Buy cialis 20mg

Over the last decade, Medicare Advantage, the private plan alternative to traditional Medicare, has taken on a larger role buy cialis 20mg in http://eastwoodrealestateservices.com/average-price-of-cialis-daily/ the Medicare program. In 2020, more than 24 million Medicare beneficiaries are enrolled in a Medicare Advantage plan. This brief provides an overview of the Medicare Advantage plans that are available for 2021 and key trends over time.Plan Offerings in 2021Number buy cialis 20mg of PlansNumber of Plans Available to Beneficiaries.

For 2021, the average Medicare beneficiary has access to 33 Medicare Advantage plans, the largest number of options available in the last decade (Figure 1).Figure 1. The average Medicare beneficiary has access to 33 Medicare Advantage plans in 2021, an increase from prior yearsAmong the 33 Medicare Advantage plans buy cialis 20mg generally available for individual enrollment to the average Medicare beneficiary, 27 of the plans include prescription drug coverage (MA-PDs). These numbers exclude employer or union-sponsored group plans, Special Needs Plans (SNPs) and PACE plans, which are only available to select populations.Total Number of Plans.

In total, 3,550 Medicare Advantage plans are available nationwide for individual enrollment in 2021 – a 13 percent increase buy cialis 20mg (402 more plans) from 2020 and the largest number of plans ever available (Figure 2. Appendix Table 1). The vast majority buy cialis 20mg (89 percent) of all Medicare Advantage plans offered include prescription drug coverage in 2021.

.As in prior years, HMOs continue to account for about two-thirds (62%) of all plans offered in 2021. The availability of local PPOs has increased rapidly over buy cialis 20mg recent years. In 2021, one-third of plans offered are local PPOs, compared to a quarter in 2018.

Between 2020 and 2021, the number of regional PPOs has remained constant, while the number of private buy cialis 20mg fee-for-service plans has continued to decline.The growth in number of plans varies across states and counties, with the preponderance of the growth occurring in Florida and California (41 more and 30 more plans, respectively. Data not shown). Virginia has 6 fewer plans available for 2021 than in 2020, while South Carolina has 3 fewer plans, and Maryland and Nebraska each have one fewer plan available in 2021 than in 2020.While many employers and unions also offer Medicare Advantage plans to their retirees, no information about these 2021 plan offerings is made available by CMS to the public during the Medicare open enrollment period because these plans are not available to the general Medicare population.One notable change for 2021 is that buy cialis 20mg people with end-stage renal disease (ESRD) are eligible to enroll in Medicare Advantage plans.

Prior to this change, people with ESRD were not able to enroll in most Medicare Advantage plans, subject to limited exceptions, such as C-SNPS for people with ESRD.Special Needs Plans (SNPs). More SNPs are available for 2021 than in any year since they were authorized, increasing from 855 plans in 2020 to 975 plans in 2021, a 14 percent increase (Figure 3). .The rise in SNPs for people who require an institutional-level of care (I-SNPs) has been particularly notable, more than doubling buy cialis 20mg from 83 plans in 2017 to 174 plans in 2021.

I-SNPs may be attractive to insurers because they tend to have much lower marketing costs than other plan types since they are often the only available option for people to receive their Medicare benefits in certain retirement communities and nursing homes. The number of SNPs for people dually eligible for Medicare and Medicaid (D-SNPs) has also increased sharply over the past five years, rising from 373 dual SNPs in 2017 to buy cialis 20mg 598 dual SNPs in 2021, a 60% increase, suggesting insurers’ continue to be interested in managing the care of this high-need population.The number of SNPs offered for people with chronic conditions (C-SNPs) is also increasing in 2021, most of which focus on people with diabetes, heart disease, or lung conditions, as has been the case since the inception of C-SNPs. For 2021, three firms are offering C-SNPs for people with dementia (the same as 2020), two firms are offering a C-SNP for people with mental health conditions (up one from 2020), three firms are offering C-SNPs for people with end-stage renal disease (one fewer than 2020) and two firms are offering C-SNPs for people with HIV/AIDS (similar to 2020).Variation in the Number of Plans, by Geographic Area.

On average, beneficiaries in metropolitan areas can choose from buy cialis 20mg about twice as many Medicare Advantage plans as beneficiaries in non-metropolitan areas (36 plans versus 20 plans, respectively).In 11 percent of counties (accounting for 41% of beneficiaries), beneficiaries can choose from more than 35 plans in 2021, including eleven counties in Ohio and five counties in Pennsylvania where more than 60 Medicare Advantage plans are available (Figure 4). In contrast, in 4 percent of counties (accounting for 1% of beneficiaries), beneficiaries can choose from two or fewer Medicare Advantage plans. The number of counties with no Medicare Advantage plans for 2021 buy cialis 20mg is 82, similar to 2020.

As in prior years, there are no Medicare Advantage plans offered in Alaska. Additionally, no Medicare buy cialis 20mg Advantage plans are available in territories other than Puerto Rico. .Access to Medicare Advantage Plans, by Plan TypeAs in recent years, virtually all Medicare beneficiaries (99%) have access to a Medicare Advantage plan as an alternative to traditional Medicare, including almost all beneficiaries in metropolitan areas (99.9%) and the vast majority of beneficiaries in non-metropolitan areas (97.7%).

In non-metropolitan counties, a smaller share of beneficiaries have access to HMOs (87% in non-metropolitan versus 99% in metropolitan counties) or local PPOs (89% in non-metropolitan versus 96% in metropolitan counties), and a slightly larger share of beneficiaries have access to regional PPOs (77% in non-metropolitan counties versus 72% in metropolitan buy cialis 20mg counties). Number of FirmsThe average Medicare beneficiary is able to choose from plans offered by 8 firms in 2021, one more than in 2020 (Figure 5). Despite most beneficiaries having access to plans operated by several different firms, enrollment is concentrated in plans operated by UnitedHealthcare, Humana, buy cialis 20mg and Blue Cross Blue Shield affiliates.Figure 5.

More than one-quarter of beneficiaries can choose among Medicare Advantage plans offered by 10 or more firmsMore than one-quarter of beneficiaries (27%) are able to choose from plans offered by 10 or more firms. Fifteen or more firms are offering Medicare Advantage plans in three counties. Orange County, California and Summit buy cialis 20mg and Medina Counties in Ohio.

In contrast, in 109 counties, most of which are rural counties with relatively few Medicare beneficiaries (1% of total), only one firm will offer Medicare Advantage plans in 2021. Over the past several years, the number of counties with a single firm offering Medicare Advantage plans has fallen substantially buy cialis 20mg. As recently as 2019, there was a single firm offering plans in nearly 200 counties.UnitedHealthcare and Humana, the two firms with the most Medicare Advantage enrollees in 2020, have large footprints across the country, offering plans in most counties.

Humana is offering plans in 84 percent of counties and UnitedHealthcare is offering plans in 66 percent of counties buy cialis 20mg in 2021 (Figure 6). More than 8 in 10 (87%) Medicare beneficiaries have access to at least one Humana plan and 86 percent have access to at least one UnitedHealthcare plans. .Most major Medicare Advantage firms have also buy cialis 20mg expanded the number of counties where they are offering plans.

UnitedHealthcare is offering plans in 2,117 counties in 2021, an increase of 245 from 2021, while Humana is offering plans in 2,703 counties in 2021, an increase of 33 from 2020. Centene is offering plans in 1,129 counties in 2021, an increase of 261 plans from 2020 buy cialis 20mg. Blue Cross Blue Shield Affiliates are offering plans in 1,181 counties, an increase of 152 plans.

CVS Health is offering buy cialis 20mg plans in 1,759 counties, an increase of 119 plans. And Cigna is offering plans in 369 counties, an increase of 67 plans. Kaiser Permanente had the smallest growth and is offering plans in 109 counties, an increase of 4 plans.New Market Entrants and ExitsMedicare Advantage continues to be an attractive market for insurers, with 14 firms entering the market for the first time in 2021, collectively accounting for about 6 percent of the growth in the number of buy cialis 20mg plans available for general enrollment and about 10 percent of the growth in SNPs (Appendix Table 2).

Nine new entrants are offering HMOs available for individual enrollment. Five of buy cialis 20mg the new entrants are offering SNPs. Three firms are offering D-SNPs for people dually eligible for Medicaid, three firms are offering C-SNPs for people with select chronic conditions, and one firm is offering an I-SNPs Four of the new firm entrants are offering plans in California, two are offering plans in Indiana, and the remainder are offering plans in at least one of ten other states (Colorado, Georgia, Illinois, Mississippi, Missouri, Ohio, Texas, Utah, and Wisconsin).Six firms that previously participated in the Medicare Advantage market are not offering plans in 2021.

Two of the firms (ApexHealth, Inc. And Clarion Health) offered plans for the first time in 2020, but did not appear buy cialis 20mg to enroll any participants. The other four firms had very low enrollment in 2020.

Three of the six exiting firms offered plans in New York.PremiumsThe buy cialis 20mg vast majority of Medicare Advantage plans for individual enrollment (89%) will include prescription drug coverage (MA-PDs), and 54 percent of these plans will charge no premium, other than the Part B premium, similar to 2020. More than nine out of ten beneficiaries (96%) have access to a MA-PD with no monthly premium in 2021. However, in Wyoming, beneficiaries do not have access to a zero-premium MA-PD, and in Idaho, less than half of beneficiaries have access to a zero-premium MA-PD.In 2020, 60 percent of enrollees in MA-PD plans buy cialis 20mg pay no premium other than the Medicare Part B premium of $144.60 per month.

Based on enrollment in March 2020, nearly one in five enrollees (18%) pay at least $50 a month, and 6 percent pay $100 or more. CMS announced that the average monthly plan premium among all buy cialis 20mg Medicare Advantage enrollees in 2021, including those who pay no premium for their Medicare Advantage plan, is expected to decrease 11 percent from 2020 to $21 a month. CMS does not disclose the methods or assumptions used in deriving their calculations, but since most Medicare Advantage enrollees pay no additional premium, the average they report is heavily influenced by zero-premium plans, and does not reflect the average premium paid by those who are in plans with an additional premium.Extra BenefitsMedicare Advantage plans may provide extra benefits that are not available in traditional Medicare, are considered “primarily health related,” and can use rebate dollars (including bonus payments) to help cover the cost of these extra benefits.

Beginning in 2019, CMS expanded the definition of “primarily health related” to buy cialis 20mg allow Medicare Advantage plans to offer additional supplemental benefits. Medicare Advantage plans may also restrict the availability of these extra benefits to certain subgroups of beneficiaries, such as those with diabetes or congestive heart failure, making different benefits available to different enrollees.Beginning in 2020, Medicare Advantage plans have also been able to offer extra benefits that are not primarily health related for chronically ill beneficiaries, known as Special Supplemental Benefits for the Chronically Ill (SSBCI). Information on the availability of SSBCI for 2021 has not yet been published by buy cialis 20mg CMS, but may include services such as pest control, food and produce (beyond a limited basis), and non-medical transportation.

Since plans are permitted to offer these benefits non-uniformly to enrollees, it will be important to examine how these benefits are distributed across subgroups of enrollees.Availability of Extra Benefits in Plans for General Enrollment. Historically, the most offered extra benefits were buy cialis 20mg fitness, dental, vision, and hearing. Nearly two-thirds of plans (68%) provide all four of these benefits for 2021.

Though these benefits are widely available, the scope of specific services varies. For example, a dental benefit buy cialis 20mg may include cleanings only or more comprehensive coverage. As of 2020, Medicare Advantage plans have also been allowed to offer more telehealth benefits than traditional Medicare (though Medicare has temporarily expanded these benefits during the cialis).

The vast majority (98%) of Medicare Advantage plans are offering telehealth in 2021 (up from 91% in 2020) (Figure buy cialis 20mg 7).Figure 7. Most Medicare Advantage plans provide fitness and dental benefits but much fewer provide in-home or caregiver supportOther extra benefits that are frequently offered for 2021 include over the counter items (75%), meal benefits, such as a cooking class, nutrition education, or meal delivery (55%), and transportation benefits (36%).Less than 10 percent of plans provide bathroom safety devices (6%) or in-home support (6%).Availability of Extra Benefits in Special Needs Plans. SNPs are designed to serve a disproportionately high-need population, and a somewhat larger buy cialis 20mg percentage of SNPs than plans for other Medicare beneficiaries provide their enrollees with over the counter items (91%), transportation benefits (85%) and meal benefits (63%).

Similar to plans available for general enrollment, a relatively small share of SNPs provide bathroom safety devices (11%) or in-home support (18%).Access to Extra Benefits. Virtually all Medicare beneficiaries live in a county where at least one Medicare Advantage plan available for general enrollment has some extra benefits not covered by traditional Medicare, with 98% having access to some dental, fitness, vision, and hearing benefits for 2021 buy cialis 20mg. The vast majority of beneficiaries also have access to telehealth benefits (99%), over the counter items (99%), transportation assistance (95%) and a meal benefit (98%), but far fewer have access to bathroom safety (55%) or in-home support (62%).DiscussionMore Medicare Advantage plans are being offered for 2021 than in any other year.

Fourteen insurers are entering the Medicare Advantage market for the first time, and six insurers are exiting the market, suggesting thatMedicare Advantage remains an attractive, profitable market for insurers buy cialis 20mg. As in prior years, some (mostly non-metropolitan) counties are less attractive to insurers, with fewer firms and plans available, though the number of areas where this is the case has declined over time. Overall, more than 99 percent of beneficiaries will have access to one or more Medicare Advantage plans buy cialis 20mg in 2021, similar to prior years.

With more firms offering SNPs and the number of SNPs rapidly growing, there may be greater focus on how well high-need, vulnerable beneficiaries are being served by Medicare Advantage plans, including SNPs as well as plans for general enrollment. As Medicare Advantage enrollment continues to buy cialis 20mg grow, insurers seem to be responding by offering more plans and choices to the people on Medicare. This analysis focuses on the Medicare Advantage marketplace in 2021 and trends over time.

The analysis includes more than 24 million enrollees in Medicare Advantage plans in 2020.Data on Medicare Advantage plan availability, enrollment, and premiums were collected from a set of data files released by the Centers for Medicare &. Medicaid Services (CMS):Medicare Advantage plan landscape files, released each fall prior to the annual enrollment periodMedicare Advantage plan and premium files, released each fallMedicare Advantage plan crosswalk files, released each fallMedicare Advantage contract/plan/state/county level enrollment files, released on a monthly basisMedicare Advantage plan benefit package files, released each fallMedicare Enrollment Dashboard files, released on a monthly basisIn previous years, KFF has used the Medicare Advantage Penetration Files to calculate buy cialis 20mg the number of Medicare beneficiaries eligible for Medicare. The Medicare Advantage Penetration Files includes people who were previously, but no longer covered by Medicare (e.g., people who obtained employer-sponsored health insurance coverage after initially enrolling in Medicare).

It also includes people within 5 months of their 65th birthday, but buy cialis 20mg not yet age 65. In addition, CMS has identified an issue where beneficiaries with multiple addresses were double counted in the Penetration File. KFF has refined its approach this year and is using the Medicare Enrollment Dashboard to calculate the number of Medicare beneficiaries because it only includes buy cialis 20mg Medicare beneficiaries with either Part A or Part B coverage, which is a more accurate estimate of the Medicare population.

The numbers published here supersede all prior estimates by KFF of the number of Medicare beneficiaries.Jeannie Fuglesten Biniek, Meredith Freed, and Tricia Neuman are with KFF.Anthony Damico is an independent consultant.During the Medicare open enrollment period from October 15 to December 7 each year, beneficiaries can enroll in a plan that provides Part D drug coverage, either a stand-alone prescription drug plan (PDP) as a supplement to traditional Medicare, or a Medicare Advantage prescription drug plan (MA-PD), which covers all Medicare benefits, including drugs. Among the 46 million buy cialis 20mg Part D enrollees in 2020, 20.2 million (44%) are in PDPs and 19.3 million (41%) are in MA-PDs (excluding the 7.0 million (15%) in employer-only group PDPs and MA-PDs). This issue brief provides an overview of Medicare Part D drug plans that will be available in 2021 and key trends over time.Part D Plan AvailabilityThe Average Medicare Beneficiary Has a Choice of Nearly 60 Medicare Plans with Part D Drug Coverage in 2021, Including 30 Medicare Stand-alone Drug Plans and 27 Medicare Advantage Drug PlansFigure 1.

The Average Medicare Beneficiary Has a Choice of Nearly 60 Medicare Plans Offering Drug Coverage in 2021, Including 30 Stand-alone Drug Plans and 27 Medicare Advantage Drug PlansA larger number of Part buy cialis 20mg D plans will be offered in 2021 than in recent years. The average Medicare beneficiary will have a choice of 30 stand-alone PDPs in 2021, two more PDP options than in 2020, and eight more than in 2017, a 36% increase (Figure 1). Although the number of PDP options in 2021 is half of what it was at the peak in 2007 (when there were 56 PDP options, on buy cialis 20mg average), this is the fourth year in a row with an increase in the average number of stand-alone drug plan options.In 2021, beneficiaries will also have access to 27 MA-PDs, on average, a 71% increase in MA-PD options since 2017 (excluding Medicare Advantage plans that do not offer the drug benefit and plans not available to all beneficiaries.

Overall, an average of 33 Medicare Advantage plan options will be available in 2021).Based on September 2020 enrollment, 8 out of 10 PDP enrollees (80%) in 2021 are projected to be in PDPs operated by just four firms. UnitedHealth, Centene (which acquired buy cialis 20mg WellCare in 2020), Humana, and CVS Health (based on PDP enrollment as of September 2020). All four firms offer PDPs in all 34 PDP regions in 2021.A Total of 996 Medicare Part D Stand-Alone Prescription Drug Plans Will Be Offered in 2021, a 5% Increase From 2020 and a 34% Increase Since 2017 Figure 2.

A Total of 996 Medicare Part D Stand-Alone Prescription Drug Plans Will Be Offered in 2021, a 5% Increase From 2020 and a 34% Increase Since 2017​A total of 996 PDPs will be offered in the 34 PDP regions in 2021 (plus another 11 PDPs in the territories), an increase of 48 PDPs (5%) over 2020, and 250 more PDPs (a 34% increase) since 2017 (Figure 2). This increase is primarily due to the Trump Administration’s elimination of the buy cialis 20mg “meaningful difference” requirement for enhanced benefit PDPs offered by the same organization in the same region. Eliminating this requirement means that PDP sponsors no longer have to demonstrate that their enhanced PDPs offered in the same region are meaningfully different in terms of enrollee out-of-pocket costs.

In 2021, 62% of PDPs (618 plans) will offer enhanced Part D benefits—a 60% increase in buy cialis 20mg the availability of enhanced-benefit PDPs since 2017, when just over half of PDPs (387 plans) offered enhanced benefits.The number of PDPs per region in 2021 will range from 25 PDPs in Alaska to 35 PDPs in Texas and will be the same or higher in 32 of the 34 PDP regions compared to 2020 (see map, Table 1). Part D PremiumsThe Estimated Average Monthly Premium for Medicare PDPs Is Projected to Increase by 9% to $41 in 2021, Based on Current EnrollmentFigure 3. The Estimated Average Monthly Premium for Medicare PDPs Is Projected to Increase by 9% to $41 in 2021, Based on Current Enrollment​The estimated national average monthly PDP premium for 2021 is projected to increase by 9% to $41, from $38 in 2020, weighted by September 2020 buy cialis 20mg enrollment (Figure 3).

It is likely that the actual average weighted premium for 2021, after taking into account enrollment choices by new enrollees and plan changes by current enrollees, will be somewhat lower than the estimated average. CMS reported that the average premium for basic Part D coverage buy cialis 20mg offered by PDPs and MA-PDs will be an estimated $30 in 2021. Our premium estimate is higher because it is based on PDPs only (excluding MA-PDs) and includes PDPs offering both basic and enhanced coverage (enhanced plans, which account for 62% of all PDPs in 2021, have higher premiums than basic plans, on average).Average Monthly Premiums for the 21 National Part D Stand-alone PDPs Are Projected to Range from $7 to $89 in 2021, with Higher Average Premiums for Enhanced Benefits and Zero-Deductible PDPsFigure 4.

Average Monthly Premiums for the 21 National Part D Stand-alone buy cialis 20mg Drug Plans Are Projected to Range from $7 to $89 in 2021​PDP premiums will vary widely across plans in 2021, as in previous years (Figure 4, Table 2). Among the 21 PDPs available nationwide, average premiums will range from a low of $7 per month for SilverScript SmartRx to a high of $89 per month for AARP MedicareRx Preferred.Changes to premiums from 2020 to 2021, averaged across regions and weighted by 2020 enrollment, also vary widely across PDPs, as do the absolute amounts of monthly premiums for 2021.The 1.9 million non-LIS enrollees in the largest PDP, CVS Health’s SilverScript Choice (which had a total of 3.9 million enrollees in 2020, including those receiving low-income subsidies) will face a modest $1 (2%) decrease in their average monthly premium, from $29 in 2020 to $28 in 2021.In contrast, the 1.8 million non-LIS enrollees in the second largest PDP, AARP MedicareRx Preferred, will face a $10 (12%) increase in their average monthly premium between 2020 and 2021, from $79 to $89. This is the highest monthly premium among the national PDPs buy cialis 20mg in 2021.The 1.3 million non-LIS enrollees in the fourth largest PDP, Humana Premier Rx, will see a $7 (13%) increase in their monthly premium, from $58 in 2020 to $65 in 2021.Most Part D stand-alone drug plans in 2021 (62% of PDPs) will offer enhanced benefits for a higher monthly premium.

Enhanced benefits can include a lower (or no) deductible, reduced cost sharing, or a higher initial coverage limit than under the standard benefit design. The average premium in 2021 for enhanced buy cialis 20mg benefit PDPs is $51, which is 55% higher than the monthly premium for PDPs offering the basic benefit ($33) (weighted by September 2020 enrollment).In 2021, a large majority of PDPs (86%) will charge a deductible, with most PDPs (67%) charging the standard amount of $445 in 2021. Across all PDPs, the average deductible in 2021 will be $345 (weighted by September 2020 enrollment).

The average monthly premium in 2021 for PDPs that charge no deductible is $88, nearly three times the monthly premium for PDPs that charge the standard deductible ($34) or a partial deductible ($31) (weighted by September 2020 enrollment).Nearly 8 in 10 Part D Stand-alone Drug Plan Enrollees Without Low-income Subsidies Will Pay Higher Premiums in 2021 If They Stay buy cialis 20mg in Their Current PlanFigure 5. Nearly 8 in 10 Part D Stand-alone Drug Plan Enrollees Without Low-income Subsidies Will Pay Higher Premiums in 2021 If They Stay in Their Current Plan​Most (78%, or 10 million) of the 13.4 million Part D PDP enrollees who are responsible for paying the entire premium (which excludes Low-Income Subsidy (LIS) recipients) will see their monthly premium increase in 2021 if they stay in their same plan, while 2.8 million (21%) will see a premium reduction if they stay in their same plan (Figure 5).Nearly 2 million non-LIS enrollees (13%) will see a premium increase of $10 or more per month, while significantly fewer (0.2 million non-LIS enrollees, or 1%) will see a premium reduction of the same magnitude. One-third (34%) of non-LIS enrollees (4.6 million) are projected to pay monthly premiums of at least $60 if they stay in their current plans, and more than 230,000 (2% of non-LIS enrollees) are projected to pay monthly premiums of at least $100.The Average Monthly Part D Premium in 2021 for the Subset of Enhanced Stand-alone Drug Plans Covering Insulin at a $35 Monthly Copay Is Substantially Higher Than Premiums for Other PDPsFigure 6.

The Average Monthly Part D Premium in 2021 for the Subset of Enhanced Stand-alone Drug Plans Covering Insulin at a $35 Monthly Copay is Substantially Higher than Premiums for Other Plans​New for 2021, beneficiaries in each state will have the option to enroll in a Part D plan participating buy cialis 20mg in the Trump Administration’s new Innovation Center model in which enhanced drug plans cover insulin products at a monthly copayment of $35 in the deductible, initial coverage, and coverage gap phases of the Part D benefit. Participating plans do not have to cover all insulin products at the $35 monthly copayment amount, just one of each dosage form (vial, pen) and insulin type (rapid-acting, short-acting, intermediate-acting, and long-acting).In 2021, a total of 1,635 enhanced Part D plans will participate in this model, which represents just over 30% of both PDPs (310 plans) and MA-PDs (1,325 plans) available in 2021, including plans in the territories. Between 8 and 10 enhanced PDPs in each buy cialis 20mg region are participating in the model, in addition to multiple MA-PDs (see map).

The average premium in 2021 for the subset of enhanced PDPs participating in the insulin $35 copay model ($59) is nearly twice as high as the monthly premium for basic PDPs ($33) and 61% higher than the average premium for enhanced PDPs that are not participating in the model ($37) (weighted by September 2020 enrollment). Part D Cost SharingPart D Enrollees Will buy cialis 20mg Pay Much Higher Cost-Sharing Amounts for Brands and Non-preferred Drugs Than For Drugs on a Generic Tier, and a Mix of Copays and Coinsurance for Different Formulary TiersFigure 7. In 2021, Part D Enrollees Will Pay Much Higher Cost-Sharing Amounts for Brands and Non-preferred Drugs than for Drugs on a Generic Tier, and a Mix of Copays and Coinsurance for Different Formulary Tiers​In 2021, as in prior years, Part D enrollees will face much higher cost-sharing amounts for brands and non-preferred drugs (which can include both brands and generics) than for drugs on a generic tier, and a mix of copayments and coinsurance for different formulary tiers (Figure 7).

The typical five-tier formulary design in Part D includes tiers for preferred generics, generics, preferred brands, non-preferred drugs, and specialty drugs buy cialis 20mg. Among all PDPs, median standard cost sharing in 2021 is $0 for preferred generics and $5 for generics (an increase from $4 in 2020), $40 for preferred brands (a decrease from $42 in 2020), 40% coinsurance for non-preferred drugs (an increase from 38% in 2020. The maximum allowed is 50%), and 25% coinsurance for specialty drugs (the same as in buy cialis 20mg 2020.

The maximum allowed is 33%).Among the 21 national PDPs, 13 PDPs, covering 9.3 million enrollees as of September 2020, are increasing cost-sharing amounts for drugs on at least one formulary tier between 2020 and 2021 (Table 3). Five PDPs are increasing copayments for generics, with increases buy cialis 20mg ranging from $1 to $4. Six PDPs are increasing copayments for preferred brands, with increases ranging from $3 to $10.

And 10 PDPs are increasing buy cialis 20mg coinsurance for non-preferred drugs, with increases ranging from 2 percentage points (e.g., from a 38% coinsurance rate to 40%) to 14 percentage points (e.g., from a 35% coinsurance rate to 49%).Low-Income Subsidy Plan AvailabilityIn 2021, 259 Part D Stand-Alone Drug Plans Will Be Premium-Free to Enrollees Receiving the Low-Income Subsidy (Benchmark Plans)Figure 8. In 2021, 259 Part D Stand-Alone Drug Plans Will Be Available Without a Premium to Enrollees Receiving the Low-Income Subsidy (“Benchmark” Plans)​In 2021, a larger number of PDPs will be premium-free benchmark plans—that is, PDPs available for no monthly premium to Medicare Part D enrollees receiving the Low-Income Subsidy (LIS)—than in recent years, with 259 premium-free benchmark plans, or roughly a quarter of all PDPs in 2021 (Figure 8). Through the Part D LIS program, enrollees with low incomes and modest assets are eligible for assistance with Part D plan premiums and cost sharing.

As of 2020, approximately 13 million Part D enrollees are receiving LIS, including 6.7 million (52%) in PDPs and 6.1 million (48%) in MA-PDs.On average (weighted by Medicare enrollment), LIS beneficiaries have eight benchmark plans available to them for 2021, or about one-fourth buy cialis 20mg the average number of PDP choices available overall. All LIS enrollees can select any plan offered in their area, but if they enroll in a non-benchmark plan, they must pay some portion of their chosen plan’s monthly premium. In 2021, 10% of all LIS PDP buy cialis 20mg enrollees who are eligible for premium-free Part D coverage (0.6 million LIS enrollees) will pay Part D premiums averaging $33 per month unless they switch or are reassigned by CMS to premium-free plans.The number of benchmark plans available in 2021 will vary by region, from five to 10 (see map).

In 2020, 89% of the 6.6 million LIS PDP enrollees are projected to be in PDPs operated by five firms. CVS Health, Centene, Humana, UnitedHealth, buy cialis 20mg and Cigna (based on 2020 enrollment). DiscussionOur analysis of the Medicare Part D stand-alone drug plan landscape for 2021 shows that millions of Part D enrollees without low-income subsidies will face premium and other cost increases in 2021 if they stay in their current stand-alone drug plan.

There are more plans available nationwide in 2021, with Medicare beneficiaries having 30 PDP choices during this year’s open enrollment buy cialis 20mg period, plus 27 Medicare Advantage drug plan options. Most Part D PDP enrollees who remain in the same plan in 2021 will be in a plan with the standard $445 deductible and will face much higher cost sharing for brands than for generic drugs, including as much as 50% coinsurance for non-preferred drugs.Some Part D enrollees who choose to stay in their current plans may see lower premiums and other costs for their drug coverage, but nearly 8 in 10 non-LIS enrollees will face higher premiums if they remain in their current plan, and many will also face higher deductibles and cost sharing for covered drugs. Some beneficiaries might find the best coverage and costs for their specific medications in a buy cialis 20mg plan with a relatively low premium, while for other beneficiaries, a higher-premium plan might be more suitable.

Because Part D plans vary in a number of ways that can have a significant effect on an enrollee’s out-of-pocket spending, beyond the monthly premium, all Part D enrollees could benefit from the opportunity to compare plans during open enrollment.Juliette Cubanski is with KFF.Anthony Damico is an independent consultant. This analysis focuses on the Medicare Part D buy cialis 20mg stand-alone prescription drug plan marketplace in 2021 and trends over time. The analysis includes 20.2 million enrollees in stand-alone PDPs, as of March 2020.

The analysis excludes 17.4 million MA-PD enrollees (non-employer), and another 4.6 million enrollees in employer-group only PDPs and 2.3 million in employer-group only MA-PDs for whom plan premium and benefits data are unavailable.Data on Part D plan availability, enrollment, and buy cialis 20mg premiums were collected from a set of data files released by the Centers for Medicare &. Medicaid Services (CMS):– Part D plan landscape files, released each fall prior to the annual enrollment period– Part D plan and premium files, released each fall– Part D plan crosswalk files, released each fall– Part D contract/plan/state/county level enrollment files, released on a monthly basis– Part D Low-Income Subsidy enrollment files, released each spring– Medicare plan benefit package files, released each fallIn this analysis, premium estimates are weighted by September 2020 enrollment unless otherwise noted. Percentage increases are calculated based on non-rounded estimates and in some cases differ from percentage calculations calculated based on rounded estimates presented in the text..

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Many people have cialis bph medicare multiple or repeated trauma. The more intense and frequent a trauma is, the more likely it is to have an impact on people. Trauma has both short-term and long-term effects. In children this might be fear of being separated from a caregiver, cialis bph medicare excessive crying or screaming, weight loss and nightmares. In older children it could be poor concentration, feelings of guilt or shame, anxiety, depression, difficulty sleeping, eating disorders, self-harming behavior, sexual acting out or use of drugs or alcohol, among other things.

These behaviors and difficulties can persist into adulthood, and may lead to difficulties getting or keeping a job, disruption in relationships or criminal behavior. When these behaviors occur in people they likely indicate some cialis bph medicare sort of traumatic past. This is because the trauma changes the way the brain functions. These struggles will sometimes lead people to seek mental health services, but sometimes people suffer without recognizing that the problems cialis bph medicare may be connected to a past traumatic event, or that they can change. As traumatized children grow into adults they are often perceived as being the problem themselves, instead of being seen as the victim of a trauma.

When friends, family, professionals and society view the person as the problem it creates a lack of compassion and ignores the healing that could occur if the trauma were recognized. When one cialis bph medicare views those with difficult behavior as a victim of their past, they will approach them with more empathy and compassion. This is the essence of being trauma informed. Trauma-informed care has been a topic of discussion for several years within the human service world. According to Trauma-Informed Care Implementation Resource Center, trauma-informed care cialis bph medicare shifts the focus from “What’s wrong with you?.

€ to “What happened to you?. € There has been a push to bring this concept outside the therapy office and into broader health care settings. This perspective, however, can be useful beyond the cialis bph medicare realm of health care. When individuals become trauma informed, they can approach all interactions differently and with more empathy and compassion. Some cialis bph medicare people, however, resist this idea.

They seem to believe that recognizing past trauma and approaching people with compassion means not holding them accountable for their behavior, and letting them “get away” with bad behavior. Handing out punishment for bad behavior while ignoring the emotional reality of the person will not fully address the problem. It may temporarily reduce the cialis bph medicare behavior, but it will likely get worse later. Compassion within trauma-informed living is recognizing the past trauma as the source of the pain that leads to difficult behavior. In the process of acknowledging the trauma and validating the emotions a door is opened to healing and learning new ways of coping.

This can be done cialis bph medicare while still holding them accountable to the consequences of the behavior. Living as a trauma-informed human means recognizing that another’s bad behavior or grumpy attitude is likely coming from a place of past trauma, and having compassion and kindness for the person, even while acknowledging that consequences happen. It is through the compassion and kindness that the healing happens. order cialis online in canada While many peoplefind healing from trauma through therapy or counseling, healing cialis bph medicare happens withinall compassionate interactions. Therefore, every person has the power to be aforce of healing in the lives of those around them, when they recognize there’sa good chance that a person’s difficult behavior is likely the result of pasttrauma, and treat them with compassion.

For those who need more intense treatment for mental health conditions, MidMichigan Health provides an intensive outpatient program called Psychiatric Partial Hospitalization cialis bph medicare Program at MidMichigan Medical Center – Gratiot. Those interested in more information about the PHP program may call (989) 466-3253. Those interested in more information on MidMichigan’s comprehensive behavioral health programs may visit www.midmichigan.org/mentalhealth.Olympic athletes train to be thebest in the world at their respective sports. They are determined, talented,capable, and display a level of grit cialis bph medicare and determination qualifying them for thehighest stage of competition. They spend years working toward a few simpleultimate goals.

Giving their best performance, honoring their country and leavingthe court, mat, field or track with a medal in their hand. When gymnast Simone Biles recentlywithdrew from the Olympic Games, it came cialis bph medicare to many as a surprise. What may havecome as even more of a surprise to some is the reason she withdrew. Her mentalhealth. This latest example of thecourage of an athlete to stand up and let the world know that mental health ishealth has brought incredible awareness to the importance cialis bph medicare of mental health inall people, even Olympians.

If you’re an athlete, or if youhave kids who play sports, you might be worried and wondering what you can doto address potential mental health struggles related to sports. Consider thesesuggestions cialis bph medicare when it comes to sports and mental health. Talk, talk, talk. Ifyou find yourself experiencing stress, anxiety or depression related to asport, consider finding a qualified counselor/therapist to discuss these issues.If you’ve got a child who plays sports, keep an open dialogue with them. Haveregular, open and honest conversations about how they’re feeling, both mentallyand physically cialis bph medicare.

Watch for warning signs. Thisis especially important if you have a child or adolescent in sports. Keep aneye out for things like mood, cialis bph medicare sleep, or behavior changes that seem concerning. Find balance. It’sokay to admit that you need help or that you need to take a break frompracticing or competing.

If you feel overwhelmed consider meditation, tryingnew cialis bph medicare things or giving your body a rest.Ask for help. Thereis no shame in seeking out help, whether it be with a therapist, psychiatristor other medical health professional. Treating a cialis bph medicare mental illness is just asimportant as treating a physical one. Protecting and prioritizing youroverall health is essential for all levels of athletes. It’s not rare to havean athlete pull out of a race, game or event due to a physical injury.

Seeingan athlete withdraw for mental health reasons is much less common, however, itsrecognition is just as important cialis bph medicare. The hope going forward is that we assistathletes in all aspects of performance and recognize that mental health is health. Thomas Bills, M.D., is a psychiatrist with a special interestin sports psychiatry. Dr. Bills is welcoming athletes to his office in theTowsley Building, located on the campus of MidMichigan Medical Center –Midland.

Those who would like to make an appointment may call the office at(989) 839-3385..

Trauma is buy cialis 20mg more prevalent that most people realize. According to the U.S Department of Health and Human Services’ Substance Abuse and Mental Health Services Administration’s website, two-thirds of people have experienced at least one traumatic event by age 16. In 2015, for every 1,000 children, 9.2 experienced some sort of child abuse buy cialis 20mg or neglect. Their research suggests that 54 percent of U.S.

Families have been affected by some type of disaster. Many people have multiple or repeated buy cialis 20mg trauma. The more intense and frequent a trauma is, the more likely it is to have an impact on people. Trauma has both short-term and long-term effects.

In children this might be fear of being separated from a caregiver, excessive crying or screaming, weight loss and buy cialis 20mg nightmares. In older children it could be poor concentration, feelings of guilt or shame, anxiety, depression, difficulty sleeping, eating disorders, self-harming behavior, sexual acting out or use of drugs or alcohol, among other things. These behaviors and difficulties can persist into adulthood, and may lead to difficulties getting or keeping a job, disruption in relationships or criminal behavior. When these behaviors occur in people they likely indicate buy cialis 20mg some sort of traumatic past.

This is because the trauma changes the way the brain functions. These struggles will sometimes lead people to seek mental buy cialis 20mg health services, but sometimes people suffer without recognizing that the problems may be connected to a past traumatic event, or that they can change. As traumatized children grow into adults they are often perceived as being the problem themselves, instead of being seen as the victim of a trauma. When friends, family, professionals and society view the person as the problem it creates a lack of compassion and ignores the healing that could occur if the trauma were recognized.

When one views those with difficult behavior as a victim of their past, they buy cialis 20mg will approach them with more empathy and compassion. This is the essence of being trauma informed. Trauma-informed care has been a topic of discussion for several years within the human service world. According to Trauma-Informed Care Implementation Resource buy cialis 20mg Center, trauma-informed care shifts the focus from “What’s wrong with you?.

€ to “What happened to you?. € There has been a push to bring this concept outside the therapy office and into broader health care settings. This perspective, however, can buy cialis 20mg be useful beyond the realm of health care. When individuals become trauma informed, they can approach all interactions differently and with more empathy and compassion.

Some people, however, buy cialis 20mg resist this idea. They seem to believe that recognizing past trauma and approaching people with compassion means not holding them accountable for their behavior, and letting them “get away” with bad behavior. Handing out punishment for bad behavior while ignoring the emotional reality of the person will not fully address the problem. It may temporarily reduce the behavior, but buy cialis 20mg it will likely get worse later.

Compassion within trauma-informed living is recognizing the past trauma as the source of the pain that leads to difficult behavior. In the process of acknowledging the trauma and validating the emotions a door is opened to healing and learning new ways of coping. This can be done while still holding them accountable to the consequences buy cialis 20mg of the behavior. Living as a trauma-informed human means recognizing that another’s bad behavior or grumpy attitude is likely coming from a place of past trauma, and having compassion and kindness for the person, even while acknowledging that consequences happen.

It is through the compassion and kindness that the healing happens. While many peoplefind healing from buy cialis 20mg trauma through therapy or counseling, healing happens withinall compassionate interactions. Therefore, every person has the power to be aforce of healing in the lives of those around them, when they recognize there’sa good chance that a person’s difficult behavior is likely the result of pasttrauma, and treat them with compassion. For those who need more intense treatment for buy cialis 20mg mental health conditions, MidMichigan Health provides an intensive outpatient program called Psychiatric Partial Hospitalization Program at MidMichigan Medical Center – Gratiot.

Those interested in more information about the PHP program may call (989) 466-3253. Those interested in more information on MidMichigan’s comprehensive behavioral health programs may visit www.midmichigan.org/mentalhealth.Olympic athletes train to be thebest in the world at their respective sports. They are determined, talented,capable, and display a level of grit and determination qualifying them for thehighest stage of buy cialis 20mg competition. They spend years working toward a few simpleultimate goals.

Giving their best performance, honoring their country and leavingthe court, mat, field or track with a medal in their hand. When gymnast Simone Biles recentlywithdrew from the Olympic Games, it came to many as a buy cialis 20mg surprise. What may havecome as even more of a surprise to some is the reason she withdrew. Her mentalhealth.

This latest example of thecourage of an athlete to stand up and buy cialis 20mg let the world know that mental health ishealth has brought incredible awareness to the importance of mental health inall people, even Olympians. If you’re an athlete, or if youhave kids who play sports, you might be worried and wondering what you can doto address potential mental health struggles related to sports. Consider thesesuggestions when it comes to sports buy cialis 20mg and mental health. Talk, talk, talk.

Ifyou find yourself experiencing stress, anxiety or depression related to asport, consider finding a qualified counselor/therapist to discuss these issues.If you’ve got a child who plays sports, keep an open dialogue with them. Haveregular, open buy cialis 20mg and honest conversations about how they’re feeling, both mentallyand physically. Watch for warning signs. Thisis especially important if you have a child or adolescent in sports.

Keep aneye out buy cialis 20mg for things like mood, sleep, or behavior changes that seem concerning. Find balance. It’sokay to admit that you need help or that you need to take a break frompracticing or competing. If you feel overwhelmed consider meditation, tryingnew buy cialis 20mg things or giving your body a rest.Ask for help.

Thereis no shame in seeking out help, whether it be with a therapist, psychiatristor other medical health professional. Treating a buy cialis 20mg mental illness is just asimportant as treating a physical one. Protecting and prioritizing youroverall health is essential for all levels of athletes. It’s not rare to havean athlete pull out of a race, game or event due to a physical injury.

Seeingan athlete withdraw for mental health reasons is much less common, however, itsrecognition is just as buy cialis 20mg important. The hope going forward is that we assistathletes in all aspects of performance and recognize that mental health is health. Thomas Bills, M.D., is a psychiatrist with a special interestin sports psychiatry. Dr.

Bills is welcoming athletes to his office in theTowsley Building, located on the campus of MidMichigan Medical Center –Midland. Those who would like to make an appointment may call the office at(989) 839-3385..

What should I watch for while using Cialis?

If you notice any changes in your vision while taking this drug, call your doctor or health care professional as soon as possible. Stop using Cialis and call your health care provider right away if you have a loss of sight in one or both eyes.

Contact you doctor or health care professional right away if the erection lasts longer than 4 hours or if it becomes painful. This may be a sign of serious problem and must be treated right away to prevent permanent damage.

If you experience symptoms of nausea, dizziness, chest pain or arm pain upon initiation of sexual activity after taking Cialis, you should refrain from further activity and call your doctor or health care professional as soon as possible.

Do not drink alcohol to excess (examples, 5 glasses of wine or 5 shots of whiskey) when taking Cialis. When taken in excess, alcohol can increase your chances of getting a headache or getting dizzy, increasing your heart rate or lowering your blood pressure.

Using Cialis does not protect you or your partner against HIV (the cialis that causes AIDS) or other sexually transmitted diseases.

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The Centers cialis advil interaction http://bocnow.com/men/ for Medicare &. Medicaid Services (CMS) and Mathematica released a fifth and final toolkit and two case studies to highlight strategies that Accountable Care Organizations (ACOs) and End-Stage Renal Disease Seamless Care Organizations (ESCOs) use to improve quality of care, lower health care costs, and enhance beneficiaries’ experience. Mathematica completed this work as part of a contract with CMS.CMS and Mathematica conducted focus groups with representatives from 13 ACOs participating in the Medicare Shared Savings Program and the Next Generation ACO Model to identify strategies for cialis advil interaction providing value-based care. With insights gained through these focus groups and other CMS-sponsored events, CMS’s ACO Learning System team developed the Operational Elements Toolkit. The toolkit presents fundamental strategies that Medicare ACOs use to begin or refine operations and considers approaches to meet the following objectives.

Establishing strategic partnerships to strengthen or expand an organization Understanding beneficiaries’ care cialis advil interaction needs and preferences Harnessing data to improve performance and support quality reportingThe Operational Elements Toolkit is part of a broader series of resources that explores how ACOs and ESCOs provide value-based care. CMS and Mathematica added to these resources with two new case studies that highlight the following strategies. Partnering with emergency departments to improve care coordination services (Reliance Healthcare) Creating an Innovation Fund that distributes grants to local organizations to improve quality, cost, and care experience (OneCare Vermont)For more information about this toolkit and other resources highlighting ACO and ESCO initiatives—including previous toolkits on care transformation, provider engagement, beneficiary engagement, and care coordination, and almost two dozen case studies—please visit CMS’s website.Parents with young children in early care and education programs like Early Head Start may also need other kinds of support. They may need affordable higher education alternatives like community college, or job training and economic support from workforce development programs cialis advil interaction. Helping clients navigate the complexities of different programs can be difficult for service providers, especially when it comes to ensuring the right coordination between services for parents and their children.

Better program coordination may lead to greater benefits for families than individual service providers could achieve alone. Coordination requires systems change, however—change achieved through active partnerships, engaged leadership, cooperative planning, data-informed decision making, strategic use cialis advil interaction of resources, and innovative problem solving. Mathematica’s new digital resource on improving family outcomes through coordinated services speaks directly to this need. Our partnership framework, which shows how local partnerships tend to evolve through stages of cooperation, coordination, and collaboration, was developed to help staff document their specific approaches to coordinated services and assess the approaches’ quality and intensity necessary to have an impact on parent and child outcomes. Beyond sharing the tools and information available now, the digital resource cialis advil interaction describes upcoming initiatives that will help programs use rapid-cycle testing to pilot their approach to coordinated services and give decision makers timely and actionable evidence on possible ways to improve program outcomes.

We also bring to light several culturally responsive best practices and innovative methods that multigenerational programs can use to overcome access disparities among communities of color and communities experiencing poverty. For more information about Mathematica’s coordinated services work, or to speak with one of our experts, email info@mathematica-mpr.com..

The Centers buy cialis 20mg for Medicare my website &. Medicaid Services (CMS) and Mathematica released a fifth and final toolkit and two case studies to highlight strategies that Accountable Care Organizations (ACOs) and End-Stage Renal Disease Seamless Care Organizations (ESCOs) use to improve quality of care, lower health care costs, and enhance beneficiaries’ experience. Mathematica completed this work as part of a contract with CMS.CMS and Mathematica conducted focus groups with representatives from 13 ACOs participating in the Medicare Shared Savings Program and the Next Generation ACO Model to identify buy cialis 20mg strategies for providing value-based care.

With insights gained through these focus groups and other CMS-sponsored events, CMS’s ACO Learning System team developed the Operational Elements Toolkit. The toolkit presents fundamental strategies that Medicare ACOs use to begin or refine operations and considers approaches to meet the following objectives. Establishing strategic partnerships to strengthen or expand an organization Understanding beneficiaries’ care needs and preferences Harnessing data to improve performance and support quality reportingThe Operational Elements Toolkit is part of a broader series of buy cialis 20mg resources that explores how ACOs and ESCOs provide value-based care.

CMS and Mathematica added to these resources with two new case studies that highlight the following strategies. Partnering with emergency departments to improve care coordination services (Reliance Healthcare) Creating an Innovation Fund that distributes grants to local organizations to improve quality, cost, and care experience (OneCare Vermont)For more information about this toolkit and other resources highlighting ACO and ESCO initiatives—including previous toolkits on care transformation, provider engagement, beneficiary engagement, and care coordination, and almost two dozen case studies—please visit CMS’s website.Parents with young children in early care and education programs like Early Head Start may also need other kinds of support. They may need affordable higher education alternatives like community college, or job training and economic support from workforce buy cialis 20mg http://www.egarciajr.com/?page_id=331 development programs.

Helping clients navigate the complexities of different programs can be difficult for service providers, especially when it comes to ensuring the right coordination between services for parents and their children. Better program coordination may lead to greater benefits for families than individual service providers could achieve alone. Coordination requires systems change, however—change achieved through active partnerships, engaged buy cialis 20mg leadership, cooperative planning, data-informed decision making, strategic use of resources, and innovative problem solving.

Mathematica’s new digital resource on improving family outcomes through coordinated services speaks directly to this need. Our partnership framework, which shows how local partnerships tend to evolve through stages of cooperation, coordination, and collaboration, was developed to help staff document their specific approaches to coordinated services and assess the approaches’ quality and intensity necessary to have an impact on parent and child outcomes. Beyond sharing the tools and information available now, the digital resource describes upcoming initiatives that will help programs use rapid-cycle testing to pilot their approach to coordinated services and give decision makers timely and actionable evidence on possible ways buy cialis 20mg to improve program outcomes.

We also bring to light several culturally responsive best practices and innovative methods that multigenerational programs can use to overcome access disparities among communities of color and communities experiencing poverty. For more information about Mathematica’s coordinated services work, or to speak with one of our experts, email info@mathematica-mpr.com..

Should you take cialis with food

The number of people experiencing numbness, tingling and pain in their feet with no known cause has should you take cialis with food been cialis online us increasing over the last two decades, according at a new study published in the October 27, 2021, online issue of Neurology®, the medical journal of the American Academy of Neurology. Called small fiber neuropathy, the condition has different symptoms than large should you take cialis with food fiber neuropathy, which can cause weakness and balance issues. But in many cases people have both types of neuropathy.For the study, researchers looked at records for everyone diagnosed with small fiber neuropathy in Olmsted County, Minn., and the adjacent counties during a 20-year period. They then should you take cialis with food compared those 94 people with 282 people of similar age and sex who did not have neuropathy.

Participants were followed for an average of six years.The study found that the should you take cialis with food condition occurred in 13.3 per 100,000 people, with the rate increasing during the study."This increase could be due in part to greater awareness," said study author Christopher J. Klein, MD, of the Mayo Clinic in Rochester, Minn., and a Fellow of the American Academy of Neurology. "Another possibility is that increasing levels of should you take cialis with food overweight and obesity in our area could be a factor in the higher rates of small fiber neuropathy. Higher body mass index, or BMI, is a risk factor for diabetes and high triglycerides, which may also lead to neuropathy."The people in the study with neuropathy had an average BMI of 30.4, compared to 28.5 for the people who did not have should you take cialis with food neuropathy.

A BMI of 18.5 to 24.9 is considered healthy. 25.0 to should you take cialis with food 29.9 is considered overweight. And 30.0 should you take cialis with food and higher is considered obese.About 50% of the people with neuropathy had buy cialis daily online diabetes, compared to 22% of those without neuropathy. advertisement The people with neuropathy were also more likely to have insomnia, at 86% compared to 54% for those without neuropathy.

They were also more likely to have heart attacks, at 46% compared to 27%."Based on these findings, people should you take cialis with food with small fiber neuropathy should be screened for heart problems and their blood glucose should be monitored for signs of diabetes," Klein said.The people with neuropathy were also more likely to take opioids for pain.For 67 of the people with neuropathy, no cause could be determined, called idiopathic neuropathy. For 14 people, the should you take cialis with food neuropathy was caused by diabetes. Other causes included Sjögren syndrome and lupus.A total of 36% of the people developed large fiber neuropathy during the study, an average of five years after they developed the small fiber version."The good news is that most people with idiopathic neuropathy do not develop major impairments or disability, but they did have many other conditions and an increased risk of heart attack, so the development of treatments and prevention methods is crucial," Klein said.The main limitation of the study was that researchers looked back in time at medical records. A study examining should you take cialis with food all people with symptoms of small fiber neuropathy and following them over time should be conducted to confirm these findings, Klein said.The study was supported by the Mayo Clinic Foundation, Mayo Clinic Center or Individualized Medicine and Mayo Clinic Center of MS and Autoimmune Neurology.

Story Source should you take cialis with food. Materials provided by American Academy of Neurology. Note. Content may be edited for style and length..

The number of people experiencing numbness, tingling and pain in their cialis 2.5mg price feet with no known cause has been increasing over the last two decades, according at a new study published in the October 27, 2021, online issue of Neurology®, the buy cialis 20mg medical journal of the American Academy of Neurology. Called small fiber neuropathy, the condition has different symptoms than buy cialis 20mg large fiber neuropathy, which can cause weakness and balance issues. But in many cases people have both types of neuropathy.For the study, researchers looked at records for everyone diagnosed with small fiber neuropathy in Olmsted County, Minn., and the adjacent counties during a 20-year period. They then compared those 94 people with 282 people of similar age and sex who did not have buy cialis 20mg neuropathy.

Participants were followed for an average of six years.The study found that the condition occurred in 13.3 per 100,000 people, with the buy cialis 20mg rate increasing during the study."This increase could be due in part to greater awareness," said study author Christopher J. Klein, MD, of the Mayo Clinic in Rochester, Minn., and a Fellow of the American Academy of Neurology. "Another possibility is that increasing levels of overweight and obesity in our area could be a factor in the higher rates of buy cialis 20mg small fiber neuropathy. Higher body mass index, or buy cialis 20mg BMI, is a risk factor for diabetes and high triglycerides, which may also lead to neuropathy."The people in the study with neuropathy had an average BMI of 30.4, compared to 28.5 for the people who did not have neuropathy.

A BMI of 18.5 to 24.9 is considered healthy. 25.0 to buy cialis 20mg 29.9 is considered overweight. And 30.0 and higher is considered additional resources obese.About 50% of the people with neuropathy had diabetes, compared to 22% of those without buy cialis 20mg neuropathy. advertisement The people with neuropathy were also more likely to have insomnia, at 86% compared to 54% for those without neuropathy.

They were also more likely to have heart attacks, at 46% compared to 27%."Based on these findings, people with small fiber neuropathy buy cialis 20mg should be screened for heart problems and their blood glucose should be monitored for signs of diabetes," Klein said.The people with neuropathy were also more likely to take opioids for pain.For 67 of the people with neuropathy, no cause could be determined, called idiopathic neuropathy. For 14 people, buy cialis 20mg the neuropathy was caused by diabetes. Other causes included Sjögren syndrome and lupus.A total of 36% of the people developed large fiber neuropathy during the study, an average of five years after they developed the small fiber version."The good news is that most people with idiopathic neuropathy do not develop major impairments or disability, but they did have many other conditions and an increased risk of heart attack, so the development of treatments and prevention methods is crucial," Klein said.The main limitation of the study was that researchers looked back in time at medical records. A study examining all people with symptoms of small fiber neuropathy and following them buy cialis 20mg over time should be conducted to confirm these findings, Klein said.The study was supported by the Mayo Clinic Foundation, Mayo Clinic Center or Individualized Medicine and Mayo Clinic Center of MS and Autoimmune Neurology.

Story Source buy cialis 20mg. Materials provided by American Academy of Neurology. Note. Content may be edited for style and length..

How to use cialis

Oct can i buy cialis in uk how to use cialis. 22, 2021 -- Pfizer says its treatment for children is 90% effective at preventing erectile dysfunction treatment s.The Pfizer treatment for kids ages 5 to 11 is 10 micrograms, roughly one-third of the dose given to adolescents and adults.In data presented to the FDA ahead of the agency’s review of its shots for children, the company described the interim results of two ongoing studies testing the safety and effectiveness of its 10-microgram shots.The treatment effectiveness data comes from a study of more than 2,000 kids ages 5 to 11. Two-thirds of the children were randomly assigned to receive a child-sized dose of the Pfizer-BioNTech treatment, while the other how to use cialis third was sorted into the placebo group.The study got underway as the Delta variant became dominant around the world. As of the first week of October, 16 participants in the placebo group had gotten a symptomatic, lab-confirmed erectile dysfunction treatment , compared with just three who caught erectile dysfunction treatment in the vaccinated group. According to the company’s analysis of its own studies, side effects how to use cialis seen in the study were nearly all mild.

The most common side effect reported was pain at the site of the shot. Kids in the group that received the treatment also had fatigue, headaches, fever, and how to use cialis chills at higher rates than were seen in the placebo group. These were most common after the second dose. Some skin reactions were seen in the study, like itching and rashes, but these were mostly mild and went away within a few days.Kids also could have swollen lymph nodes after their vaccinations, how to use cialis as adults sometimes do, but these reactions were temporary.One child developed a tic, a recurring involuntary muscle twitch or vocal sound, that came one week after their second dose of the treatment. It was judged by study investigators to be related to the treatment.

The company how to use cialis says it was going away by the time the study was being published.Reassuringly, no cases of heart inflammation called myocarditis were found in the study. Myocarditis is rare and temporary, but it requires hospital care. The highest rates of myocarditis have been seen in males younger than 30. That group has a risk of about 11 cases for every 100,000 doses given, according to a recent study in the New England Journal of Medicine..

Oct https://www.profi-parkett.com/produkt/weitzer-provital-oel/ buy cialis 20mg. 22, 2021 -- Pfizer says its treatment for children is 90% effective at preventing erectile dysfunction treatment s.The Pfizer treatment for kids ages 5 to 11 is 10 micrograms, roughly one-third of the dose given to adolescents and adults.In data presented to the FDA ahead of the agency’s review of its shots for children, the company described the interim results of two ongoing studies testing the safety and effectiveness of its 10-microgram shots.The treatment effectiveness data comes from a study of more than 2,000 kids ages 5 to 11. Two-thirds of the children were randomly assigned to receive a child-sized dose of the Pfizer-BioNTech treatment, while buy cialis 20mg the other third was sorted into the placebo group.The study got underway as the Delta variant became dominant around the world.

As of the first week of October, 16 participants in the placebo group had gotten a symptomatic, lab-confirmed erectile dysfunction treatment , compared with just three who caught erectile dysfunction treatment in the vaccinated group. According to the company’s analysis of its own studies, side effects seen in the study were nearly all mild buy cialis 20mg. The most common side effect reported was pain at the site of the shot.

Kids in the group that received the treatment also had fatigue, headaches, fever, and chills buy cialis 20mg at higher rates than were seen in the placebo group. These were most common after the second dose. Some skin buy cialis 20mg reactions were seen in the study, like itching and rashes, but these were mostly mild and went away within a few days.Kids also could have swollen lymph nodes after their vaccinations, as adults sometimes do, but these reactions were temporary.One child developed a tic, a recurring involuntary muscle twitch or vocal sound, that came one week after their second dose of the treatment.

It was judged by study investigators to be related to the treatment. The company says it buy cialis 20mg was going away by the time the study was being published.Reassuringly, no cases of heart inflammation called myocarditis were found in the study. Myocarditis is rare and temporary, but it requires hospital care.

The highest rates of myocarditis have been seen in males younger than 30. That group has a risk of about 11 cases for every 100,000 doses given, according to a recent study in the New England Journal of Medicine..

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How to cite this Order zithromax for chlamydia article:Singh cialis precio O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J cialis precio Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went into cialis precio a frenzy as newspapers, news channels, and social media were full of stories providing minute details of the suicidal act.

Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private and personal details were freely and cialis precio 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 cialis precio suicidal ideation.

This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of cialis precio 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 cialis precio 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 cialis precio this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental health professionals cialis precio were called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to cialis precio the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules cialis precio 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 cialis precio documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as cialis precio 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 - cialis precio 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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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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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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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.

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

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

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

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

How to buy cialis 20mg cite this article:Singh O Order zithromax for chlamydia P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized buy cialis 20mg 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 buy cialis 20mg 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, buy cialis 20mg 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 buy cialis 20mg distress calls from their patients in despair with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has buy cialis 20mg 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 buy cialis 20mg 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 buy cialis 20mg the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident.

Many psychiatrists and mental health professionals were called by media houses to comment on buy cialis 20mg the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so. There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist.

These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to buy cialis 20mg doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of buy cialis 20mg 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, buy cialis 20mg and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion.

It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, buy cialis 20mg and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

O P SinghAA 304, buy cialis 20mg Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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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].