Symbicort prices walmart

AbstractBrazil is currently home to the you could check here largest Japanese population outside of Japan symbicort prices walmart. In Brazil today, Japanese-Brazilians are considered to be successful members of Brazilian society. This was not symbicort prices walmart always the case, however, and Japanese immigrants to Brazil endured much hardship to attain their current level of prestige. This essay explores this community’s trajectory towards the formation of the Japanese-Brazilian identity and the issues of mental health that arise in this immigrant community. Through the analysis of Japanese-Brazilian novels, TV shows, film and public health studies, I seek to disentangle the themes of gender and modernisation, and how these themes concurrently grapple with Japanese-Brazilian mental health issues.

These fictional narratives provide a lens into the experience of the Japanese-Brazilian community that is unavailable in traditional medical studies about their mental health.filmliterature and medicinemental health caregender studiesmedical humanitiesData availability symbicort prices walmart statementData are available in a public, open access repository.Introduction and philosophical backgroundWork in the medical humanities has noted the importance of the ‘medical gaze’ and how it may ‘see’ the patient in ways which are specific, while possessing broad significance, in relation to developing medical knowledge. To diagnosis. And to the social position of the medical profession.1 Some authors have emphasised that vision is a distinctive modality of perception symbicort prices walmart which merits its own consideration, and which may have a particular role to play in medical education and understanding.2 3 The clothing we wear has a strong impact on how we are perceived. For example, commentary in this journal on the ‘white coat’ observes that while it may rob the medical doctor of individuality, it nonetheless grants an elevated status4. In contrast, the patient hospital gown may rob patients of individuality in a way that stigmatises them,5 reducing their status in the ward, and ultimately dehumanises them, in conflict with the humanistic approaches seen as central to the best practice in the care of older patients, and particularly those living with dementia.6The broad context of our concern is the visibility of patients and their needs.

We draw on observations made during an ethnographic study of the everyday care of people symbicort prices walmart living with dementia within acute hospital wards, to consider how patients’ clothing may impact on the way they were perceived by themselves and by others. Hence, we draw on this ethnography to contribute to discussion of the ‘medical gaze’ in a specific and informative context.The acute setting illustrates a situation in which there are great many biomedical, technical, recording, and timetabled routine task-oriented demands, organised and delivered by different staff members, together with demands for care and attention to particular individuals and an awareness of their needs. Within this ward setting, we focus on patients who are living with dementia, since this group may be particularly vulnerable to a dehumanising gaze.6 We frame our discussion within the broader context of the general philosophical question of how we acquire knowledge of different types, and the moral consequences of this, particularly knowledge through visual perception.Debates throughout the history of philosophy raise questions about the nature and sources of our knowledge. Contrasts are symbicort prices walmart often drawn between more reliable or less reliable knowledge. And between knowledge that is more technical or ‘objective’, and knowledge that is more emotionally based or more ‘subjective’.

A frequent point of discussion is the reliability and characteristics of perception symbicort prices walmart as a source of knowledge. This epistemological discussion is mostly focused on vision, indicating its particular importance as a mode of perception to humans.7Likewise, in ethics, there is discussion of the origin of our moral knowledge and the particular role of perception.8 There is frequent recognition that the observer has some significant role in acquiring moral knowledge. Attention to qualities of the moral observer is not in itself a denial of moral reality. Indeed, it is the very essence of an ethical response to the world to recognise the deep reality symbicort prices walmart of others as separate persons. The nature of ethical attention to the world and to those around us is debated and has been articulated in various ways.

The quality of ethical attention may vary and achieving a high level of ethical attention may require certain conditions, certain virtues, and the time and mental space to attend to the situation and claims of the other.9Consideration has already been given to how different modes of attention to the world might be of relevance to the practice of medicine. Work that examines different ways of processing information, and of interacting with and being in symbicort prices walmart the world, can be found in Iain McGilchrist’s The Master and His Emissary,10 where he draws on neurological discoveries and applies his ideas to the development of human culture. McGilchrist has recently expanded on the relevance of understanding two different approaches to knowledge for the practice of medicine.11 He argues that task-oriented perception, and a wider, more emotionally attuned awareness of the environment are necessary partners, but may in some circumstances compete, with the competitive edge often being given to the narrower, task-based attention.There has been critique of McGilchrist’s arguments as well as much support. We find his work a useful framework for understanding important debates in the ethics of medicine and of nursing about relationships of staff symbicort prices walmart to patients. In particular, it helps to illuminate the consequences of patients’ dress and personal appearance for how they are seen and treated.Dementia and personal appearanceOur work focuses on patients living with dementia admitted to acute hospital wards.

Here, they are a large group, present alongside older patients unaffected by dementia, as well as younger patients. This mixed population provides a useful setting to consider the impact of personal appearance on different patient groups.The role of appearance in the presentation of the self has been symbicort prices walmart explored extensively by Tseëlon,12 13 drawing on Goffman’s work on stigma5 and the presentation of the self14 using interactionist approaches. Drawing on the experiences on women in the UK, Tseëlon argues Goffman’s interactionist approach best supports how we understand the relationship appearance plays in self presentation, and its relationships with other signs and interactions surrounding it. Tseëlon suggests that understandings in this area, in the role appearance and clothing have in the presentation of the self, have been restricted by the perceived trivialities of the topic and limited to the field of fashion studies.15The personal appearance of older patients, and patients living with dementia in particular, has, more recently, been shown to be worthy of attention and of particular significance. Older people are often assumed to be left out of fashion, yet a concern with appearance remains.16 17 Lack of attention to clothing and to personal care may be one sign of the varied symptoms associated with cognitive impairment or dementia, and so conversely, attention to appearance is one way of combatting symbicort prices walmart the stigma associated with dementia.

Families and carers may also feel the importance of personal appearance. The significant body of work by Twigg and Buse in this field in particular draws attention to the role clothing has on preserving the identity and dignity or people living with dementia, while also constraining and enabling elements of care within long-term community settings.16–19 Within this paper, we examine the ways in which these phenomena can be even more acutely felt within the impersonal setting of the symbicort prices walmart acute hospital.Work has also shown how people living with dementia strongly retain a felt, bodily appreciation for the importance of personal appearance. The comfort and sensuous feel of familiar clothing may remain, even after cognitive capacities such as the ability to recognise oneself in a mirror, or verbal fluency, are lost.18 More strongly still, Kontos,20–22 drawing on the work of Merleau-Ponty and of Bourdieu, has convincingly argued that this attention to clothing and personal appearance is an important aspect of the maintenance of a bodily sense of self, which is also socially mediated, in part via such attention to appearance. Our observations lend support to Kontos’ hypothesis.Much of this previous work has considered clothing in the everyday life of people living with dementia in the context of community or long-term residential care.18 Here, we look at the visual impact of clothing and appearance in the different setting of the hospital ward and consider the consequent implications for patient care. This setting enables us to consider how the short-term and unfamiliar environments of the acute ward, together with the contrast between personal and institutional attire, impact on the perception of the patient by self and by others.There is a body of literature that examines the work of restoring the symbicort prices walmart appearance of residents within long-term community care settings, for instance Ward et al’s work that demonstrates the importance of hair and grooming as a key component of care.23 24 The work of Iltanen-Tähkävuori25 examines the usage of garments designed for long-term care settings, exploring the conflict between clothing used to prevent undressing or facilitate the delivery of care, and the distress such clothing can cause, being powerfully symbolic of lower social status and associated with reduced autonomy.26 27Within this literature, there has also been a significant focus on the role of clothing, appearance and the tasks of personal care surrounding it, on the older female body.

A corpus of feminist literature has examined the ageing process and the use of clothing to conceal ageing, the presentation of a younger self, or a ‘certain’ age28 It argues that once the ability to conceal the ageing process through clothing and grooming has been lost, the aged person must instead conceal themselves, dressing to hide themselves and becoming invisible in the process.29 This paper will explore how institutional clothing within hospital wards affects both the male and female body, the presentation of the ageing body and its role in reinforcing the invisibility of older people, at a time when they are paradoxically most visible, unclothed and undressed, or wearing institutional clothing within the hospital ward.Institutional clothing is designed and used to fulfil a practical function. Its use may therefore perhaps incline us towards a ‘task-based’ mode of attention, which as McGilchrist argues,10 while having a vital place in our understanding of the world, may on occasion interfere with the forms of attention that may be needed to deliver good person-oriented care responsive to individual needs.MethodsEthnography involves the in-depth study of people’s actions and accounts within their natural everyday setting, collecting relatively unstructured data from a range of sources.30 Importantly, it can take into account the perspectives of patients, carers and hospital staff.31 Our approach to ethnography is informed by the symbolic interactionist research tradition, which aims to provide an interpretive understanding of the social world, with an emphasis on interaction, focusing on understanding how action and meaning are constructed within a setting.32 The value of this approach is the depth of understanding and theory generation it can provide.33The goal of ethnography is to identify social processes within the data. There are multiple complex and nuanced interactions within these clinical settings that are capable of ‘communicating many messages at once, even of subverting on one level what it appears to be “saying” on another’.34 Thus, symbicort prices walmart it is important to observe interaction and performance. How everyday care work is organised and delivered. By obtaining observational data from within each institution on the symbicort prices walmart everyday work of hospital wards, their family carers and the nursing and healthcare assistants (HCAs) who carry out this work, we can explore the ways in which hospital organisation, procedures and everyday care impact on care during a hospital admission.

It remedies a common weakness in many qualitative studies, that what people say in interviews may differ from what they do or their private justifications to others.35Data collection (observations and interviews) and analysis were informed by the analytic tradition of grounded theory.36 There was no prior hypothesis testing and we used the constant comparative method and theoretical sampling whereby data collection (observation and interview data) and analysis are inter-related,36 37 and are carried out concurrently.38 39 The flexible nature of this approach is important, because it can allow us to increase the ‘analytic incisiveness’35 of the study. Preliminary analysis of data collected from individual sites informed the focus of later stages of sampling, data collection and analysis in other sites.Thus, sampling requires a flexible, pragmatic approach and purposive and maximum variation sampling (theoretical sampling) was used. This included five hospitals selected to represent a range of symbicort prices walmart hospitals types, geographies and socioeconomic catchments. Five hospitals were purposefully selected to represent a range of hospitals types. Two large university teaching hospitals, two medium-sized general hospitals and one smaller general hospital.

This included one urban, two inner city and two hospitals covering a mix of rural and suburban catchment areas, all situated within England and Wales.These sites represented a range of expertise and interventions in caring for people with dementia, from no formal expertise to the deployment of symbicort prices walmart specialist dementia workers. Fractures, nutritional disorders, urinary tract and pneumonia40 41 are among the principal causes of admission to acute hospital settings among people with dementia. Thus, we focused observation within trauma and orthopaedic wards (80 days) symbicort prices walmart and medical assessment units (MAU. 75 days).Across these sites, 155 days of observational fieldwork were carried out. At each of the five sites, a minimum of 30 days observation took place, split between the two ward types.

Observations were carried out by two researchers, symbicort prices walmart each working in clusters of 2–4 days over a 6-week period at each site. A single day of observation could last a minimum of 2 hours and a maximum of 12 hours. A total of 684 hours of observation were conducted for this study. This produced symbicort prices walmart approximately 600 000 words of observational fieldnotes that were transcribed, cleaned and anonymised (by KF and AN). We also carried out ethnographic (during observation) interviews with trauma and orthopaedic ward (192 ethnographic interviews and 22 group interviews) and MAU (222 ethnographic interviews) staff (including nurses, HCAs, auxiliary and support staff and medical teams) as they cared for this patient group.

This allowed us to question what they are doing and why, and what are the caring practices of ward staff when interacting with people living with dementia.Patients within these settings with a diagnosis of dementia were identified through ward nursing handover notes, patient records and symbicort prices walmart board data with the assistance of ward staff. Following the provision of written and verbal information about the study, and the expression of willingness to take part, written consent was taken from patients, staff and visitors directly observed or spoken to as part of the study.To optimise the generalisability of our findings,42 our approach emphasises the importance of comparisons across sites,43 with theoretical saturation achieved following the search for negative cases, and on exploring a diverse and wide range of data. When no additional empirical data were found, we concluded that the analytical categories were saturated.36 44Grounded theory and ethnography are complementary traditions, with grounded theory strengthening the ethnographic aims of achieving a theoretical interpretation of the data, while the ethnographic approach prevents a rigid application of grounded theory.35 Using an ethnographic approach can mean that everything within a setting is treated as data, which can lead to large volumes of unconnected data and a descriptive analysis.45 This approach provides a middle ground in which the ethnographer, often seen as a passive observer of the social world, uses grounded theory to provide a systematic approach to data collection and analysis that can be used to develop theory to address the interpretive realities of participants within this setting.35Patient and public involvementThe data presented in this paper are drawn from a wider ethnographic study supported by an advisory group of people living with dementia and their family carers. It was this symbicort prices walmart advisory group that informed us of the need of a better understanding of the impacts of the everyday care received by people living with dementia in acute hospital settings. The authors met with this group on a regular basis throughout the study, and received guidance on both the design of the study and the format of written materials used to recruit participants to the study.

The external oversight group for this study included, and was chaired, by carers of people living with dementia. Once data analysis was complete, the advisory symbicort prices walmart group commented on our initial findings and recommendations. During and on completion of the analysis, a series of public consultation events were held with people living with dementia and family carers to ensure their involvement in discussing, informing and refining our analysis.FindingsWithin this paper, we focus on exploring the medical gaze through the embedded institutional cultures of patient clothing, and the implications this have for patients living with dementia within acute hospital wards. These findings emerged from our wider analysis of our ethnographic study examining ward cultures of care and the experiences of people living with dementia symbicort prices walmart. Here, we examine the ways in which the cultures of clothing within wards impact on the visibility of patients within it, what clothing and identity mean within the ward and the ways in which clothing can be a source of distress.

We will look at how personal grooming and appearance can affect status within the ward, and finally explore the removal of clothing, and the impacts of its absence.Ward clothing culturesAcross our sites, there was variation in the cultures of patient clothing and dress. Within many wards, it was typical for all older patients to be dressed in hospital-issued institutional gowns and pyjamas (typically in pastel blue, pink, green or peach), paired with hospital supplied socks (usually bright red, although there was some small variation) with non-slip grip soles, while in symbicort prices walmart other wards, it was standard practice for people to be supported to dress in their own clothes. Across all these wards, we observed that younger patients (middle aged/working age) were more likely to be able to wear their own clothes while admitted to a ward, than older patients and those with a dementia diagnosis.Among key signifiers of social status and individuality are the material things around the person, which in these hospital wards included the accoutrements around the bedside. Significantly, it was observed that people living with dementia were more likely to be wearing an institutional hospital gown or institutional pyjamas, and to have little to individuate the person at the bedside, on either their cabinet or the mobile tray table at their bedside. The wearing of institutional clothing was typically connected to fewer personal items symbicort prices walmart on display or within reach of the patient, with any items tidied away out of sight.

In contrast, younger working age patients often had many personal belongings, cards, gadgets, books, media players, with young adults also often having a range of ‘get well soon’ gifts, balloons and so on from the hospital gift shop) on display. This both afforded some elements of familiarity, but also marked the person symbicort prices walmart out as someone with individuality and a certain social standing and place.Visibility of patients on a wardThe significance of the obscurity or invisibility of the patient in artworks depicting doctors has been commented on.4 Likewise, we observed that some patients within these wards were much more ‘visible’ to staff than others. It was often apparent how the wearing of personal clothing could make the patient and their needs more readily visible to others as a person. This may be especially so given the contrast in appearance clothing may produce in this particular setting. On occasion, this may be remarked on symbicort prices walmart by staff, and the resulting attention received favourably by the patient.A member of the bay team returned to a patient and found her freshly dressed in a white tee shirt, navy slacks and black velvet slippers and exclaimed aloud and appreciatively, ‘Wow, look at you!.

€™ The patient looked pleased as she sat and combed her hair [site 3 day 1].Such a simple act of recognition as someone with a socially approved appearance takes on a special significance in the context of an acute hospital ward, and for patients living with dementia whose personhood may be overlooked in various ways.46This question of visibility of patients may also be particularly important when people living with dementia may be less able to make their needs and presence known. In this example, a whole bay of patients was seemingly ‘invisible’. Here, the ethnographer is observing a four-bed bay occupied by male patients symbicort prices walmart living with dementia.The man in bed 17 is sitting in his bedside chair. He is dressed in green hospital issue pyjamas and yellow grip socks. At 10 a.m., the symbicort prices walmart physiotherapy team come and see him.

The physiotherapist crouches down in front of him and asks him how he is. He says he is unhappy, and the physiotherapist explains that she’ll be back later to see him again. The nurse checks on him, asks him if he wants a pillow, and puts symbicort prices walmart it behind his head explaining to him, ‘You need to sit in the chair for a bit’. She pulls his bedside trolley near to him. With the help of a Healthcare Assistant they make the bed.

The Healthcare Assistant chats to him, puts cake symbicort prices walmart out for him, and puts a blanket over his legs. He is shaking slightly and I wonder if he is cold.The nurse explains to me, ‘The problem is this is a really unstimulating environment’, then says to the patient, ‘All done, let’s have a bit of a tidy up,’ before wheeling the equipment out.The neighbouring patient in bed 18, is now sitting in his bedside chair, wearing (his own) striped pyjamas. His eyes are open, and symbicort prices walmart he is looking around. After a while, he closes his eyes and dozes. The team chat to patient 19 behind the curtains.

He says he doesn’t want to sit, and they say that is fine symbicort prices walmart unless the doctors tell them otherwise.The nurse puts music on an old radio with a CD player which is at the doorway near the ward entrance. It sounds like music from a musical and the ward it is quite noisy suddenly. She turns down the volume a bit, but it is very jaunty and upbeat. The man symbicort prices walmart in bed 19 quietly sings along to the songs. €˜I am going to see my baby when I go home on victory day…’At ten thirty, the nurse goes off on her break.

The rest of the team are spread around symbicort prices walmart the other bays and side rooms. There are long distances between bays within this ward. After all the earlier activity it is now very calm and peaceful in the bay. Patient 20 is sitting symbicort prices walmart in the chair tapping his feet to the music. He has taken out a large hessian shopping bag out of his cabinet and is sorting through the contents.

There is symbicort prices walmart a lot of paperwork in it which he is reading through closely and sorting.Opposite, patient 17 looks very uncomfortable. He is sitting with two pillows behind his back but has slipped down the chair. His head is in his hands and he suddenly looks in pain. He hasn’t symbicort prices walmart touched his tea, and is talking to himself. The junior medic was aware that 17 was not comfortable, and it had looked like she was going to get some advice, but she hasn’t come back.

18 drinks his tea and looks at a wool twiddle mitt sleeve, puts it down, and dozes. 19 has finished all his coffee and manages to put the cup down on the trolley.Everyone is tapping their feet or wiggling their toes to the music, or singing quietly to it, when a student nurse, who is working at the computer station in symbicort prices walmart the corridor outside the room, comes in. She has a strong purposeful stride and looks irritated as she switches the music off. It feels like a jolt to symbicort prices walmart the room. She turns and looks at me and says, ‘Sorry were you listening to it?.

€™ I tell her that I think these gentlemen were listening to it.She suddenly looks very startled and surprised and looks at the men in the room for the first time. They have all stopped symbicort prices walmart tapping their toes and stopped singing along. She turns it back on but asks me if she can turn it down. She leaves and goes back to her paperwork outside. Once it is turned back on everyone starts tapping their symbicort prices walmart toes again.

The music plays on. €˜There’ll be bluebirds over the white cliffs of Dover, just you wait and see…’[Site 3 day 3]The music was played by staff to help combat the drab and unstimulating environment of this hospital ward for the patients, the very people the ward is meant symbicort prices walmart to serve. Yet for this member of ward staff the music was perceived as a nuisance, the men for whom the music was playing seemingly did not register to her awareness. Only an individual of ‘higher’ status, the researcher, sitting at the end of this room was visible to her. This example illustrates symbicort prices walmart the general question of the visibility or otherwise of patients.

Focusing on our immediate topic, there may be complex pathways through which clothing may impact on how patients living with dementia are perceived, and on their self-perception.Clothing and identityOn these wards, we also observed how important familiar aspects of appearance were to relatives. Family members may be distressed if they find the person they knew so well, looking markedly different. In the example symbicort prices walmart below, a mother and two adult daughters visit the father of the family, who is not visible to them as the person they were so familiar with. His is not wearing his glasses, which are missing, and his daughters find this very difficult. Even though he looks very different following his admission—he has symbicort prices walmart lost a large amount of weight and has sunken cheekbones, and his skin has taken on a darker hue—it is his glasses which are a key concern for the family in their recognition of their father:As I enter the corridor to go back to the ward, I meet the wife and daughter of the patient in bed 2 in the hall and walk with them back to the ward.

Their father looks very frail, his head is back, and his face is immobile, his eyes are closed, and his mouth is open. His skin looks darker than before, and his cheekbones and eye sockets are extremely prominent from weight loss. €˜I am like a bird symbicort prices walmart I want to fly away…’ plays softly in the radio in the bay. I sit with them for a bit and we chat—his wife holds his hand as we talk. His wife has to take two busses to get to the hospital and we talk about the potential care home they expect her husband will be discharged to.

They hope it will be close because she does symbicort prices walmart not drive. He isn’t wearing his glasses and his daughter tells me that they can’t find them. We look in symbicort prices walmart the bedside cabinet. She has never seen her dad without his glasses. €˜He doesn’t look like my dad without his glasses’ [Site 2 day 15].It was often these small aspects of personal clothing and grooming that prompted powerful responses from visiting family members.

Missing glasses and missing teeth were notable in this regard (and with symbicort prices walmart the follow-up visits from the relatives of discharged patients trying to retrieve these now lost objects). The location of these possessions, which could have a medical purpose in the case of glasses, dental prosthetics, hearing aids or accessories which contained personal and important aspects of a patient’s identity, such as wallets or keys, and particularly, for female patients, handbags, could be a prominent source of distress for individuals. These accessories to personal clothing were notable on these wards by their everyday absence, hidden away in bedside cupboards or simply not brought in with the patient at admission, and by the frequency with which patients requested and called out for them or tried to look for them, often in repetitive cycles that indicated their underlying anxiety about these belongings, but which would become invisible to staff, becoming an everyday background intrusion to the work of the wards.When considering the visibility and recognition of individual persons, missing glasses, especially glasses for distance vision, have a particular significance, for without them, a person may be less able to recognise and interact visually with others. Their presence facilitates the subject of the gaze, symbicort prices walmart in gazing back, and hence helps to ground meaningful and reciprocal relationships of recognition. This may be one factor behind the distress of relatives in finding their loved ones’ glasses to be absent.Clothing as a source of distressAcross all sites, we observed patients living with dementia who exhibited obvious distress at aspects of their institutional apparel and at the absence of their own personal clothing.

Some older patients were symbicort prices walmart clearly able to verbalise their understandings of the impacts of wearing institutional clothing. One patient remarked to a nurse of her hospital blue tracksuit. €˜I look like an Olympian or Wentworth prison in this outfit!. The latter I expect…’ The staff laughed as they walked symbicort prices walmart her out of the bay (site 3 day 1).Institutional clothing may be a source of distress to patients, although they may be unable to express this verbally. Kontos has shown how people living with dementia may retain an awareness at a bodily level of the demands of etiquette.20 Likewise, in our study, a man living with dementia, wearing a very large institutional pyjama top, which had no collar and a very low V neck, continually tried to pull it up to cover his chest.

The neckline was particularly low, because the pyjamas were far too large for him. He continued to fiddle with his very low-necked top even when his lunch symbicort prices walmart tray was placed in front of him. He clearly felt very uncomfortable with such clothing. He continued using his hands to try to pull symbicort prices walmart it up to cover his exposed chest, during and after the meal was finished (site 3 day 5).For some patients, the communication of this distress in relation to clothing may be liable to misinterpretation and may have further impacts on how they are viewed within the ward. Here, a patient living with dementia recently admitted to this ward became tearful and upset after having a shower.

She had no fresh clothes, and so the team had provided her with a pink hospital gown to wear.‘I want my trousers, where is my bra, I’ve got no bra on.’ It is clear she doesn’t feel right without her own clothes on. The one-to-one healthcare assistant assigned to this symbicort prices walmart patient tells her, ‘Your bra is dirty, do you want to wear that?. €™ She replies, ‘No I want a clean one. Where are my trousers?. I want them, I’ve lost them.’ The healthcare assistant repeats the explaination that her clothes are dirty, symbicort prices walmart and asks her, ‘Do you want your dirty ones?.

€™ She is very teary ‘No, I want my clean ones.’ The carer again explains that they are dirty.The cleaner who always works in the ward arrives to clean the floor and sweeps around the patient as she sits in her chair, and as he does this, he says ‘Hello’ to her. She is very teary and explains that she symbicort prices walmart has lost her clothes. The cleaner listens sympathetically as she continues ‘I am all confused. I have lost my clothes. I am all confused symbicort prices walmart.

How am I going to go to the shops with no clothes on!. €™ (site 5 day 5).This person experienced significant distress because of her absent clothes, but this would often be simply attributed to confusion, seen as a feature of her dementia. This then may solidify staff perceptions symbicort prices walmart of her condition. However, we need to consider that rather than her condition (her diagnosis of dementia) causing distress about clothing, the direction of causation may be the reverse. The absence of her own familiar clothing contributes significantly to her symbicort prices walmart distress and disorientation.

Others have argued that people with limited verbal capacity and limited cognitive comprehension will have a direct appreciation of the grounding familiarity of wearing their own clothes, which give a bodily felt notion of comfort and familiarity.18 47 Familiar clothing may then be an essential prop to anchor the wearer within a recognisable social and meaningful space. To simply see clothing from a task-oriented point of view, as fulfilling a simply mechanical function, and that all clothing, whether personal or institutional have the same value and role, might be to interpret the desire to wear familiar clothing as an ‘optional extra’. However, for symbicort prices walmart those patients most at risk of disorientation and distress within an unfamiliar environment, it could be a valuable necessity.Personal grooming and social statusIncluding in our consideration of clothing, we observed other aspects of the role of personal grooming. Personal grooming was notable by its absence beyond the necessary cleaning required for reasons of immediate hygiene and clinical need (such as the prevention of pressure ulcers). Older patients, and particular those living with dementia who were unable to carry out ‘self-care’ independently and were not able to request support with personal grooming, could, over their admission, become visibly unkempt and scruffy, hair could be left unwashed, uncombed and unstyled, while men could become hirsute through a lack of shaving.

The simple act of a visitor dressing and grooming a patient as they prepared for discharge could transform symbicort prices walmart their appearance and leave that patient looking more alert, appear to having increased capacity, than when sitting ungroomed in their bed or bedside chair.It is important to consider the impact of appearance and of personal care in the context of an acute ward. Kontos’ work examining life in a care home, referred to earlier, noted that people living with dementia may be acutely aware of transgressions in grooming and appearance, and noted many acts of self-care with personal appearance, such as stopping to apply lipstick, and conformity with high standards of table manners. Clothing, etiquette and personal grooming are important indicators of social class and hence an aspect of belonging and identity, symbicort prices walmart and of how an individual relates to a wider group. In Kontos’ findings, these rituals and standards of appearance were also observed in negative reactions, such as expressions of disgust, towards those residents who breached these standards. Hence, even in cases where an individual may be assessed as having considerable cognitive impairment, the importance of personal appearance must not be overlooked.For some patients within these wards, routine practices of everyday care at the bedside can increase the potential to influence whether they feel and appear socially acceptable.

The delivery of routine timetabled care at the bedside can impact on people’s appearance in ways that may mark them out as failing to symbicort prices walmart achieve accepted standards of embodied personhood. The task-oriented timetabling of mealtimes may have significance. It was a typical observed feature of this routine, when a mealtime has ended, that people living with dementia were left with visible signs and features of the mealtime through spillages on faces, clothes, bed sheets and bedsides, that leave them at risk of being assessed as less socially acceptable and marked as having reduced independence. For example, a volunteer attempts to ‘feed’ a person living with dementia, when she gives up and leave the bedside (this woman living with dementia has resisted her attempts and explicitly says symbicort prices walmart ‘no’), remnants of the food is left spread around her mouth (site E). In a different ward, the mealtime has ended, yet a large white plastic bib to prevent food spillages remains attached around the neck of a person living with dementia who is unable to remove it (site X).Of note, an adult would not normally wear a white plastic bib at home or in a restaurant.

It signifies a task-based apparel that is demeaning to an individual’s symbicort prices walmart social status. This example also contrasts poignantly with examples from Kontos’ work,20 such as that of a female who had little or no ability to verbalise, but who nonetheless would routinely take her pearl necklace out from under her bib at mealtimes, showing she retained an acute awareness of her own appearance and the ‘right’ way to display this symbol of individuality, femininity and status. Likewise, Kontos gives the example of a resident who at mealtimes ‘placed her hand on her chest, to prevent her blouse from touching the food as she leaned over her plate’.20Patients who are less robust, who have cognitive impairments, who may be liable to disorientation and whose agency and personhood are most vulnerable are thus those for whom appropriate and familiar clothing may be most advantageous. However, we found the ‘Matthew effect’ to be frequently in symbicort prices walmart operation. To those who have the least, even that which they have will be taken away.48 Although there may be institutional and organisational rationales for putting a plastic cover over a patient, leaving it on for an extended period following a meal may act as a marker of dehumanising loss of social status.

By being able to maintain familiar clothing and adornment to visually display social standing and identity, a person living with dementia may maintain a continuity of selfhood.However, it is also possible that dressing and grooming an older person may itself be a task-oriented institutional activity in certain contexts, as discussed by Lee-Treweek49 in the context of a nursing home preparing residents for ‘lounge view’ where visitors would see them, using residents to ‘create a visual product for others’ sometimes to the detriment of residents’ needs. Our observations regarding the importance symbicort prices walmart of patient appearance must therefore be considered as part of the care of the whole person and a significant feature of the institutional culture.Patient status and appearanceWithin these wards, a new grouping of class could become imposed on patients. We understand class not simply as socioeconomic class but as an indicator of the strata of local social organisation to which an individual belongs. Those in the lowest symbicort prices walmart classes may have limited opportunities to participate in society, and we observed the ways in which this applied to the people living with dementia within these acute wards. The differential impact of clothing as signifiers of social status has also been observed in a comparison of the white coat and the patient gown.4 It has been argued that while these both may help to mask individuality, they have quite different effects on social status on a ward.

One might say that the white coat increases visibility as a person of standing and the attribution of agency, the patient gown diminishes both of these. (Within these wards, although white coats were not to be found, the dress code of medical staff did make them symbicort prices walmart stand out. For male doctors, for example, the uniform rarely strayed beyond chinos paired with a blue oxford button down shirt, sleeves rolled up, while women wore a wider range of smart casual office wear.) Likewise, we observed that the same arrangement of attire could be attributed to entirely different meanings for older patients with or without dementia.Removal of clothes and exposureWithin these wards, we observed high levels of behaviour perceived by ward staff as people living with dementia displaying ‘resistance’ to care.50 This included ‘resistance’ towards institutional clothing. This could include pulling up or removing hospital gowns, removing institutional pyjama trousers or pulling up gowns, and standing with gowns untied and exposed at the back (although this last example is an unavoidable design feature of the clothing itself). Importantly, the removal of clothing was limited to institutional gowns and pyjamas and we did not see any patients removing their own symbicort prices walmart clothing.

This also included the removal of institutional bedding, with instances of patients pulling or kicking sheets from their bed. These acts could and was symbicort prices walmart often interpreted by ward staff as a patient’s ‘resistance’ to care. There was some variation in this interpretation. However, when an individual patient response to their institutional clothing and bedding was repeated during a shift, it was more likely to be conceived by the ward team as a form of resistance to their care, and responded to by the replacement and reinforcement of the clothing and bedding to recover the person.The removal of gowns, pyjamas and bedsheets often resulted in a patient exposing their genitalia or continence products (continence pads could be visible as a large diaper or nappy or a pad visibly held in place by transparent net pants), and as such, was disruptive to the norms and highly visible to staff and other visitor to these wards. Notably, unlike other behaviours considered by staff to be symbicort prices walmart disruptive or inappropriate within these wards such as shouting or crying out, the removal of bedsheets and the subsequent bodily exposure would always be immediately corrected, the sheet replaced and the patient covered by either the nurse or HCA.

The act of removal was typically interpreted by ward staff as representing a feature of the person’s dementia and staff responses were framed as an issue of patient dignity, or the dignity and embarrassment of other patients and visitors to the ward. However, such responses to removal could lead to further symbicort prices walmart cycles of removal and replacement, leading to an escalation of distress in the person. This was important, because the recording of ‘refusal of care’, or presumed ‘confusion’ associated with this, could have significant impacts on the care and discharge pathways available and prescribed for the individual patient.Consider the case of a woman living with dementia who is 90 years old (patient 1), in the example below. Despite having no immediate medical needs, she has been admitted to the MAU from a care home (following her husband’s stroke, he could no longer care for her). Across the previous evening and symbicort prices walmart morning shift, she was shouting, refusing all food and care and has received assistance from the specialist dementia care worker.

However, during this shift, she has become calmer following a visit from her husband earlier in the day, has since eaten and requested drinks. Her care home would not readmit her, which meant she was not able to be discharged from the unit (an overflow unit due to a high number of admissions to the emergency department during a patch of exceptionally hot weather) until alternative arrangements could be made by social services.During our observations, she remains calm for the first 2 hours. When she does talk, she is very loud and high pitched, but this is normal for her and not symbicort prices walmart a sign of distress. For staff working on this bay, their attention is elsewhere, because of the other six patients on the unit, one is ‘on suicide watch’ and another is ‘refusing their medication’ (but does not have a diagnosis of dementia). At 15:10 patient 1 begins symbicort prices walmart to remove her sheets:15:10.

The unit seems chaotic today. Patient 1 has begun to loudly drum her fingers on the tray table. She still has not been symbicort prices walmart brought more milk, which she requested from the HCA an hour earlier. The bay that patient 1 is admitted to is a temporary overflow unit and as a result staff do not know where things are. 1 has moved her sheets off her legs, her bare knees peeking out over the top of piled sheets.15:15.

The nurse in charge symbicort prices walmart says, ‘Hello,’ when she walks past 1’s bed. 1 looks across and smiles back at her. The nurse in charge explains to her that she needs to shuffle up symbicort prices walmart the bed. 1 asks the nurse about her husband. The nurse reminds 1 that her husband was there this morning and that he is coming back tomorrow.

1 says that he hasn’t been and she does not believe the symbicort prices walmart nurse.15:25. I overhear the nurse in charge question, under her breath to herself, ‘Why 1 has been left on the unit?. €™ 1 has started asking for somebody to come and see her. The nurse in charge tells 1 that she needs to do some jobs first and then symbicort prices walmart will come and talk to her.15:30. 1 has once again kicked her sheets off of her legs.

A social worker comes symbicort prices walmart onto the unit. 1 shouts, ‘Excuse me’ to her. The social worker replies, ‘Sorry I’m not staff, I don’t work here’ and leaves the bay.15:40. 1 keeps kicking sheets off her bed, symbicort prices walmart otherwise the unit is quiet. She now whimpers whenever anyone passes her bed, which is whenever anyone comes through the unit’s door.

1 is the only elderly patient on the unit. Again, the nurse in charge is heard sympathizing symbicort prices walmart that this is not the right place for her.16:30. A doctor approaches 1, tells her that she is on her list of people to say hello to, she is quite friendly. 1 tells symbicort prices walmart her that she has been here for 3 days, (the rest is inaudible because of pitch). The doctor tries to cover 1 up, raising her bed sheet back over the bed, but 1 loudly refuses this.

The doctor responds by ending the interaction, ‘See you later’, and leaves the unit.16:40. 1 attempts to talk to the new nurse assigned to symbicort prices walmart the unit. She goes over to 1 and says, ‘What’s up my darling?. €™ It’s hard to follow 1 now as she sounds very upset. The RN’s symbicort prices walmart first instinct, like with the doctor and the nurse in charge, is to cover up 1 s legs with her bed sheet.

When 1 reacts to this she talks to her and they agree to cover up her knees. 1 is talking about how her husband won’t come and visit her, and still sounds really upset symbicort prices walmart about this. [Site 3, Day 13]Of note is that between days 6 and 15 at this site, observed over a particularly warm summer, this unit was uncomfortably hot and stuffy. The need to be uncovered could be viewed as a reasonable response, and in fact was considered acceptable for patients without a classification of dementia, provided they were otherwise clothed, such as the hospital gown patient 1 was wearing. This is an example of an aspect of care where the choice and autonomy granted to patients assessed as having (or assumed to have) cognitive capacity is not available to people who are considered to have impaired cognitive capacity (a diagnosis of dementia) and carries the additional moral judgements of the appropriateness of behaviour symbicort prices walmart and bodily exposure.

In the example given above, the actions were linked to the patient’s resistance to their admission to the hospital, driven by her desire to return home and to be with her husband. Throughout observations over this 10-day period, patients perceived by staff as rational agents were allowed to strip down their bedding for comfort, whereas patients living with dementia who responded in this way were often viewed by staff as ‘undressing’, which would be interpreted as a feature of their condition, to be challenged and corrected by staff.Note how the same visual data triggered opposing interpretations of personal autonomy. Just as in the example above where distress over loss of familiar clothing may be interpreted as an aspect of confusion, yet lead to, or symbicort prices walmart exacerbate, distress and disorientation. So ‘deviant’ bedding may be interpreted, for some patients only, in ways that solidify notions of lack of agency and confusion, is another example of the Matthew effect48 at work through the organisational expectations of the clothed appearance of patients.Within wards, it is not unusual to see patients, especially those with a diagnosis of dementia or cognitive impairment, walking in the corridor inadvertently in some state of undress, typically exposed from behind by their hospital gowns. This exposure in itself is of course, an intrinsic functional feature of the design of the flimsy back-opening institutional clothing the patient has been symbicort prices walmart placed in.

This task-based clothing does not even fulfil this basic function very adequately. However, this inadvertent exposure could often be interpreted as an overt act of resistance to the ward and towards staff, especially when it led to exposed genitalia or continence products (pads or nappies).We speculate that the interpretation of resistance may be triggered by the visual prompt of disarrayed clothing and the meanings assumed to follow, where lack of decorum in attire is interpreted as indicating more general behavioural incompetence, cognitive impairment and/or standing outside the social order.DiscussionPrevious studies examining the significance of the visual, particularly Twigg and Buse’s work16–19 exploring the materialities of appearance, emphasise its key role in self-presentation, visibility, dignity and autonomy for older people and especially those living with dementia in care home settings. Similarly, care home studies have demonstrated that institutional clothing, designed to facilitate task-based care, can be potentially dehumanising or and distressing.25 symbicort prices walmart 26 Our findings resonate with this work, but find that for people living with dementia within a key site of care, the acute ward, the impact of institutional clothing on the individual patient living with dementia, is poorly recognised, but is significant for the quality and humanity of their care.Our ethnographic approach enabled the researchers to observe the organisation and delivery of task-oriented fast-paced nature of the work of the ward and bedside care. Nonetheless, it should also be emphasised the instances in which staff such as HCAs and specialist dementia staff within these wards took time to take note of personal appearance and physical caring for patients and how important this can be for overall well-being. None of our observations should be read as critical of any individual staff, but reflects longstanding institutional cultures.Our previous work has examined how readily a person living with dementia within a hospital wards is vulnerable to dehumanisation,51 and to their behaviour within these wards being interpreted as a feature of their condition, rather than a response to the ways in which timetabled care is delivered at their bedside.50 We have also examined the ways in which visual stimuli within these wards in the form of signs and symbols indicating a diagnosis of dementia may inadvertently focus attention away from the individual patient and may incline towards simplified and inaccurate categorisation of both needs and the diagnostic category of dementia.52Our work supports the analysis of the two forms of attention arising from McGilchrist’s work.10 The institutional culture of the wards produces an organisational task-based technical attention, which we found appeared to compete with and reduce the opportunity for ward staff to seek a finer emotional attunement to the person they are caring for and their needs.

Focus on efficiency, pace and record keeping that measures individual task symbicort prices walmart completion within a timetable of care may worsen all these effects. Indeed, other work has shown that in some contexts, attention to visual appearance may itself be little more than a ‘task’ to achieve.49 McGilchrist makes clear, and we agree, that both forms of attention are vital, but more needs to be done to enable staff to find a balance.Previous work has shown how important appearance is to older people, and to people living with dementia in particular, both in terms of how they are perceived by others, but also how for this group, people living with dementia, clothing and personal grooming may act as a particularly important anchor into a familiar social world. These twin aspects of clothing and appearance—self-perception and perception by others—may be especially important in the fast-paced context of an acute ward environment, where patients living with dementia may be struggling with the impacts of an additional acute medical condition within in a highly timetabled and regimented and symbicort prices walmart unfamiliar environment of the ward, and where staff perceptions of them may feed into clinical assessments of their condition and subsequent treatment and discharge pathways. We have seen above, for instance, how behaviour in relation to appearance may be seen as ‘resisting care’ in one group of patients, but as the natural expression of personal preference in patients viewed as being without cognitive impairments. Likewise, personal grooming might impact favourably on a patient’s alertness, visibility and status within the ward.Prior work has demonstrated the importance of the medical gaze for the perceptions of the patient.

Other work has also shown how older people, and in particular people living with dementia, may be thought to be beyond concern for appearance, yet this does not accurately reflect the importance of appearance we found for symbicort prices walmart this patient group. Indeed, we argue that our work, along with the work of others such as Kontos,20 21 shows that if anything, visual appearance is especially important for people living with dementia particularly within clinical settings. In considering the task of washing the patient, Pols53 considered ‘dignitas’ in terms of aesthetic values, in comparison to humanitas conceived as citizen values of equality between persons. Attention to dignitas in the form of appearance may symbicort prices walmart be a way of facilitating the treatment by others of a person with humanitas, and helping to realise dignity of patients.Data availability statementNo data are available. Data are unavailable to protect anonymity.Ethics statementsPatient consent for publicationNot required.Ethics approvalEthics committee approval for the study was granted by the NHS Research Ethics Service (15/WA/0191).AcknowledgmentsThe authors acknowledge funding support from the NIHR.Notes1.

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(2017). "The art of medicine. Arts-based training in observation and mindfulness for fostering the empathic response in medical residents.” Medical Humanities. Medhum-2016-011180.3. E Forde (2018).

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Contemporary Epistemology, John Wiley and Sons.8. D McNaughton (1988). Moral Vision. Blackwell.9. S Weil (1953).

Gravity and Grace. U of Nebraska Press.10. I McGilchrist (2009). The Master and his Emissary. The divided brain and the making of the western world.

New Haven and London, Yale University Press.11. Iain McGilchrist (2011). €œPaying attention to the bipartite brain.” The Lancet 377 (9771). 1068–1069.12. Efrat Tseëlon (1992).

€œSelf presentation through appearance. A manipulative vs a dramaturgical approach”. Symbolic Interaction, 15(4). 501–514.13. E Tseëlon (1995).

The masque of femininity. The presentation of woman in everyday life. London. Sage.14. E Goffman (1990b).

The Presentation of Self in Everyday Life Penguin15. Efrat Tseëlon (2001). €œFashion research and its discontents”. Fashion Theory, 5 (4). 435–451.16.

Julia Twigg (2010a). €œClothing and dementia. A neglected dimension?. € Journal of Ageing Studies 24(4). 223–230.17.

Julia Twigg and Christina E Buse (2013). €œDress, dementia and the embodiment of identity.” Dementia 12(3). 326–336.18. C. E Buse and J.

Twigg (2015). €œClothing, embodied identity and dementia. Maintaining the self through dress.” Age, Culture, Humanities (2).19. Christina Buse and Julia Twigg (2018). €œDressing disrupted.

Negotiating care through the materiality of dress in the context of dementia.” Sociology of Health &. Illness, 40(2). 340-352.20. PIA C Kontos (2004). Ethnographic reflections on selfhood, embodiment and Alzheimer's disease.

Ageing &. Society, 24(6). 829–849.21. P. C Kontos (2005).

€œEmbodied selfhood in Alzheimer's disease. Rethinking person-centred care.” Dementia 4 (4). 553–570.22. P. C Kontos and G.

Naglie (2007). €œBridging theory and practice. Imagination, the body, and person-centred dementia care.” Dementia 6 (4). 549–569.23. Richard Ward et al.

(2016a). €œâ€˜Gonna make yer gorgeous’. Everyday transformation, resistance and belonging in the care-based hair salon.” Dementia, 15(3). 395–413.24. Richard Ward, Sarah Campbell, and John Keady (2016b).

€œAssembling the salon. Learning from alternative forms of body work in dementia care.” Sociology of Health &. Illness, 38(8). 1287–1302.25. Sonja Iltanen-Tähkävuori, Minttu Wikberg, and Päivi Topo (2012).

Design and dementia. A case of garments designed to prevent undressing. Dementia, 11(1). 49–59.26. Päivi Topo and Sonja Iltanen-Tähkävuori (2010).

€œScripting patienthood with patient clothing.” Social Science &. Medicine, 70(11). 1682–1689.27. Julia Twigg (2010b). €œWelfare embodied.

The materiality of hospital dress. A commentary on Topo and Iltanen-Tähkävuori”. Social Science and Medicine, 70(11), 1690–1692.28. Kathleen Woodward (2006). €œPerforming age, performing gender” National Women’s Studies Association (NWSA) Journal 18(1).

162–89.29. K.M Woodward (1999). Introduction. In K.M. Woodward (ed.), Figuring Age.

Women, Bodies and Generations (pp. Ix-xxix). Bloomington. Indiana University Press.30. M Hammersley and P Atkinson (1989).

Ethnography. Principles in practice. London. Routledge.31. V.

J Caracelli (2006). Enhancing the policy process through the use of ethnography and other study frameworks. A mixed-method strategy. Research in the Schools, 13(1). 84–92.32.

W Housley and P Atkinson (2003). Interactionism, Sage33. M Hammersley (1987) What's Wrong with Ethnography?. Methodological Explorations. London.

Routledge34. V Turner and E Bruner (1986). The Anthropology of Experience New York. PAJ Publications. 2435.

K Charmaz and RG Mitchell (2001). €˜Grounded theory in ethnography’ in Atkinson P. (Ed) Handbook of Ethnography, 2001. 160-174. Sage.

London36. B Glaser and A Strauss (1967). The Discovery of Grounded Theory. London. Weidenfeld and Nicholson, 24(25).

288–30437. Juliet M. Corbin and Anselm Strauss (1990). Grounded theoryrResearch. Procedures, canons, and evaluative criteria.

Qual. Sociol. 13. 3–21.38. J Green (1998).

Commentary. Grounded theory and the constant comparative method. BMJ (Clinical research ed.), 316 (7137),:1064.39. Roy Suddaby (2006). €œFrom the editors.

What grounded theory is not.” Academy of management journal, 49(4). 633–642.40. Elizabeth L Sampson et al. (2009). €œDementia in the acute hospital.

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45. 728–734.42. Robert E Herriott and William A. Firestone (1983) “Multisite qualitative policy research. Optimising description and generalizability”.

Education Research 12:14–1943. F Vogt (2002). €œNo ethnography without comparison. The methodological significance of comparison in ethnographic research” Studies in Education Ethnography 6:23–4244. Benjamin Saunders et al.

(2018). €œSaturation in qualitative research. Exploring its conceptualization and operationalization.” Quality and Quantity 52 (4). 1893–1907.45. A Coffey and P Atkinson (1996).

Making sense of qualitative data. Complementary research strategies. Sage Publications, Inc.46. Paula Boddington and Katie Featherstone (2018). €œThe canary in the coal mine.

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Dignity and aesthetic values in nursing care” Nursing Philosophy, 14(3). 186–200.

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A great deal has occurred, however, since Whitehead characterised his culture’s confusions 100 years ago. In our time, I suggest, experience is no longer construed as an invalid second cousin of bodily states in philosophy, in medicine or in the culture at large. More importantly, we must evaluate medical can you overdose on symbicort inhaler explanations before we reach for philosophical alternatives. The National Institutes of Health and the Institute of Medicine have concluded that ME/CFS is, in fact, a biomedical disease, and all US governmental health organisations now agree.

Although it would be productive for Sharpe and Greco to state and support their disagreement with the other side of the disease debate, it is no longer tenable, or safe, to ignore the possibility of disease in patients with ME/CFS, or to recommend that clinicians should do so. When we find ourselves in a framework that suggests the possibility of medical need is somehow beside the point for medical providers, it is time to reconsider our conceptual foundations.medical humanitiespsychiatrymedical ethics/bioethicsphilosophy of medicine/health carehealth policy.

AbstractIn ‘Chronic fatigue syndrome and an symbicort prices walmart illness-focused approach to care Cheap cialis online canadian. Controversy, morality and paradox’, authors Michael Sharpe and Monica Greco begin by characterising myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) as illness-without-disease. On that basis they ask why patients reject treatments for illness-without-disease, and they answer with a philosophical idea. Whitehead’s ‘bifurcation of nature’, they suggest, still symbicort prices walmart dominates public and professional thinking, and that conceptual confusion leads patients to reject the treatment they need.

A great deal has occurred, however, since Whitehead characterised his culture’s confusions 100 years ago. In our time, I suggest, experience is no longer construed as an invalid second cousin of bodily states in philosophy, in medicine or in the culture at large. More importantly, we must evaluate medical explanations before we reach symbicort prices walmart for philosophical alternatives. The National Institutes of Health and the Institute of Medicine have concluded that ME/CFS is, in fact, a biomedical disease, and all US governmental health organisations now agree.

Although it would be productive for Sharpe and Greco to state and support their disagreement with the other side of the disease debate, it is no longer tenable, or safe, to ignore the possibility of disease in patients with ME/CFS, or to recommend that clinicians should do so. When we find ourselves in a framework that suggests the possibility of medical need is somehow beside the point for medical providers, it is time to reconsider our conceptual foundations.medical humanitiespsychiatrymedical ethics/bioethicsphilosophy of medicine/health carehealth policy.

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In low-and-middle-income countries (LMICs), there remain critical gaps in view website the get symbicort prescription online quality of surgical care. Comparatively high rates of surgical adverse events occur and are likely highly preventable.1–3 There has been substantial focus on improving access to health services, including surgical care in LMICs, yet quality oversight and improvement practices remain limited in these settings.4 Over the past decade, get symbicort prescription online surgical volume has doubled in the most resource-poor settings. Between 2004 and 2012, the annual number of operations jumped from 234 million to 313 million, with the biggest growth occurring in countries with the lowest amount of healthcare spending.5 6 This signals a profound shift.

Whereas prior efforts were focused on s and maternal health, non-communicable diseases such as cancers and get symbicort prescription online trauma are an increasing priority for LMIC health systems. With the rapid growth in surgical delivery, the quality and safety of care are critically important. Poor outcomes and high morbidity breed mistrust, scepticism and fear among local populations, and thus hinder the mission of health systems to provide get symbicort prescription online timely and essential services, especially risky ones like surgery.In this issue of the Journal, two articles shed some light on the challenges and opportunities for improving and maintaining high-quality surgical and anaesthetic services in LMICs.

The first explores variation in the determinants of surgical quality across 10 hospitals in Tanzania that participated in the Safe Surgery 2020 (SS2020) programme.7 The investigators identified significant differences between what they termed high-performing and low-performing institutions. These included the perception and application of the SS2020 surgical quality improvement interventions meant to boost get symbicort prescription online adherence to safety practices, enhance teamwork and communication, and improve completeness of documentation in patient records. These practices were aimed at get symbicort prescription online reducing postsurgical s in hospitals implementing the intervention.

The programme worked to change organisational culture, build capacity to deliver evidence-based practices in safe surgery and anaesthesia, and facilitate the sustainability of the first and second phases through in-person and virtual mentorship.The authors noted that the high-performing sites had a strong prior culture of teamwork, with references to surgery as a team effort, collective problem-solving and support of co-workers, as well as a flattened hierarchy with open communication. These facilities used get symbicort prescription online the Surgical Safety Checklist (SSC) as a tool to strengthen teamwork and communication. Lower performing sites gave more emphasis to individual learning than organisational learning, thought of the SSC as a means to improve outcomes rather than encourage teamwork, considered SS2020 as a programme for surgeons rather than for all members of the perioperative team and expressed higher levels of reluctance to engage in open communication because of hierarchy.The second article describes surgical service monitoring and quality control systems at district hospitals Malawi, Tanzania and Zambia.8 The authors investigated surgical surveillance at a facility level and the types of quality processes and controls in place to assess service capacity, volume, outcomes and adherence to standards.

After evaluating 75 district hospitals, the authors noted get symbicort prescription online a number of major challenges, including that data registry and recording formats were not standardised. In fact, over half of hospitals surveyed had two or more systems in place. Hospitals also get symbicort prescription online lacked accountability mechanisms.

Of the 75 hospitals, only 43 created mortality reports for review, 11 conducted surgical audits of any kind and 22 used the SSC routinely despite get symbicort prescription online numerous studies confirming its benefit to patient safety in these environments.Each study has its own limitations. In the article by Alidina et al, the grading used to classify high and low performers was subjectively set by the study team, the sample size of facilities was relatively small, and interviewee responses were potentially affected by recall and social desirability biases. Furthermore, high-performer hospitals were overwhelmingly from smaller-sized facilities, indicating a strong clustering effect get symbicort prescription online.

In the article by Clarke et al, self-reported information also introduces a potential for bias, there was limited interviewing of hospital administration and other stakeholders outside of perioperative providers, and the focus on district hospitals might miss more robust practices in urban and teaching hospitals.Although there have been proposals for standardised surgical and anaesthesia metrics to track service delivery and quality, there is not a firm consensus on minimum standards or an organising body to incentivise monitoring.9–12 Yet proper data collection using standardised and comparable metrics is essential for service planning, as the routine and appropriate monitoring of such information is critical for implementation of quality surgical services. As these two articles make clear, such processes are still rudimentary in many LMIC environments get symbicort prescription online. The challenges to improving them include a lack of properly developed registries, inappropriate formatting, technological barriers for centralised data recording and storage, absence of data interpretation and feedback, and gaps in planning mechanisms.13 These challenges are overwhelmingly due to lack of dedicated leadership in the oversight of surgical service provision and fundamental gaps in basic service management, without any proper linkage of data capture to future planning or improvement interventions.

Without adequate and complete get symbicort prescription online data, assessments of patient outcomes and safety process gap identification at the institutional level is impossible. Furthermore, strong management is critical for ensuring adherence to standards and clear standard operating procedures. While leadership training is get symbicort prescription online the focus of much discussion, as it was in the article by Alidina, little has been done to elevate and promote management skills that are essential for efficient service provision.

Work in Ghana, for example, has demonstrated that good get symbicort prescription online management practices can avoid depletion of critical supplies14. Yet even when service delivery increases, facility readiness and the practices that must accompany increased volume do not necessarily follow.15 16There are a number of solutions to these challenges. Hospital leaders need to emphasise quality as central get symbicort prescription online to the hospital mission.

Lessons from high-performing hospitals have demonstrated that a focus on quality by hospital leadership can raise the standards of care delivery, although under specific conditions that promote quality through accountability and transparency and with evidence from relatively small numbers of hospitals.13 Such efforts require a standardised approach to data collection and robust assessments of processes, such as compliance with critical standards of care (eg, prevention standards such as hand hygiene and antimicrobial stewardship). When implemented in a rigorous way in surgery, high-quality data and strong process adherence have tremendous beneficial effects.17 18Improvements in quality and safety also require infrastructure and a management team that sets targets for performance, benchmarks quality standards, allocates resources and assigns people with skill sets matched to clinical service needs to drive improvements.19 20 Good management practices have been correlated with improved outcomes and better compliance with known standards of care.21Unfortunately, studies from LMICs show substantial variability in the way in which quality of care is measured.22 Furthermore, get symbicort prescription online there is a fundamental lack of appropriate guidelines and management protocols, and those that do exist are not easily implemented. Our experience indicates that integrating a proper monitoring and evaluation programme into institutional efforts to improve perioperative processes have powerful positive effects on outcomes.18 We have done this in our work through the use of process mapping, an exercise that takes a quality improvement team through the pathway of a care routine or a standard operating procedure in order to gain a complete understanding of the barriers to appropriate compliance.23 This type of process was developed for industry but has been applied in healthcare as a means of improving compliance by aligning tasks with specific process goals.

The work requires data-driven, quality-controlled surgical services structured in a manner that allow changes to be made to the care routine and associated processes get symbicort prescription online. Assessing baseline data, understanding barriers to quality services and care, seeking local solutions, addressing knowledge gaps, standardising monitoring and rewarding improvements get symbicort prescription online must all be integrated to achieve such change. Appropriate surgical monitoring and evaluation tools can help measure quantitative and qualitative improvements to surgical care in LMICs.24Like politics, all quality improvement is local, so a deep understanding of local context and circumstances is essential.

As surgical and anaesthetic services continue to expand, hospital-based surgical programmes will need to engage more concertedly in get symbicort prescription online research and quality improvement initiatives in order to decrease adverse outcomes and raise the quality and safety of surgical services in LMICs. As the authors of both articles note, however, these improvement mechanisms are not without substantial challenges, many will not be effective, and all require a more coordinated approach and a strengthening of management practices to ensure the quality and safety of care.Ethics statementsPatient consent for publicationNot required.In this issue we are presented with two novel and important studies in English primary care addressing the epidemiology of patient safety. The first study, by Reeves and colleagues, retrospectively reviewed 2057 randomly selected consultations in 21 general get symbicort prescription online practices to identify missed diagnostic opportunities, in order to estimate their incidence, origins and potential harms.1 They conclude that diagnostic errors occur in up to 4% of consultations, are multifactorial, and that 40% of them have the potential to result in moderate or severe patient harm.

The second study recruited 12 randomly selected general practices and reviewed the case notes of an ‘enhanced’ sample of 14 407 patients with significant health problems.2 In this second study, Avery and colleagues were interested in actual harms that could be considered avoidable, in order to estimate their incidence and to quantify and classify the context from which they arose. They identified 74 cases of avoidable significant harm, a rate of 36/100 000 patient years, with diagnosis problems accounting for the majority (61%).Although the field of patient safety research goes back to the 1980s, much of it was initially focused on specialist care and hospital settings, where rates of adverse events as high as 10% were reported.3 4 In contrast, studies in primary care found that rates of adverse events were much lower, but the potential for harm, notably from prescribing errors, was significant.5 This led to developments such as PINCER, a pharmacist-led intervention to reduce clinically important medication errors that has since been widely adopted in England,6 and in the USA to a focus on preventing ‘Never Events’ or serious, preventable medical errors.7 More recently, the importance of diagnostic error in patient safety has come to the fore, with a landmark report from the US Institute of Medicine (IoM)8 and recognition that this aspect of patient safety is distinct from errors in the management of patients with a diagnosis and that it represents a global concern.9 10 The latter has been driven by early diagnosis being a policy focus in many high-income countries, particularly in relation to cancer, with misdiagnosis one of the most common reasons for malpractice claims11 and evidence that early cancer diagnosis leads to better outcomes.Diagnostic error was defined in the IoM report Improving Diagnosis in Healthcare as the ‘failure to make an accurate and timely explanation of the patient’s health problem, or to communicate get symbicort prescription online that explanation to the patient’.8 The concept of ‘missed diagnostic opportunities’, proposed by Singh and colleagues and applied in the study by Reeves and colleagues, is one that works well for primary care, since it takes account of the evolving course of a patient’s presenting problem, sometimes over multiple consultations.12Preventable or avoidable harm is by definition attributable to medical error, although many errors do not lead to harm. Harm can also be a broad concept, ranging from transient anxiety through to death.

Avery and colleagues have been particularly diligent in their definitions of avoidability and significant harm, deriving the latter from that provided by WHO,13 get symbicort prescription online which in turn lies between the definitions of moderate and severe harm described by England’s National Patient Safety Agency and by Panesar and colleagues.14By drawing our attention to the extent to which errors and avoidable harms occur, these two studies also prompt us to consider ways in which we might take action to improve diagnostic safety in primary care. One is to identify errors as soon as, or right after, they are made, which then provides an opportunity to forestall any ensuing harm or get symbicort prescription online reduce its severity. Safety-netting is a well-established if ill-defined consultation technique where the patient is advised on the anticipated course of events and the action(s) to take if these do not follow within a specified timeframe.15 It is specifically advocated in English national guidance on management and referral of suspected cancer.16 A more systematic and technical approach is the use of e-triggers, signals of a likely error or adverse event, generated by the systematic mining of electronic patient data.

These can prompt clinicians to the correct actions or can generate reminders when the correct actions are not performed in a timely way.17 Singh and others have also proposed the SaferDx e-Trigger Tool Framework for the future development of tools that monitor diagnostic errors and intervene for specific patients when needed.17Another way to take action to improve diagnostic safety is to use retrospective get symbicort prescription online clinical record review to identify the circumstances and types of events that might threaten patient safety during the diagnostic process, in order to address these circumstances in the future. Examples include a Danish study that found ‘quality deviations’ in 30% of the 5711 patients presenting with symptoms subsequently found to be due to cancer,18 and an English national audit of 14 259 patients with cancer where GPs reported avoidable delays in 24% of the sample.19 ‘Quality deviations’ and other avoidable delays can potentially be prevented, but only with a strong professional culture that values identifying them in the first place. A culture of identifying and reflecting on safety incidents is well established in many countries where strong primary care systems get symbicort prescription online pertain.

In the UK, significant event audit is widely practised and is part of the Royal College of General Practitioners’ patient safety toolkit. Changes in clinical practice or quality of care are often reported although not easily verified.20 However, qualitative analysis of multiple significant event get symbicort prescription online audits has been used to identify opportunities for quality improvement in the diagnostic process for lung cancer.21 On the other hand, reporting of patient safety incidents to a central body, such as the National Reporting and Learning System in England has not been widely adopted in primary care, in contrast to secondary care, which accounts for more than 99% of patient safety incident reports. Incident reporting has also not generally been as successful as it could be in the USA, get symbicort prescription online despite strong models of its importance for improvement in other fields, such as aviation.22These various approaches to identifying errors and harms that occur in primary care can all inform the design of safer systems and/or safer diagnosticians, to reduce the risk of error in the first place.

By learning about which processes lead to errors, one can try to improve those processes and prevent errors occurring. In this way, e-triggers, for example, could provide the information needed for a healthcare system to identify targets get symbicort prescription online for diagnostic safety, as suggested in the SaferDx framework. For example, if triggers identified frequent failures in a particular healthcare system in the follow-up on abnormal test results, a system re-design could be put in place to prevent these.

Alternatively, one might provide clinicians with tools that enhance get symbicort prescription online their diagnostic capabilities. These could include better access to diagnostic tests or the provision of electronic clinical decision support systems. A recent systematic review confirmed get symbicort prescription online that these have the capacity to improve diagnostic decision making for cancer in primary care.23 The two studies in this issue of the journal clearly describe the problems.

Action is now needed to address them in a concerted and systematic way.Ethics statementsPatient consent for publicationNot required..

In low-and-middle-income countries (LMICs), there remain critical gaps in the quality of surgical care symbicort prices walmart. Comparatively high rates of surgical adverse events occur and are likely highly preventable.1–3 There has been substantial focus on improving access symbicort prices walmart to health services, including surgical care in LMICs, yet quality oversight and improvement practices remain limited in these settings.4 Over the past decade, surgical volume has doubled in the most resource-poor settings. Between 2004 and 2012, the annual number of operations jumped from 234 million to 313 million, with the biggest growth occurring in countries with the lowest amount of healthcare spending.5 6 This signals a profound shift.

Whereas prior efforts were focused on s and maternal health, non-communicable diseases such symbicort prices walmart as cancers and trauma are an increasing priority for LMIC health systems. With the rapid growth in surgical delivery, the quality and safety of care are critically important. Poor outcomes and high morbidity breed mistrust, scepticism and fear among local populations, and thus hinder the mission of health systems to provide timely and essential services, especially risky ones like surgery.In this issue of the Journal, symbicort prices walmart two articles shed some light on the challenges and opportunities for improving and maintaining high-quality surgical and anaesthetic services in LMICs.

The first explores variation in the determinants of surgical quality across 10 hospitals in Tanzania that participated in the Safe Surgery 2020 (SS2020) programme.7 The investigators identified significant differences between what they termed high-performing and low-performing institutions. These included the perception and application of the SS2020 surgical quality improvement interventions meant to boost symbicort prices walmart adherence to safety practices, enhance teamwork and communication, and improve completeness of documentation in patient records. These practices symbicort prices walmart were aimed at reducing postsurgical s in hospitals implementing the intervention.

The programme worked to change organisational culture, build capacity to deliver evidence-based practices in safe surgery and anaesthesia, and facilitate the sustainability of the first and second phases through in-person and virtual mentorship.The authors noted that the high-performing sites had a strong prior culture of teamwork, with references to surgery as a team effort, collective problem-solving and support of co-workers, as well as a flattened hierarchy with open communication. These facilities used the Surgical Safety Checklist (SSC) as a tool to symbicort prices walmart strengthen teamwork and communication. Lower performing sites gave more emphasis to individual learning than organisational learning, thought of the SSC as a means to improve outcomes rather than encourage teamwork, considered SS2020 as a programme for surgeons rather than for all members of the perioperative team and expressed higher levels of reluctance to engage in open communication because of hierarchy.The second article describes surgical service monitoring and quality control systems at district hospitals Malawi, Tanzania and Zambia.8 The authors investigated surgical surveillance at a facility level and the types of quality processes and controls in place to assess service capacity, volume, outcomes and adherence to standards.

After evaluating 75 district hospitals, the authors symbicort prices walmart noted a number of major challenges, including that data registry and recording formats were not standardised. In fact, over half of hospitals surveyed had two or more systems in place. Hospitals also lacked accountability mechanisms symbicort prices walmart.

Of the 75 hospitals, only 43 created mortality reports for review, 11 conducted surgical audits of any kind and 22 used symbicort prices walmart the SSC routinely despite numerous studies confirming its benefit to patient safety in these environments.Each study has its own limitations. In the article by Alidina et al, the grading used to classify high and low performers was subjectively set by the study team, the sample size of facilities was relatively small, and interviewee responses were potentially affected by recall and social desirability biases. Furthermore, high-performer hospitals were overwhelmingly from symbicort prices walmart smaller-sized facilities, indicating a strong clustering effect.

In the article by Clarke et al, self-reported information also introduces a potential for bias, there was limited interviewing of hospital administration and other stakeholders outside of perioperative providers, and the focus on district hospitals might miss more robust practices in urban and teaching hospitals.Although there have been proposals for standardised surgical and anaesthesia metrics to track service delivery and quality, there is not a firm consensus on minimum standards or an organising body to incentivise monitoring.9–12 Yet proper data collection using standardised and comparable metrics is essential for service planning, as the routine and appropriate monitoring of such information is critical for implementation of quality surgical services. As these symbicort prices walmart two articles make clear, such processes are still rudimentary in many LMIC environments. The challenges to improving them include a lack of properly developed registries, inappropriate formatting, technological barriers for centralised data recording and storage, absence of data interpretation and feedback, and gaps in planning mechanisms.13 These challenges are overwhelmingly due to lack of dedicated leadership in the oversight of surgical service provision and fundamental gaps in basic service management, without any proper linkage of data capture to future planning or improvement interventions.

Without adequate and complete data, assessments of patient outcomes and safety process gap identification at the institutional level symbicort prices walmart is impossible. Furthermore, strong management is critical for ensuring adherence to standards and clear standard operating procedures. While leadership training is the focus of much discussion, as it was in the article by Alidina, little has been done to elevate and promote symbicort prices walmart management skills that are essential for efficient service provision.

Work in Ghana, for example, has demonstrated that good management practices can avoid depletion of symbicort prices walmart critical supplies14. Yet even when service delivery increases, facility readiness and the practices that must accompany increased volume do not necessarily follow.15 16There are a number of solutions to these challenges. Hospital leaders need to emphasise quality as central to the hospital symbicort prices walmart mission.

Lessons from high-performing hospitals have demonstrated that a focus on quality by hospital leadership can raise the standards of care delivery, although under specific conditions that promote quality through accountability and transparency and with evidence from relatively small numbers of hospitals.13 Such efforts require a standardised approach to data collection and robust assessments of processes, such as compliance with critical standards of care (eg, prevention standards such as hand hygiene and antimicrobial stewardship). When implemented in a rigorous way in surgery, high-quality data symbicort prices walmart and strong process adherence have tremendous beneficial effects.17 18Improvements in quality and safety also require infrastructure and a management team that sets targets for performance, benchmarks quality standards, allocates resources and assigns people with skill sets matched to clinical service needs to drive improvements.19 20 Good management practices have been correlated with improved outcomes and better compliance with known standards of care.21Unfortunately, studies from LMICs show substantial variability in the way in which quality of care is measured.22 Furthermore, there is a fundamental lack of appropriate guidelines and management protocols, and those that do exist are not easily implemented. Our experience indicates that integrating a proper monitoring and evaluation programme into institutional efforts to improve perioperative processes have powerful positive effects on outcomes.18 We have done this in our work through the use of process mapping, an exercise that takes a quality improvement team through the pathway of a care routine or a standard operating procedure in order to gain a complete understanding of the barriers to appropriate compliance.23 This type of process was developed for industry but has been applied in healthcare as a means of improving compliance by aligning tasks with specific process goals.

The work requires data-driven, quality-controlled surgical services structured in a manner that allow changes to symbicort prices walmart be made to the care routine and associated processes. Assessing baseline data, understanding barriers to quality services and care, seeking local solutions, addressing knowledge gaps, standardising symbicort prices walmart monitoring and rewarding improvements must all be integrated to achieve such change. Appropriate surgical monitoring and evaluation tools can help measure quantitative and qualitative improvements to surgical care in LMICs.24Like politics, all quality improvement is local, so a deep understanding of local context and circumstances is essential.

As surgical and anaesthetic services continue to expand, hospital-based surgical programmes will need to engage more concertedly in research and quality improvement initiatives in order symbicort prices walmart to decrease adverse outcomes and raise the quality and safety of surgical services in LMICs. As the authors of both articles note, however, these improvement mechanisms are not without substantial challenges, many will not be effective, and all require a more coordinated approach and a strengthening of management practices to ensure the quality and safety of care.Ethics statementsPatient consent for publicationNot required.In this issue we are presented with two novel and important studies in English primary care addressing the epidemiology of patient safety. The first symbicort prices walmart study, by Reeves and colleagues, retrospectively reviewed 2057 randomly selected consultations in 21 general practices to identify missed diagnostic opportunities, in order to estimate their incidence, origins and potential harms.1 They conclude that diagnostic errors occur in up to 4% of consultations, are multifactorial, and that 40% of them have the potential to result in moderate or severe patient harm.

The second study recruited 12 randomly selected general practices and reviewed the case notes of an ‘enhanced’ sample of 14 407 patients with significant health problems.2 In this second study, Avery and colleagues were interested in actual harms that could be considered avoidable, in order to estimate their incidence and to quantify and classify the context from which they arose. They identified 74 cases of avoidable significant harm, a rate of 36/100 000 patient years, with diagnosis problems accounting for the majority (61%).Although the field of patient safety research goes back to the 1980s, much of it was initially focused on specialist care and hospital settings, where rates of adverse events as high as 10% were reported.3 4 In contrast, studies in primary care found that rates of adverse events were much lower, but the potential for harm, notably from prescribing errors, was significant.5 This led to developments such as PINCER, a pharmacist-led intervention to reduce clinically important medication errors that has since been widely adopted in England,6 and in the USA to a focus on preventing ‘Never Events’ or serious, preventable medical errors.7 More recently, the importance of diagnostic error symbicort prices walmart in patient safety has come to the fore, with a landmark report from the US Institute of Medicine (IoM)8 and recognition that this aspect of patient safety is distinct from errors in the management of patients with a diagnosis and that it represents a global concern.9 10 The latter has been driven by early diagnosis being a policy focus in many high-income countries, particularly in relation to cancer, with misdiagnosis one of the most common reasons for malpractice claims11 and evidence that early cancer diagnosis leads to better outcomes.Diagnostic error was defined in the IoM report Improving Diagnosis in Healthcare as the ‘failure to make an accurate and timely explanation of the patient’s health problem, or to communicate that explanation to the patient’.8 The concept of ‘missed diagnostic opportunities’, proposed by Singh and colleagues and applied in the study by Reeves and colleagues, is one that works well for primary care, since it takes account of the evolving course of a patient’s presenting problem, sometimes over multiple consultations.12Preventable or avoidable harm is by definition attributable to medical error, although many errors do not lead to harm. Harm can also be a broad concept, ranging from transient anxiety through to death.

Avery and colleagues have been particularly diligent in their definitions of avoidability and significant harm, deriving the latter from that symbicort prices walmart provided by WHO,13 which in turn lies between the definitions of moderate and severe harm described by England’s National Patient Safety Agency and by Panesar and colleagues.14By drawing our attention to the extent to which errors and avoidable harms occur, these two studies also prompt us to consider ways in which we might take action to improve diagnostic safety in primary care. One is to identify errors as soon as, or right after, they are made, symbicort prices walmart which then provides an opportunity to forestall any ensuing harm or reduce its severity. Safety-netting is a well-established if ill-defined consultation technique where the patient is advised on the anticipated course of events and the action(s) to take if these do not follow within a specified timeframe.15 It is specifically advocated in English national guidance on management and referral of suspected cancer.16 A more systematic and technical approach is the use of e-triggers, signals of a likely error or adverse event, generated by the systematic mining of electronic patient data.

These can prompt clinicians to the correct actions or can generate reminders when the correct actions are not performed in a timely way.17 Singh and others have also proposed the SaferDx e-Trigger Tool Framework for the future development of tools that monitor diagnostic errors and intervene for specific patients symbicort prices walmart when needed.17Another way to take action to improve diagnostic safety is to use retrospective clinical record review to identify the circumstances and types of events that might threaten patient safety during the diagnostic process, in order to address these circumstances in the future. Examples include a Danish study that found ‘quality deviations’ in 30% of the 5711 patients presenting with symptoms subsequently found to be due to cancer,18 and an English national audit of 14 259 patients with cancer where GPs reported avoidable delays in 24% of the sample.19 ‘Quality deviations’ and other avoidable delays can potentially be prevented, but only with a strong professional culture that values identifying them in the first place. A culture of identifying and reflecting on safety incidents is well established in many countries where strong primary care symbicort prices walmart systems pertain.

In the UK, significant event audit is widely practised and is part of the Royal College of General Practitioners’ patient safety toolkit. Changes in clinical practice or quality of care are often reported although not easily verified.20 However, qualitative analysis of multiple significant event audits has been used to identify opportunities for quality improvement in the diagnostic process for lung cancer.21 On the other hand, symbicort prices walmart reporting of patient safety incidents to a central body, such as the National Reporting and Learning System in England has not been widely adopted in primary care, in contrast to secondary care, which accounts for more than 99% of patient safety incident reports. Incident reporting has also not generally been as successful as it could be in the symbicort prices walmart USA, despite strong models of its importance for improvement in other fields, such as aviation.22These various approaches to identifying errors and harms that occur in primary care can all inform the design of safer systems and/or safer diagnosticians, to reduce the risk of error in the first place.

By learning about which processes lead to errors, one can try to improve those processes and prevent errors occurring. In this way, e-triggers, for example, could provide the information needed for a healthcare system to identify targets symbicort prices walmart for diagnostic safety, as suggested in the SaferDx framework. For example, if triggers identified frequent failures in a particular healthcare system in the follow-up on abnormal test results, a system re-design could be put in place to prevent these.

Alternatively, one might provide clinicians with tools that symbicort prices walmart enhance their diagnostic capabilities. These could include better access to diagnostic tests or the provision of electronic clinical decision support systems. A recent systematic review confirmed that these have the capacity to improve diagnostic decision making for cancer in symbicort prices walmart primary care.23 The two studies in this issue of the journal clearly describe the problems.

Action is now needed to address them in a concerted and systematic way.Ethics statementsPatient consent for publicationNot required..

Symbicort spc

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

As expected, the media went into a frenzy as newspapers, news channels, and social media were full of stories providing minute symbicort spc 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 symbicort spc 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 symbicort spc with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of symbicort spc photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and illness and also symbicort spc 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 symbicort spc 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 symbicort spc 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, symbicort spc and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements symbicort spc and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have symbicort spc guidelines and resource books for interacting with media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media.

Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, 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 symbicort spc 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 symbicort spc SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest.

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

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

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

However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords. Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update.

Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al. In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies. The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time.

Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness. However, there are obvious ethical issues in designing human studies that are designed to answer this specific question. Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions.

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

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

In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today. The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain. The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes.

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

Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al. Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al.

That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies. In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al.

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

Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms. Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al. In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression.

It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus. The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe.

It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al. Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population. It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder.

The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al. In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered.

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

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

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

Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite. However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies. It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations.

The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis. Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

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

Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results. The ACC is another area which has been studied in some detail utilizing the MRSI technique. In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT.

This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al. In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al. Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity.

A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al. In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al.

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

This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT. However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development.

The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect. It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT. Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder.

The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration. However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory.

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

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

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

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

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

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

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

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J Psychiatry Neurosci 2017;42:6-16. 40.Cano M, Martínez-Zalacaín I, Bernabéu-Sanz Á, Contreras-Rodríguez O, Hernández-Ribas R, Via E, et al. Brain volumetric and metabolic correlates of electroconvulsive therapy for treatment-resistant depression. A longitudinal neuroimaging study.

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

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50.Bramham CR, Messaoudi E. BDNF function in adult synaptic plasticity. The synaptic consolidation hypothesis. Prog Neurobiol 2005;76:99-125.

51.Duman RS, Monteggia LM. A neurotrophic model for stress-related mood disorders. Biol Psychiatry 2006;59:1116-27. 52.Bocchio-Chiavetto L, Bagnardi V, Zanardini R, Molteni R, Nielsen MG, Placentino A, et al.

Serum and plasma BDNF levels in major depression. A replication study and meta-analyses. World J Biol Psychiatry 2010;11:763-73. 53.Brunoni AR, Lopes M, Fregni F.

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

Increased BDNF levels after electroconvulsive therapy in patients with major depressive disorder. A meta-analysis study. J Psychiatr Res 2016;83:47-53. 55.UK ECT Review Group.

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73.Frith CD, Stevens M, Johnstone EC, Deakin JF, Lawler P, Crow TJ. Effects of ECT and depression on various aspects of memory. Br J Psychiatry 1983;142:610-7. 74.Ng C, Schweitzer I, Alexopoulos P, Celi E, Wong L, Tuckwell V, et al.

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

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

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

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

How to http://lmatecha.com/get-amoxil-prescription-online cite this symbicort prices walmart article:Singh O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is symbicort prices walmart 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 channels, and social media were full of stories providing symbicort prices walmart 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, symbicort prices walmart reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress calls from their patients in despair with increased symbicort prices walmart 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 symbicort prices walmart 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 symbicort prices walmart full 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 symbicort prices walmart the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way 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 symbicort prices walmart 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 symbicort prices walmart stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists symbicort prices walmart reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions. Methods and principles of interaction with media should form a part of our training curriculum.

Many professional societies have guidelines and resource books for interacting with media, and psychiatrists should symbicort prices walmart familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should symbicort prices walmart 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, symbicort prices walmart Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Is symbicort covered by medicare

Latest anti-inflammatories Read More Here News By is symbicort covered by medicare Steven Reinberg HealthDay ReporterTHURSDAY, Sept. 2, 2021 (HealthDay News) As the new school year begins, teachers can take comfort in a new report that finds they have no greater risk of catching or being hospitalized for severe anti inflammatory drugs than anyone else. Researchers in Scotland say that might be because many schools is symbicort covered by medicare take precautions that other workplaces don't. It's also possible that the teachers in the study were younger and healthier than other workers, the authors said.

"Teachers are about average in terms of their risk of hospitalization with anti inflammatory drugs, when compared to other working-age adults," said lead researcher Dr. David McAllister, a professor is symbicort covered by medicare of clinical epidemiology and medical informatics at the Institute of Health and Wellbeing at the University of Glasgow. "Unlike health care workers, teachers are not at increased risk of hospitalization with anti inflammatory drugs, even when schools are open." Using data from March 2020 to July 2021, McAllister and his colleagues collected information on more than 132,000 people with anti inflammatory drugs, ages 21 to 65, and more than 1.3 million people from the general population, all in Scotland. They compared the risk of anti inflammatory drugs among teachers and their family members with health care workers and others.

Over the study period, the risk of being hospitalized is symbicort covered by medicare with anti inflammatory drugs was less than 1% for teachers, health care workers and other adults, the researchers found. After taking into account factors such as age, sex, ethnicity and economic status, the risk of being hospitalized with anti inflammatory drugs was about 50% lower among teachers and their family members than among the general population, the researchers noted. Over the same period, the risk was almost four times higher among health care workers and almost twice as high among their families, the researchers found. During the first period of full school opening in the fall of 2020, the risk of hospitalization among teachers increased by 2.4-fold, reaching a level similar to that is symbicort covered by medicare in the general population.

By the summer of 2021, when vaccinations were underway, a smaller increase of 1.7 times was seen. The report was published online Sept. 1 in the journal BMJ is symbicort covered by medicare. It's not surprising that the risk to teachers is not higher than other groups, said Douglas Harris, Schlieder Foundation Chair in public education at Tulane University in New Orleans, and director of the Education Research Alliance for New Orleans.

In schools where masks and social distancing are mandated, the risk of spreading anti inflammatory drugs is cut dramatically, is symbicort covered by medicare he said. "I think, for the most part, schools are handling it in a sensible way and I think, for the most part, it's sensible keeping the kids in school when it's safe," Harris said. Of course, vaccination is the key to beating the symbicort, he added. "I think in the U.S., there's is symbicort covered by medicare an ongoing debate about whether treatments can be mandated.

That's the elephant in the room. I think that that almost has to happen if we're really going to get back to normal," Harris said. Harris believes that school systems should mandate anti inflammatory drugs vaccinations for teachers and all students, including is symbicort covered by medicare young children once a treatment has been approved. "We already do that for, for children, they're already required to get vaccinated for other things," he said.

"It's hard to see why you wouldn't require it. In this case and really that is the only way we get back to normal, this could go on for years." is symbicort covered by medicare As more adults are vaccinated, the symbicort will attack mostly the unvaccinated, especially children, Harris said. But everything should be done to minimize the spread of the symbicort and keep schools open, he said. "There are health consequences to closing schools," Harris said.

"We tend to focus on the immediate effect of schools opening is symbicort covered by medicare and spreading the symbicort, which is clearly important and probably the first consideration, but when you close the schools you create a new set of problems, mental illness and child abuse, and all sorts of economic side effects." More information For more on anti inflammatory drugs and schools, see the U.S. Centers for Disease Control and Prevention. SOURCES. David McAllister, MD, MPH, professor, clinical epidemiology and medical informatics, Institute of Health and Wellbeing, University of Glasgow, Scotland.

Douglas Harris, PhD, professor, economics, and Schlieder Foundation Chair, public education, Tulane University, New Orleans, and director, Education Research Alliance for New Orleans. BMJ , Sept. 1, 2021, online Copyright © 2021 HealthDay. All rights reserved.Latest anti-inflammatories News THURSDAY, Sept.

2, 2021 (HealthDay News) The prescribing, dispensing and use of ivermectin to prevent or treat anti inflammatory drugs outside of clinical trials must end immediately, the American Medical Association, American Pharmacists Association and American Society of Health-System Pharmacists say. The drug has U.S. Food and Drug Administration approval to treat people with s caused by internal and external parasites, but is not approved to prevent or treat anti inflammatory drugs. Ivermectin is also available for veterinary use in horses and other animals, but medications intended for animals should not be used by humans.

"We are alarmed by reports that outpatient prescribing for and dispensing of ivermectin have increased 24-fold since before the symbicort and increased exponentially over the past few months," the groups said in a statement. They noted that calls to poison control centers related to ivermectin have increased fivefold compared to before the symbicort. The FDA has also received multiple reports of people who have been hospitalized after "self-medicating with ivermectin intended for horses," the agency said in a consumer update on. "You are not a horse.

You are not a cow. Seriously, y'all. Stop it," the FDA tweeted on Aug.21. No form of ivermectin has been approved to treat or prevent anti inflammatory drugs, the FDA emphasized.

It said it was compelled to issue a warning due to "a lot of misinformation" around the drug, according to the update. "You may have heard that it's okay to take large doses of ivermectin. That is wrong," the FDA said. .The U.S.

Centers for Disease Control and Prevention also issued an advisory saying ivermectin is not authorized or approved for the prevention or treatment of anti inflammatory drugs. The CDC has warned about the potentially toxic effects of the drug, including "nausea, vomiting and diarrhea. Overdoses are associated with hypotension [low blood pressure] and neurologic effects such as decreased consciousness, confusion, hallucinations, seizures, coma and death." More information Visit the U.S. Centers for Disease Control and Prevention for more on anti inflammatory drugs treatments.

SOURCE. American Medical Association, American Pharmacists Association, American Society of Health-System Pharmacists, news release, Sept. 1, 2021 Robert Preidt Copyright © 2021 HealthDay. All rights reserved.Latest Infectious Disease News By Amy Norton HealthDay ReporterTHURSDAY, Sept.

2, 2021 (HealthDay News) The anti inflammatory drugs symbicort has spurred a resurgence in other s that strike hospitalized patients, a U.S. Government study finds. The study, by the U.S. Centers for Disease Control and Prevention, highlights the broad toll the symbicort has taken.

It found that rates of several types of hospital-acquired s rose after the symbicort reached U.S. Shores in 2020. More hospital patients suffered potentially deadly s related to medical devices, including ventilators and tubes placed in blood vessels compared to the same period in 2019. There was a similar rise in antibiotic-resistant staph s, which can infiate the bloodstream and lungs.

The trend is disconcerting, in part, because U.S. Hospitals had been making steady progress in preventing those s before the symbicort. "What we've learned during this symbicort is that the impact of anti inflammatory drugs is far-reaching," said Dr. Arjun Srinivasan, associate director of the CDC's health care-associated prevention programs.

The unfortunate fact, he said, is that anti inflammatory drugs created a "perfect storm" of circumstances that fed the increase in hospital-acquired s. There was the sheer number of patients flooding many hospitals -- people who were very ill and often required intensive care. Plus, Srinivasan said, those patients commonly had preexisting medical conditions and often needed to stay on ventilators and other medical devices for prolonged periods -- all of which raise the risk of s. Add to that the challenges faced by health care providers.

Earlier in the symbicort, Srinivasan said, "we didn't have enough gowns, we didn't have enough masks, we didn't have enough respirators." As a result, protective equipment meant to be thrown away after one use was sometimes being reused. And, Srinivasan said, health care workers were falling ill or needing to quarantine -- which fed staffing shortages and added to providers' exhaustion. "This is, in no way, saying that health care workers failed to do their job," Srinivasan stressed. "This was a failure of the system." The findings -- published Sept.

2 in the journal Control &. Hospital Epidemiology -- are based on data from a national surveillance system that tracks health care-linked s. CDC epidemiologist Lindsey Weiner-Lastinger led the study. Researchers found that in the early part of 2020, those s were generally declining compared to the same period in 2019.

That changed with the symbicort. The biggest increase was in blood s related to central lines, which are catheters placed into large arteries to deliver medications or fluids. Those s were up by about 47% in the latter half of 2020. s related to ventilators, urinary catheters and antibiotic-resistant Staphylococcus aureus bacteria were all up as well.

"This isn't surprising to those of us on the ground," said Dr. Cornelius Clancy, a professor of medicine at the University of Pittsburgh. "The national data reflect what we've seen." He pointed to the general strain on hospital systems, and the "inordinate resources" that anti inflammatory drugs care demanded, as factors. Some "bread-and-butter" practices that prevent health care-associated s, Clancy said, could not get the same attention they do during normal times.

"This is another example of how you can't separate anti inflammatory drugs from everything else that goes on in health care," said Clancy, who is also with the Infectious Diseases Society of America. anti inflammatory drugs affects not only the people who are sickened with it, he said, but the wider health care system. That is not to say people should fear going to the hospital, both Clancy and Srinivasan emphasized. "People certainly need to seek any care they need," Clancy said.

And even in the midst of new anti inflammatory drugs surges at some U.S. Hospitals, there are reasons to expect that the risks of hospital-acquired s might be less, versus last year. For one, Srinivasan said, hospitals are more aware of the issue now. Health care workers are also more experienced in managing anti inflammatory drugs patients, and more protected from through vaccination.

As for the general public, the study underscores the importance of getting vaccinated to cut the risk of falling seriously ill with anti inflammatory drugs. SLIDESHOW Urinary Incontinence in Women. Types, Causes, and Treatments for Bladder Control See Slideshow "One of the best ways to prevent health care-associated s is through vaccination," Srinivasan said. "Even with the delta variant," he added, "the treatments are tremendously effective at preventing hospitalization." Clancy agreed.

"The data on vaccination are incontrovertible," he said. More information The U.S. Centers for Disease Control and Prevention has advice for patients on lowering their risk of health care-associated s. SOURCES.

Arjun Srinivasan, MD, associate director, healthcare-associated prevention programs, U.S. Centers for Disease Control and Prevention, Atlanta. Cornelius J. Clancy, MD, professor, medicine, University of Pittsburgh School of Medicine.

Control &. Hospital Epidemiology, online, Sept. 2, 2021 Copyright © 2021 HealthDay. All rights reserved.

From Women's Health Resources Featured Centers Health Solutions From Our SponsorsLatest Heart News THURSDAY, Sept. 2, 2021 (American Heart Association News) At 13, Alison Conklin passed out while playing in a basketball tournament. When she collapsed again during a competitive game of floor hockey, her mother took her to see a cardiologist. An echocardiogram of Alison's heart showed the wall between the two bottom chambers of her heart was bigger than it should be.

She was diagnosed with hypertrophic cardiomyopathy. HCM causes heart walls to thicken, in turn becoming stiff and reducing the amount of blood taken in and pumped out to the body with each heartbeat. Fainting is a symptom of HCM, along with shortness of breath, abnormal heart rhythms and dizziness. Frightening as that was, Alison had someone to help walk her through it.

Her mom, who also had HCM. Then, five months later, everything changed. "My mom and I were sitting in the kitchen," Alison said. "It was my first day at my first real job at the public library, and she said she didn't feel well, and she collapsed." Alison had just taken a babysitting class at the hospital and learned CPR.

She called 911 and started giving her mom chest compressions until paramedics arrived and took over. "It was terrifying!. You can take as many classes as you want, and whether you can actually implement these things in the heat of the moment, I tried," Alison said. "I was begging her to wake up." At 42, Alison's mother did not survive that day in July 1994.

And her grieving teenage daughter – who already was struggling with knowing she had HCM – just saw the condition kill her mom. Alison continued to struggle with it. Throughout high school, she passed out often enough that she became a patient at the National Institutes of Health. She underwent many surgeries and tests as doctors tried to help improve her symptoms.

Finally, when she was 20, her cardiologist mentioned a new device – an implantable cardioverter defibrillator. It was a machine that would send an electric shock to her heart if a dangerously irregular heartbeat was detected, thus reducing her risk of sudden cardiac death. "He said, 'There's this technology that would have saved your mother's life that is readily available now. It's an ICD.

You're a perfect candidate for one because you have sudden death in your family. Would you like it?. '" Alison recalled. "Obviously, it was a yes." Doctors implanted an ICD in Alison's chest in 2001.

Fast forward to 2015. She was mom to a 12-year-old son. They'd just finished climbing five flights of stairs to get to an orthodontist appointment. "I had the same deadly heart rhythm my mom had on the day she died," Alison said.

"My device saved my life." Thankful her son didn't have to experience what she did at about his age, Alison had an epiphany. "I was always angry at (my mom) that she didn't try to live or angry at myself that I couldn't save her. And it wasn't until that same exact scenario happened to me that I realized it really wasn't anybody's to control," she said. Alison's husband, Geoff Conklin, rushed her to the hospital.

One of the nurses started crying when she read Alison's chart. "Thank God for the device working," the woman told Alison. The couple is grateful neither of their two sons have HCM, which is the most common form of genetic heart disease. Alison went on to have open-heart surgery in 2018 to help relieve her symptoms.

The surgeon removed part of her bulging heart wall to improve blood flow. Now 41 and having faced health challenges for most of her life – including battling a brain tumor that temporarily left her blind – Alison doesn't let that define her. The busy mom runs her own photography business in Emmaus, Pennsylvania. Photography is a passion that grew out of her mother's death.

Her father brought out old photos, negatives and slides of her mom. After that, Alison started carrying a camera everywhere. "I always cherish moments that could be taken for granted," she said. While photographing a Go Red for Women event for the American Heart Association, Alison noticed many women in the room bore scars like hers.

She then came up with the idea of taking portraits of 11 women affected by heart disease and one man whose wife died from it. QUESTION In the U.S., 1 in every 4 deaths is caused by heart disease. See Answer "I think it is really powerful. There is something very important about storytelling," Alison said.

"I think for me, it's just being able to know that I'm not the only person in the world that has experienced these experiences. It makes me feel better, less alone." American Heart Association News covers heart and brain health. Not all views expressed in this story reflect the official position of the American Heart Association. Copyright is owned or held by the American Heart Association, Inc., and all rights are reserved.

If you have questions or comments about this story, please email [email protected] By Stefani Kopenec American Heart Association News Copyright © 2021 HealthDay. All rights reserved. From Healthy Heart Resources Featured Centers Health Solutions From Our SponsorsLatest anti-inflammatories News By Amy Norton HealthDay ReporterTHURSDAY, Sept. 2, 2021 (HealthDay News) People hospitalized for anti inflammatory drugs, and even some with milder cases, may suffer lasting damage to their kidneys, new research finds.

The study of more than 1.7 million patients in the U.S. Veterans Affairs system adds to concerns about the lingering effects of anti inflammatory drugs -- particularly among people sick enough to need hospitalization. Researchers found that months after their initial , anti inflammatory drugs survivors were at increased risk of various types of kidney damage -- from reduced kidney function to advanced kidney failure. People who'd been most severely ill -- requiring ICU care -- had the highest risk of long-term kidney damage.

Similarly, patients who'd developed acute kidney injury during their anti inflammatory drugs hospitalization had higher risks than anti inflammatory drugs patients with no apparent kidney problems during their hospital stay. But what's striking is that those latter patients were not out of the woods, said Dr. F. Perry Wilson, a kidney specialist who was not involved in the study.

They were still about two to five times more likely to develop some degree of kidney dysfunction or disease than VA patients who were not diagnosed with anti inflammatory drugs. "What stood out to me is that across the board, you see these risks even in patients who did not have acute kidney injury when they were hospitalized," said Wilson, an associate professor at Yale School of Medicine in New Haven, Conn. There is some question about the degree to which the kidney problems are related to anti inflammatory drugs specifically, or to being sick in the hospital, according to Wilson. It's unclear, for instance, how their kidney function would compare against that of patients hospitalized for the flu.

But the study found that even VA patients who were sick at home with anti inflammatory drugs were at increased risk of kidney problems. Inflammation to blame?. "There were risks, albeit smaller, among these patients who never had major problems when they were sick," said senior researcher Dr. Ziyad Al-Aly, an assistant professor at Washington University School of Medicine in St.

Louis. Wilson said the "big question" is why?. "Is this reflecting some ongoing immune system stimulation and inflammation?. " he said.

"It will take more research to figure that out." The findings -- published Sept. 1 in the Journal of the American Society of Nephrology -- are based on medical records from more than 1.7 million VA patients. Of those, 89,216 were diagnosed with anti inflammatory drugs between March 2020 and March 2021, and were still alive 30 days later. The study looked at patients' risk of developing various types of kidney problems in the months after that 30-day mark.

Overall, anti inflammatory drugs patients were more likely to show a substantial drop in the kidneys' glomerular fiation rate (GFR), a measure of how well the organs are filtering waste from the blood. Just over 5% of anti inflammatory drugs patients had a GFR decline of 30% or more, the study found. And compared with the general VA patient population, their risk was 25% higher. Since adults naturally lose about 1% of their kidney function per year, a 30% decline in GFR is akin to losing 30 years of kidney function, according to Wilson.

The study also examined the risk of acute kidney injury, where the organs suddenly lose function. It can cause symptoms such as swelling in the legs, fatigue and breathing difficulty, but sometimes causes no overt problems. anti inflammatory drugs patients were nearly twice as likely to develop acute kidney injury, though it varied according to initial anti inflammatory drugs severity. Will the damage last?.

Those who'd been hospitalized were five to eight times more likely than non-anti inflammatory drugs patients to develop acute kidney injury. People who'd been sick at home with anti inflammatory drugs had a 30% higher risk, versus the non-anti inflammatory drugs group. It's not yet known what it all means for anti inflammatory drugs patients' long-term kidney health, Al-Aly said. One question now, he noted, is whether the GFR declines in some patients will level off.

As for acute kidney injury, people can recover from it with no lasting harm, Wilson said. And if a drop in GFR is related to acute kidney injury, he noted, it may well rebound. Some patients in the study did develop end-stage kidney failure. Those odds were greatest among anti inflammatory drugs patients who'd been in the ICU.

They developed the disease at a rate of about 21 cases per 1,000 patients per year -- making their risk 13 times higher than other VA patients'. Smaller risks were also seen among other anti inflammatory drugs patients, hospitalized or not. A limitation of the study is that the VA patients were mostly older men. It's unclear how the results apply more broadly, according to Al-Aly.

The risks presented to non-hospitalized patients are also somewhat murky. They are far from a uniform group, both doctors said. Wilson suspects that people only mildly affected by anti inflammatory drugs would be unlikely to develop kidney problems, whereas those who are "really knocked out for weeks" might have a relatively greater risk. SLIDESHOW Kidney Stones.

Symptoms, Causes, and Treatment See Slideshow The good news, Al-Aly said, is that kidney dysfunction is readily detectable through basic blood work done at primary care visits. Wilson said that kind of check-up might be worthwhile for people who were more severely ill with anti inflammatory drugs. More information The National Kidney Foundation has more on anti inflammatory drugs and kidney disease. SOURCES.

Ziyad Al-Aly, MD, assistant professor, medicine, Washington University School of Medicine in St. Louis. F. Perry Wilson, MD, associate professor, medicine, Yale School of Medicine, New Haven, Conn..

Journal of the American Society of Nephrology, online, Sept. 1, 2021 Copyright © 2021 HealthDay. All rights reserved. From Healthy Resources Featured Centers Health Solutions From Our Sponsors.

Latest anti-inflammatories News By symbicort prices walmart Can i buy symbicort over the counter Steven Reinberg HealthDay ReporterTHURSDAY, Sept. 2, 2021 (HealthDay News) As the new school year begins, teachers can take comfort in a new report that finds they have no greater risk of catching or being hospitalized for severe anti inflammatory drugs than anyone else. Researchers in Scotland say that might be because symbicort prices walmart many schools take precautions that other workplaces don't. It's also possible that the teachers in the study were younger and healthier than other workers, the authors said. "Teachers are about average in terms of their risk of hospitalization with anti inflammatory drugs, when compared to other working-age adults," said lead researcher Dr.

David McAllister, a professor of clinical epidemiology and medical informatics at the Institute of Health and Wellbeing at the University symbicort prices walmart of Glasgow. "Unlike health care workers, teachers are not at increased risk of hospitalization with anti inflammatory drugs, even when schools are open." Using data from March 2020 to July 2021, McAllister and his colleagues collected information on more than 132,000 people with anti inflammatory drugs, ages 21 to 65, and more than 1.3 million people from the general population, all in Scotland. They compared the risk of anti inflammatory drugs among teachers and their family members with health care workers and others. Over the study period, the risk of being hospitalized with anti inflammatory drugs was less than 1% for teachers, health care workers symbicort prices walmart and other adults, the researchers found. After taking into account factors such as age, sex, ethnicity and economic status, the risk of being hospitalized with anti inflammatory drugs was about 50% lower among teachers and their family members than among the general population, the researchers noted.

Over the same period, the risk was almost four times higher among health care workers and almost twice as high among their families, the researchers found. During the first period of full school opening in the fall of 2020, the risk of hospitalization symbicort prices walmart among teachers increased by 2.4-fold, reaching a level similar to that in the general population. By the summer of 2021, when vaccinations were underway, a smaller increase of 1.7 times was seen. The report was published online Sept. 1 in the symbicort prices walmart journal BMJ.

It's not surprising that the risk to teachers is not higher than other groups, said Douglas Harris, Schlieder Foundation Chair in public education at Tulane University in New Orleans, and director of the Education Research Alliance for New Orleans. In schools where masks and social distancing are mandated, the risk of spreading anti inflammatory drugs is cut dramatically, symbicort prices walmart he said. "I think, for the most part, schools are handling it in a sensible way and I think, for the most part, it's sensible keeping the kids in school when it's safe," Harris said. Of course, vaccination is the key to beating the symbicort, he added. "I think symbicort prices walmart in the U.S., there's an ongoing debate about whether treatments can be mandated.

That's the elephant in the room. I think that that almost has to happen if we're really going to get back to normal," Harris said. Harris believes that school systems should mandate anti inflammatory drugs vaccinations for teachers and all students, including young children once a symbicort prices walmart treatment has been approved. "We already do that for, for children, they're already required to get vaccinated for other things," he said. "It's hard to see why you wouldn't require it.

In this case and really that is the only way we get symbicort prices walmart back to normal, this could go on for years." As more adults are vaccinated, the symbicort will attack mostly the unvaccinated, especially children, Harris said. But everything should be done to minimize the spread of the symbicort and keep schools open, he said. "There are health consequences to closing schools," Harris said. "We tend to focus on the immediate effect of schools opening and spreading the symbicort, which is clearly symbicort prices walmart important and probably the first consideration, but when you close the schools you create a new set of problems, mental illness and child abuse, and all sorts of economic side effects." More information For more on anti inflammatory drugs and schools, see the U.S. Centers for Disease Control and Prevention.

SOURCES. David McAllister, MD, MPH, professor, clinical epidemiology and medical informatics, Institute of Health and Wellbeing, University of Glasgow, Scotland. Douglas Harris, PhD, professor, economics, and Schlieder Foundation Chair, public education, Tulane University, New Orleans, and director, Education Research Alliance for New Orleans. BMJ , Sept. 1, 2021, online Copyright © 2021 HealthDay.

All rights reserved.Latest anti-inflammatories News THURSDAY, Sept. 2, 2021 (HealthDay News) The prescribing, dispensing and use of ivermectin to prevent or treat anti inflammatory drugs outside of clinical trials must end immediately, the American Medical Association, American Pharmacists Association and American Society of Health-System Pharmacists say. The drug has U.S. Food and Drug Administration approval to treat people with s caused by internal and external parasites, but is not approved to prevent or treat anti inflammatory drugs. Ivermectin is also available for veterinary use in horses and other animals, but medications intended for animals should not be used by humans.

"We are alarmed by reports that outpatient prescribing for and dispensing of ivermectin have increased 24-fold since before the symbicort and increased exponentially over the past few months," the groups said in a statement. They noted that calls to poison control centers related to ivermectin have increased fivefold compared to before the symbicort. The FDA has also received multiple reports of people who have been hospitalized after "self-medicating with ivermectin intended for horses," the agency said in a consumer update on. "You are not a horse. You are not a cow.

Seriously, y'all. Stop it," the FDA tweeted on Aug.21. No form of ivermectin has been approved to treat or prevent anti inflammatory drugs, the FDA emphasized. It said it was compelled to issue a warning due to "a lot of misinformation" around the drug, according to the update. "You may have heard that it's okay to take large doses of ivermectin.

That is wrong," the FDA said. .The U.S. Centers for Disease Control and Prevention also issued an advisory saying ivermectin is not authorized or approved for the prevention or treatment of anti inflammatory drugs. The CDC has warned about the potentially toxic effects of the drug, including "nausea, vomiting and diarrhea. Overdoses are associated with hypotension [low blood pressure] and neurologic effects such as decreased consciousness, confusion, hallucinations, seizures, coma and death." More information Visit the U.S.

Centers for Disease Control and Prevention for more on anti inflammatory drugs treatments. SOURCE. American Medical Association, American Pharmacists Association, American Society of Health-System Pharmacists, news release, Sept. 1, 2021 Robert Preidt Copyright © 2021 HealthDay. All rights reserved.Latest Infectious Disease News By Amy Norton HealthDay ReporterTHURSDAY, Sept.

2, 2021 (HealthDay News) The anti inflammatory drugs symbicort has spurred a resurgence in other s that strike hospitalized patients, a U.S. Government study finds. The study, by the U.S. Centers for Disease Control and Prevention, highlights the broad toll the symbicort has taken. It found that rates of several types of hospital-acquired s rose after the symbicort reached U.S.

Shores in 2020. More hospital patients suffered potentially deadly s related to medical devices, including ventilators and tubes placed in blood vessels compared to the same period in 2019. There was a similar rise in antibiotic-resistant staph s, which can infiate the bloodstream and lungs. The trend is disconcerting, in part, because U.S. Hospitals had been making steady progress in preventing those s before the symbicort.

"What we've learned during this symbicort is that the impact of anti inflammatory drugs is far-reaching," said Dr. Arjun Srinivasan, associate director of the CDC's health care-associated prevention programs. The unfortunate fact, he said, is that anti inflammatory drugs created a "perfect storm" of circumstances that fed the increase in hospital-acquired s. There was the sheer number of patients flooding many hospitals -- people who were very ill and often required intensive care. Plus, Srinivasan said, those patients commonly had preexisting medical conditions and often needed to stay on ventilators and other medical devices for prolonged periods -- all of which raise the risk of s.

Add to that the challenges faced by health care providers. Earlier in the symbicort, Srinivasan said, "we didn't have enough gowns, we didn't have enough masks, we didn't have enough respirators." As a result, protective equipment meant to be thrown away after one use was sometimes being reused. And, Srinivasan said, health care workers were falling ill or needing to quarantine -- which fed staffing shortages and added to providers' exhaustion. "This is, in no way, saying that health care workers failed to do their job," Srinivasan stressed. "This was a failure of the system." The findings -- published Sept.

2 in the journal Control &. Hospital Epidemiology -- are based on data from a national surveillance system that tracks health care-linked s. CDC epidemiologist Lindsey Weiner-Lastinger led the study. Researchers found that in the early part of 2020, those s were generally declining compared to the same period in 2019. That changed with the symbicort.

The biggest increase was in blood s related to central lines, which are catheters placed into large arteries to deliver medications or fluids. Those s were up by about 47% in the latter half of 2020. s related to ventilators, urinary catheters and antibiotic-resistant Staphylococcus aureus bacteria were all up as well. "This isn't surprising to those of us on the ground," said Dr. Cornelius Clancy, a professor of medicine at the University of Pittsburgh.

"The national data reflect what we've seen." He pointed to the general strain on hospital systems, and the "inordinate resources" that anti inflammatory drugs care demanded, as factors. Some "bread-and-butter" practices that prevent health care-associated s, Clancy said, could not get the same attention they do during normal times. "This is another example of how you can't separate anti inflammatory drugs from everything else that goes on in health care," said Clancy, who is also with the Infectious Diseases Society of America. anti inflammatory drugs affects not only the people who are sickened with it, he said, but the wider health care system. That is not to say people should fear going to the hospital, both Clancy and Srinivasan emphasized.

"People certainly need to seek any care they need," Clancy said. And even in the midst of new anti inflammatory drugs surges at some U.S. Hospitals, there are reasons to expect that the risks of hospital-acquired s might be less, versus last year. For one, Srinivasan said, hospitals are more aware of the issue now. Health care workers are also more experienced in managing anti inflammatory drugs patients, and more protected from through vaccination.

As for the general public, the study underscores the importance of getting vaccinated to cut the risk of falling seriously ill with anti inflammatory drugs. SLIDESHOW Urinary Incontinence in Women. Types, Causes, and Treatments for Bladder Control See Slideshow "One of the best ways to prevent health care-associated s is through vaccination," Srinivasan said. "Even with the delta variant," he added, "the treatments are tremendously effective at preventing hospitalization." Clancy agreed. "The data on vaccination are incontrovertible," he said.

More information The U.S. Centers for Disease Control and Prevention has advice for patients on lowering their risk of health care-associated s. SOURCES. Arjun Srinivasan, MD, associate director, healthcare-associated prevention programs, U.S. Centers for Disease Control and Prevention, Atlanta.

Cornelius J. Clancy, MD, professor, medicine, University of Pittsburgh School of Medicine. Control &. Hospital Epidemiology, online, Sept. 2, 2021 Copyright © 2021 HealthDay.

All rights reserved. From Women's Health Resources Featured Centers Health Solutions From Our SponsorsLatest Heart News THURSDAY, Sept. 2, 2021 (American Heart Association News) At 13, Alison Conklin passed out while playing in a basketball tournament. When she collapsed again during a competitive game of floor hockey, her mother took her to see a cardiologist. An echocardiogram of Alison's heart showed the wall between the two bottom chambers of her heart was bigger than it should be.

She was diagnosed with hypertrophic cardiomyopathy. HCM causes heart walls to thicken, in turn becoming stiff and reducing the amount of blood taken in and pumped out to the body with each heartbeat. Fainting is a symptom of HCM, along with shortness of breath, abnormal heart rhythms and dizziness. Frightening as that was, Alison had someone to help walk her through it. Her mom, who also had HCM.

Then, five months later, everything changed. "My mom and I were sitting in the kitchen," Alison said. "It was my first day at my first real job at the public library, and she said she didn't feel well, and she collapsed." Alison had just taken a babysitting class at the hospital and learned CPR. She called 911 and started giving her mom chest compressions until paramedics arrived and took over. "It was terrifying!.

You can take as many classes as you want, and whether you can actually implement these things in the heat of the moment, I tried," Alison said. "I was begging her to wake up." At 42, Alison's mother did not survive that day in July 1994. And her grieving teenage daughter – who already was struggling with knowing she had HCM – just saw the condition kill her mom. Alison continued to struggle with it. Throughout high school, she passed out often enough that she became a patient at the National Institutes of Health.

She underwent many surgeries and tests as doctors tried to help improve her symptoms. Finally, when she was 20, her cardiologist mentioned a new device – an implantable cardioverter defibrillator. It was a machine that would send an electric shock to her heart if a dangerously irregular heartbeat was detected, thus reducing her risk of sudden cardiac death. "He said, 'There's this technology that would have saved your mother's life that is readily available now. It's an ICD.

You're a perfect candidate for one because you have sudden death in your family. Would you like it?. '" Alison recalled. "Obviously, it was a yes." Doctors implanted an ICD in Alison's chest in 2001. Fast forward to 2015.

She was mom to a 12-year-old son. They'd just finished climbing five flights of stairs to get to an orthodontist appointment. "I had the same deadly heart rhythm my mom had on the day she died," Alison said. "My device saved my life." Thankful her son didn't have to experience what she did at about his age, Alison had an epiphany. "I was always angry at (my mom) that she didn't try to live or angry at myself that I couldn't save her.

And it wasn't until that same exact scenario happened to me that I realized it really wasn't anybody's to control," she said. Alison's husband, Geoff Conklin, rushed her to the hospital. One of the nurses started crying when she read Alison's chart. "Thank God for the device working," the woman told Alison. The couple is grateful neither of their two sons have HCM, which is the most common form of genetic heart disease.

Alison went on to have open-heart surgery in 2018 to help relieve her symptoms. The surgeon removed part of her bulging heart wall to improve blood flow. Now 41 and having faced health challenges for most of her life – including battling a brain tumor that temporarily left her blind – Alison doesn't let that define her. The busy mom runs her own photography business in Emmaus, Pennsylvania. Photography is a passion that grew out of her mother's death.

Her father brought out old photos, negatives and slides of her mom. After that, Alison started carrying a camera everywhere. "I always cherish moments that could be taken for granted," she said. While photographing a Go Red for Women event for the American Heart Association, Alison noticed many women in the room bore scars like hers. She then came up with the idea of taking portraits of 11 women affected by heart disease and one man whose wife died from it.

QUESTION In the U.S., 1 in every 4 deaths is caused by heart disease. See Answer "I think it is really powerful. There is something very important about storytelling," Alison said. "I think for me, it's just being able to know that I'm not the only person in the world that has experienced these experiences. It makes me feel better, less alone." American Heart Association News covers heart and brain health.

Not all views expressed in this story reflect the official position of the American Heart Association. Copyright is owned or held by the American Heart Association, Inc., and all rights are reserved. If you have questions or comments about this story, please email [email protected] By Stefani Kopenec American Heart Association News Copyright © 2021 HealthDay. All rights reserved. From Healthy Heart Resources Featured Centers Health Solutions From Our SponsorsLatest anti-inflammatories News By Amy Norton HealthDay ReporterTHURSDAY, Sept.

2, 2021 (HealthDay News) People hospitalized for anti inflammatory drugs, and even some with milder cases, may suffer lasting damage to their kidneys, new research finds. The study of more than 1.7 million patients in the U.S. Veterans Affairs system adds to concerns about the lingering effects of anti inflammatory drugs -- particularly among people sick enough to need hospitalization. Researchers found that months after their initial , anti inflammatory drugs survivors were at increased risk of various types of kidney damage -- from reduced kidney function to advanced kidney failure. People who'd been most severely ill -- requiring ICU care -- had the highest risk of long-term kidney damage.

Similarly, patients who'd developed acute kidney injury during their anti inflammatory drugs hospitalization had higher risks than anti inflammatory drugs patients with no apparent kidney problems during their hospital stay. But what's striking is that those latter patients were not out of the woods, said Dr. F. Perry Wilson, a kidney specialist who was not involved in the study. They were still about two to five times more likely to develop some degree of kidney dysfunction or disease than VA patients who were not diagnosed with anti inflammatory drugs.

"What stood out to me is that across the board, you see these risks even in patients who did not have acute kidney injury when they were hospitalized," said Wilson, an associate professor at Yale School of Medicine in New Haven, Conn. There is some question about the degree to which the kidney problems are related to anti inflammatory drugs specifically, or to being sick in the hospital, according to Wilson. It's unclear, for instance, how their kidney function would compare against that of patients hospitalized for the flu. But the study found that even VA patients who were sick at home with anti inflammatory drugs were at increased risk of kidney problems. Inflammation to blame?.

"There were risks, albeit smaller, among these patients who never had major problems when they were sick," said senior researcher Dr. Ziyad Al-Aly, an assistant professor at Washington University School of Medicine in St. Louis. Wilson said the "big question" is why?. "Is this reflecting some ongoing immune system stimulation and inflammation?.

" he said. "It will take more research to figure that out." The findings -- published Sept. 1 in the Journal of the American Society of Nephrology -- are based on medical records from more than 1.7 million VA patients. Of those, 89,216 were diagnosed with anti inflammatory drugs between March 2020 and March 2021, and were still alive 30 days later. The study looked at patients' risk of developing various types of kidney problems in the months after that 30-day mark.

Overall, anti inflammatory drugs patients were more likely to show a substantial drop in the kidneys' glomerular fiation rate (GFR), a measure of how well the organs are filtering waste from the blood. Just over 5% of anti inflammatory drugs patients had a GFR decline of 30% or more, the study found. And compared with the general VA patient population, their risk was 25% higher. Since adults naturally lose about 1% of their kidney function per year, a 30% decline in GFR is akin to losing 30 years of kidney function, according to Wilson. The study also examined the risk of acute kidney injury, where the organs suddenly lose function.

It can cause symptoms such as swelling in the legs, fatigue and breathing difficulty, but sometimes causes no overt problems. anti inflammatory drugs patients were nearly twice as likely to develop acute kidney injury, though it varied according to initial anti inflammatory drugs severity. Will the damage last?. Those who'd been hospitalized were five to eight times more likely than non-anti inflammatory drugs patients to develop acute kidney injury. People who'd been sick at home with anti inflammatory drugs had a 30% higher risk, versus the non-anti inflammatory drugs group.

It's not yet known what it all means for anti inflammatory drugs patients' long-term kidney health, Al-Aly said. One question now, he noted, is whether the GFR declines in some patients will level off. As for acute kidney injury, people can recover from it with no lasting harm, Wilson said. And if a drop in GFR is related to acute kidney injury, he noted, it may well rebound. Some patients in the study did develop end-stage kidney failure.

Those odds were greatest among anti inflammatory drugs patients who'd been in the ICU. They developed the disease at a rate of about 21 cases per 1,000 patients per year -- making their risk 13 times higher than other VA patients'. Smaller risks were also seen among other anti inflammatory drugs patients, hospitalized or not. A limitation of the study is that the VA patients were mostly older men. It's unclear how the results apply more broadly, according to Al-Aly.

The risks presented to non-hospitalized patients are also somewhat murky. They are far from a uniform group, both doctors said. Wilson suspects that people only mildly affected by anti inflammatory drugs would be unlikely to develop kidney problems, whereas those who are "really knocked out for weeks" might have a relatively greater risk. SLIDESHOW Kidney Stones. Symptoms, Causes, and Treatment See Slideshow The good news, Al-Aly said, is that kidney dysfunction is readily detectable through basic blood work done at primary care visits.

Wilson said that kind of check-up might be worthwhile for people who were more severely ill with anti inflammatory drugs. More information The National Kidney Foundation has more on anti inflammatory drugs and kidney disease. SOURCES. Ziyad Al-Aly, MD, assistant professor, medicine, Washington University School of Medicine in St. Louis.

F. Perry Wilson, MD, associate professor, medicine, Yale School of Medicine, New Haven, Conn.. Journal of the American Society of Nephrology, online, Sept. 1, 2021 Copyright © 2021 HealthDay. All rights reserved.

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Airduo respiclick vs symbicort

€‚For the podcast associated with this article, please visit https://academic.oup.com/eurheartj/pages/Podcasts.This issue begins with the Special Article ‘An EAPCI Expert Consensus http://geolistening.com/levitra-cialis-online/ Document on Ischaemia with Non-Obstructive Coronary Arteries in Collaboration with European Society of Cardiology Working Group airduo respiclick vs symbicort on Coronary Pathophysiology &. Microcirculation Endorsed by Coronary Vasomotor Disorders International Study Group’ by Vijay Kunadian from Newcastle University in the UK, and colleagues.1 While for many years our attention has been focused on coronary stenoses, growing evidence suggests that functional alterations of the coronary circulation play an important role in all clinical manifestations of ischaemic heart disease.2,3 The current contribution is an expert consensus document on ischaemia with non-obstructive coronary arteries (INOCA). Angina pectoris affects ∼112 million people globally airduo respiclick vs symbicort. Up to 70% of patients undergoing invasive angiography do not have obstructive coronary artery disease, more common in women than in men, and a large proportion have INOCA as a cause of their symptoms.

INOCA patients airduo respiclick vs symbicort present with a wide spectrum of symptoms and signs that are often misdiagnosed as non-cardiac, leading to underdiagnosis/investigation and undertreatment. INOCA can result from several mechanism including coronary vasospasm and microvascular dysfunction, and is not a benign condition. Compared with asymptomatic individuals, INOCA is associated with increased incidence of cardiovascular events, repeated hospital admissions, as well as impaired quality of life and associated increased healthcare costs. This document provides a definition of INOCA and guidance to the community on the diagnostic approach and management of INOCA based on existing evidence from research and best available clinical airduo respiclick vs symbicort practice, noting gaps in knowledge and potential areas for investigation.This issue then continues with a focus on acute coronary syndromes (ACS) which represent the most dramatic presentation of ischaemic heart disease.

The abrupt clinical presentation of ACS gives a strong signal of discontinuity in the natural history of atherothrombosis.4,5 While experimental models of atherogenesis have provided a growing body of information about molecular mechanisms of plaque growth, the transition from coronary stability to instability is less well understood. This issue provides novel important information in this fascinating area of cardiovascular medicine.6In a clinical research manuscript entitled airduo respiclick vs symbicort ‘Long-term beta-blocker therapy and clinical outcomes after acute myocardial infarction in patients without heart failure. Nationwide cohort study’, Jihoon Kim from the University School of Medicine in Seoul, South Korea and colleagues investigate the association between long-term beta-blocker therapy and clinical outcomes in patients without heart failure (HF) after acute myocardial infarction (MI).7 Between 2010 and 2015, a total of 28 970 patients who underwent coronary revascularization for acute MI with beta-blocker prescription at hospital discharge, and were event-free from death, recurrent MI, or HF for 1 year were enrolled from Korean nationwide medical insurance data. The primary outcome was all-cause death.

The secondary outcome was a airduo respiclick vs symbicort composite of all-cause death, recurrent MI, or hospitalization for new HF. Outcomes were compared between beta-blocker therapy for ≥1 year (n = 22707) and beta-blocker therapy for <1 year (n = 6263) using landmark analysis at 1 year after the index MI. Compared with patients receiving beta-blocker therapy for <1 year, those receiving beta-blocker therapy for ≥1 year had a significant 19% lower risk of all-cause death and a airduo respiclick vs symbicort significant 18% lower risk of the composite of all-cause death, recurrent MI, or hospitalization for new HF. The lower risk of all-cause death associated with persistent beta-blocker therapy was observed beyond 2 years but not beyond 3 years after MI (Figure 1).

Figure 1Cumulative incidences of clinical outcomes since 1 year after myocardial infarction. (A) All-cause death, (B) recurrent MI, (C) hospitalization for new heart failure, and airduo respiclick vs symbicort (D) a composite of all-cause death, recurrent MI, or hospitalization for new heart failure. MI, myocardial infarction (from Kim J, Kang D, Park H, Kang M, Park TK, Lee JM, Yang JH, Song JB, Choi J-H, Choi S-H, Gwon H-C, Guallar E, Cho J, Hahn J-Y. Long-term β-blocker therapy and clinical outcomes after acute airduo respiclick vs symbicort myocardial infarction in patients without heart failure.

Nationwide cohort study. See pages 3521–3529).Figure 1Cumulative incidences of clinical outcomes since 1 year after myocardial infarction. (A) All-cause airduo respiclick vs symbicort death, (B) recurrent MI, (C) hospitalization for new heart failure, and (D) a composite of all-cause death, recurrent MI, or hospitalization for new heart failure. MI, myocardial infarction (from Kim J, Kang D, Park H, Kang M, Park TK, Lee JM, Yang JH, Song JB, Choi J-H, Choi S-H, Gwon H-C, Guallar E, Cho J, Hahn J-Y.

Long-term β-blocker therapy and clinical outcomes after acute myocardial infarction in airduo respiclick vs symbicort patients without heart failure. Nationwide cohort study. See pages 3521–3529).The authors conclude that in this nationwide cohort, beta-blocker therapy for ≥1 year after MI was associated with reduced all-cause death among patients with acute MI without HF. The manuscript is accompanied by an Editorial by Rafael Harari and Sripal Bangalore from the New York University School of Medicine in the USA, who conclude that a drug that has been widely used clinically for over half a century is now in urgent need of reappraisal from contemporary trials.8In a clinical research article entitled ‘Ticagrelor alone versus ticagrelor plus aspirin following percutaneous coronary intervention in patients with airduo respiclick vs symbicort non-ST-segment elevation acute coronary syndromes.

TWILIGHT-ACS’, Roxana Mehran from Mount Sinai School of Medicine in New York, USA and colleagues determined the effect of ticagrelor monotherapy on clinically relevant bleeding and major ischaemic events in relation to clinical presentation with and without non-ST elevation acute coronary syndromes (NSTE-ACS) among patients undergoing percutaneous coronary intervention (PCI) with drug-eluting stents (DES).9 The authors conducted a pre-specified subgroup analysis of The Ticagrelor With Aspirin or Alone in High-Risk Patients After Coronary Intervention (TWILIGHT) trial, which enrolled 9006 patients with high-risk features undergoing PCI with DES. After 3 months of dual antiplatelet therapy (DAPT) with ticagrelor plus aspirin, 7119 adherent and event-free patients were randomized in a double-blind airduo respiclick vs symbicort manner to ticagrelor plus placebo vs. Ticagrelor plus aspirin for 12 months. The primary outcome was Bleeding Academic Research Consortium (BARC) type 2, 3, or 5 bleeding, while the composite of all-cause death, MI, or stroke was the key secondary outcome.

Ticagrelor monotherapy significantly reduced BARC 2, 3, or 5 bleeding by a significant 54% among NSTE-ACS patients and by airduo respiclick vs symbicort a non-significant 24% among stable patients (P for interaction 0.03). Rates of all-cause death, MI, or stroke were similar between treatment arms irrespective of clinical presentation.Mehran et al. Conclude that among patients with or without NSTE-ACS who have completed an initial 3-month course of DAPT following PCI with DES, ticagrelor monotherapy reduced clinically airduo respiclick vs symbicort meaningful bleeding events without increasing ischaemic risk as compared with ticagrelor plus aspirin. The benefits of ticagrelor monotherapy with respect to bleeding events were more pronounced in patients with NSTE-ACS.

This manuscript is accompanied by an Editorial by Robert Storey from the University of Sheffield in the UK10 who wonders if one should switch from ticagrelor monotherapy to aspirin monotherapy at 12 months or continue ticagrelor monotherapy long term, and suggests that that part of the journey remains largely unexplored. Figure 2In total, 150 patients were included into the prospective airduo respiclick vs symbicort translational OPTICO-ACS study (A) and the culprit lesions were characterized by OCT as well as by local and systematic immunophenotyping. Culprit lesion assessment revealed differential immunological signature with an enrichment in T-lymphocytes, both CD4+ and CD8+ T-cell subpopulations (B) as well as increased T-cell effector molecules at the culprit site distinguishing acute coronary syndromes with intact fibrous cap from ruptured fibrous cap-acute coronary syndrome. Since acute coronary syndromes with intact fibrous cap-lesion were often located at bifurcations, endothelial cells were subjected to culture in disturbed airduo respiclick vs symbicort laminar flow conditions (C), i.e.

To simulate coronary flow near a bifurcation, demonstrated an enhanced adhesion of CD8+ T cells. Finally, both CD8+ T cells and their cytotoxic effector molecules caused endothelial cell death, a key pathophysiological mechanism in acute coronary syndromes with intact fibrous cap (from Leistner DM, Kränkel N, Meteva D, Abdelwahed YS, Seppelt C, Stähli BE, Rai H, Skurk C, Lauten A, Mochmann H-C, Fröhlich G, Rauch-Kröhnert U, Flores E, Riedel M, Sieronski L, Kia S, Strässler E, Haghikia A, Dirks F, Steiner JK, Mueller DN, Volk H-D, Klotsche J, Joner M, Libby P, Landmesser U. Differential immunological signature at the culprit site distinguishes acute coronary syndrome airduo respiclick vs symbicort with intact from acute coronary syndrome with ruptured fibrous cap. Results from the prospective translational OPTICO-ACS study.

See pages 3549–3560).Figure 2In total, 150 patients were included into the prospective translational OPTICO-ACS study (A) and the culprit lesions were characterized by OCT as well as airduo respiclick vs symbicort by local and systematic immunophenotyping. Culprit lesion assessment revealed differential immunological signature with an enrichment in T-lymphocytes, both CD4+ and CD8+ T-cell subpopulations (B) as well as increased T-cell effector molecules at the culprit site distinguishing acute coronary syndromes with intact fibrous cap from ruptured fibrous cap-acute coronary syndrome. Since acute coronary syndromes with intact fibrous cap-lesion were often located airduo respiclick vs symbicort at bifurcations, endothelial cells were subjected to culture in disturbed laminar flow conditions (C), i.e. To simulate coronary flow near a bifurcation, demonstrated an enhanced adhesion of CD8+ T cells.

Finally, both CD8+ T cells and their cytotoxic effector molecules caused endothelial cell death, a key pathophysiological mechanism in acute coronary syndromes with intact fibrous cap (from Leistner DM, Kränkel N, Meteva D, Abdelwahed YS, Seppelt C, Stähli BE, Rai H, Skurk C, Lauten A, Mochmann H-C, Fröhlich G, Rauch-Kröhnert U, Flores E, Riedel M, Sieronski L, Kia S, Strässler E, Haghikia A, Dirks F, Steiner JK, Mueller DN, Volk H-D, Klotsche J, Joner M, Libby P, Landmesser U. Differential immunological airduo respiclick vs symbicort signature at the culprit site distinguishes acute coronary syndrome with intact from acute coronary syndrome with ruptured fibrous cap. Results from the prospective translational OPTICO-ACS study. See pages 3549–3560).ACS with airduo respiclick vs symbicort an intact fibrous cap (IFC), i.e.

Caused by coronary plaque erosion, account for approximately one-third of ACS cases. However, the underlying pathophysiological mechanisms as compared with ACS caused by a ruptured fibrous cap (RFC) remain largely undefined.11–14 In a clinical research article entitled ‘Differential immunological signature at the culprit site distinguishes acute coronary syndrome with intact from acute coronary syndrome with ruptured fibrous cap. Results from the prospective translational OPTICO-ACS study’, David Leistner from the Charite Universitatsmedizin airduo respiclick vs symbicort Berlin in Germany and colleagues compared the microenvironment of culprit lesions (CLs) with IFC vs. Those with RFC.15 The CL of 170 consecutive ACS patients was investigated by optical coherence tomography (OCT) and simultaneous immunophenotyping by flow cytometric analysis as well as by effector molecule concentration measurements across the CL.

Within the study cohort, IFC CLs caused 25% of ACS while RFC CLs caused the remaining 75%, as determined and validated airduo respiclick vs symbicort by two independent OCT core laboratories. IFC CLs were characterized by lower lipid content, less calcification, a thicker overlying fibrous cap, and largely localized near a coronary bifurcation as compared with RFC CLs. The microenvironment of IFC CLs demonstrated selective enrichment in both CD4+ and CD8+ T lymphocytes as compared with RFC CLs. T cell-associated extracellular circulating microvesicles were more pronounced in IFC CLs, and a significantly higher amount of CD8+ T lymphocytes was detectable in thrombi aspirated from IFC CLs as airduo respiclick vs symbicort compared with RFC CLs.

Furthermore, IFC CLs showed significantly increased levels of the T-cell effector molecules granzyme A (+22%), perforin (+59%), and granulysin (+75%) as compared with RFC CLs. Endothelial cells subjected to culture in disturbed airduo respiclick vs symbicort laminar flow conditions to simulate coronary flow near a bifurcation demonstrated an enhanced adhesion of CD8+ T cells. Finally, both CD8+ T cells and their cytotoxic effector molecules caused endothelial cell death, a key potential pathophysiological mechanism in IFC CLs.Thus, the OPTICO-ACS study emphasizes a novel mechanism in the pathogenesis of IFC CLs, favouring participation of the adaptive immune system, particularly CD8+ T cells and their effector molecules. The manuscript is accompanied by an Editorial by Giovanna Liuzzo and colleagues (myself included) from the Catholic University16 who conclude that we are learning a lot about plaque erosion but we should not forget the words of Winston Churchill.

€˜Now this airduo respiclick vs symbicort is not the end. It is not even the beginning of the end. But it is, perhaps, the end of the beginning.’Balance between inflammatory and reparative leucocytes allows optimal healing after MI.17 In a clinical research article ‘Molecular imaging-guided repair after acute myocardial infarction by targeting the chemokine receptor CXCR4’, Annika Hess from the Hannover Medical School in airduo respiclick vs symbicort Germany and colleagues aimed to characterize infarct chemokine CXC receptor 4 (CXCR4) expression using positron emission tomography (PET) and establish its relationship to cardiac outcome. The authors tested whether image-guided early CXCR4-directed therapy attenuates chronic dysfunction.18 A total of 180 mice underwent coronary ligation or sham surgery and serial PET imaging over 7 days.

Infarct CXCR4 content was significantly higher over 3 days after MI compared with sham, confirmed by flow cytometry and histopathology. Mice that airduo respiclick vs symbicort died of left ventricular (LV) rupture exhibited persistent inflammation at 3 days compared with survivors. Higher CXCR4 signal at 1 and 3 days independently predicted significantly worse functional outcome at 6 weeks assessed by cardiac magnetic resonance. Following the imaging time-course, mice were airduo respiclick vs symbicort treated with AMD3100, a CXCR4 blocker.

CXCR4 blockade at 3 days significantly lowered LV rupture incidence vs. Untreated MI (8% vs. 25%), and significantly airduo respiclick vs symbicort improved contractile function at 6 weeks. CXCR4 blockade at 7 days failed to improve the outcome.

Flow cytometry analysis revealed lower LV airduo respiclick vs symbicort neutrophil and Ly6C high monocyte content after CXCR4 blockade at 3 days. A total of 50 patients underwent CXCR4 PET imaging and functional assessment early after MI. CXCR4 expression correlated with contractile function.Hess and colleagues conclude that PET imaging identifies early CXCR4 up-regulation which predicts acute rupture and chronic contractile dysfunction. Imaging-guided CXCR4 inhibition accelerates inflammatory resolution and airduo respiclick vs symbicort improves outcome.

This supports a molecular imaging-based theranostic approach to guide therapy after MI. The manuscript is accompanied by an Editorial by Christian Weber from the Ludwig-Maximilians-Universität in Munich, Germany and colleagues.19 The authors point out that the study of Hess airduo respiclick vs symbicort et al. Building on the virtues of molecular PET imaging for non-invasive analysis of biomarker expression within injured tissue, in a pre-clinical as well as in a clinical setting, demonstrates the value of CXCR4 PET imaging in identifying the best time point of anti-inflammatory treatment by CXCR4 antagonism with respect to chronic cardiac function.In a clinical review article entitled ‘Management of non-culprit coronary plaques in patients with acute coronary syndrome’, Rocco Montone from the Fondazione Policlinico Universitario A. Gemelli IRCCS in Rome, Italy, and colleagues (including myself) note that ∼50% of patients with ST-segment elevation myocardial infarction (STEMI) have multivessel coronary artery disease, a condition associated with an increased incidence of recurrent ischaemic events and higher mortality.20,21 Based on recent evidence, a strategy of staged PCI of obstructive non-culprit lesions should be considered the gold standard for the management of these patients.22 However, several issues remain unresolved.

Indeed, what the optimal timing of staged PCI is airduo respiclick vs symbicort has not been completely defined. Moreover, assessment of intermediate non-culprit lesions still represents a clinical conundrum, as pressure-wire indexes do not seem able to correctly identify those patients in whom deferral is safe. Intracoronary imaging may help to identify untreated non-culprit lesions containing vulnerable plaques that may portend a higher risk of airduo respiclick vs symbicort future cardiovascular events. However, there are hitherto no studies demonstrating that preventive PCI of vulnerable plaques or more intensive pharmacological treatment is associated with an improved clinical outcome.

In this review, the authors discuss the recent evolving concepts about management of non-culprit plaques in STEMI patients, proposing a diagnostic and therapeutic algorithm to guide physicians in clinical practice. They also airduo respiclick vs symbicort underscore the several knowledge gaps which need to be addressed in future studies.This issue is also complemented by two Discussion Forum contributions. In a contribution entitled ‘Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest in relation to organ donation’, Stefan Roest from the Erasmus MC in Amsterdam, the Netherlands and colleagues comment on the recent publication entitled ‘Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest. A registry study’ by Wulfran Bougouin from the Paris Cardiovascular Research Center airduo respiclick vs symbicort (PARCC) in France, and his colleagues the Sudden Death Expertise Center investigators.23,24 Bougouin et al.

Respond in a separate comment.25The editors hope that readers of this issue of the European Heart Journal will find it of interest.With thanks to Amelia Meier-Batschelet, Johanna Hugger, and Martin Meyer for help with compilation of this article. References1Kunadian V, Chieffo A, Camici PG, Berry C, Escaned J, Maas A, Prescott E, Karam N, airduo respiclick vs symbicort Appelman Y, Fraccaro C, Louise Buchanan G, Manzo-Silberman S, Al-Lamee R, Regar E, Lansky A, Abbott JD, Badimon L, Duncker DJ, Mehran R, Capodanno D, Baumbach A. An EAPCI Expert Consensus Document on Ischaemia with Non-Obstructive Coronary Arteries in Collaboration with European Society of Cardiology Working Group on Coronary Pathophysiology &. Microcirculation Endorsed by Coronary Vasomotor Disorders International Study Group.

Eur Heart J 2020;41:3504–3520.2Crea F, Camici airduo respiclick vs symbicort PG, Bairey Merz CN. Coronary microvascular dysfunction. An update airduo respiclick vs symbicort. Eur Heart J 2014;35:1101–1111.3Berry C, Duncker D, Guzik T.

Coronary microvascular dysfunction in Cardiovascular Research. Time to airduo respiclick vs symbicort turn on the spotlight!. Eur Heart J 2020;41:612–613.4Lüscher TF. Improving outcomes after acute coronary events airduo respiclick vs symbicort.

What works and what doesn’t. Eur Heart J 2018;39:2691–2694.5Crea F, Liuzzo G. Anti-inflammatory treatment airduo respiclick vs symbicort of acute coronary syndromes. The need for precision medicine.

Eur Heart J 2016;37:2414–2416.6Collet JP, Thiele H, Barbato E, Barthélémy O, Bauersachs J, Bhatt DL, Dendale P, Dorobantu M, Edvardsen T, Folliguet T, Gale CP, Gilard M, Jobs A, Jüni P, airduo respiclick vs symbicort Lambrinou E, Lewis BS, Mehilli J, Meliga E, Merkely B, Mueller C, Roffi M, Rutten FH, Sibbing D, Siontis GCM. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J 2020;doi:10.1093/eurheartj/ehaa575.7Kim J, Kang D, Park H, Kang M, Park TK, Lee JM, Yang JH, Song YB, Choi JH, Choi SH, Gwon HC, Guallar E, Cho J, Hahn JY. Long-term beta-blocker therapy and clinical outcomes after acute myocardial infarction in patients without heart failure airduo respiclick vs symbicort.

Nationwide cohort study. Eur Heart airduo respiclick vs symbicort J 2020;41:3521–3529.8Harari R, Bangalore S. Beta-blockers after acute myocardial infarction. An old drug in urgent need of new evidence!.

Eur Heart J 2020;41:3530–3532.9Baber U, Dangas G, Angiolillo DJ, Cohen DJ, Sharma SK, Nicolas J, Briguori C, Cha JY, Collier T, Dudek D, Džavik V, Escaned J, Gil R, Gurbel P, Hamm CW, Henry T, Huber K, Kastrati airduo respiclick vs symbicort A, Kaul U, Kornowski R, Krucoff M, Kunadian V, Marx SO, Mehta SR, Moliterno D, Ohman EM, Oldroyd K, Sardella G, Sartori S, Shlofmitz R, Steg PG, Weisz G, Witzenbichler B, Han Y-L, Pocock S, Gibson CM, Mehran R. Ticagrelor alone versus ticagrelor plus aspirin following percutaneous coronary intervention in patients with non-ST-segment elevation acute coronary syndromes. TWILIGHT-ACS. Eur Heart J 2020;41:3533–3545.10Storey RF.

The long journey of individualizing antiplatelet therapy after acute coronary syndromes. Eur Heart J 2020;41:3546–3548.11Partida RA, Libby P, Crea F, Jang IK. Plaque erosion. A new in vivo diagnosis and a potential major shift in the management of patients with acute coronary syndromes.

Eur Heart J 2018;39:2070–2076.12Jia H, Dai J, Hou J, Xing L, Ma L, Liu H, Xu M, Yao Y, Hu S, Yamamoto E, Lee H, Zhang S, Yu B, Jang IK. Effective anti-thrombotic therapy without stenting. Intravascular optical coherence tomography-based management in plaque erosion (the EROSION study). Eur Heart J 2017;38:792–800.13Libby P.

Superficial erosion and the precision management of acute coronary syndromes. Not one-size-fits-all. Eur Heart J 2017;38:801–803.14Quillard T, Araújo HA, Franck G, Shvartz E, Sukhova G, Libby P. TLR2 and neutrophils potentiate endothelial stress, apoptosis and detachment.

Implications for superficial erosion. Eur Heart J 2015;36:1394–404.15Leistner DM, Kränkel N, Meteva D, Abdelwahed YS, Seppelt C, Stähli, Rai H, Skurk C, Lauten A, Mochmann HC, Fröhlich G, Rauch-Kröhnert U, Flores E, Riedel M, Sieronski L, Kia S, Strässler E, Haghikia A, Dirks F, Steiner J, Mueller DN, Volk HD, Klotsche J, Joner M, Libby P, Landmesser U. Differential immunological signature at the culprit site distinguishes acute coronary syndrome with intact from acute coronary syndrome with ruptured fibrous cap. Results from the prospective translational OPTICO-ACS study.

Eur Heart J 2020;41:3549–3560.16Liuzzo G, Pedicino D, Vinci R, Crea F. CD8 lymphocytes and plaque erosion. A new piece in the jigsaw. Eur Heart J 2020;41:3561–3563.17Montecucco F, Carbone F, Schindler TH.

Pathophysiology of ST-segment elevation myocardial infarction. Novel mechanisms and treatments. Eur Heart J 2016;37:1268–1283.18Hess A, Derlin T, Koenig T, Diekmann J, Wittneben A, Wang Y, Wester HJ, Ross TL, Wollert KC, Bauersachs J, Bengel FM, Thackeray JT. Molecular imaging-guided repair after acute myocardial infarction by targeting the chemokine receptor CXCR4.

Eur Heart J 2020;41:3564–3575.19Döring Y, Noels H, van der Vorst E, Weber C. Seeing is repairing. How imaging-based timely interference with CXCR4 could improve repair after myocardial infarction. Eur Heart J 2020;41:3576–3578.20Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, Caforio ALP, Crea F, Goudevenos JA, Halvorsen S, Hindricks G, Kastrati A, Lenzen MJ, Prescott E, Roffi M, Valgimigli M, Varenhorst C, Vranckx P, Widimský P.

2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2018;39:119–177.21Montone RA, Niccoli G, Crea F, Jang IK. Management of non-culprit coronary plaques in patients with acute coronary syndrome.

Eur Heart J 2020;41:3579–3586.22Pavasini R, Biscaglia S, Barbato E, Tebaldi M, Dudek D, Escaned J, Casella G, Santarelli A, Guiducci V, Gutierrez-Ibanes E, Di Pasquale G, Politi L, Saglietto A, D’Ascenzo F, Campo G. Complete revascularization reduces cardiovascular death in patients with ST-segment elevation myocardial infarction and multivessel disease. Systematic review and meta-analysis of randomized clinical trials. Eur Heart J 2019;doi:10.1093/eurheartj/ehz896.23Roest S, Bunge JJH, Manintveld OC.

Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest in relation to organ donation. Eur Heart J 2020;41:3587.24Bougouin W, Dumas F, Lamhaut L, Marijon E, Carli P, Combes A, Pirracchio R, Aissaoui N, Karam N, Deye N, Sideris G, Beganton F, Jost D, Cariou A, Jouven X. Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest. A registry study.

Eur Heart J 2020;41:1961–1971.25Bougouin W, Cariou A, Jouven X. Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest. Do not neglect potential for organ donation!. Eur Heart J 2020;41:3588.

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email.

Journals.permissions@oup.com.The Ten ‘Commandments’(1) DiagnosisChest discomfort without persistent ST-segment elevation (NSTE-ACS) is the leading symptom initiating the diagnostic and therapeutic cascade. The correlated pathology at the myocardial level is cardiomyocyte necrosis, measured by troponin release, or, less frequently, myocardial ischaemia without cell damage (unstable angina).(2) Troponin assaysHigh-sensitivity troponin assay (hs-cTn) measurements are recommended over less sensitive ones. However, many cardiac pathologies other than MI may also result in cardiac troponin elevations.(3) Rapid ‘rule-in’ and ‘rule-out’ algorithmsIt is recommended to use the 0 h/1 h algorithm (best option) or the 0 h/2 h algorithm. Used in conjunction with clinical and ECG findings, the 0 h/1 h and 0 h/2 h hs-cTn algorithms allow identification of appropriate candidates for early discharge and outpatient management.(4) Ischaemic/bleeding risk assessmentInitial hs-cTn levels add prognostic information in terms of short- and long-term mortality to clinical and ECG variables.

The Global Registry of Acute Coronary Events (GRACE) risk score is superior to (subjective) physician assessment for the occurrence of death or MI. The Academic Research Consortium-High Bleeding Risk may be used to assess the bleeding risk.(5) Non-invasive imagingEven after the rule-out of MI, elective non-invasive or invasive imaging may be indicated according to clinical assessment. Coronary computed tomography angiography or stress imaging may be options based on risk assessment.(6) Risk stratification for an invasive approachAn early routine invasive approach within 24 h of admission is recommended for Non ST segment elevation myocardial infarction (NSTEMI) based on hs-cTn measurements, GRACE risk score >140, and dynamic new or presumably new ST-segment changes. Immediate invasive angiography is required in highly unstable patients according to hemodynamic status, arrhythmias, acute heart failure, or persistent chest pain.

In all other clinical presentations, a selective invasive approach may be performed according to non-invasive testing or clinical risk assessment.(7) Revascularization strategiesRadial access is recommended as the preferred approach in NSTE-ACS patients undergoing invasive assessment. Percutaneous coronary intervention of the culprit lesion is the treatment of choice. In multivessel disease, timing and completeness of revascularization should be decided according to the functional relevance of stenoses, age, general patient condition, comorbidities, and left ventricular function.(8) MINOCAMyocardial infarction with non-obstructive coronary arteries incorporates a heterogeneous group of underlying causes that may involve both coronary and non-coronary pathological conditions. Cardiac magnetic resonance imaging is one of the key diagnostic tools as it allows to identify the underlying cause in the majority of patients.(9) Post-treatment antiplatelet therapyDual antiplatelet therapy consisting of a potent P2Y12 receptor inhibitor in addition to aspirin is generally recommended for 12 months unless there are contraindications.

Dual antiplatelet therapy duration can be shortened (<12 months), extended (>12 months), or modified by switching DAPT or de-escalation depending on individual clinical judgement driven by ischaemic and bleeding risk.(10) Triple antithrombotic therapyNon-vitamin K oral anticoagulants (NOACs) are preferred over vitamin K antagonists in patients undergoing PCI with an indication for long-term oral anticoagulation. Dual antithrombotic therapy with a NOAC and single antiplatelet therapy is recommended as the default strategy up to 12 months after a short period of up to 1 week of TAT. Triple antithrombotic therapy may be prolonged up to 1 month when the ischaemic risk outweighs the bleeding risk..

€‚For the podcast associated with this article, please visit http://geolistening.com/levitra-cialis-online/ https://academic.oup.com/eurheartj/pages/Podcasts.This issue begins with the Special Article ‘An EAPCI Expert Consensus Document symbicort prices walmart on Ischaemia with Non-Obstructive Coronary Arteries in Collaboration with European Society of Cardiology Working Group on Coronary Pathophysiology &. Microcirculation Endorsed by Coronary Vasomotor Disorders International Study Group’ by Vijay Kunadian from Newcastle University in the UK, and colleagues.1 While for many years our attention has been focused on coronary stenoses, growing evidence suggests that functional alterations of the coronary circulation play an important role in all clinical manifestations of ischaemic heart disease.2,3 The current contribution is an expert consensus document on ischaemia with non-obstructive coronary arteries (INOCA). Angina pectoris affects symbicort prices walmart ∼112 million people globally.

Up to 70% of patients undergoing invasive angiography do not have obstructive coronary artery disease, more common in women than in men, and a large proportion have INOCA as a cause of their symptoms. INOCA patients symbicort prices walmart present with a wide spectrum of symptoms and signs that are often misdiagnosed as non-cardiac, leading to underdiagnosis/investigation and undertreatment. INOCA can result from several mechanism including coronary vasospasm and microvascular dysfunction, and is not a benign condition.

Compared with asymptomatic individuals, INOCA is associated with increased incidence of cardiovascular events, repeated hospital admissions, as well as impaired quality of life and associated increased healthcare costs. This document provides a definition of INOCA and guidance to the community on the diagnostic approach and management of INOCA based on existing evidence from research and best available clinical practice, noting gaps in knowledge and symbicort prices walmart potential areas for investigation.This issue then continues with a focus on acute coronary syndromes (ACS) which represent the most dramatic presentation of ischaemic heart disease. The abrupt clinical presentation of ACS gives a strong signal of discontinuity in the natural history of atherothrombosis.4,5 While experimental models of atherogenesis have provided a growing body of information about molecular mechanisms of plaque growth, the transition from coronary stability to instability is less well understood.

This issue provides novel important information in this fascinating area symbicort prices walmart of cardiovascular medicine.6In a clinical research manuscript entitled ‘Long-term beta-blocker therapy and clinical outcomes after acute myocardial infarction in patients without heart failure. Nationwide cohort study’, Jihoon Kim from the University School of Medicine in Seoul, South Korea and colleagues investigate the association between long-term beta-blocker therapy and clinical outcomes in patients without heart failure (HF) after acute myocardial infarction (MI).7 Between 2010 and 2015, a total of 28 970 patients who underwent coronary revascularization for acute MI with beta-blocker prescription at hospital discharge, and were event-free from death, recurrent MI, or HF for 1 year were enrolled from Korean nationwide medical insurance data. The primary outcome was all-cause death.

The secondary outcome was a composite symbicort prices walmart of all-cause death, recurrent MI, or hospitalization for new HF. Outcomes were compared between beta-blocker therapy for ≥1 year (n = 22707) and beta-blocker therapy for <1 year (n = 6263) using landmark analysis at 1 year after the index MI. Compared with patients receiving beta-blocker therapy for <1 year, those receiving beta-blocker therapy for ≥1 symbicort prices walmart year had a significant 19% lower risk of all-cause death and a significant 18% lower risk of the composite of all-cause death, recurrent MI, or hospitalization for new HF.

The lower risk of all-cause death associated with persistent beta-blocker therapy was observed beyond 2 years but not beyond 3 years after MI (Figure 1). Figure 1Cumulative incidences of clinical outcomes since 1 year after myocardial infarction. (A) All-cause death, (B) recurrent MI, (C) hospitalization for new heart failure, symbicort prices walmart and (D) a composite of all-cause death, recurrent MI, or hospitalization for new heart failure.

MI, myocardial infarction (from Kim J, Kang D, Park H, Kang M, Park TK, Lee JM, Yang JH, Song JB, Choi J-H, Choi S-H, Gwon H-C, Guallar E, Cho J, Hahn J-Y. Long-term β-blocker symbicort prices walmart therapy and clinical outcomes after acute myocardial infarction in patients without heart failure. Nationwide cohort study.

See pages 3521–3529).Figure 1Cumulative incidences of clinical outcomes since 1 year after myocardial infarction. (A) All-cause death, (B) recurrent MI, (C) hospitalization for new heart failure, and symbicort prices walmart (D) a composite of all-cause death, recurrent MI, or hospitalization for new heart failure. MI, myocardial infarction (from Kim J, Kang D, Park H, Kang M, Park TK, Lee JM, Yang JH, Song JB, Choi J-H, Choi S-H, Gwon H-C, Guallar E, Cho J, Hahn J-Y.

Long-term β-blocker therapy and clinical outcomes after acute myocardial infarction in patients without symbicort prices walmart heart failure. Nationwide cohort study. See pages 3521–3529).The authors conclude that in this nationwide cohort, beta-blocker therapy for ≥1 year after MI was associated with reduced all-cause death among patients with acute MI without HF.

The manuscript is accompanied by an Editorial by Rafael Harari and Sripal Bangalore from the New York symbicort prices walmart University School of Medicine in the USA, who conclude that a drug that has been widely used clinically for over half a century is now in urgent need of reappraisal from contemporary trials.8In a clinical research article entitled ‘Ticagrelor alone versus ticagrelor plus aspirin following percutaneous coronary intervention in patients with non-ST-segment elevation acute coronary syndromes. TWILIGHT-ACS’, Roxana Mehran from Mount Sinai School of Medicine in New York, USA and colleagues determined the effect of ticagrelor monotherapy on clinically relevant bleeding and major ischaemic events in relation to clinical presentation with and without non-ST elevation acute coronary syndromes (NSTE-ACS) among patients undergoing percutaneous coronary intervention (PCI) with drug-eluting stents (DES).9 The authors conducted a pre-specified subgroup analysis of The Ticagrelor With Aspirin or Alone in High-Risk Patients After Coronary Intervention (TWILIGHT) trial, which enrolled 9006 patients with high-risk features undergoing PCI with DES. After 3 months of dual antiplatelet therapy (DAPT) with ticagrelor plus aspirin, symbicort prices walmart 7119 adherent and event-free patients were randomized in a double-blind manner to ticagrelor plus placebo vs.

Ticagrelor plus aspirin for 12 months. The primary outcome was Bleeding Academic Research Consortium (BARC) type 2, 3, or 5 bleeding, while the composite of all-cause death, MI, or stroke was the key secondary outcome. Ticagrelor monotherapy significantly reduced BARC 2, 3, or 5 bleeding by a significant 54% symbicort prices walmart among NSTE-ACS patients and by a non-significant 24% among stable patients (P for interaction 0.03).

Rates of all-cause death, MI, or stroke were similar between treatment arms irrespective of clinical presentation.Mehran et al. Conclude that among patients with or without NSTE-ACS who have completed an initial 3-month course of DAPT following PCI with DES, ticagrelor monotherapy reduced clinically meaningful bleeding events without increasing ischaemic risk as compared symbicort prices walmart with ticagrelor plus aspirin. The benefits of ticagrelor monotherapy with respect to bleeding events were more pronounced in patients with NSTE-ACS.

This manuscript is accompanied by an Editorial by Robert Storey from the University of Sheffield in the UK10 who wonders if one should switch from ticagrelor monotherapy to aspirin monotherapy at 12 months or continue ticagrelor monotherapy long term, and suggests that that part of the journey remains largely unexplored. Figure 2In total, 150 patients were included into the prospective translational OPTICO-ACS study (A) and the culprit lesions were characterized by OCT as well as by local and symbicort prices walmart systematic immunophenotyping. Culprit lesion assessment revealed differential immunological signature with an enrichment in T-lymphocytes, both CD4+ and CD8+ T-cell subpopulations (B) as well as increased T-cell effector molecules at the culprit site distinguishing acute coronary syndromes with intact fibrous cap from ruptured fibrous cap-acute coronary syndrome.

Since acute coronary syndromes with intact fibrous cap-lesion were often located at bifurcations, endothelial symbicort prices walmart cells were subjected to culture in disturbed laminar flow conditions (C), i.e. To simulate coronary flow near a bifurcation, demonstrated an enhanced adhesion of CD8+ T cells. Finally, both CD8+ T cells and their cytotoxic effector molecules caused endothelial cell death, a key pathophysiological mechanism in acute coronary syndromes with intact fibrous cap (from Leistner DM, Kränkel N, Meteva D, Abdelwahed YS, Seppelt C, Stähli BE, Rai H, Skurk C, Lauten A, Mochmann H-C, Fröhlich G, Rauch-Kröhnert U, Flores E, Riedel M, Sieronski L, Kia S, Strässler E, Haghikia A, Dirks F, Steiner JK, Mueller DN, Volk H-D, Klotsche J, Joner M, Libby P, Landmesser U.

Differential immunological signature at the culprit site distinguishes acute coronary syndrome with intact from acute coronary syndrome symbicort prices walmart with ruptured fibrous cap. Results from the prospective translational OPTICO-ACS study. See pages 3549–3560).Figure 2In total, 150 patients symbicort prices walmart were included into the prospective translational OPTICO-ACS study (A) and the culprit lesions were characterized by OCT as well as by local and systematic immunophenotyping.

Culprit lesion assessment revealed differential immunological signature with an enrichment in T-lymphocytes, both CD4+ and CD8+ T-cell subpopulations (B) as well as increased T-cell effector molecules at the culprit site distinguishing acute coronary syndromes with intact fibrous cap from ruptured fibrous cap-acute coronary syndrome. Since acute coronary syndromes with intact fibrous cap-lesion were often located at bifurcations, endothelial cells were symbicort prices walmart subjected to culture in disturbed laminar flow conditions (C), i.e. To simulate coronary flow near a bifurcation, demonstrated an enhanced adhesion of CD8+ T cells.

Finally, both CD8+ T cells and their cytotoxic effector molecules caused endothelial cell death, a key pathophysiological mechanism in acute coronary syndromes with intact fibrous cap (from Leistner DM, Kränkel N, Meteva D, Abdelwahed YS, Seppelt C, Stähli BE, Rai H, Skurk C, Lauten A, Mochmann H-C, Fröhlich G, Rauch-Kröhnert U, Flores E, Riedel M, Sieronski L, Kia S, Strässler E, Haghikia A, Dirks F, Steiner JK, Mueller DN, Volk H-D, Klotsche J, Joner M, Libby P, Landmesser U. Differential immunological signature at the culprit site distinguishes acute coronary syndrome with intact from acute symbicort prices walmart coronary syndrome with ruptured fibrous cap. Results from the prospective translational OPTICO-ACS study.

See pages symbicort prices walmart 3549–3560).ACS with an intact fibrous cap (IFC), i.e. Caused by coronary plaque erosion, account for approximately one-third of ACS cases. However, the underlying pathophysiological mechanisms as compared with ACS caused by a ruptured fibrous cap (RFC) remain largely undefined.11–14 In a clinical research article entitled ‘Differential immunological signature at the culprit site distinguishes acute coronary syndrome with intact from acute coronary syndrome with ruptured fibrous cap.

Results from the prospective translational OPTICO-ACS study’, David Leistner from the Charite Universitatsmedizin Berlin in Germany and colleagues compared the microenvironment of culprit symbicort prices walmart lesions (CLs) with IFC vs. Those with RFC.15 The CL of 170 consecutive ACS patients was investigated by optical coherence tomography (OCT) and simultaneous immunophenotyping by flow cytometric analysis as well as by effector molecule concentration measurements across the CL. Within the study cohort, IFC CLs caused 25% of ACS while RFC CLs caused the remaining 75%, as determined and validated by two independent symbicort prices walmart OCT core laboratories.

IFC CLs were characterized by lower lipid content, less calcification, a thicker overlying fibrous cap, and largely localized near a coronary bifurcation as compared with RFC CLs. The microenvironment of IFC CLs demonstrated selective enrichment in both CD4+ and CD8+ T lymphocytes as compared with RFC CLs. T cell-associated extracellular circulating symbicort prices walmart microvesicles were more pronounced in IFC CLs, and a significantly higher amount of CD8+ T lymphocytes was detectable in thrombi aspirated from IFC CLs as compared with RFC CLs.

Furthermore, IFC CLs showed significantly increased levels of the T-cell effector molecules granzyme A (+22%), perforin (+59%), and granulysin (+75%) as compared with RFC CLs. Endothelial cells subjected to culture in disturbed laminar flow conditions to simulate coronary symbicort prices walmart flow near a bifurcation demonstrated an enhanced adhesion of CD8+ T cells. Finally, both CD8+ T cells and their cytotoxic effector molecules caused endothelial cell death, a key potential pathophysiological mechanism in IFC CLs.Thus, the OPTICO-ACS study emphasizes a novel mechanism in the pathogenesis of IFC CLs, favouring participation of the adaptive immune system, particularly CD8+ T cells and their effector molecules.

The manuscript is accompanied by an Editorial by Giovanna Liuzzo and colleagues (myself included) from the Catholic University16 who conclude that we are learning a lot about plaque erosion but we should not forget the words of Winston Churchill. €˜Now this symbicort prices walmart is not the end. It is not even the beginning of the end.

But it is, perhaps, the end of the beginning.’Balance between inflammatory and reparative leucocytes allows optimal healing after MI.17 In a clinical research article ‘Molecular imaging-guided repair after acute myocardial infarction by targeting the chemokine receptor symbicort prices walmart CXCR4’, Annika Hess from the Hannover Medical School in Germany and colleagues aimed to characterize infarct chemokine CXC receptor 4 (CXCR4) expression using positron emission tomography (PET) and establish its relationship to cardiac outcome. The authors tested whether image-guided early CXCR4-directed therapy attenuates chronic dysfunction.18 A total of 180 mice underwent coronary ligation or sham surgery and serial PET imaging over 7 days. Infarct CXCR4 content was significantly higher over 3 days after MI compared with sham, confirmed by flow cytometry and histopathology.

Mice that died of left ventricular (LV) rupture exhibited persistent inflammation at 3 days compared with survivors symbicort prices walmart. Higher CXCR4 signal at 1 and 3 days independently predicted significantly worse functional outcome at 6 weeks assessed by cardiac magnetic resonance. Following the imaging time-course, mice were treated with AMD3100, a CXCR4 symbicort prices walmart blocker.

CXCR4 blockade at 3 days significantly lowered LV rupture incidence vs. Untreated MI (8% vs. 25%), and significantly improved symbicort prices walmart contractile function at 6 weeks.

CXCR4 blockade at 7 days failed to improve the outcome. Flow cytometry analysis revealed lower LV neutrophil and Ly6C high monocyte content after CXCR4 blockade at symbicort prices walmart 3 days. A total of 50 patients underwent CXCR4 PET imaging and functional assessment early after MI.

CXCR4 expression correlated with contractile function.Hess and colleagues conclude that PET imaging identifies early CXCR4 up-regulation which predicts acute rupture and chronic contractile dysfunction. Imaging-guided CXCR4 inhibition accelerates inflammatory resolution symbicort prices walmart and improves outcome. This supports a molecular imaging-based theranostic approach to guide therapy after MI.

The manuscript is accompanied by an Editorial by Christian Weber from the Ludwig-Maximilians-Universität in Munich, Germany and colleagues.19 The authors point out symbicort prices walmart that the study of Hess et al. Building on the virtues of molecular PET imaging for non-invasive analysis of biomarker expression within injured tissue, in a pre-clinical as well as in a clinical setting, demonstrates the value of CXCR4 PET imaging in identifying the best time point of anti-inflammatory treatment by CXCR4 antagonism with respect to chronic cardiac function.In a clinical review article entitled ‘Management of non-culprit coronary plaques in patients with acute coronary syndrome’, Rocco Montone from the Fondazione Policlinico Universitario A. Gemelli IRCCS in Rome, Italy, and colleagues (including myself) note that ∼50% of patients with ST-segment elevation myocardial infarction (STEMI) have multivessel coronary artery disease, a condition associated with an increased incidence of recurrent ischaemic events and higher mortality.20,21 Based on recent evidence, a strategy of staged PCI of obstructive non-culprit lesions should be considered the gold standard for the management of these patients.22 However, several issues remain unresolved.

Indeed, what the optimal timing of staged PCI is has not been symbicort prices walmart completely defined. Moreover, assessment of intermediate non-culprit lesions still represents a clinical conundrum, as pressure-wire indexes do not seem able to correctly identify those patients in whom deferral is safe. Intracoronary imaging may help to identify untreated symbicort prices walmart non-culprit lesions containing vulnerable plaques that may portend a higher risk of future cardiovascular events.

However, there are hitherto no studies demonstrating that preventive PCI of vulnerable plaques or more intensive pharmacological treatment is associated with an improved clinical outcome. In this review, the authors discuss the recent evolving concepts about management of non-culprit plaques in STEMI patients, proposing a diagnostic and therapeutic algorithm to guide physicians in clinical practice. They also underscore the several knowledge gaps which need to be addressed in future studies.This issue symbicort prices walmart is also complemented by two Discussion Forum contributions.

In a contribution entitled ‘Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest in relation to organ donation’, Stefan Roest from the Erasmus MC in Amsterdam, the Netherlands and colleagues comment on the recent publication entitled ‘Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest. A registry study’ by Wulfran Bougouin from the Paris symbicort prices walmart Cardiovascular Research Center (PARCC) in France, and his colleagues the Sudden Death Expertise Center investigators.23,24 Bougouin et al. Respond in a separate comment.25The editors hope that readers of this issue of the European Heart Journal will find it of interest.With thanks to Amelia Meier-Batschelet, Johanna Hugger, and Martin Meyer for help with compilation of this article.

References1Kunadian V, Chieffo A, Camici PG, Berry C, Escaned symbicort prices walmart J, Maas A, Prescott E, Karam N, Appelman Y, Fraccaro C, Louise Buchanan G, Manzo-Silberman S, Al-Lamee R, Regar E, Lansky A, Abbott JD, Badimon L, Duncker DJ, Mehran R, Capodanno D, Baumbach A. An EAPCI Expert Consensus Document on Ischaemia with Non-Obstructive Coronary Arteries in Collaboration with European Society of Cardiology Working Group on Coronary Pathophysiology &. Microcirculation Endorsed by Coronary Vasomotor Disorders International Study Group.

Eur Heart J 2020;41:3504–3520.2Crea F, Camici PG, Bairey Merz CN symbicort prices walmart. Coronary microvascular dysfunction. An update symbicort prices walmart.

Eur Heart J 2014;35:1101–1111.3Berry C, Duncker D, Guzik T. Coronary microvascular dysfunction in Cardiovascular Research. Time to turn symbicort prices walmart on the spotlight!.

Eur Heart J 2020;41:612–613.4Lüscher TF. Improving outcomes after acute symbicort prices walmart coronary events. What works and what doesn’t.

Eur Heart J 2018;39:2691–2694.5Crea F, Liuzzo G. Anti-inflammatory treatment symbicort prices walmart of acute coronary syndromes. The need for precision medicine.

Eur Heart J symbicort prices walmart 2016;37:2414–2416.6Collet JP, Thiele H, Barbato E, Barthélémy O, Bauersachs J, Bhatt DL, Dendale P, Dorobantu M, Edvardsen T, Folliguet T, Gale CP, Gilard M, Jobs A, Jüni P, Lambrinou E, Lewis BS, Mehilli J, Meliga E, Merkely B, Mueller C, Roffi M, Rutten FH, Sibbing D, Siontis GCM. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J 2020;doi:10.1093/eurheartj/ehaa575.7Kim J, Kang D, Park H, Kang M, Park TK, Lee JM, Yang JH, Song YB, Choi JH, Choi SH, Gwon HC, Guallar E, Cho J, Hahn JY.

Long-term beta-blocker therapy and clinical outcomes after acute myocardial infarction in symbicort prices walmart patients without heart failure. Nationwide cohort study. Eur Heart J 2020;41:3521–3529.8Harari R, Bangalore S symbicort prices walmart.

Beta-blockers after acute myocardial infarction. An old drug in urgent need of new evidence!. Eur Heart J 2020;41:3530–3532.9Baber U, Dangas G, Angiolillo DJ, Cohen DJ, Sharma SK, Nicolas J, Briguori C, Cha JY, Collier T, Dudek D, Džavik V, Escaned J, Gil R, Gurbel P, Hamm CW, Henry T, Huber K, Kastrati A, Kaul U, Kornowski R, Krucoff M, Kunadian V, Marx SO, Mehta SR, Moliterno D, Ohman EM, Oldroyd K, symbicort prices walmart Sardella G, Sartori S, Shlofmitz R, Steg PG, Weisz G, Witzenbichler B, Han Y-L, Pocock S, Gibson CM, Mehran R.

Ticagrelor alone versus ticagrelor plus aspirin following percutaneous coronary intervention in patients with non-ST-segment elevation acute coronary syndromes. TWILIGHT-ACS. Eur Heart J 2020;41:3533–3545.10Storey RF.

The long journey of individualizing antiplatelet therapy after acute coronary syndromes. Eur Heart J 2020;41:3546–3548.11Partida RA, Libby P, Crea F, Jang IK. Plaque erosion.

A new in vivo diagnosis and a potential major shift in the management of patients with acute coronary syndromes. Eur Heart J 2018;39:2070–2076.12Jia H, Dai J, Hou J, Xing L, Ma L, Liu H, Xu M, Yao Y, Hu S, Yamamoto E, Lee H, Zhang S, Yu B, Jang IK. Effective anti-thrombotic therapy without stenting.

Intravascular optical coherence tomography-based management in plaque erosion (the EROSION study). Eur Heart J 2017;38:792–800.13Libby P. Superficial erosion and the precision management of acute coronary syndromes.

Not one-size-fits-all. Eur Heart J 2017;38:801–803.14Quillard T, Araújo HA, Franck G, Shvartz E, Sukhova G, Libby P. TLR2 and neutrophils potentiate endothelial stress, apoptosis and detachment.

Implications for superficial erosion. Eur Heart J 2015;36:1394–404.15Leistner DM, Kränkel N, Meteva D, Abdelwahed YS, Seppelt C, Stähli, Rai H, Skurk C, Lauten A, Mochmann HC, Fröhlich G, Rauch-Kröhnert U, Flores E, Riedel M, Sieronski L, Kia S, Strässler E, Haghikia A, Dirks F, Steiner J, Mueller DN, Volk HD, Klotsche J, Joner M, Libby P, Landmesser U. Differential immunological signature at the culprit site distinguishes acute coronary syndrome with intact from acute coronary syndrome with ruptured fibrous cap.

Results from the prospective translational OPTICO-ACS study. Eur Heart J 2020;41:3549–3560.16Liuzzo G, Pedicino D, Vinci R, Crea F. CD8 lymphocytes and plaque erosion.

A new piece in the jigsaw. Eur Heart J 2020;41:3561–3563.17Montecucco F, Carbone F, Schindler TH. Pathophysiology of ST-segment elevation myocardial infarction.

Novel mechanisms and treatments. Eur Heart J 2016;37:1268–1283.18Hess A, Derlin T, Koenig T, Diekmann J, Wittneben A, Wang Y, Wester HJ, Ross TL, Wollert KC, Bauersachs J, Bengel FM, Thackeray JT. Molecular imaging-guided repair after acute myocardial infarction by targeting the chemokine receptor CXCR4.

Eur Heart J 2020;41:3564–3575.19Döring Y, Noels H, van der Vorst E, Weber C. Seeing is repairing. How imaging-based timely interference with CXCR4 could improve repair after myocardial infarction.

Eur Heart J 2020;41:3576–3578.20Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, Caforio ALP, Crea F, Goudevenos JA, Halvorsen S, Hindricks G, Kastrati A, Lenzen MJ, Prescott E, Roffi M, Valgimigli M, Varenhorst C, Vranckx P, Widimský P. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC).

Eur Heart J 2018;39:119–177.21Montone RA, Niccoli G, Crea F, Jang IK. Management of non-culprit coronary plaques in patients with acute coronary syndrome. Eur Heart J 2020;41:3579–3586.22Pavasini R, Biscaglia S, Barbato E, Tebaldi M, Dudek D, Escaned J, Casella G, Santarelli A, Guiducci V, Gutierrez-Ibanes E, Di Pasquale G, Politi L, Saglietto A, D’Ascenzo F, Campo G.

Complete revascularization reduces cardiovascular death in patients with ST-segment elevation myocardial infarction and multivessel disease. Systematic review and meta-analysis of randomized clinical trials. Eur Heart J 2019;doi:10.1093/eurheartj/ehz896.23Roest S, Bunge JJH, Manintveld OC.

Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest in relation to organ donation. Eur Heart J 2020;41:3587.24Bougouin W, Dumas F, Lamhaut L, Marijon E, Carli P, Combes A, Pirracchio R, Aissaoui N, Karam N, Deye N, Sideris G, Beganton F, Jost D, Cariou A, Jouven X. Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest.

A registry study. Eur Heart J 2020;41:1961–1971.25Bougouin W, Cariou A, Jouven X. Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest.

Do not neglect potential for organ donation!. Eur Heart J 2020;41:3588. Published on behalf of the European Society of Cardiology.

All rights reserved. © The Author(s) 2020. For permissions, please email.

Journals.permissions@oup.com.The Ten ‘Commandments’(1) DiagnosisChest discomfort without persistent ST-segment elevation (NSTE-ACS) is the leading symptom initiating the diagnostic and therapeutic cascade. The correlated pathology at the myocardial level is cardiomyocyte necrosis, measured by troponin release, or, less frequently, myocardial ischaemia without cell damage (unstable angina).(2) Troponin assaysHigh-sensitivity troponin assay (hs-cTn) measurements are recommended over less sensitive ones. However, many cardiac pathologies other than MI may also result in cardiac troponin elevations.(3) Rapid ‘rule-in’ and ‘rule-out’ algorithmsIt is recommended to use the 0 h/1 h algorithm (best option) or the 0 h/2 h algorithm.

Used in conjunction with clinical and ECG findings, the 0 h/1 h and 0 h/2 h hs-cTn algorithms allow identification of appropriate candidates for early discharge and outpatient management.(4) Ischaemic/bleeding risk assessmentInitial hs-cTn levels add prognostic information in terms of short- and long-term mortality to clinical and ECG variables. The Global Registry of Acute Coronary Events (GRACE) risk score is superior to (subjective) physician assessment for the occurrence of death or MI. The Academic Research Consortium-High Bleeding Risk may be used to assess the bleeding risk.(5) Non-invasive imagingEven after the rule-out of MI, elective non-invasive or invasive imaging may be indicated according to clinical assessment.

Coronary computed tomography angiography or stress imaging may be options based on risk assessment.(6) Risk stratification for an invasive approachAn early routine invasive approach within 24 h of admission is recommended for Non ST segment elevation myocardial infarction (NSTEMI) based on hs-cTn measurements, GRACE risk score >140, and dynamic new or presumably new ST-segment changes. Immediate invasive angiography is required in highly unstable patients according to hemodynamic status, arrhythmias, acute heart failure, or persistent chest pain. In all other clinical presentations, a selective invasive approach may be performed according to non-invasive testing or clinical risk assessment.(7) Revascularization strategiesRadial access is recommended as the preferred approach in NSTE-ACS patients undergoing invasive assessment.

Percutaneous coronary intervention of the culprit lesion is the treatment of choice. In multivessel disease, timing and completeness of revascularization should be decided according to the functional relevance of stenoses, age, general patient condition, comorbidities, and left ventricular function.(8) MINOCAMyocardial infarction with non-obstructive coronary arteries incorporates a heterogeneous group of underlying causes that may involve both coronary and non-coronary pathological conditions. Cardiac magnetic resonance imaging is one of the key diagnostic tools as it allows to identify the underlying cause in the majority of patients.(9) Post-treatment antiplatelet therapyDual antiplatelet therapy consisting of a potent P2Y12 receptor inhibitor in addition to aspirin is generally recommended for 12 months unless there are contraindications.

Dual antiplatelet therapy duration can be shortened (<12 months), extended (>12 months), or modified by switching DAPT or de-escalation depending on individual clinical judgement driven by ischaemic and bleeding risk.(10) Triple antithrombotic therapyNon-vitamin K oral anticoagulants (NOACs) are preferred over vitamin K antagonists in patients undergoing PCI with an indication for long-term oral anticoagulation. Dual antithrombotic therapy with a NOAC and single antiplatelet therapy is recommended as the default strategy up to 12 months after a short period of up to 1 week of TAT. Triple antithrombotic therapy may be prolonged up to 1 month when the ischaemic risk outweighs the bleeding risk..