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How to cite this amoxil dosage for dogs article:Singh Can you buy zithromax over the counter O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized events in our amoxil dosage for dogs 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 amoxil dosage for dogs full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor.

All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast amoxil dosage for dogs 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 amoxil dosage for dogs started getting distress calls from their patients in despair with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has amoxil dosage for dogs 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 amoxil dosage for dogs the person's mental condition and illness and also his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking amoxil dosage for dogs for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident.

Many psychiatrists and mental health professionals were called by media houses to comment on the episode amoxil dosage for dogs. 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, amoxil dosage for dogs 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 amoxil dosage for dogs 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 amoxil dosage for dogs 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 amoxil dosage for dogs 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, amoxil dosage for dogs 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. However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J.

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

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

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

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

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

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

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

Oxford, England. New York. Oxford University Press.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

How to amoxil best buy cite this article:Singh O you could check here P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is amoxil best buy 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, amoxil best buy the media went into a frenzy as newspapers, news channels, and social media were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor.

All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private and personal details were freely amoxil best buy 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 amoxil best buy their patients in despair with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of amoxil best buy 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 amoxil best buy 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 amoxil best buy to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident.

Many psychiatrists and mental health professionals amoxil best buy were called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so. There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist.

These types of viewpoints perpetuate stigma, myths, amoxil best buy 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 amoxil best buy 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 amoxil best buy have guidelines and resource books for interacting with media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion.

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

O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, amoxil best buy Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Oxford, England. New York. Oxford University Press.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Late-stage studies of AstraZeneca's buy antibiotics treatment candidate are on temporary hold while the company investigates whether a patient suffered a serious side effect or if the where can i get amoxil illness had nothing to do with the shot.In a statement issued Tuesday evening, the company said its "standard review process triggered a pause to vaccination to allow review of safety data."AstraZeneca didn't reveal any information about the possible side effect except to call it "a potentially unexplained illness." The health news site STAT first reported the pause in who can buy amoxil online testing, saying the possible side effect occurred in the United Kingdom.An AstraZeneca spokesperson confirmed the pause in vaccinations covers studies in the U.S. And other where can i get amoxil countries. Late last month, AstraZeneca began recruiting 30,000 people where can i get amoxil in the U.S. For its where can i get amoxil largest study of the treatment.

It also is testing the treatment, developed by Oxford University, in thousands of people in Britain, and in smaller studies in Brazil and South Africa.Two other treatments are in huge, final-stage tests in the United States, one made by Moderna Inc. And the other by Pfizer and where can i get amoxil Germany's BioNTech. Those two treatments work differently than AstraZeneca's, and the studies already have recruited about two-thirds of where can i get amoxil the needed volunteers.Temporary holds of large medical studies aren't unusual, and investigating any serious or unexpected reaction is a mandatory part of safety testing. AstraZeneca pointed out that it's possible the problem could be a where can i get amoxil coincidence.

Illnesses of all sorts could arise in studies of thousands of people."We are working to expedite the review of the single event to minimize any potential impact on the trial timeline," the where can i get amoxil company statement said.Dr. Ashish Jha of Brown University said via Twitter that the significance of the interruption was unclear but that he was "still optimistic" that an effective treatment will be found in the coming months."But optimism isn't evidence," he wrote. "Let's let science drive this process."During the third and final stage of testing, where can i get amoxil researchers look for any signs of possible side effects that may have gone undetected in earlier patient research. Because of their large size, the studies are considered the most important phase of study for picking less common side effects and establishing safety.The trials also assess effectiveness by tracking who gets sick and who doesn't between patients getting the treatment and those receiving a dummy shot.The development came the same day that AstraZeneca and where can i get amoxil eight other drugmakers issued an unusual pledge, vowing to uphold the highest ethical and scientific standards in developing their treatments.The announcement follows worries that President Donald Trump will pressure the U.S.

Food and Drug Administration to approve a treatment before it's proven to be safe and where can i get amoxil effective.The U.S. Has invested billions of dollars in efforts to quickly develop multiple treatments against where can i get amoxil buy antibiotics. But public fears that a treatment is unsafe or ineffective could be disastrous, derailing the effort to vaccinate millions of Americans.Representatives for the FDA did not immediately respond to requests for comment Tuesday evening.AstraZeneca's U.S.-traded shares fell more than 6% in after-hours trading following reports of the trial being paused..

Late-stage studies of AstraZeneca's buy antibiotics treatment candidate are on temporary hold while the company investigates whether a patient suffered a serious side effect or if the illness had nothing to do with the shot.In a statement issued Tuesday evening, the company said its "standard review process triggered a pause to vaccination to allow review of safety data."AstraZeneca didn't reveal any information about the possible side effect can you buy amoxil online except to call it "a potentially unexplained illness." The health news site STAT first reported the pause in testing, saying the possible side amoxil best buy effect occurred in the United Kingdom.An AstraZeneca spokesperson confirmed the pause in vaccinations covers studies in the U.S. And other amoxil best buy countries. Late last month, AstraZeneca began recruiting 30,000 amoxil best buy people in the U.S. For its largest study of the treatment amoxil best buy. It also is testing the treatment, developed by Oxford University, in thousands of people in Britain, and in smaller studies in Brazil and South Africa.Two other treatments are in huge, final-stage tests in the United States, one made by Moderna Inc.

And the other amoxil best buy by Pfizer and Germany's BioNTech. Those two treatments work amoxil best buy differently than AstraZeneca's, and the studies already have recruited about two-thirds of the needed volunteers.Temporary holds of large medical studies aren't unusual, and investigating any serious or unexpected reaction is a mandatory part of safety testing. AstraZeneca pointed out that it's possible the problem could be amoxil best buy a coincidence. Illnesses of all sorts could arise in studies of thousands of people."We are working to expedite the review of the single event amoxil best buy to minimize any potential impact on the trial timeline," the company statement said.Dr. Ashish Jha of Brown University said via Twitter that the significance of the interruption was unclear but that he was "still optimistic" that an effective treatment will be found in the coming months."But optimism isn't evidence," he wrote.

"Let's let science drive this process."During the third and final stage of testing, researchers look for any signs of amoxil best buy possible side effects that may have gone undetected in earlier patient research. Because of their large size, the studies are considered the most important phase of study for picking less common side effects and establishing safety.The trials also assess effectiveness by tracking who gets sick and who doesn't between patients getting the treatment and those receiving a dummy shot.The amoxil best buy development came the same day that AstraZeneca and eight other drugmakers issued an unusual pledge, vowing to uphold the highest ethical and scientific standards in developing their treatments.The announcement follows worries that President Donald Trump will pressure the U.S. Food and Drug Administration to approve a treatment before it's proven amoxil best buy to be safe and effective.The U.S. Has invested amoxil best buy billions of dollars in efforts to quickly develop multiple treatments against buy antibiotics. But public fears that a treatment is unsafe or ineffective could be disastrous, derailing the effort to vaccinate millions of Americans.Representatives for the FDA did not immediately respond to requests for comment Tuesday evening.AstraZeneca's U.S.-traded shares fell more than 6% in after-hours trading following reports of the trial being paused..

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IntroductionEarly warning http://bobmackin.ca/?p=453 or ‘track-and-trigger’ scores (EWSs) are used to identify the deteriorating patient and reduce unwarranted variation in the incidence of adverse events.1 They were developed to enable timely escalation of sick patients to medical staff and where to get amoxil pills are used in everyday clinical practice to guide changes in clinical management, admission to intensive care units (ICUs) and initiation of end-of-life care. Early track-and-trigger scores were based on aggregate vital signs. Many have been externally validated in hospital and prehospital settings where to get amoxil pills as predictors of ICU admission and survival for sepsis,2 exacerbations of chronic obstructive pulmonary disease3 and trauma.4 Machine learning and the rollout of integrated electronic health records have accelerated the development of sophisticated EWSs incorporating blood test and imaging results. These scores may provide ‘real-time’ information about ongoing clinical deterioration or a more rounded overall assessment of prognosis.

Some of these tools may improve outcomes in patients with life-threatening pathology,5 but others are methodologically flawed and may have no or even adverse effects on patient care.1EWSs lose their salience when they fail to identify deteriorating patients and when staffing and resource limitations in overstretched healthcare where to get amoxil pills systems prevent clinicians from taking timely action. The buy antibiotics amoxil has placed immense pressure on health systems across the world, and adults with buy antibiotics may deteriorate rapidly and unexpectedly.6 There is widespread concern that existing EWSs may underestimate illness severity in patients with buy antibiotics, providing clinicians with false reassurance and thus delaying treatment escalation.7 8 Several groups have therefore sought to assess the utility of existing track-and-trigger scores and develop and validate novel tools for adults with buy antibiotics. This article will outline the pitfalls of existing EWSs for adult patients with buy antibiotics, highlight key findings from studies of novel EWSs for buy antibiotics and discuss the ideal properties of where to get amoxil pills a track-and-trigger score for buy antibiotics suitable for use around the world.What are EWSs and why are they useful in healthcare settings?. The first EWS emerged in the late 1990s.

Early versions assigned numerical values to different vital signs, and other factors such as clinical intuition, with aggregate scores triggering escalation to medical staff where to get amoxil pills. They were designed primarily to reduce the incidence of avoidable in-hospital cardiac arrests in ward settings by enabling timely transfer of sick patients to ICU. Scores were where to get amoxil pills developed with poor methodological rigour and in a haphazard fashion with local and regional variations, until regulatory bodies and professional organisations pressed for and developed standardised tools. For example, in the UK, the Royal College of Physicians developed the National Early Warning Score (NEWS), which was launched in 2012 and soon became mandatory in National Health Service hospitals.9 To reflect differences in physiological norms, distinct EWSs have been developed for adult, paediatric and obstetric populations.

In recent years, novel or adapted scores have focused on different outcomes, such as cause-specific or all-cause mortality, and have been designed for use in different settings (such as the emergency department (ED) and in primary and where to get amoxil pills prehospital care).There is some evidence that implementation of EWSs improves outcomes for patients with sepsis,10 and several studies support their utility in identifying critical illness in hospital and prehospital settings.11 12 EWSs also provide a common language for ‘sickness’ and aid triage and resource allocation, particularly in a amoxil setting. Nonetheless, frontline professionals are aware of their pitfalls, particularly for those scores based on physiological parameters. Isolated values must be interpreted with regard to trajectory and placed within a clinical context—junior doctors are often informed of a patient ‘triggering’ when they have had a high score for hours or even days and already where to get amoxil pills been reviewed. EWS based on vital signs can also provide false reassurance.

Shocked patients on beta blockers may not mount a tachycardia, and patients with acute renal failure may show no respiratory, cardiovascular or neurological where to get amoxil pills compromise despite requiring urgent renal replacement therapy.What are the problems with existing EWSs in relation to buy antibiotics?. Where clinically appropriate, the deteriorating patient with buy antibiotics requires urgent clinical review to determine the need for non-invasive ventilation (NIV) or intubation and mechanical ventilation (IMV). Delays in accessing these where to get amoxil pills time-critical interventions may result in adverse outcomes. Depending on the patient’s age, comorbidities, level of frailty and the nature of their acute illness, their ceiling of care may be limited to NIV or even ward-based treatment, in which case deterioration may represent a terminal event and prompt a switch to end-of-life care.

Clinical signs of deterioration in hospitalised adults with buy antibiotics include a rising oxygen requirement, raised respiratory rate, use of accessory muscles of respiration and altered mental state.In NEWS2, the most where to get amoxil pills widely used EWS in the UK, supplemental oxygen therapy scores two points, but once a patient is on oxygen this score does not change to reflect flow rate or oxygen delivery device. Work of breathing is not included in NEWS2, though it has been used as an inclusion criterion for NIV in buy antibiotics.13 NEWS2 was developed with a focus on sepsis and therefore assigns significant value to tachycardia and hypotension. However, cardiovascular compromise is relatively uncommon in moderate to severe buy antibiotics and may indicate additional pathology such as bacterial sepsis or pulmonary embolism.14 While respiratory rate may rise as patients with buy antibiotics deteriorate, there are widespread reports of ‘happy hypoxia’ in which the typical physiological response (tachypnoea and increased work of breathing) to and subjective experience of hypoxia (dyspnoea) are absent.15 16 A recent report suggesting that pulse oximetry monitoring may underestimate the frequency of hypoxaemia in black patients is of particular concern in the context of buy antibiotics.17Development of novel early warning and prognostic scores for buy antibioticsVarious research groups have investigated whether existing scores can accurately identify where to get amoxil pills hospitalised patients with buy antibiotics who are at risk of clinical deterioration. Several studies have suggested that EWSs such as NEWS2 and the quick Sequential (Sepsis-related) Organ Failure Assessment, and prognostic tools such as CURB-65 perform poorly in cohorts of inpatients with buy antibiotics.18 19 This has spurred the development of dozens of bespoke early warning and prognostic scores for buy antibiotics through retrospective multivariable logistic regression of patient-level data.While outcomes of interest and time horizons vary, most models have combined vital signs with demographic factors, comorbidities and laboratory and imaging indices which reflect risk factors for severe disease or death.

Variables of interest have typically been identified by expert clinicians or derived from observational studies highlighting risk factors for where to get amoxil pills adverse outcomes in early buy antibiotics cohorts and for other respiratory illnesses such as bacterial pneumonia and influenza. Researchers have developed these composite scores by assigning differential weight to each variable and then evaluating the clinical sensitivity and specificity of candidate models at different thresholds for clinical deterioration. Scores favouring variables derived from the wisdom of frontline clinicians may be more tractable in clinical where to get amoxil pills settings but may lack the discriminative power offered by data-driven scores based on statistical analysis of routinely collected patient-level data. Several groups have sought to balance these tensions by asking panels of clinicians to review the relevance of candidate variables identified by statistical analyses.The trade-off between each model’s sensitivity and specificity can be represented by receiver operator characteristics (ROCs), which can be displayed graphically.

By quantifying the ‘area under the ROC curve’ (AUROC) for where to get amoxil pills new and existing models, it is possible to compare their performance. For existing and novel scores evaluated in buy antibiotics cohorts, this could mean discrimination between stable and deteriorating hospitalised patients—where deterioration is defined by the subsequent need for IMV or ICU level care—or patients at high or low risk of mortality at first presentation to the ED. AUROC values always where to get amoxil pills lie between 0 and 1. A value of 0.5 suggests that a model’s discrimination is no better than chance.

We would consider an AUROC value over 0.75 to represent good clinical discrimination.20As outcomes such as ICU admission and mortality are relatively rare events, models derived from small populations are at risk where to get amoxil pills of ‘overfitting’. Providing perfect results under study conditions but performing poorly in the real world. Some prognostic scores have combined where to get amoxil pills the risk of antibiotics exposure with the risk of severe buy antibiotics, despite differences in their respective risk factors. These risk prediction tools become less useful as exposures deviate from those seen in study conditions.

This is particularly relevant to the issue of ethnic group differences in hospitalisation and mortality from buy antibiotics in the UK and USA, which likely reflect differences in exposure to antibiotics and confounding factors such as deprivation rather than any genetic differences in underlying risk profiles.21Furthermore, most novel prognostic and EWSs for buy antibiotics have been developed without prospective external validation in large and diverse patient cohorts. Unsurprisingly, a systematic review of prognostic scores for buy antibiotics where to get amoxil pills suggests that most novel scores are poorly reported and likely overestimate their true predictive performance.22 This is supported by a recent single-centre external validation study, which found that NEWS2 score was a better predictor of clinical deterioration at 24 hours than 22 novel prognostic scores in a cohort of 411 hospitalised adults with buy antibiotics, with an AUROC of 0.76.23 The sole high-quality novel scores with similar performance to NEWS2 after external validation are the antibiotics Clinical Characterisation Consortium (4C) mortality (AUROC 0.78) and deterioration scores. Derived from multiethnic cohorts of over 30 000 hospitalised patients, these scores show real promise and have been widely adopted in the UK and beyond.The 4C mortality score combines patient age. Sex at where to get amoxil pills birth.

Number of comorbidities. Respiratory rate, peripheral where to get amoxil pills oxygen saturations and Glasgow Coma Scale at admission. And serum urea and C reactive protein concentrations to provide an estimate of untreated in-hospital mortality.24 Patients receive an aggregate score out of 21, with age alone providing up to 8 points. By providing an early where to get amoxil pills assessment of prognosis at the front door, the 4C score might be used to guide treatment decisions, triage and clinical disposition.

However, it is important to note that it predicts mortality rather than the need for NIV, IMV or ICU admission. As such, it may be most useful at its where to get amoxil pills extremes. Giving clinicians confidence to discharge patients with low mortality scores or prompt early conversations around treatment escalation with older patients requiring oxygen. The 4C deterioration score incorporates 11 variables and defines clinical deterioration more broadly, to encompass death, ICU admission and IMV.25 It can be used at first where to get amoxil pills presentation to ED for community-acquired buy antibiotics or immediately after identification of nosocomial disease.

This score may help to optimise resource allocation—for example, by prompting early transfer of high-risk patients to higher acuity settings—and inform discussions with patients and families to give them time to prepare for expected deterioration. Future studies should assess where to get amoxil pills reattendance rates and ICU admissions among patients discharged from ED with low 4C mortality and deterioration scores.An important drawback of both scores is that their use may be impractical in low and middle-income countries (LMICs). A recent postmortem surveillance study suggests that buy antibiotics rates may have been significantly under-reported in Africa due to poor access to testing.26 The 4C scores are only useful after a diagnosis of buy antibiotics is confirmed. However, with restricted access to antibiotics antigen tests in the community and hospital settings, where to get amoxil pills diagnosis is often made on clinical grounds alone.

It can be difficult to distinguish buy antibiotics from decompensated heart failure and bacterial pneumonia. This confers a risk of misdiagnosis and inappropriate treatment and management based on irrelevant prognostic scores.Restricted access to ancillary where to get amoxil pills diagnostic facilities may make it challenging to identify early signs of deterioration or determine prognosis in buy antibiotics even where it is possible to establish a diagnosis. In rural LMIC settings, poor access to blood tests and X-ray facilities will make it impossible to calculate the 4C scores. This serves as an urgent reminder of the importance of health systems strengthening in remote LMIC settings, but even with sustained investment and political will where to get amoxil pills it will take years to improve diagnostic capabilities and train local staff.

As such, triage tools based on vital signs alone may be more practical and reproducible in these settings. The utility of routinely where to get amoxil pills used EWSs already validated in LMICs—such as the universal vital assessment score developed in sub-Saharan Africa27—should be assessed in buy antibiotics cohorts alongside external validation of novel models like the PRIEST score developed in high-income settings.28 Simpler univariate scoring systems may also be effective. Among 411 adults admitted to a UK urban teaching hospital with buy antibiotics, admission oxygen saturation on room air alone was a strong predictor of deterioration and mortality.23 Healthcare workers and technicians could be rapidly trained to use pulse oximeters and flag patients with hypoxia to medical staff. This would also support judicious use of precious oxygen therapy.29 Unfortunately, oximeters remain scarce in countries such as Ethiopia,30 and their mass distribution in LMICs should be a priority as the amoxil evolves.Future workResearchers must reassess novel early warning and prognostic scores in light of growing population immunity to prevailing antibiotics strains through prior or vaccination, and the emergence of new variants associated with higher mortality.31 Most where to get amoxil pills prognostic scores for buy antibiotics have a short time horizon.

They use vital signs and other prognostic markers measured at an index ED attendance or inpatient admission to predict short-term outcomes such as in-hospital mortality and discharge from hospital. However, with a recent retrospective cohort study demonstrating high rates of multiorgan dysfunction and all-cause mortality in buy antibiotics survivors at 140 days after hospital discharge,32 we need to develop models capable of predicting long-term survival and adverse consequences where to get amoxil pills. Cox regression analyses, which, unlike standard ROC curve analyses, account for the time taken for an adverse event to occur,33 would be well suited to the development of these models.To date, most researchers have taken a crude approach to developing buy antibiotics scoring systems, using data from large populations of hospitalised adults assumed to be homogeneous. While evidence is mixed,34 some studies support the existence of distinct disease phenotypes, notably a hyperinflammatory subtype associated with higher risks of next-day escalation to higher level respiratory care and higher rates of ICU admission and mortality.35 We may see the emergence of novel scores for specific buy antibiotics phenotypes and must balance the tension between any where to get amoxil pills additional discriminative benefits they offer and the extra cognitive load they place on overstretched healthcare professionals.In high-income settings, technology may help to ease this cognitive load and identify high-risk patients across the hospital as close to real time as possible, to aid resource allocation.

Future studies should assess whether integration of scores into electronic health records reduces unwarranted variation in treatment escalation and disease outcomes. Scores could be calculated automatically with electronic where to get amoxil pills alerts notifying clinicians of risk and prompting guideline-based clinical management. This could be used to support safe discharge of low-risk patients from the ED and gold-standard prescribing of remdesivir, dexamethasone and tocilizumab at different points in the disease course. The introduction of similar electronic alerts designed to improve the recognition and management of sepsis at a multisite London hospital Trust has previously been shown to reduce mortality.5Future studies which describe the development and validation of novel prognostic scores for buy antibiotics must be transparent where to get amoxil pills about their intended purpose.

It is often unclear if a score is designed for routine clinical use. To inform risk stratification in interventional studies or where to get amoxil pills to separate different disease phenotypes in observational studies. Prospective external validation may confirm that a novel score reliably discriminates between stable and deteriorating patients, but if the score is difficult to use or understand, it will not be widely adopted. In the UK, one of the key characteristics of the NEWS2 score is that it provides a universal ‘language for sickness’ which is widely understood by healthcare professionals of where to get amoxil pills different stripes and seniority.

Close collaboration between clinicians and statisticians at all stages of the research process should aid the development of robust scores which are clinically relevant, easy to use and align with workflow.Risk prediction tools such as Qbuy antibiotics have also been developed for patients in the community, to identify those at high risk of acquiring and poor outcomes and inform shielding guidelines.36 While they may help clinicians and public health agencies to implement targeted risk mitigation measures, they cannot discriminate between patients who can be managed safely in the community and those who require hospital care after acquiring buy antibiotics. The prevalidation RECAP-V0 is a promising tool which could help to identify patients in a community setting with suspected or confirmed buy antibiotics who require further evaluation in secondary care settings.37 Future work must seek to determine whether this and similar scores can support more integrated care across whole healthcare systems. For example, early admission of high-risk patients identified in the community may help to avoid spikes of critically ill patients presenting to ED in where to get amoxil pills extremis and enable more equitable distribution of patients across wider hospital networks. This is particularly important in LMICs, where access to advanced respiratory support and critical care is limited.ConclusionEWSs can support timely recognition of clinical deterioration and escalation to critical care or palliation.

There are widespread concerns that existing scores such as NEWS2 may fail to identify the deteriorating patient with buy antibiotics as they place a premium on cardiovascular instability rather than respiratory where to get amoxil pills dysfunction. Several research groups have used advanced statistical techniques to develop novel early warning and prognostic scores for patients hospitalised with buy antibiotics. While many of these scores are at high risk of where to get amoxil pills bias, the 4C mortality and deterioration scores have been externally validated in high-income settings and offer useful insights which can inform clinical care. These scores might be used to optimise resource allocation, support discussions around treatment escalation and inform protocols for safe discharge.

Unfortunately, limited access to virological testing and laboratory and imaging facilities may blunt their utility where to get amoxil pills in LMICs, where physiological scores may be more practical. Future work should focus on predicting long-term outcomes in buy antibiotics, improving user experience and identifying the optimum balance between the extra discrimination afforded by novel scores and their ease of use in everyday clinical practice.Ethics statementsPatient consent for publicationNot required.‘Of or belonging to another, not one’s own, foreign, strange.’From the Latin alienus, the etymology of the word ‘alien’ signifies much of what the word connotes. A certain where to get amoxil pills unnatural and inhuman nature. Nonetheless, ever since the Alien and Sedition Acts in 1798, the dehumanising term ‘alien’ has repeatedly been used to refer to immigrants in the USA.

On his first day in office, President Biden sent Congress the US Citizenship Act of 2021, which notably sought to change the term where to get amoxil pills ‘alien’ to ‘non-citizen’ in our immigration laws. Much attention, therefore, has been given to this change and its implications within the realm of immigration, but we must also recognise the importance of similar semantic alterations within healthcare. For instance, the Affordable Care Act (ACA) repeatedly refers to ‘non-citizens’ as ‘aliens,’ and where to get amoxil pills such terminology is ubiquitous throughout health policy and the literature more broadly. Eliciting notions of segregation, the term ‘alien’ relegates important communities to a second-class status.

The buy antibiotics amoxil has exacerbated deep-rooted fissures of trust in the federal government and healthcare institutions, as demonstrated by a palpable hesitancy to receive the three authorised antibiotics treatments where to get amoxil pills among non-citizen communities.1 2 In our efforts to curb the buy antibiotics amoxil, we cannot permit our diction to further intensify bias and, in turn, alienate immigrants from vaccination.Already, non-citizens in the USA face difficulties as they endeavour to navigate our complex healthcare system. These realities manifest themselves in disproportionately low levels of health insurance among non-citizens. 77% of lawfully present immigrants where to get amoxil pills and 55% of undocumented immigrants as compared with 91% of citizens.3 While undocumented immigrants are entirely ineligible for Medicaid and ACA coverage, lawfully present immigrants are often precluded from these federal programmes because of fear, confusion and literacy challenges, as well as worries about being labelled as a ‘public charge’ (ie, receiving government benefits can make one ineligible for a green card or visa). Unfortunately, the prior administration empowered an Immigration and Customs Enforcement agency that aggressively targeted non-citizens, and, more broadly, our political climate has elevated rhetoric that voraciously maligns all immigrants.

As such, it should come to no surprise that immigrants of all documentation statuses have quietly retreated from the public sphere and the healthcare system altogether.1 Countless reports have found that non-citizens increasingly avoid scheduling doctor’s appointments and refuse to answer the door for home health visits, which may help to explain why immigrants are less likely to receive preventive care services and are more likely to suffer from chronic diseases.1 4 5 While it may be secondary where to get amoxil pills to challenges regarding access, exorbitant costs associated with care, or an unwillingness to put themselves and their families at risk,4 the health consequences are disastrous. In the context of buy antibiotics, non-citizens may avoid seeking medical advice until the last possible moment when the amoxil has already wrought immense damage on their bodies. Alienated from traditional avenues of care, non-citizens are often caught only in the fraying safety nets of urgent care clinics and emergency rooms with their severely exacerbated conditions.We have already where to get amoxil pills seen the consequences of such disparities as it relates to the amoxil. Constituting 13.7% of the US population, immigrant essential workers represent 16.3% of essential healthcare operations, 18.4% of essential retail and 20.2% of essential services, disproportionately serving as frontline personnel and sustaining countless industries on the backs of their labour.6 Whether it be this work as essential workers or high rates of poverty and other social risk factors, immigrants are at least twice as likely to be infected with buy antibiotics as native-born individuals and face significantly higher mortality rates.1 7 For instance, in the Dallas Fort-Worth Area, which sees one of the largest populations of undocumented immigrants in the nation, middle-aged Latino men are eight times more likely to die from buy antibiotics than their non-Latino white peers.2 While immigrants do not necessarily have significantly higher rates of underlying health conditions,8 various structural barriers and injustices prevent non-citizens from accessing care, contributing to these higher rates of and worse outcomes.These challenges and the resultant adverse health consequences can erode trust among non-citizens in health systems and federal institutions.

Trust is broken in wake of discrimination in clinics where to get amoxil pills. Trust is broken when non-citizens, without insurance, have to pay exorbitant sums to access healthcare. Trust is broken when trips to the hospital put one at risk of being where to get amoxil pills deported. Trust is broken when non-citizens see community members dying needlessly from buy antibiotics.

In a amoxil that has burdened immigrants in particular, subtle mental assaults through stigmatising language only where to get amoxil pills further deteriorate trust. Indeed, the term ‘alien’ implicitly removes non-citizens from the healthcare system and risks excluding them from the buy antibiotics vaccination rollout, exacerbating existing structural issues such as limited treatment availability in these communities.It is already well known that labelling individuals as ‘illegal aliens’ subjects them to more prejudice and discrimination than does the term ‘non-citizens’.9 Indeed, one study found that mental health professionals who thought about Latino immigrants as ‘undocumented immigrants’ viewed them more positively than those asked to think about Latino immigrants as ‘illegal aliens’.10 This finding should come to no surprise given that the derogatory term ‘alien’ defines someone by their immigration status rather than as a person with an immigration status. While ‘non-citizen’ does not entirely resolve the matter of people-first language, it represents a crucial step where to get amoxil pills forward and conveys greater humanity to these individuals. If we cannot purge ‘alien’ from the medical vocabulary entirely, we betray the foundational ideal of equal healthcare for all and turn a blind eye to non-citizens, who represent 14% of the US population.Certainly, President Biden’s efforts to remove ‘alien’ from our immigration laws is a long-overdue first step to mitigate bias and build trust, but we must broaden our vision towards all realms, including healthcare.

The federal government represents where to get amoxil pills the face of the buy antibiotics treatment rollout, yet non-citizens largely do not trust the government to protect them and their communities. This paucity of trust is complex and multifactorial, and revamping diction within complicated pieces of legislation may not have any immediate implications for rebuilding that faith. But the words that pervade policy—and their connotations—set the tone for how we collectively address these communities, as well as the dignity and respect they where to get amoxil pills receive. A semantic transition towards ‘non-citizens’ may ultimately beget public health messaging which comes from bilingual community leaders, assurances that vaccination is free and does not carry a deportation risk, and local efforts to make the treatment accessible to all immigrants.

These steps, in turn, may engender the political will where to get amoxil pills to combat structural barriers that non-citizens face in navigating health institutions. At the end of the day, words matter, humanity matters. During a amoxil indifferent to matters of citizenship, we must make sincere overtures to bridge access to care and deracinate stigmatising, dehumanising language from our vocabulary.Ethics statementsPatient consent for publicationNot required..

IntroductionEarly warning or ‘track-and-trigger’ scores (EWSs) are used to identify the deteriorating patient and reduce unwarranted variation in the incidence of adverse events.1 They amoxil best buy were developed to enable timely escalation of sick patients to medical staff and are used in everyday clinical practice to guide changes in clinical management, admission to intensive care units (ICUs) and initiation of end-of-life care. Early track-and-trigger scores were based on aggregate vital signs. Many have been amoxil best buy externally validated in hospital and prehospital settings as predictors of ICU admission and survival for sepsis,2 exacerbations of chronic obstructive pulmonary disease3 and trauma.4 Machine learning and the rollout of integrated electronic health records have accelerated the development of sophisticated EWSs incorporating blood test and imaging results.

These scores may provide ‘real-time’ information about ongoing clinical deterioration or a more rounded overall assessment of prognosis. Some of these tools may improve outcomes in patients with life-threatening pathology,5 amoxil best buy but others are methodologically flawed and may have no or even adverse effects on patient care.1EWSs lose their salience when they fail to identify deteriorating patients and when staffing and resource limitations in overstretched healthcare systems prevent clinicians from taking timely action. The buy antibiotics amoxil has placed immense pressure on health systems across the world, and adults with buy antibiotics may deteriorate rapidly and unexpectedly.6 There is widespread concern that existing EWSs may underestimate illness severity in patients with buy antibiotics, providing clinicians with false reassurance and thus delaying treatment escalation.7 8 Several groups have therefore sought to assess the utility of existing track-and-trigger scores and develop and validate novel tools for adults with buy antibiotics.

This article amoxil best buy will outline the pitfalls of existing EWSs for adult patients with buy antibiotics, highlight key findings from studies of novel EWSs for buy antibiotics and discuss the ideal properties of a track-and-trigger score for buy antibiotics suitable for use around the world.What are EWSs and why are they useful in healthcare settings?. The first EWS emerged in the late 1990s. Early versions assigned amoxil best buy numerical values to different vital signs, and other factors such as clinical intuition, with aggregate scores triggering escalation to medical staff.

They were designed primarily to reduce the incidence of avoidable in-hospital cardiac arrests in ward settings by enabling timely transfer of sick patients to ICU. Scores were developed with poor methodological rigour and in a haphazard fashion with local and regional variations, until regulatory bodies and professional organisations amoxil best buy pressed for and developed standardised tools. For example, in the UK, the Royal College of Physicians developed the National Early Warning Score (NEWS), which was launched in 2012 and soon became mandatory in National Health Service hospitals.9 To reflect differences in physiological norms, distinct EWSs have been developed for adult, paediatric and obstetric populations.

In recent years, novel or adapted scores have focused on different outcomes, such as cause-specific or all-cause mortality, and have been designed for use in different settings (such as the emergency department (ED) and in primary and prehospital care).There is some evidence amoxil best buy that implementation of EWSs improves outcomes for patients with sepsis,10 and several studies support their utility in identifying critical illness in hospital and prehospital settings.11 12 EWSs also provide a common language for ‘sickness’ and aid triage and resource allocation, particularly in a amoxil setting. Nonetheless, frontline professionals are aware of their pitfalls, particularly for those scores based on physiological parameters. Isolated values must amoxil best buy be interpreted with regard to trajectory and placed within a clinical context—junior doctors are often informed of a patient ‘triggering’ when they have had a high score for hours or even days and already been reviewed.

EWS based on vital signs can also provide false reassurance. Shocked patients on beta blockers may not mount a tachycardia, and patients with acute renal failure may show no respiratory, amoxil best buy cardiovascular or neurological compromise despite requiring urgent renal replacement therapy.What are the problems with existing EWSs in relation to buy antibiotics?. Where clinically appropriate, the deteriorating patient with buy antibiotics requires urgent clinical review to determine the need for non-invasive ventilation (NIV) or intubation and mechanical ventilation (IMV).

Delays in accessing these time-critical interventions may amoxil best buy result in adverse outcomes. Depending on the patient’s age, comorbidities, level of frailty and the nature of their acute illness, their ceiling of care may be limited to NIV or even ward-based treatment, in which case deterioration may represent a terminal event and prompt a switch to end-of-life care. Clinical signs of deterioration in hospitalised adults with buy antibiotics include a rising oxygen requirement, raised respiratory rate, use of accessory muscles of respiration and altered mental state.In NEWS2, the most widely used EWS in the UK, supplemental oxygen therapy scores two points, but once a patient is on oxygen amoxil best buy this score does not change to reflect flow rate or oxygen delivery device.

Work of breathing is not included in NEWS2, though it has been used as an inclusion criterion for NIV in buy antibiotics.13 NEWS2 was developed with a focus on sepsis and therefore assigns significant value to tachycardia and hypotension. However, cardiovascular compromise is relatively uncommon in moderate to severe buy antibiotics and may indicate additional amoxil best buy pathology such as bacterial sepsis or pulmonary embolism.14 While respiratory rate may rise as patients with buy antibiotics deteriorate, there are widespread reports of ‘happy hypoxia’ in which the typical physiological response (tachypnoea and increased work of breathing) to and subjective experience of hypoxia (dyspnoea) are absent.15 16 A recent report suggesting that pulse oximetry monitoring may underestimate the frequency of hypoxaemia in black patients is of particular concern in the context of buy antibiotics.17Development of novel early warning and prognostic scores for buy antibioticsVarious research groups have investigated whether existing scores can accurately identify hospitalised patients with buy antibiotics who are at risk of clinical deterioration. Several studies have suggested that EWSs such as NEWS2 and the quick Sequential (Sepsis-related) Organ Failure Assessment, and prognostic tools such as CURB-65 perform poorly in cohorts of inpatients with buy antibiotics.18 19 This has spurred the development of dozens of bespoke early warning and prognostic scores for buy antibiotics through retrospective multivariable logistic regression of patient-level data.While outcomes of interest and time horizons vary, most models have combined vital signs with demographic factors, comorbidities and laboratory and imaging indices which reflect risk factors for severe disease or death.

Variables of interest have typically been identified by expert clinicians or derived from observational studies highlighting risk factors for adverse amoxil best buy outcomes in early buy antibiotics cohorts and for other respiratory illnesses such as bacterial pneumonia and influenza. Researchers have developed these composite scores by assigning differential weight to each variable and then evaluating the clinical sensitivity and specificity of candidate models at different thresholds for clinical deterioration. Scores favouring variables derived from the wisdom of frontline clinicians may be more tractable in clinical settings but may lack the discriminative power offered amoxil best buy by data-driven scores based on statistical analysis of routinely collected patient-level data.

Several groups have sought to balance these tensions by asking panels of clinicians to review the relevance of candidate variables identified by statistical analyses.The trade-off between each model’s sensitivity and specificity can be represented by receiver operator characteristics (ROCs), which can be displayed graphically. By quantifying the ‘area under the ROC curve’ (AUROC) for new and existing models, amoxil best buy it is possible to compare their performance. For existing and novel scores evaluated in buy antibiotics cohorts, this could mean discrimination between stable and deteriorating hospitalised patients—where deterioration is defined by the subsequent need for IMV or ICU level care—or patients at high or low risk of mortality at first presentation to the ED.

AUROC values always lie between 0 and 1 amoxil best buy. A value of 0.5 suggests that a model’s discrimination is no better than chance. We would consider an AUROC value over 0.75 to represent good clinical discrimination.20As outcomes such as ICU admission and mortality are relatively rare events, models derived from small populations are at risk amoxil best buy of ‘overfitting’.

Providing perfect results under study conditions but performing poorly in the real world. Some prognostic scores have combined the risk of antibiotics exposure with the risk of severe buy antibiotics, despite differences amoxil best buy in their respective risk factors. These risk prediction tools become less useful as exposures deviate from those seen in study conditions.

This is particularly relevant to the issue of ethnic group differences in hospitalisation and mortality from buy antibiotics in the UK and USA, which likely reflect differences in exposure to antibiotics and confounding factors such as deprivation rather than any genetic differences in underlying risk profiles.21Furthermore, most novel prognostic and EWSs for buy antibiotics have been developed without prospective external validation in large and diverse patient cohorts. Unsurprisingly, a systematic review of prognostic scores for buy antibiotics suggests that most novel scores are poorly reported and likely overestimate their true predictive performance.22 This is supported by a recent single-centre external validation study, which found that NEWS2 score was a better predictor of clinical amoxil best buy deterioration at 24 hours than 22 novel prognostic scores in a cohort of 411 hospitalised adults with buy antibiotics, with an AUROC of 0.76.23 The sole high-quality novel scores with similar performance to NEWS2 after external validation are the antibiotics Clinical Characterisation Consortium (4C) mortality (AUROC 0.78) and deterioration scores. Derived from multiethnic cohorts of over 30 000 hospitalised patients, these scores show real promise and have been widely adopted in the UK and beyond.The 4C mortality score combines patient age.

Sex at birth amoxil best buy. Number of comorbidities. Respiratory rate, peripheral oxygen saturations and Glasgow Coma Scale at amoxil best buy admission.

And serum urea and C reactive protein concentrations to provide an estimate of untreated in-hospital mortality.24 Patients receive an aggregate score out of 21, with age alone providing up to 8 points. By providing amoxil best buy an early assessment of prognosis at the front door, the 4C score might be used to guide treatment decisions, triage and clinical disposition. However, it is important to note that it predicts mortality rather than the need for NIV, IMV or ICU admission.

As such, amoxil best buy it may be most useful at its extremes. Giving clinicians confidence to discharge patients with low mortality scores or prompt early conversations around treatment escalation with older patients requiring oxygen. The 4C deterioration score incorporates 11 variables and defines clinical deterioration more broadly, to encompass death, ICU admission and IMV.25 It can be used at first amoxil best buy presentation to ED for community-acquired buy antibiotics or immediately after identification of nosocomial disease.

This score may help to optimise resource allocation—for example, by prompting early transfer of high-risk patients to higher acuity settings—and inform discussions with patients and families to give them time to prepare for expected deterioration. Future studies should assess reattendance rates and ICU admissions among patients discharged from ED with low 4C mortality and deterioration scores.An important drawback of both scores is amoxil best buy that their use may be impractical in low and middle-income countries (LMICs). A recent postmortem surveillance study suggests that buy antibiotics rates may have been significantly under-reported in Africa due to poor access to testing.26 The 4C scores are only useful after a diagnosis of buy antibiotics is confirmed.

However, with restricted access to antibiotics antigen tests in the community and amoxil best buy hospital settings, diagnosis is often made on clinical grounds alone. It can be difficult to distinguish buy antibiotics from decompensated heart failure and bacterial pneumonia. This confers a risk of misdiagnosis amoxil best buy and inappropriate treatment and management based on irrelevant prognostic scores.Restricted access to ancillary diagnostic facilities may make it challenging to identify early signs of deterioration or determine prognosis in buy antibiotics even where it is possible to establish a diagnosis.

In rural LMIC settings, poor access to blood tests and X-ray facilities will make it impossible to calculate the 4C scores. This serves amoxil best buy as an urgent reminder of the importance of health systems strengthening in remote LMIC settings, but even with sustained investment and political will it will take years to improve diagnostic capabilities and train local staff. As such, triage tools based on vital signs alone may be more practical and reproducible in these settings.

The utility of routinely used EWSs already validated in LMICs—such as the universal vital assessment score developed in amoxil best buy sub-Saharan Africa27—should be assessed in buy antibiotics cohorts alongside external validation of novel models like the PRIEST score developed in high-income settings.28 Simpler univariate scoring systems may also be effective. Among 411 adults admitted to a UK urban teaching hospital with buy antibiotics, admission oxygen saturation on room air alone was a strong predictor of deterioration and mortality.23 Healthcare workers and technicians could be rapidly trained to use pulse oximeters and flag patients with hypoxia to medical staff. This would also support judicious use of precious oxygen therapy.29 Unfortunately, oximeters remain scarce in amoxil best buy countries such as Ethiopia,30 and their mass distribution in LMICs should be a priority as the amoxil evolves.Future workResearchers must reassess novel early warning and prognostic scores in light of growing population immunity to prevailing antibiotics strains through prior or vaccination, and the emergence of new variants associated with higher mortality.31 Most prognostic scores for buy antibiotics have a short time horizon.

They use vital signs and other prognostic markers measured at an index ED attendance or inpatient admission to predict short-term outcomes such as in-hospital mortality and discharge from hospital. However, with a recent retrospective cohort study demonstrating high rates of multiorgan dysfunction and all-cause mortality in buy antibiotics survivors at 140 amoxil best buy days after hospital discharge,32 we need to develop models capable of predicting long-term survival and adverse consequences. Cox regression analyses, which, unlike standard ROC curve analyses, account for the time taken for an adverse event to occur,33 would be well suited to the development of these models.To date, most researchers have taken a crude approach to developing buy antibiotics scoring systems, using data from large populations of hospitalised adults assumed to be homogeneous.

While evidence is mixed,34 some studies support the existence of distinct disease phenotypes, notably a hyperinflammatory subtype associated with higher risks of next-day escalation to higher level respiratory care and higher rates of ICU admission and mortality.35 We may see the emergence of novel scores for specific buy antibiotics phenotypes and must balance the tension amoxil best buy between any additional discriminative benefits they offer and the extra cognitive load they place on overstretched healthcare professionals.In high-income settings, technology may help to ease this cognitive load and identify high-risk patients across the hospital as close to real time as possible, to aid resource allocation. Future studies should assess whether integration of scores into electronic health records reduces unwarranted variation in treatment escalation and disease outcomes. Scores could be calculated automatically with electronic alerts notifying amoxil best buy clinicians of risk and prompting guideline-based clinical management.

This could be used to support safe discharge of low-risk patients from the ED and gold-standard prescribing of remdesivir, dexamethasone and tocilizumab at different points in the disease course. The introduction of similar electronic alerts amoxil best buy designed to improve the recognition and management of sepsis at a multisite London hospital Trust has previously been shown to reduce mortality.5Future studies which describe the development and validation of novel prognostic scores for buy antibiotics must be transparent about their intended purpose. It is often unclear if a score is designed for routine clinical use.

To inform risk stratification in interventional amoxil best buy studies or to separate different disease phenotypes in observational studies. Prospective external validation may confirm that a novel score reliably discriminates between stable and deteriorating patients, but if the score is difficult to use or understand, it will not be widely adopted. In the UK, one of the key characteristics of the NEWS2 score is that it provides a universal ‘language for sickness’ which amoxil best buy is widely understood by healthcare professionals of different stripes and seniority.

Close collaboration between clinicians and statisticians at all stages of the research process should aid the development of robust scores which are clinically relevant, easy to use and align with workflow.Risk prediction tools such as Qbuy antibiotics have also been developed for patients in the community, to identify those at high risk of acquiring and poor outcomes and inform shielding guidelines.36 While they may help clinicians and public health agencies to implement targeted risk mitigation measures, they cannot discriminate between patients who can be managed safely in the community and those who require hospital care after acquiring buy antibiotics. The prevalidation RECAP-V0 is a promising tool which could help to identify patients in a community setting with suspected or confirmed buy antibiotics who require further evaluation in secondary care settings.37 Future work must seek to determine whether this and similar scores can support more integrated care across whole healthcare systems. For example, early admission of high-risk patients identified in the community may help to avoid spikes of critically ill patients presenting to ED in extremis and enable more equitable distribution of patients amoxil best buy across wider hospital networks.

This is particularly important in LMICs, where access to advanced respiratory support and critical care is limited.ConclusionEWSs can support timely recognition of clinical deterioration and escalation to critical care or palliation. There are widespread concerns that existing scores such as NEWS2 may fail to identify amoxil best buy the deteriorating patient with buy antibiotics as they place a premium on cardiovascular instability rather than respiratory dysfunction. Several research groups have used advanced statistical techniques to develop novel early warning and prognostic scores for patients hospitalised with buy antibiotics.

While many of these scores are at amoxil best buy high risk of bias, the 4C mortality and deterioration scores have been externally validated in high-income settings and offer useful insights which can inform clinical care. These scores might be used to optimise resource allocation, support discussions around treatment escalation and inform protocols for safe discharge. Unfortunately, limited access to virological testing amoxil best buy and laboratory and imaging facilities may blunt their utility in LMICs, where physiological scores may be more practical.

Future work should focus on predicting long-term outcomes in buy antibiotics, improving user experience and identifying the optimum balance between the extra discrimination afforded by novel scores and their ease of use in everyday clinical practice.Ethics statementsPatient consent for publicationNot required.‘Of or belonging to another, not one’s own, foreign, strange.’From the Latin alienus, the etymology of the word ‘alien’ signifies much of what the word connotes. A certain unnatural and inhuman nature amoxil best buy. Nonetheless, ever since the Alien and Sedition Acts in 1798, the dehumanising term ‘alien’ has repeatedly been used to refer to immigrants in the USA.

On his first day in office, President Biden sent Congress the US Citizenship Act of 2021, which notably sought to change the term ‘alien’ to ‘non-citizen’ amoxil best buy in our immigration laws. Much attention, therefore, has been given to this change and its implications within the realm of immigration, but we must also recognise the importance of similar semantic alterations within healthcare. For instance, the Affordable Care Act (ACA) repeatedly refers to ‘non-citizens’ as ‘aliens,’ and such terminology is ubiquitous throughout health policy and the amoxil best buy literature more broadly.

Eliciting notions of segregation, the term ‘alien’ relegates important communities to a second-class status. The buy antibiotics amoxil has exacerbated deep-rooted fissures of trust in the federal government and healthcare institutions, as demonstrated by a palpable hesitancy to receive the three authorised antibiotics treatments among non-citizen communities.1 2 In our efforts to curb the buy antibiotics amoxil, we cannot permit our diction to further intensify bias and, in turn, alienate immigrants from vaccination.Already, non-citizens in the USA face difficulties as they endeavour to amoxil best buy navigate our complex healthcare system. These realities manifest themselves in disproportionately low levels of health insurance among non-citizens.

77% of lawfully present immigrants and 55% of undocumented immigrants as compared with 91% of citizens.3 While undocumented immigrants are entirely ineligible for Medicaid and ACA coverage, lawfully present immigrants are often precluded from these federal programmes because of fear, amoxil best buy confusion and literacy challenges, as well as worries about being labelled as a ‘public charge’ (ie, receiving government benefits can make one ineligible for a green card or visa). Unfortunately, the prior administration empowered an Immigration and Customs Enforcement agency that aggressively targeted non-citizens, and, more broadly, our political climate has elevated rhetoric that voraciously maligns all immigrants. As such, it should come to no surprise that immigrants of all documentation statuses have quietly retreated from the public sphere and the healthcare system altogether.1 Countless reports have found that non-citizens increasingly avoid scheduling doctor’s appointments and refuse to answer the door for home health visits, which may help to explain why immigrants are less likely to receive preventive care amoxil best buy services and are more likely to suffer from chronic diseases.1 4 5 While it may be secondary to challenges regarding access, exorbitant costs associated with care, or an unwillingness to put themselves and their families at risk,4 the health consequences are disastrous.

In the context of buy antibiotics, non-citizens may avoid seeking medical advice until the last possible moment when the amoxil has already wrought immense damage on their bodies. Alienated from traditional avenues of care, non-citizens are often caught only in the fraying safety nets of urgent care clinics and emergency rooms with their severely exacerbated conditions.We have already seen the consequences of such disparities as it amoxil best buy relates to the amoxil. Constituting 13.7% of the US population, immigrant essential workers represent 16.3% of essential healthcare operations, 18.4% of essential retail and 20.2% of essential services, disproportionately serving as frontline personnel and sustaining countless industries on the backs of their labour.6 Whether it be this work as essential workers or high rates of poverty and other social risk factors, immigrants are at least twice as likely to be infected with buy antibiotics as native-born individuals and face significantly higher mortality rates.1 7 For instance, in the Dallas Fort-Worth Area, which sees one of the largest populations of undocumented immigrants in the nation, middle-aged Latino men are eight times more likely to die from buy antibiotics than their non-Latino white peers.2 While immigrants do not necessarily have significantly higher rates of underlying health conditions,8 various structural barriers and injustices prevent non-citizens from accessing care, contributing to these higher rates of and worse outcomes.These challenges and the resultant adverse health consequences can erode trust among non-citizens in health systems and federal institutions.

Trust is broken in wake amoxil best buy of discrimination in clinics. Trust is broken when non-citizens, without insurance, have to pay exorbitant sums to access healthcare. Trust is broken when trips to amoxil best buy the hospital put one at risk of being deported.

Trust is broken when non-citizens see community members dying needlessly from buy antibiotics. In a amoxil that has burdened immigrants in amoxil best buy particular, subtle mental assaults through stigmatising language only further deteriorate trust. Indeed, the term ‘alien’ implicitly removes non-citizens from the healthcare system and risks excluding them from the buy antibiotics vaccination rollout, exacerbating existing structural issues such as limited treatment availability in these communities.It is already well known that labelling individuals as ‘illegal aliens’ subjects them to more prejudice and discrimination than does the term ‘non-citizens’.9 Indeed, one study found that mental health professionals who thought about Latino immigrants as ‘undocumented immigrants’ viewed them more positively than those asked to think about Latino immigrants as ‘illegal aliens’.10 This finding should come to no surprise given that the derogatory term ‘alien’ defines someone by their immigration status rather than as a person with an immigration status.

While ‘non-citizen’ does not entirely resolve the matter of people-first language, amoxil best buy it represents a crucial step forward and conveys greater humanity to these individuals. If we cannot purge ‘alien’ from the medical vocabulary entirely, we betray the foundational ideal of equal healthcare for all and turn a blind eye to non-citizens, who represent 14% of the US population.Certainly, President Biden’s efforts to remove ‘alien’ from our immigration laws is a long-overdue first step to mitigate bias and build trust, but we must broaden our vision towards all realms, including healthcare. The federal government represents the face amoxil best buy of the buy antibiotics treatment rollout, yet non-citizens largely do not trust the government to protect them and their communities.

This paucity of trust is complex and multifactorial, and revamping diction within complicated pieces of legislation may not have any immediate implications for rebuilding that faith. But the words that pervade policy—and their connotations—set the tone for amoxil best buy how we collectively address these communities, as well as the dignity and respect they receive. A semantic transition towards ‘non-citizens’ may ultimately beget public health messaging which comes from bilingual community leaders, assurances that vaccination is free and does not carry a deportation risk, and local efforts to make the treatment accessible to all immigrants.

These steps, in turn, may engender the political will to combat structural barriers that non-citizens face in navigating health institutions. At the end of the day, words matter, humanity matters. During a amoxil indifferent to matters of citizenship, we must make sincere overtures to bridge access to care and deracinate stigmatising, dehumanising language from our vocabulary.Ethics statementsPatient consent for publicationNot required..

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About This TrackerThis tracker provides the number of confirmed cases and deaths from novel antibiotics by country, the trend in confirmed case and death counts by country, and a global map showing which amoxil capsules 500mg chemist warehouse countries have confirmed cases and deaths. The data are drawn from the Johns Hopkins University (JHU) antibiotics Resource Center’s buy antibiotics Map and the World Health Organization’s (WHO) antibiotics Disease (buy antibiotics-2019) amoxil capsules 500mg chemist warehouse situation reports.This tracker will be updated regularly, as new data are released.Related Content. About buy antibiotics antibioticsIn late 2019, a new antibiotics emerged in central China to cause disease in humans.

Cases of this disease, known as amoxil capsules 500mg chemist warehouse buy antibiotics, have since been reported across around the globe. On January 30, 2020, amoxil capsules 500mg chemist warehouse the World Health Organization (WHO) declared the amoxil represents a public health emergency of international concern, and on January 31, 2020, the U.S. Department of Health and Human Services declared it to be a health emergency for the United States.With increased attention to the global need for buy antibiotics treatments and the Biden administration’s announcement today about how it plans to distribute the first portion of the 80 million doses it will share by the end of this month, the latest KFF Health Tracking Poll finds that two-thirds of the public (66%) say that the U.S.

Should play at least a “major role” in distributing buy antibiotics treatments to other countries, including about a quarter (27%) who say it should play a “leading role.”Nearly 9 in 10 Democrats support amoxil capsules 500mg chemist warehouse the U.S. Taking at least amoxil capsules 500mg chemist warehouse a “major role” (87%), while most Republicans (57%) say the U.S. Should play a “minor role” or “no role at all,” a larger share than the 41% who want the U.S.

To play amoxil capsules 500mg chemist warehouse a “leading” or “major role.”The shares who say the U.S. Should take at least a major role increase when people are told amoxil capsules 500mg chemist warehouse that the U.S. Has enough buy antibiotics treatment to help other countries without hurting its own supply (78%), that the amoxil is much worse in other countries and they need access to the treatments to stop its spread (77%), or that providing treatments to other countries could help the U.S.

Achieve the immunity necessary to amoxil capsules 500mg chemist warehouse curb the amoxil (76%). After hearing each of these messages, at amoxil capsules 500mg chemist warehouse least half of Republicans say the U.S. Should take a leading or major role in treatment distribution overseas.The poll also gauges the public’s health policy priorities, and finds large shares of the public consider each of nine proposals tested as “top” or “important” priorities for Congress.This includes at least 8 in 10 who say so about allowing the federal government to negotiate lower prices directly with drug makers (92%), expanding Medicare coverage to include hearing aids, dental and vision coverage (90%), placing a limit on out-of-pocket costs that seniors have to pay each year for things like prescription drugs (88%), and continuing efforts to make sure U.S.

Residents are able to receive a buy antibiotics treatment (81%).Other priorities for Congress include expanding public health coverage for low-income people in states that have not expanded their Medicaid program (78%), creating a public option to compete with private insurance (71%), or lowering the age of Medicare eligibility (66%).Democrats are generally more likely than Republicans to prioritize each of these amoxil capsules 500mg chemist warehouse health issues as priorities for Congress. The policies aimed at addressing drug costs are the only ones that majorities of Democrats, independents, and Republicans identify as “top” priorities.When asked directly amoxil capsules 500mg chemist warehouse whether they support or oppose allowing the federal government to negotiate with drug makers to reduce prices for both Medicare and private insurance, the vast majority of the public (88%) is in favor. The poll suggests those views could change in a national debate with arguments being made for and against the approach.Support inches higher (to 90%) when the public hears that people could save money on their prescription drugs if this policy were implemented.

On the flip side, nearly two thirds (65%) say they oppose such a policy after being told that “it could lead to less research and development of new amoxil capsules 500mg chemist warehouse drugs” or that “it could limit people’s access to newer prescription drugs.” These arguments are similarly effective with Democrats and Republicans.Other findings include:The buy antibiotics relief law enacted in March provides additional financial assistance to people who buy their own health insurance through the Affordable Care Act’s marketplace. Few (7%) of those who could be eligible for this assistance are aware of this fact.Far amoxil capsules 500mg chemist warehouse more continue to view the Affordable Care Act favorably (53%) than unfavorably (35%). This reflects a huge partisan divide, with most Democrats (85%) and a narrow majority of independents (54%) viewing it favorably, and most Republicans (77%) viewing it unfavorably.Larger majorities, including most Republicans, view both Medicare (78%) and Medicaid (74%) favorably.Designed and analyzed by public opinion researchers at KFF, the KFF Health Tracking Poll was conducted from May 18-25 among a nationally representative random digit dial telephone sample of 1,526 adults.

Interviews were conducted in English and Spanish by landline amoxil capsules 500mg chemist warehouse (248) and cell phone (1,278). The margin of sampling error is amoxil capsules 500mg chemist warehouse plus or minus 3 percentage points for the full sample. For results based on subgroups, the margin of sampling error may be higher..

About This TrackerThis tracker provides the number of confirmed cases and deaths from novel antibiotics by country, the trend in confirmed case and death counts by country, and a global map showing amoxil best buy which countries have confirmed cases and deaths. The data are drawn from the Johns Hopkins University (JHU) antibiotics Resource Center’s buy antibiotics Map and the amoxil best buy World Health Organization’s (WHO) antibiotics Disease (buy antibiotics-2019) situation reports.This tracker will be updated regularly, as new data are released.Related Content. About buy antibiotics antibioticsIn late 2019, a new antibiotics emerged in central China to cause disease in humans. Cases of this disease, known as buy antibiotics, have since been reported amoxil best buy across around the globe. On January 30, 2020, the World Health Organization (WHO) declared the amoxil represents a public health emergency of international concern, and on January amoxil best buy 31, 2020, the U.S.

Department of Health and Human Services declared it to be a health emergency for the United States.With increased attention to the global need for buy antibiotics treatments and the Biden administration’s announcement today about how it plans to distribute the first portion of the 80 million doses it will share by the end of this month, the latest KFF Health Tracking Poll finds that two-thirds of the public (66%) say that the U.S. Should play at least a “major role” in distributing buy antibiotics treatments to other countries, including about a amoxil best buy quarter (27%) who say it should play a “leading role.”Nearly 9 in 10 Democrats support the U.S. Taking at least amoxil best buy a “major role” (87%), while most Republicans (57%) say the U.S. Should play a “minor role” or “no role at all,” a larger share than the 41% who want the U.S. To play a “leading” amoxil best buy or “major role.”The shares who say the U.S.

Should take at least a major role increase when people are told that the U.S amoxil best buy. Has enough buy antibiotics treatment to help other countries without hurting its own supply (78%), that the amoxil is much worse in other countries and they need access to the treatments to stop its spread (77%), or that providing treatments to other countries could help the U.S. Achieve the amoxil best buy immunity necessary to curb the amoxil (76%). After hearing each of these messages, at least half of Republicans amoxil best buy say the U.S. Should take a leading or major role in treatment distribution overseas.The poll also gauges the public’s health policy priorities, and finds large shares of the public consider each of nine proposals tested as “top” or “important” priorities for Congress.This includes at least 8 in 10 who say so about allowing the federal government to negotiate lower prices directly with drug makers (92%), expanding Medicare coverage to include hearing aids, dental and vision coverage (90%), placing a limit on out-of-pocket costs that seniors have to pay each year for things like prescription drugs (88%), and continuing efforts to make sure U.S.

Residents are able to receive a buy antibiotics treatment (81%).Other priorities for Congress include expanding public health coverage for low-income people in states amoxil best buy that have not expanded their Medicaid program (78%), creating a public option to compete with private insurance (71%), or lowering the age of Medicare eligibility (66%).Democrats are generally more likely than Republicans to prioritize each of these health issues as priorities for Congress. The policies aimed at addressing drug costs are the only ones that majorities of Democrats, independents, and Republicans identify as “top” priorities.When asked directly whether they support or oppose allowing the federal government to negotiate amoxil best buy with drug makers to reduce prices for both Medicare and private insurance, the vast majority of the public (88%) is in favor. The poll suggests those views could change in a national debate with arguments being made for and against the approach.Support inches higher (to 90%) when the public hears that people could save money on their prescription drugs if this policy were implemented. On the flip side, nearly two thirds (65%) say they oppose such a policy after being told that “it could lead to less research and amoxil best buy development of new drugs” or that “it could limit people’s access to newer prescription drugs.” These arguments are similarly effective with Democrats and Republicans.Other findings include:The buy antibiotics relief law enacted in March provides additional financial assistance to people who buy their own health insurance through the Affordable Care Act’s marketplace. Few (7%) of those who could be eligible for this assistance are aware of this fact.Far more continue to view amoxil best buy the Affordable Care Act favorably (53%) than unfavorably (35%).

This reflects a huge partisan divide, with most Democrats (85%) and a narrow majority of independents (54%) viewing it favorably, and most Republicans (77%) viewing it unfavorably.Larger majorities, including most Republicans, view both Medicare (78%) and Medicaid (74%) favorably.Designed and analyzed by public opinion researchers at KFF, the KFF Health Tracking Poll was conducted from May 18-25 among a nationally representative random digit dial telephone sample of 1,526 adults. Interviews were conducted in English and Spanish by amoxil best buy landline (248) and cell phone (1,278). The margin of sampling amoxil best buy error is plus or minus 3 percentage points for the full sample. For results based on subgroups, the margin of sampling error may be higher..