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We live in unprecedented times keflex 500mg price at walmart. But what makes them without parallel is not the current pandemic crisis nor the continued problems facing minorities in our institutions. Rather, it’s that for the first keflex 500mg price at walmart time, the problems of accessibility, rights and freedoms are now invading privileged spaces.

There can be no ‘getting back to normal’, because ‘normal’ only ever benefited the white, Western, patriarchal, abled and cis ideals. For many, the world is not suddenly on fire keflex 500mg price at walmart. It has long been burning.The present pandemic lays bare systemic prejudice against the most vulnerable among us.

We at Medical Humanities, with our focus on global health and social justice, welcome discussion about how the crisis has disproportionately affected racial and fiscal minorities, those from the disabled community, those who are LGBTQA+ and other vulnerable groups. What we focus on here, now, can lead to greater accessibility and equity in the future.In this expanded issue, we offer some of the incredible work keflex 500mg price at walmart being done across the field of medical humanities prior to the COVID-19 crisis, and we are already reviewing articles on the role of health humanities during the pandemic. The process of academic publishing tends not to lend itself to immediacy, however, and the challenges of pandemic means greater pressure on everyone, from the authors to the reviewers and readers.To remedy this, we at Medical Humanities have been increasing the work on our blog platform, a place where content can be quickly updated, and where conversations can occur among readers and writers.

We openly invite submissions concerning the virus, as well as topics relevant to our wider CFP (call for posts/papers) this keflex 500mg price at walmart year on social justice and health, to both blog and journal. We will do our best to expedite. Finally, we have also been addressing social justice and access in our podcast, where we interviewed disability activist Alice Wong and most recently Dr Oni Blackstock, primary care physician and HIV specialist in New York.

We hope to keflex 500mg price at walmart have many more on these critical subjects.We wish all of you good health and safety and know that many of you are yet on the front lines. Thank you for being part of the community of Medical Humanities.IntroductionMinecraft is a computer game with no specific goals to accomplish. The gameworld consists of three-dimensional (3D) keflex 500mg price at walmart cubes and objects which the player (Steve) can mine and build into infinitely complex (and logically impossible) structures.

Steve sometimes encounters other characters (‘mobs’), such as animals and hostile creatures. He can ‘spawn’ and destroy them. While it looks like a harmless game of logical construction, it keflex 500mg price at walmart conveys some worryingly delusive ideas about the real world.

The difference between real and imagined structures is at the heart of the age-old debate around categorising mental disorders.Classification in mental health has had various forms throughout history. Mack and colleagues set out a history of psychiatric classification beginning in 2600 BC with Egyptian references to keflex 500mg price at walmart melancholia and hysteria. Through the Ancient Greeks with Hippocrates’ phrenitis, mania, melancholia, epilepsy, hysteria and Scythian disease.

Through the Renaissance period. Through to 19th-century psychiatry featuring Pinel (known as the first psychiatrist), Kraepelin (known for observational classification) and Freud (known for classifying neurosis and psychosis).1Although the keflex 500mg price at walmart history of psychiatric classification identifies some common trends such as the labels ‘melancholia’ and ‘hysteria’ which have survived millennia, the label ‘depression’ is relatively new. The earliest usage noted by Snaith is from 1899.

€˜in simple pathological depression…the patient exhibits a growing indifference to his former pursuits…’.2 Snaith noted that early 20th-century psychiatrists keflex 500mg price at walmart like Adolf Meyer hoped that ‘depression’ would come to encompass a broad category under which descriptions of subtypes would emerge. This did not happen until the middle of the 20th century. With the publication of the sixth International Classification of Diseases (ICD) in 1948 and the Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1952 and their subsequent revisions, the latter half of the 20th century has seen depression subtype labels proliferate.

In their study of the social determinants of diagnostic labels in depression, McPherson and Armstrong illustrate how the codification of depression subtypes in the latter half of the 20th century has been shaped keflex 500mg price at walmart by the evolving context of psychiatry, including power struggles within the profession, a move to community care and the development of psychopharmacology.3During this period, McPherson and Armstrong describe how subsequent versions of the DSM served as battlegrounds for professional disputes and philosophical quarrels around categorisation of mental disorders. DSM I and DSM II have been described as products of an American Psychiatric Association dominated by psychoanalytic psychiatrists.4 DSM III and DSM III-R have been described as a radical rejection of psychoanalytic thinking, a ‘neo-Kraepelinian revolution’, a reference to the observational descriptive techniques of 19th-century psychiatrist Emil Kraepelin who classified mental disorders into two broad categories. €˜dementia praecox’ keflex 500mg price at walmart and ‘manic-depression’.5 DSM III was seen by some as a turning point in the use of the medical model of mental illness, through provision of specific inclusion and exclusion criteria, and use of field trials and a multiaxial system.6 These latter technocratic additions to psychiatric labelling served to engender a much closer alignment between psychiatry, science and medicine.The codification of mental disorders in manuals has been described by Thomas Schacht as intrinsic to the relationship between science and politics and the way in which psychiatrists gain significant social power by aligning themselves to science.7 His argument drew on Szasz, who saw the mental health establishment as a therapeutic state.

Zimbardo, who described psychiatric care as a controlling force. And Foucault, who described the categorisation of the mentally ill as a force for isolating ‘the other’. Diagnostic critique has been further developed through a cultural relativist lens in that what Western psychiatrists classify as a depression is constructed differently in other cultures.8 Considering these limitations, some critics have gone so far as to argue that psychiatric diagnostic systems should be abolished.9Yet architects keflex 500mg price at walmart of DSM manuals have worked hard to ensure the technology of classification is regarded as genuine scientific activity with sound roots in philosophy of science.

In their philosophical defence of DSM IV, Allen Frances and colleagues address their critics under the headings ‘nominalism vs realism’, ‘empiricism vs rationalism’ and ‘categorical vs dimensional’.10 The implication is that there are opposing stances in which a choice must be made or a middle ground forged by those reasonable enough to recognise the need for pragmatism in the service of clinical utility. The nominalism–realism debate is illustrated using as metaphor three different stances a cricket umpire might take on keflex 500mg price at walmart calling strikes and balls. The discussion sets out two of these as extreme views.

€˜at one extreme…those who take a reductionistically realistic view of the world’ versus ‘the solipsistic nominalists…might content that nothing exists’. Szasz, who is characterised as holding particularly extreme views, is named as keflex 500mg price at walmart an archetypal solipsist. There is implied to be a degree of arrogance associated with this view in the illustrative example in which the umpire states ‘there are no balls and there are no strikes until I call them’.

Frances therefore sets up a means of grouping two kinds of people as philosophical extremists who can be dismissed, while avoiding addressing the philosophical problems they pose.Frances provides little if any justification for the middle ground stance, ‘There are balls and there are strikes and I call them as I see them’, other than to focus on its clinical utility and the lack of clinical keflex 500mg price at walmart utility in the alternatives ‘naïve realism’ and ‘heuristically barren solipsism’. The natural conclusion the reader is invited to reach is that a middle ground of a heuristic concept is naturally right because it is not extreme and is naturally useful clinically, without specifying in what way this stance is coherent, resolves the two alternatives, and in what way a heuristic construct that is not ‘real’ can be subject to scientific testing.Similarly, in discussing the ‘categorical vs dimensional’, Frances promotes the ‘prototype approach’. Those holding opposing views are labelled as ‘dualists’ or ‘dichotomisers’.

The prototypical approach is again put forward as a clinically useful keflex 500mg price at walmart middle ground. Illustrations are drawn from natural science. €˜a triangle and a square are never the same’, inciting the reader to keflex 500mg price at walmart consider science as value-free.

The prototypical approach emerges as a natural solution, yet the authors do not address how a diagnostic prototype resolves the issues posed by the two alternatives, nor how a prototype can be subjected to natural science methods.The argument presented here is not a defence of solipsism or dualism. Rather it aims to illustrate that if for pragmatic purposes clinicians and policymakers choose to gloss over the philosophical flaws in classification practices, it is then risky to move beyond the heuristic and apply natural science methods to these constructs adding multiple layers of technocratic subclassification. Doing so is more like playing Minecraft than cricket keflex 500mg price at walmart.

The National Institute for Health and Care Excellence (NICE) guideline for depression is taken as an example of the philosophical errors that can follow from playing Minecraft with unsound heuristic devices, specifically subcategories of persistent forms of depression. As well as serving a clinical purpose, diagnosis in medicine is a way of allocating keflex 500mg price at walmart resources for insurance companies and constructing clinical guidelines, which in turn determine rationing within the National Health Service. The consequences for recipients of healthcare are therefore significant.

Clinical utility is arguably not being served at all and patients are left at risk of poor-quality care.Heterogeneity of persistent depressionAndrea Jobst and colleagues note that ‘because of their chronic clinical course, approximately 40% of CD [chronic depression] patients also fulfil criteria for TRD [treatment resistant depression]…usually defined by the number of non-successful biological treatments’.11 This position is reflected in the DSM VAmerican Psychiatric Association (2013), the European Psychiatric Association (EPA) guidance and the ICD-11(World Health Organisation, 2018), which all use a ‘persistent’ depression category, acknowledging a loosely defined mixed group of long-term, difficult-to-treat depressive conditions, often associated with dysthymia and comorbid common mental disorders, various personality traits and psychosocial disability.In contrast, the NICE 2018 draft guideline separates treatments into those for ‘new episodes’ of depression. €˜further-line’ treatment of depression keflex 500mg price at walmart (equivalent to TRD), CD and ‘depression with co-morbidities’. The latter is subdivided into treatments for ‘complex depression’ and ‘psychotic depression’.

These categories and subcategories keflex 500mg price at walmart introduce an unfortunate sense of certainty as though these labels represent real things. An analysis follows of how these definitions play out in terms of grouping of randomised controlled trials in the NICE evidence review. Specifically, the analysis reveals the overlap between populations in trials which have been separated into discrete categories, revealing significant limitations to the utility of the category labels.The NICE definition of CD requires trial samples to meet the criteria for major depressive disorder (MDD) for 2 years.

Dysthymia and keflex 500mg price at walmart double depression (MDD superimposed on dysthymia) were included. If 75% of the trial population met these criteria, the trial was reviewed in the CD category.12 The definition of TRD (or ‘further-line treatments’) required that the trial sample had demonstrated a ‘limited response to previous treatment’ and randomised to the further-line treatment at this point. If 80% of the trial participants met these criteria, it was reviewed in the TRD category.13 Complex depression was defined keflex 500mg price at walmart as ‘depression co-existing with personality disorder’.

To be classed as complex, 51% of trial participants had to have personality disorder (PD).14It is immediately clear from these definitions that there is a potential problem with attempting to categorise trial populations into just one of these categories. These populations are likely to overlap, whether or not a trial protocol sets out to explicitly record all of this information. The analysis below will illustrate this using examples from within the NICE review.Cataloguing complexity in trial populationsWithin the category keflex 500mg price at walmart of further-line treatments (TRD), 64 trials were reviewed.

Comparisons within these trials were further subcategorised into ‘dose escalation strategies’, ‘augmentation strategies’ and ‘switching strategies’. In drilling down by way of illustration, this analysis considers the keflex 500mg price at walmart 51 trials in the augmentation strategy evidence review. Of these, two were classified by the reviewers as also fulfilling the criteria for CD but were not analysed in the CD category (Study IDs.

Fonagy 2015 and Kocsis 200915). About half of the trials (23/51) did not report keflex 500mg price at walmart the mean duration of episode, meaning that it is not possible to know what percentage of participants also met the criteria for CD. Of trials that did report episode duration, 17 reported a mean duration longer than 24 months.

While the standard deviations varied keflex 500mg price at walmart in size or were unreported, the mean indicates a good likelihood that a significant proportion of the participants across these 51 trials met the criteria for CD.Details of baseline employment, trauma history, suicidality, physical comorbidity, axis I comorbidity and PD (all clinical indicators of complexity, severity and chronicity) were not collated by NICE. For the present analysis, all 51 publications were examined and data compiled concerning clinical complexity in the trial populations. Only 14 of 51 trials report employment data.

Of those that do, unemployment ranges from 12% to keflex 500mg price at walmart 56% across trial samples. None of the trials report trauma history. About half of the trials (26/51) excluded people who were considered keflex 500mg price at walmart a suicide risk.

The others did not.A large proportion of trials (30/51) did not provide any data on axis 1 comorbidity. Of these, 18 did not exclude any diagnoses, while 12 excluded some (but not all) disorders. The most keflex 500mg price at walmart common diagnoses excluded were psychotic disorders, substance or alcohol abuse, and bipolar disorder (excluded in 26, 25 and 23 trials, respectively).

Only 7 of 51 trials clearly stated that all axis 1 diagnoses were excluded. This leaves only keflex 500mg price at walmart 13 studies providing any data about comorbidity. Of these, 9 gave partial data on one or two conditions, while 4 reported either the mean number of disorders (range 1.96–2.9) or the percentage of participants (range 68.1–96.7) with any comorbid diagnosis (Nierenberg 2003a, Nierenberg 2006, Watkins 2011a, Town 201715).The majority of trials (46/51) did not report the prevalence of PD.

Many stated PD as an exclusion criterion but without defining a threshold for exclusion. For example, PD could be excluded if it ‘impacted’ the depression, keflex 500mg price at walmart if it was ‘significant’, ‘severe’ or ‘persistent’. Some excluded certain PDs (such as antisocial or borderline) and not others but without reporting the prevalence of those not excluded.

In the keflex 500mg price at walmart five trials where prevalence was clear, prevalence ranged from 0% (Ravindran 2008a15), where all PDs were excluded, to 87.5% of the sample (Town 201715). Two studies reported the mean number of PDs. 2.0 (Nierenberg 2003a) and 0.85 (Watkins 2011a15).The majority of trials (43/51) did not report the prevalence of physical illness.

Many stated keflex 500mg price at walmart illness as an exclusion criterion, but the definitions and thresholds were vague and could be interpreted in different ways. For example, illness could be excluded if it was ‘unstable’, ‘serious’, ‘significant’, ‘relevant’, or would ‘contraindicate’ or ‘impact’ the medication. Of the eight trials reporting information about physical health, keflex 500mg price at walmart there was a wide variation.

Four reported prevalence varying from 7.6% having a disability (Eisendrath 201615) to 90.9% having an illness or disability (Town 201715). Four used scales of physical health. Two indicating mild problems (Nierenberg 2006, Lavretsky 201115) and two indicating moderately high keflex 500mg price at walmart levels of illness (Thase 2007, Fang 201015).The NICE review also divided trial populations into a dichotomy of ‘more severe’ and ‘less severe’ on the grounds that this would be a clinically useful classification for general practitioners.

NICE applied a bespoke methodology for creating this dichotomy, abandoning validated measure thresholds in order first to generate two ‘homogeneous’ groups to ‘facilitate analysis’, and second to create an algorithm to ‘read across’ different measures (such as the Beck Depression Inventory, the Hamilton Rating Scale for Depression (HRSD) and the Montgomery-Asberg Depression Rating Scale).16 Examining trials which use more than one of these measures reveals problems in the algorithm. Of the 51 trials, there are 6 instances in which the study population falls into NICE’s more severe category according to one measure and into the less severe keflex 500mg price at walmart category according to another. In four of these trials, NICE chose the less severe category (Souza 2016, Watkins 2011a, Fonagy 2015, Town 201715).

The other two trials were designated more severe (Barbee 2011, Dunner 200715). Only 17 of 51 trials reported two or more depression scale measures, leaving much unknown about whether other keflex 500mg price at walmart study populations could count as both more severe and less severe.Absence of knowledge or knowledge of absence?. A key philosophical error in science is to confuse an absence of knowledge with knowledge of absence.

It is likely that some of the keflex 500mg price at walmart study populations deemed lacking in complexity or severity could actually have high degrees of complexity and/or severity. Data to demonstrate this may either fall foul of a guideline committee decision to prioritise certain information over other conflicting information (as in the severity algorithm). The information may be non-existent as it was not collected.

It may keflex 500mg price at walmart be somewhere in the publication pipeline. Or it may be sitting in a database with a research team that has run out of funds for supplementary analyses. Wherever those data are or are not, their keflex 500mg price at walmart absence from published articles does not define the phenomenology of depression for the patients who took part.

As a case in point, data from the Fonagy 2015 trial presented at conferences but not published reveal that PD prevalence data would place the trial well within the NICE complex depression category, and that the sample had high levels of past trauma and physical condition comorbidity. The trial also meets the guideline criteria for CD according to the guideline’s own appendices.17 Reported axis 1 comorbidity was high (75.2% had anxiety disorder, 18.6% had substance abuse disorder, 13.2% had eating disorder).18 The mean depression scores at baseline were 36.5 on the Beck Depression Inventory and 20.1 on the HRSD (severe and very severe, respectively, according to published cut-off scores). NICE categorised this population as less severe TRD, not CD and not complex.Notes1 keflex 500mg price at walmart.

Avram H. Mack et al keflex 500mg price at walmart. (1994), “A Brief History of Psychiatric Classification.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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The General Medical Council’s (GMC) motto of ‘Working with doctors, working for patients’ is at the heart of the work we carry out does keflex affect birth control pills to ensure medical schools and you could check here postgraduate medical training is of the high standard that patients demand, and rightly deserve. However, we know delivering world-class healthcare is taking its toll on doctors and carrying out research into how we can ease the burden and find how burnout can be prevented is becoming a key focus of our work.While still delivering our important statutory functions of controlling access to the register and investigating when things go wrong, we are actively supporting professionals to maintain and improve standards of good medical practice. Additionally, there is a vast amount of work taking place behind the scenes at the GMC to adapt to the ever-evolving environment we are training doctors to work in.SHAPING TRAINING TO MEET does keflex affect birth control pills THE NEEDS OF WORKFORCE AND PATIENTSThe UK population is continuously changing. We have an ageing and consequently increasingly frail population with more people with complex and comorbid diseases. We have more patients with disabilities related to mental and physical health problems—which we expect will does keflex affect birth control pills continue to rise due to does keflex cause c diff the COVID-19 pandemic.

In addition, more young people tend to live in urban areas, whereas there are more older people generally residing in more rural areas.This in turn places a demand on services meaning we need to train more doctors with more generalist, flexible skills and have doctors located in the right geographical areas to treat patients. The ongoing COVID-19 pandemic has highlighted does keflex affect birth control pills the importance of doctors working flexibly.The medical workforce is also ever-varying. Our most recent ‘The state of medical education and practice in the UK’1 report showed we are seeing more female doctors on the register. Increasingly, female doctors make up a higher proportion of the workforce as male ….

The General Medical Council’s (GMC) motto of ‘Working with doctors, working for patients’ is at the heart of keflex 500mg price at walmart the work we carry out to ensure medical schools and postgraduate medical training is of the high standard that patients demand, and https://www.voiture-et-handicap.fr/cheap-generic-keflex/ rightly deserve. However, we know delivering world-class healthcare is taking its toll on doctors and carrying out research into how we can ease the burden and find how burnout can be prevented is becoming a key focus of our work.While still delivering our important statutory functions of controlling access to the register and investigating when things go wrong, we are actively supporting professionals to maintain and improve standards of good medical practice. Additionally, there is a vast amount of work taking place behind the scenes at the GMC to adapt to the ever-evolving environment we are training doctors to work in.SHAPING TRAINING TO MEET THE NEEDS OF keflex 500mg price at walmart WORKFORCE AND PATIENTSThe UK population is continuously changing. We have an ageing and consequently increasingly frail population with more people with complex and comorbid diseases. We have more patients with keflex 500mg price at walmart disabilities related to mental and physical health problems—which we is keflex good for kidney infection expect will continue to rise due to the COVID-19 pandemic.

In addition, more young people tend to live in urban areas, whereas there are more older people generally residing in more rural areas.This in turn places a demand on services meaning we need to train more doctors with more generalist, flexible skills and have doctors located in the right geographical areas to treat patients. The ongoing COVID-19 pandemic has highlighted the importance of doctors working flexibly.The keflex 500mg price at walmart medical workforce is also ever-varying. Our most recent ‘The state of medical education and practice in the UK’1 report showed we are seeing more female doctors on the register. Increasingly, female doctors make up a higher proportion of the workforce as male ….

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Bactrim vs keflex

More than 90% bactrim vs keflex of babies born with heart defects survive into adulthood. As a result, there are now more adults living with congenital heart disease than children. These adults have a chronic, lifelong condition and the European Society of Cardiology (ESC) has bactrim vs keflex produced advice to give the best chance of a normal life. The guidelines are published online today in European Heart Journal,1 and on the ESC website.2Congenital heart disease refers to any structural defect of the heart and/or great vessels (those directly connected to the heart) present at birth. Congenital heart disease affects all aspects of bactrim vs keflex life, including physical and mental health, socialising, and work.

Most patients are unable to exercise at the same level as their peers which, along with the awareness of having a chronic condition, affects mental wellbeing."Having a congenital heart disease, with a need for long-term follow-up and treatment, can also have an impact on social life, limit employment options and make it difficult to get insurance," said Professor Helmut Baumgartner, Chairperson of the guidelines Task Force and head of Adult Congenital and Valvular Heart Disease at the University Hospital of Münster, Germany. "Guiding and supporting patients in all of these processes is an inherent part of their care."All adults with congenital heart disease should have at least one appointment at a specialist centre to determine how often they need to be seen. Teams at bactrim vs keflex these centres should include specialist nurses, psychologists and social workers given that anxiety and depression are common concerns.Pregnancy is contraindicated in women with certain conditions such high blood pressure in the arteries of the lungs. "Pre-conception counselling is recommended for women and men to discuss the risk of the defect in offspring and the option of foetal screening," said Professor Julie De Backer, Chairperson of the guidelines Task Force and cardiologist and clinical geneticist at Ghent University Hospital, Belgium.Concerning sports, recommendations are provided for each condition. Professor De bactrim vs keflex Backer said.

"All adults with congenital heart disease should be encouraged to exercise, taking into account the nature of the underlying defect and their own abilities."The guidelines state when and how to diagnose complications. This includes proactively monitoring for arrhythmias, cardiac imaging and blood tests to detect problems with heart function.Detailed bactrim vs keflex recommendations are provided on how and when to treat complications. Arrhythmias are an important cause of sickness and death and the guidelines stress the importance of correct and timely referral to a specialised treatment centre. They also list when particular treatments should be considered such as ablation (a procedure to destroy heart tissue and stop faulty electrical signals) and device implantation.For several defects, there are new recommendations for catheter-based treatment. "Catheter-based treatment should be performed by specialists in adult congenital heart disease working within a bactrim vs keflex multidisciplinary team," said Professor Baumgartner.

Story Source. Materials provided by European Society of Cardiology bactrim vs keflex. Note. Content may be edited for style and length..

More than keflex 500mg price at walmart 90% of babies born with heart defects survive is keflex good for kidney infection into adulthood. As a result, there are now more adults living with congenital heart disease than children. These adults have a chronic, lifelong condition and the European Society of Cardiology (ESC) has keflex 500mg price at walmart produced advice to give the best chance of a normal life. The guidelines are published online today in European Heart Journal,1 and on the ESC website.2Congenital heart disease refers to any structural defect of the heart and/or great vessels (those directly connected to the heart) present at birth.

Congenital heart disease affects all aspects of life, including physical and mental keflex 500mg price at walmart health, socialising, and work. Most patients are unable to exercise at the same level as their peers which, along with the awareness of having a chronic condition, affects mental wellbeing."Having a congenital heart disease, with a need for long-term follow-up and treatment, can also have an impact on social life, limit employment options and make it difficult to get insurance," said Professor Helmut Baumgartner, Chairperson of the guidelines Task Force and head of Adult Congenital and Valvular Heart Disease at the University Hospital of Münster, Germany. "Guiding and supporting patients in all of these processes is an inherent part of their care."All adults with congenital heart disease should have at least one appointment at a specialist centre to determine how often they need to be seen. Teams at these centres should keflex 500mg price at walmart include specialist nurses, psychologists and social workers given that anxiety and depression are common concerns.Pregnancy is contraindicated in women with certain conditions such high blood pressure in the arteries of the lungs.

"Pre-conception counselling is recommended for women and men to discuss the risk of the defect in offspring and the option of foetal screening," said Professor Julie De Backer, Chairperson of the guidelines Task Force and cardiologist and clinical geneticist at Ghent University Hospital, Belgium.Concerning sports, recommendations are provided for each condition. Professor De keflex 500mg price at walmart Backer said. "All adults with congenital heart disease should be encouraged to exercise, taking into account the nature of the underlying defect and their own abilities."The guidelines state when and how to diagnose complications. This includes proactively monitoring for arrhythmias, cardiac imaging and keflex 500mg price at walmart blood tests to detect problems with heart function.Detailed recommendations are provided on how and when to treat complications.

Arrhythmias are an important cause of sickness and death and the guidelines stress the importance of correct and timely referral to a specialised treatment centre. They also list when particular treatments should be considered such as ablation (a procedure to destroy heart tissue and stop faulty electrical signals) and device implantation.For several defects, there are new recommendations for catheter-based treatment. "Catheter-based treatment should be performed by specialists in adult congenital heart disease keflex 500mg price at walmart working within a multidisciplinary team," said Professor Baumgartner. Story Source.

Materials provided keflex 500mg price at walmart by European Society of Cardiology. Note. Content may be edited for style and length..

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A strict permit does keflex treat uti system is in place for all flights arriving in NSW https://www.voiture-et-handicap.fr/cheap-generic-keflex/ from Victoria and passengers undergo comprehensive police and health checks upon arrival. Health Minister Brad Hazzard said all flights are met by NSW Health staff and police officers to ensure anyone entering NSW complies with the current health orders. “There are only limited reasons does keflex treat uti anyone from Victoria should be entering NSW and people have been turned back despite being allowed on the plane in Melbourne,” Mr Hazzard said.

€œVictorian residents are not permitted into NSW at all unless they are needed for specific purposes and even then have to apply for and get a permit. €œWe are constantly reviewing the situation in Victoria and will adjust the health orders as necessary to protect the people of NSW.” Anyone who flies into NSW from Victoria must either be a NSW resident or have a does keflex treat uti relevant permit that allows entry into NSW – that can include:defence officialsdoctors and nursescritical workers in energy, mining and constructionchild protection workersdisability workers.All travellers are provided with a pack of two masks and hand sanitiser by the airlines. Upon arrival into NSW all passengers from Victoria are.

given masks if they left them on the planetemperature checkedasked relevant questions about their health. And their permit is checked to ensure it complies with the strict permit system.Anyone without a valid permit is referred to NSW Police and taken to does keflex treat uti the Special Health Accommodation to complete 14 days of quarantine. Strict instructions and rules are in place for those going into ‘Home Isolation’ including.

Recommended they be collected in a private car by family or friendsnot to use public transport to get hometo only sit in the back seat of a car with the windows open and air conditioning not on recirculationtold to wear their face masks and observe hand hygiene recommendations, andcalled to make sure they arrive home.NSW Health is provided the contact details of everyone who enters NSW does keflex treat uti from Victoria. NSW Police is conducting regular compliance checks for people told to go into ‘Home Isolation’ as well as responding to reports from the community in relation to suspected breaches. Over the weekend, NSW Police visited almost 600 homes to check that those that were meant to be self-isolating were does keflex treat uti doing so.

In addition to that, over the same period NSW Police received 374 calls to Crime Stoppers reporting suspected breaches of the health orders, the majority of which were for people suspected of not following self-isolation rules. ​Seven cutting-edge is keflex good for kidney infection NSW research projects have been awarded almost $15 million in NSW Government grants to improve the health of people with spinal cord injuries (SCI).Treasurer Dominic Perrottet and Minister for Health and Medical Research Brad Hazzard today announced the grants at the opening of the Neuroscience Research Australia (NeuRA) Spinal Cord Injury Research Centre at Randwick where three of the projects will be carried out. €œThe investment of close to $15 million over four years was a centrepiece of our last Budget and it’s exciting to see the range of research does keflex treat uti projects now underway,” Mr Perrottet said.

€œThis is about improving the health and wellbeing of people with spinal cord injuries, and these projects could help people not just in NSW but right around the world.” Minister Hazzard said every one of the innovative projects holds tremendous promise to improve treatment for people living with spinal cord injuries, giving back muscle function, sense of touch and other abilities that most of us take for granted. €œA spinal injury brings very substantial life challenges, but does keflex treat uti advances in research now mean survivors can have a better quality of life – and even the hope of a cure,” Mr Hazzard said. €œThese projects have great scope, from investigating ways to restore touch sensation through immersive virtual reality through to using electrical stimulation to improve breathing for people affected by the most severe form of paralysis.” The following grant recipients will conduct their research at the new NeuRA centre.

Associate Professor Sylvia Gustin, The University of NSW, does keflex treat uti Neuroscience Research Australia – received $2.5 million for her research project on using virtual reality training to restore touch sensation. Professor Jane Butler – Neuroscience Research Australia, The University of NSW, received $1.5 million to develop a treatment to restore voluntary function after spinal cord injury. And Dr Euan McCaughey, Neuroscience Research Australia, The University of NSW, received $2.4 million for his research into using muscle stimulation to improve respiratory function for people with tetraplegia.

The projects have been awarded through the NSW Government’s Spinal Cord Injury Research Grants program, does keflex treat uti launched in November 2019, with guidance from an advisory committee of spinal cord injury experts. NeuRA CEO, Professor Peter Schofield, said the range and scope of the funded research projects held exciting promise for health related outcomes. €œNeuroscience Research does keflex treat uti Australia is at the forefront of spinal cord injury research in Australia.

Our new Spinal Cord Injury Research Centre and these research projects will dramatically improve Australia’s understanding of how to best treat people with these life-long injuries,” Professor Schofield said. €œNeuRA thanks the NSW Government for funding the Spinal Cord Injury Research Grants Program, and SpinalCure Australia for its tireless efforts in campaigning for more research funding to improve the quality of life for people with a spinal cord injury.” Information on grant recipients and their research projects is available on the OHMR Funded Research Directory​​.​​​.

A strict permit system is in place for all flights arriving in NSW from Victoria keflex for cyst and keflex 500mg price at walmart passengers undergo comprehensive police and health checks upon arrival. Health Minister Brad Hazzard said all flights are met by NSW Health staff and police officers to ensure anyone entering NSW complies with the current health orders. “There are only limited reasons anyone from Victoria should be entering NSW and people have been turned back despite being allowed on the plane keflex 500mg price at walmart in Melbourne,” Mr Hazzard said.

€œVictorian residents are not permitted into NSW at all unless they are needed for specific purposes and even then have to apply for and get a permit. €œWe are constantly reviewing the situation in Victoria and will adjust the health orders as necessary to protect the people of NSW.” Anyone who flies into NSW from Victoria must either be a NSW resident or have a relevant permit that allows entry into NSW – that can include:defence keflex 500mg price at walmart officialsdoctors and nursescritical workers in energy, mining and constructionchild protection workersdisability workers.All travellers are provided with a pack of two masks and hand sanitiser by the airlines. Upon arrival into NSW all passengers from Victoria are.

given masks if they left them on the planetemperature checkedasked relevant questions about their health. And their permit is checked to ensure it complies with the keflex 500mg price at walmart strict permit system.Anyone without a valid permit is referred to NSW Police and taken to the Special Health Accommodation to complete 14 days of quarantine. Strict instructions and rules are in place for those going into ‘Home Isolation’ including.

Recommended they be collected in a private car by family or friendsnot to use public transport to get hometo only sit in the back seat of a car with the windows open and air conditioning not on recirculationtold to keflex 500mg price at walmart wear their face masks and observe hand hygiene recommendations, andcalled to make sure they arrive home.NSW Health is provided the contact details of everyone who enters NSW from Victoria. NSW Police is conducting regular compliance checks for people told to go into ‘Home Isolation’ as well as responding to reports from the community in relation to suspected breaches. Over the weekend, NSW Police visited almost 600 homes to keflex 500mg price at walmart check that those that were meant to be self-isolating were doing so.

In addition to that, over the same period NSW Police received 374 calls to Crime Stoppers reporting suspected breaches of the health orders, the majority of which were for people suspected of not following self-isolation rules. ​Seven cutting-edge NSW research projects have been awarded almost $15 million in NSW Government grants to improve the health of people with spinal cord injuries (SCI).Treasurer Dominic Perrottet and Minister for Health and Medical Research Brad Hazzard today announced the grants at the opening of the Neuroscience Research Australia (NeuRA) Spinal Cord Injury Research Centre at Randwick where three of the projects will be carried out. €œThe investment of close to $15 million over four years was a centrepiece of our last Budget and it’s exciting to see the keflex 500mg price at walmart range of research projects now underway,” Mr Perrottet said.

€œThis is about improving the health and wellbeing of people with spinal cord injuries, and these projects could help people not just in NSW but right around the world.” Minister Hazzard said every one of the innovative projects holds tremendous promise to improve treatment for people living with spinal cord injuries, giving back muscle function, sense of touch and other abilities that most of us take for granted. €œA spinal injury brings very substantial life challenges, but advances in research now mean survivors can have a better quality keflex 500mg price at walmart of life – and even the hope of a cure,” Mr Hazzard said. €œThese projects have great scope, from investigating ways to restore touch sensation through immersive virtual reality through to using electrical stimulation to improve breathing for people affected by the most severe form of paralysis.” The following grant recipients will conduct their research at the new NeuRA centre.

Associate Professor Sylvia Gustin, The University of NSW, Neuroscience Research Australia – received $2.5 keflex 500mg price at walmart million for her research project on using virtual reality training to restore touch sensation. Professor Jane Butler – Neuroscience Research Australia, The University of NSW, received $1.5 million to develop a treatment to restore voluntary function after spinal cord injury. And Dr Euan McCaughey, Neuroscience Research Australia, The University of NSW, received $2.4 million for his research into using muscle stimulation to improve respiratory function for people with tetraplegia.

The projects have been awarded through the NSW Government’s Spinal Cord Injury Research Grants program, launched in November 2019, with guidance from an advisory committee of spinal keflex 500mg price at walmart cord injury experts. NeuRA CEO, Professor Peter Schofield, said the range and scope of the funded research projects held exciting promise for health related outcomes. €œNeuroscience Research Australia is at the keflex 500mg price at walmart forefront of spinal cord injury research in Australia.

Our new Spinal Cord Injury Research Centre and these research projects will dramatically improve Australia’s understanding of how to best treat people with these life-long injuries,” Professor Schofield said. €œNeuRA thanks the NSW Government for funding the Spinal Cord Injury Research Grants Program, and SpinalCure Australia for its tireless efforts in campaigning for more research funding to improve the quality of life for people with a spinal cord injury.” Information on grant recipients and their research projects is available on the OHMR Funded Research Directory​​.​​​.

Keflex antibiotics for mastitis

How to cite keflex antibiotics for mastitis this article:Singh keflex for cyst O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is keflex antibiotics for mastitis one of the highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide.

As expected, the media went into a frenzy as newspapers, news keflex antibiotics for mastitis channels, and social media were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed keflex antibiotics for mastitis on electronic, print, and social media.

We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress calls from their patients in despair with keflex antibiotics for mastitis 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 keflex antibiotics for mastitis of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full keflex antibiotics for mastitis of speculations about the person's mental condition and illness and also his relationships and finances. Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him.

The Indian Psychiatric Society has written to the Press Council of India underlining this concern and keflex antibiotics for mastitis asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental health professionals were called by media houses to comment keflex antibiotics for mastitis 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 keflex antibiotics for mastitis 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 keflex antibiotics for mastitis be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and resource books keflex antibiotics for mastitis 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 keflex antibiotics for mastitis 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 available at the moment. References Correspondence Address:Dr. O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata keflex antibiotics for mastitis - 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.

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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 keflex 500mg price at walmart cite this https://www.voiture-et-handicap.fr/cheap-generic-keflex/ 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 publicized events keflex 500mg price at walmart in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide.

As expected, the media went into keflex 500mg price at walmart 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 keflex 500mg price at walmart many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media.

We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress calls from their patients in despair with keflex 500mg price at walmart 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 keflex 500mg price at walmart 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 keflex 500mg price at walmart about the person's mental condition and illness and also his relationships and finances. Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him.

The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative keflex 500mg price at walmart 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 keflex 500mg price at walmart 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 keflex 500mg price at walmart 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 keflex 500mg price at walmart to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and resource books for interacting with media, and keflex 500mg price at walmart 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 keflex 500mg price at walmart 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 available at the moment. References Correspondence Address:Dr. O P SinghAA 304, Ashabari Apartments, keflex 500mg price at walmart 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.

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

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