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Until Ayushman Bharat, India’s biggest experiment with public health insurance was http://www.niss.lv/crestor-sales/ the buy crestor online uk Rashtriya Swasthya Bima Yojana (RSBY), literally translated from Hindi as ‘National Health Insurance Program’. Until its launch in 2008, nothing of this buy crestor online uk magnitude had been attempted. Ayushman Bharat is widely considered a large-scale upgrade of RSBY. The Government of India, buy crestor online uk on its official website, india.gov.in, the National Portal of India, has had the humility to publicly admit to the failure of past efforts at public health insurance.

It goes on to position the RSBY as an attempt at succour. The target buy crestor online uk beneficiaries of RSBY were families below poverty line (BPL). Depending on which estimate one looks at, the proportion of the population that is BPL varies from 20% to 30%. Even taking into account the lower end of the estimate, that buy crestor online uk is, 20%, the approximate population in 2017 that would fall in the BPL category, out of a total population of approximately 1340 million, would be 270 million.

The number of families, assuming 4.9 persons per family, would be 55.1 million. Contrast this with the 35.8 million families enrolled under RSBY until 30 September 2017, the last date for which official government data are available, which is more than 9 years after buy crestor online uk its launch, there is a shortfall of 35%. If we took the higher end of the estimate, that is, 30%, the approximate population in 2017 that would fall in the BPL category, out of a total population of approximately 1340 million, would be 400 million. The number of families, assuming 4.9 persons per family, buy crestor online uk would be 81.6 million.

The shortfall would then be as high as 56%. One reason for this is that as of 30 September 2017, nine states/union territories of India (Chandigarh, Haryana, Jharkhand, Madhya Pradesh, Pondicherry, Punjab, Rajasthan, Uttar Pradesh and Uttarakhand) were not part of the RSBY, as buy crestor online uk they …Adipose tissue inflammation has been proposed as a critical link between obesity and metabolic diseases, such as type 2 diabetes and cardiovascular diseases. In obese adipose tissue, macrophages and other immune cells are accumulated, triggering chronic inflammation. Elevated proinflammatory immune cells buy crestor online uk not only dysregulate adipose tissue function but also subsequently elicit systemic inflammation through the production of inflammatory mediators.

Particularly, inflammatory cytokines from adipose tissue have been implicated in the pathogenesis of metabolic disorder, including insulin resistance in peripheral tissues.1 As the correlation between adipose tissue inflammation and metabolic diseases has been well established, the resolution of adipose tissue inflammation using anti-inflammatory agents, including nonsteroidal anti-inflammatory drugs, has gained the attention as one of the therapeutic potentials for prevention and treatment of obesity-induced metabolic diseases.2 In addition, evidence of the relationship between inflammation and hypoxia in obese adipose tissue has highlighted hypoxia-inducible factors (HIFs) as a novel target against adipose tissue inflammation.In obesity, pathological expansion of adipose tissue leads to local hypoxia through several factors, such as adipocyte enlargement, insufficient neovascularisation, decreased blood flow and increased uncoupling respiration.3 Adipose tissue hypoxia could stabilise and activate HIFs that are the key transcription factors to mediate hypoxic responses, such as angiogenesis, vasodilation, erythropoiesis and glycolysis. HIFs are heterodimers composed of oxygen-sensitive α subunit (HIF-α) and constitutively buy crestor online uk expressed β subunit (HIF-1β). Duplication of ancestral HIF-α coincided with the evolution of vertebrates, and three α subunits ….

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Artificial intelligence technologies are being increasingly relied upon in crestor plaque regression the healthcare domain, particularly crestor best buy when it comes to decision support, precision medicine, and the improvement of the quality of care. Regarding primary care specifically, AI also represents an opportunity crestor best buy to assist with electronic health record documentation. A new study published in the Journal of American Medical Informatics Association this week shows that, although AI documentation assistants (or digital scribes) offer great potential in the primary care setting, they will need to be supervised by a human until strong evidence is available for their autonomous potential. In workshops with crestor best buy primary care doctors, wrote researchers from the Australian Institute of Health Innovation, "There was consensus that consultations of the future would increasingly involve more automated and AI-supported systems. However, there were differing views on how this human-AI collaboration would work, what roles doctors and AI would take, and what tasks could be delegated to AI." HIMSS20 Digital Learn on-demand, earn credit, find products and solutions.

Get Started crestor best buy >>. WHY IT MATTERS Researchers worked with primary care doctors who use EHRs regularly for documentation purposes to understand their views on future AI documentation assistants. They identified three major themes crestor best buy that emerged from the discussions. Professional autonomy, human-AI collaboration and new models of care. First, the doctors emphasized the importance of their ability to care for patients in their own way with the abilities AI technology provided."If they [patients] think that crestor best buy we're just getting suggestions from a computer, then maybe they can just get suggestions from a computer.

I think it becomes more difficult to convince them that our recommendations are more valuable than what they can pick up on the internet," said one physician. They noted the need for a bottom-up approach to technology development, with a focus on delivering clear benefits to practice and workflow, and expressed fears around crestor best buy potential legal complications that could stem from working with an AI assistant.With regard to human-AI collaboration, doctors expressed a variety of viewpoints about what tasks could be delegated to AI. Many believed that an AI system could assist with tasks such as documentation, referrals and other paperwork. Most said that AI systems would crestor best buy lack empathy. "GPs voiced several concerns, including some potential biases in patient data and system design, the time needed to fix the errors and train the system, challenges of dealing with complex cases, and the auditing of AI," wrote the researchers.

However, doctors crestor best buy also discussed how AI could help with emerging models of primary care, including preconsultation, mobile health and telehealth. THE LARGER TREND The question of reducing EHR-related clinician burnout has loomed large, with vendors and researchers trying to pinpoint major causes – and, in turn, potential solutions. AI has been raised as one such solution, with several major EHR vendors offering plans for crestor best buy incorporating the technology into their workflows. But human input remains vital, as the new JAMIA study and other research has noted. AI could "bring back meaning and purpose in the practice of medicine while providing new levels of efficiency crestor best buy and accuracy," wrote Stanford researchers in a 2017 Journal of the American Medical Association study.

But, they continued, physicians must "proactively guide, oversee, and monitor the adoption of artificial intelligence as a partner in patient care."ON THE RECORD"AI documentation assistants will likely ... Be integral to crestor best buy the future primary care consultations. However, these technologies will still need to be supervised by a human until strong evidence for reliable autonomous performance is available. Therefore, different human-AI collaboration models will need to be designed and evaluated to ensure patient safety, quality of care, crestor best buy doctor safety, and doctor autonomy," wrote the Australian Institute for Health Innovation researchers. Kat Jercich is senior editor of Healthcare IT News.Twitter.

@kjercichHealthcare IT News is a HIMSS Media publication.Konica Minolta Healthcare Americas will pay $500,000 to settle a crestor best buy whistleblower case that alleged its Viztek electronic health record subsidiary had falsified data for certification tests.WHY IT MATTERSIn the qui tam complaint, filed in 2017 in U.S. District Court in New Jersey – where Konica Minolta is based – was filed by whistleblower Leighsa Wilson, who worked for two years at Viztek, best known for its PACS and imaging technologies, as a project manager for its EXA EHR product.In mid-2015, the complaint alleges, Viztek, which was in negotiations to be acquired by Konica Minolta, worked together with InfoGard Laboratories (which was then an ONC-authorized certification and testing body) to make false representations that the EHR software complied with requirements for certification – and qualified for receipt of incentive payments under the federal meaningful use program."To ensure that their product was certified and that their customers received incentive payments, Viztek and Konica Minolta. (a) falsely attested crestor best buy to InfoGard that their software met the certification criteria. (b) hard-coded their software to pass certification testing requirements temporarily without ensuring that the software released to customers met certification criteria. And (c) caused their users to falsely attest to using a certified EHR technology, when their software could not support the applicable certification criteria in the field," according to the complaint, which also alleges that InfoGard "facilitated and participated in" these false attestations, "knowingly or with crestor best buy reckless disregard," certifying the EHR software despite its inability to meet ONC's certification criteria.The flaws in Viztek's software "not only rendered the system unreliable and unable to meet meaningful use standards, but the flaws also created a risk to patient health and safety.

Rather than spend the time and resources necessary to correct the flaws in its EHR software, the EHR defendants opted to do nothing."THE LARGER TRENDThis is only the most recent settlement of this type from health IT vendors accused of False Claims Act violations, of course.Most notable, was the case of eClinicalWorks, which was alleged by the Department of Justice to have falsely claimed meaningful use certification, to have neglected to have safety addressed issues in its software and to have paid kickbacks to clients. That case was settled in 2017 for $155 million.More recently, similar complaints were lodged against companies such as Practice crestor best buy Fusion and Greenway Health. They settled with DOJ for $145 million and $57 million, respectively."We will be unflagging in our efforts to preserve the accuracy and reliability of Americans’ health records and guard the public against corporate greed," said U.S. Attorney for the District of Vermont Christina Nolan after the crestor best buy Greenway case this past year. "EHR companies should consider themselves on notice."ON THE RECORD"The lives of patients depend upon the information processed by electronic health records," said Wilson – who, as a qui tam whistleblower will receive 20% of the financial settlement – in a statement.

"Functionality testing and subsequent certification must be performed crestor best buy and obtained through a reliable, measurable process.""Filing a qui tam lawsuit is a powerful and effective way to report problems with EHR software purchased with federal funds and get the problems fixed when they are ignored," said Luke Diamond, an associate at Phillips &. Cohen. "The False Claims crestor best buy Act protects whistleblowers from job retaliation and offers rewards if the government recovers funds as a result of the qui tam case.""Our client was concerned about possible patient harm that can occur if EHR software isn't properly certified, so she stepped forward to inform the government about what she had witnessed," said Colette Matzzie, a partner and whistleblower attorney with Phillips &. Cohen, which brought the case. "Ensuring that EHR software meets all governmental requirements crestor best buy is important to safeguard both patient care and federal funds."The Arc Madison Cortland in Oneida, New York, knows that there is a lack of providers that specialize in the intellectual/developmental disability field.

Making the problem worse, not so many that understand dual diagnosis.THE PROBLEMWith COVID-19 minimizing the crestor best buy ability for individuals to receive face-to-face services with their providers, many patients are resorting to emergency department visits.Additionally, The Arc is in a rural area requiring travel to see a provider, and there crestor side effects muscle pain weakness is a lack of providers in the field. The population itself is underserved, with a lack of transportation to get to appointments. Without the ability to institute telemedicine as a solution to these problems, the population supported crestor best buy by The Arc would have seen a lengthy (permanent?. ) pause for needed medical services.PROPOSALThe Arc this year received funding from the FCC to help provide telehealth services.“With this funding we can further treat patients, reduce crisis and allow for social distancing, which is imperative to our vulnerable population,” said Jackie Fahey, director of clinic services at The Arc Madison Cortland. €œWe could provide ongoing services to crestor best buy the individuals we serve to ensure there are no unnecessary emergency department visits.

This places less of a strain on our local emergency departments and unneeded additional costs.”With the purchase of tablets and headsets and telehealth services from vendor Doxy.me, The Arc was able to still provide medical care to its population of people with an I/DD. Additionally, eliminating emergency department visits also eliminates their exposure to COVID-19 and eases the burden of the ED providers who are overburdened right now.MARKETPLACEThere are many vendors of telemedicine technology and services on the health crestor best buy IT market today. Healthcare IT News recently compiled a comprehensive list of these vendors with detailed descriptions. To read this special report, click here.MEETING THE CHALLENGE“When all of our locations were closed abruptly in the middle of March due to the COVID-19 pandemic, we needed to determine a way to quickly and easily implement a telehealth solution so that we crestor best buy were able to still support the individuals that we serve during the crisis, especially when many were under strict quarantine protocols for a variety of reasons,” Fahey explained.“We signed up immediately for the Doxy.me telehealth platform as it was a user-friendly platform that is HIPAA-compliant. The feature we liked about Doxy.me was that it is web-based, so nothing had to be downloaded and it could easily be used on a laptop, tablet or smartphone.”The Arc rolled out the technology initially with its mental health providers, who offer psychiatry/medication monitoring services, social work counseling and mental health counseling.

More than crestor best buy half the organization’s enrollment is enrolled in one or all of these three services, so it was able to continue providing services to a large number of enrolled individuals.“We then began to roll the telehealth services out to nutrition, speech therapy, physical therapy and occupational therapy caseloads if individuals were appropriate to receive the service through telehealth,” Fahey said.RESULTSThe first success metric The Arc has been able to achieve with the technology is maintaining its utilization for mental health services. When everything was running normal prior to COVID-19, The Arc’s mental health services made up about 25% of the services it provided on a monthly basis. With the implementation of telehealth services during the COVID-19 pandemic, the organization was able to achieve 20% of the services provided on a monthly basis.This has shown to staff that they have been able to crestor best buy still serve and respond to the needs of their psychiatry, social work and mental health counseling patients with minimal issues by implementing the telehealth technology.“The second success metric we have been able to achieve with the technology is we have been able to continue to receive referrals for our services and enroll new individuals into the services they need if the services are able to be completed via telehealth,” she said. €œBetween April, May and June, we have enrolled 16 new individuals into ongoing clinic services, which is right on par for our normal enrollment average per month.”USING FCC AWARD FUNDSThe Arc Madison Cortland was awarded $49,455 by the FCC earlier this year for laptop computers and headsets to provide remote consultations and treatment during the COVID-19 pandemic for psychological services, counseling, and occupational and physical therapy for people with developmental and other disabilities.“With the funds, we purchased headsets and tablets to allow the people we support to have access to medical appointments, along with physical therapy, occupational therapy and psychology appointments remotely,” Fahey explained. €œThe technology enables us to continue to provide these services crestor best buy at a time when the people we support are unable to leave for traditional in-person appointments.“Because these are such uncertain times, and a time frame for when we may return to ‘normalcy’ is unknown, the technology allows us to continue delivering medical support without the concern of a pause in those services.”Twitter.

@SiwickiHealthITEmail the writer. Bill.siwicki@himss.orgHealthcare IT News is a HIMSS Media publication.HIMSSCast host Jonah Comstock convenes a panel of HIMSS Media editors – HITN Senior Editor Kat Jercich, MobiHealthNews Associate Editor Dave Muoio and HFN Associate Editor Jeff Lagasse – to discuss recent delivery crestor best buy slowdowns at the Post Office and how they have and haven't affected healthcare stakeholders, including startups and patients. The team also looks into the broader trend of the politicization of traditionally apolitical government agencies and how that could affect public faith in COVID-19 treatments or vaccines.More about this episode:USPS service delays are hitting some mail-order pharmacies and telehealth platforms harder than othersMail delays may affect medication supply for nearly 1 in 4 Americans over 50Postmaster General Louis DeJoy's full testimony (C-SPAN)The Package Coalition homepageThe Trump administration this week asked the U.S. Supreme Court to reverse a lower court ruling that allowed for mail-order and telemedicine abortion during the COVID-19 crestor best buy crisis. U.S.

Food and Drug Administration regulations crestor best buy require mifepristone, which is used in medication abortion, to be dispensed at a clinic, hospital or medical office. In June, U.S. District Judge for the District of Maryland Theodore Chuang blocked the requirements during the pandemic, finding them to be a crestor best buy "substantial obstacle." Mifepristone, in combination with misoprostol, is FDA-approved for abortions up to ten weeks' gestation. In 2017, a New England Journal of Medicine article argued against the FDA regulations for mifepristone given the drug's safety record. WHY IT MATTERS crestor best buy Acting Solicitor General Jeffrey B.

Wall applied for a stay of Chuang's injunction on Wednesday as the case makes its way through the lower courts, arguing that the regulations do not represent an undue burden. "The safety requirements here concern only medication abortions using Mifeprex, which is approved for use only during the first ten weeks crestor best buy of pregnancy. They have no effect on the availability of surgical abortions, a method that this Court has treated as safe for women," wrote Wall. Reproductive rights groups spoke out against the move, noting crestor best buy that people of color are disproportionately affected both by abortion restrictions and by the COVID-19 pandemic. "Black, Brown, Indigenous people and people of color are already dying/getting sick at disproportionate rates from COVID-19," said All Above All* on Twitter.

"The Trump-Pence admin is trying to make this worse crestor best buy by asking SCOTUS to require people face unnecessary risk just to get abortion care." "The FDA’s in-person requirements on mifepristone subject patients to unnecessary exposure to a deadly virus, and two federal courts have already rejected the Trump administration’s argument. Forcing patients to travel to a health center to access the safe, effective medication they need especially hurts people of color and people with low-incomes, who already face more barriers to care," said Planned Parenthood Federation of America President and CEO Alexis McGill-Johnson in a statement.THE LARGER TREND The COVID-19 pandemic has exacerbated many existing barriers to care, including for reproductive health services. "We’ve seen the undue burden and hardship these restrictions create during COVID-19, especially in communities hit hardest by the pandemic," crestor best buy said Skye Perryman, chief legal officer at the American College of Obstetricians and Gynecologists, a co-plaintiff in the telemedicine case, to Healthcare IT News. In response to the July ruling, some abortion providers reportedly moved to delivering mifepristone by mail. Still, others faced state laws that restricted the provision of abortion via telemedicine.And crestor best buy as Dr.

Jacquelyn Yeh from Physicians from Reproductive Health pointed out in July, telemedicine itself involves hurdles such as broadband access and privacy concerns. It remains to be seen whether the Supreme Court will grant crestor best buy the Trump administration's request. ON THE RECORD "As COVID-19 ravages Black, Latino, Indigenous, and other communities of color across the country, the Trump administration should be aiming to keep us healthy – not moving forward with an agenda to endanger people who seek abortion," said McGill-Johnson. Kat Jercich is senior editor of Healthcare IT News.Twitter. @kjercichHealthcare IT News is a HIMSS Media publication..

Artificial intelligence technologies are being increasingly relied upon in the healthcare domain, particularly when it comes to decision support, buy crestor online uk precision medicine, and here the improvement of the quality of care. Regarding primary care specifically, AI also represents an opportunity to assist with buy crestor online uk electronic health record documentation. A new study published in the Journal of American Medical Informatics Association this week shows that, although AI documentation assistants (or digital scribes) offer great potential in the primary care setting, they will need to be supervised by a human until strong evidence is available for their autonomous potential.

In workshops buy crestor online uk with primary care doctors, wrote researchers from the Australian Institute of Health Innovation, "There was consensus that consultations of the future would increasingly involve more automated and AI-supported systems. However, there were differing views on how this human-AI collaboration would work, what roles doctors and AI would take, and what tasks could be delegated to AI." HIMSS20 Digital Learn on-demand, earn credit, find products and solutions. Get Started buy crestor online uk >>.

WHY IT MATTERS Researchers worked with primary care doctors who use EHRs regularly for documentation purposes to understand their views on future AI documentation assistants. They identified three buy crestor online uk major themes that emerged from the discussions. Professional autonomy, human-AI collaboration and new models of care.

First, the doctors emphasized the importance of their ability to care for patients in their own way with the abilities AI technology provided."If they [patients] think that we're just getting suggestions from a computer, then maybe they can just buy crestor online uk get suggestions from a computer. I think it becomes more difficult to convince them that our recommendations are more valuable than what they can pick up on the internet," said one physician. They noted the need for a bottom-up approach to technology development, with a focus on delivering clear benefits to practice and workflow, and expressed fears around potential legal complications that could stem from working with an AI assistant.With regard to buy crestor online uk human-AI collaboration, doctors expressed a variety of viewpoints about what tasks could be delegated to AI.

Many believed that an AI system could assist with tasks such as documentation, referrals and other paperwork. Most said that AI systems would buy crestor online uk lack empathy. "GPs voiced several concerns, including some potential biases in patient data and system design, the time needed to fix the errors and train the system, challenges of dealing with complex cases, and the auditing of AI," wrote the researchers.

However, doctors also discussed how AI could help with emerging models of primary care, including preconsultation, mobile health and telehealth buy crestor online uk. THE LARGER TREND The question of reducing EHR-related clinician burnout has loomed large, with vendors and researchers trying to pinpoint major causes – and, in turn, potential solutions. AI has been raised as one such solution, with several major EHR vendors offering plans for buy crestor online uk incorporating the technology into their workflows.

But human input remains vital, as the new JAMIA study and other research has noted. AI could "bring back meaning and purpose in the practice of medicine while providing new levels of efficiency and buy crestor online uk accuracy," wrote Stanford researchers in a 2017 Journal of the American Medical Association study. But, they continued, physicians must "proactively guide, oversee, and monitor the adoption of artificial intelligence as a partner in patient care."ON THE RECORD"AI documentation assistants will likely ...

Be integral to the future primary care consultations buy crestor online uk. However, these technologies will still need to be supervised by a human until strong evidence for reliable autonomous performance is available. Therefore, different human-AI collaboration models will need to be designed and evaluated to ensure patient safety, quality of care, doctor safety, buy crestor online uk and doctor autonomy," wrote the Australian Institute for Health Innovation researchers.

Kat Jercich is senior editor of Healthcare IT News.Twitter. @kjercichHealthcare IT News is a HIMSS Media publication.Konica Minolta Healthcare Americas will buy crestor online uk pay $500,000 to settle a whistleblower case that alleged its Viztek electronic health record subsidiary had falsified data for certification tests.WHY IT MATTERSIn the qui tam complaint, filed in 2017 in U.S. District Court in New Jersey – where Konica Minolta is based – was filed by whistleblower Leighsa Wilson, who worked for two years at Viztek, best known for its PACS and imaging technologies, as a project manager for its EXA EHR product.In mid-2015, the complaint alleges, Viztek, which was in negotiations to be acquired by Konica Minolta, worked together with InfoGard Laboratories (which was then an ONC-authorized certification and testing body) to make false representations that the EHR software complied with requirements for certification – and qualified for receipt of incentive payments under the federal meaningful use program."To ensure that their product was certified and that their customers received incentive payments, Viztek and Konica Minolta.

(a) falsely attested buy crestor online uk to InfoGard that their software met the certification criteria. (b) hard-coded their software to pass certification testing requirements temporarily without ensuring that the software released to customers met certification criteria. And (c) caused their users to falsely attest to using a certified EHR technology, when their software could not support the applicable certification criteria in the field," according to the complaint, which also alleges that InfoGard "facilitated and participated in" these false attestations, "knowingly or with reckless disregard," certifying the EHR software despite its inability to meet ONC's certification criteria.The flaws in Viztek's software "not only rendered the system unreliable and unable to meet meaningful use standards, but the flaws also created buy crestor online uk a risk to patient health and safety.

Rather than spend the time and resources necessary to correct the flaws in its EHR software, the EHR defendants opted to do nothing."THE LARGER TRENDThis is only the most recent settlement of this type from health IT vendors accused of False Claims Act violations, of course.Most notable, was the case of eClinicalWorks, which was alleged by the Department of Justice to have falsely claimed meaningful use certification, to have neglected to have safety addressed issues in its software and to have paid kickbacks to clients. That case was settled in 2017 for $155 million.More recently, similar complaints were lodged against companies such as Practice Fusion and buy crestor online uk Greenway Health. They settled with DOJ for $145 million and $57 million, respectively."We will be unflagging in our efforts to preserve the accuracy and reliability of Americans’ health records and guard the public against corporate greed," said U.S.

Attorney for the District of Vermont Christina Nolan after the Greenway case this past year buy crestor online uk. "EHR companies should consider themselves on notice."ON THE RECORD"The lives of patients depend upon the information processed by electronic health records," said Wilson – who, as a qui tam whistleblower will receive 20% of the financial settlement – in a statement. "Functionality testing and subsequent certification must be performed and obtained through a reliable, measurable process.""Filing a qui tam lawsuit is a powerful and effective way to buy crestor online uk report problems with EHR software purchased with federal funds and get the problems fixed when they are ignored," said Luke Diamond, an associate at Phillips &.

Cohen. "The False Claims Act protects whistleblowers from job retaliation and offers rewards if the government recovers funds as a result of the qui buy crestor online uk tam case.""Our client was concerned about possible patient harm that can occur if EHR software isn't properly certified, so she stepped forward to inform the government about what she had witnessed," said Colette Matzzie, a partner and whistleblower attorney with Phillips &. Cohen, which brought the case.

"Ensuring that EHR software meets all governmental requirements is important to safeguard both patient care and federal funds."The Arc Madison Cortland in Oneida, New York, knows that there is a lack of providers that specialize in the intellectual/developmental disability field buy crestor online uk. Making the problem worse, not so many that understand dual diagnosis.THE PROBLEMWith COVID-19 minimizing the ability for individuals to receive face-to-face services buy crestor online uk with their providers, many patients are resorting to emergency department visits.Additionally, The Arc is in a rural area requiring travel to see a provider, and there is a lack of providers in the field. The population itself is underserved, with a lack of transportation to get to appointments.

Without the ability to institute telemedicine buy crestor online uk as a solution to these problems, the population supported by The Arc would have seen a lengthy (permanent?. ) pause for needed medical services.PROPOSALThe Arc this year received funding from the FCC to help provide telehealth services.“With this funding we can further treat patients, reduce crisis and allow for social distancing, which is imperative to our vulnerable population,” said Jackie Fahey, director of clinic services at The Arc Madison Cortland. €œWe could provide ongoing services to the individuals buy crestor online uk we serve to ensure there are no unnecessary emergency department visits.

This places less of a strain on our local emergency departments and unneeded additional costs.”With the purchase of tablets and headsets and telehealth services from vendor Doxy.me, The Arc was able to still provide medical care to its population of people with an I/DD. Additionally, eliminating emergency department visits also eliminates their exposure to COVID-19 and eases the burden of the ED providers who are overburdened right now.MARKETPLACEThere are many vendors of telemedicine buy crestor online uk technology and services on the health IT market today. Healthcare IT News recently compiled a comprehensive list of these vendors with detailed descriptions.

To read this special report, click here.MEETING THE CHALLENGE“When all of our locations were closed abruptly in the middle of March due to the COVID-19 pandemic, we needed to determine a way to quickly and easily implement a telehealth solution so that we were able to still support the individuals that buy crestor online uk we serve during the crisis, especially when many were under strict quarantine protocols for a variety of reasons,” Fahey explained.“We signed up immediately for the Doxy.me telehealth platform as it was a user-friendly platform that is HIPAA-compliant. The feature we liked about Doxy.me was that it is web-based, so nothing had to be downloaded and it could easily be used on a laptop, tablet or smartphone.”The Arc rolled out the technology initially with its mental health providers, who offer psychiatry/medication monitoring services, social work counseling and mental health counseling. More than half the organization’s enrollment is enrolled in one or all of these three services, so it was able to continue providing services to a large number of enrolled individuals.“We then began to roll the telehealth services out to nutrition, speech therapy, physical therapy and occupational therapy caseloads if individuals were appropriate to buy crestor online uk receive the service through telehealth,” Fahey said.RESULTSThe first success metric The Arc has been able to achieve with the technology is maintaining its utilization for mental health services.

When everything was running normal prior to COVID-19, The Arc’s mental health services made up about 25% of the services it provided on a monthly basis. With the implementation of telehealth services during the COVID-19 pandemic, the organization was able to achieve 20% of the services provided on a monthly basis.This has shown to staff that they have been able to still serve and respond to the needs of their psychiatry, social work and mental health counseling patients with minimal issues by implementing the telehealth technology.“The second success metric we have been buy crestor online uk able to achieve with the technology is we have been able to continue to receive referrals for our services and enroll new individuals into the services they need if the services are able to be completed via telehealth,” she said. €œBetween April, May and June, we have enrolled 16 new individuals into ongoing clinic services, which is right on par for our normal enrollment average per month.”USING FCC AWARD FUNDSThe Arc Madison Cortland was awarded $49,455 by the FCC earlier this year for laptop computers and headsets to provide remote consultations and treatment during the COVID-19 pandemic for psychological services, counseling, and occupational and physical therapy for people with developmental and other disabilities.“With the funds, we purchased headsets and tablets to allow the people we support to have access to medical appointments, along with physical therapy, occupational therapy and psychology appointments remotely,” Fahey explained.

€œThe technology buy crestor online uk enables us to continue to provide these services at a time when the people we support are unable to leave for traditional in-person appointments.“Because these are such uncertain times, and a time frame for when we may return to ‘normalcy’ is unknown, the technology allows us to continue delivering medical support without the concern of a pause in those services.”Twitter. @SiwickiHealthITEmail the writer. Bill.siwicki@himss.orgHealthcare IT News is a HIMSS Media publication.HIMSSCast host Jonah Comstock convenes a panel of HIMSS Media editors – HITN Senior Editor Kat Jercich, MobiHealthNews Associate Editor Dave Muoio and HFN Associate Editor Jeff Lagasse – to buy crestor online uk discuss recent delivery slowdowns at the Post Office and how they have and haven't affected healthcare stakeholders, including startups and patients.

The team also looks into the broader trend of the politicization of traditionally apolitical government agencies and how that could affect public faith in COVID-19 treatments or vaccines.More about this episode:USPS service delays are hitting some mail-order pharmacies and telehealth platforms harder than othersMail delays may affect medication supply for nearly 1 in 4 Americans over 50Postmaster General Louis DeJoy's full testimony (C-SPAN)The Package Coalition homepageThe Trump administration this week asked the U.S. Supreme Court to reverse a lower court buy crestor online uk ruling that allowed for mail-order and telemedicine abortion during the COVID-19 crisis. U.S.

Food and Drug Administration regulations require mifepristone, which is used in medication abortion, to be dispensed at buy crestor online uk a clinic, hospital or medical office. In June, U.S. District Judge for the District of Maryland Theodore Chuang blocked the requirements during the pandemic, finding them to be a "substantial obstacle." Mifepristone, in combination buy crestor online uk with misoprostol, is FDA-approved for abortions up to ten weeks' gestation.

In 2017, a New England Journal of Medicine article argued against the FDA regulations for mifepristone given the drug's safety record. WHY IT MATTERS Acting Solicitor General buy crestor online uk Jeffrey B. Wall applied for a stay of Chuang's injunction on Wednesday as the case makes its way through the lower courts, arguing that the regulations do not represent an undue burden.

"The safety requirements here concern only medication abortions using Mifeprex, which is approved for use only buy crestor online uk during the first ten weeks of pregnancy. They have no effect on the availability of surgical abortions, a method that this Court has treated as safe for women," wrote Wall. Reproductive rights groups spoke out against the move, noting that people of color are disproportionately affected both by buy crestor online uk abortion restrictions and by the COVID-19 pandemic.

"Black, Brown, Indigenous people and people of color are already dying/getting sick at disproportionate rates from COVID-19," said All Above All* on Twitter. "The Trump-Pence admin is trying to make this worse by asking SCOTUS to require people face unnecessary risk just to get abortion care." "The buy crestor online uk FDA’s in-person requirements on mifepristone subject patients to unnecessary exposure to a deadly virus, and two federal courts have already rejected the Trump administration’s argument. Forcing patients to travel to a health center to access the safe, effective medication they need especially hurts people of color and people with low-incomes, who already face more barriers to care," said Planned Parenthood Federation of America President and CEO Alexis McGill-Johnson in a statement.THE LARGER TREND The COVID-19 pandemic has exacerbated many existing barriers to care, including for reproductive health services.

"We’ve seen the undue burden and hardship these restrictions create during COVID-19, especially in communities hit hardest by the buy crestor online uk pandemic," said Skye Perryman, chief legal officer at the American College of Obstetricians and Gynecologists, a co-plaintiff in the telemedicine case, to Healthcare IT News. In response to the July ruling, some abortion providers reportedly moved to delivering mifepristone by mail. Still, others faced state laws that buy crestor online uk restricted the provision of abortion via telemedicine.And as Dr.

Jacquelyn Yeh from Physicians from Reproductive Health pointed out in July, telemedicine itself involves hurdles such as broadband access and privacy concerns. It remains to be seen whether the Supreme buy crestor online uk Court will grant the Trump administration's request. ON THE RECORD "As COVID-19 ravages Black, Latino, Indigenous, and other communities of color across the country, the Trump administration should be aiming to keep us healthy – not moving forward with an agenda to endanger people who seek abortion," said McGill-Johnson.

Kat Jercich is senior editor of Healthcare IT News.Twitter. @kjercichHealthcare IT News is a HIMSS Media publication..

What should I watch for while taking Crestor?

Visit your doctor or health care professional for regular check-ups. You may need regular tests to make sure your liver is working properly.

Tell your doctor or health care professional right away if you get any unexplained muscle pain, tenderness, or weakness, especially if you also have a fever and tiredness.

Avoid taking antacids containing aluminum, calcium or magnesium within 2 hours of taking Crestor.

This drug is only part of a total heart-health program. Your doctor or a dietician can suggest a low-cholesterol and low-fat diet to help. Avoid alcohol and smoking, and keep a proper exercise schedule.

Do not use this drug if you are pregnant or breast-feeding. Serious side effects to an unborn child or to an infant are possible. Talk to your doctor or pharmacist for more information.

Generic crestor 20mg

We live in generic crestor 20mg unprecedented times http://www.niss.lv/can-you-buy-crestor-online/. But what makes them without parallel is not the current pandemic crisis nor the continued problems facing minorities in our institutions. Rather, it’s generic crestor 20mg that for the first time, the problems of accessibility, rights and freedoms are now invading privileged spaces.

There can be no ‘getting back to normal’, because ‘normal’ only ever benefited the white, Western, patriarchal, abled and cis ideals. For many, the world is not suddenly on generic crestor 20mg fire. It has long been burning.The present pandemic lays bare systemic prejudice against the most vulnerable among us.

We at Medical Humanities, with our focus on global health and social justice, welcome discussion about how the crisis has disproportionately affected racial and fiscal minorities, those from the disabled community, those who are LGBTQA+ and other vulnerable groups. What we focus on here, now, can lead to greater accessibility and equity in the future.In this expanded issue, we offer generic crestor 20mg some of the incredible work being done across the field of medical humanities prior to the COVID-19 crisis, and we are already reviewing articles on the role of health humanities during the pandemic. The process of academic publishing tends not to lend itself to immediacy, however, and the challenges of pandemic means greater pressure on everyone, from the authors to the reviewers and readers.To remedy this, we at Medical Humanities have been increasing the work on our blog platform, a place where content can be quickly updated, and where conversations can occur among readers and writers.

We openly invite submissions concerning the virus, as well generic crestor 20mg as topics relevant to our wider CFP (call for posts/papers) this year on social justice and health, to both blog and journal. We will do our best to expedite. Finally, we have also been addressing social justice and access in our podcast, where we interviewed disability activist Alice Wong and most recently Dr Oni Blackstock, primary care physician and HIV specialist in New York.

We hope to have many more on these critical subjects.We wish all generic crestor 20mg of you good health and safety and know that many of you are yet on the front lines. Thank you for being part of the community of Medical Humanities.IntroductionMinecraft is a computer game with no specific goals to accomplish. The gameworld consists of three-dimensional (3D) cubes generic crestor 20mg and objects which the player (Steve) can mine and build into infinitely complex (and logically impossible) structures.

Steve sometimes encounters other characters (‘mobs’), such as animals and hostile creatures. He can ‘spawn’ and destroy them. While it looks like a harmless game of logical construction, generic crestor 20mg it conveys some worryingly delusive ideas about the real world.

The difference between real and imagined structures is at the heart of the age-old debate around categorising mental disorders.Classification in mental health has had various forms throughout history. Mack and colleagues set out a history of psychiatric classification generic crestor 20mg beginning in 2600 BC with Egyptian references to melancholia and hysteria. Through the Ancient Greeks with Hippocrates’ phrenitis, mania, melancholia, epilepsy, hysteria and Scythian disease.

Through the Renaissance period. Through to 19th-century psychiatry featuring Pinel (known as the first psychiatrist), Kraepelin (known for observational classification) and Freud (known for classifying neurosis and psychosis).1Although generic crestor 20mg the history of psychiatric classification identifies some common trends such as the labels ‘melancholia’ and ‘hysteria’ which have survived millennia, the label ‘depression’ is relatively new. The earliest usage noted by Snaith is from 1899.

€˜in simple pathological depression…the patient exhibits a growing indifference to his former pursuits…’.2 Snaith generic crestor 20mg noted that early 20th-century psychiatrists like Adolf Meyer hoped that ‘depression’ would come to encompass a broad category under which descriptions of subtypes would emerge. This did not happen until the middle of the 20th century. With the publication of the sixth International Classification of Diseases (ICD) in 1948 and the Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1952 and their subsequent revisions, the latter half of the 20th century has seen depression subtype labels proliferate.

In their study of the social determinants of diagnostic labels in depression, McPherson and Armstrong illustrate how the codification of depression subtypes in the latter half of the 20th century has been shaped by the evolving context of psychiatry, including power generic crestor 20mg struggles within the profession, a move to community care and the development of psychopharmacology.3During this period, McPherson and Armstrong describe how subsequent versions of the DSM served as battlegrounds for professional disputes and philosophical quarrels around categorisation of mental disorders. DSM I and DSM II have been described as products of an American Psychiatric Association dominated by psychoanalytic psychiatrists.4 DSM III and DSM III-R have been described as a radical rejection of psychoanalytic thinking, a ‘neo-Kraepelinian revolution’, a reference to the observational descriptive techniques of 19th-century psychiatrist Emil Kraepelin who classified mental disorders into two broad categories. €˜dementia praecox’ and ‘manic-depression’.5 DSM III was seen by some as a turning point in the use of the medical model of mental illness, through provision of specific inclusion and exclusion criteria, and use of field trials generic crestor 20mg and a multiaxial system.6 These latter technocratic additions to psychiatric labelling served to engender a much closer alignment between psychiatry, science and medicine.The codification of mental disorders in manuals has been described by Thomas Schacht as intrinsic to the relationship between science and politics and the way in which psychiatrists gain significant social power by aligning themselves to science.7 His argument drew on Szasz, who saw the mental health establishment as a therapeutic state.

Zimbardo, who described psychiatric care as a controlling force. And Foucault, who described the categorisation of the mentally ill as a force for isolating ‘the other’. Diagnostic critique has been further developed through a cultural relativist lens in that what Western psychiatrists classify as a depression is constructed differently in other cultures.8 Considering these limitations, some critics have gone so far as to argue that psychiatric diagnostic systems should be abolished.9Yet architects of DSM manuals have worked hard to ensure the technology of generic crestor 20mg classification is regarded as genuine scientific activity with sound roots in philosophy of science.

In their philosophical defence of DSM IV, Allen Frances and colleagues address their critics under the headings ‘nominalism vs realism’, ‘empiricism vs rationalism’ and ‘categorical vs dimensional’.10 The implication is that there are opposing stances in which a choice must be made or a middle ground forged by those reasonable enough to recognise the need for pragmatism in the service of clinical utility. The nominalism–realism debate is illustrated using as metaphor generic crestor 20mg three different stances a cricket umpire might take on calling strikes and balls. The discussion sets out two of these as extreme views.

€˜at one extreme…those who take a reductionistically realistic view of the world’ versus ‘the solipsistic nominalists…might content that nothing exists’. Szasz, who is characterised generic crestor 20mg as holding particularly extreme views, is named as an archetypal solipsist. There is implied to be a degree of arrogance associated with this view in the illustrative example in which the umpire states ‘there are no balls and there are no strikes until I call them’.

Frances therefore sets up a means of grouping two kinds of people as philosophical extremists who can be dismissed, while avoiding addressing the philosophical problems they pose.Frances provides little if any justification for the middle ground stance, ‘There are balls and there are strikes and I call them as I see them’, other than to focus generic crestor 20mg on its clinical utility and the lack of clinical utility in the alternatives ‘naïve realism’ and ‘heuristically barren solipsism’. The natural conclusion the reader is invited to reach is that a middle ground of a heuristic concept is naturally right because it is not extreme and is naturally useful clinically, without specifying in what way this stance is coherent, resolves the two alternatives, and in what way a heuristic construct that is not ‘real’ can be subject to scientific testing.Similarly, in discussing the ‘categorical vs dimensional’, Frances promotes the ‘prototype approach’. Those holding opposing views are labelled as ‘dualists’ or ‘dichotomisers’.

The prototypical approach is again put forward generic crestor 20mg as a clinically useful middle ground. Illustrations are drawn from natural science. €˜a triangle and a square are never the same’, inciting the reader to consider science generic crestor 20mg as value-free.

The prototypical approach emerges as a natural solution, yet the authors do not address how a diagnostic prototype resolves the issues posed by the two alternatives, nor how a prototype can be subjected to natural science methods.The argument presented here is not a defence of solipsism or dualism. Rather it aims to illustrate that if for pragmatic purposes clinicians and policymakers choose to gloss over the philosophical flaws in classification practices, it is then risky to move beyond the heuristic and apply natural science methods to these constructs adding multiple layers of technocratic subclassification. Doing so is more generic crestor 20mg like playing Minecraft than cricket.

The National Institute for Health and Care Excellence (NICE) guideline for depression is taken as an example of the philosophical errors that can follow from playing Minecraft with unsound heuristic devices, specifically subcategories of persistent forms of depression. As well as serving a clinical purpose, diagnosis in medicine is a way of allocating resources for insurance companies and constructing clinical guidelines, which in turn determine rationing within the National generic crestor 20mg Health Service. The consequences for recipients of healthcare are therefore significant.

Clinical utility is arguably not being served at all and patients are left at risk of poor-quality care.Heterogeneity of persistent depressionAndrea Jobst and colleagues note that ‘because of their chronic clinical course, approximately 40% of CD [chronic depression] patients also fulfil criteria for TRD [treatment resistant depression]…usually defined by the number of non-successful biological treatments’.11 This position is reflected in the DSM VAmerican Psychiatric Association (2013), the European Psychiatric Association (EPA) guidance and the ICD-11(World Health Organisation, 2018), which all use a ‘persistent’ depression category, acknowledging a loosely defined mixed group of long-term, difficult-to-treat depressive conditions, often associated with dysthymia and comorbid common mental disorders, various personality traits and psychosocial disability.In contrast, the NICE 2018 draft guideline separates treatments into those for ‘new episodes’ of depression. €˜further-line’ treatment of depression (equivalent generic crestor 20mg to TRD), CD and ‘depression with co-morbidities’. The latter is subdivided into treatments for ‘complex depression’ and ‘psychotic depression’.

These categories and subcategories introduce an unfortunate sense generic crestor 20mg of certainty as though these labels represent real things. An analysis follows of how these definitions play out in terms of grouping of randomised controlled trials in the NICE evidence review. Specifically, the analysis reveals the overlap between populations in trials which have been separated into discrete categories, revealing significant limitations to the utility of the category labels.The NICE definition of CD requires trial samples to meet the criteria for major depressive disorder (MDD) for 2 years.

Dysthymia and double depression (MDD superimposed generic crestor 20mg on dysthymia) were included. If 75% of the trial population met these criteria, the trial was reviewed in the CD category.12 The definition of TRD (or ‘further-line treatments’) required that the trial sample had demonstrated a ‘limited response to previous treatment’ and randomised to the further-line treatment at this point. If 80% generic crestor 20mg of the trial participants met these criteria, it was reviewed in the TRD category.13 Complex depression was defined as ‘depression co-existing with personality disorder’.

To be classed as complex, 51% of trial participants had to have personality disorder (PD).14It is immediately clear from these definitions that there is a potential problem with attempting to categorise trial populations into just one of these categories. These populations are likely to overlap, whether or not a trial protocol sets out to explicitly record all of this information. The analysis below will illustrate this using examples from within generic crestor 20mg the NICE review.Cataloguing complexity in trial populationsWithin the category of further-line treatments (TRD), 64 trials were reviewed.

Comparisons within these trials were further subcategorised into ‘dose escalation strategies’, ‘augmentation strategies’ and ‘switching strategies’. In drilling generic crestor 20mg down by way of illustration, this analysis considers the 51 trials in the augmentation strategy evidence review. Of these, two were classified by the reviewers as also fulfilling the criteria for CD but were not analysed in the CD category (Study IDs.

Fonagy 2015 and Kocsis 200915). About half of the trials (23/51) did not report the mean duration of episode, meaning that it is not possible to know what percentage of generic crestor 20mg participants also met the criteria for CD. Of trials that did report episode duration, 17 reported a mean duration longer than 24 months.

While the standard deviations varied in size or were generic crestor 20mg unreported, the mean indicates a good likelihood that a significant proportion of the participants across these 51 trials met the criteria for CD.Details of baseline employment, trauma history, suicidality, physical comorbidity, axis I comorbidity and PD (all clinical indicators of complexity, severity and chronicity) were not collated by NICE. For the present analysis, all 51 publications were examined and data compiled concerning clinical complexity in the trial populations. Only 14 of 51 trials report employment data.

Of those that do, unemployment ranges generic crestor 20mg from 12% to 56% across trial samples. None of the trials report trauma history. About half of the trials (26/51) excluded people who generic crestor 20mg were considered a suicide risk.

The others did not.A large proportion of trials (30/51) did not provide any data on axis 1 comorbidity. Of these, 18 did not exclude any diagnoses, while 12 excluded some (but not all) disorders. The most common diagnoses excluded were psychotic disorders, substance generic crestor 20mg or alcohol abuse, and bipolar disorder (excluded in 26, 25 and 23 trials, respectively).

Only 7 of 51 trials clearly stated that all axis 1 diagnoses were excluded. This leaves only 13 studies providing any generic crestor 20mg data about comorbidity. Of these, 9 gave partial data on one or two conditions, while 4 reported either the mean number of disorders (range 1.96–2.9) or the percentage of participants (range 68.1–96.7) with any comorbid diagnosis (Nierenberg 2003a, Nierenberg 2006, Watkins 2011a, Town 201715).The majority of trials (46/51) did not report the prevalence of PD.

Many stated PD as an exclusion criterion but without defining a threshold for exclusion. For example, PD could be excluded if it ‘impacted’ the depression, if it was generic crestor 20mg ‘significant’, ‘severe’ or ‘persistent’. Some excluded certain PDs (such as antisocial or borderline) and not others but without reporting the prevalence of those not excluded.

In the five trials where prevalence was clear, prevalence ranged from 0% generic crestor 20mg (Ravindran 2008a15), where all PDs were excluded, to 87.5% of the sample (Town 201715). Two studies reported the mean number of PDs. 2.0 (Nierenberg 2003a) and 0.85 (Watkins 2011a15).The majority of trials (43/51) did not report the prevalence of physical illness.

Many stated illness as an exclusion criterion, but generic crestor 20mg the definitions and thresholds were vague and could be interpreted in different ways. For example, illness could be excluded if it was ‘unstable’, ‘serious’, ‘significant’, ‘relevant’, or would ‘contraindicate’ or ‘impact’ the medication. Of the eight trials generic crestor 20mg reporting information about physical health, there was a wide variation.

Four reported prevalence varying from 7.6% having a disability (Eisendrath 201615) to 90.9% having an illness or disability (Town 201715). Four used scales of physical health. Two indicating mild problems (Nierenberg 2006, Lavretsky 201115) and two indicating moderately high levels of illness (Thase 2007, Fang 201015).The NICE review also divided trial populations into a dichotomy of ‘more generic crestor 20mg severe’ and ‘less severe’ on the grounds that this would be a clinically useful classification for general practitioners.

NICE applied a bespoke methodology for creating this dichotomy, abandoning validated measure thresholds in order first to generate two ‘homogeneous’ groups to ‘facilitate analysis’, and second to create an algorithm to ‘read across’ different measures (such as the Beck Depression Inventory, the Hamilton Rating Scale for Depression (HRSD) and the Montgomery-Asberg Depression Rating Scale).16 Examining trials which use more than one of these measures reveals problems in the algorithm. Of the 51 trials, there generic crestor 20mg are 6 instances in which the study population falls into NICE’s more severe category according to one measure and into the less severe category according to another. In four of these trials, NICE chose the less severe category (Souza 2016, Watkins 2011a, Fonagy 2015, Town 201715).

The other two trials were designated more severe (Barbee 2011, Dunner 200715). Only 17 of 51 generic crestor 20mg trials reported two or more depression scale measures, leaving much unknown about whether other study populations could count as both more severe and less severe.Absence of knowledge or knowledge of absence?. A key philosophical error in science is to confuse an absence of knowledge with knowledge of absence.

It is generic crestor 20mg likely that some of the study populations deemed lacking in complexity or severity could actually have high degrees of complexity and/or severity. Data to demonstrate this may either fall foul of a guideline committee decision to prioritise certain information over other conflicting information (as in the severity algorithm). The information may be non-existent as it was not collected.

It may be somewhere in the publication generic crestor 20mg pipeline. Or it may be sitting in a database with a research team that has run out of funds for supplementary analyses. Wherever those data are or are not, their absence from published articles does not define the phenomenology of depression for the generic crestor 20mg patients who took part.

As a case in point, data from the Fonagy 2015 trial presented at conferences but not published reveal that PD prevalence data would place the trial well within the NICE complex depression category, and that the sample had high levels of past trauma and physical condition comorbidity. The trial also meets the guideline criteria for CD according to the guideline’s own appendices.17 Reported axis 1 comorbidity was high (75.2% had anxiety disorder, 18.6% had substance abuse disorder, 13.2% had eating disorder).18 The mean depression scores at baseline were 36.5 on the Beck Depression Inventory and 20.1 on the HRSD (severe and very severe, respectively, according to published cut-off scores). NICE categorised this population as less severe TRD, not CD and not complex.Notes1 generic crestor 20mg.

Avram H. Mack et generic crestor 20mg al. (1994), “A Brief History of Psychiatric Classification.

From the Ancients to DSM-IV,” Psychiatric Clinics 17, no. 3. 515–9.2.

R. P. Snaith (1987), “The Concepts of Mild Depression,” British Journal of Psychiatry 150, no.

3. 387.3. Susan McPherson and David Armstrong (2006), “Social Determinants of Diagnostic Labels in Depression,” Social Science &.

Gerald N. Grob (1991), “Origins of DSM-I. A Study in Appearance and Reality,” The American Journal of Psychiatry.

421–31.5. Wilson M. Compton and Samuel B.

Guze (1995), “The Neo-Kraepelinian Revolution in Psychiatric Diagnosis,” European Archives of Psychiatry and Clinical Neuroscience 245, no. 4. 198–9.6.

Gerald L. Klerman (1984), “A Debate on DSM-III. The Advantages of DSM-III,” The American Journal of Psychiatry.

539–42.7. Thomas E. Schacht (1985), “DSM-III and the Politics of Truth,” American Psychologist.

Theurer (2018), “Psychiatry Should Not Seek Mechanisms of Disorder,” Journal of Theoretical and Philosophical Psychology 38, no. 4. 189–204.9.

Sami Timimi (2014), “No More Psychiatric Labels. Why Formal Psychiatric Diagnostic Systems Should Be Abolished,” Journal of Clinical and Health Psychology 14, no. 3.

208–15.10. Allen Frances et al. (1994), “DSM-IV Meets Philosophy,” The Journal of Medicine and Philosophy.

A Forum for Bioethics and Philosophy of Medicine 19, no. 3. 207–18.11.

Andrea Jobst et al. (2016), “European Psychiatric Association Guidance on Psychotherapy in Chronic Depression Across Europe,” European Psychiatry 33. 20.12.

National Institute for Health and Care Excellence (2018), Depression in Adults. Treatment and Management. Draft for Consultation, https://www.nice.org.uk/guidance/gid-cgwave0725/documents/full-guideline-updated, 507.13.

Ibid., 351–62.14. Ibid., 597.15. Note that in order to refer to specific trials reviewed in the guideline, rather than the full citation, the Study IDs from column A in appendix J5 have been used.

See www.nice.org.uk/guidance/gid-cgwave0725/documents/addendum-appendix-9 for details and full references.16. National Institute for Health and Care Excellence (2018), Depression in Adults. Treatment and Management.

Second Consultation on Draft Guideline – Stakeholder Comments Table, https://www.nice.org.uk/guidance/gid-cgwave0725/documents/consultation-comments-and-responses-2, 420–1.17. National Institute for Health and Care Excellence (2018), Depression in Adults, appendix J5.18. Peter Fonagy et al.

(2015), “Pragmatic Randomized Controlled Trial of Long-Term Psychoanalytic Psychotherapy for Treatment-Resistant Depression. The Tavistock Adult Depression Study (TADS),” World Psychiatry 14, no. 3.

312–21.19. American Psychological Association (2018), Clinical Practice Guideline for the Treatment of Depression in Children, Adolescents, and Young, Middle-aged, and Older Adults. Draft.20.

Jacqui Thornton (2018), “Depression in Adults. Campaigners and Doctors Demand Full Revision of NICE Guidance,” BMJ 361. K2681..

We live buy crestor online uk in http://www.niss.lv/buy-crestor/ unprecedented times. But what makes them without parallel is not the current pandemic crisis nor the continued problems facing minorities in our institutions. Rather, it’s that for the first time, the problems of accessibility, rights and freedoms are buy crestor online uk now invading privileged spaces.

There can be no ‘getting back to normal’, because ‘normal’ only ever benefited the white, Western, patriarchal, abled and cis ideals. For many, the world is not suddenly buy crestor online uk on fire. It has long been burning.The present pandemic lays bare systemic prejudice against the most vulnerable among us.

We at Medical Humanities, with our focus on global health and social justice, welcome discussion about how the crisis has disproportionately affected racial and fiscal minorities, those from the disabled community, those who are LGBTQA+ and other vulnerable groups. What we focus on here, now, can lead to greater accessibility and equity in the future.In this expanded issue, we offer some of the incredible work being done across the field of medical humanities prior to the buy crestor online uk COVID-19 crisis, and we are already reviewing articles on the role of health humanities during the pandemic. The process of academic publishing tends not to lend itself to immediacy, however, and the challenges of pandemic means greater pressure on everyone, from the authors to the reviewers and readers.To remedy this, we at Medical Humanities have been increasing the work on our blog platform, a place where content can be quickly updated, and where conversations can occur among readers and writers.

We openly invite submissions concerning the virus, as well as topics relevant to our wider CFP (call for buy crestor online uk posts/papers) this year on social justice and health, to both blog and journal. We will do our best to expedite. Finally, we have also been addressing social justice and access in our podcast, where we interviewed disability activist Alice Wong and most recently Dr Oni Blackstock, primary care physician and HIV specialist in New York.

We hope buy crestor online uk to have many more on these critical subjects.We wish all of you good health and safety and know that many of you are yet on the front lines. Thank you for being part of the community of Medical Humanities.IntroductionMinecraft is a computer game with no specific goals to accomplish. The gameworld consists of three-dimensional (3D) cubes buy crestor online uk and objects which the player (Steve) can mine and build into infinitely complex (and logically impossible) structures.

Steve sometimes encounters other characters (‘mobs’), such as animals and hostile creatures. He can ‘spawn’ and destroy them. While it looks like a harmless game of logical construction, it conveys some worryingly delusive ideas about the real buy crestor online uk world.

The difference between real and imagined structures is at the heart of the age-old debate around categorising mental disorders.Classification in mental health has had various forms throughout history. Mack and colleagues set out a history of psychiatric classification buy crestor online uk beginning in 2600 BC with Egyptian references to melancholia and hysteria. Through the Ancient Greeks with Hippocrates’ phrenitis, mania, melancholia, epilepsy, hysteria and Scythian disease.

Through the Renaissance period. Through to 19th-century psychiatry featuring Pinel (known as the first psychiatrist), Kraepelin (known for observational classification) and Freud (known for classifying neurosis and psychosis).1Although the buy crestor online uk history of psychiatric classification identifies some common trends such as the labels ‘melancholia’ and ‘hysteria’ which have survived millennia, the label ‘depression’ is relatively new. The earliest usage noted by Snaith is from 1899.

€˜in simple pathological depression…the patient exhibits a growing indifference to his former pursuits…’.2 Snaith noted that early 20th-century psychiatrists like Adolf Meyer hoped that ‘depression’ buy crestor online uk would come to encompass a broad category under which descriptions of subtypes would emerge. This did not happen until the middle of the 20th century. With the publication of the sixth International Classification of Diseases (ICD) in 1948 and the Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1952 and their subsequent revisions, the latter half of the 20th century has seen depression subtype labels proliferate.

In their study of the social determinants of diagnostic labels in depression, McPherson and Armstrong illustrate how the codification of depression subtypes in the latter half of the 20th century has been shaped by the evolving context of psychiatry, including power struggles within the profession, a move to community care and the development of psychopharmacology.3During this period, McPherson and Armstrong describe how subsequent versions of the DSM served as battlegrounds for professional disputes and buy crestor online uk philosophical quarrels around categorisation of mental disorders. DSM I and DSM II have been described as products of an American Psychiatric Association dominated by psychoanalytic psychiatrists.4 DSM III and DSM III-R have been described as a radical rejection of psychoanalytic thinking, a ‘neo-Kraepelinian revolution’, a reference to the observational descriptive techniques of 19th-century psychiatrist Emil Kraepelin who classified mental disorders into two broad categories. €˜dementia praecox’ and ‘manic-depression’.5 DSM III was seen by some as a turning point in the use of the medical model of mental illness, through provision of specific inclusion and exclusion criteria, and use of field trials and a multiaxial system.6 These latter technocratic additions to psychiatric labelling served to engender a much closer alignment between psychiatry, science and medicine.The codification of mental disorders in manuals has been described by Thomas Schacht as intrinsic to the relationship between science and politics and the way in which psychiatrists gain significant social power by aligning themselves to science.7 His argument drew on Szasz, who saw buy crestor online uk the mental health establishment as a therapeutic state.

Zimbardo, who described psychiatric care as a controlling force. And Foucault, who described the categorisation of the mentally ill as a force for isolating ‘the other’. Diagnostic critique has been further developed through a cultural relativist lens in that what Western psychiatrists classify as a depression is constructed differently in other cultures.8 Considering these limitations, some critics have gone so far as to argue buy crestor online uk that psychiatric diagnostic systems should be abolished.9Yet architects of DSM manuals have worked hard to ensure the technology of classification is regarded as genuine scientific activity with sound roots in philosophy of science.

In their philosophical defence of DSM IV, Allen Frances and colleagues address their critics under the headings ‘nominalism vs realism’, ‘empiricism vs rationalism’ and ‘categorical vs dimensional’.10 The implication is that there are opposing stances in which a choice must be made or a middle ground forged by those reasonable enough to recognise the need for pragmatism in the service of clinical utility. The nominalism–realism debate is illustrated using buy crestor online uk as metaphor three different stances a cricket umpire might take on calling strikes and balls. The discussion sets out two of these as extreme views.

€˜at one extreme…those who take a reductionistically realistic view of the world’ versus ‘the solipsistic nominalists…might content that nothing exists’. Szasz, who buy crestor online uk is characterised as holding particularly extreme views, is named as an archetypal solipsist. There is implied to be a degree of arrogance associated with this view in the illustrative example in which the umpire states ‘there are no balls and there are no strikes until I call them’.

Frances therefore sets up a means of grouping two kinds of people as philosophical extremists who can be dismissed, while avoiding addressing the philosophical problems they pose.Frances provides little if any justification for the middle ground stance, ‘There are balls and there are strikes and I call them as I see them’, other than to focus on its clinical utility and the lack of clinical utility in buy crestor online uk the alternatives ‘naïve realism’ and ‘heuristically barren solipsism’. The natural conclusion the reader is invited to reach is that a middle ground of a heuristic concept is naturally right because it is not extreme and is naturally useful clinically, without specifying in what way this stance is coherent, resolves the two alternatives, and in what way a heuristic construct that is not ‘real’ can be subject to scientific testing.Similarly, in discussing the ‘categorical vs dimensional’, Frances promotes the ‘prototype approach’. Those holding opposing views are labelled as ‘dualists’ or ‘dichotomisers’.

The prototypical approach is again put forward as buy crestor online uk a clinically useful middle ground. Illustrations are drawn from natural science. €˜a triangle and a square are never the same’, inciting the reader to consider science as value-free buy crestor online uk.

The prototypical approach emerges as a natural solution, yet the authors do not address how a diagnostic prototype resolves the issues posed by the two alternatives, nor how a prototype can be subjected to natural science methods.The argument presented here is not a defence of solipsism or dualism. Rather it aims to illustrate that if for pragmatic purposes clinicians and policymakers choose to gloss over the philosophical flaws in classification practices, it is then risky to move beyond the heuristic and apply natural science methods to these constructs adding multiple layers of technocratic subclassification. Doing so is more like playing Minecraft than buy crestor online uk cricket.

The National Institute for Health and Care Excellence (NICE) guideline for depression is taken as an example of the philosophical errors that can follow from playing Minecraft with unsound heuristic devices, specifically subcategories of persistent forms of depression. As well as buy crestor online uk serving a clinical purpose, diagnosis in medicine is a way of allocating resources for insurance companies and constructing clinical guidelines, which in turn determine rationing within the National Health Service. The consequences for recipients of healthcare are therefore significant.

Clinical utility is arguably not being served at all and patients are left at risk of poor-quality care.Heterogeneity of persistent depressionAndrea Jobst and colleagues note that ‘because of their chronic clinical course, approximately 40% of CD [chronic depression] patients also fulfil criteria for TRD [treatment resistant depression]…usually defined by the number of non-successful biological treatments’.11 This position is reflected in the DSM VAmerican Psychiatric Association (2013), the European Psychiatric Association (EPA) guidance and the ICD-11(World Health Organisation, 2018), which all use a ‘persistent’ depression category, acknowledging a loosely defined mixed group of long-term, difficult-to-treat depressive conditions, often associated with dysthymia and comorbid common mental disorders, various personality traits and psychosocial disability.In contrast, the NICE 2018 draft guideline separates treatments into those for ‘new episodes’ of depression. €˜further-line’ treatment of depression buy crestor online uk (equivalent to TRD), CD and ‘depression with co-morbidities’. The latter is subdivided into treatments for ‘complex depression’ and ‘psychotic depression’.

These categories and subcategories introduce an unfortunate sense of certainty as though these labels represent buy crestor online uk real things. An analysis follows of how these definitions play out in terms of grouping of randomised controlled trials in the NICE evidence review. Specifically, the analysis reveals the overlap between populations in trials which have been separated into discrete categories, revealing significant limitations to the utility of the category labels.The NICE definition of CD requires trial samples to meet the criteria for major depressive disorder (MDD) for 2 years.

Dysthymia and double depression (MDD superimposed on dysthymia) were buy crestor online uk included. If 75% of the trial population met these criteria, the trial was reviewed in the CD category.12 The definition of TRD (or ‘further-line treatments’) required that the trial sample had demonstrated a ‘limited response to previous treatment’ and randomised to the further-line treatment at this point. If 80% of the trial participants buy crestor online uk met these criteria, it was reviewed in the TRD category.13 Complex depression was defined as ‘depression co-existing with personality disorder’.

To be classed as complex, 51% of trial participants had to have personality disorder (PD).14It is immediately clear from these definitions that there is a potential problem with attempting to categorise trial populations into just one of these categories. These populations are likely to overlap, whether or not a trial protocol sets out to explicitly record all of this information. The analysis below will illustrate this using examples from within the NICE review.Cataloguing complexity in trial populationsWithin the category buy crestor online uk of further-line treatments (TRD), 64 trials were reviewed.

Comparisons within these trials were further subcategorised into ‘dose escalation strategies’, ‘augmentation strategies’ and ‘switching strategies’. In drilling down by way of illustration, this analysis considers the 51 trials in the augmentation strategy buy crestor online uk evidence review. Of these, two were classified by the reviewers as also fulfilling the criteria for CD but were not analysed in the CD category (Study IDs.

Fonagy 2015 and Kocsis 200915). About half of the trials buy crestor online uk (23/51) did not report the mean duration of episode, meaning that it is not possible to know what percentage of participants also met the criteria for CD. Of trials that did report episode duration, 17 reported a mean duration longer than 24 months.

While the standard deviations varied in size or were unreported, the mean indicates a good likelihood that a significant buy crestor online uk proportion of the participants across these 51 trials met the criteria for CD.Details of baseline employment, trauma history, suicidality, physical comorbidity, axis I comorbidity and PD (all clinical indicators of complexity, severity and chronicity) were not collated by NICE. For the present analysis, all 51 publications were examined and data compiled concerning clinical complexity in the trial populations. Only 14 of 51 trials report employment data.

Of those buy crestor online uk that do, unemployment ranges from 12% to 56% across trial samples. None of the trials report trauma history. About half of the trials buy crestor online uk (26/51) excluded people who were considered a suicide risk.

The others did not.A large proportion of trials (30/51) did not provide any data on axis 1 comorbidity. Of these, 18 did not exclude any diagnoses, while 12 excluded some (but not all) disorders. The most common diagnoses excluded were psychotic disorders, substance or alcohol abuse, and bipolar disorder (excluded in 26, 25 buy crestor online uk and 23 trials, respectively).

Only 7 of 51 trials clearly stated that all axis 1 diagnoses were excluded. This leaves only 13 studies providing any data about buy crestor online uk comorbidity. Of these, 9 gave partial data on one or two conditions, while 4 reported either the mean number of disorders (range 1.96–2.9) or the percentage of participants (range 68.1–96.7) with any comorbid diagnosis (Nierenberg 2003a, Nierenberg 2006, Watkins 2011a, Town 201715).The majority of trials (46/51) did not report the prevalence of PD.

Many stated PD as an exclusion criterion but without defining a threshold for exclusion. For example, buy crestor online uk PD could be excluded if it ‘impacted’ the depression, if it was ‘significant’, ‘severe’ or ‘persistent’. Some excluded certain PDs (such as antisocial or borderline) and not others but without reporting the prevalence of those not excluded.

In the five trials where prevalence was clear, prevalence ranged from 0% buy crestor online uk (Ravindran 2008a15), where all PDs were excluded, to 87.5% of the sample (Town 201715). Two studies reported the mean number of PDs. 2.0 (Nierenberg 2003a) and 0.85 (Watkins 2011a15).The majority of trials (43/51) did not report the prevalence of physical illness.

Many stated illness as an exclusion criterion, buy crestor online uk but the definitions and thresholds were vague and could be interpreted in different ways. For example, illness could be excluded if it was ‘unstable’, ‘serious’, ‘significant’, ‘relevant’, or would ‘contraindicate’ or crestor allergy ‘impact’ the medication. Of the eight trials reporting buy crestor online uk information about physical health, there was a wide variation.

Four reported prevalence varying from 7.6% having a disability (Eisendrath 201615) to 90.9% having an illness or disability (Town 201715). Four used scales of physical health. Two indicating mild problems (Nierenberg 2006, Lavretsky 201115) and two indicating moderately high levels of illness (Thase 2007, Fang buy crestor online uk 201015).The NICE review also divided trial populations into a dichotomy of ‘more severe’ and ‘less severe’ on the grounds that this would be a clinically useful classification for general practitioners.

NICE applied a bespoke methodology for creating this dichotomy, abandoning validated measure thresholds in order first to generate two ‘homogeneous’ groups to ‘facilitate analysis’, and second to create an algorithm to ‘read across’ different measures (such as the Beck Depression Inventory, the Hamilton Rating Scale for Depression (HRSD) and the Montgomery-Asberg Depression Rating Scale).16 Examining trials which use more than one of these measures reveals problems in the algorithm. Of the 51 trials, there are buy crestor online uk 6 instances in which the study population falls into NICE’s more severe category according to one measure and into the less severe category according to another. In four of these trials, NICE chose the less severe category (Souza 2016, Watkins 2011a, Fonagy 2015, Town 201715).

The other two trials were designated more severe (Barbee 2011, Dunner 200715). Only 17 of 51 trials reported two or more depression scale measures, leaving much unknown about whether other study populations could count buy crestor online uk as both more severe and less severe.Absence of knowledge or knowledge of absence?. A key philosophical error in science is to confuse an absence of knowledge with knowledge of absence.

It is likely that some of the study populations deemed lacking in complexity or severity buy crestor online uk could actually have high degrees of complexity and/or severity. Data to demonstrate this may either fall foul of a guideline committee decision to prioritise certain information over other conflicting information (as in the severity algorithm). The information may be non-existent as it was not collected.

It may buy crestor online uk be somewhere in the publication pipeline. Or it may be sitting in a database with a research team that has run out of funds for supplementary analyses. Wherever those data are or are not, their absence from published articles does not define the phenomenology of depression for the patients who took buy crestor online uk part.

As a case in point, data from the Fonagy 2015 trial presented at conferences but not published reveal that PD prevalence data would place the trial well within the NICE complex depression category, and that the sample had high levels of past trauma and physical condition comorbidity. The trial also meets the guideline criteria for CD according to the guideline’s own appendices.17 Reported axis 1 comorbidity was high (75.2% had anxiety disorder, 18.6% had substance abuse disorder, 13.2% had eating disorder).18 The mean depression scores at baseline were 36.5 on the Beck Depression Inventory and 20.1 on the HRSD (severe and very severe, respectively, according to published cut-off scores). NICE categorised this population as less severe TRD, not CD buy crestor online uk and not complex.Notes1.

Avram H. Mack et al buy crestor online uk. (1994), “A Brief History of Psychiatric Classification.

From the Ancients to DSM-IV,” Psychiatric Clinics 17, no. 3. 515–9.2.

R. P. Snaith (1987), “The Concepts of Mild Depression,” British Journal of Psychiatry 150, no.

3. 387.3. Susan McPherson and David Armstrong (2006), “Social Determinants of Diagnostic Labels in Depression,” Social Science &.

Gerald N. Grob (1991), “Origins of DSM-I. A Study in Appearance and Reality,” The American Journal of Psychiatry.

421–31.5. Wilson M. Compton and Samuel B.

Guze (1995), “The Neo-Kraepelinian Revolution in Psychiatric Diagnosis,” European Archives of Psychiatry and Clinical Neuroscience 245, no. 4. 198–9.6.

Gerald L. Klerman (1984), “A Debate on DSM-III. The Advantages of DSM-III,” The American Journal of Psychiatry.

539–42.7. Thomas E. Schacht (1985), “DSM-III and the Politics of Truth,” American Psychologist.

Theurer (2018), “Psychiatry Should Not Seek Mechanisms of Disorder,” Journal of Theoretical and Philosophical Psychology 38, no. 4. 189–204.9.

Sami Timimi (2014), “No More Psychiatric Labels. Why Formal Psychiatric Diagnostic Systems Should Be Abolished,” Journal of Clinical and Health Psychology 14, no. 3.

208–15.10. Allen Frances et al. (1994), “DSM-IV Meets Philosophy,” The Journal of Medicine and Philosophy.

A Forum for Bioethics and Philosophy of Medicine 19, no. 3. 207–18.11.

Andrea Jobst et al. (2016), “European Psychiatric Association Guidance on Psychotherapy in Chronic Depression Across Europe,” European Psychiatry 33. 20.12.

National Institute for Health and Care Excellence (2018), Depression in Adults. Treatment and Management. Draft for Consultation, https://www.nice.org.uk/guidance/gid-cgwave0725/documents/full-guideline-updated, 507.13.

Ibid., 351–62.14. Ibid., 597.15. Note that in order to refer to specific trials reviewed in the guideline, rather than the full citation, the Study IDs from column A in appendix J5 have been used.

See www.nice.org.uk/guidance/gid-cgwave0725/documents/addendum-appendix-9 for details and full references.16. National Institute for Health and Care Excellence (2018), Depression in Adults. Treatment and Management.

Second Consultation on Draft Guideline – Stakeholder Comments Table, https://www.nice.org.uk/guidance/gid-cgwave0725/documents/consultation-comments-and-responses-2, 420–1.17. National Institute for Health and Care Excellence (2018), Depression in Adults, appendix J5.18. Peter Fonagy et al.

(2015), “Pragmatic Randomized Controlled Trial of Long-Term Psychoanalytic Psychotherapy for Treatment-Resistant Depression. The Tavistock Adult Depression Study (TADS),” World Psychiatry 14, no. 3.

312–21.19. American Psychological Association (2018), Clinical Practice Guideline for the Treatment of Depression in Children, Adolescents, and Young, Middle-aged, and Older Adults. Draft.20.

Jacqui Thornton (2018), “Depression in Adults. Campaigners and Doctors Demand Full Revision of NICE Guidance,” BMJ 361. K2681..

Buy crestor online canada

Start Preamble buy crestor online canada Centers http://www.niss.lv/buy-crestor/ for Medicare &. Medicaid Services (CMS), HHS. Continuation of effectiveness and extension of timeline for publication of buy crestor online canada the final rule.

This document announces the continuation of, effectiveness of, and the extension of the timeline for publication of a final rule. We are issuing this document in accordance with section 1871(a)(3)(C) of the Social Security Act (the Act), which allows an interim final rule to remain in effect after the expiration of the timeline specified in section 1871(a)(3)(B) of the Act if the Secretary publishes a notice of continuation explaining why we did not comply with the regular publication timeline. Effective September 4, 2020, the Medicare provisions adopted in the interim final rule published on September 6, 2016 (81 FR buy crestor online canada 61538), continue in effect and the regular timeline for publication of the final rule is extended for an additional year, until September 6, 2021.

Start Further Info Steve Forry (410) 786-1564 or Jaqueline Cipa (410) 786-3259. End Further Info End Preamble Start Supplemental Information Section 1871(a) of the Social Security Act (the Act) sets forth certain procedures for promulgating regulations necessary to carry out the administration of the insurance programs under Title XVIII of the Act. Section 1871(a)(3)(A) of the Act requires the Secretary, in consultation with the Director of the Office of Management and Budget (OMB), buy crestor online canada to establish a regular timeline for the publication of final regulations based on the previous publication of a proposed rule or an interim final rule.

In accordance with section 1871(a)(3)(B) of the Act, such timeline may vary among different rules, based on the complexity of the rule, the number and scope of the comments received, and other relevant factors. However, the timeline for publishing the final rule, cannot exceed 3 years from the date of publication of the proposed or interim final rule, unless there are exceptional circumstances. After consultation with the Director of OMB, the Secretary published a document, which appeared in the December 30, 2004 Federal Register on (69 FR 78442), establishing a general 3-year timeline for publishing Medicare final rules after the buy crestor online canada publication of a proposed or interim final rule.

Section 1871(a)(3)(C) of the Act states that upon expiration of the regular timeline for the publication of a final regulation after opportunity for public comment, a Medicare interim final rule shall not continue in effect unless the Secretary publishes a notice of continuation of the regulation that includes an explanation of why the regular timeline was not met. Upon publication of such notice, the regular timeline for publication of the final regulation is treated as having been extended for 1 additional year. On September 6, 2016 Federal Register (81 FR 61538), the Department of Health and Human Services (HHS) issued a department-wide interim final rule titled “Adjustment of Civil Monetary Penalties for Inflation” that established new regulations at 45 CFR part 102 to adjust for inflation the maximum civil monetary penalty amounts for the various civil monetary penalty authorities for all agencies within the Department buy crestor online canada.

HHS took this action to comply with the Federal Civil Penalties Inflation Adjustment Act of 1990 (the Inflation Adjustment Act) (28 U.S.C. 2461 note 2(a)), as amended by the Federal Civil Penalties Inflation Adjustment Act Improvements Act of 2015 (section 701 of the Bipartisan Budget Act of 2015, (Pub. L.

114-74), enacted on November 2, 2015). In addition, this September 2016 interim final rule included updates to certain agency-specific regulations to reflect the new provisions governing the adjustment of civil monetary penalties for inflation in 45 CFR part 102. One of the purposes of the Inflation Adjustment Act was to create a mechanism to allow for regular inflationary adjustments to federal civil monetary penalties.

Section 2(b)(1) of the Inflation Adjustment Act. The 2015 amendments removed an inflation update exclusion that previously Start Printed Page 55386applied to the Social Security Act as well as to the Occupational Safety and Health Act. The 2015 amendments also “reset” the inflation calculations by excluding prior inflationary adjustments under the Inflation Adjustment Act and requiring agencies to identify, for each penalty, the year and corresponding amount(s) for which the maximum penalty level or range of minimum and maximum penalties was established (that is, originally enacted by Congress) or last adjusted other than pursuant to the Inflation Adjustment Act.

In accordance with section 4 of the Inflation Adjustment Act, agencies were required to. (1) Adjust the level of civil monetary penalties with an initial “catch-up” adjustment through an interim final rulemaking (IFR) to take effect by August 1, 2016. And (2) make subsequent annual adjustments for inflation.

In the September 2016 interim final rule, HHS adopted new regulations at 45 CFR part how much is crestor without insurance 102 to govern adjustment of civil monetary penalties for inflation. The regulation at 45 CFR 102.1 provides that part 102 applies to each statutory provision under the laws administered by the Department of Health and Human Services concerning civil monetary penalties, and that the regulations in part 102 supersede existing HHS regulations setting forth civil monetary penalty amounts. The civil money penalties and the adjusted penalty amounts administered by all HHS agencies are listed in tabular form in 45 CFR 102.3.

In addition to codifying the adjusted penalty amounts identified in § 102.3, the HHS-wide interim final rule included several technical conforming updates to certain agency-specific regulations, including various CMS regulations, to identify their updated information, and incorporate a cross-reference to the location of HHS-wide regulations. Because the conforming changes to the Medicare provisions were part of a larger, omnibus departmental interim final rule, we inadvertently missed setting a target date for the final rule to make permanent the changes to the Medicare regulations in accordance with section 1871(a)(3)(A) of the Act and the procedures outlined in the December 2004 document. Therefore, in the January 2, 2020 Federal Register (85 FR 7), we published a document continuing the effectiveness of effect and the regular timeline for publication of the final rule for an additional year, until September 6, 2020.

Consistent with section 1871(a)(3)(C) of the Act, we are publishing this second notice of continuation extending the effectiveness of the technical conforming changes to the Medicare regulations that were implemented through interim final rule and to allow time to publish a final rule. On January 31, 2020, pursuant to section 319 of the Public Health Service Act (PHSA), the Secretary determined that a Public Health Emergency (PHE) exists for the United States to aid the nation's healthcare community in responding to COVID-19. On March 11, 2020, the World Health Organization (WHO) publicly declared COVID-19 a pandemic.

On March 13, 2020, the President declared the COVID-19 pandemic a national emergency. This declaration, along with the Secretary's January 31, 2020 declaration of a PHE, conferred on the Secretary certain waiver authorities under section 1135 of the Act. On March 13, 2020, the Secretary authorized waivers under section 1135 of the Act, effective March 1, 2020.[] Effective July 25, 2020, the Secretary renewed the January 31, 2020 determination that was previously renewed on April 21, 2020, that a PHE exists and has existed since January 27, 2020.

The unprecedented nature of this national emergency has placed enormous responsibilities upon CMS to respond appropriately, and resources have had to be re-allocated throughout the agency in order to be responsive. Therefore, the Medicare provisions adopted in interim final regulation continue in effect and the regular timeline for publication of the final rule is extended for an additional year, until September 6, 2021. Start Signature Wilma M.

Robinson, Deputy Executive Secretary to the Department, Department of Health and Human Services. End Signature End Supplemental Information [FR Doc. 2020-19657 Filed 9-4-20.

8:45 am]BILLING CODE 4120-01-PThis document is unpublished. It is scheduled to be published on 09/18/2020. Once it is published it will be available on this page in an official form.

Until then, you can download the unpublished PDF version. Although we make a concerted effort to reproduce the original document in full on our Public Inspection pages, in some cases graphics may not be displayed, and non-substantive markup language may appear alongside substantive text. If you are using public inspection listings for legal research, you should verify the contents of documents against a final, official edition of the Federal Register.

Only official editions of the Federal Register provide legal notice to the public and judicial notice to the courts under 44 U.S.C. 1503 &. 1507.

Start Preamble Centers for buy crestor online uk Medicare &. Medicaid Services (CMS), HHS. Continuation of buy crestor online uk effectiveness and extension of timeline for publication of the final rule. This document announces the continuation of, effectiveness of, and the extension of the timeline for publication of a final rule. We are issuing this document in accordance with section 1871(a)(3)(C) of the Social Security Act (the Act), which allows an interim final rule to remain in effect after the expiration of the timeline specified in section 1871(a)(3)(B) of the Act if the Secretary publishes a notice of continuation explaining why we did not comply with the regular publication timeline.

Effective September 4, 2020, the Medicare provisions adopted in the interim final rule published on September 6, 2016 (81 buy crestor online uk FR 61538), continue in effect and the regular timeline for publication of the final rule is extended for an additional year, until September 6, 2021. Start Further Info Steve Forry (410) 786-1564 or Jaqueline Cipa (410) 786-3259. End Further Info End Preamble Start Supplemental Information Section 1871(a) of the Social Security Act (the Act) sets forth certain procedures for promulgating regulations necessary to carry out the administration of the insurance programs under Title XVIII of the Act. Section 1871(a)(3)(A) of the Act requires the Secretary, in consultation with the Director of the Office of Management and Budget (OMB), to establish a regular timeline for the publication of final regulations based on the previous publication of a proposed rule or an interim final rule buy crestor online uk. In accordance with section 1871(a)(3)(B) of the Act, such timeline may vary among different rules, based on the complexity of the rule, the number and scope of the comments received, and other relevant factors.

However, the timeline for publishing the final rule, cannot exceed 3 years from the date of publication of the proposed or interim final rule, unless there are exceptional circumstances. After consultation with the Director of OMB, the Secretary published a document, which appeared in the December 30, 2004 Federal Register on (69 FR 78442), buy crestor online uk establishing a general 3-year timeline for publishing Medicare final rules after the publication of a proposed or interim final rule. Section 1871(a)(3)(C) of the Act states that upon expiration of the regular timeline for the publication of a final regulation after opportunity for public comment, a Medicare interim final rule shall not continue in effect unless the Secretary publishes a notice of continuation of the regulation that includes an explanation of why the regular timeline was not met. Upon publication of such notice, the regular timeline for publication of the final regulation is treated as having been extended for 1 additional year. On September 6, 2016 Federal Register (81 FR 61538), the Department of Health and Human Services (HHS) issued a department-wide interim final rule titled “Adjustment of Civil Monetary Penalties for Inflation” that established new regulations at 45 CFR part 102 to adjust for inflation the maximum civil buy crestor online uk monetary penalty amounts for the various civil monetary penalty authorities for all agencies within the Department.

HHS took this action to comply with the Federal Civil Penalties Inflation Adjustment Act of 1990 (the Inflation Adjustment Act) (28 U.S.C. 2461 note 2(a)), as amended by the Federal Civil Penalties Inflation Adjustment Act Improvements Act of 2015 (section 701 of the Bipartisan Budget Act of 2015, (Pub. L. 114-74), enacted on November 2, 2015). In addition, this September 2016 interim final rule included updates to certain agency-specific regulations to reflect the new provisions governing the adjustment of civil monetary penalties for inflation in 45 CFR part 102.

One of the purposes of the Inflation Adjustment Act was to create a mechanism to allow for regular inflationary adjustments to federal civil monetary penalties. Section 2(b)(1) of the Inflation Adjustment Act. The 2015 amendments removed an inflation update exclusion that previously Start Printed Page 55386applied to the Social Security Act as well as to the Occupational Safety and Health Act. The 2015 amendments also “reset” the inflation calculations by excluding prior inflationary adjustments under the Inflation Adjustment Act and requiring agencies to identify, for each penalty, the year and corresponding amount(s) for which the maximum penalty level or range of minimum and maximum penalties was established (that is, originally enacted by Congress) or last adjusted other than pursuant to the Inflation Adjustment Act. In accordance with section 4 of the Inflation Adjustment Act, agencies were required to.

(1) Adjust the level of civil monetary penalties with an initial “catch-up” adjustment through an interim final rulemaking (IFR) to take effect by August 1, 2016. And (2) make subsequent annual adjustments for inflation. In the September 2016 interim final rule, HHS adopted new regulations at 45 CFR part 102 to govern adjustment of civil monetary penalties for inflation. The regulation at 45 CFR 102.1 provides that part 102 applies to each statutory provision under the laws administered by the Department of Health and Human Services concerning civil monetary penalties, and that the regulations in part 102 supersede existing HHS regulations setting forth civil monetary penalty amounts. The civil money penalties and the adjusted penalty amounts administered by all HHS agencies are listed in tabular form in 45 CFR 102.3.

In addition to codifying the adjusted penalty amounts identified in § 102.3, the HHS-wide interim final rule included several technical conforming updates to certain agency-specific regulations, including various CMS regulations, to identify their updated information, and incorporate a cross-reference to the location of HHS-wide regulations. Because the conforming changes to the Medicare provisions were part of a larger, omnibus departmental interim final rule, we inadvertently missed setting a target date for the final rule to make permanent the changes to the Medicare regulations in accordance with section 1871(a)(3)(A) of the Act and the procedures outlined in the December 2004 document. Therefore, in the January 2, 2020 Federal Register (85 FR 7), we published a document continuing the effectiveness of effect and the regular timeline for publication of the final rule for an additional year, until September 6, 2020. Consistent with section 1871(a)(3)(C) of the Act, we are publishing this second notice of continuation extending the effectiveness of the technical conforming changes to the Medicare regulations that were implemented through interim final rule and to allow time to publish a final rule. On January 31, 2020, pursuant to section 319 of the Public Health Service Act (PHSA), the Secretary determined that a Public Health Emergency (PHE) exists for the United States to aid the nation's healthcare community in responding to COVID-19.

On March 11, 2020, the World Health Organization (WHO) publicly declared COVID-19 a pandemic. On March 13, 2020, the President declared the COVID-19 pandemic a national emergency. This declaration, along with the Secretary's January 31, 2020 declaration of a PHE, conferred on the Secretary certain waiver authorities under section 1135 of the Act. On March 13, 2020, the Secretary authorized waivers under section 1135 of the Act, effective March 1, 2020.[] Effective July 25, 2020, the Secretary renewed the January 31, 2020 determination that was previously renewed on April 21, 2020, that a PHE exists and has existed since January 27, 2020. The unprecedented nature of this national emergency has placed enormous responsibilities upon CMS to respond appropriately, and resources have had to be re-allocated throughout the agency in order to be responsive.

Therefore, the Medicare provisions adopted in interim final regulation continue in effect and the regular timeline for publication of the final rule is extended for an additional year, until September 6, 2021. Start Signature Wilma M. Robinson, Deputy Executive Secretary to the Department, Department of Health and Human Services. End Signature End Supplemental Information [FR Doc. 2020-19657 Filed 9-4-20.

8:45 am]BILLING CODE 4120-01-PThis document is unpublished. It is scheduled to be published on 09/18/2020. Once it is published it will be available on this page in an official form. Until then, you can download the unpublished PDF version. Although we make a concerted effort to reproduce the original document in full on our Public Inspection pages, in some cases graphics may not be displayed, and non-substantive markup language may appear alongside substantive text.

If you are using public inspection listings for legal research, you should verify the contents of documents against a final, official edition of the Federal Register. Only official editions of the Federal Register provide legal notice to the public and judicial notice to the courts under 44 U.S.C. 1503 &. 1507. Learn more here..

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Shutterstock An event in Smyrna, Del., provided opioid rescue kits to residents efectos secundarios de crestor and free training http://www.niss.lv/crestor-sales/ Wednesday. The event was aimed at those who are at risk of experiencing an overdose or for the loved ones of those at risk.Each rescue kit contained two doses of Naloxone, an opioid overdose reversal drug.The training lasted efectos secundarios de crestor approximately 10 minutes. Attendees were taught how to recognize and respond to an opioid overdose emergency. They also were informed about local treatment and support resources.“Amidst the COVID-19 pandemic, we can’t forget about efectos secundarios de crestor crestor brand the opioid epidemic.

Addiction has its grip on our community, and with this event and others, we can make sure that Naloxone gets to individuals and families who may need it during an opioid overdose emergency,” Trinidad Navarro, the insurance commissioner, said. €œWhile we continue to work to ensure that treatment for those with drug dependencies is affordable and accessible, events like these offer an opportunity to increase awareness and education life-saving techniques and tools.”Navarro hosted the event efectos secundarios de crestor in collaboration with Public Health’s Kent County Community Response Team, the First Presbyterian Church of Smyrna, and the Smyrna-Clayton Ministerium. The event was outdoors and offered drive-through and walk-up options..

Shutterstock An event in Smyrna, Del., buy crestor online uk provided opioid rescue kits to residents and free training Wednesday. The event was aimed at those who are at risk of experiencing an overdose or for the loved ones of those at risk.Each rescue kit contained two doses of Naloxone, an opioid overdose reversal drug.The training buy crestor online uk lasted approximately 10 minutes. Attendees were taught how to recognize and respond to an opioid overdose emergency. They also were informed about local treatment and support resources.“Amidst buy crestor online uk the COVID-19 pandemic, we can’t forget about the opioid epidemic. Addiction has its grip on our community, and with this event and others, we can make sure that Naloxone gets to individuals and families who may need it during an opioid overdose emergency,” Trinidad Navarro, the insurance commissioner, said.

€œWhile we continue to work to ensure that treatment for those with drug dependencies is affordable and accessible, events like these offer an buy crestor online uk opportunity to increase awareness and education life-saving techniques and tools.”Navarro hosted the event in collaboration with Public Health’s Kent County Community Response Team, the First Presbyterian Church of Smyrna, and the Smyrna-Clayton Ministerium. The event was outdoors and offered drive-through and walk-up options..

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21 August, side effects stopping crestor cold turkey 2020. The National Clinical Terminology Service (NCTS) is pleased to announce that the August combined release of SNOMED CT®-AU and the Australian Medicines Terminology (AMT) is now available to registered users from the NCTS website. Important InformationThird party reference setsThe following new reference sets are now available to support systems with the identification of the AMT Trade Product Unit of Use (TPUU) and Containered Trade Product Pack (CTPP) concepts that are reportable within South Australia and Queensland for Electronic Recording and Reporting of Controlled Drugs (ERRCD) requirements;South Australia reportable Schedule 4 trade medications reference set.Queensland Health QScript side effects stopping crestor cold turkey Schedule 4 monitored medicines reference set.These complement the existing Tasmania and Victoria reportable Schedule 4 trade medications reference sets and the Schedule 8 medications reference set.The full description of each reference set can be viewed by selecting it within Reference Sets from the ACCESS tab.Document Library updateThe following document has been added to the Document Library.

Please refer to the NCTS Document Library Release Note v2.22 in Recent Updates for further details.LicensingSNOMED CT-AU inclusive of the Australian Medicines Terminology is updated monthly and is available to download for free to registered license holders. To register for an account please go to the registration page.Licensing terms can be side effects stopping crestor cold turkey found here.FeedbackDevelopment by the NCTS relies on the input and cooperation of the Australian healthcare community. We value your feedback and encourage questions, comments, or suggestions about our products.

You can contact us by completing the online support request form, emailing [email protected], or calling 1300 901 001.Thank you for your continued support.- Joint communique - 17 August, 2020 side effects stopping crestor cold turkey. To support those people most at risk from COVID-19, the rollout of electronic prescriptions across Greater Melbourne will be expanded beyond the current communities of interest. This follows successful testing since side effects stopping crestor cold turkey May 2020.

Electronic prescribing is being implemented in General Practices and Community Pharmacies across Australia. To date, this has occurred through a managed approach of testing and continuous improvement across a growing number of ‘communities of interest’.Given the current COVID-19 crisis in Melbourne the Royal side effects stopping crestor cold turkey Australian College of General Practitioners (RACGP) and the Pharmacy Guild of Australia are working together with the Australian Department of Health and the Australian Digital Health Agency to support doctors and pharmacists in the Greater Melbourne area to access this new technology faster. This will support a safer and more convenient supply of medicines for patients.

Previous communications have stated electronic prescriptions should only be written side effects stopping crestor cold turkey or dispensed as part of the communities of interest trials. This is now being expanded to the Greater Melbourne area. If you have made the preparations outlined below, you can and should commence electronic prescribing in Greater Melbourne, starting with the side effects stopping crestor cold turkey patient’s preferred choice of how they receive their prescriptions and medicines.

With an immediate focus on general practices and community pharmacies in greater metropolitan Melbourne to substantially increase electronic prescription capability over the coming weeks we all need to work together. The following steps will help your pharmacy or general practice get ready.General side effects stopping crestor cold turkey practice and pharmacy readiness.Step 1. Software activation - contact your software supplier and ask them to activate your electronic prescribing functionality.Step 2.

Communication between local pharmacies and side effects stopping crestor cold turkey general practices is critical - this will ensure everyone is ready to write and dispense an electronic prescription (noting some pharmacies may require more time and resources to get their dispensing workflow ready).Patients may experience a delay in accessing their medicines including having to return to general practice for a paper prescription if this step is not undertaken.Step 3. Stay informed - attend webinars and education sessions run by the Australian Digital Health Agency, the Pharmacy Guild and the RACGP to learn more about electronic prescribing and how it works.Practices and pharmacies in other areas of Australia are being advised to prepare for a broader rollout by getting software ready and participating in training opportunities being provided by the Agency, peak bodies and software providers. Schedule 8 and 4D medicinesAll medicines, including Schedule 8 and side effects stopping crestor cold turkey 4D medicines, can be prescribed and dispensed through an electronic prescription providing patients with a safe and secure way of obtaining medicines remotely.

Unlike a request for a Schedule 8 or 4D medicine using a digital image prescription via fax or email, the prescriber is not required to send an original hard copy of the prescription to the pharmacy - the electronic (paperless) prescription is the legal order to prescribe and supply.Patient ChoiceIt’s important to remember that electronic prescriptions are an alternative to paper. If a patient’s preferred local pharmacy is not ready for electronic prescriptions, patients can still choose to get a paper prescription from their doctor.ResourcesFor more information about electronic prescribing and electronic prescriptions, see:Department of HealthAustralian Digital Health AgencyAustralian Digital Health Agency electronic prescription eLearningAustralian Digital Health Agency electronic prescription upcoming webinarsThe RACGP side effects stopping crestor cold turkey information for GP’s and patientsPharmaceutical Society of Australia Dedicated Electronic Prescriptions Support Line for pharmacies:1300 955 162. Available 08:30am to 7:00pm AESTMedia contactAustralian Digital Health Agency Media TeamMobile.

0428 772 side effects stopping crestor cold turkey 421Email. [email protected] About the Australian Digital Health AgencyThe Agency is tasked with improving health outcomes for all Australians through the delivery of digital healthcare systems, and implementing Australia’s National Digital Health Strategy – Safe, Seamless, and Secure. Evolving health and care side effects stopping crestor cold turkey to meet the needs of modern Australia in collaboration with partners across the community.

The Agency is the System Operator of My Health Record, and provides leadership, coordination, and delivery of a collaborative and innovative approach to utilising technology to support and enhance a clinically safe and connected national health system. These improvements will give individuals more control of their health and their health information, and support healthcare providers to deliver informed healthcare through access side effects stopping crestor cold turkey to current clinical and treatment information. Further information.

Www.digitalhealth.gov.auMedia release - Electronic prescriptions rolling out to support Melbourne.docx (168KB)Media release - Electronic prescriptions rolling out to support Melbourne.pdf (76KB).

21 August, buy crestor online uk 2020. The National Clinical Terminology Service (NCTS) is pleased to announce that the August combined release of SNOMED CT®-AU and the Australian Medicines Terminology (AMT) is now available to registered users from the NCTS website. Important InformationThird party reference setsThe following new reference sets are now available to support systems with the identification of the AMT Trade Product Unit of Use (TPUU) and Containered Trade Product Pack (CTPP) concepts that are reportable within South Australia and Queensland for Electronic Recording and Reporting of Controlled Drugs (ERRCD) requirements;South Australia reportable Schedule 4 trade medications reference set.Queensland Health QScript Schedule 4 monitored medicines reference set.These complement the existing Tasmania and Victoria reportable Schedule 4 trade medications reference sets and the Schedule 8 medications reference set.The full description of each reference buy crestor online uk set can be viewed by selecting it within Reference Sets from the ACCESS tab.Document Library updateThe following document has been added to the Document Library. Please refer to the NCTS Document Library Release Note v2.22 in Recent Updates for further details.LicensingSNOMED CT-AU inclusive of the Australian Medicines Terminology is updated monthly and is available to download for free to registered license holders. To register for an account please go to the registration page.Licensing terms can be found here.FeedbackDevelopment by the NCTS relies on the input and cooperation buy crestor online uk of the Australian healthcare community.

We value your feedback and encourage questions, comments, or suggestions about our products. You can contact buy crestor online uk us by completing the online support request form, emailing [email protected], or calling 1300 901 001.Thank you for your continued support.- Joint communique - 17 August, 2020. To support those people most at risk from COVID-19, the rollout of electronic prescriptions across Greater Melbourne will be expanded beyond the current communities of interest. This follows successful testing since buy crestor online uk May 2020. Electronic prescribing is being implemented in General Practices and Community Pharmacies across Australia.

To date, this has occurred through a managed approach of testing and continuous improvement across a growing number of ‘communities of interest’.Given the current COVID-19 crisis in Melbourne the Royal Australian College of General Practitioners (RACGP) and the Pharmacy Guild of Australia are working together with the buy crestor online uk Australian Department of Health and the Australian Digital Health Agency to support doctors and pharmacists in the Greater Melbourne area to access this new technology faster. This will support a safer and more convenient supply of medicines for patients. Previous communications have stated electronic prescriptions buy crestor online uk should only be written or dispensed as part of the communities of interest trials. This is now being expanded to the Greater Melbourne area. If you have made the preparations outlined below, you can buy crestor online uk and should commence electronic prescribing in Greater Melbourne, starting with the patient’s preferred choice of how they receive their prescriptions and medicines.

With an immediate focus on general practices and community pharmacies in greater metropolitan Melbourne to substantially increase electronic prescription capability over the coming weeks we all need to work together. The following buy crestor online uk steps will help your pharmacy or general practice get ready.General practice and pharmacy readiness.Step 1. Software activation - contact your software supplier and ask them to activate your electronic prescribing functionality.Step 2. Communication between local pharmacies and general practices is critical - this will ensure everyone is ready to write and dispense an electronic prescription (noting some pharmacies may require more time and resources to get their dispensing workflow ready).Patients may experience a delay in accessing their medicines including having to buy crestor online uk return to general practice for a paper prescription if this step is not undertaken.Step 3. Stay informed - attend webinars and education sessions run by the Australian Digital Health Agency, the Pharmacy Guild and the RACGP to learn more about electronic prescribing and how it works.Practices and pharmacies in other areas of Australia are being advised to prepare for a broader rollout by getting software ready and participating in training opportunities being provided by the Agency, peak bodies and software providers.

Schedule 8 and 4D medicinesAll medicines, including Schedule 8 and 4D medicines, can buy crestor online uk be prescribed and dispensed through an electronic prescription providing patients with a safe and secure way of obtaining medicines remotely. Unlike a request for a Schedule 8 or 4D medicine using a digital image prescription via fax or email, the prescriber is not required to send an original hard copy of the prescription to the pharmacy - the electronic (paperless) prescription is the legal order to prescribe and supply.Patient ChoiceIt’s important to remember that electronic prescriptions are an alternative to paper. If a patient’s preferred local pharmacy is buy crestor online uk not ready for electronic prescriptions, patients can still choose to get a paper prescription from their doctor.ResourcesFor more information about electronic prescribing and electronic prescriptions, see:Department of HealthAustralian Digital Health AgencyAustralian Digital Health Agency electronic prescription eLearningAustralian Digital Health Agency electronic prescription upcoming webinarsThe RACGP information for GP’s and patientsPharmaceutical Society of Australia Dedicated Electronic Prescriptions Support Line for pharmacies:1300 955 162. Available 08:30am to 7:00pm AESTMedia contactAustralian Digital Health Agency Media TeamMobile. 0428 772 buy crestor online uk 421Email.

[email protected] About the Australian Digital Health AgencyThe Agency is tasked with improving health outcomes for all Australians through the delivery of digital healthcare systems, and implementing Australia’s National Digital Health Strategy – Safe, Seamless, and Secure. Evolving health and care to meet the needs of modern Australia in collaboration with buy crestor online uk partners across the community. The Agency is the System Operator of My Health Record, and provides leadership, coordination, and delivery of a collaborative and innovative approach to utilising technology to support and enhance a clinically safe and connected national health system. These improvements will give individuals more control of their health and their health information, and support healthcare providers to deliver informed healthcare through access to current clinical and buy crestor online uk treatment information. Further information.

Www.digitalhealth.gov.auMedia release - Electronic prescriptions rolling out to support Melbourne.docx (168KB)Media release - Electronic prescriptions rolling out to support Melbourne.pdf (76KB).

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Mathematica is crestor food interactions committed to advancing public health by applying our expertise across disciplines that constitute some of the most critical areas of public health today. The following focus areas highlight how we’re working to progress together to improve public well-being.APHA Public Health Film Festival. Helping Families Affected by Substance UseThe APHA selected a short film that Mathematica produced with support from the crestor food interactions Administration for Children and Families to show at the APHA Public Health Film Festival. The film focuses on how the Regional Partnership Grant program improves the safety, permanency, and well-being of children affected by parent’s substance use disorders.

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Social Determinants of HealthPolicymakers and practitioners are increasingly interested in social determinants of health—the conditions in which people are born, grow, live, work, and age—to address upstream social risks, such as food insecurity and lack of affordable housing, that, in turn, improve health care outcomes. Mathematica data and policy experts recently produced a series of blog posts and research on how different stakeholders can improve and leverage data crestor food interactions on social determinants of health to maximize the health and well-being of children and adults in the United States.COVID-19 ServicesResponding to the current public health crisis and illuminating the path forward to safely re-open businesses, schools, workplaces, and community services requires a seasoned partner with trusted solutions. Built on our foundation of rigorous data and evidence, Mathematica’s scalable services provide state and local agencies, as well as private-sector employers, with the confidence and clarity they need to take on the complex challenges of COVID-19. Some of our services include contact tracing, workforce planning, modeling and forecasting, and wastewater testing and analysis.Data Analytics and Survey ExpertiseAt Mathematica, we apply our expertise at the intersection of data science and social science to produce efficient, high quality, and action-oriented analysis that advances your mission.Using advanced technologies, reusable and scalable platforms, and high-performance secure cloud infrastructure, we enable our partners to target areas of opportunity and make the most of their data.

We collect the data you need, manage data as a secure asset, analyze to surface insights, and place this knowledge in the hands of those who need it most.Mental Health and Substance UseMathematica understands crestor food interactions the pressing challenges faced by our partners working to improve the delivery system, innovative value-based service models, and financing strategies that states and payers are testing—strategies that could improve the prevention and treatment of behavioral health conditions. We’re leading efforts to address the opioid crisis, increase access to care while controlling costs, and support the integration of behavioral health services with other health care and social services.Our staff have in-depth knowledge of the complex array of intersecting public and private programs and eligibility requirements that create challenges for consumers to get the help they need. Our work involves evaluating a wide range of behavioral health service delivery crestor food interactions and payment models, helping partners establish programs that implement new services and policies and fill data gaps, fielding large-scale behavioral health surveys, developing and implementing behavioral health quality measures, and analyzing policy to guide decision making. For more than two decades, we’ve conducted national surveys of every known mental health and substance use disorder treatment facility in the country.

Our analyses of T-MSIS data for the Centers for Medicare &. Medicaid Services provide critical information on patterns of substance use disorders and treatment across states as evidenced by the T-MSIS Substance Use Disorder (SUD) Data Book crestor food interactions and a series of supporting data quality briefs.Publisher. Regional Educational Laboratory Mid‑Atlantic Oct 13, 2020 Authors Regional Educational Laboratory Mid‑Atlantic Teacher turnover is a widespread issue. High turnover rates may be costly to the district, disrupt operations, and lower student achievement.

Project Mathematica Leads the Regional Educational Laboratory (REL) for the Mid-Atlantic Region crestor food interactions Funders U.S. Department of Education, National Center for Education Evaluation U.S. Department of Education, Institute of Education Sciences Time Frame 2017-2022.

Mathematica is buy crestor online uk committed to advancing http://www.niss.lv/buy-crestor/ public health by applying our expertise across disciplines that constitute some of the most critical areas of public health today. The following focus areas highlight how we’re working to progress together to improve public well-being.APHA Public Health Film Festival. Helping Families Affected by Substance UseThe APHA selected a short film that Mathematica produced with support from buy crestor online uk the Administration for Children and Families to show at the APHA Public Health Film Festival. The film focuses on how the Regional Partnership Grant program improves the safety, permanency, and well-being of children affected by parent’s substance use disorders.

Starting October 19, registered APHA Annual Meeting attendees can watch the film on demand. Registered attendees can also submit questions to Debra Strong a senior researcher for the Regional Partnership Grant National Cross-Site Evaluation, using a discussion board that will be available with the buy crestor online uk film. Please visit APHA’s page about public health films focusing on substance use and addiction treatment for more information. Diversity, Equity, and InclusionWhat does it take for organizations to progress together?.

It takes a common purpose, shared values, a complementary array buy crestor online uk of resources and capabilities, and a mutual desire to learn from and with each other. Our ongoing diversity, equity, and inclusion journey is driving necessary changes in who we are. How we relate to each other, our partners, buy crestor online uk and our communities. And how we approach our work.

Social Determinants of HealthPolicymakers and practitioners are increasingly interested in social determinants of health—the conditions in which people are born, grow, live, work, and age—to address upstream social risks, such as food insecurity and lack of affordable housing, that, in turn, improve health care outcomes. Mathematica data and policy experts recently produced a series of blog posts and research on how different stakeholders can improve and leverage data on social determinants of health to maximize the health buy crestor online uk and well-being of children and adults in the United States.COVID-19 ServicesResponding to the current public health crisis and illuminating the path forward to safely re-open businesses, schools, workplaces, and community services requires a seasoned partner with trusted solutions. Built on our foundation of rigorous data and evidence, Mathematica’s scalable services provide state and local agencies, as well as private-sector employers, with the confidence and clarity they need to take on the complex challenges of COVID-19. Some of our services include contact tracing, workforce planning, modeling and forecasting, and wastewater testing and analysis.Data Analytics and Survey ExpertiseAt Mathematica, we apply our expertise at the intersection of data science and social science to produce efficient, high quality, and action-oriented analysis that advances your mission.Using advanced technologies, reusable and scalable platforms, and high-performance secure cloud infrastructure, we enable our partners to target areas of opportunity and make the most of their data.

We collect the data you need, manage data as a secure asset, analyze to buy crestor online uk surface insights, and place this knowledge in the hands of those who need it most.Mental Health and Substance UseMathematica understands the pressing challenges faced by our partners working to improve the delivery system, innovative value-based service models, and financing strategies that states and payers are testing—strategies that could improve the prevention and treatment of behavioral health conditions. We’re leading efforts to address the opioid crisis, increase access to care while controlling costs, and support the integration of behavioral health services with other health care and social services.Our staff have in-depth knowledge of the complex array of intersecting public and private programs and eligibility requirements that create challenges for consumers to get the help they need. Our work involves evaluating a wide range of behavioral health service delivery buy crestor online uk and payment models, helping partners establish programs that implement new services and policies and fill data gaps, fielding large-scale behavioral health surveys, developing and implementing behavioral health quality measures, and analyzing policy to guide decision making. For more than two decades, we’ve conducted national surveys of every known mental health and substance use disorder treatment facility in the country.

Our analyses of T-MSIS data for the Centers for Medicare &. Medicaid Services provide critical information on patterns of substance use disorders and treatment across states as evidenced buy crestor online uk by the T-MSIS Substance Use Disorder (SUD) Data Book and a series of supporting data quality briefs.Publisher. Regional Educational Laboratory Mid‑Atlantic Oct 13, 2020 Authors Regional Educational Laboratory Mid‑Atlantic Teacher turnover is a widespread issue. High turnover rates may be costly to the district, disrupt operations, and lower student achievement.

Project Mathematica Leads the Regional Educational Laboratory (REL) for the buy crestor online uk Mid-Atlantic Region Funders U.S. Department of Education, National Center for Education Evaluation U.S. Department of Education, Institute of Education Sciences Time Frame 2017-2022.

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How to crestor knee joint pain what is the difference between crestor and rosuvastatin calcium cite this article:Singh O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J crestor knee joint pain Psychiatry 2020;62:337-8Celebrity suicide 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 crestor knee joint pain 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 crestor knee joint pain discussed on electronic, print, and social media.

We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress calls from their patients in despair crestor knee joint pain 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 Organization report on Preventing crestor knee joint pain Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and illness and also his relationships and finances crestor knee joint pain. 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 crestor knee joint pain a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental health professionals were called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the crestor knee joint pain life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm crestor knee joint pain 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 crestor knee joint pain 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and resource books for interacting with media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely crestor knee joint pain 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” crestor knee joint pain as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr. O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict crestor knee joint pain of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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, crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain SM. Does electroconvulsive therapy cause brain damage. An update crestor knee joint pain.

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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain [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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain. 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain. 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain [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 crestor knee joint pain 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 crestor knee joint pain. 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 crestor knee joint pain 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, crestor knee joint pain 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 crestor knee joint pain. In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al.

In 2015 failed to crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain 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 crestor knee joint pain in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT. However, these cannot be construed as brain damage as is usually understood. Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question.

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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]No AbstractNo Reference information available - sign in for access.

No Supplementary Data.No Article MediaNo MetricsDocument Type. Research ArticleAffiliations:1. Department of Rehabilitation, University of Zimbabwe College of Health Sciences, Harare, Zimbabwe 2. 3.

UCSF Pulmonary Rehabilitation and Sleep Disorders Center 4. Division of Pulmonary and Critical Care Medicine, Zuckerberg San Francisco General Hospital and Trauma Center, University of California San Francisco, San Francisco, CA, USA, , Email. [email protected]Publication date:01 July 2020More about this publication?. The International Journal of Tuberculosis and Lung Disease publishes articles on all aspects of lung health, including public health-related issues such as training programmes, cost-benefit analysis, legislation, epidemiology, intervention studies and health systems research.

The IJTLD is dedicated to the continuing education of physicians and health personnel and the dissemination of information on lung health world-wide. To share scientific research of immediate concern as rapidly as possible, The Union is fast-tracking the publication of certain articles from the IJTLD and publishing them on The Union website, prior to their publication in the Journal. Read fast-track articles.Certain IJTLD articles are also selected for translation into French, Spanish, Chinese or Russian. These are available on the Union website.Editorial BoardInformation for AuthorsSubscribe to this TitleInternational Journal of Tuberculosis and Lung DiseasePublic Health ActionIngenta Connect is not responsible for the content or availability of external websitesNo AbstractNo Reference information available - sign in for access.

No Supplementary Data.No Article MediaNo MetricsDocument Type. Research ArticleAffiliations:1. Faculdade de Medicina, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil 2. Center for Infectious Disease Epidemiology and Surveillance, National Institute of Public Health and the Environment, Bilthoven, The Netherlands, , Email.

[email protected]Publication date:01 July 2020More about this publication?. The International Journal of Tuberculosis and Lung Disease publishes articles on all aspects of lung health, including public health-related issues such as training programmes, cost-benefit analysis, legislation, epidemiology, intervention studies and health systems research. The IJTLD is dedicated to the continuing education of physicians and health personnel and the dissemination of information on lung health world-wide. To share scientific research of immediate concern as rapidly as possible, The Union is fast-tracking the publication of certain articles from the IJTLD and publishing them on The Union website, prior to their publication in the Journal.

Read fast-track articles.Certain IJTLD articles are also selected for translation into French, Spanish, Chinese or Russian. These are available on the Union website.Editorial BoardInformation for AuthorsSubscribe to this TitleInternational Journal of Tuberculosis and Lung DiseasePublic Health ActionIngenta Connect is not responsible for the content or availability of external websites.

How to cite this Read Full Report article:Singh buy crestor online uk 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 buy crestor online uk our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went into a frenzy as newspapers, news channels, buy crestor online uk 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 on electronic, print, and buy crestor online uk social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress calls from their patients in despair with buy crestor online uk increased suicidal ideation.

This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids buy crestor online uk publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide. A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition buy crestor online uk and illness and also his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While buy crestor online uk there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental health professionals were called by media houses 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 buy crestor online uk had no “professional authority” to do so.

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

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

O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest buy crestor online uk. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update buy crestor online uk. 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk.

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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk. 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk.

In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al. In 2015 failed to buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk. 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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, buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk 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 buy crestor online uk.

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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.

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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.

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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]No AbstractNo Reference information available - sign in for access. No Supplementary Data.No Article MediaNo MetricsDocument Type. Research ArticleAffiliations:1. Department of Rehabilitation, University of Zimbabwe College of Health Sciences, Harare, Zimbabwe 2.

3. UCSF Pulmonary Rehabilitation and Sleep Disorders Center 4. Division of Pulmonary and Critical Care Medicine, Zuckerberg San Francisco General Hospital and Trauma Center, University of California San Francisco, San Francisco, CA, USA, , Email. [email protected]Publication date:01 July 2020More about this publication?. The International Journal of Tuberculosis and Lung Disease publishes articles on all aspects of lung health, including public health-related issues such as training programmes, cost-benefit analysis, legislation, epidemiology, intervention studies and health systems research.

The IJTLD is dedicated to the continuing education of physicians and health personnel and the dissemination of information on lung health world-wide. To share scientific research of immediate concern as rapidly as possible, The Union is fast-tracking the publication of certain articles from the IJTLD and publishing them on The Union website, prior to their publication in the Journal. Read fast-track articles.Certain IJTLD articles are also selected for translation into French, Spanish, Chinese or Russian. These are available on the Union website.Editorial BoardInformation for AuthorsSubscribe to this TitleInternational Journal of Tuberculosis and Lung DiseasePublic Health ActionIngenta Connect is not responsible for the content or availability of external websitesNo AbstractNo Reference information available - sign in for access. No Supplementary Data.No Article MediaNo MetricsDocument Type.

Research ArticleAffiliations:1. Faculdade de Medicina, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil 2. Center for Infectious Disease Epidemiology and Surveillance, National Institute of Public Health and the Environment, Bilthoven, The Netherlands, , Email. [email protected]Publication date:01 July 2020More about this publication?. The International Journal of Tuberculosis and Lung Disease publishes articles on all aspects of lung health, including public health-related issues such as training programmes, cost-benefit analysis, legislation, epidemiology, intervention studies and health systems research.

The IJTLD is dedicated to the continuing education of physicians and health personnel and the dissemination of information on lung health world-wide. To share scientific research of immediate concern as rapidly as possible, The Union is fast-tracking the publication of certain articles from the IJTLD and publishing them on The Union website, prior to their publication in the Journal. Read fast-track articles.Certain IJTLD articles are also selected for translation into French, Spanish, Chinese or Russian. These are available on the Union website.Editorial BoardInformation for AuthorsSubscribe to this TitleInternational Journal of Tuberculosis and Lung DiseasePublic Health ActionIngenta Connect is not responsible for the content or availability of external websites.

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