless compared to the U.S., Fung says.

€œThey have both the fortunate and misfortune of the impact of SARS in 2003.” In between the cipros, consistent mask-wearing in parts of Asia evolved into an occasional polite choice someone might make if they had a cold or cough and were out in public. Masks, along with other buy antibiotics protocols like hand washing and social distancing, can reduce the odds of someone spreading other illnesses like the seasonal flu. In the U.S., a similar scenario — a population scarred by a cipro comes to realize how useful the masks are for other illnesses — might play out. Granted, mask use has become political in the U.S.

In a way it hasn’t in many other places, Fung points out. But throughout the cipro, Pew Research Center surveys have shown that the partisan divide on masking behaviors lessened over time.Christos Lynteris, a social anthropologist at the University of St Andrews in Scotland, thinks future consistent mask use might stand a chance in part because the cipro won’t end with one theatrical, celebratory announcement. If the health crisis was suddenly “over” one day, some people might reject masks completely from there on out. €œThrowing your mask away [could be] like you're unshackling yourself from the epidemic, which is over,” Lynteris says.

But it’s more likely the cipro could see seasonal resurgences like the flu and draw out for a while. In that case, the longer battle with antibiotics could help individuals see masks as a more consistent part of life that comes with other health benefits. Too Close for ComfortThe realization of the perpetual benefits of masks might take hold in cities best, particularly if many residents rely on public transit, Fung says. When people don’t own cars and need to get around via packed buses or train cars, they spend a lot more time in close contact with other people.

It’s hard to be in that environment daily and not see the value of a face covering, Fung says. In large swathes of the U.S. Where people commute in their own cars or rely on relatively-empty public transportation, the appeal of wearing masks might not be as strong.Future mask use could also depend on how well people transform the face-covering into an effective but appealing — maybe even fashionable — accessory. If public health departments had wanted to make mask-wearing a more consistent part of long-term healthy behaviors, the institutions could have been more intentional about encouraging this transition, Lynteris says.

€œYou need to allow people to adopt the mask as their own thing,” he says. Meeting with different communities and encouraging people to make masks look the way they want them to could make them more appealing. In parts of Asia, people pulled off this exact transition with masks over the years. People sell and purchase masks that coordinate with outfits, and when it is part of the wardrobe, the face-covering becomes even more likely to be worn, Fung says.

If covering faces in public persists for years to come, the well-meaning action would be more likely to be effective if people had a better idea of how to handle the masks. In fact, this is a part of mask education that Fung thinks could be improved right now during the cipro. €œThis part of health education I do not see happening in the U.S.,” he says. €œWe are only focusing on wearing it, not how to properly take it off or wash it.” Handling masks correctly can reduce the likelihood that any cipro on the material doesn’t make its way into your nose or mouth.

And while the CDC has guidelines on appropriate behavior, simply having online information available for those who search for it isn’t quite enough, Lynteris notes. Appropriate mask protocols are another topic public health officials should discuss with communities. A chance to ask questions — about when masks should be cleaned or how to dispose of them, for example — or even hear from others about the mistakes they’ve made can familiarize people with what they need to do themselves. €œIf you don’t use the mask correctly but think it's protecting you, you may be engaging in behavior where you put yourself and others at risk,” Lynteris says.

€œIt’s an important conversation we’re not having.”Alcohol consumption in the U.S. Surged in 2020. Booze delivery services gained popularity while market reports relayed information about higher sales volumes. Even academic surveys found people were drinking more — one sample representing roughly 1,500 American adults found that on average, three of every four individuals were pouring themselves a drink an extra day every month.Of course, having a beer one extra day of the month doesn’t necessarily mean someone is drinking too much.

But when it comes to self-assessing booze habits, people tend to define the problem in a way that somehow leaves their own habits in good standing, says Patricia E. Molina, the director of the Alcohol and Drug Abuse Center of Excellence at LSU Health Sciences Center New Orleans. €œWhat the lay public tends to do is pay attention or focus on one aspect that is convenient for their definition." Beyond Binge DrinkingTypically, people use the term binge drinking as a benchmark of whether or not they’ve had one too many. The term refers to booze consumption that brings someone’s blood alcohol content (BAC) to .08g/dl or above — the legal limit for driving in the U.S.

Most men reach that value after having five drinks in two hours, while women typically reach it after having four drinks in the same time span. Binge drinking is the most common and deadly form of excessive drinking in the U.S., according to the CDC, as it’s associated with a wide range of health consequences. Some stem from the impact alcohol has on the body, such as alcohol poisoning, while others are due to the way alcohol disrupts our ability to function, like injuries from car accidents. But even when people haven't reached excessive BAC levels, it doesn’t exempt them, or others, from harm.

€œOne could make the argument that, okay, if I don't drink that much in two hours, but over a longer period of time, is that okay?. € Molina says. €œWell, not completely.” Besides binge drinking, the CDC also labels heavy drinking as a risky, harmful behavior, and is a concept Molina thinks should be a larger part of alcohol education campaigns. Classified as eight or more drinks a week for women and 15 or more a week for men, heavy drinking is less likely to cause short-term issues, like car accidents.

But over time, the habit can lead to a range of cancers, liver disease and heart problems, as well as depression and anxiety. So while someone might be able to drive their car after tailgating all Saturday, they may still have put away several drinks over the entire afternoon, Molina says, pushing the limit of what qualifies as a week of heavy drinking. Ultimately, the fewer drinks someone has, the better. To keep the health consequences of alcohol low, the official USDA dietary guidelines for 2020 to 2025 cap moderate drinking at two drinks a day for men and one drink a day for women.

However, the scientific advisory group that helps craft these guidelines has recommended that the cap be one drink a day for everyone. No Sense of StandardEven if someone was keeping track of their beer habit and trying to stick to these quantities, a lot of people don’t know or can’t estimate what qualifies as a single drink, Molina says. In the U.S., a standard drink contains 14 grams of alcohol. Since different kinds of drinks have a range of alcohol content, that serving size pans out to be 12 ounces of a 5 percent alcohol beer, five ounces of wine and one and a half ounces of liquor.

These volumes don’t always match what someone might perceive as a single serving, like an oversized can of beer or a restaurant pour of wine, which is often closer to eight ounces, Molina says. Studies have shown that people tend to overestimate what qualifies as a standard drink anyways, and when asked to pour out a single serving, are too generous. If people drink more than they think they do, then their threshold for what it takes to feel buzzed is likely higher than they thought, too. How people develop alcohol tolerance — where a given number of drinks has less of an effect on their ability to function over time — isn’t well understood by researchers, though there are likely genetic and social influences at work.

But increasing tolerance is often associated with alcohol use disorder or alcohol dependence. The more someone drinks, Molina says, the more they need to achieve the relaxation or buzz they’re seeking through alcohol. At the same time, “you increase the risk of falling into a pattern of drinking to avoid negative feelings,” she says.For anyone curious about the best ways to recalibrate their drinking patterns, Molina recommends Rethinking Drinking, a National Institute of Health resource that spells out serving sizes, how those compare to what standard drink containers hold, and what different drinking habits look like..

Cipro el salvador

How to cite this article:Singh how much cipro cost O cipro el salvador P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized events in cipro el salvador 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, cipro el salvador and social media were full of stories providing minute details of the suicidal act.

Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched cipro el salvador and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly cipro el salvador started getting distress calls from their patients in despair with increased suicidal ideation.

This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health cipro el salvador Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report 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 cipro el salvador 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 cipro el salvador Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental health professionals were called by media houses cipro el salvador to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints cipro el salvador perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a cipro el salvador 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 cipro el salvador books for interacting with media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely cipro el salvador recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

How to cite this article:Singh where to buy cheap cipro click to find out more O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized where to buy cheap cipro events in our country.

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

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

Psychiatrists suddenly started getting distress calls from their where to buy cheap cipro 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 where to buy cheap cipro 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 where to buy cheap cipro also his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more where to buy cheap cipro 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 where to buy cheap cipro comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so. There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist.

These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the where to buy cheap cipro 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 where to buy cheap cipro 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional where to buy cheap cipro societies have guidelines and resource books for interacting with media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion.

It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely where to buy cheap cipro recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of where to buy cheap cipro Support. None, Conflict of Interest. NoneDOI.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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