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How to cite this article:Singh O P low price amoxil can u buy amoxil over the counter. Aftermath of celebrity suicide â Media coverage and role of psychiatrists. Indian J low price amoxil Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, low price amoxil 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 low price amoxil process, reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress calls from their patients in despair with increased low price amoxil 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 low price amoxil publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide. A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and illness and also his low price amoxil relationships and finances.
Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure low price amoxil 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 low price amoxil the episode. Many psychiatrists were quoted, or âÂÂmisquoted,â or âÂÂquoted out of context,â commenting on the life of a person whom they had never examined and had no âÂÂprofessional authorityâ to do so.
There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and âÂÂmisleading conceptsâ about psychiatry and are detrimental to the image of psychiatry in addition low price amoxil 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 âÂÂThe Goldwater Ruleâ 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 âÂÂstatements to the mediaâ can be a double-edged sword, and we should know about the rules low price amoxil of engagements and boundaries of interactions. Methods and principles of interaction with media should form a part of our training curriculum.
Many professional societies have guidelines and resource books for interacting with media, and psychiatrists should familiarize themselves with these documents low price amoxil. 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 âÂÂoff the recordâ as the media person is most likely recording the low price amoxil interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made â professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.
O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support low price amoxil. 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 â 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 bloodâÂÂbrain 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 amygdalaâÂÂhippocampal 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 â amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study â Nordanskog et al., 2014 â has followed study patients for a long term â 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 â 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 â 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 doseâÂÂresponse 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 â 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 â 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 â 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 â 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 â 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 â 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 â Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 â have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] â 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 â 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 â 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 â 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 1âÂÂ2 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 â 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 â 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 â 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 â due to the transient inflammation â and the long-term improvement in mood â neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT.
However, these cannot be construed as brain damage as is usually understood. Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question. However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J. Electroconvulsive therapy.
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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.
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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.
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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 à  , 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 where can i buy amoxil over the counter cite this article:Singh O P. Aftermath of celebrity suicide â Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity where can i buy amoxil over the counter suicide is one of the highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide.
As expected, the media went into a where can i buy amoxil over the counter 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 where can i buy amoxil over the counter 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 where can i buy amoxil over the counter 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 where can i buy amoxil over the counter Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing 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 where can i buy amoxil over the counter the person's mental condition and illness and also his relationships and finances. Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him.
The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the where can i buy amoxil over the counter 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 where can i buy amoxil over the counter comment on the episode. Many psychiatrists were quoted, or âÂÂmisquoted,â or âÂÂquoted out of context,â commenting on the life of a person whom they had never examined and had no âÂÂprofessional authorityâ to do so.
There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and âÂÂmisleading conceptsâ about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our where can i buy amoxil over the counter 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 âÂÂThe Goldwater Ruleâ 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 where can i buy amoxil over the counter âÂÂstatements to the mediaâ can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.
Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and resource books for interacting with media, and where can i buy amoxil over the counter 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 where can i buy amoxil over the counter assumed that no statement goes âÂÂoff the recordâ 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 â 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 where can i buy amoxil over the counter SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest.
NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment. The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage.
This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically. Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods.
These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies. And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain.
However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords. Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update.
Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al. In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas â 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 bloodâÂÂbrain 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 amygdalaâÂÂhippocampal 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 â amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study â Nordanskog et al., 2014 â has followed study patients for a long term â 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 â 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 â 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 doseâÂÂresponse 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 â 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 â 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 â 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 â 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 â 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 â 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 â Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 â have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] â 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 â 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 â 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 â 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 1âÂÂ2 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 â 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 â 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 â 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 â due to the transient inflammation â and the long-term improvement in mood â 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.
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Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].
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Viner et al1 produced a rapid systematic review that concludes that school closures have less impact on how to get amoxil in the us rate and mortality than other social distancing measures. Many countries have closed their schools for less time than the UK and have already started to reopen with several protective measures in place.2Concerns about the long-term economic, social and mental impact of lockdown led to the generation of plans to âÂÂget back to businessâÂÂ. This was conveyed to the population of the UK on how to get amoxil in the us 10 May by the UK prime minister, Boris Johnson.
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In a joint statement nine unions representing teachers stated that they thought 1 June was too early to be safe.4 They recognise that the opening of schools is a vital part of restarting the UK economy, but they have concerns about the safety and welfare of children and others.Meanwhile, the education how to get amoxil in the us secretary, Gavin Williamson, spoke at a press conference on 16 May stating that scientific evidence backed their decision. Interestingly, much of his statement was not about the scientific evidence but setting out an emotive argument that school was essential for safe and happy children.There is a consequence to this, the longer that schools are closed the more that children miss out. Teachers know that there are children out there that have not spoken or played with another child their own how to get amoxil in the us age for the last twoâÂÂmonths.
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The Institute for Fiscal Studies has produced a briefing note on childrenâÂÂs experiences of learning during lockdown.5 This is being widely cited as a rationale for reopening schools because children from vulnerable backgrounds are disproportionately affected by not being able to attend school. This has caused concern about the attainment gap, but as Quinn6 points out fewer children from disadvantaged backgrounds are likely to return to how to get amoxil in the us school than those from more affluent backgrounds.Government ministers and spokespeople reiterated that scientific evidence and observation of other European countries where schools had reopened demonstrated their decision was the correct one. However, there were no links provided to the scientific evidence and unions were quick to seize on this (eg, NASUWT7).The chief scientific advisor to the Department for Education, Osama Rahman, made a statement in a parliamentary science and technology committee meeting on 13 May that:There is a low degree of confidence in evidence that [children] might transmit it less.Carol Monaghan, the Scottish National Party education spokesperson, replied:WeâÂÂre putting together hundreds of potential vectors that can then go on and transmit.
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Rahman had already stated that the Scientific Advisory Group for Emergencies (SAGE) was collecting and considering evidence that was new and emerging, and that confidence was low in the evidence relating to transmission because there was very little evidence.8 However, this normal scientific caution in the evidence base was not discussed, and therefore it was assumed that low or moderate confidence in the evidence means a high-risk strategy is being mooted.There appear to be two major concerns about lifting the lockdown for children. First is the risk to children of how to get amoxil in the us developing antibiotics disease. The second is the risk to others of children transmitting antibiotics disease, either while being symptomatic or asymptomatic.
Here are some of the available evidence.Morbidity and mortality in children from antibiotics diseaseChildren appear to be less likely to acquire antibiotics disease in various nations.9âÂÂ11 Barton et al12 found that children account for 1.9% of confirmed cases (data collected from government websites and publications) how to get amoxil in the us. Of these 8113 paediatric cases, 14% required hospital admission. The admission rate to critical care was 2.2% of confirmed cases (7.2% of how to get amoxil in the us admitted children).
Death was reported in 15 cases how to get amoxil in the us (0.18%). This adds to other evidence suggesting that children are at a relatively low risk from the amoxil, with other estimates coming in at around 0.01%.13 14 This is likely to be because they appear to have a stronger immune response to the amoxil.15There are concerns that children who have been infected with the amoxil can develop a postviral inflammatory reaction (Kawasaki disease) and this can be severe,16 but the research evidence for this is not well developed yet.Transmission by childrenChildren can be asymptomatic and test positive for buy antibiotics, and in the absence of effective community testing it will be impossible to know if they are carrying the amoxil. Children also can have normal or abnormal signs (eg, chest imaging) when they have tested positive.17 In short, it is difficult to determine how to get amoxil in the us without much more extensive testing if a child can transmit the .Arav et al18 found that the contact route was much more important than the airborne route, which they concluded had a negligible contribution.
They suggest protective measures would therefore be good hand hygiene, careful cleaning and avoiding physical contact.Given that there are quite low numbers of symptomatic cases and an unknown quantity of asymptomatic cases, it is very difficult to determine whether children are a significant vector for the disease. Studies cited by the Royal College of Paediatrics and Child Health that explored family clusters of suggest that the child was unlikely to be the index case.The riskThis evidence suggests that there is a case for reopening schools to limited numbers of pupilsâÂÂthe risk to pupils and the adults how to get amoxil in the us they come into contact with seems to be small, and the potential gains for children may outweigh them. There is a big proviso with this however, and that is that the overall incidence of buy antibiotics has fallen below specified threshold.
This is quite a contentious issue and depends on us meeting the five key tests for easing lockdown.Making sure the National Health Service can cope.A sustained and consistent fall in the daily death rate.Rate of decreasing to manageable levels.Ensuring that personal protective equipment supply can meet demand.Being confident that any adjustments would not risk a second peak.These conditions are open to interpretation, and there appears to be a lack of trust by the public and by how to get amoxil in the us professionals from education and health in the information that the government and their scientific advisors are sharing. An example of this is a group of scientists who have come together to challenge the government about their decision-making.19 The concern about whether the evidence and advice that we are given are biased in any way has also been increased by concerns that a government advisor (Dominic Cummings) has attended what were supposed to be politically independent meetings of the SAGE.Scientific evidence continues to emerge, but weighing up the risks and benefits is not easy. Decisions about how to get amoxil in the us whether to reopen schools are taken on a national level with a distance from personal concerns and fears.
Individuals who are making decisions often rely on media translations of the evidence, and there is a level of mistrust in politicians and the media.20 Individuals are often irrational in their risk perception and management (eg, continuing to smoke or drink alcohol despite strong scientific evidence about the risk).21 22Overall, we are information-poor and opinion-rich. It is how to get amoxil in the us a difficult path to navigate. The debate about whether the benefits outweigh the risks of returning to school reminds me of the post-Wakefield Measles Mumps and Rubella vaccination situation.
Parents were being asked to believe that MMR was a safe treatment in the face of a massive and emotive campaign that promoted the âÂÂriskâ of how to get amoxil in the us having the treatment above all else. This situation is even more complex than that as we have increased access to opinion and how to get amoxil in the us difficulty in understanding if or how much that information is biased. It is no wonder that decision-making is difficult.
It is likely that evidence will continue to emerge how to get amoxil in the us and gradually the choice will become easier to make. For now, however, we can understand the difficulties that parents, teachers and councils face.IntroductionWhenever developing training competencies, tools to support clinical practice or a response to a professional issue, seeking the opinion of experts is a common approach. By working to identify a consensus position, researchers can report findings on a specific how to get amoxil in the us question (or set of questions) that are based on the knowledge and experience of experts in their field.However, there are challenges to this approach.
For example, what should be done when consensus cannot be reached?. How can experts be engaged in a way that allows them to consider objectively the views of others andâÂÂwhere appropriateâÂÂchange their own opinions in response? how to get amoxil in the us. One approach that attempts to provide a clear method for gathering expert opinion is the Delphi technique.The Delphi technique was first developed in the 1950s by Norman Dalkey and Olaf Helmer in an attempt to gain reliable expert consensus.
Specifically, they developed an approachâÂÂnamed after the Ancient Greek Oracle of Delphi, who could predict the futureâÂÂwhich promoted anonymity and avoided how to get amoxil in the us direct confrontation between experts, so that the methods employed âÂÂâ¦appear to be more conducive to independent thought on the part of the experts and to aid them in the gradual formation of a considered opinionâÂÂ.1 Though the original Delphi study was linked to the defence industry, the technique has spread to other research areas, including nursing.2Characteristics of Delphi studiesAs with all research methods, the Delphi technique has evolved since it was first reported on in the 1960s. However, many of the fundamental characteristics of the approach still remain from Dalkey and HelmerâÂÂs original outline. First, the overarching approach is based on a series of âÂÂroundsâÂÂ, where a set of how to get amoxil in the us experts are asked their opinions on a particular issue.
The questions for each round are based in part of the findings of the previous one, allowing the study to evolve over time in response to earlier findings.Second, participants are able to see the results of previous roundsâÂÂincluding their own responsesâÂÂallowing them to reflect on the views of others and reposition their own opinions accordingly.2 This also gives them the opportunity to consider and feedback on what they perceive to be the strengths and weaknesses of otherâÂÂs responses. Finally, the findings of each round are always shared with the broader group anonymously how to get amoxil in the us. This avoids any bias that might result from participants being concerned about their own views being viewed negatively or from their own opinions being biased by personal factors how to get amoxil in the us.
This framework of expert opinion rounds, with each round built on previous findings and each allowing for responses to be reconsidered by participants, is designed to allow the development of a consensus view that answers the research question.Within this broad approach, there can be variation in areas such as how many rounds there are, how the questions are delivered and responses collected, and how âÂÂconsensusâ is judged. For example, a study of human factors that contributed to nursing errors used only how to get amoxil in the us two rounds. The first took the form of an online survey asking 25 experts to list all the âÂÂhumanâ causes of nursing errors that they could.
Analysis of responses resulted in a list of 28 potential reasonsâÂÂthis list was sent back to the same group of experts for the second round, asking them how to get amoxil in the us to score each one for importance. Analysis of this scoring then allowed for consensus conclusions on the top 10 human factors that contributed to nursing errors (with fatigue, heavy workload and communication problems the top three).3In another example, nurse practitioners (NPs) were recruited to participate in a Delphi study to achieve consensus related to NP advance care planning competencies. In round 1, how to get amoxil in the us draft competencies were developed from the findings of a survey of NP beliefs, knowledge and level of implementation of advance care planning.
Round 2 included engagement with 29 NPs who evaluated the draft competencies and their components. Revisions were made based on the original feedback, and a third round how to get amoxil in the us was conducted where 15 of the original NP participants confirmed their consensus with the final document. The final document includes four competencies, each with several elements.
Clinical Practice, Consultation and Communication, Advocacy and Therapeutic Management.4Strengths and weaknesses of Delphi studiesThe Delphi technique offers a flexible approach to gathering the views of experts on an how to get amoxil in the us area of interest. The ability for participants to reconsider their views in light of the contribution of others allows for an element of reflection that is missing from studies based on single interviews or focus groups. The anonymity among the expert groups that underpins Delphi studies promotes honesty among participants and reduces the risk of the âÂÂhalo effectâ where views from dominant or high-profile members of the group are given extra credence.5However, Delphi studies canâÂÂby their very natureâÂÂbe complex and time how to get amoxil in the us consuming.
The need for participants to complete multiple rounds can lead to high drop-out rates which impacts on validity how to get amoxil in the us of the study. The ability of participants to amend or alter their views at each round is also something of a double-edged sword. It provides those taking part with the opportunity to reflect and reconsider their position in response to how to get amoxil in the us additional information, which is an important part of nursing practice.
Conversely though, there is a danger that this flexibility introduces bias, with participants altering their response to comply with what they view to be the majority view (sometime called the âÂÂbandwagon effectâÂÂ).5Delphi studies can be criticised due to a lack of clarity on what is meant by âÂÂconsensusâÂÂ. Even with the level of flexibility how to get amoxil in the us and reflexivity present in Delphi studies, it is still unlikely that a group of experts will demonstrate 100% agreement on issues. However, because consensus is a requirement of a Delphi study, there does need to be a judgement on when this point is reached.
This is where there is inconsistency across studies and authors, with the suggested level how to get amoxil in the us of consensus ranging from 51% to 100%.2 In addition, it has been identified that in some areas, consensus is not predefined as part of the study method. For example, a review of Delphi studies in nurse education found that fewer than half of the papers appraised included a predefined level at which consensus was judged to have been achieved.6 In addition, the identification of an objective level consensus is only possible when gathering quantifiable dataâÂÂthe judgement on consensus being reached in some qualitative Delphi studies will always be rather more subjective on the part of the researcher, and therefore potentially open to bias.By their nature, Delphi studies often rely purely on expert opinion to generate findings. A further limitation is therefore related to the quality of evidence, with expert opinion viewed as providing a poor basis for making judgements on healthcare interventions.7 This does not mean that the findings of Delphi studies how to get amoxil in the us are intrinsically unreliable or invalid.
It does mean that researchers should consider whether their research question is one that can be answered through expert consensus or whether other approaches (such as a systematic review of research evidence) are more appropriate.ConclusionThe Delphi technique is a well-established approach to answering a research question through the identification of a consensus view across subject experts. It allows for reflection among participants, who are able to nuance and reconsider their opinion based on the anonymised opinions how to get amoxil in the us of others. However, researchers must take steps to enhance robustness of the studies.
It is important how to get amoxil in the us to try and prevent participants from simply resorting to agreeing with the majority view. Studies must also predefine what is meant by âÂÂconsensusâ and how it will be established.With careful and clear design though, Delphi studies can make a valuable contribution to the nursing evidence base by tapping into the professionâÂÂs most precious resourceâÂÂthe knowledge and expertise of its practitioners..
The past week has seen an blog link explosion of media commentary about whether children in the UK should go back to where can i buy amoxil over the counter school. Since âÂÂlockdownâ (23 March 2020) began schools have been open to vulnerable children and where can i buy amoxil over the counter young people, and to the children of âÂÂkey workersâÂÂ. Right from the start there have been differing opinions about the necessity or wisdom of closing schools. Viner et where can i buy amoxil over the counter al1 produced a rapid systematic review that concludes that school closures have less impact on rate and mortality than other social distancing measures. Many countries have closed their schools for less time than the UK and have already started to reopen with several protective measures in place.2Concerns about the long-term economic, social and mental impact of lockdown led to the generation of plans to âÂÂget back to businessâÂÂ.
This was conveyed to the population of the UK on 10 May by where can i buy amoxil over the counter the UK prime minister, Boris Johnson. He announced a range of measures to gradually reduce the level of lockdown. This is in keeping with modelling undertaken by various groups, including a preprint (not peer-reviewed) where can i buy amoxil over the counter modelling exercise by Zhang et al.3Mr Johnson announced that there would be a phased return (in England) of some children to school from 1 June. There are no national guidelines as it is recognised that school have differences that require a flexible approach, but there are a broad set of principles relating to social distancing and hygiene.Government ministers and teachersâ unions have opposing views on the safety of reopening schools. In a joint statement nine unions representing where can i buy amoxil over the counter teachers stated that they thought 1 June was too early to be safe.4 They recognise that the opening of schools is a vital part of restarting the UK economy, but they have concerns about the safety and welfare of children and others.Meanwhile, the education secretary, Gavin Williamson, spoke at a press conference on 16 May stating that scientific evidence backed their decision.
Interestingly, much of his statement was not about the scientific evidence but setting out an emotive argument that school was essential for safe and happy children.There is a consequence to this, the longer that schools are closed the more that children miss out. Teachers know where can i buy amoxil over the counter that there are children out there that have not spoken or played with another child their own age for the last twoâÂÂmonths. They know there are children from difficult or very unhappy homes for whom school is the happiest moment in their week, and itâÂÂs also the safest place for them to be. The poorest children will be the where can i buy amoxil over the counter ones who fall further behind if we keep school gates closed. This phased return is in line with what other European countries are doing.There ensued an at times ill-tempered debate where can i buy amoxil over the counter and a flurry of tweets and news articles identifying problems in enacting the government plan and the illogical nature of WilliamsonâÂÂs statement.
The Institute for Fiscal Studies has produced a briefing note on childrenâÂÂs experiences of learning during lockdown.5 This is being widely cited as a rationale for reopening schools because children from vulnerable backgrounds are disproportionately affected by not being able to attend school. This has caused concern about the attainment gap, but as Quinn6 points out fewer children from disadvantaged backgrounds are likely to return to school than those from more affluent backgrounds.Government ministers and spokespeople reiterated that scientific evidence and observation of other where can i buy amoxil over the counter European countries where schools had reopened demonstrated their decision was the correct one. However, there were no links provided to the scientific evidence and unions were quick to seize on this (eg, NASUWT7).The chief scientific advisor to the Department for Education, Osama Rahman, made a statement in a parliamentary science and technology committee meeting on 13 May that:There is a low degree of confidence in evidence that [children] might transmit it less.Carol Monaghan, the Scottish National Party education spokesperson, replied:WeâÂÂre putting together hundreds of potential vectors that can then go on and transmit. Is that where can i buy amoxil over the counter correct?. Osama Rahman responded:Possibly, depending on school sizes.His final statement contains layers of complexity but can be interpreted simply as âÂÂwe donâÂÂt knowâÂÂ.
This provoked a great where can i buy amoxil over the counter deal of disquiet. Rahman had already stated that the Scientific Advisory Group for Emergencies (SAGE) was collecting and considering evidence that was new and emerging, and that confidence was low in the evidence relating to transmission because there was very little evidence.8 However, this normal scientific caution in the evidence base was not discussed, and therefore it was assumed that low or moderate confidence in the evidence means a high-risk strategy is being mooted.There appear to be two major concerns about lifting the lockdown for children. First is the risk to children where can i buy amoxil over the counter of developing antibiotics disease. The second is the risk to others of children transmitting antibiotics disease, either while being symptomatic or asymptomatic. Here are some of the available evidence.Morbidity and mortality in children from antibiotics diseaseChildren appear to be less likely to acquire antibiotics disease where can i buy amoxil over the counter in various nations.9âÂÂ11 Barton et al12 found that children account for 1.9% of confirmed cases (data collected from government websites and publications).
Of these 8113 paediatric cases, 14% required hospital admission. The admission rate to critical care was 2.2% of where can i buy amoxil over the counter confirmed cases (7.2% of admitted children). Death was reported where can i buy amoxil over the counter in 15 cases (0.18%). This adds to other evidence suggesting that children are at a relatively low risk from the amoxil, with other estimates coming in at around 0.01%.13 14 This is likely to be because they appear to have a stronger immune response to the amoxil.15There are concerns that children who have been infected with the amoxil can develop a postviral inflammatory reaction (Kawasaki disease) and this can be severe,16 but the research evidence for this is not well developed yet.Transmission by childrenChildren can be asymptomatic and test positive for buy antibiotics, and in the absence of effective community testing it will be impossible to know if they are carrying the amoxil. Children also can have normal or where can i buy amoxil over the counter abnormal signs (eg, chest imaging) when they have tested positive.17 In short, it is difficult to determine without much more extensive testing if a child can transmit the .Arav et al18 found that the contact route was much more important than the airborne route, which they concluded had a negligible contribution.
They suggest protective measures would therefore be good hand hygiene, careful cleaning and avoiding physical contact.Given that there are quite low numbers of symptomatic cases and an unknown quantity of asymptomatic cases, it is very difficult to determine whether children are a significant vector for the disease. Studies cited by the Royal College of Paediatrics and Child Health that explored family clusters of suggest that the child was unlikely to be the index case.The riskThis evidence suggests that there is a case for reopening schools where can i buy amoxil over the counter to limited numbers of pupilsâÂÂthe risk to pupils and the adults they come into contact with seems to be small, and the potential gains for children may outweigh them. There is a big proviso with this however, and that is that the overall incidence of buy antibiotics has fallen below specified threshold. This is quite a contentious issue and depends on us meeting the five key tests for easing lockdown.Making sure the where can i buy amoxil over the counter National Health Service can cope.A sustained and consistent fall in the daily death rate.Rate of decreasing to manageable levels.Ensuring that personal protective equipment supply can meet demand.Being confident that any adjustments would not risk a second peak.These conditions are open to interpretation, and there appears to be a lack of trust by the public and by professionals from education and health in the information that the government and their scientific advisors are sharing. An example of this is a group of scientists who have come together to challenge the government about their decision-making.19 The concern about whether the evidence and advice that we are given are biased in any way has also been increased by concerns that a government advisor (Dominic Cummings) has attended what were supposed to be politically independent meetings of the SAGE.Scientific evidence continues to emerge, but weighing up the risks and benefits is not easy.
Decisions about whether to reopen schools are taken on a national level with a distance from personal concerns and fears where can i buy amoxil over the counter. Individuals who are making decisions often rely on media translations of the evidence, and there is a level of mistrust in politicians and the media.20 Individuals are often irrational in their risk perception and management (eg, continuing to smoke or drink alcohol despite strong scientific evidence about the risk).21 22Overall, we are information-poor and opinion-rich. It is where can i buy amoxil over the counter a difficult path to navigate. The debate about whether the benefits outweigh the risks of returning to school reminds me of the post-Wakefield Measles Mumps and Rubella vaccination situation. Parents were being asked to believe that MMR was a safe treatment in the face of a massive and emotive campaign that where can i buy amoxil over the counter promoted the âÂÂriskâ of having the treatment above all else.
This situation is even more complex than that as we have increased access to opinion and difficulty in understanding if or how much that information where can i buy amoxil over the counter is biased http://www.aspenridgegoldendoodles.com/testimonials/. It is no wonder that decision-making is difficult. It is likely that evidence will continue to emerge and gradually the where can i buy amoxil over the counter choice will become easier to make. For now, however, we can understand the difficulties that parents, teachers and councils face.IntroductionWhenever developing training competencies, tools to support clinical practice or a response to a professional issue, seeking the opinion of experts is a common approach. By working to identify a consensus position, researchers can report findings on a specific question (or set of questions) that are based on the knowledge and experience of experts in where can i buy amoxil over the counter their field.However, there are challenges to this approach.
For example, what should be done when consensus cannot be reached?. How can experts be engaged in a way that allows where can i buy amoxil over the counter them to consider objectively the views of others andâÂÂwhere appropriateâÂÂchange their own opinions in response?. One approach that attempts to provide a clear method for gathering expert opinion is the Delphi technique.The Delphi technique was first developed in the 1950s by Norman Dalkey and Olaf Helmer in an attempt to gain reliable expert consensus. Specifically, they developed where can i buy amoxil over the counter an approachâÂÂnamed after the Ancient Greek Oracle of Delphi, who could predict the futureâÂÂwhich promoted anonymity and avoided direct confrontation between experts, so that the methods employed âÂÂâ¦appear to be more conducive to independent thought on the part of the experts and to aid them in the gradual formation of a considered opinionâÂÂ.1 Though the original Delphi study was linked to the defence industry, the technique has spread to other research areas, including nursing.2Characteristics of Delphi studiesAs with all research methods, the Delphi technique has evolved since it was first reported on in the 1960s. However, many of the fundamental characteristics of the approach still remain from Dalkey and HelmerâÂÂs original outline.
First, the overarching approach is based on a series of âÂÂroundsâÂÂ, where a set of experts are asked their opinions where can i buy amoxil over the counter on a particular issue. The questions for each round are based in part of the findings of the previous one, allowing the study to evolve over time in response to earlier findings.Second, participants are able to see the results of previous roundsâÂÂincluding their own responsesâÂÂallowing them to reflect on the views of others and reposition their own opinions accordingly.2 This also gives them the opportunity to consider and feedback on what they perceive to be the strengths and weaknesses of otherâÂÂs responses. Finally, the findings of each round are always shared with the broader group anonymously where can i buy amoxil over the counter. This avoids any bias that might result from participants being concerned about their own views being viewed negatively or where can i buy amoxil over the counter from their own opinions being biased by personal factors. This framework of expert opinion rounds, with each round built on previous findings and each allowing for responses to be reconsidered by participants, is designed to allow the development of a consensus view that answers the research question.Within this broad approach, there can be variation in areas such as how many rounds there are, how the questions are delivered and responses collected, and how âÂÂconsensusâ is judged.
For example, a where can i buy amoxil over the counter study of human factors that contributed to nursing errors used only two rounds. The first took the form of an online survey asking 25 experts to list all the âÂÂhumanâ causes of nursing errors that they could. Analysis of responses resulted in a list of 28 potential reasonsâÂÂthis list was sent back to the same group of experts for the second round, asking them to where can i buy amoxil over the counter score each one for importance. Analysis of this scoring then allowed for consensus conclusions on the top 10 human factors that contributed to nursing errors (with fatigue, heavy workload and communication problems the top three).3In another example, nurse practitioners (NPs) were recruited to participate in a Delphi study to achieve consensus related to NP advance care planning competencies. In round where can i buy amoxil over the counter 1, draft competencies were developed from the findings of a survey of NP beliefs, knowledge and level of implementation of advance care planning.
Round 2 included engagement with 29 NPs who evaluated the draft competencies and their components. Revisions were made based on the original feedback, and a third round was conducted where 15 of the where can i buy amoxil over the counter original NP participants confirmed their consensus with the final document. The final document includes four competencies, each with several elements. Clinical Practice, Consultation where can i buy amoxil over the counter and Communication, Advocacy and Therapeutic Management.4Strengths and weaknesses of Delphi studiesThe Delphi technique offers a flexible approach to gathering the views of experts on an area of interest. The ability for participants to reconsider their views in light of the contribution of others allows for an element of reflection that is missing from studies based on single interviews or focus groups.
The anonymity among the expert groups that underpins where can i buy amoxil over the counter Delphi studies promotes honesty among participants and reduces the risk of the âÂÂhalo effectâ where views from dominant or high-profile members of the group are given extra credence.5However, Delphi studies canâÂÂby their very natureâÂÂbe complex and time consuming. The need for participants to complete multiple rounds where can i buy amoxil over the counter can lead to high drop-out rates which impacts on validity of the study. The ability of participants to amend or alter their views at each round is also something of a double-edged sword. It provides those taking part with the opportunity to reflect where can i buy amoxil over the counter and reconsider their position in response to additional information, which is an important part of nursing practice. Conversely though, there is a danger that this flexibility introduces bias, with participants altering their response to comply with what they view to be the majority view (sometime called the âÂÂbandwagon effectâÂÂ).5Delphi studies can be criticised due to a lack of clarity on what is meant by âÂÂconsensusâÂÂ.
Even with the level of flexibility and reflexivity present in Delphi studies, it where can i buy amoxil over the counter is still unlikely that a group of experts will demonstrate 100% agreement on issues. However, because consensus is a requirement of a Delphi study, there does need to be a judgement on when this point is reached. This is where there is inconsistency across studies and authors, with the suggested level of consensus ranging from 51% to 100%.2 In addition, it has been identified that where can i buy amoxil over the counter in some areas, consensus is not predefined as part of the study method. For example, a review of Delphi studies in nurse education found that fewer than half of the papers appraised included a predefined level at which consensus was judged to have been achieved.6 In addition, the identification of an objective level consensus is only possible when gathering quantifiable dataâÂÂthe judgement on consensus being reached in some qualitative Delphi studies will always be rather more subjective on the part of the researcher, and therefore potentially open to bias.By their nature, Delphi studies often rely purely on expert opinion to generate findings. A further limitation is therefore related to the quality of evidence, with expert opinion viewed as providing a poor basis for making judgements on healthcare interventions.7 This does not mean that the findings of where can i buy amoxil over the counter Delphi studies are intrinsically unreliable or invalid.
It does mean that researchers should consider whether their research question is one that can be answered through expert consensus or whether other approaches (such as a systematic review of research evidence) are more appropriate.ConclusionThe Delphi technique is a well-established approach to answering a research question through the identification of a consensus view across subject experts. It allows where can i buy amoxil over the counter for reflection among participants, who are able to nuance and reconsider their opinion based on the anonymised opinions of others. However, researchers must take steps to enhance robustness of the studies. It is important where can i buy amoxil over the counter to try and prevent participants from simply resorting to agreeing with the majority view. Studies must also predefine what is meant by âÂÂconsensusâ and how it will be established.With careful and clear design though, Delphi studies can make a valuable contribution to the nursing evidence base by tapping into the professionâÂÂs most precious resourceâÂÂthe knowledge and expertise of its practitioners..
Amoxil suspension 250mg
WASHINGTON, DC amoxil suspension 250mg â buy amoxil usa The U.S. Department of LaborâÂÂs Wage and Hour Division (WHD) today posted revisions to regulations that implemented the paid sick leave and expanded family and medical leave provisions of the Families First antibiotics Response Act (FFCRA). The revisions made by the new rule clarify workersâ rights and employersâ amoxil suspension 250mg responsibilities under the FFCRAâÂÂs paid leave provisions, in light of the U.S. District Court for the Southern District of New York in an Aug.
3, 2020, decision that found portions of the regulations invalid. The revisions amoxil suspension 250mg do the following. Reaffirm and provide additional explanation for the requirement that employees may take FFCRA leave only if work would otherwise be available to them. Reaffirm and provide additional explanation for the requirement that an employee have employer approval to amoxil suspension 250mg take FFCRA leave intermittently.
Revise the definition of âÂÂhealthcare providerâ to include only employees who meet the definition of that term under the Family and Medical Leave Act regulations or who are employed to provide diagnostic services, preventative services, treatment services or other services that are integrated with and necessary to the provision of patient care which, if not provided, would adversely impact patient care. Clarify that employees must provide required documentation supporting their need for FFCRA leave to their employers as soon as practicable. Correct an inconsistency regarding when employees may be required to provide notice of a need to take expanded family and medical leave to their employers.âÂÂAs the economy continues to rebound, more businesses return to full capacity, and schools reopen, the need for clarity regarding the Families First antibiotics Response amoxil suspension 250mg Act paid leave provisions may be greater than ever,â said Wage and Hour Administrator Cheryl Stanton. ÃÂÂTodayâÂÂs updates respond to this evolving situation and address some of the challenges the American workforce faces.
Our continuing robust response to this amoxil balances amoxil suspension 250mg support for workers and employers alike, and remains our priority.â The Department issued its initial temporary rule implementing provisions under the FFCRA on April 1, 2020. Read the revisions to that temporary rule, which will become effective Sept. 16, 2020 in the Federal Register. The amoxil suspension 250mg FFCRA helps the U.S.
Combat and defeat the workplace effects of the antibiotics by giving tax credits to American businesses with fewer than 500 employees to provide employees with paid leave for certain reasons related to the antibiotics. Please visit WHDâÂÂs âÂÂQuick Benefits Tipsâ for information about how much leave workers may qualify to use, and the wages employers amoxil suspension 250mg must pay. The law enables employers to provide paid leave reimbursed by tax credits, while at the same time ensuring that workers are not forced to choose between their paychecks and the public health measures needed to combat the amoxil. WHD continues to provide updated information on its website and through extensive outreach efforts to ensure that workers and employers have the information they need about the benefits and protections of the FFCRA.
The agency also provides additional information on common issues employers and employees face when responding to the antibiotics amoxil suspension 250mg and its effects on wages and hours worked under the Fair Labor Standards Act and on job-protected leave under the Family and Medical Leave Act at https://www.dol.gov/agencies/whd/amoxil. WHDâÂÂs mission is to promote http://www.em-achenheim.ac-strasbourg.fr/qr-codes/ and achieve compliance with labor standards to protect and enhance the welfare of the nationâÂÂs workforce. WHD enforces federal minimum wage, overtime pay, recordkeeping, and child labor requirements of the FLSA amoxil suspension 250mg. WHD also enforces the paid sick leave and expanded family and medical leave requirements of the Families First antibiotics Response Act, the Migrant and Seasonal Agricultural Worker Protection Act, the Employee Polygraph Protection Act, the Family and Medical Leave Act, wage garnishment provisions of the Consumer Credit Protection Act, and a number of employment standards and worker protections as provided in several immigration related statutes.
Additionally, WHD administers and enforces the prevailing wage requirements of the Davis Bacon Act and the Service Contract Act and other statutes applicable to Federal contracts for construction and for the provision of goods and services. The mission of the Department amoxil suspension 250mg of Labor is to foster, promote and develop the welfare of the wage earners, job seekers and retirees of the United States. Improve working conditions. Advance opportunities amoxil suspension 250mg for profitable employment.
And assure work-related benefits and rights.PARAMUS, NJ â The U.S. Department of LaborâÂÂs Occupational Safety and Health Administration (OSHA) has cited CarePlus Bergen Inc., doing business as Bergen New Bridge Medical Center, for violating respiratory protection standards at its Paramus, New Jersey, location. OSHA cited the hospital for two serious violations, with proposed penalties of $9,639.Based on a amoxil suspension 250mg antibiotics-related inspection, OSHA cited the Bergen New Bridge Medical Center for failing to fit test tight-fitting face piece respirators on employees who were required to use them. The hospital also failed to train employees on proper respirator use and ensure employees understood when to wear a respirator.
âÂÂEmployers must take action to protect their employees during the amoxil, including implementing amoxil suspension 250mg effective respiratory protection programs,â said OSHA Hasbrouck Heights Area Office Director Lisa Levy. ÃÂÂOSHA standards require healthcare workers to be fit-tested to ensure the respirators they use provide adequate protection.â Employers with questions on compliance with OSHA standards should contact their local OSHA office for guidance and assistance at 800-321-OSHA (6742). OSHAâÂÂs buy antibiotics response webpage offers extensive resources for addressing safety and health hazards during the evolving antibiotics amoxil. The company has 15 amoxil suspension 250mg business days from receipt of the citations and penalties to comply, request an informal conference with OSHAâÂÂs area director or contest the findings before the independent Occupational Safety and Health Review Commission.
Under the Occupational Safety and Health Act of 1970, employers are responsible for providing safe and healthful workplaces for their employees. OSHAâÂÂs role is to help ensure these conditions for AmericaâÂÂs working men and women amoxil suspension 250mg by setting and enforcing standards, and providing training, education and assistance. For more information, visit http://www.osha.gov. The mission of the Department of Labor is to foster, promote and develop the welfare of the wage earners, job seekers and retirees of the United States.
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WASHINGTON, DC buy amoxil usa â where can i buy amoxil over the counter The U.S. Department of LaborâÂÂs Wage and Hour Division (WHD) today posted revisions to regulations that implemented the paid sick leave and expanded family and medical leave provisions of the Families First antibiotics Response Act (FFCRA). The revisions made by the new rule clarify where can i buy amoxil over the counter workersâ rights and employersâ responsibilities under the FFCRAâÂÂs paid leave provisions, in light of the U.S.
District Court for the Southern District of New York in an Aug. 3, 2020, decision that found portions of the regulations invalid. The where can i buy amoxil over the counter revisions do the following.
Reaffirm and provide additional explanation for the requirement that employees may take FFCRA leave only if work would otherwise be available to them. Reaffirm and provide additional explanation for the requirement that an employee have employer approval to take FFCRA where can i buy amoxil over the counter leave intermittently. Revise the definition of âÂÂhealthcare providerâ to include only employees who meet the definition of that term under the Family and Medical Leave Act regulations or who are employed to provide diagnostic services, preventative services, treatment services or other services that are integrated with and necessary to the provision of patient care which, if not provided, would adversely impact patient care.
Clarify that employees must provide required documentation supporting their need for FFCRA leave to their employers as soon as practicable. Correct an inconsistency regarding when employees may be required to provide notice of a need to where can i buy amoxil over the counter take expanded family and medical leave to their employers.âÂÂAs the economy continues to rebound, more businesses return to full capacity, and schools reopen, the need for clarity regarding the Families First antibiotics Response Act paid leave provisions may be greater than ever,â said Wage and Hour Administrator Cheryl Stanton. ÃÂÂTodayâÂÂs updates respond to this evolving situation and address some of the challenges the American workforce faces.
Our continuing where can i buy amoxil over the counter robust response to this amoxil balances support for workers and employers alike, and remains our priority.â The Department issued its initial temporary rule implementing provisions under the FFCRA on April 1, 2020. Read the revisions to that temporary rule, which will become effective Sept. 16, 2020 in the Federal Register.
The FFCRA helps the where can i buy amoxil over the counter U.S. Combat and defeat the workplace effects of the antibiotics by giving tax credits to American businesses with fewer than 500 employees to provide employees with paid leave for certain reasons related to the antibiotics. Please visit WHDâÂÂs âÂÂQuick Benefits Tipsâ for information about where can i buy amoxil over the counter how much leave workers may qualify to use, and the wages employers must pay.
The law enables employers to provide paid leave reimbursed by tax credits, while at the same time ensuring that workers are not forced to choose between their paychecks and the public health measures needed to combat the amoxil. WHD continues to provide updated information on its website and through extensive outreach efforts to ensure that workers and employers have the information they need about the benefits and protections of the FFCRA. The agency also provides additional information on common issues employers and employees face when responding to the antibiotics and its effects on wages and hours worked under the Fair Labor Standards Act where can i buy amoxil over the counter and on job-protected leave under the Family and Medical Leave Act at https://www.dol.gov/agencies/whd/amoxil.
WHDâÂÂs mission is to promote and achieve compliance check my source with labor standards to protect and enhance the welfare of the nationâÂÂs workforce. WHD enforces federal minimum wage, where can i buy amoxil over the counter overtime pay, recordkeeping, and child labor requirements of the FLSA. WHD also enforces the paid sick leave and expanded family and medical leave requirements of the Families First antibiotics Response Act, the Migrant and Seasonal Agricultural Worker Protection Act, the Employee Polygraph Protection Act, the Family and Medical Leave Act, wage garnishment provisions of the Consumer Credit Protection Act, and a number of employment standards and worker protections as provided in several immigration related statutes.
Additionally, WHD administers and enforces the prevailing wage requirements of the Davis Bacon Act and the Service Contract Act and other statutes applicable to Federal contracts for construction and for the provision of goods and services. The mission of the Department of Labor is where can i buy amoxil over the counter to foster, promote and develop the welfare of the wage earners, job seekers and retirees of the United States. Improve working conditions.
Advance opportunities where can i buy amoxil over the counter for profitable employment. And assure work-related benefits and rights.PARAMUS, NJ â The U.S. Department of LaborâÂÂs Occupational Safety and Health Administration (OSHA) has cited CarePlus Bergen Inc., doing business as Bergen New Bridge Medical Center, for violating respiratory protection standards at its Paramus, New Jersey, location.
OSHA cited the hospital for two serious violations, with proposed penalties of $9,639.Based on a antibiotics-related inspection, OSHA cited the Bergen New Bridge Medical Center for failing to fit test tight-fitting face piece respirators on employees who were required to use them where can i buy amoxil over the counter. The hospital also failed to train employees on proper respirator use and ensure employees understood when to wear a respirator. âÂÂEmployers must take action to protect their employees during the amoxil, including implementing effective respiratory protection programs,â said OSHA where can i buy amoxil over the counter Hasbrouck Heights Area Office Director Lisa Levy.
ÃÂÂOSHA standards require healthcare workers to be fit-tested to ensure the respirators they use provide adequate protection.â Employers with questions on compliance with OSHA standards should contact their local OSHA office for guidance and assistance at 800-321-OSHA (6742). OSHAâÂÂs buy antibiotics response webpage offers extensive resources for addressing safety and health hazards during the evolving antibiotics amoxil. The company has 15 business days from receipt of the citations and penalties to comply, request an informal conference with OSHAâÂÂs area director or contest the findings before the independent Occupational Safety where can i buy amoxil over the counter and Health Review Commission.
Under the Occupational Safety and Health Act of 1970, employers are responsible for providing safe and healthful workplaces for their employees. OSHAâÂÂs role is to help ensure these conditions for AmericaâÂÂs working men and women by setting and enforcing standards, and providing where can i buy amoxil over the counter training, education and assistance. For more information, visit http://www.osha.gov.
The mission of the Department of Labor is to foster, promote and develop the welfare of the wage earners, job seekers and retirees of the United States. Improve working conditions where can i buy amoxil over the counter. Advance opportunities for profitable employment.
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