Where to buy zithromax

Vision Team tilbyder løsninger baseret på
Typo3, Drupal og Wordpress, klik her for at komme videre >>

Where to buy zithromax

Where to buy zithromax

€˜None of us will be where to buy zithromax safe until everyone is safe. Global access to antibiotics treatments, tests and treatments where to buy zithromax for everyone who needs them, anywhere, is the only way out’. This statement by Dr Tedros Adhanom Ghebreyesus, Director-General of the WHO and Ursula von der Leyen, President of the European Commission1 has become the rallying call for buy antibiotics vaccination.

The success of a safe and efficacious buy antibiotics treatment depends just not only on production and availability but also crucially on uptake.In where to buy zithromax countries such as the UK where buy antibiotics treatment prioritisation and rollout are proceeding quickly, attitudes to vaccination have rapidly become a priority.2 treatment hesitancy (‘behavioural delay in acceptance or refusal of treatments despite availability of treatment services’)3 is not a single entity. Reasons vary and there is a continuum from complete acceptance to refusal of all treatments, with treatment hesitancy lying between the two where to buy zithromax poles. Factors involved include confidence (trusting or not the treatment or provider), complacency (seeing the need or value of a treatment) and convenience (easy, convenient access to the treatment).3 4 Importantly, attitudes to vaccination can change and people who are initially hesitant can still come to see a treatment’s safety, efficacy and necessity.5Developing strategies to address hesitancy is key.6 The expedited development and relative novelty of the buy antibiotics treatments have led to public uncertainty.4 In addition, efforts to explain the mode of action of these treatments involve a degree of complexity (eg, immune response and genetic mechanisms), which is difficult to communicate quickly and simply.

There are genuine knowledge voids (eg, long-term where to buy zithromax safety data), which in some cases have been filled with misinformation.7 Recent studies have assessed potential acceptance rates specifically for the buy antibiotics treatment. A UK where to buy zithromax study of more than 5000 adults using a validated scale found 71.7% were willing to be vaccinated, 16.6% were very unsure and 11.7% were strongly hesitant, with hesitancy relatively evenly spread across the population.8 Willingness to take a treatment was closely bound to recognition of the collective importance of this decision as well as beliefs about the likelihood of buy antibiotics , the efficacy, speed of development and side effects of the treatment. This implies that public information emphasising social benefits may be especially effective, at least in a majority of a population, and information that encourages mistrust or undermines social cohesion will lower treatment uptake.We also need to consider more focused strategies about treatment hesitancy for particular groups, including those groups who are most at risk of hesitancy and severe course of illness.

As mental health clinicians, we assessed the impact of mental health conditions on buy antibiotics treatment hesitancy and searched for current guidance in this area using a validated approach.9 where to buy zithromax We found that there is currently no specific guidance in addressing treatment hesitancy in those with mental health difficulties,10 although it is recognised that this is a high-risk group who should be monitored. People with mental health issues, particularly with severe mental illness (SMI), are at particular risk both for with buy antibiotics and for more severe complications and higher mortality.11 Historically, the uptake of similar treatments such as the influenza treatment in those with SMI can be as low as 25%,12 and where to buy zithromax so, similar to other low uptake groups, focused efforts are needed to increase this. Suggestions for change include offering specific discussions from mental health professionals and peer workers, treatment education and awareness focused for those with SMI, vaccination programmes within mental health services (with coexistent organisational change to facilitate this), alignment with other preventative health strategies (such as influenza vaccination, smoking cessation, metabolic monitoring), focused outreach and monitoring uptake.13Monitoring of vulnerable groups treatment uptake itself presents problems.

In the example of the UK, monitoring where to buy zithromax of treatment coverage of most routine immunisation programmes relies on data extracted from primary care systems. To monitor vulnerable where to buy zithromax groups, the data need to be specifically recorded. For example, Public Health England’s national immunisation equity audit in 2019 identified inequalities in uptake by a number of important variables (such as age, geography, ethnicity) but could not assess others including mental illness due to a lack of systematically collected data.14 Inequalities that were assessed by the audit were not only in overall coverage but also in timing of treatments and completion of treatment schedules.

In addition, the extent of a particular inequality varies when it intersects with where to buy zithromax one or more other factors. In the case of mental illness, multiple long-term conditions across mental and physical health domains as well as socio-economic factors means that both vulnerability and inequality are likely to be additive.11 However, treatment impact may be greater among the where to buy zithromax most vulnerable despite lower treatment uptake because the baseline absolute risk is so high.15 Therefore, in the context of a buy antibiotics treatment programme, even if treatment uptake falls short in some high-risk groups, even small increases in treatment uptake will still have significant health benefits.14Uptake of vaccination is crucial both for the individual and protection of others. It is in everyone’s interests to ensure that groups where a low uptake is predicted have extra care and input.

At the moment there is little formal guidance on where to buy zithromax how to support those with mental health issues to access clear and reliable information, and practical and easy access to vaccination for those who are willing. If we are to ensure that ‘everyone is safe’, we need a concerted and global effort16 to guide and focus strategies to support and inform those who are both potentially most hesitant and most vulnerable, including and prioritising those with mental health difficulties..

Side effects of zithromax in children

Zithromax
Myambutol
Chloromycetin
Terramycin
Ampicillin
Neggram
Can you get a sample
Online
Yes
No
No
Online
Yes
Duration of action
Buy in Pharmacy
Buy
Buy online
Purchase in online Pharmacy
Buy in online Pharmacy
Purchase online
Buy with echeck
4h
3h
1h
5h
3h
8h
Buy with amex
Drugstore on the corner
Drugstore on the corner
On the market
At walgreens
Order online
Canadian Pharmacy
Does work at first time
Ask your Doctor
No
Yes
You need consultation
Ask your Doctor
Yes
Great Britain pharmacy price
67
58
43
58
41
48
Long term side effects
3h
24h
14h
6h
23h
2h

Green manufacturing is becoming an increasingly critical process across industries, propelled buy zithromax 500mg online by a growing awareness of the negative environmental and health impacts associated with traditional side effects of zithromax in children practices. In the biomaterials industry, electrospinning is a universal fabrication method used around the world to produce nano- to microscale fibrous meshes that closely resemble native tissue architecture. The process, however, has traditionally used solvents that not only are environmentally hazardous but also pose a significant barrier to industrial scale-up, clinical translation, and, ultimately, widespread use.Researchers at Columbia Engineering report that they have developed a "green electrospinning" process that addresses many of side effects of zithromax in children the challenges to scaling up this fabrication method, from managing the environmental risks of volatile solvent storage and disposal at large volumes to meeting health and safety standards during both fabrication and implementation. The team's new study, published June 28, 2021, by Biofabrication, details how they have modernized the nanofiber fabrication of widely utilized biological and synthetic polymers (e.g. Poly-α-hydroxyesters, collagen), side effects of zithromax in children polymer blends, and polymer-ceramic composites.The study also underscores the superiority of green manufacturing.

The group's "green" fibers exhibited exceptional mechanical properties and preserved growth factor bioactivity relative to traditional fiber counterparts, which is essential for drug delivery and tissue engineering applications.Regenerative medicine is a $156 billion global industry, one that is growing exponentially. The team of researchers, led by Helen H. Lu, Percy K side effects of zithromax in children. And Vida L.W. Hudson Professor of Biomedical Engineering, wanted to address the challenge of establishing scalable green manufacturing practices for biomimetic biomaterials and scaffolds used in regenerative medicine."We think this is a paradigm shift in biofabrication, and will accelerate the translation of scalable biomaterials and biomimetic scaffolds for tissue engineering and regenerative medicine," said Lu, a leader in research on tissue interfaces, particularly the design of biomaterials and therapeutic strategies for recreating the side effects of zithromax in children body's natural synchrony between tissues.

"Green electrospinning not only preserves the composition, chemistry, architecture, and biocompatibility of traditionally electrospun fibers, but it also improves their mechanical properties by doubling the ductility of traditional fibers without compromising yield or ultimate tensile strength. Our work provides both a more biocompatible and sustainable solution for scalable nanomaterial fabrication."The team, which included several BME doctoral students from Lu's group, Christopher Mosher PhD'20 and Philip Brudnicki, as well as Theanne Schiros, an expert in eco-conscious textile synthesis who is also a research scientist at Columbia MRSEC and assistant professor at FIT, applied sustainability principles to biomaterial production, and developed a green electrospinning process by systematically testing what the FDA considers as biologically benign solvents (Q3C Class 3).They identified acetic acid as a green solvent that exhibits low ecological impact (Sustainable Minds® Life Cycle Assessment) and supports a stable electrospinning jet under routine fabrication conditions. By tuning electrospinning parameters, such as needle-plate distance and flow rate, the researchers were able to ameliorate the fabrication of research and industry-standard biomedical polymers, cutting the detrimental manufacturing impacts of the electrospinning process by three to six times.Green electrospun materials can be used in a broad range of applications side effects of zithromax in children. Lu's team is currently working on further innovating these materials for orthopaedic and dental applications, and expanding this eco-conscious fabrication process for scalable production of regenerative materials."Biofabrication has been referred to as the 'fourth industrial revolution' following steam engines, electrical power, and the digital age for automating mass production," noted Mosher, the study's first author. "This work is side effects of zithromax in children an important step towards developing sustainable practices in the next generation of biomaterials manufacturing, which has become paramount amidst the global climate crisis."Symptoms for early buy antibiotics differ among age groups and between men and women, new research has found.

These differences are most notable between younger age groups (16 to 59 years) compared to older age groups (60 to 80 years and over), and men have different symptoms compared to women in the early stages of buy antibiotics .The paper, published today in The Lancet Digital Health, and led by researchers from King's College London analyses data from the ZOE buy antibiotics Symptom Study app between April 20th to 15th October 2020. App contributors are invited to get tested as soon as they report any new symptoms, thanks to a joint initiative with the Department of Health and side effects of zithromax in children Social Care. The researchers modelled the early signs of buy antibiotics and successfully detected 80% of cases when using three days of self-reported symptoms.Researchers compared the ability to predict early signs of buy antibiotics using current National Health Service UK diagnostic criteria and a Hierarchical Gaussian Process model, a type of machine learning.This machine learning model was able to incorporate some characteristics about the person affected, such as age, sex, and health conditions, and showed that symptoms of early buy antibiotics are different among various groups.18 symptoms were examined, which had different relevance for early detection in different groups. The most important symptoms for earliest detection of buy antibiotics overall included loss of smell, chest pain, persistent cough, abdominal pain, blisters on the feet, eye soreness and unusual muscle pain. However, loss of smell lost significance in people side effects of zithromax in children over 60 years of age and was not relevant for subjects over 80.

Other early symptoms such as diarrhoea were key in older age groups (60-79 and >80). Fever, while a known symptom of disease, was not an early feature of the disease in any age group.Men were more side effects of zithromax in children likely to report shortness of breath, fatigue, chills and shivers, whereas women were more likely to report loss of smell, chest pain and a persistent cough.While these models were generated in the buy antibiotics Symptom study app, models were replicated across time suggesting they would also apply to non-app contributors. Although the models were used on the first strain of the zithromax and Alpha variants, the key findings suggest the symptoms of the Delta variant and subsequent variants will also differ across population groups.Lead author, Claire Steves, Reader at King's College London said. "Its important people know the earliest symptoms are wide-ranging and may look different for each member of a family or household. Testing guidance could be updated to enable cases to be picked up earlier, especially in the face of new variants which side effects of zithromax in children are highly transmissible.

This could include using widely available lateral flow tests for people with any of these non-core symptoms."Dr Liane dos Santos Canas, first author from King's College London, said. "Currently, in the UK, side effects of zithromax in children only a few symptoms are used to recommend self-isolation and further testing. Using a larger number of symptoms and only after a few days of being unwell, using AI, we can better detect buy antibiotics positive cases. We hope such a method is used to encourage more people to get tested as early as possible to minimise the risk of spread."Dr Marc Modat, Senior Lecturer at King's College London, said. "As part of our study, we have been able side effects of zithromax in children to identify that the profile of symptoms due to buy antibiotics differs from one group to another.

This suggests that the criteria to encourage people to get tested should be personalised using individuals' information such as age. Alternatively, a larger set of symptoms could be side effects of zithromax in children considered, so the different manifestations of the disease across different groups are taken into account." Story Source. Materials provided by King's College London. Note. Content may be edited for style and length.The mutations that give rise to melanoma result from a chemical conversion in DNA fueled by sunlight -- not just a DNA copying error as previously believed, reports a study by Van Andel Institute scientists published today in Science Advances.The findings upend long-held beliefs about the mechanisms underlying the disease, reinforce the importance of prevention efforts and offer a path forward for investigating the origins of other cancer types."Cancers result from DNA mutations that allow defective cells to survive and invade other tissues.

However, in most cases, the source of these mutations is not clear, which complicates development of therapies and prevention methods," said Gerd Pfeifer, Ph.D., a VAI professor and the study's corresponding author. "In melanoma, we've now shown that damage from sunlight primes the DNA by creating 'premutations' that then give way to full mutations during DNA replication."Melanoma is a serious type of skin cancer that begins in pigment-producing skin cells. Although less common than other types of skin cancer, melanoma is more likely to spread and invade other tissues, which significantly reduces patient survival. Previous large-scale sequencing studies have shown that melanoma has the most DNA mutations of any cancer. Like other skin cancers, melanoma is linked to sun exposure, specifically a type of radiation called UVB.

Exposure to UVB damages skin cells as well as the DNA within cells.Most cancers are thought to begin when DNA damage directly causes a mutation that is then copied into subsequent generations of cells during normal cellular replication. In the case of melanoma, however, Pfeifer and his team found a different mechanism that produces disease-causing mutations -- the introduction of a chemical base not normally found in DNA that makes it prone to mutation.DNA comprises four chemical bases that exist in pairs -- adenine (A) and thymine (T), and cytosine (C) and guanine (G). Different sequences of these pairs encode all of the instructions for life. In melanoma, the problem occurs when UVB radiation from the sun hits certain sequences of bases -- CC, TT, TC and CT -- causing them to chemically link together and become unstable. The resulting instability causes a chemical change to cytosine that transforms it into uracil, a chemical base found in the messenger molecule RNA but not in DNA.

This change, called a "premutation," primes the DNA to mutate during normal cell replication, thereby causing alterations that underlie melanoma.These mutations may not cause disease right away. Instead, they may lay dormant for years. They also can accumulate as time goes on and a person's lifetime exposure to sunlight increases, resulting in a tough-to-treat cancer that evades many therapeutic options."Safe sun practices are very important. In our study, 10-15 minutes of exposure to UVB light was equivalent to what a person would experience at high noon, and was sufficient to cause premutations," Pfeifer said. "While our cells have built-in safeguards to repair DNA damage, this process occasionally lets something slip by.

Protecting the skin is generally the best bet when it comes to melanoma prevention."The findings were made possible using a method developed by Pfeifer's lab called Circle Damage Sequencing, which allows scientists to "break" DNA at each point where damage occurs. They then coax the DNA into circles, which are replicated thousands of times using a technology called PCR. Once they have enough DNA, they use next-generation sequencing to identify which DNA bases are present at the breaks. Going forward, Pfeifer and colleagues plan to use this powerful technique to investigate other types of DNA damage in different kinds of cancer.Other authors include Seung-Gi Jin, Ph.D., Dean Pettinga, Jennifer Johnson and Peipei Li, Ph.D., of VAI. Story Source.

Materials provided by Van Andel Research Institute. Note. Content may be edited for style and length.UT Southwestern faculty have discovered what appears to be an Achilles' heel in ovarian cancers, as well as new biomarkers that could point to which patients are the best candidates for possible new treatments.The finding, published in the journal Cell, was made in part using a research tool invented in a UT Southwestern lab in the Cecil H. And Ida Green Center for Reproductive Biology Sciences.The research was led by W. Lee Kraus, Ph.D., Professor of Obstetrics and Gynecology and Pharmacology and a member of the Harold C.

Simmons Comprehensive Cancer Center."Many researchers are trying to find dependencies in cancers by asking why a cancer cell amplifies a gene, increases the levels of a protein, or upregulates a critical cellular pathway. These changes give that cancer a selective advantage, but at the same time they can become an Achilles' heel -- something that, if the alteration was blocked, would kill the cancer or stop its growth," he said.Dr. Kraus and his team, including lead author Sridevi Challa, Ph.D., a postdoctoral researcher in the lab, found that ovarian cancers massively amplify an enzyme, NMNAT-2, that makes NAD+. NAD+ is the substrate for a family of enzymes called PARPs, which chemically modify proteins with ADP-ribose from NAD+. In this study, the team found that one PARP family member, PARP-16, uses NAD+ to modify ribosomes, the protein synthesizing machines of the cell.A challenge for this work was that a single ADP-ribose group attached to a protein is difficult to detect.

Dr. Kraus and his team overcame this problem by developing a synthetic mono(ADP-ribose) detection reagent made up of natural protein domains fused together, which can be used to detect ADP-ribosylated proteins in cells and patient samples. advertisement In collaboration with UT Southwestern clinicians, led by Jayanthi Lea, M.D., Professor of Obstetrics and Gynecology and member of the Simmons Cancer Center, Dr. Kraus and his team screened human ovarian cancer patient samples using the mono(ADP-ribose) detection reagent to identify those with low or high levels of mono(ADP-ribose)."We were able to show that when ribosomes are mono(ADP-ribosyl)ated in ovarian cancer cells, the modification changes the way they translate mRNAs into proteins," Dr. Kraus said.

"The ovarian cancers amplify NMNAT-2 to increase the levels of NAD+ available for PARP-16 to mono(ADP-ribosyl)ate ribosomes, giving them a selective advantage by allowing them to fine-tune the levels of translation and prevent toxic protein aggregation. But that selective advantage also becomes their Achilles' heel. They're addicted to NMNAT-2, so inhibition or reduction of NMNAT-2 inhibits the growth of the cancer cells."This study identified mono(ADP-ribose) and NMNAT-2 as potential biomarkers for ovarian cancers, which may allow clinicians to determine which ovarian cancer patients may respond well and which will not. Even more ovarian cancer patients might do well if an inhibitor is developed for PARP-16, which blocks ribosome mono(ADP-ribosyl)ation.Dr. Kraus, an expert in PARPs, said medical science has had great success in developing FDA-approved PARP-1 inhibitors, and an inhibitor for PARP-16 is likely."No PARP-16 inhibitors are currently in clinical trials, but labs in academia and the pharmaceutical industry are developing specific and potent inhibitors of PARP-16.

Such a drug could be an effective therapeutic for treating ovarian cancers," he said. advertisement Dr. Kraus is a founder and consultant for Ribon Therapeutics Inc., and ARase Therapeutics Inc. He is also co-holder of U.S. Patent 9,599,606 covering the mono(ADP-ribose) detection reagent, which has been licensed to and is sold by EMD Millipore."Dr.

Kraus' research is not just a great advance in basic science. It has real promise for clinician investigators and cancer care practitioners because it shows a biomarker and a pathway a future drug could target. The fact that technology developed in his laboratory helped make these findings shows how our faculty builds on their findings to break new ground," said Carlos L. Arteaga, M.D., Director of the Simmons Cancer Center.Other researchers who contributed to this study include Beman R. Khulpateea, Tulip Nandu, Cristel V.

Camacho, Keun W. Ryu, Hao Chen, and Yan Peng.The research work was supported by a grant from the National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK069710) as well as funds from the Cecil H. And Ida Green Center for Reproductive Biology Sciences Endowment to Kraus, and a postdoctoral fellowship from the Ovarian Cancer Research Alliance (GAA202103-0003) to Challa.Dr. Arteaga holds the The Lisa K. Simmons Distinguished Chair in Comprehensive Oncology.

Kraus holds the Cecil H. And Ida Green Distinguished Chair in Reproductive Biology Sciences. Dr. Lea holds the Patricia Duniven Fletcher Distinguished Professorship in Gynecological Oncology.[embedded content] “CBS This Morning,” in partnership with KHN and NPR, interviews Phil Gaimon, a cyclist who had hoped to be in Tokyo next week as a competitor in the track events on the USA Cycling national team. Instead, a crash on the velodrome track in Pennsylvania in 2019 ended his Olympic dream and left him with huge medical bills — even after his two insurance policies paid portions of the treatment.

KHN Editor-in-Chief Elisabeth Rosenthal said Gaimon hit three health care land mines. Out-of-network hospitals, out-of-state care and gold-plated charges from the hospitals. Two years after the crash, Gaimon is still fielding calls from collection agencies. Related Topics Contact Us Submit a Story TipNot so long ago, laws governing abortion in Massachusetts and Rhode Island were far more restrictive than those in the Deep South, as state legislators throughout New England regularly banned the procedure, no matter the circumstances, during the 1960s and ’70s. Nowadays, however, the American South represents a hub of anti-abortion fervor, home to a series of laws and regulations that have eroded Roe v.

Wade, as liberal states in the Northeast and elsewhere have enacted laws to codify that landmark 1973 Supreme Court decision. How that regional reversal came to pass touches on demographic and ideological shifts, as well as a political environment in which few governors or state legislators anywhere claim to be moderates on the issue. More than anything, the switch can be traced to religion, and how Christian faiths have in some cases become as polarized on the issue of abortion as the views of elected officials who rely on votes of the religious faithful. Q. Why was famously liberal New England so opposed to abortion?.

Two words. The pope. Daniel Williams, author of “God’s Own Party. The Making of the Christian Right” and “Defenders of the Unborn. The Pro-Life Movement Before Roe v.

Wade,” said that in the early 1970s the strongest opposition to abortion came not from Southern evangelicals but from states with strong Catholic ties in the Northeast. Even as states like Connecticut and Maine were passing bans, states that were home to large populations of more conservative religious denominations allowed women to safely end pregnancies in cases of rape, incest, fetal deformities and when a woman’s life was at risk. North Carolina was one of the first states to allow for limited legal access to abortion in 1967. Georgia followed in 1968, and South Carolina and Arkansas in 1970. In Texas, a poll taken in 1970 by the Baptist Standard, the periodical of the Baptist convention, found that 90% of its readers — largely pastors and deacons — believed Texas’ abortion laws were too harsh.

Religious scholars say white evangelical Protestants did not support unfettered abortion rights, but without a strong theology about when human life begins, less restrictive abortion laws were not a moral threat. Evangelicals viewed abortion as a Catholic cause. €œThe general view among Southern evangelicals in the 1960s and early 1970s was that abortion was ethically problematic,” said Williams, who serves as a professor of history at the University of West Georgia. €œBut there was no firm biblical support for the Catholic claim that human life began at conception.” Q. So, why did the South — and Southern evangelicals — change their minds?.

One could say it started offshore. In March 1970, Hawaii became the first state to decriminalize abortion, though the law applied only to state residents. Later that year, New York, then led by a Republican governor, Nelson Rockefeller, and a Republican-dominated legislature, went further, allowing women from any state to receive abortion care. In 1972, some 200,000 women had legal abortions in New York, and 3 of 5 were from out of state. That alarmed many Southerners, who feared that the procedure was being used — and abused — by unmarried women.

€œMany of the Baptists in Texas might have thought if a married woman experienced problems with a pregnancy” she should have the option of a safe, legal abortion, said Williams. €œThey were not envisioning there would be 200,000. This was clearly not a limited procedure in a small number of instances.” Q. Was it just abortion that worried evangelicals?. Aversion to women’s rights was not limited to reproductive issues.

Disaffected by the sexual revolution and the feminist movement, Christian conservative leaders campaigned against the Equal Rights Amendment. They also battled to protect the tax-exempt status of racially segregated private schools and pushed to ban gay teachers from public schools and restore classroom prayer. As opposition to abortion among Catholic voters and lawmakers eased, white evangelicals and fundamentalists grew more strident on the issue. By the late 1970s, white evangelicals had fully embraced the position that legal abortion was an assault on moral values. As biblicists, committed to the text of the Bible, evangelical leaders found new meaning in certain verses they believed gave credence to prenatal life.

€œThe connection these conservative evangelicals saw was that when Americans drifted away from God in public life, a change in gender roles came in,” said Williams. €œChristianity was being replaced by secular, humanistic, sexual ethics, and Roe v. Wade became the symbol for all of that.” Q. What role did politics play in the shift?. A major one.

While Catholics are fairly dispersed around the country, white evangelicals are heavily concentrated in Southern states, where true believers often also hold elected office, and thus the power to make laws, said Andrew Lewis, associate professor of political science at the University of Cincinnati. Mary Ziegler, a professor at Florida State University College of Law and author of “Abortion and the Law in America. Roe v. Wade to the Present,” describes a trifecta that reinforced abortion opposition in the South. €œThere are a lot of white evangelicals, a lot of Republicans and a lot of gerrymandered swing states,” she said.

The acceleration of state-level abortion restrictions arose from grassroots conservative activists and socially conservative state legislators, not from national Republican Party strategists. €œOnce the Republican Party took over the South, it did so largely through the efforts of the Christian Coalition” of America, said Williams. And that connection between white evangelicals and the GOP intensified as the decades passed. By 2009, white evangelicals made up 35% of the Republican Party. Q.

Where does it all stand now?. Nearly 50 years after the U.S. Supreme Court legalized abortion, the South is the most fervently anti-abortion region in the country. And year after year, Southern legislatures have outdone one another, passing ever more restrictive measures on abortion care and criminal punishment to those who provide it. For instance, a 99-year prison sentence for doctors who perform abortions in Alabama.

A ban on nearly all abortions after 15 weeks of pregnancy in Mississippi and six weeks in Texas. Rape crisis counselors are subject to lawsuits from private citizens if a woman chooses to end her pregnancy. Few of these laws have taken effect. Most have been struck down or frozen by the courts and, until last month, the Supreme Court declined to consider many of them. But state legislators, often acting without guidance from national anti-abortion organizations, have continued to introduce anti-abortion bills at a fevered pace.

And with the Supreme Court’s rightward shift, many in the movement sense their moment has arrived. The Democratic Party in the South “generally doesn’t fight” abortion restrictions, Williams said. The party, which counts on the support of Black and Hispanic voters, tends to focus on other priorities, he said. €œThere is much greater interest in talking about health care and jobs.” And while many voters, even conservative ones, have shifted to the left on issues like gay rights, Williams said, younger evangelicals are more likely than their parents to oppose abortion. €œThe Republican Party has a lot of staying power in Georgia and Alabama and across much of the South for the foreseeable future,” Williams said.

Sarah Varney. svarney@kff.org, @SarahVarney4 Related Topics Contact Us Submit a Story Tip.

Green manufacturing is becoming an where to buy zithromax increasingly critical process zithromax z pak cost walmart across industries, propelled by a growing awareness of the negative environmental and health impacts associated with traditional practices. In the biomaterials industry, electrospinning is a universal fabrication method used around the world to produce nano- to microscale fibrous meshes that closely resemble native tissue architecture. The process, however, has traditionally used solvents that not only are environmentally hazardous but also pose a significant barrier to industrial scale-up, clinical translation, and, ultimately, widespread use.Researchers at Columbia Engineering report that they have developed a "green electrospinning" process that addresses many of the challenges to scaling up this fabrication method, from managing the environmental risks of volatile solvent storage and disposal where to buy zithromax at large volumes to meeting health and safety standards during both fabrication and implementation.

The team's new study, published June 28, 2021, by Biofabrication, details how they have modernized the nanofiber fabrication of widely utilized biological and synthetic polymers (e.g. Poly-α-hydroxyesters, collagen), polymer blends, and polymer-ceramic composites.The study also where to buy zithromax underscores the superiority of green manufacturing. The group's "green" fibers exhibited exceptional mechanical properties and preserved growth factor bioactivity relative to traditional fiber counterparts, which is essential for drug delivery and tissue engineering applications.Regenerative medicine is a $156 billion global industry, one that is growing exponentially.

The team of researchers, led by Helen H. Lu, Percy K where to buy zithromax. And Vida L.W.

Hudson Professor of Biomedical Engineering, wanted to address the challenge of establishing scalable green manufacturing practices for biomimetic biomaterials and scaffolds used in regenerative medicine."We where to buy zithromax think this is a paradigm shift in biofabrication, and will accelerate the translation of scalable biomaterials and biomimetic scaffolds for tissue engineering and regenerative medicine," said Lu, a leader in research on tissue interfaces, particularly the design of biomaterials and therapeutic strategies for recreating the body's natural synchrony between tissues. "Green electrospinning not only preserves the composition, chemistry, architecture, and biocompatibility of traditionally electrospun fibers, but it also improves their mechanical properties by doubling the ductility of traditional fibers without compromising yield or ultimate tensile strength. Our work provides both a more biocompatible and sustainable solution for scalable nanomaterial fabrication."The team, which included several BME doctoral students from Lu's group, Christopher Mosher PhD'20 and Philip Brudnicki, as well as Theanne Schiros, an expert in eco-conscious textile synthesis who is also a research scientist at Columbia MRSEC and assistant professor at FIT, applied sustainability principles to biomaterial production, and developed a green electrospinning process by systematically testing what the FDA considers as biologically benign solvents (Q3C Class 3).They identified acetic acid as a green solvent that exhibits low ecological impact (Sustainable Minds® Life Cycle Assessment) and supports a stable electrospinning jet under routine fabrication conditions.

By tuning electrospinning parameters, such as needle-plate distance and flow rate, the researchers were able to ameliorate the fabrication of research and industry-standard biomedical polymers, cutting the detrimental manufacturing impacts of the electrospinning process by three to six times.Green electrospun materials can where to buy zithromax be used in a broad range of applications. Lu's team is currently working on further innovating these materials for orthopaedic and dental applications, and expanding this eco-conscious fabrication process for scalable production of regenerative materials."Biofabrication has been referred to as the 'fourth industrial revolution' following steam engines, electrical power, and the digital age for automating mass production," noted Mosher, the study's first author. "This work is an important step towards developing sustainable practices in the next generation of biomaterials manufacturing, which has become paramount amidst where to buy zithromax the global climate crisis."Symptoms for early buy antibiotics differ among age groups and between men and women, new research has found.

These differences are most notable between younger age groups (16 to 59 years) compared to older age groups (60 to 80 years and over), and men have different symptoms compared to women in the early stages of buy antibiotics .The paper, published today in The Lancet Digital Health, and led by researchers from King's College London analyses data from the ZOE buy antibiotics Symptom Study app between April 20th to 15th October 2020. App contributors are invited to where to buy zithromax get tested as soon as they report any new symptoms, thanks to a joint initiative with the Department of Health and Social Care. The researchers modelled the early signs of buy antibiotics and successfully detected 80% of cases when using three days of self-reported symptoms.Researchers compared the ability to predict early signs of buy antibiotics using current National Health Service UK diagnostic criteria and a Hierarchical Gaussian Process model, a type of machine learning.This machine learning model was able to incorporate some characteristics about the person affected, such as age, sex, and health conditions, and showed that symptoms of early buy antibiotics are different among various groups.18 symptoms were examined, which had different relevance for early detection in different groups.

The most important symptoms for earliest detection of buy antibiotics overall included loss of smell, chest pain, persistent cough, abdominal pain, blisters on the feet, eye soreness and unusual muscle pain. However, loss of smell lost significance in people where to buy zithromax over 60 years of age and was not relevant for subjects over 80. Other early symptoms such as diarrhoea were key in older age groups (60-79 and >80).

Fever, while a known symptom of disease, where to buy zithromax was not an early feature of the disease in any age group.Men were more likely to report shortness of breath, fatigue, chills and shivers, whereas women were more likely to report loss of smell, chest pain and a persistent cough.While these models were generated in the buy antibiotics Symptom study app, models were replicated across time suggesting they would also apply to non-app contributors. Although the models were used on the first strain of the zithromax and Alpha variants, the key findings suggest the symptoms of the Delta variant and subsequent variants will also differ across population groups.Lead author, Claire Steves, Reader at King's College London said. "Its important people know the earliest symptoms are wide-ranging and may look different for each member of a family or household.

Testing guidance could be updated to enable cases to be picked up earlier, especially in the face of new where to buy zithromax variants which are highly transmissible. This could include using widely available lateral flow tests for people with any of these non-core symptoms."Dr Liane dos Santos Canas, first author from King's College London, said. "Currently, in the UK, only a few symptoms are used to where to buy zithromax recommend self-isolation and further testing.

Using a larger number of symptoms and only after a few days of being unwell, using AI, we can better detect buy antibiotics positive cases. We hope such a method is used to encourage more people to get tested as early as possible to minimise the risk of spread."Dr Marc Modat, Senior Lecturer at King's College London, said. "As part of our study, we have been able to where to buy zithromax identify that the profile of symptoms due to buy antibiotics differs from one group to another.

This suggests that the criteria to encourage people to get tested should be personalised using individuals' information such as age. Alternatively, a larger where to buy zithromax set of symptoms could be considered, so the different manifestations of the disease across different groups are taken into account." Story Source. Materials provided by King's College London.

Note. Content may be edited for style and length.The mutations that give rise to melanoma result from a chemical conversion in DNA fueled by sunlight -- not just a DNA copying error as previously believed, reports a study by Van Andel Institute scientists published today in Science Advances.The findings upend long-held beliefs about the mechanisms underlying the disease, reinforce the importance of prevention efforts and offer a path forward for investigating the origins of other cancer types."Cancers result from DNA mutations that allow defective cells to survive and invade other tissues. However, in most cases, the source of these mutations is not clear, which complicates development of therapies and prevention methods," said Gerd Pfeifer, Ph.D., a VAI professor and the study's corresponding author.

"In melanoma, we've now shown that damage from sunlight primes the DNA by creating 'premutations' that then give way to full mutations during DNA replication."Melanoma is a serious type of skin cancer that begins in pigment-producing skin cells. Although less common than other types of skin cancer, melanoma is more likely to spread and invade other tissues, which significantly reduces patient survival. Previous large-scale sequencing studies have shown that melanoma has the most DNA mutations of any cancer.

Like other skin cancers, melanoma is linked to sun exposure, specifically a type of radiation called UVB. Exposure to UVB damages skin cells as well as the DNA within cells.Most cancers are thought to begin when DNA damage directly causes a mutation that is then copied into subsequent generations of cells during normal cellular replication. In the case of melanoma, however, Pfeifer and his team found a different mechanism that produces disease-causing mutations -- the introduction of a chemical base not normally found in DNA that makes it prone to mutation.DNA comprises four chemical bases that exist in pairs -- adenine (A) and thymine (T), and cytosine (C) and guanine (G).

Different sequences of these pairs encode all of the instructions for life. In melanoma, the problem occurs when UVB radiation from the sun hits certain sequences of bases -- CC, TT, TC and CT -- causing them to chemically link together and become unstable. The resulting instability causes a chemical change to cytosine that transforms it into uracil, a chemical base found in the messenger molecule RNA but not in DNA.

This change, called a "premutation," primes the DNA to mutate during normal cell replication, thereby causing alterations that underlie melanoma.These mutations may not cause disease right away. Instead, they may lay dormant for years. They also can accumulate as time goes on and a person's lifetime exposure to sunlight increases, resulting in a tough-to-treat cancer that evades many therapeutic options."Safe sun practices are very important.

In our study, 10-15 minutes of exposure to UVB light was equivalent to what a person would experience at high noon, and was sufficient to cause premutations," Pfeifer said. "While our cells have built-in safeguards to repair DNA damage, this process occasionally lets something slip by. Protecting the skin is generally the best bet when it comes to melanoma prevention."The findings were made possible using a method developed by Pfeifer's lab called Circle Damage Sequencing, which allows scientists to "break" DNA at each point where damage occurs.

They then coax the DNA into circles, which are replicated thousands of times using a technology called PCR. Once they have enough DNA, they use next-generation sequencing to identify which DNA bases are present at the breaks. Going forward, Pfeifer and colleagues plan to use this powerful technique to investigate other types of DNA damage in different kinds of cancer.Other authors include Seung-Gi Jin, Ph.D., Dean Pettinga, Jennifer Johnson and Peipei Li, Ph.D., of VAI.

Story Source. Materials provided by Van Andel Research Institute. Note.

Content may be edited for style and length.UT Southwestern faculty have discovered what appears to be an Achilles' heel in ovarian cancers, as well as new biomarkers that could point to which patients are the best candidates for possible new treatments.The finding, published in the journal Cell, was made in part using a research tool invented in a UT Southwestern lab in the Cecil H. And Ida Green Center for Reproductive Biology Sciences.The research was led by W. Lee Kraus, Ph.D., Professor of Obstetrics and Gynecology and Pharmacology and a member of the Harold C.

Simmons Comprehensive Cancer Center."Many researchers are trying to find dependencies in cancers by asking why a cancer cell amplifies a gene, increases the levels of a protein, or upregulates a critical cellular pathway. These changes give that cancer a selective advantage, but at the same time they can become an Achilles' heel -- something that, if the alteration was blocked, would kill the cancer or stop its growth," he said.Dr. Kraus and his team, including lead author Sridevi Challa, Ph.D., a postdoctoral researcher in the lab, found that ovarian cancers massively amplify an enzyme, NMNAT-2, that makes NAD+.

NAD+ is the substrate for a family of enzymes called PARPs, which chemically modify proteins with ADP-ribose from NAD+. In this study, the team found that one PARP family member, PARP-16, uses NAD+ to modify ribosomes, the protein synthesizing machines of the cell.A challenge for this work was that a single ADP-ribose group attached to a protein is difficult to detect. Dr.

Kraus and his team overcame this problem by developing a synthetic mono(ADP-ribose) detection reagent made up of natural protein domains fused together, which can be used to detect ADP-ribosylated proteins in cells and patient samples. advertisement In collaboration with UT Southwestern clinicians, led by Jayanthi Lea, M.D., Professor of Obstetrics and Gynecology and member of the Simmons Cancer Center, Dr. Kraus and his team screened human ovarian cancer patient samples using the mono(ADP-ribose) detection reagent to identify those with low or high levels of mono(ADP-ribose)."We were able to show that when ribosomes are mono(ADP-ribosyl)ated in ovarian cancer cells, the modification changes the way they translate mRNAs into proteins," Dr.

Kraus said. "The ovarian cancers amplify NMNAT-2 to increase the levels of NAD+ available for PARP-16 to mono(ADP-ribosyl)ate ribosomes, giving them a selective advantage by allowing them to fine-tune the levels of translation and prevent toxic protein aggregation. But that selective advantage also becomes their Achilles' heel.

They're addicted to NMNAT-2, so inhibition or reduction of NMNAT-2 inhibits the growth of the cancer cells."This study identified mono(ADP-ribose) and NMNAT-2 as potential biomarkers for ovarian cancers, which may allow clinicians to determine which ovarian cancer patients may respond well and which will not. Even more ovarian cancer patients might do well if an inhibitor is developed for PARP-16, which blocks ribosome mono(ADP-ribosyl)ation.Dr. Kraus, an expert in PARPs, said medical science has had great success in developing FDA-approved PARP-1 inhibitors, and an inhibitor for PARP-16 is likely."No PARP-16 inhibitors are currently in clinical trials, but labs in academia and the pharmaceutical industry are developing specific and potent inhibitors of PARP-16.

Such a drug could be an effective therapeutic for treating ovarian cancers," he said. advertisement Dr. Kraus is a founder and consultant for Ribon Therapeutics Inc., and ARase Therapeutics Inc.

He is also co-holder of U.S. Patent 9,599,606 covering the mono(ADP-ribose) detection reagent, which has been licensed to and is sold by EMD Millipore."Dr. Kraus' research is not just a great advance in basic science.

It has real promise for clinician investigators and cancer care practitioners because it shows a biomarker and a pathway a future drug could target. The fact that technology developed in his laboratory helped make these findings shows how our faculty builds on their findings to break new ground," said Carlos L. Arteaga, M.D., Director of http://thetrunkseries.com/?p=179 the Simmons Cancer Center.Other researchers who contributed to this study include Beman R.

Khulpateea, Tulip Nandu, Cristel V. Camacho, Keun W. Ryu, Hao Chen, and Yan Peng.The research work was supported by a grant from the National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK069710) as well as funds from the Cecil H.

And Ida Green Center for Reproductive Biology Sciences Endowment to Kraus, and a postdoctoral fellowship from the Ovarian Cancer Research Alliance (GAA202103-0003) to Challa.Dr. Arteaga holds the The Lisa K. Simmons Distinguished Chair in Comprehensive Oncology.

Kraus holds the Cecil H. And Ida Green Distinguished Chair in Reproductive Biology Sciences. Dr.

Lea holds the Patricia Duniven Fletcher Distinguished Professorship in Gynecological Oncology.[embedded content] “CBS This Morning,” in partnership with KHN and NPR, interviews Phil Gaimon, a cyclist who had hoped to be in Tokyo next week as a competitor in the track events on the USA Cycling national team. Instead, a crash on the velodrome track in Pennsylvania in 2019 ended his Olympic dream and left him with huge medical bills — even after his two insurance policies paid portions of the treatment. KHN Editor-in-Chief Elisabeth Rosenthal said Gaimon hit three health care land mines.

Out-of-network hospitals, out-of-state care and gold-plated charges from the hospitals. Two years after the crash, Gaimon is still fielding calls from collection agencies. Related Topics Contact Us Submit a Story TipNot so long ago, laws governing abortion in Massachusetts and Rhode Island were far more restrictive than those in the Deep South, as state legislators throughout New England regularly banned the procedure, no matter the circumstances, during the 1960s and ’70s.

Nowadays, however, the American South represents a hub of anti-abortion fervor, home to a series of laws and regulations that have eroded Roe v. Wade, as liberal states in the Northeast and elsewhere have enacted laws to codify that landmark 1973 Supreme Court decision. How that regional reversal came to pass touches on demographic and ideological shifts, as well as a political environment in which few governors or state legislators anywhere claim to be moderates on the issue.

More than anything, the switch can be traced to religion, and how Christian faiths have in some cases become as polarized on the issue of abortion as the views of elected officials who rely on votes of the religious faithful. Q. Why was famously liberal New England so opposed to abortion?.

Two words. The pope. Daniel Williams, author of “God’s Own Party.

The Making of the Christian Right” and “Defenders of the Unborn. The Pro-Life Movement Before Roe v. Wade,” said that in the early 1970s the strongest opposition to abortion came not from Southern evangelicals but from states with strong Catholic ties in the Northeast.

Even as states like Connecticut and Maine were passing bans, states that were home to large populations of more conservative religious denominations allowed women to safely end pregnancies in cases of rape, incest, fetal deformities and when a woman’s life was at risk. North Carolina was one of the first states to allow for limited legal access to abortion in 1967. Georgia followed in 1968, and South Carolina and Arkansas in 1970.

In Texas, a poll taken in 1970 by the Baptist Standard, the periodical of the Baptist convention, found that 90% of its readers — largely pastors and deacons — believed Texas’ abortion laws were too harsh. Religious scholars say white evangelical Protestants did not support unfettered abortion rights, but without a strong theology about when human life begins, less restrictive abortion laws were not a moral threat. Evangelicals viewed abortion as a Catholic cause.

€œThe general view among Southern evangelicals in the 1960s and early 1970s was that abortion was ethically problematic,” said Williams, who serves as a professor of history at the University of West Georgia. €œBut there was no firm biblical support for the Catholic claim that human life began at conception.” Q. So, why did the South — and Southern evangelicals — change their minds?.

One could say it started offshore. In March 1970, Hawaii became the first state to decriminalize abortion, though the law applied only to state residents. Later that year, New York, then led by a Republican governor, Nelson Rockefeller, and a Republican-dominated legislature, went further, allowing women from any state to receive abortion care.

In 1972, some 200,000 women had legal abortions in New York, and 3 of 5 were from out of state. That alarmed many Southerners, who feared that the procedure was being used — and abused — by unmarried women. €œMany of the Baptists in Texas might have thought if a married woman experienced problems with a pregnancy” she should have the option of a safe, legal abortion, said Williams.

€œThey were not envisioning there would be 200,000. This was clearly not a limited procedure in a small number of instances.” Q. Was it just abortion that worried evangelicals?.

Aversion to women’s rights was not limited to reproductive issues. Disaffected by the sexual revolution and the feminist movement, Christian conservative leaders campaigned against the Equal Rights Amendment. They also battled to protect the tax-exempt status of racially segregated private schools and pushed to ban gay teachers from public schools and restore classroom prayer.

As opposition to abortion among Catholic voters and lawmakers eased, white evangelicals and fundamentalists grew more strident on the issue. By the late 1970s, white evangelicals had fully embraced the position that legal abortion was an assault on moral values. As biblicists, committed to the text of the Bible, evangelical leaders found new meaning in certain verses they believed gave credence to prenatal life.

€œThe connection these conservative evangelicals saw was that when Americans drifted away from God in public life, a change in gender roles came in,” said Williams. €œChristianity was being replaced by secular, humanistic, sexual ethics, and Roe v. Wade became the symbol for all of that.” Q.

What role did politics play in the shift?. A major one. While Catholics are fairly dispersed around the country, white evangelicals are heavily concentrated in Southern states, where true believers often also hold elected office, and thus the power to make laws, said Andrew Lewis, associate professor of political science at the University of Cincinnati.

Mary Ziegler, a professor at Florida State University College of Law and author of “Abortion and the Law in America. Roe v. Wade to the Present,” describes a trifecta that reinforced abortion opposition in the South.

€œThere are a lot of white evangelicals, a lot of Republicans and a lot of gerrymandered swing states,” she said. The acceleration of state-level abortion restrictions arose from grassroots conservative activists and socially conservative state legislators, not from national Republican Party strategists. €œOnce the Republican Party took over the South, it did so largely through the efforts of the Christian Coalition” of America, said Williams.

And that connection between white evangelicals and the GOP intensified as the decades passed. By 2009, white evangelicals made up 35% of the Republican Party. Q.

Where does it all stand now?. Nearly 50 years after the U.S. Supreme Court legalized abortion, the South is the most fervently anti-abortion region in the country.

And year after year, Southern legislatures have outdone one another, passing ever more restrictive measures on abortion care and criminal punishment to those who provide it. For instance, a 99-year prison sentence for doctors who perform abortions in Alabama. A ban on nearly all abortions after 15 weeks of pregnancy in Mississippi and six weeks in Texas.

Rape crisis counselors are subject to lawsuits from private citizens if a woman chooses to end her pregnancy. Few of these laws have taken effect. Most have been struck down or frozen by the courts and, until last month, the Supreme Court declined to consider many of them.

But state legislators, often acting without guidance from national anti-abortion organizations, have continued to introduce anti-abortion bills at a fevered pace. And with the Supreme Court’s rightward shift, many in the movement sense their moment has arrived. The Democratic Party in the South “generally doesn’t fight” abortion restrictions, Williams said.

The party, which counts on the support of Black and Hispanic voters, tends to focus on other priorities, he said. €œThere is much greater interest in talking about health care and jobs.” And while many voters, even conservative ones, have shifted to the left on issues like gay rights, Williams said, younger evangelicals are more likely than their parents to oppose abortion. €œThe Republican Party has a lot of staying power in Georgia and Alabama and across much of the South for the foreseeable future,” Williams said.

Sarah Varney. svarney@kff.org, @SarahVarney4 Related Topics Contact Us Submit a Story Tip.

What may interact with Zithromax?

  • antacids
  • astemizole; digoxin
  • dihydroergotamine
  • ergotamine
  • magnesium salts
  • terfenadine
  • triazolam
  • warfarin

Tell your prescriber or health care professional about all other medicines you are taking, including non-prescription medicines, nutritional supplements, or herbal products. Also tell your prescriber or health care professional if you are a frequent user of drinks with caffeine or alcohol, if you smoke, or if you use illegal drugs. These may affect the way your medicine works. Check with your health care professional before stopping or starting any of your medicines.

Zithromax z pak 250mg side effects

Former Editor-in-Chief of the Postgraduate Medical Journal Dr Barry Ian Hoffbrand died suddenly on April 24, 2020 at the age of 86.A prominent member of zithromax z pak 250mg side effects a generation of very bright young doctors at University College Hospital (UCH) in London who went on to distinguished careers, he was much admired for his keen intellect, clinical perception and skills, gentle good humour and kindly nature, combined with a wonderfully sharp intelligence. Professor Dame Jane Dacre remembered him as ‘a kind, witty, clever man, and a great physician’.He was born in Bradford, West Yorkshire, to Philip Hoffbrand, a bespoke tailor, and Minnie (née Freedman), both from Jewish families from Eastern Europe. After Bradford Grammar School, he went up to read medicine from 1952 zithromax z pak 250mg side effects to 1956 at The Queen’s College, Oxford, where he was a keen member of the college cricket team—the Quondams.

He was pleased to feature in the 1950s on the silver Quondams Cup. Clinical training on a Goldsmid scholarship followed from 1956 to 1958 at UCH Medical School, London, where he was awarded prizes in clinical pathology and haematology. His postgraduate medical training was mainly at UCH, where he was house physician to Max (later Lord) Rosenheim, after an zithromax z pak 250mg side effects initial 6 months at St Luke’s Hospital, Bradford.

He also spent a year as senior research fellow from 1967 to 1968 at the Cardiovascular Research Institute, at the University of California Medical Center in San Francisco. Barry’s research on cardiovascular physiology lead to a DM in 1971 from Oxford University.Barry was appointed in 1970 as a consultant physician at the Whittington Hospital and honorary senior clinical lecturer at UCH Medical School, with interests in general and …INTRODUCTIONAs cardiac arrest occurs in around 20% of the patients with severe buy antibiotics, a large number of them will require immediate resuscitative efforts.1 Cardiopulmonary resuscitation (CPR) in buy antibiotics zithromax has become a source of speculation and debate worldwide. Healthcare professionals (HCPs) resuscitating this subset of patients are subject to fears and enormous mental stress pertaining to risk of transmission, breach in personal protective equipment zithromax z pak 250mg side effects (PPE), unsure effectiveness of PPE and nevertheless bleak positive outcomes in patients despite best resuscitative measures.2 CPR, which is conventionally deemed to be life-saving for patients, appears as an aerosol-generating procedure risking lives of HCPs caring for patients with buy antibiotics.

Protected code blue algorithm has been formulated to address both performer and patient safety.3POCUS-INTEGRATED CPR. WHY THE zithromax z pak 250mg side effects NEED IN buy antibiotics?. Danilo Buonsenso and colleagues have described buy antibiotics era as demanding less stethoscope and more ultrasound usage in clinical practice.4 PPE is now an essential measure for HCP protection, and goggles used as a part of PPE are associated with fogging and poor visibility.

This coupled with the inability to confirm endotracheal tube position with stethoscope due to poor accessibility in PPE, increases the risk of oesophageal intubation, re-intubation attempts, aerosol generation and thus HCP exposure. Bedside ultrasound zithromax z pak 250mg side effects could act as visual stethoscope in the described scenario. Sono-CPR in buy antibiotics can help intervene quickly in treatable cases and reduce the time spent by HCP in futile resuscitative efforts.

Reduced time spent equates to reduced duration of aerosol exposure and thus reduced risk of transmission. Various algorithms are described for sono-cardiopulmonary resuscitation (sono-CPR) during cardiac arrest, zithromax z pak 250mg side effects but none are discussed to address patients with buy antibiotics.5 It would hence be wise to integrate bedside point-of-care ultrasound (POCUS) in the code blue algorithm.HOW THE BEDSIDE TOOL HELPS?. Hypoxemia and respiratory failure attribute over 80% aetiology of cardiac arrest in patients with buy antibiotics.1 Prioritising oxygenation and ventilation using definitive airway and use of high-efficiency particulate air filters reduces airborne transmission, thereby making early intubation the dictum of resuscitation.3 Considering poor visualisation due to fogging with the goggles and face shield, inability to use stethoscope and lack of availability of end-tidal CO2 (EtCO2) in resource constraint settings, ultrasound-guided real-time intubation by trained HCP or endotracheal tube (ETT) placement confirmation post intubation could prove beneficial.

Confirming ETT placement and direct visualisation of oesophagal lumen can be done using a linear ultrasound probe.6 In cases of oesophageal intubation, tissue-air hyperechoic lines are visualised in both trachea and oesophagus, referred to as ‘double-track sign’.State of hypercoagulability zithromax z pak 250mg side effects and myocardial dysfunction exist in patients with buy antibiotics, hence increasing the likelihood of myocardial infarction or pulmonary thromboembolism as aetiologies of cardiac arrest.7 Regional wall motion abnormality, dilated right atrium or right ventricle, plethoric inferior vena cava are easily identified by goal-directed echocardiography. Pneumothorax has been reported in patients with buy antibiotics, and ultrasound can identify absence of lung sliding, helping in quick needle thoracocentesis in arrest and peri-arrest cases. Few cases of cardiac tamponade owing to myopericarditis have also been reported and bedside ultrasound can help diagnose and perform pericardiocentesis in such patients.Literature suggests that the chances of Return Of Spontaneous Circulation (ROSC) and survival to hospital admission at 24 hours is better in patients with baseline cardiac activity rather than no baseline cardiac activity.

In patients with no baseline cardiac activity on arrival, one can withhold CPR, thereby protecting the HCP in this resource-intensive, aerosol-generating futile resuscitative effort.8 Asystole could be the disguised entity of fine ventricular zithromax z pak 250mg side effects fibrillation, which can be confirmed by fibrillatory cardiac activity on transthoracic echocardiography and can be defibrillated, thereby increasing the chances of earlier ROSC.9POCUS-INTEGRATED CPR. THE PROPOSED ALGORITHMCPR is a chaotic scenario, and to prevent added chaos, there is a need for a well-trained ultrasound performer placed in an appropriate area (figure 1). Intubating room needs to consist of minimal necessary number of HCPs, and all of them should be equipped with full PPE.

Ultrasound device could be a potential fomite facilitating cross-transmission zithromax z pak 250mg side effects and requires adequate protection of machine and its components with a transparent cover, sheet or bag. When unavailable, low-level disinfectant solution should be used between each patient.Proposed algorithm for integration of POCUS during CPR in patients with buy antibiotics with team dynamics. The illustration zithromax z pak 250mg side effects is original work of the authors Dr Brunda RL and colleagues.

CPR, cardiopulmonary resuscitation. HCP, healthcare professional. POCUS, point-of-care zithromax z pak 250mg side effects ultrasound.

PPE, personal protective equipment. RA, right atrium. RV, right ventricle zithromax z pak 250mg side effects.

VF, ventricular fibrillation. USG, ultrasonography." data-icon-position data-hide-link-title="0">Figure 1 Proposed algorithm for integration of POCUS during CPR in patients with buy antibiotics with team dynamics. The illustration is original work of zithromax z pak 250mg side effects the authors Dr Brunda RL and colleagues.

CPR, cardiopulmonary resuscitation. HCP, healthcare zithromax z pak 250mg side effects professional. POCUS, point-of-care ultrasound.

PPE, personal protective equipment. RA, right atrium zithromax z pak 250mg side effects. RV, right ventricle.

VF, ventricular fibrillation. USG, ultrasonography.When a patient experiences cardiac arrest, there zithromax z pak 250mg side effects is a need for HCPs with full PPE to check pulse and begin CPR as per standard guidelines. After 2 min of CPR, if there is no ROSC, during the 10 second pause for rhythm assessment, a trained HCP can perform POCUS in a stepwise manner.

Each step needs to be performed individually during 10 zithromax z pak 250mg side effects second pause without prolonging delay between chest compressions and compromising the quality of CPR. Any treatable aetiology identified during the algorithm requires immediate intervention.Step 1. Assess cardiac activity—Sub-xiphoid view can be procured and cardiac activity assessed.

If absent, consider termination of efforts, and if present, resuscitative efforts can be continued.After repeating 2 min cycle zithromax z pak 250mg side effects of CPR, if there has been no ROSC, consider hypoxic aetiology as the cause of arrest in patients with buy antibiotics and intubate without delay. Withholding chest compressions during intubation is recommended.3Step 2. Assess ETT placement—At the level of thyroid gland, above the suprasternal notch, place ultrasound probe transversely and visualise the oesophagus.10 If the posterior wall of oesophagus is obscured by a dark acoustic shadow or if there is ‘double-track’ sign, consider failed endotracheal intubation and perform immediate re-intubation.Step 3.

Assess lung for pneumothorax—Assess lung sliding, and if zithromax z pak 250mg side effects absent look for ‘stratosphere sign’ in M-mode of ultrasound.10 If detected, perform immediate needle thoracocentesis.Step 4. Assess for Cardiac etiology of arrest—Obtain sub-xiphoid window preferably, and look for the presence of cardiac tamponade, chamber dilatation or collapse, regional wall motion abnormality and cardiac contractility.Availability of trained personnel and smaller portable ultrasound devices makes its use during cardiac arrest plausible.CPR with the help of POCUS could thus prove to improve chances of ROSC and also reduced transmission to HCP by early identification, treatment of reversible causes and avoidance of prolonged efforts. Sono-CPR appears to be more HCP-friendly than prolonged blind CPR and necessitates its utility in the era of buy antibiotics addressing performer safety as well as patient safety..

Former Editor-in-Chief of the Postgraduate Medical Journal Dr Barry Ian Hoffbrand died suddenly on April 24, 2020 at the age of 86.A prominent member of a generation of very bright young doctors at University College Hospital (UCH) in London who went on to distinguished where to buy zithromax careers, he was much admired for his keen intellect, clinical perception and skills, gentle good humour and kindly nature, combined with a wonderfully sharp intelligence. Professor Dame Jane Dacre remembered him as ‘a kind, witty, clever man, and a great physician’.He was born in Bradford, West Yorkshire, to Philip Hoffbrand, a bespoke tailor, and Minnie (née Freedman), both from Jewish families from Eastern Europe. After Bradford Grammar School, he went up to read medicine from 1952 to 1956 at The Queen’s College, Oxford, where he was a where to buy zithromax keen member of the college cricket team—the Quondams. He was pleased to feature in the 1950s on the silver Quondams Cup. Clinical training on a Goldsmid scholarship followed from 1956 to 1958 at UCH Medical School, London, where he was awarded prizes in clinical pathology and haematology.

His postgraduate medical training was mainly at UCH, where where to buy zithromax he was house physician to Max (later Lord) Rosenheim, after an initial 6 months at St Luke’s Hospital, Bradford. He also spent a year as senior research fellow from 1967 to 1968 at the Cardiovascular Research Institute, at the University of California Medical Center in San Francisco. Barry’s research on cardiovascular physiology lead to a DM in 1971 from Oxford University.Barry was appointed in 1970 as a consultant physician at the Whittington Hospital and honorary senior clinical lecturer at UCH Medical School, with interests in general and …INTRODUCTIONAs cardiac arrest occurs in around 20% of the patients with severe buy antibiotics, a large number of them will require immediate resuscitative efforts.1 Cardiopulmonary resuscitation (CPR) in buy antibiotics zithromax has become a source of speculation and debate worldwide. Healthcare professionals (HCPs) resuscitating this subset of patients are subject to fears and enormous mental stress pertaining to risk of transmission, breach in personal protective equipment (PPE), unsure effectiveness of PPE and nevertheless bleak positive outcomes in patients despite best resuscitative measures.2 CPR, which is conventionally deemed to be where to buy zithromax life-saving for patients, appears as an aerosol-generating procedure risking lives of HCPs caring for patients with buy antibiotics. Protected code blue algorithm has been formulated to address both performer and patient safety.3POCUS-INTEGRATED CPR.

WHY THE NEED where to buy zithromax IN buy antibiotics?. Danilo Buonsenso and colleagues have described buy antibiotics era as demanding less stethoscope and more ultrasound usage in clinical practice.4 PPE is now an essential measure for HCP protection, and goggles used as a part of PPE are associated with fogging and poor visibility. This coupled with the inability to confirm endotracheal tube position with stethoscope due to poor accessibility in PPE, increases the risk of oesophageal intubation, re-intubation attempts, aerosol generation and thus HCP exposure. Bedside ultrasound where to buy zithromax could act as visual stethoscope in the described scenario. Sono-CPR in buy antibiotics can help intervene quickly in treatable cases and reduce the time spent by HCP in futile resuscitative efforts.

Reduced time spent equates to reduced duration of aerosol exposure and thus reduced risk of transmission. Various algorithms are described for sono-cardiopulmonary resuscitation (sono-CPR) during cardiac arrest, but none are discussed to address patients with buy antibiotics.5 It where to buy zithromax would hence be wise to integrate bedside point-of-care ultrasound (POCUS) in the code blue algorithm.HOW THE BEDSIDE TOOL HELPS?. Hypoxemia and respiratory failure attribute over 80% aetiology of cardiac arrest in patients with buy antibiotics.1 Prioritising oxygenation and ventilation using definitive airway and use of high-efficiency particulate air filters reduces airborne transmission, thereby making early intubation the dictum of resuscitation.3 Considering poor visualisation due to fogging with the goggles and face shield, inability to use stethoscope and lack of availability of end-tidal CO2 (EtCO2) in resource constraint settings, ultrasound-guided real-time intubation by trained HCP or endotracheal tube (ETT) placement confirmation post intubation could prove beneficial. Confirming ETT placement and direct visualisation of oesophagal lumen can be done using a linear ultrasound probe.6 In cases of oesophageal intubation, tissue-air hyperechoic lines are visualised in both trachea and oesophagus, referred to as ‘double-track sign’.State where to buy zithromax of hypercoagulability and myocardial dysfunction exist in patients with buy antibiotics, hence increasing the likelihood of myocardial infarction or pulmonary thromboembolism as aetiologies of cardiac arrest.7 Regional wall motion abnormality, dilated right atrium or right ventricle, plethoric inferior vena cava are easily identified by goal-directed echocardiography. Pneumothorax has been reported in patients with buy antibiotics, and ultrasound can identify absence of lung sliding, helping in quick needle thoracocentesis in arrest and peri-arrest cases.

Few cases of cardiac tamponade owing to myopericarditis have also been reported and bedside ultrasound can help diagnose and perform pericardiocentesis in such patients.Literature suggests that the chances of Return Of Spontaneous Circulation (ROSC) and survival to hospital admission at 24 hours is better in patients with baseline cardiac activity rather than no baseline cardiac activity. In patients with no baseline cardiac activity on arrival, one can withhold CPR, thereby protecting the HCP in this resource-intensive, aerosol-generating futile resuscitative where to buy zithromax effort.8 Asystole could be the disguised entity of fine ventricular fibrillation, which can be confirmed by fibrillatory cardiac activity on transthoracic echocardiography and can be defibrillated, thereby increasing the chances of earlier ROSC.9POCUS-INTEGRATED CPR. THE PROPOSED ALGORITHMCPR is a chaotic scenario, and to prevent added chaos, there is a need for a well-trained ultrasound performer placed in an appropriate area (figure 1). Intubating room needs to consist of minimal necessary number of HCPs, and all of them should be equipped with full PPE. Ultrasound device could be a potential fomite facilitating cross-transmission and requires adequate protection of machine and its components with a transparent cover, where to buy zithromax sheet or bag.

When unavailable, low-level disinfectant solution should be used between each patient.Proposed algorithm for integration of POCUS during CPR in patients with buy antibiotics with team dynamics. The illustration is original work of the authors Dr Brunda RL and where to buy zithromax colleagues. CPR, cardiopulmonary resuscitation. HCP, healthcare professional. POCUS, point-of-care ultrasound where to buy zithromax.

PPE, personal protective equipment. RA, right atrium. RV, right where to buy zithromax ventricle. VF, ventricular fibrillation. USG, ultrasonography." data-icon-position data-hide-link-title="0">Figure 1 Proposed algorithm for integration of POCUS during CPR in patients with buy antibiotics with team dynamics.

The illustration is original work of the authors Dr where to buy zithromax Brunda RL and colleagues. CPR, cardiopulmonary resuscitation. HCP, healthcare where to buy zithromax professional. POCUS, point-of-care ultrasound. PPE, personal protective equipment.

RA, right where to buy zithromax atrium. RV, right ventricle. VF, ventricular fibrillation. USG, ultrasonography.When a patient experiences cardiac arrest, there is a need for HCPs with full PPE to check pulse and begin where to buy zithromax CPR as per standard guidelines. After 2 min of CPR, if there is no ROSC, during the 10 second pause for rhythm assessment, a trained HCP can perform POCUS in a stepwise manner.

Each step needs where to buy zithromax to be performed individually during 10 second pause without prolonging delay between chest compressions and compromising the quality of CPR. Any treatable aetiology identified during the algorithm requires immediate intervention.Step 1. Assess cardiac activity—Sub-xiphoid view can be procured and cardiac activity assessed. If absent, consider termination where to buy zithromax of efforts, and if present, resuscitative efforts can be continued.After repeating 2 min cycle of CPR, if there has been no ROSC, consider hypoxic aetiology as the cause of arrest in patients with buy antibiotics and intubate without delay. Withholding chest compressions during intubation is recommended.3Step 2.

Assess ETT placement—At the level of thyroid gland, above the suprasternal notch, place ultrasound probe transversely and visualise the oesophagus.10 If the posterior wall of oesophagus is obscured by a dark acoustic shadow or if there is ‘double-track’ sign, consider failed endotracheal intubation and perform immediate re-intubation.Step 3. Assess lung for pneumothorax—Assess lung sliding, and if absent look for ‘stratosphere sign’ in M-mode of ultrasound.10 If detected, perform immediate needle where to buy zithromax thoracocentesis.Step 4. Assess for Cardiac etiology of arrest—Obtain sub-xiphoid window preferably, and look for the presence of cardiac tamponade, chamber dilatation or collapse, regional wall motion abnormality and cardiac contractility.Availability of trained personnel and smaller portable ultrasound devices makes its use during cardiac arrest plausible.CPR with the help of POCUS could thus prove to improve chances of ROSC and also reduced transmission to HCP by early identification, treatment of reversible causes and avoidance of prolonged efforts. Sono-CPR appears to be more HCP-friendly than prolonged blind CPR and necessitates its utility in the era of buy antibiotics addressing performer safety as well as patient safety..

Zithromax brand and generic name

The Fairy Meadow community will soon receive its own ambulance station under the NSW Government’s $232 million what do you need to buy zithromax Rural Ambulance Infrastructure Reconfiguration (RAIR) program.Minister for Health Brad Hazzard said Fairy Meadow was identified as the ideal location to base a new station to provide the best ambulance coverage across the Illawarra region, now and in the future.“This is a first for Fairy Meadow, providing paramedics with a modern zithromax brand and generic name facility with state-of-the-art equipment to help them carry out their vital job of saving lives in the local Illawarra communities,” Mr Hazzard said.“The next step will be choosing the best site in Fairy Meadow to build the ambulance station. To do this we have expert help from tried and tested international software which maps Triple Zero calls.”NSW Ambulance Assistant Commissioner Clare Lorenzen said the announcement was another welcome NSW Government initiative for regional and rural communities.“Operating from a new base in Fairy Meadow, our local paramedics will be well positioned to continue to provide the best possible high-quality emergency medical care to residents of local communities,” Ms Lorenzen said.“The additional ambulance service in Fairy Meadow will support the Bulli and Wollongong ambulance stations to strengthen the coverage of the Illawarra region.” zithromax brand and generic name The RAIR program is the single largest investment in regional NSW Ambulance’s 126-year history, with 24 new or upgraded ambulance stations already delivered or under construction as part of the $132 million Stage 1 program. The new station for the Illawarra community is part of the NSW Government’s additional $100 million investment in Stage 2 of the RAIR program.In 2020-21, the NSW Government is investing more than $1 billion in services and capital works for NSW Ambulance.This includes $27 million of funding for 180 new NSW Ambulance staff across NSW, as zithromax brand and generic name part of the third tranche of the June 2018 commitment to recruit 750 additional paramedic and control centre staff over four years.Work has started on installing additional security fencing on the Sydney Trains network to prevent trespassing and reduce self-harm incidents in the rail corridor.Minister for Transport and Roads Andrew Constance said the $4.5 million of new fencing is being installed across 2.3 kilometres of the rail corridor by the end of 2021.“This new fencing will not only improve safety and stop people accessing the rail network illegally, it will also help save lives,” Mr Constance said.“Tragically, 16 people lost their lives on the NSW rail network last year. There were also 155 near misses and 54 people injured from trespassing or entering the Sydney Trains rail corridor.”Minister for Mental Health Bronnie Taylor said any death by suicide is a tragedy that has a profound impact on the whole community.“We know that when we erect physical barriers in identified suicide ‘hot spots’, it significantly reduces the immediate risk to that individual’s life,” Mrs Taylor said.“I encourage anyone who is having suicidal thoughts to seek help, or talk to a trusted friend about their feelings immediately.”Sydney Trains Acting Chief Executive Pete Church said while most of the Sydney Trains network is already fenced, there are a few locations where people have been able to access the rail corridor.“When people trespass in the rail corridor, they not only risk their life, but their actions can have a long lasting impact for their friends and family, as well as our customers and staff,” Mr Church said.TrackSAFE zithromax brand and generic name Executive Director Heather Neil said they work closely with Sydney Trains to raise awareness of rail safety issues, and to reduce near misses on the rail network.“Reducing accessibility to train lines through the installation of fences and other physical barriers is known to be a successful method of reducing trespass and self-harm incidents,” Ms Neil said.There were more than 2,600 trespassing incidents on the network, including nine people caught train surfing, in the 2019-20 financial year. The minimum fine for trespassing is $400 but can be as high as $5,500.Other Sydney Trains initiatives to prevent trespassing and self-harm incidents include:Training for frontline staff to help them recognise the warning signs for suicide.Emergency help points on every platform, which are directly linked to trained security operators 24 hours a day.More than 12,000 CCTV cameras monitoring the network, including high-definition cameras with stronger capabilities to identify trespassers.If you, or someone you know, is thinking about suicide or experiencing a personal crisis or zithromax brand and generic name distress, please seek help immediately by calling 000 or one of these services:Lifeline 13 11 14Suicide Call Back Service 1300 659 467NSW Mental Health Line 1800 011 511.

The Fairy Meadow community will soon receive its own ambulance station under the NSW Government’s $232 million Rural Ambulance Infrastructure Reconfiguration (RAIR) program.Minister for Health Brad Hazzard said where to buy zithromax Fairy Meadow was identified as the ideal location to base a new station zithromax 500mg cost to provide the best ambulance coverage across the Illawarra region, now and in the future.“This is a first for Fairy Meadow, providing paramedics with a modern facility with state-of-the-art equipment to help them carry out their vital job of saving lives in the local Illawarra communities,” Mr Hazzard said.“The next step will be choosing the best site in Fairy Meadow to build the ambulance station. To do this we have expert help from tried and tested international software which maps Triple Zero calls.”NSW Ambulance Assistant Commissioner Clare Lorenzen said the announcement was another welcome NSW Government initiative for regional and where to buy zithromax rural communities.“Operating from a new base in Fairy Meadow, our local paramedics will be well positioned to continue to provide the best possible high-quality emergency medical care to residents of local communities,” Ms Lorenzen said.“The additional ambulance service in Fairy Meadow will support the Bulli and Wollongong ambulance stations to strengthen the coverage of the Illawarra region.” The RAIR program is the single largest investment in regional NSW Ambulance’s 126-year history, with 24 new or upgraded ambulance stations already delivered or under construction as part of the $132 million Stage 1 program. The new station for the http://hid-design.de/2017/12/22/nymphenburg/ Illawarra community is part of the NSW Government’s additional $100 million investment in Stage 2 of the RAIR program.In 2020-21, the NSW Government is investing more than $1 billion in services and capital works for NSW Ambulance.This includes $27 million of funding for 180 new NSW Ambulance staff across NSW, as part of the third tranche of the June 2018 commitment to recruit 750 additional paramedic and control centre staff over four years.Work has started on installing additional security fencing on the Sydney Trains network to prevent trespassing and reduce self-harm incidents in the rail corridor.Minister for Transport and Roads Andrew Constance said the $4.5 million of new fencing is being installed across 2.3 kilometres of the rail corridor by the end of 2021.“This new fencing will not only improve safety and stop people accessing the rail network illegally, it will also help save lives,” Mr Constance said.“Tragically, 16 people lost where to buy zithromax their lives on the NSW rail network last year. There were also 155 near misses and 54 people injured from trespassing or entering the Sydney where to buy zithromax Trains rail corridor.”Minister for Mental Health Bronnie Taylor said any death by suicide is a tragedy that has a profound impact on the whole community.“We know that when we erect physical barriers in identified suicide ‘hot spots’, it significantly reduces the immediate risk to that individual’s life,” Mrs Taylor said.“I encourage anyone who is having suicidal thoughts to seek help, or talk to a trusted friend about their feelings immediately.”Sydney Trains Acting Chief Executive Pete Church said while most of the Sydney Trains network is already fenced, there are a few locations where people have been able to access the rail corridor.“When people trespass in the rail corridor, they not only risk their life, but their actions can have a long lasting impact for their friends and family, as well as our customers and staff,” Mr Church said.TrackSAFE Executive Director Heather Neil said they work closely with Sydney Trains to raise awareness of rail safety issues, and to reduce near misses on the rail network.“Reducing accessibility to train lines through the installation of fences and other physical barriers is known to be a successful method of reducing trespass and self-harm incidents,” Ms Neil said.There were more than 2,600 trespassing incidents on the network, including nine people caught train surfing, in the 2019-20 financial year. The minimum fine for trespassing is $400 but can be as high as $5,500.Other Sydney Trains initiatives to prevent trespassing and self-harm incidents include:Training for frontline staff to help them recognise the warning signs for suicide.Emergency help points on every platform, which are directly linked to trained security operators 24 hours a day.More than 12,000 CCTV cameras monitoring the network, including high-definition cameras with stronger capabilities to identify trespassers.If you, or someone you know, is thinking about suicide or experiencing where to buy zithromax a personal crisis or distress, please seek help immediately by calling 000 or one of these services:Lifeline 13 11 14Suicide Call Back Service 1300 659 467NSW Mental Health Line 1800 011 511.

Zithromax generic cost

Protecting the Buy kamagra london safety and health zithromax generic cost of essential workers who support America’s food security—including the meat, poultry, and pork processing industries—is a top priority for the Occupational Safety and Health Administration (OSHA). OSHA and the Centers for Disease Control and Prevention issued additional guidance to reduce the risk of exposure to the antibiotics and keep workers safe and healthy in the meatpacking and meat processing industries —including those involved in beef, pork, and poultry operations. This new guidance provides specific recommendations for employers to meet their obligations to protect workers in these facilities, zithromax generic cost where people normally work closely together and share workspaces and equipment. Here are eight ways to help minimize meat processing workers’ exposure to the antibiotics.

Screen workers before they enter the workplace. If a worker becomes sick, send them home zithromax generic cost and disinfect their workstation and any tools they used. Move workstations farther apart. Install partitions between workstations using strip curtains, plexiglass, or zithromax generic cost similar materials.

To limit spread between groups, assign the same workers to the same shifts with the same coworkers. Prevent workers from using other workers’ equipment. Allow workers to wear zithromax generic cost face coverings when entering, inside, and exiting the facility. Encourage workers to report any safety and health concerns to their supervisors.

OSHA is committed to ensuring that workers and employers in essential industries zithromax generic cost have clear guidance to keep workers safe and healthy from the antibiotics—including guidance for essential workers in construction, manufacturing, package delivery, and retail. Workers and employers who have questions or concerns about workplace safety can contact OSHA online or by phone at 1-800-321-6742 (OSHA). You can find additional resources and learn more about OSHA’s response to the antibiotics at www.osha.gov/antibiotics. Loren Sweatt is the Principal Deputy Assistant Secretary for zithromax generic cost the U.S.

Department of Labor’s Occupation Safety and Health Administration Editor’s Note. It is important to note that information and guidance zithromax generic cost about buy antibiotics continually evolve as conditions change. Workers and employers are encouraged to regularly refer to the resources below for updates:The Derda family following a promotion ceremony on Sept. 2, 2020, at Camp Murray, Washington.

Photo. National GuardWith the holiday season here, there is no better time to reflect on our blessings and show our appreciation for the people who keep our nation safe. As we close out National Veterans and Military Families Appreciation Month, we want to recognize the sacrifices of the men and women who protect our freedom and their families. There are 1.9 million women veterans, according to the Bureau of Labor Statistics.

Of nearly 1 million military spouses, nearly 92% are women and three-quarters have children at home. The U.S. Department of Labor has a number of initiatives that benefit veterans and military spouses. One is promoting occupational licensing reform, which can help more military spouses and veterans get good jobs when they move across state lines.

In 2018, the U.S. Department of Labor provided $7 million in grants to help states review and streamline their occupational licensing rules, including $1.5 million to help transitioning service members and veterans meet educational requirements for employment in selected licensed occupations. Throughout 2019, the Department’s Women’s Bureau hosted listening sessions to learn more about the unique challenges facing military spouses and their employment options. These listening sessions provided insights on occupational licensing reform, expanding Transition Assistance Program offerings for military spouses, and the kinds of resources we can provide to employers that will best assist military families.

In 2020, it became increasingly clear that career reentry is a top consideration for military spouses, as for many women. Military spouses represent a tremendous talent pool that employers should consider. That’s why the Women’s Bureau worked closely this year with the Department’s Veterans’ Employment and Training Service to develop four pilot courses for military spouses on entering the workforce or experiencing a career change. And this November, we hosted a webinar, “What You Need to Know about Hiring Military Spouses,” with Elizabeth Larsen from Hiring Our Heroes and Carol Fishman Cohen of iRelaunch, to share resources to help employers connect with women veterans and military spouses.

As the workforce changes, so does the need for employment opportunities for veterans and military spouses. Many are highly skilled and can help sustain and strengthen America’s economic recovery. We encourage everyone to join us in honoring veterans and expressing our gratitude for the military families whose support makes their loved one’s service possible. Visit our website to learn more about the Women’s Bureau and our centennial initiative.

Dol.gov/wb. The U.S. Department of Labor offers employment resources for military spouses. Laurie Todd-Smith, Ph.D., is the director of the U.S.

Department of Labor’s Women’s Bureau. Follow the Women’s Bureau on Twitter at @WB_DOL..

Protecting the this page safety and health of essential workers who support America’s food security—including the meat, poultry, where to buy zithromax and pork processing industries—is a top priority for the Occupational Safety and Health Administration (OSHA). OSHA and the Centers for Disease Control and Prevention issued additional guidance to reduce the risk of exposure to the antibiotics and keep workers safe and healthy in the meatpacking and meat processing industries —including those involved in beef, pork, and poultry operations. This new guidance provides specific recommendations for employers to meet their obligations to where to buy zithromax protect workers in these facilities, where people normally work closely together and share workspaces and equipment.

Here are eight ways to help minimize meat processing workers’ exposure to the antibiotics. Screen workers before they enter the workplace. If a worker becomes sick, send them home and disinfect their workstation and any tools they used where to buy zithromax.

Move workstations farther apart. Install partitions between workstations using strip where to buy zithromax curtains, plexiglass, or similar materials. To limit spread between groups, assign the same workers to the same shifts with the same coworkers.

Prevent workers from using other workers’ equipment. Allow workers to wear face coverings when where to buy zithromax entering, inside, and exiting the facility. Encourage workers to report any safety and health concerns to their supervisors.

OSHA is committed to ensuring that workers and employers in essential industries have clear guidance to keep workers safe and healthy where to buy zithromax from the antibiotics—including guidance for essential workers in construction, manufacturing, package delivery, and retail. Workers and employers who have questions or concerns about workplace safety can contact OSHA online or by phone at 1-800-321-6742 (OSHA). You can find additional resources and learn more about OSHA’s response to the antibiotics at www.osha.gov/antibiotics.

Loren Sweatt where to buy zithromax is the Principal Deputy Assistant Secretary for the U.S. Department of Labor’s Occupation Safety and Health Administration Editor’s Note. It is important to note that information and guidance about buy antibiotics continually evolve where to buy zithromax as conditions change.

Workers and employers are encouraged to regularly refer to the resources below for updates:The Derda family following a promotion ceremony on Sept. 2, 2020, at Camp Murray, Washington. Photo.

National GuardWith the holiday season here, there is no better time to reflect on our blessings and show our appreciation for the people who keep our nation safe. As we close out National Veterans and Military Families Appreciation Month, we want to recognize the sacrifices of the men and women who protect our freedom and their families. There are 1.9 million women veterans, according to the Bureau of Labor Statistics.

Of nearly 1 million military spouses, nearly 92% are women and three-quarters have children at home. The U.S. Department of Labor has a number of initiatives that benefit veterans and military spouses.

One is promoting occupational licensing reform, which can help more military spouses and veterans get good jobs when they move across state lines. In 2018, the U.S. Department of Labor provided $7 million in grants to help states review and streamline their occupational licensing rules, including $1.5 million to help transitioning service members and veterans meet educational requirements for employment in selected licensed occupations.

Throughout 2019, the Department’s Women’s Bureau hosted listening sessions to learn more about the unique challenges facing military spouses and their employment options. These listening sessions provided insights on occupational licensing reform, expanding Transition Assistance Program offerings for military spouses, and the kinds of resources we can provide to employers that will best assist military families. In 2020, it became increasingly clear that career reentry is a top consideration for military spouses, as for many women.

Military spouses represent a tremendous talent pool that employers should consider. That’s why the Women’s Bureau worked closely this year with the Department’s Veterans’ Employment and Training Service to develop four pilot courses for military spouses on entering the workforce or experiencing a career change. And this November, we hosted a webinar, “What You Need to Know about Hiring Military Spouses,” with Elizabeth Larsen from Hiring Our Heroes and Carol Fishman Cohen of iRelaunch, to share resources to help employers connect with women veterans and military spouses.

As the workforce changes, so does the need for employment opportunities for veterans and military spouses. Many are highly skilled and can help sustain and strengthen America’s economic recovery. We encourage everyone to join us in honoring veterans and expressing our gratitude for the military families whose support makes their loved one’s service possible.

Visit our website to learn more about the Women’s Bureau and our centennial initiative. Dol.gov/wb. The U.S.

Department of Labor offers employment resources for military spouses. Laurie Todd-Smith, Ph.D., is the director of the U.S. Department of Labor’s Women’s Bureau.

Follow the Women’s Bureau on Twitter at @WB_DOL..

Zithromax online canada

How to cite this zithromax online canada article:Singh O view website P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide zithromax online canada is one of the highly publicized events in our country.

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

All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed zithromax online canada 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 zithromax online canada from their patients in despair with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health zithromax online canada 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 zithromax online canada 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 urgent need for zithromax online canada training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident.

Many psychiatrists and mental health professionals were called by media houses to comment zithromax online canada 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 zithromax online canada of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. 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 zithromax online canada information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

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

It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, zithromax online canada 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, zithromax online canada 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. Part I. A perspective on the evolution and current practice of ECT.

J Psychiatr Pract 2009;15:346-68. 2.Lauber C, Nordt C, Falcato L, Rössler W. Can a seizure help?.

The public's attitude toward electroconvulsive therapy. Psychiatry Res 2005;134:205-9. 3.Stefanazzi M.

Is electroconvulsive therapy (ECT) ever ethically justified?. If so, under what circumstances. HEC Forum 2013;25:79-94.

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

5.Devanand DP. Does electroconvulsive therapy damage brain cells?. Semin Neurol 1995;15:351-7.

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

Oxford, England. New York. Oxford University Press.

1996. 7.Collin PH. Dictionary of Medical Terms.

2004. 8.Hajdu SI. Entries on laboratory medicine in the first illustrated medical dictionary.

Ann Clin Lab Sci 2005;35:465-8. 9.Mander AJ, Whitfield A, Kean DM, Smith MA, Douglas RH, Kendell RE. Cerebral and brain stem changes after ECT revealed by nuclear magnetic resonance imaging.

Br J Psychiatry 1987;151:69-71. 10.Coffey CE, Weiner RD, Djang WT, Figiel GS, Soady SA, Patterson LJ, et al. Brain anatomic effects of electroconvulsive therapy.

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

Time course of cerebral magnetic resonance changes after electroconvulsive therapy. Br J Psychiatry 1990;156:551-3. 12.Pande AC, Grunhaus LJ, Aisen AM, Haskett RF.

A preliminary magnetic resonance imaging study of ECT-treated depressed patients. Biol Psychiatry 1990;27:102-4. 13.Coffey CE, Figiel GS, Djang WT, Sullivan DC, Herfkens RJ, Weiner RD.

Effects of ECT on brain structure. A pilot prospective magnetic resonance imaging study. Am J Psychiatry 1988;145:701-6.

14.Qiu H, Li X, Zhao W, Du L, Huang P, Fu Y, et al. Electroconvulsive therapy-Induced brain structural and functional changes in major depressive disorders. A longitudinal study.

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

Indian J Psychiatry 2007;49:195-9. [PUBMED] [Full text] 16.Pirnia T, Joshi SH, Leaver AM, Vasavada M, Njau S, Woods RP, et al. Electroconvulsive therapy and structural neuroplasticity in neocortical, limbic and paralimbic cortex.

Transl Psychiatry 2016;6:e832. 17.Szabo K, Hirsch JG, Krause M, Ende G, Henn FA, Sartorius A, et al. Diffusion weighted MRI in the early phase after electroconvulsive therapy.

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

A volumetric magnetic resonance imaging study. J ECT 2010;26:62-7. 19.Nordanskog P, Larsson MR, Larsson EM, Johanson A.

Hippocampal volume in relation to clinical and cognitive outcome after electroconvulsive therapy in depression. Acta Psychiatr Scand 2014;129:303-11. 20.Tendolkar I, van Beek M, van Oostrom I, Mulder M, Janzing J, Voshaar RO, et al.

Electroconvulsive therapy increases hippocampal and amygdala volume in therapy refractory depression. A longitudinal pilot study. Psychiatry Res 2013;214:197-203.

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

22.Abbott CC, Jones T, Lemke NT, Gallegos P, McClintock SM, Mayer AR, et al. Hippocampal structural and functional changes associated with electroconvulsive therapy response. Transl Psychiatry 2014;4:e483.

23.Lyden H, Espinoza RT, Pirnia T, Clark K, Joshi SH, Leaver AM, et al. Electroconvulsive therapy mediates neuroplasticity of white matter microstructure in major depression. Transl Psychiatry 2014;4:e380.

24.Bouckaert F, De Winter FL, Emsell L, Dols A, Rhebergen D, Wampers M, et al. Grey matter volume increase following electroconvulsive therapy in patients with late life depression. A longitudinal MRI study.

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

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

Neural Plast 2015;2015:271674. 27.van Eijndhoven P, Mulders P, Kwekkeboom L, van Oostrom I, van Beek M, Janzing J, et al. Bilateral ECT induces bilateral increases in regional cortical thickness.

Transl Psychiatry 2016;6:e874. 28.Bouckaert F, Dols A, Emsell L, De Winter FL, Vansteelandt K, Claes L, et al. Relationship between hippocampal volume, serum BDNF, and depression severity following electroconvulsive therapy in late-life depression.

Neuropsychopharmacology 2016;41:2741-8. 29.Depping MS, Nolte HM, Hirjak D, Palm E, Hofer S, Stieltjes B, et al. Cerebellar volume change in response to electroconvulsive therapy in patients with major depression.

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

Biol Psychiatry 2016;79:282-92. 31.Wade BS, Joshi SH, Njau S, Leaver AM, Vasavada M, Woods RP, et al. Effect of electroconvulsive therapy on striatal morphometry in major depressive disorder.

Neuropsychopharmacology 2016;41:2481-91. 32.Wolf RC, Nolte HM, Hirjak D, Hofer S, Seidl U, Depping MS, et al. Structural network changes in patients with major depression and schizophrenia treated with electroconvulsive therapy.

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

A proton magnetic resonance spectroscopic imaging study. Arch Gen Psychiatry 2000;57:937-43. 34.Michael N, Erfurth A, Ohrmann P, Arolt V, Heindel W, Pfleiderer B.

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

Neurotrophic effects of electroconvulsive therapy. A proton magnetic resonance study of the left amygdalar region in patients with treatment-resistant depression. Neuropsychopharmacology 2003;28:720-5.

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

37.Merkl A, Schubert F, Quante A, Luborzewski A, Brakemeier EL, Grimm S, et al. Abnormal cingulate and prefrontal cortical neurochemistry in major depression after electroconvulsive therapy. Biol Psychiatry 2011;69:772-9.

38.Jorgensen A, Magnusson P, Hanson LG, Kirkegaard T, Benveniste H, Lee H, et al. Regional brain volumes, diffusivity, and metabolite changes after electroconvulsive therapy for severe depression. Acta Psychiatr Scand 2016;133:154-64.

39.Njau S, Joshi SH, Espinoza R, Leaver AM, Vasavada M, Marquina A, et al. Neurochemical correlates of rapid treatment response to electroconvulsive therapy in patients with major depression. J Psychiatry Neurosci 2017;42:6-16.

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

Transl Psychiatry 2017;7:e1023. 41.Figiel GS, Krishnan KR, Doraiswamy PM. Subcortical structural changes in ECT-induced delirium.

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

Shocking relations. Neural Plast 2014;2014:723915. 43.Singh A, Kar SK.

How electroconvulsive therapy works?. Understanding the neurobiological mechanisms. Clin Psychopharmacol Neurosci 2017;15:210-21.

44.Gbyl K, Videbech P. Electroconvulsive therapy increases brain volume in major depression. A systematic review and meta-analysis.

Acta Psychiatr Scand 2018;138:180-95. 45.Oltedal L, Narr KL, Abbott C, Anand A, Argyelan M, Bartsch H, et al. Volume of the human hippocampus and clinical response following electroconvulsive therapy.

Biol Psychiatry 2018;84:574-81. 46.Breggin PR. Brain-Disabling Treatments in Psychiatry.

Drugs, Electroshock, and the Role of the FDA. New York. Springer Pub.

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

MR spectroscopic imaging. Principles and recent advances. J Magn Reson Imaging 2013;37:1301-25.

48.Simmons ML, Frondoza CG, Coyle JT. Immunocytochemical localization of N-acetyl-aspartate with monoclonal antibodies. Neuroscience 1991;45:37-45.

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

50.Bramham CR, Messaoudi E. BDNF function in adult synaptic plasticity. The synaptic consolidation hypothesis.

Prog Neurobiol 2005;76:99-125. 51.Duman RS, Monteggia LM. A neurotrophic model for stress-related mood disorders.

Biol Psychiatry 2006;59:1116-27. 52.Bocchio-Chiavetto L, Bagnardi V, Zanardini R, Molteni R, Nielsen MG, Placentino A, et al. Serum and plasma BDNF levels in major depression.

A replication study and meta-analyses. World J Biol Psychiatry 2010;11:763-73. 53.Brunoni AR, Lopes M, Fregni F.

A systematic review and meta-analysis of clinical studies on major depression and BDNF levels. Implications for the role of neuroplasticity in depression. Int J Neuropsychopharmacol 2008;11:1169-80.

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

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

A systematic review and meta-analysis. Lancet 2003;361:799-808. 56.57.Semkovska M, McLoughlin DM.

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

58.Tulving E, Madigan SA. Memory and verbal learning. Annu Rev Psychol 1970;21:437-84.

59.Rose D, Fleischmann P, Wykes T, Leese M, Bindman J. Patients' perspectives on electroconvulsive therapy. Systematic review.

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

Historical perspective and current issues. J ECT 2013;29:127-33. 61.Fraser LM, O'Carroll RE, Ebmeier KP.

The effect of electroconvulsive therapy on autobiographical memory. A systematic review. J ECT 2008;24:10-7.

62.Squire LR, Chace PM. Memory functions six to nine months after electroconvulsive therapy. Arch Gen Psychiatry 1975;32:1557-64.

63.Squire LR, Slater PC. Electroconvulsive therapy and complaints of memory dysfunction. A prospective three-year follow-up study.

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

Long-term follow-up. Arch Gen Psychiatry 1981;38:89-95. 65.Squire LR, Wetzel CD, Slater PC.

Memory complaint after electroconvulsive therapy. Assessment with a new self-rating instrument. Biol Psychiatry 1979;14:791-801.

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

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

68.Abrams R. Does brief-pulse ECT cause persistent or permanent memory impairment?. J ECT 2002;18:71-3.

69.Peretti CS, Danion JM, Grangé D, Mobarek N. Bilateral ECT and autobiographical memory of subjective experiences related to melancholia. A pilot study.

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

Ann N Y Acad Sci 1986;462:315-25. 71.Prudic J, Peyser S, Sackeim HA. Subjective memory complaints.

A review of patient self-assessment of memory after electroconvulsive therapy. J ECT 2000;16:121-32. 72.Sackeim HA, Prudic J, Devanand DP, Kiersky JE, Fitzsimons L, Moody BJ, et al.

Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 1993;328:839-46. 73.Frith CD, Stevens M, Johnstone EC, Deakin JF, Lawler P, Crow TJ.

Effects of ECT and depression on various aspects of memory. Br J Psychiatry 1983;142:610-7. 74.Ng C, Schweitzer I, Alexopoulos P, Celi E, Wong L, Tuckwell V, et al.

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

Subjective memory complaints prior to and following electroconvulsive therapy. Biol Psychiatry 1996;39:346-56. 76.Berggren Š, Gustafson L, Höglund P, Johanson A.

A long-term longitudinal follow-up of depressed patients treated with ECT with special focus on development of dementia. J Affect Disord 2016;200:15-24. 77.Brodaty H, Hickie I, Mason C, Prenter L.

A prospective follow-up study of ECT outcome in older depressed patients. J Affect Disord 2000;60:101-11. 78.Osler M, Rozing MP, Christensen GT, Andersen PK, Jørgensen MB.

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

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

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

How to cite this http://www.adhvikdecor.com/purchase-antabuse/ article:Singh where to buy zithromax O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized events in our where to buy zithromax country.

Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went into a frenzy as newspapers, news channels, and social media were full of stories providing minute details of where to buy zithromax 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, where to buy zithromax reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident.

Psychiatrists suddenly started getting distress calls from where to buy zithromax their patients in despair with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without where to buy zithromax his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and illness and also his relationships and where to buy zithromax 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, where to buy zithromax 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 where to buy zithromax called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so. There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist.

These types of viewpoints perpetuate where to buy zithromax 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 where to buy zithromax reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

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

It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the where to buy zithromax 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 where to buy zithromax of Support. None, Conflict of Interest. NoneDOI.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Electroconvulsive therapy. Part I. A perspective on the evolution and current practice of ECT.

J Psychiatr Pract 2009;15:346-68. 2.Lauber C, Nordt C, Falcato L, Rössler W. Can a seizure help?.

The public's attitude toward electroconvulsive therapy. Psychiatry Res 2005;134:205-9. 3.Stefanazzi M.

Is electroconvulsive therapy (ECT) ever ethically justified?. If so, under what circumstances. HEC Forum 2013;25:79-94.

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

5.Devanand DP. Does electroconvulsive therapy damage brain cells?. Semin Neurol 1995;15:351-7.

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

Oxford, England. New York. Oxford University Press.

1996. 7.Collin PH. Dictionary of Medical Terms.

2004. 8.Hajdu SI. Entries on laboratory medicine in the first illustrated medical dictionary.

Ann Clin Lab Sci 2005;35:465-8. 9.Mander AJ, Whitfield A, Kean DM, Smith MA, Douglas RH, Kendell RE. Cerebral and brain stem changes after ECT revealed by nuclear magnetic resonance imaging.

Br J Psychiatry 1987;151:69-71. 10.Coffey CE, Weiner RD, Djang WT, Figiel GS, Soady SA, Patterson LJ, et al. Brain anatomic effects of electroconvulsive therapy.

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

Time course of cerebral magnetic resonance changes after electroconvulsive therapy. Br J Psychiatry 1990;156:551-3. 12.Pande AC, Grunhaus LJ, Aisen AM, Haskett RF.

A preliminary magnetic resonance imaging study of ECT-treated depressed patients. Biol Psychiatry 1990;27:102-4. 13.Coffey CE, Figiel GS, Djang WT, Sullivan DC, Herfkens RJ, Weiner RD.

Effects of ECT on brain structure. A pilot prospective magnetic resonance imaging study. Am J Psychiatry 1988;145:701-6.

14.Qiu H, Li X, Zhao W, Du L, Huang P, Fu Y, et al. Electroconvulsive therapy-Induced brain structural and functional changes in major depressive disorders. A longitudinal study.

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

Indian J Psychiatry 2007;49:195-9. [PUBMED] [Full text] 16.Pirnia T, Joshi SH, Leaver AM, Vasavada M, Njau S, Woods RP, et al. Electroconvulsive therapy and structural neuroplasticity in neocortical, limbic and paralimbic cortex.

Transl Psychiatry 2016;6:e832. 17.Szabo K, Hirsch JG, Krause M, Ende G, Henn FA, Sartorius A, et al. Diffusion weighted MRI in the early phase after electroconvulsive therapy.

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

A volumetric magnetic resonance imaging study. J ECT 2010;26:62-7. 19.Nordanskog P, Larsson MR, Larsson EM, Johanson A.

Hippocampal volume in relation to clinical and cognitive outcome after electroconvulsive therapy in depression. Acta Psychiatr Scand 2014;129:303-11. 20.Tendolkar I, van Beek M, van Oostrom I, Mulder M, Janzing J, Voshaar RO, et al.

Electroconvulsive therapy increases hippocampal and amygdala volume in therapy refractory depression. A longitudinal pilot study. Psychiatry Res 2013;214:197-203.

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

22.Abbott CC, Jones T, Lemke NT, Gallegos P, McClintock SM, Mayer AR, et al. Hippocampal structural and functional changes associated with electroconvulsive therapy response. Transl Psychiatry 2014;4:e483.

23.Lyden H, Espinoza RT, Pirnia T, Clark K, Joshi SH, Leaver AM, et al. Electroconvulsive therapy mediates neuroplasticity of white matter microstructure in major depression. Transl Psychiatry 2014;4:e380.

24.Bouckaert F, De Winter FL, Emsell L, Dols A, Rhebergen D, Wampers M, et al. Grey matter volume increase following electroconvulsive therapy in patients with late life depression. A longitudinal MRI study.

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

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

Neural Plast 2015;2015:271674. 27.van Eijndhoven P, Mulders P, Kwekkeboom L, van Oostrom I, van Beek M, Janzing J, et al. Bilateral ECT induces bilateral increases in regional cortical thickness.

Transl Psychiatry 2016;6:e874. 28.Bouckaert F, Dols A, Emsell L, De Winter FL, Vansteelandt K, Claes L, et al. Relationship between hippocampal volume, serum BDNF, and depression severity following electroconvulsive therapy in late-life depression.

Neuropsychopharmacology 2016;41:2741-8. 29.Depping MS, Nolte HM, Hirjak D, Palm E, Hofer S, Stieltjes B, et al. Cerebellar volume change in response to electroconvulsive therapy in patients with major depression.

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

Biol Psychiatry 2016;79:282-92. 31.Wade BS, Joshi SH, Njau S, Leaver AM, Vasavada M, Woods RP, et al. Effect of electroconvulsive therapy on striatal morphometry in major depressive disorder.

Neuropsychopharmacology 2016;41:2481-91. 32.Wolf RC, Nolte HM, Hirjak D, Hofer S, Seidl U, Depping MS, et al. Structural network changes in patients with major depression and schizophrenia treated with electroconvulsive therapy.

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

A proton magnetic resonance spectroscopic imaging study. Arch Gen Psychiatry 2000;57:937-43. 34.Michael N, Erfurth A, Ohrmann P, Arolt V, Heindel W, Pfleiderer B.

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

Neurotrophic effects of electroconvulsive therapy. A proton magnetic resonance study of the left amygdalar region in patients with treatment-resistant depression. Neuropsychopharmacology 2003;28:720-5.

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

37.Merkl A, Schubert F, Quante A, Luborzewski A, Brakemeier EL, Grimm S, et al. Abnormal cingulate and prefrontal cortical neurochemistry in major depression after electroconvulsive therapy. Biol Psychiatry 2011;69:772-9.

38.Jorgensen A, Magnusson P, Hanson LG, Kirkegaard T, Benveniste H, Lee H, et al. Regional brain volumes, diffusivity, and metabolite changes after electroconvulsive therapy for severe depression. Acta Psychiatr Scand 2016;133:154-64.

39.Njau S, Joshi SH, Espinoza R, Leaver AM, Vasavada M, Marquina A, et al. Neurochemical correlates of rapid treatment response to electroconvulsive therapy in patients with major depression. J Psychiatry Neurosci 2017;42:6-16.

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

Transl Psychiatry 2017;7:e1023. 41.Figiel GS, Krishnan KR, Doraiswamy PM. Subcortical structural changes in ECT-induced delirium.

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

Shocking relations. Neural Plast 2014;2014:723915. 43.Singh A, Kar SK.

How electroconvulsive therapy works?. Understanding the neurobiological mechanisms. Clin Psychopharmacol Neurosci 2017;15:210-21.

44.Gbyl K, Videbech P. Electroconvulsive therapy increases brain volume in major depression. A systematic review and meta-analysis.

Acta Psychiatr Scand 2018;138:180-95. 45.Oltedal L, Narr KL, Abbott C, Anand A, Argyelan M, Bartsch H, et al. Volume of the human hippocampus and clinical response following electroconvulsive therapy.

Biol Psychiatry 2018;84:574-81. 46.Breggin PR. Brain-Disabling Treatments in Psychiatry.

Drugs, Electroshock, and the Role of the FDA. New York. Springer Pub.

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

MR spectroscopic imaging. Principles and recent advances. J Magn Reson Imaging 2013;37:1301-25.

48.Simmons ML, Frondoza CG, Coyle JT. Immunocytochemical localization of N-acetyl-aspartate with monoclonal antibodies. Neuroscience 1991;45:37-45.

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

50.Bramham CR, Messaoudi E. BDNF function in adult synaptic plasticity. The synaptic consolidation hypothesis.

Prog Neurobiol 2005;76:99-125. 51.Duman RS, Monteggia LM. A neurotrophic model for stress-related mood disorders.

Biol Psychiatry 2006;59:1116-27. 52.Bocchio-Chiavetto L, Bagnardi V, Zanardini R, Molteni R, Nielsen MG, Placentino A, et al. Serum and plasma BDNF levels in major depression.

A replication study and meta-analyses. World J Biol Psychiatry 2010;11:763-73. 53.Brunoni AR, Lopes M, Fregni F.

A systematic review and meta-analysis of clinical studies on major depression and BDNF levels. Implications for the role of neuroplasticity in depression. Int J Neuropsychopharmacol 2008;11:1169-80.

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

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

A systematic review and meta-analysis. Lancet 2003;361:799-808. 56.57.Semkovska M, McLoughlin DM.

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

58.Tulving E, Madigan SA. Memory and verbal learning. Annu Rev Psychol 1970;21:437-84.

59.Rose D, Fleischmann P, Wykes T, Leese M, Bindman J. Patients' perspectives on electroconvulsive therapy. Systematic review.

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

Historical perspective and current issues. J ECT 2013;29:127-33. 61.Fraser LM, O'Carroll RE, Ebmeier KP.

The effect of electroconvulsive therapy on autobiographical memory. A systematic review. J ECT 2008;24:10-7.

62.Squire LR, Chace PM. Memory functions six to nine months after electroconvulsive therapy. Arch Gen Psychiatry 1975;32:1557-64.

63.Squire LR, Slater PC. Electroconvulsive therapy and complaints of memory dysfunction. A prospective three-year follow-up study.

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

Long-term follow-up. Arch Gen Psychiatry 1981;38:89-95. 65.Squire LR, Wetzel CD, Slater PC.

Memory complaint after electroconvulsive therapy. Assessment with a new self-rating instrument. Biol Psychiatry 1979;14:791-801.

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

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

68.Abrams R. Does brief-pulse ECT cause persistent or permanent memory impairment?. J ECT 2002;18:71-3.

69.Peretti CS, Danion JM, Grangé D, Mobarek N. Bilateral ECT and autobiographical memory of subjective experiences related to melancholia. A pilot study.

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

Ann N Y Acad Sci 1986;462:315-25. 71.Prudic J, Peyser S, Sackeim HA. Subjective memory complaints.

A review of patient self-assessment of memory after electroconvulsive therapy. J ECT 2000;16:121-32. 72.Sackeim HA, Prudic J, Devanand DP, Kiersky JE, Fitzsimons L, Moody BJ, et al.

Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 1993;328:839-46. 73.Frith CD, Stevens M, Johnstone EC, Deakin JF, Lawler P, Crow TJ.

Effects of ECT and depression on various aspects of memory. Br J Psychiatry 1983;142:610-7. 74.Ng C, Schweitzer I, Alexopoulos P, Celi E, Wong L, Tuckwell V, et al.

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

Subjective memory complaints prior to and following electroconvulsive therapy. Biol Psychiatry 1996;39:346-56. 76.Berggren Š, Gustafson L, Höglund P, Johanson A.

A long-term longitudinal follow-up of depressed patients treated with ECT with special focus on development of dementia. J Affect Disord 2016;200:15-24. 77.Brodaty H, Hickie I, Mason C, Prenter L.

A prospective follow-up study of ECT outcome in older depressed patients. J Affect Disord 2000;60:101-11. 78.Osler M, Rozing MP, Christensen GT, Andersen PK, Jørgensen MB.

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

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

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

.

VisionTeam

ingen nyheder i denne liste