Where to buy ventolin pills

The transpopulation represents a vulnerable population segment where to buy ventolin pills both socially and medically, with a higher incidence of mental health issues. During the asthma treatment outbreak, transgender persons have faced additional social, psychological and physical difficulties.1 2 In Italy and in several other countries access where to buy ventolin pills to healthcare has been difficult or impossible thereby hindering the start or continuation of hormonal and psychological treatments. Furthermore, several where to buy ventolin pills planned gender-affirming surgeries have been postponed. These obstacles may have caused an additional psychological burden given the positive effects of medical and surgical treatments on well-being, directly and indirectly, reducing stressors such as where to buy ventolin pills workplace discrimination and social inequalities.3 Some organisational aspects should also be considered. Binary gender policies may where to buy ventolin pills worsen inequalities and marginalisation of transgender subjects potentially increasing the risk of morbidity and mortality.As with the general population, during the lockdown, the Internet and social media were useful in reducing isolation and, in this particular population, were also relevant for keeping in touch with associations and healthcare facilities with the support of telemedicine services.4 Addressing the role of the telemedicine in the transpopulation, between May and June 2020 we conducted an anonymous web-based survey among transgenders living in Italy (ClinicalTrials.gov Identifier NCT04448418).

Among the 108 respondents, with a mean age of 34.3±11.7 years, 73.1% were transmen and 26.9% transwomen and 88.9% were undergoing gender-affirming hormonal treatment (GAHT). One in four subjects (24.1%) presented a moderate-to-severe impact of the where to buy ventolin pills ventolin event (Impact of Event Scale score ≥26). The availability of telematic endocrinological visit was associated with better Mental Health Scores in the 12-items Short Form Health Survey(SF-12) (p=0.030) and better IES (p=0.006).Our survey suggests a positive effect where to buy ventolin pills of telemedicine as the availability of telematic endocrinological consultations may have relieved the distress caused by the ventolin by offering the opportunity to avoid halting GAHT. In fact, where to buy ventolin pills deprivation of GAHT may result in several negative effects such as the increase in short-term self-medication and in depression and suicidal behaviour not only for those waiting for the start of treatment but also for those already using hormones.5 In conclusion, particular attention should be paid to vulnerable groups like the transpopulation who may pay a higher price during the ventolin. The use of telemedicine where to buy ventolin pills for continuation and monitoring of GAHT may be an effective tool for mitigating the negative effects of the ventolin.AcknowledgmentsThe authors thank Julie Norbury for English copy editing.The British Medical Association recently published their report on the impact of asthma treatment on mental health in England, highlighting the urgent need for investment in mental health services and further recruitment of mental health staff.1 Like many others, they have predicted a substantial increase in demand on mental health services in the coming months.

Their recommendations include a call for detailed workforce planning at local, national and system levels where to buy ventolin pills. This coincides with the publication of the ‘NHS People Plan’ which also emphasised the need to maximise staff potential.2 The message from both is clear, it is time for Trusts to revise and improve how where to buy ventolin pills they use their multidisciplinary workforce, including non-medical prescribers (NMPs).Pharmacists have been able to register as independent prescribers since 20063 and as such, can work autonomously to prescribe any medicine for any medical condition within their areas of competency.4 There has been a slow uptake of pharmacists into this role5 and while a recent General Pharmaceutical Council survey found only a small increase between the number of active prescribers from 2013 (1.094) to 2019 (1.590), almost a quarter of prescribers included mental health within their prescribing practice.6 More recently, we have started to see increasing reports of the value of pharmacist independent prescribers in mental health services.7 8Pharmacists bring a unique perspective to patient consultation. Their expertise in pharmacology and medicine use means they are ideally placed to help patients optimise their medicines treatment4 and to ensure that patients are involved in decisions about their medicines, taking into account individual views and preferences. This approach is consistent with the guidance on medicines optimisation from the National Institute for Health and Care Excellence9 and the Royal Pharmaceutical Society,10 and the Department of Health’s drive to involve patients actively in clinical decisions.11 An increased focus on precision psychiatry in urging clinicians to tailor medicines to patients according to evidence about individualised risks and benefits.12 13 However, it takes time to discuss medicine choices where to buy ventolin pills and to explore individual beliefs about medicines. This is especially relevant in Psychiatry, where a large group of where to buy ventolin pills medicines (eg, antipsychotics) may have a wide range of potential side effects.

Prescribing pharmacists could provide leadership and support in tailoring medicines for patients, as part of where to buy ventolin pills the wider multidisciplinary team.10The recent news that Priadel, the most commonly used brand of lithium in the UK, is planned to be discontinued14 is another example where a new and unexpected burden on psychiatric services could be eased by sharing the workload with prescribing pharmacists. The Medicines and Healthcare Products Regulatory where to buy ventolin pills Agency recommends that patients should have an individualised medication review in order to switch from one brand of lithium to another.14 This is work that can be done by prescribing pharmacists who have an in-depth knowledge of the pharmacokinetics of lithium formulations.Importantly, this is a role that can be delivered using telepsychiatry and enhanced by the use of digital tools. Patients can meet pharmacists from the comfort of their own home where to buy ventolin pills using video conferencing. Pharmacists can upload and share medicines information on the screen while discussing the benefits, risks and individual medication needs with each client. Increasingly organisations are using technology whereby prescriptions can be prepared electronically and sent securely to patients or their medicines providers.15We know from systematic reviews that NMPs in general are considered to provide a responsive, efficient and convenient service5 and to deliver similar prescribing outcomes as doctors.16 Medical professionals who have worked with NMPs have found that this support permits them to concentrate on clinical issues that require medical expertise.5 A patient survey carried out in 2013 indicated that independent non‐medical prescribing was valued highly by patients and that generally there were few perceived differences in the care received from respondents’ NMP and their usual doctor.17 The literature also suggests that an NMP’s role is more likely to flourish when linked to where to buy ventolin pills a strategic vision of NMPs within an National Health Service (NHS) Trust, along with a well-defined area of practice.18Mental health trusts are being asked to prepare for a surge in referrals and as part of this planning, they will need to ensure that they get the most out of their highly skilled workforce.

There are active pharmacist prescribers in many trusts, however, this role is not yet commonplace.19 Health Education England has already identified that this is an important area of transformation for pharmacy and has called on mental health pharmacy teams to develop and share innovative ways of working.19 The ‘NHS People Plan’ outlines a commitment to train 50 community-based specialist mental health pharmacists within the next 2 years, along with a plan to extend the pharmacy foundation training to create a sustainable supply of prescribing pharmacists in future years.2We suggest that Mental Health Trusts should urgently develop prescribing roles for specialist mental health where to buy ventolin pills pharmacists, which are integrated within mental health teams. In these roles, prescribing pharmacists can where to buy ventolin pills actively support their multidisciplinary colleagues in case discussion meetings. Furthermore, they should host regular medication review where to buy ventolin pills clinics, where patients can be referred to discuss their medicine options and, as advancements in precision therapeutics continue, have their treatment individually tailored to their needs. This is the way forward for a modern and patient-oriented NHS in the UK..

Can you get ventolin over the counter australia

Ventolin
Advair diskus
Pulmicort
Promethazine
Ventolin inhaler
Ventolin inhalator
Buy with echeck
Online
Yes
Online
Yes
No
No
How long does work
Order online
On the market
Yes
Canadian Pharmacy
At walgreens
No
Over the counter
11h
17h
14h
17h
5h
21h
Female dosage
Yes
No
Small dose
No
Small dose
Small dose
Best way to get
6h
18h
14h
24h
3h
9h
Does work at first time
No
Offline
Yes
At walgreens
Offline

Universal HIV test-and-treat intervention in African correctional settingsWhile people who are incarcerated have a higher burden of HIV and other STIs, delivering sexual health services How to get cialis over the counter in correctional settings is can you get ventolin over the counter australia difficult. A mixed methods cohort study examined the implementation of a universal test-and-treat intervention at 10 correctional units (6 for men, 3 for women, 1 for youth) in South Africa and Zambia. Same-day anti-retroviral therapy (ART) initiation, training and support, ensuring ART supply, and viral can you get ventolin over the counter australia load monitoring were evaluated among 975 inmates living with HIV.

Median time from enrolment to ART initiation was 0 days (IQR 0–8) and the proportion of people retained in care with viral load monitoring was high (94%, 327/346) among those still incarcerated at 6 months. This study demonstrates the feasibility of implementing comprehensive HIV interventions in can you get ventolin over the counter australia selected settings.Herce ME, Hoffmann CJ, Fielding K, et al. Universal test-and-treat in Zambian and South African correctional facilities.

A multisite prospective can you get ventolin over the counter australia cohort study (published online ahead of print, 2020 Aug 4). Lancet HIV. 2020;S2352-3018(20)30188-0.

Doi:10.1016/S2352-3018(20)30188-0Therapeutic HIV treatment sheds light on HIV remission in humansART does not eliminate the HIV reservoir completely, suggesting the need for innovative therapies to achieve HIV remission. Several HIV remission studies have focused on people with acute HIV who have a smaller reservoir. A double-blind two-arm placebo-controlled randomised controlled trial of 27 people with acute HIV in Thailand gave a modified vaccinia therapeutic treatment to examine safety and duration of viraemic control after treatment interruption.

The treatment was well tolerated and created strong immune responses. However, time to viral rebound was only moderately increased in the treatment group (median 21 days, range 8–44 days) compared with the placebo group (15 days, range 10–164 days). Further research is needed to inform future study designs in HIV remission research.Colby DJ, Sarnecki M, Barouch DH, et al.

Safety and immunogenicity of Ad26 and MVA treatments in acutely treated HIV and effect on viral rebound after antiretroviral therapy interruption. Nat Med. 2020;26(4):498–501.

Doi:10.1038/s41591-020-0774-yPharyngeal gonorrhoea testing among heterosexual menAlthough pharyngeal gonorrhoea testing is no longer recommended in the UK for heterosexual men with urethral or those who are known contacts, one sexual health service continued this practice, testing 232 heterosexual men over 2 years. Of those with urethral gonorrhoea, 33% (35/106) tested positive for pharyngeal gonorrhoea, including one who retained pharyngeal positivity after treatment that cleared the urethral . Among asymptomatic contacts, 20% (17/86) had pharyngeal , the majority of whom (10/17) did not have concurrent urethral .

Had pharyngeal testing not occurred in asymptomatic contacts, more than 10% of s would not have been diagnosed or treated, potentially leading to onward transmission through kissing or orogenital/rectal contact. These results indicate that pharyngeal testing is warranted and should be considered in future guidelines.Dresser M and Hussey J. (2020).

Testing for pharyngeal gonorrhoea in heterosexual men. Should we revisit national guidelines?. International Journal of STD &.

AIDS, 31(6), 593–595.HIV risk behaviours, STI testing and PrEP uptake among Australian MSMThe HIV prevention landscape has significantly changed with the implementation of pre-exposure prophylaxis (PrEP), treatment as prevention programmes and campaigns to increase testing. To assess the impact of these strategies and determine prevalence of undiagnosed HIV, two large cross-sectional studies among men who have sex with men (MSM) were conducted in Sydney, Australia in 2014 (n=2222) and 2018 (n=2158). Prevalence of undiagnosed HIV was low (13.8% (2014) vs 5.3% (2018), ns).

HIV and STI testing increased significantly (from 49.6% to 56.3%, and from 61.7% to 69.2%, respectively), as did PrEP uptake (from 2.1% to 23.0%). However, in 2018, MSM were more likely to report behaviours associated with HIV/STI risk and past-year STI diagnosis. Results indicate that despite increasing risk behaviour, prevalence of undiagnosed HIV remains low suggesting the combined effectiveness of treatment and prevention strategies.Keen P, Lee E, Grulich AE, Prestage G, Guy R, Stoove MA,… and Duck T (2020).

Sustained, low prevalence of undiagnosed HIV among gay and bisexual men in Sydney, Australia coincident with increased testing and pre-exposure prophylaxis use. Results from repeated, bio-behavioural studies 2014–2018. JAIDS.

Online ahead of print.Rapid gonorrhoea and chlamydia resultsRapid point-of-care (POC) tests for gonorrhoea and chlamydia could enable testing and treatment to occur in a single visit, reducing complications of untreated s, attendance burden and risk of onward transmission. In a prospective cross-sectional study, swabs from 1523 women and first catch urine from 922 men were tested by non-laboratory-trained staff using a POC assay and compared with laboratory assay results. Sensitivities and specificities for chlamydia and gonorrhoea using the POC test were greater than the target of 95% in both women and men, except for sensitivity of the chlamydia test in men (92.5%, 95% CI 86.4% to 96.0%).

Further assessment of these tests is needed in rectal and oropharyngeal samples and cost-effectiveness analyses will be helpful to understand their utility.Van Der Pol B, Taylor SN, Mena L, et al. Evaluation of the Performance of a Point-of-Care Test for Chlamydia and Gonorrhea. JAMA Netw Open.

2020;3(5):e204819. Published 2020 May 1. Doi:10.1001/jamanetworkopen.2020.4819Role of syphilis partner notification in ending the HIV epidemicSyphilis partner notification is an opportunity to case find newly diagnosed syphilis and HIV in known contacts.

A retrospective record review of 984 syphilis cases found that 1457 cases and partners received HIV/STI prevention counselling, 400 partners were tested and treated for STIs (including 63 new syphilis diagnoses) and 168 PrEP referrals were made. Three hundred and fifty-two partners were tested for HIV, 22 received new HIV diagnoses, 68% were retained in care and 60% were virally suppressed. Previously undiagnosed HIV positivity was 14% and 3.5% among partners of co-occurrent HIV and syphilis cases and among partners to HIV-negative cases, respectively.

Partner notification for syphilis provides a key opportunity to deliver combination prevention with behavioural counselling for STIs and HIV, early testing and treatment.DiOrio D, Collins D, Hanley S. Ending the HIV Epidemic. Contributions Resulting From Syphilis Partner Services.

Sex Transm Dis. 2020;47(8):511–515. Doi:10.1097/OLQ.0000000000001201The National Health Service is facing rising demands for services, issues of funding, variations in quality and safety, and labour challenges.1 2 These challenges are felt acutely within genitourinary medicine, which has one of the lowest fill rates nationally,3 one-third of sexual and reproductive consultants are due to retire in the next 5 years and sexual health services face budget cuts of more than 20%.4A range of solutions have been proposed, including new models of care and modernisation of the workforce.1 2 5 Modernising the workforce will involve securing the supply of staff, creating a flexible workforce, widening participation and broadening career pathways5 and the development of extended and advanced practice roles.1 2 5 It is anticipated these solutions will increase efficiency and efficacy, facilitate professionals to work at the top of their licence, thus reducing variations in practice and improve standards of care.5To support ….

Universal HIV test-and-treat intervention in African correctional where to buy ventolin pills settingsWhile people who are incarcerated have a higher burden of HIV and other STIs, delivering sexual health services in correctional settings is difficult. A mixed methods cohort study examined the implementation of a universal test-and-treat intervention at 10 correctional units (6 for men, 3 for women, 1 for youth) in South Africa and Zambia. Same-day anti-retroviral therapy (ART) initiation, training and where to buy ventolin pills support, ensuring ART supply, and viral load monitoring were evaluated among 975 inmates living with HIV. Median time from enrolment to ART initiation was 0 days (IQR 0–8) and the proportion of people retained in care with viral load monitoring was high (94%, 327/346) among those still incarcerated at 6 months.

This study demonstrates the feasibility of implementing comprehensive where to buy ventolin pills HIV interventions in selected settings.Herce ME, Hoffmann CJ, Fielding K, et al. Universal test-and-treat in Zambian and South African correctional facilities. A multisite prospective cohort study where to buy ventolin pills (published online ahead of print, 2020 Aug 4). Lancet HIV.

2020;S2352-3018(20)30188-0. Doi:10.1016/S2352-3018(20)30188-0Therapeutic HIV treatment sheds light on HIV remission in humansART does not eliminate the HIV reservoir completely, suggesting the need for innovative therapies to achieve HIV remission. Several HIV remission studies have focused on people with acute HIV who have a smaller reservoir. A double-blind two-arm placebo-controlled randomised controlled trial of 27 people with acute HIV in Thailand gave a modified vaccinia therapeutic treatment to examine safety and duration of viraemic control after treatment interruption.

The treatment was well tolerated and created strong immune responses. However, time to viral rebound was only moderately increased in the treatment group (median 21 days, range 8–44 days) compared with the placebo group (15 days, range 10–164 days). Further research is needed to inform future study designs in HIV remission research.Colby DJ, Sarnecki M, Barouch DH, et al. Safety and immunogenicity of Ad26 and MVA treatments in acutely treated HIV and effect on viral rebound after antiretroviral therapy interruption.

Nat Med. 2020;26(4):498–501. Doi:10.1038/s41591-020-0774-yPharyngeal gonorrhoea testing among heterosexual menAlthough pharyngeal gonorrhoea testing is no longer recommended in the UK for heterosexual men with urethral or those who are known contacts, one sexual health service continued this practice, testing 232 heterosexual men over 2 years. Of those with urethral gonorrhoea, 33% (35/106) tested positive for pharyngeal gonorrhoea, including one who retained pharyngeal positivity after treatment that cleared the urethral .

Among asymptomatic contacts, 20% (17/86) had pharyngeal , the majority of whom (10/17) did not have concurrent urethral . Had pharyngeal testing not occurred in asymptomatic contacts, more than 10% of s would not have been diagnosed or treated, potentially leading to onward transmission through kissing or orogenital/rectal contact. These results indicate that pharyngeal testing is warranted and should be considered in future guidelines.Dresser M and Hussey J. (2020).

Testing for pharyngeal gonorrhoea in heterosexual men. Should we revisit national guidelines?. International Journal of STD &. AIDS, 31(6), 593–595.HIV risk behaviours, STI testing and PrEP uptake among Australian MSMThe HIV prevention landscape has significantly changed with the implementation of pre-exposure prophylaxis (PrEP), treatment as prevention programmes and campaigns to increase testing.

To assess the impact of these strategies and determine prevalence of undiagnosed HIV, two large cross-sectional studies among men who have sex with men (MSM) were conducted in Sydney, Australia in 2014 (n=2222) and 2018 (n=2158). Prevalence of undiagnosed HIV was low (13.8% (2014) vs 5.3% (2018), ns). HIV and STI testing increased significantly (from 49.6% to 56.3%, and from 61.7% to 69.2%, respectively), as did PrEP uptake (from 2.1% to 23.0%). However, in 2018, MSM were more likely to report behaviours associated with HIV/STI risk and past-year STI diagnosis.

Results indicate that despite increasing risk behaviour, prevalence of undiagnosed HIV remains low suggesting the combined effectiveness of treatment and prevention strategies.Keen P, Lee E, Grulich AE, Prestage G, Guy R, Stoove MA,… and Duck T (2020). Sustained, low prevalence of undiagnosed HIV among gay and bisexual men in Sydney, Australia coincident with increased testing and pre-exposure prophylaxis use. Results from repeated, bio-behavioural studies 2014–2018. JAIDS.

Online ahead of print.Rapid gonorrhoea and chlamydia resultsRapid point-of-care (POC) tests for gonorrhoea and chlamydia could enable testing and treatment to occur in a single visit, reducing complications of untreated s, attendance burden and risk of onward transmission. In a prospective cross-sectional study, swabs from 1523 women and first catch urine from 922 men were tested by non-laboratory-trained staff using a POC assay and compared with laboratory assay results. Sensitivities and specificities for chlamydia and gonorrhoea using the POC test were greater than the target of 95% in both women and men, except for sensitivity of the chlamydia test in men (92.5%, 95% CI 86.4% to 96.0%). Further assessment of these tests is needed in rectal and oropharyngeal samples and cost-effectiveness analyses will be helpful to understand their utility.Van Der Pol B, Taylor SN, Mena L, et al.

Evaluation of the Performance of a Point-of-Care Test for Chlamydia and Gonorrhea. JAMA Netw Open. 2020;3(5):e204819. Published 2020 May 1.

Doi:10.1001/jamanetworkopen.2020.4819Role of syphilis partner notification in ending the HIV epidemicSyphilis partner notification is an opportunity to case find newly diagnosed syphilis and HIV in known contacts. A retrospective record review of 984 syphilis cases found that 1457 cases and partners received HIV/STI prevention counselling, 400 partners were tested and treated for STIs (including 63 new syphilis diagnoses) and 168 PrEP referrals were made. Three hundred and fifty-two partners were tested for HIV, 22 received new HIV diagnoses, 68% were retained in care and 60% were virally suppressed. Previously undiagnosed HIV positivity was 14% and 3.5% among partners of co-occurrent HIV and syphilis cases and among partners to HIV-negative cases, respectively.

Partner notification for syphilis provides a key opportunity to deliver combination prevention with behavioural counselling for STIs and HIV, early testing and treatment.DiOrio D, Collins D, Hanley S. Ending the HIV Epidemic. Contributions Resulting From Syphilis Partner Services. Sex Transm Dis.

2020;47(8):511–515. Doi:10.1097/OLQ.0000000000001201The National Health Service is facing rising demands for services, issues of funding, variations in quality and safety, and labour challenges.1 2 These challenges are felt acutely within genitourinary medicine, which has one of the lowest fill rates nationally,3 one-third of sexual and reproductive consultants are due to retire in the next 5 years and sexual health services face budget cuts of more than 20%.4A range of solutions have been proposed, including new models of care and modernisation of the workforce.1 2 5 Modernising the workforce will involve securing the supply of staff, creating a flexible workforce, widening participation and broadening career pathways5 and the development of extended and advanced practice roles.1 2 5 It is anticipated these solutions will increase efficiency and efficacy, facilitate professionals to work at the top of their licence, thus reducing variations in practice and improve standards of care.5To support ….

Where should I keep Ventolin?

Keep out of the reach of children. Store albuterol tablets in the refrigerator (36 to 46 degrees F). Other tablets may be stored at room temperature (59 to 86 degrees F), check the packaging or ask your pharmacist. Keep container closed tightly. Throw away any unused medicine after the expiration date.

Generic name of ventolin

From. Health CanadaDate. July 16, 2021As of July 16, 2021, Health Canada will no longer accept applications for certain categories of medical devices under Interim Order No.

2 if it has been determined there's no longer an urgent public health need for those devices. On this page BackgroundMechanisms in place to expedite access to medical devices during the asthma treatment ventolin include Interim Order No. 2 (IO No.

2). This interim order was signed by the Minister of Health in March 2021.For a asthma treatment medical device to be authorized for importation or sale under IO No. 2, the Minister must determine if there is an urgent public health need (UPHN) for that device.

A UPHN exists if immediate action is required to protect or improve the health of individuals or communities in Canada. Determining urgent public health needTo determine if there's an UPHN for a medical device, Health Canada considers a number of factors, including. Its supply and demand its lifecycle (how long it lasts) its clinical need the status of the asthma treatment ventolin in CanadaEach IO application for a device undergoes a UPHN assessment.

If there's not enough evidence of a UPHN, the applicant will receive a screening deficiency letter asking for evidence that a UPHN exists for their medical device. An attestation from a Canadian health authority stating that a UPHN exists for that medical device is an example of such evidence.Health Canada will reject applications that don't have enough evidence of a UPHN. Medical devices that no longer have UPHN statusAs the ventolin evolves, Health Canada is assessing whether there's an urgent public health need for certain categories of medical devices.

Table 1 lists the categories of asthma treatment medical devices that no longer have UPHN status. We will reassess the status of these devices from time to time as the ventolin evolves and if the supply and demand for certain categories of devices changes.This approach allows us to better focus resources on assessing urgently needed devices to ensure they're quickly available to Canadians. Table 1.

Categories of asthma treatment medical devices that no longer have UPHN status Device category* Assessment date Thermometers 2021-07-16 Ventilators 2021-07-16 *IO approval may still be possible for devices listed in Table 1 if the applicant provides enough UPHN evidence for the device. Health Canada will consider the supporting evidence and inform the applicant of the decision taken as per our service standards.The device categories listed in Table 1 only affect applications filed after the assessment date identified in the table. Applications that were submitted before that date and are still being processed or authorizations already issued under the IO before that date are not affected.The Medical Devices Regulations pathway remains open for obtaining medical device establishment licences (Class I) and medical device licences (Class II to IV) for all types of medical devices.

To obtain a medical device licence and medical device establishment licence under this pathway, see the following guidance documents. If you have any questions, please contact the Medical Devices Directorate at hc.mddpolicy-politiquesdim.sc@canada.ca. Related linksNew policy and updated submission requirements Date.

July 9, 2021 On this page Background and purpose Rapid antigen tests are easy to use and provide results in 15 minutes on average. However, their sensitivity is lower than that of molecular RT-PCR tests. On September 29, 2020, Health Canada published a notice on the minimum value for sensitivity of rapid antigen testing devices.

Tests with sensitivity below 80% will not be authorized. This position aligns with the minimum value required by other regulatory agencies (for example, U.S. FDA, WHO, U.K.

MHRA, Germany’s PEI). Recent scientific and medical studies show that serial testing may. increase the overall sensitivity of an antigen test and make it possible for less sensitive tests to meet the established 80% sensitivity requirement As such, Health Canada is introducing more flexibility during the review process of antigen tests that use serial testing for individuals without symptoms.The purpose of this notice is to communicate to industry this new policy and submission requirements.

New policy position Health Canada may authorize an antigen test that uses serial testing for asymptomatic individuals without the support of pre-market clinical evidence.This new policy is based on. early reports on the possible similarity of viral loads between people with and without symptoms technical reports and key messages on the use of rapid antigen tests strategies implemented by our international regulatory partners recent U.S. FDA recommendations to allow for more flexibility during pre-market evaluation of asthma treatment testing devices during the ventolin New policy details and submission requirements Manufacturers may consider a claim for serial testing of patients without symptoms and where there’s no pre-market clinical evidence if the test.

has undergone clinical evaluation with symptomatic individuals in a laboratory or a point-of-care (POC) setting and has a sensitivity of at least 80%, with 70% at the lower bound of the 2-sided 95% confidence interval If these requirements are met, a screening claim for an asymptomatic population intended for use as part of a testing program may be granted. This is achieved by imposing an agreed-upon condition to the interim order (IO) authorization. The condition will require a clinical study establishing the performance of the assay in an asymptomatic population.

The clinical study should include at least 20 positive asymptomatic patients and the clinical data will need to be submitted within a specified timeframe. Study samples must represent the viral loads expected, with 10% to 20% of the samples falling in the low positive category stratification. Analysis of the results by PCR Ct values should also be provided.If manufacturers are unable to obtain the required 20 positive samples from asymptomatic individuals to support their clinical claims, they may present the results from 10 positive samples from asymptomatic individuals if.

The data from symptomatic individuals are also submitted the analysis of cycle threshold (Ct) values demonstrates reasonably similar distribution of viral loads Authorization is conditional on Health Canada receiving data from the remaining 10 positive clinical specimens.As part of the conditional IO authorization for antigen tests, manufacturers will be required to submit a quarterly post-market report. This report must include. The number of devices sold in and outside Canada a summary of problem reports on the performance of the assay, number of false positive, false negative, invalid results and major complaints on the robustness of the assay published peer-reviewed articles on the performance of your device The test labelling must include the following statement in the intended use.

€œIndividuals without symptoms or other epidemiological reasons to suspect asthma treatment , when tested twice over 2 (or 3) days with at least 24 hours (and no more than 36 hours) between tests.” In both the limitations and clinical performance sections of the Instructions for Use (IFU), manufacturers must clearly state that. clinical studies in asymptomatic patients using serial testing are ongoing to establish clinical performance the performance of this test has not yet been clinically validated for use in patients without signs and symptoms of respiratory or for serial screening applications note that performance may differ in these populations How to apply If manufacturers are applying for a new authorization, all requirements outlined in the following antigen guidance documents published by Health Canada and the FDA apply. For an application that is currently under evaluation by Health Canada and meets the requirement of the new policy.

If you have not submitted an application and you believe your device meets these criteria, you may include the claim in your indications for use along with the required labelling..

From ventolin hfa purchase where to buy ventolin pills. Health CanadaDate. July 16, 2021As of July 16, 2021, Health Canada will no longer accept applications for certain categories of medical devices under Interim Order No where to buy ventolin pills.

2 if it has been determined there's no longer an urgent public health need for those devices. On this page BackgroundMechanisms in place to expedite access to medical devices during the asthma treatment ventolin include Interim Order No. 2 (IO where to buy ventolin pills No.

2). This interim order was signed by the Minister of Health in March 2021.For a asthma treatment medical device to be authorized for importation or sale under IO No. 2, the Minister must determine if there is an urgent public health need (UPHN) for that where to buy ventolin pills device.

A UPHN exists if immediate action is required to protect or improve the health of individuals or communities in Canada. Determining urgent public health needTo determine if there's an UPHN for a medical device, Health Canada considers a number of factors, including. Its supply and demand where to buy ventolin pills its lifecycle (how long it lasts) its clinical need the status of the asthma treatment ventolin in CanadaEach IO application for a device undergoes a UPHN assessment.

If there's not enough evidence of a UPHN, the applicant will receive a screening deficiency letter asking for evidence that a UPHN exists for their medical device. An attestation from a Canadian health authority stating that a UPHN exists for that medical device is an example of such evidence.Health Canada will reject applications that don't have enough evidence of a UPHN. Medical devices that no longer have UPHN statusAs the ventolin evolves, Health Canada is assessing whether there's an urgent public health where to buy ventolin pills need for certain categories of medical devices.

Table 1 lists the categories of asthma treatment medical devices that no longer have UPHN status. We will reassess the status of these devices from time to time as the ventolin evolves and if the supply and demand for certain categories of devices changes.This approach allows us to better focus resources on assessing urgently needed devices to ensure they're quickly available to Canadians. Table 1 where to buy ventolin pills.

Categories of asthma treatment medical devices that no longer have UPHN status Device category* Assessment date Thermometers 2021-07-16 Ventilators 2021-07-16 *IO approval may still be possible for devices listed in Table 1 if the applicant provides enough UPHN evidence for the device. Health Canada will consider the supporting evidence and inform the applicant of the decision taken as per our service standards.The device categories listed in Table 1 only affect applications filed after the assessment date identified in the table. Applications that were submitted before that date and are still being processed or authorizations already issued under the IO before that date are not affected.The Medical Devices Regulations pathway remains open for obtaining medical device establishment licences (Class I) and where to buy ventolin pills medical device licences (Class II to IV) for all types of medical devices.

To obtain a medical device licence and medical device establishment licence under this pathway, see the following guidance documents. If you have any questions, please contact the Medical Devices Directorate at hc.mddpolicy-politiquesdim.sc@canada.ca. Related linksNew policy and updated where to buy ventolin pills submission requirements Date.

July 9, 2021 On http://adisamba.com/archives/515 this page Background and purpose Rapid antigen tests are easy to use and provide results in 15 minutes on average. However, their where to buy ventolin pills sensitivity is lower than that of molecular RT-PCR tests. On September 29, 2020, Health Canada published a notice on the minimum value for sensitivity of rapid antigen testing devices.

Tests with sensitivity below 80% will not be authorized. This position where to buy ventolin pills aligns with the minimum value required by other regulatory agencies (for example, U.S. FDA, WHO, U.K.

MHRA, Germany’s PEI). Recent scientific and where to buy ventolin pills medical studies show that serial testing may. increase the overall sensitivity of an antigen test and make it possible for less sensitive tests to meet the established 80% sensitivity requirement As such, Health Canada is introducing more flexibility during the review process of antigen tests that use serial testing for individuals without symptoms.The purpose of this notice is to communicate to industry this new policy and submission requirements.

New policy position Health Canada may authorize an antigen test that uses serial testing for asymptomatic individuals without the support of pre-market clinical evidence.This new policy is based on. early reports on the possible similarity of viral loads between people with and without symptoms technical reports and key messages on the use of rapid antigen tests strategies implemented by our international regulatory partners recent U.S where to buy ventolin pills. FDA recommendations to allow for more flexibility during pre-market evaluation of asthma treatment testing devices during the ventolin New policy details and submission requirements Manufacturers may consider a claim for serial testing of patients without symptoms and where there’s no pre-market clinical evidence if the test.

has undergone clinical evaluation with symptomatic individuals in a laboratory or a point-of-care (POC) setting and has a sensitivity of at least 80%, with 70% at the lower bound of the 2-sided 95% confidence interval If these requirements are met, a screening claim for an asymptomatic population intended for use as part of a testing program may be granted. This is achieved by imposing an agreed-upon condition to where to buy ventolin pills the interim order (IO) authorization. The condition will require a clinical study establishing the performance of the assay in an asymptomatic population.

The clinical study should include at least 20 positive asymptomatic patients and the clinical data will need to be submitted within a specified timeframe. Study samples must represent the viral loads expected, with 10% to 20% of the samples falling in the where to buy ventolin pills low positive category stratification. Analysis of the results by PCR Ct values should also be provided.If manufacturers are unable to obtain the required 20 positive samples from asymptomatic individuals to support their clinical claims, they may present the results from 10 positive samples from asymptomatic individuals if.

The data from symptomatic individuals are also submitted the analysis of cycle threshold (Ct) values demonstrates reasonably similar distribution of viral loads Authorization is conditional on Health Canada receiving data from the remaining 10 positive clinical specimens.As part of the conditional IO authorization for antigen tests, manufacturers will be required to submit a quarterly post-market report. This report must where to buy ventolin pills include. The number of devices sold in and outside Canada a summary of problem reports on the performance of the assay, number of false positive, false negative, invalid results and major complaints on the robustness of the assay published peer-reviewed articles on the performance of your device The test labelling must include the following statement in the intended use.

€œIndividuals without symptoms or other epidemiological reasons to suspect asthma treatment , when tested twice over 2 (or 3) days with at least 24 hours (and no more than 36 hours) between tests.” In both the limitations and clinical performance sections of the Instructions for Use (IFU), manufacturers must clearly state that. clinical studies in asymptomatic patients using serial testing are ongoing to establish clinical performance the performance of this test has not yet been clinically validated for use in patients without signs and symptoms of respiratory or for serial screening applications note that performance may differ in these populations How to apply If manufacturers are applying for a new authorization, all requirements outlined in the following antigen guidance documents published by Health Canada and the FDA apply. For an application that is currently under evaluation by Health Canada and meets the requirement of the new policy.

If you have not submitted an application and you believe your device meets these criteria, you may include the claim in your indications for use along with the required labelling..

Can u buy ventolin over the counter

Photo. Geber86/Getty ImagesWalmart's announcement last week that it would acquire telehealth company MeMD to provide virtual care nationwide for primary, urgent and behavioral healthcare is a bigger deal than Amazon's March rollout of its virtual primary care services, according to consultant Paul Keckley of The Keckley Report."I think it's a strategic play. I think it's bigger than Amazon," Keckley said. "Amazon does not have the bricks to accompany the clicks.

They don't have the presence that Walmart has."Walmart Health is acquiring MeMD for an undisclosed price in a deal expected to close in months, should it pass regulatory approval. Keckley believes there will be pushback on the acquisition and possibly court challenges from those who view the move as infringement, but thinks that Walmart probably has regulatory approval in its corner.Walmart has a broad underserved population base, which will be to its regulatory advantage. The question will boil down to how Walmart can effectively manage costs at a discount, Keckley said. This fits perfectly with Walmart's business plan.MeMD, founded in 2010, provides on-demand, online care for common illnesses, injuries and behavioral health issues.

The service complements in-person care at Walmart Health centers."MeMD's mission fits perfectly with Walmart's dedicated focus to help people save money and live better, and now we can impact millions more by being part of Walmart," the company said by released statement."Today people expect omnichannel access to care, and adding telehealth to our Walmart Health care strategies allows us to provide in-person and digital care across our multiple assets and solutions," said Dr. Cheryl Pegus, executive vice president, Health &. Wellness for Walmart. WHY THIS MATTERSWalmart's move is the latest foray by a non-provider into traditional provider care.

The mega-retailer is a threat because it has a strong digital platform to help customers manage their health and also manage their food through their neighborhood markets.Other players wanting a piece of the provider pie through telehealth are Amazon Care, Transcarent for the self-insured market and insurers. Cigna's MDLive, which is part of its Evernorth portfolio, helped propel the insurer to strong first quarter results.Transcarent, headed by Livongo founder Glen Tullman, is betting on consumer's desire to chat by app.Amazon Care, which promises virtual care in all 50 states starting this summer, puts the big tech firm directly in the healthcare services business.Hospitals and physician practices are at a crossroads on what to do about telehealth post-ventolin. Providers are currently getting payment parity for a telehealth visit, but there is uncertainty moving forward whether that will continue. Prior to the asthma treatment ventolin, insurers paid 20-40% less for a telehealth visit than for an in-person visit.CFOs have digital health priorities that include telehealth, but hospitals must also have the cooperation of doctors."Walmart doesn't," Keckley said.With this competition, hospitals will be forced to move into telehealth, whether they are paid at parity or not.Keckley, who works with healthcare executives, believes providers will integrate telehealth into operations one clinical program at a time.

To do nothing means being left behind."I think this time, the train has left the station through the ventolin, the [American] Rescue Plan and relief funds," Keckley said. Telehealth has particularly made inroads in behavioral healthcare, which "has always been touted as the gap in the system," Keckley said.Insurers see telehealth as a way to help members manage chronic conditions, as in the shake-up $18.5 billion merger between telehealth platform Teladoc and chronic care management program Livongo last year. WHAT'S HAPPENING TO MAKE TELEHEALTH HAPPENCongress has numerous bills and proposals under consideration for the future of telehealth payments once the public health emergency ends and the waivers put into place by the Centers for Medicare and Medicaid Services expire.The main question is over concern of potential overutilization as consumers visit the doctor both virtually and in person. There are also questions over geographic barriers, interstate licensure and establishing a national framework for multistate employers.While only a few states have their own payment parity laws for telehealth, payment parity is now the focus of numerous state bills, according to Health Affairs.

"Payment parity is particularly important for small practices and those located in underserved communities, who may not have the financial means to offer telehealth if reimbursement is substantially lower," Health Affairs said. During a House Ways and Means Health Subcommittee hearing on April 28 entitled "Charting the Path Forward for Telehealth," panelists debated the parity question.Ellen Kelsay, president and CEO of the Business Group on Health, which represents employers, said the focus is on telehealth utilization and that everyone should exercise caution to determine when in-person rather than virtual care is more medically appropriate."We cannot ignore cost," Kelsay said. "How it might increase costs over time. A telehealth visit is often followed by an in-person visit for the same purpose."Dr.

Thomas Kim, chief behavioral health officer for Prism Health North Texas, said telehealth is not a replacement or an additive to traditional care. Payment should be made at the same rate, he said.Dr. Ateev Mehrotra, associate professor at the department of healthcare policy at Harvard Medical School, said he would advocate to pay for virtual visits at a lower rate. Provider costs for telemedicine visits are lower, and payment should reflect that, Mehrotra said.Subcommittee Chairman LloydDoggett said, "With CMS telehealth waivers currently extended through years' end, we need a plan in place to assure no abrupt suspension.

Though recognizing the great promise of telehealth, the Medicare Payment Advisory Commission last month noted that our understanding of the impact of telehealth is largely limited to data and experience covering only a few months."MedPAC has recommended that Congress initially provide a limited extension to permit additional time for gathering evidence about the impact of telehealth on access, quality and cost, he said. "While pay parity between telemedicine and in-person care has spurred rapid adoption, we must evaluate that impact on Medicare spending and ensure a telemedicine appointment is not duplicating an in-person visit," Doggett said.A bipartisan group of 50 Senators has reintroduced the CONNECT for Health Act. American Telemedicine Association CEO Ann Mond Johnson said, "The telehealth cliff is looming, casting much uncertainty and concern for the health and safety of Medicare beneficiaries, and the sustainability of our already overburdened healthcare system. By ensuring Medicare beneficiaries do not lose access to telehealth after the asthma treatment public health emergency ends, the CONNECT ACT would protect seniors from the telehealth cliff.

We urge Congress to recognize telehealth as a bipartisan, commonsense solution and speedily advance comprehensive policy that will allow permanent access to telehealth and virtual care." THE LARGER TRENDTelehealth came into its own during the height of the ventolin.CMS granted Medicare waivers to cover 144 telehealth services during the public health emergency. The agency waived geographic areas, site restrictions, expanded the services and increased tech options. "Though some providers say it adds costs and unnecessary services, most think telehealth savings can be significant if integrated in care management effectively and geographic restrictions lifted," Keckley said in The Keckley Report. The bigger question, according to Keckley, is where healthcare delivery is going, when care is increasingly being provided outside of the physician's office or hospital and insurers no longer remain in the traditional insurance business."This [Walmart] deal symbolizes the widening gap between healthcare's future and its past," Keckley said.

"Walmart aspires to be a major player in its future."Twitter. @SusanJMorseEmail the writer. Susan.morse@himssmedia.com.

Photo Where can i buy lasix over the counter usa where to buy ventolin pills. Geber86/Getty ImagesWalmart's announcement last week that it would acquire telehealth company MeMD to provide virtual care nationwide for primary, urgent and behavioral healthcare is a bigger deal than Amazon's March rollout of its virtual primary where to buy ventolin pills care services, according to consultant Paul Keckley of The Keckley Report."I think it's a strategic play. I think it's bigger than Amazon," Keckley said. "Amazon does where to buy ventolin pills not have the bricks to accompany the clicks.

They don't have the presence that Walmart has."Walmart Health is acquiring MeMD for an undisclosed price in a deal expected to close in months, should it pass regulatory approval. Keckley believes there will be pushback on the acquisition and possibly court challenges from those who view where to buy ventolin pills the move as infringement, but thinks that Walmart probably has regulatory approval in its corner.Walmart has a broad underserved population base, which will be to its regulatory advantage. The question will boil down to how Walmart can effectively manage costs at a discount, Keckley said. This fits where to buy ventolin pills perfectly with Walmart's business plan.MeMD, founded in 2010, provides on-demand, online care for common illnesses, injuries and behavioral health issues.

The service complements in-person care at Walmart Health centers."MeMD's mission fits perfectly with Walmart's dedicated focus to help people save money and live better, and now we can impact millions more by being part of Walmart," the company said where to buy ventolin pills by released statement."Today people expect omnichannel access to care, and adding telehealth to our Walmart Health care strategies allows us to provide in-person and digital care across our multiple assets and solutions," said Dr. Cheryl Pegus, executive vice president, Health &. Wellness for Walmart where to buy ventolin pills. WHY THIS MATTERSWalmart's move is the latest foray by a non-provider into traditional provider care.

The mega-retailer is a threat because it has a strong digital platform to help customers manage their health and also manage their food through their where to buy ventolin pills neighborhood markets.Other players wanting a piece of the provider pie through telehealth are Amazon Care, Transcarent for the self-insured market and insurers. Cigna's MDLive, which is part of its Evernorth portfolio, helped propel the insurer to strong first quarter results.Transcarent, headed by Livongo founder Glen Tullman, is betting on consumer's desire to chat by app.Amazon Care, which promises virtual care in all 50 states starting this summer, puts the big tech firm directly in the healthcare services business.Hospitals and physician practices are at a crossroads on what to do about telehealth post-ventolin. Providers are where to buy ventolin pills currently getting payment parity for a telehealth visit, but there is uncertainty moving forward whether that will continue. Prior to the asthma treatment ventolin, insurers paid 20-40% less for a telehealth visit than for an in-person visit.CFOs have digital health priorities that include telehealth, but hospitals must also have the cooperation of doctors."Walmart doesn't," Keckley where to buy ventolin pills said.With this competition, hospitals will be forced to move into telehealth, whether they are paid at parity or not.Keckley, who works with healthcare executives, believes providers will integrate telehealth into operations one clinical program at a time.

To do nothing means being left behind."I think this time, the train has left the station through the ventolin, the [American] Rescue Plan and relief funds," Keckley said. Telehealth has particularly made inroads in behavioral where to buy ventolin pills healthcare, which "has always been touted as the gap in the system," Keckley said.Insurers see telehealth as a way to help members manage chronic conditions, as in the shake-up $18.5 billion merger between telehealth platform Teladoc and chronic care management program Livongo last year. WHAT'S HAPPENING TO MAKE TELEHEALTH HAPPENCongress has numerous bills and proposals under consideration for the future of telehealth payments once the public health emergency ends and the waivers put into place by the Centers for Medicare and Medicaid Services expire.The main question is over concern of potential overutilization as consumers visit the doctor both virtually and in person. There are also questions where to buy ventolin pills over geographic barriers, interstate licensure and establishing a national framework for multistate employers.While only a few states have their own payment parity laws for telehealth, payment parity is now the focus of numerous state bills, according to Health Affairs.

"Payment parity is particularly important for small practices and those located in underserved communities, who may not have the financial means to offer telehealth if reimbursement is substantially lower," Health Affairs said. During a House Ways and Means Health Subcommittee hearing on April 28 entitled "Charting the Path Forward for Telehealth," panelists debated the parity question.Ellen Kelsay, president and CEO of the Business Group on Health, which represents employers, said the focus is on telehealth utilization and that everyone should where to buy ventolin pills exercise caution to determine when in-person rather than virtual care is more medically appropriate."We cannot ignore cost," Kelsay said. "How it might increase costs over time. A telehealth visit is often followed where to buy ventolin pills by an in-person visit for the same purpose."Dr.

Thomas Kim, where to buy ventolin pills chief behavioral health officer for Prism Health North Texas, said telehealth is not a replacement or an additive to traditional care. Payment should be made at the same rate, he said.Dr. Ateev Mehrotra, associate professor at the department of healthcare policy at Harvard Medical where to buy ventolin pills School, said he would advocate to pay for virtual visits at a lower rate. Provider costs for telemedicine visits are lower, and payment should reflect that, Mehrotra said.Subcommittee Chairman LloydDoggett said, "With CMS telehealth waivers currently extended through years' end, we need a plan in place to assure no abrupt suspension.

Though recognizing the great promise of telehealth, the Medicare Payment Advisory Commission last month noted that our understanding of the impact of telehealth is largely limited to data and experience covering only a few months."MedPAC has recommended that Congress initially provide a limited extension to permit where to buy ventolin pills additional time for gathering evidence about the impact of telehealth on access, quality and cost, he said. "While pay parity between telemedicine and in-person care has spurred rapid adoption, we must evaluate that impact on Medicare spending and ensure a telemedicine appointment is not duplicating an in-person visit," Doggett said.A bipartisan group of 50 Senators has reintroduced the CONNECT for Health Act. American Telemedicine where to buy ventolin pills Association CEO Ann Mond Johnson said, "The telehealth cliff is looming, casting much uncertainty and concern for the health and safety of Medicare beneficiaries, and the sustainability of our already overburdened healthcare system. By ensuring Medicare beneficiaries do not lose access to telehealth after the where to buy ventolin pills asthma treatment public health emergency ends, the CONNECT ACT would protect seniors from the telehealth cliff.

We urge Congress to recognize telehealth as a bipartisan, commonsense solution and speedily advance comprehensive policy that will allow permanent access to telehealth and virtual care." THE LARGER TRENDTelehealth came into its own during the height of the ventolin.CMS granted Medicare waivers to cover 144 telehealth services during the public health emergency. The agency waived where to buy ventolin pills geographic areas, site restrictions, expanded the services and increased tech options. "Though some providers say it adds costs and unnecessary services, most think telehealth savings can be significant if integrated in care management effectively and geographic restrictions lifted," Keckley said in The Keckley Report. The bigger question, according to Keckley, is where healthcare delivery is going, when care is increasingly being provided outside of the physician's office or hospital and insurers no longer remain in the traditional insurance business."This [Walmart] deal symbolizes the widening gap between healthcare's future and its past," Keckley said.

"Walmart aspires to be a major player in its future."Twitter. @SusanJMorseEmail the writer. Susan.morse@himssmedia.com.

Gsk ventolin recall

How to gsk ventolin recall cite this article:Singh O P http://www.grundschule-muehlenberg.de/online-doctor-zithromax/. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized events in our country gsk ventolin recall. 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, gsk ventolin recall 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, gsk ventolin recall 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 gsk ventolin recall despair with increased suicidal ideation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Part I. A perspective on the evolution and current practice of ECT. J Psychiatr Pract 2009;15:346-68. 2.Lauber C, Nordt C, Falcato L, Rössler W. Can a seizure help?.

The public's attitude toward electroconvulsive therapy. Psychiatry Res 2005;134:205-9. 3.Stefanazzi M. Is electroconvulsive therapy (ECT) ever ethically justified?. If so, under what circumstances.

HEC Forum 2013;25:79-94. 4.Devanand DP, Dwork AJ, Hutchinson ER, Bolwig TG, Sackeim HA. Does ECT alter brain structure?. Am J Psychiatry 1994;151:957-70. 5.Devanand DP.

Does electroconvulsive therapy damage brain cells?. Semin Neurol 1995;15:351-7. 6.Pearsall J, Trumble B, editors. The Oxford English Reference Dictionary. 2nd ed.

Oxford, England. New York. Oxford University Press. 1996. 7.Collin PH.

Dictionary of Medical Terms. 4th ed. London. Bloomsbury. 2004.

8.Hajdu SI. Entries on laboratory medicine in the first illustrated medical dictionary. Ann Clin Lab Sci 2005;35:465-8. 9.Mander AJ, Whitfield A, Kean DM, Smith MA, Douglas RH, Kendell RE. Cerebral and brain stem changes after ECT revealed by nuclear magnetic resonance imaging.

Br J Psychiatry 1987;151:69-71. 10.Coffey CE, Weiner RD, Djang WT, Figiel GS, Soady SA, Patterson LJ, et al. Brain anatomic effects of electroconvulsive therapy. A prospective magnetic resonance imaging study. Arch Gen Psychiatry 1991;48:1013-21.

11.Scott AI, Douglas RH, Whitfield A, Kendell RE. Time course of cerebral magnetic resonance changes after electroconvulsive therapy. Br J Psychiatry 1990;156:551-3. 12.Pande AC, Grunhaus LJ, Aisen AM, Haskett RF. A preliminary magnetic resonance imaging study of ECT-treated depressed patients.

Biol Psychiatry 1990;27:102-4. 13.Coffey CE, Figiel GS, Djang WT, Sullivan DC, Herfkens RJ, Weiner RD. Effects of ECT on brain structure. A pilot prospective magnetic resonance imaging study. Am J Psychiatry 1988;145:701-6.

14.Qiu H, Li X, Zhao W, Du L, Huang P, Fu Y, et al. Electroconvulsive therapy-Induced brain structural and functional changes in major depressive disorders. A longitudinal study. Med Sci Monit 2016;22:4577-86. 15.Kunigiri G, Jayakumar PN, Janakiramaiah N, Gangadhar BN.

MRI T2 relaxometry of brain regions and cognitive dysfunction following electroconvulsive therapy. Indian J Psychiatry 2007;49:195-9. [PUBMED] [Full text] 16.Pirnia T, Joshi SH, Leaver AM, Vasavada M, Njau S, Woods RP, et al. Electroconvulsive therapy and structural neuroplasticity in neocortical, limbic and paralimbic cortex. Transl Psychiatry 2016;6:e832.

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

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

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

Electroconvulsive therapy-induced brain plasticity determines therapeutic outcome in mood disorders. Proc Natl Acad Sci U S A 2014;111:1156-61. 22.Abbott CC, Jones T, Lemke NT, Gallegos P, McClintock SM, Mayer AR, et al. Hippocampal structural and functional changes associated with electroconvulsive therapy response. Transl Psychiatry 2014;4:e483.

23.Lyden H, Espinoza RT, Pirnia T, Clark K, Joshi SH, Leaver AM, et al. Electroconvulsive therapy mediates neuroplasticity of white matter microstructure in major depression. Transl Psychiatry 2014;4:e380. 24.Bouckaert F, De Winter FL, Emsell L, Dols A, Rhebergen D, Wampers M, et al. Grey matter volume increase following electroconvulsive therapy in patients with late life depression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Springer Pub. Co.. 1997. 47.Posse S, Otazo R, Dager SR, Alger J. MR spectroscopic imaging.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

How to Go Here cite this where to buy ventolin pills article:Singh 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 where to buy ventolin pills 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 where to buy ventolin pills into a frenzy as newspapers, news channels, and social media were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor.

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

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

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and illness and where to buy ventolin pills also his relationships and finances.

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

These types of viewpoints perpetuate stigma, where to buy ventolin pills myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements where to buy ventolin pills 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 where to buy ventolin pills interacting with media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion.

It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be where to buy ventolin pills 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, where to buy ventolin pills O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Oxford, England. New York. Oxford University Press.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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