Linda Andre’s New Book, “Doctors of Deception: What They Don’t Want You to Know About Shock Treatment,” Just Out From Rutgers University Press!

If you buy and read only one book on ECT, this should be the one. Andre is not only a survivor of ECT, but has spent the past 25 years listening to, and documenting the experiences of, other survivors. With her exhaustive knowledge of what passes for scientific research on the subject, and an insider’s knowledge of the politics behind that “science” as well as the pronouncements of supposedly trustworthy authorities like the FDA, no one is more qualified to demolish the claims of the shock industry. Andre does so with thoroughness, style, and even wit. Everything she says is documented, but never before has all this information been gathered in one volume.
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The Top Three Questions

What follows are the three most frequently asked questions sent via email:

1. Where can I find a facility that gives ECT?

I don’t have a master list of ECT providers. I am concerned, however, that you would be seeking out ECT on your own. It is unlikely that you would find a clinic or hospital that would give you ECT without a doctor’s recommendation.

This is something that should be discussed with your psychiatrist. Your doctor will know of facilities that perform ECT and will give you a recommendation if s/he feels ECT would be beneficial. If you do not have a relationship with a psychiatrist and wish to have ECT, you will have to find a psychiatrist who will fully evaluate you.

2. I had ECT and it was successful. Why is it necessary to put so much negative information on the web?

I am always curious about one thing when I get this question: if ECT was successful, why are you searching the Internet for ECT information? It seems to me that you would simply accept that it worked and move on to other more interesting pursuits. (I do not doubt your enthusiasm, but it’s something that has always puzzled me – I’m interested in responses!)

That said; why NOT put it on the web? I sincerely believe that patients should be told all sides of the ECT story before making their decision. Anything less is unfair and it’s patronizing.

Until recently there appears to have been a general reluctance among psychiatrists to admit that ECT could cause memory or other cognitive problems that are severe, persistent and disabling.” This bold statement comes from a recent article in the British medical journal Advances in Psychiatric Treatment. (1)

The majority of people who find their way to ect.org AFTER ECT are at the very least disappointed. At worst, they’re devastated. If they had known before ECT that it causes a number of side effects (with discouraging efficacy and high relapse rates), they could have at least gone into it armed with information and lowered expectations. It’s less devastating to know the possibilities beforehand than to be caught completely blindsided. The latter leaves patients feeling deceived and swindled. That is much of the reason there is so much anger on the part of ECT patients who have a bad outcome. If they had clearly known the risks, they likely would have made the same decision to have ECT, but would not end up feeling so mislead.

Robertson and Pryor emphasized that “prospective patients should be warned of the significant risk of permanent amnesia and the possibility of permanent memory and cognitive disability.” (2)

You may have had a good outcome, but many do not. The negative side of ECT is discussed on ect.org to provide the full set of facts instead of the sanitized version many ECT practitioners choose to supply. Additionally, after a person is left bewildered, with no answers, this site provides a sense of fellowship with others, knowledge that they are not alone.

ECT is NOT a cure and any doctor who sells it as such is guilty of snake-oil salesmanship.

3. I told my doctor I searched the Internet and found information contrary to what s/he told me regarding ECT. His/her response was that the Internet is full of material not based on scientific facts and I should ignore it and stay off the web. Why would s/he be dishonest? What reasons could my doctor possibly have to hide these things from his/her patients?

Two simple answers followed up by more thorough discussion:

1. They are unaware or more commonly, don’t listen to their patients and have their heads in the sand.

2. They are paternalistic and think they know what’s best for you. They know if they provided a full set of facts, some patients would reject ECT.

Neither explanation means that your psychiatrist is a demon or a bad doctor. The very nature of psychiatry is based on paternalism, a view that you are mentally ill and therefore are incapable of decision-making. By removing some of the variables (information), your decision is easier to make. Unfortunately, this point of view is strongly rooted in psychiatry and in the public perception. That doesn’t make psychiatrists bad, just old fashioned and in need of a makeover.

Paternalism

“Persons with mental illness cannot make decisions on their own.” Most are lumped into that category. Yes, there are some individuals who are so ill they cannot function and make a decision. But you are obviously well enough to surf the Internet, to perform a search and find ect.org, and you’re well enough to compose an email to me, type in the email address and operate your computer to send the mail. You’re very likely well enough to make an informed decision, based on ALL the facts, not the selected few chosen by the person in charge.

There is a debate within the ECT industry concerning when ECT should be prescribed. Should it be used early in a depressive episode, or saved for those who are the most severely ill, desperate and treatment resistant? One of the leading psychiatrists in the latter camp once said that if a person is well enough to surf the Internet, he or she is not ill enough to consider ECT. (Many would disagree with that statement, but I toss it out as an interesting observation.)

Without a clue

I did a small research study called “Voices” a decade ago. An unsurprising finding from that study was that when ECT patients tell their doctors that they HAVE suffered devastating memory loss and other side effects, the doctors dismiss their complaints. But there was a highly surprising finding: many of those patients get frustrated at their psychiatrists but feel trying to convince them of the existence of the effects is futile. They move on to a new psychiatrist, or give up on psychiatry completely.

That treating psychiatrist, who has already discounted that they had side effects, never sees the individual again. S/he logically assumes that the person got better and moved on. Another success story! And since the doctor had not listened to the patient’s complaints, those complaints are never registered in the psychiatrist’s mind, and therefore, do not exist.

You can make up a variety of scenarios regarding the psychiatrist’s thinking along that path, but the bottom line is that to the psychiatrist, that patient did not have side effects. It’s a misperception, based on a refusal to acknowledge the patient’s complaints, but the doctor probably genuinely does not know it.

The second scenario is of course knowing the truth, but failing to share it. That sounds a bit more devious that I believe it is. I don’t think it’s a case of an evil doctor knowing and not telling because s/he’s a bad person. I think it’s just more of a case of this paternalism I keep talking about, a view that the doctor knows what’s best for you, so why bog you down with too much information, particularly negative information.

Another possibility is that your doctor simply has not kept up with the literature. What your doctor may consider “scientific fact” may be the statistic that has been quoted for many years, that only 1 in 200 persons suffer severe memory loss. Several years ago, that statistic was shown to be, depending on your point of view, either misleading or an outright lie. Harold Sackeim, considered the King of ECT, admitted it on a television show, although it softened the blow by calling the number “Impressionistic.”

impressionistic:

adjective

1. of or relating to or based on an impression rather than on facts or reasoning; “a surprisingly impressionistic review bearing marks of hasty composition”; “she had impressionistic memories of her childhood”

In more recent writings and testimonies, Mr. Sackeim has said that now it’s known ECT does, in fact, cause severe memory loss much more often than has been acknowledged. In his defense, he said the industry “Just didn’t know,” and that he has been trying to get industry leaders and doctors in the field to acknowledge what is now known.

For seventy years, patients have been reporting the same complaints, but “they just didn’t know.” Sackeim claims that they only discovered the hard science a few years ago.

The information is now out there, it’s being published, and your doctor’s only excuse will soon be that s/he’s not keeping up with current literature.

If your doctor is promoting ECT as a cure for depression, consider that a red flag and get a second opinion. Even the most enthusiastic ECT cheerleaders will tell you it’s most often a temporary fix, one that will require regular treatments indefinitely.

References:

1. Mangaoang, M. & Lucey, J. (2007) Cognitive rehabilitation: assessment and treatment of persistent memory impairments following ECT. Advances in Psychiatric Treatment, 13, 90-100.

2. Robertson, H. & Pryor, R. (2006) Memory and cognitive effects of ECT: informing and assessing patients. Advances in Psychiatric Treatment, 12,228-237.

Cognitive Rehab After ECT: New Journal Article

Advances in Psychiatric Treatment (2007), vol. 13, 90-100 doi: 10.1192/apt.bp.106.002899

Cognitive rehabilitation: assessment and treatment of persistent memory impairments following ECT

Maeve A. Mangaoang & Jim V. Lucey

Abstract
Few tests address the types of memory problem commonly reported after electroconvulsive therapy (ECT). Here, we focus on the importance of neuropsychological assessment in ECT-treated patients and describe a number of tasks that may be useful in measuring the everyday memory problems of such patients with ongoing memory difficulties. At the time of writing, no attempts have been made to rehabilitate patients who experience persistent adverse cognitive effects, but clinicians should be aware of the potential beneficial role of cognitive rehabilitation in the treatment and management of these effects.

In a recent issue of APT, Robertson & Pryor (2006) drew attention to a number of issues regarding the assessment of cognitive function in patients treated with electroconvulsive therapy (ECT). In particular, they highlighted the paucity of tests that are sensitive and relevant to the specific memory problems commonly reported after ECT. Here, Mangaoang & Lucey return to this problem, discussing neuropsychological assessment in ECT-treated patients.

Electroconvulsive therapy (ECT) has been used for many years, but it remains one of the most controversial psychiatric treatments. In recent years, a considerable amount of research has attempted to highlight the efficacy and safety of ECT, in addition to emphasising the overall improvements in current ECT techniques, equipment and standards (Sharma, 2001; Chung, 2002; UK ECT Review Group, 2003; Prudic et al, 2004). However, there also exists a growing body of research consistently reporting the adverse cognitive and psychological consequences of ECT among a substantial minority of patients (Johnstone, 1999; Service User Research Enterprise, 2002; Koopowitz et al, 2003; Rose et al, 2003; Scott, 2005). Although discrepancies exist between clinician-led or hospital-based studies and those undertaken in collaboration with patients regarding the nature and extent of adverse side-effects, there is a general consensus that memory loss (Box 1) is the most frequently and consistently reported side-effect following ECT (Rose et al, 2003). There have been many conflicting accounts of the severity and duration of the memory and other cognitive difficulties (Weeks et al, 1980; Squire et al, 1981; Templer & Veleber, 1982; Squire & Slater, 1983; Lisanby et al, 2000; Brodaty et al, 2000), but to date there has been a distinct lack of routine neuropsychological assessment of individuals receiving ECT at any stage during their treatment.

Designing an assessment battery that is sensitive to the nature of the everyday problems experienced by patients with memory and/or cognitive disability is challenging, and standard neuropsychological tests may not adequately reflect the levels of impairment experienced by patients on a daily basis (Robertson & Pryor, 2006). Thus, the use of novel, personally relevant memory tasks such as those described below may be warranted.

Furthermore, no attempts have been made to provide any form of memory rehabilitation or cognitive retraining to patients who experience persistent memory and other cognitive problems in these areas following ECT. Here we argue that cognitive rehabilitation could be offered to such patients as a means of addressing these difficulties in a constructive way.

The importance of assessment

What is striking from the literature in this area is the lack of routine, formal assessment of patients’ neuropsychological performance following a course of ECT, despite the long-known risk to memory functioning (Squire & Chace, 1975; Squire et al, 1975; Freeman et al, 1980; Squire & Slater, 1983; Robertson & Pryor, 2006). Furthermore, the lack of consistency in the types of measures used to assess patients has made it difficult to clarify the extent and duration of the reported cognitive problems and the impact they may have on the individual’s overall quality of life and sense of self.

In Ireland, for example, there is no published research on the long-term effects of ECT on cognitive functioning among Irish patients. The failure to conduct such assessments means that there may be a significant delay in detecting patients who have experienced a marked decline in memory function.

Guidelines

The importance of assessing and monitoring patients’ cognitive function throughout their treatment has been recognised in guidelines on the commissioning of ECT services within the National Health Service (NHS) (Royal College of Psychiatrists, 1995,1999), and the ECT Accreditation Service (ECT Accreditation Service, 2005) includes assessment and monitoring of cognitive function as standards required for accreditation of a clinic. However, there has been a relative neglect to include such measures in routine clinical practice. It appears that even when they have been explicitly recommended (Freeman et al, 1980; Salford Community Health Council, 1998 ; Royal College of Psychiatrists, 2005) patients who report persistent memory loss have not been systematically followed-up or referred for neuropsychological assessment. As a result, their progress or deterioration over time in terms of cognitive performance has not been monitored.

Monitoring patients’ self-reports of adverse side-effects to ECT has also been recommended by the Royal College of Psychiatrists (1995, 2005) and the National Institute for Clinical Excellence (NICE, 2003). Benbow & Crentsil (2004) have shown the importance of measuring such experiences during treatment, as it allowed the ECT staff to take immediate action to try to relieve the problems. For instance, if patients reported persistent confusion or memory difficulties, staff could change from bilateral to unilateral ECT or increase the interval between treatments.

Longer-term implications

The failure to adequately provide neuropsychological assessments to patients receiving ECT means that the impact of additional, subsequent episodes of depression and/or future courses of ECT on overall cognitive functioning remains unknown (Robertson & Pryor, 2006). Establishing a baseline of functioning before an individual’s first ECT treatment is extremely important in terms of its association with ‘cognitive reserve’. This concept refers to individual differences in factors such as education and occupation, which may be protective against ECT’s adverse effects on memory functioning (Legendre et al, 2003).

The Society for Cognitive Rehabilitation (SCR; Malia et al, 2004) recommends that a combination of standard and novel tasks to assess current cognitive status should be administered to patients. Objective and subjective self-report questionnaires and collateral information from family or caregivers should be used, and the assessment battery should provide sufficient information to form hypotheses about the underlying cognitive impairments and deficits that interfere with the individual’s cognitive functioning. These recommendations concur with Robertson & Pryor’s (2006) proposal that ECT-treated patients who report ongoing memory disability should be referred for neuropsychological assessment. The purpose of this is both to determine their general cognitive abilities and to measure specific cognitive functions, such as attention, concentration and information processing, that may be related to memory functioning in everyday life (Ponds & Hendriks, 2006).

Making use of assessments results

Rather than merely describing problems, the results of neuropsychological assessments should be explained in terms that the patient can understand and explicitly related back to the functional problems that have been identified (Mateer et al, 2005). They should be interpreted in a holistic way that takes account of the individual’s personality and emotional characteristics and used to inform decisions about preparing a suitable rehabilitation programme (Malia et al, 2004).

Neuropsychological assessment of memory

There are many factors to consider in the neuropsychological assessment of patients receiving ECT. These include the selection or development of appropriate testing materials, the timing of testing sessions (Robertson & Pryor, 2006) and the effects of factors such as mood, metamemory and memory self-efficacy on performance (Mateer et al, 2005; Ponds & Hendriks, 2006). Additional problems, such as limited access to neuropsychology services, financial and time constraints, may have an impact on the number and frequency of assessment sessions that can be undertaken.

Design of appropriate tests

Although Robertson & Pryor (2006) recommend that patients who have had ECT should be assessed with the kind of neuropsychological tests that are used for patients with known or suspected brain injury, they acknowledge some of the problems associated with these traditional, standardised tasks. The main challenge appears to be designing tests that are sensitive to the memory and other cognitive demands placed on patients in their everyday lives. This task is made even more difficult by the realisation that patients with memory disability may not be able to give reliable self-reports of their memory functioning (Cronholm & Ottosson, 1963; Robertson & Pryor, 2006). Rose et al (2003) note that neuropsychological assessment of the extent of memory loss in ECT patients has tended to focus on the ability to form new memories (anterograde memory, Box 1), whereas patients have commonly reported the loss of autobiographical memory (retrograde amnesia, Box 1) following ECT (Coleman et al, 1996; Peretri et al, 1996; Donahue, 2000). However, loss of autobiographical memory does not appear to have been adequately investigated (Robertson & Pryor, 2006). Furthermore, alternative versions of tests may be required to reduce practice effects over repeated assessments.

Timing of testing

As mentioned above, encouraging patients who are undergoing a course of ECT to give self-reports of any adverse side-effects can be beneficial in terms of allowing staff to take immediate actions to reduce or relieve these effects (Benbow & Crentsil, 2004). However, in many studies the premature assessment of memory and overall cognitive functioning following ECT has led to inaccuracies and underestimations of patients’ impairment (Squire & Slater, 1983; Weiner et al, 1986; Coleman et al, 1996; Peretti et al, 1996; Donahue, 2000; Rogers et al, 2002; Robertson & Pryor, 2006). It may take a number of months for patients to gain a more stable view of permanent changes in their memory and cognition (Weiner et al, 1986; Coleman et al, 1996; Donahue, 2000).

A further problem relates to the ambiguity of meaning in the phrase ‘short-term memory loss’. Does it refer to type of memory or duration of loss? Robertson & Pryor (2006) recommend that the phrase ‘temporary memory loss’ should be used when referring to duration. Patients who interpret short-term memory loss in terms of duration may not be inclined to complain about memory difficulties, believing that they are to be expected and will resolve within the ‘short term’. This may lead to an underreporting of memory problems among patients who are assessed only a few days or weeks after the completion of ECT and highlights the importance of scheduling follow-up assessments after the 6-month time point (Service User Research Enterprise, 2002; Robertson & Pryor, 2006).

Effects of mood and emotional valence on performance

Many studies have shown that individuals who are depressed are more likely to recall negative events than positive or neutral ones (Teasdale et al, 1980; Parrott & Sabiny, 1990; Williams et al, 1988; Lemogne et al, 2005). The performance of people without depression on tasks measuring memory and cognition may also be influenced by their current mood. Recently, Beatty et al‘s (2006) study involving healthy adults showed the significance of both current mood and emotional valence (the subjective emotions associated with an event) on participants’ ability to recall events they had experienced over the past year. Therefore, any assessments of cognitive and memory functioning in patients who have received ECT should take account of the individual’s mood at the time of testing and also whether they perceive the event recalled as positive, negative or neutral.

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The concept is strongly linked to Mateer et al‘s (2005) theory of metamemory, which is defned as an awareness of one’s own memory processes, knowledge and use of memory strategies, self-perceptions of one’s memory abilities and beliefs about the functioning of ones’ own memory.

Memory self-efficacy and metamemory

According to Ponds & Hendriks (2006), patients’ complaints about their memory do not necessarily reflect memory deficits; furthermore, there may be large discrepancies between the severity of memory disturbances as measured by memory tests and the impact of these problems in daily life. Finding only moderate correlations between self-reported memory problems and objective results on standardised neuropsychological assessments, Ponds & Hendriks introduced the idea of memory self-efficacy (Box 2) to explain this discrepancy. They argue that an individual’s beliefs and perceptions about their memory may be extremely influential in determining their level of engagement and performance during memory assessment. The belief that one has a poor memory may lead to increased dependence on others, avoidance of memory challenges, and a pattern of helplessness and demoralisation when faced with memory difficulties (Elliot & Lachman, 1989). Additional evidence of the impact of self-perceived memory capacity on control of memory efficiency (Cavanaugh & Poon, 1989; Hertzog et al, 1990; Jonker et al, 1997) supports the argument that neuropsychological assessments of patients who have had ECT should take account of the patient’s own metamemory or sense of memory self-efficacy.

Novel tasks for measuring everyday memory

A few years ago one of us (M. M.) was involved in a study of the effects of surgery for temporal lobe epilepsy (Mangaoang et al, 2004). The study team developed tasks for assessing aspects of everyday memory functioning and spatial representation in patients after surgery (Box 3). These have since been administered to large numbers of healthy control individuals of all ages and to people with chronic major depression (McMackin et al, 2005). These tasks, which are outlined in this section, might be considered for use with patients following ECT.

Sensitivity to the nature of the patients’ memory problems

Episodic and autobiographical memory

The Mundane Memory Questionnaire specifically measures personally relevant episodic memory of typical daily events over the previous four consecutive days. Participants are asked to indicate (by circling either ‘yes’ or ‘no’) whether they recall a particular event, for example, watching television or eating lunch. If the event is recalled, they are asked to give additional information such as what programmes they watched or what food they ate. If participants are unable to provide additional details, they are asked to proceed to the next question.

This measure was extremely sensitive to the types of everyday memory problem experienced by the patients in our study of temporal lobe epilepsy (Mangaoang et al, 2004). It differs from questionnaires such as the Everyday Memory Questionnaire (Sunderland et al, 1984), the Prospective and Retrospective Memory Questionnaire (Smith et al, 2000) and the Cognitive Failures Questionnaire (Broadbent et al, 1982) in that it does not require patients to rate their own memory performance, thereby taking account of the observation that some people with memory problems cannot accurately rate the level of their impairment.

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The Everyday Memory Interview is based on an interview used by Eldridge et al (1994) in their assessment of the role of schemas in autobiographical memory. In a tape-recorded interview, the participant is asked to describe, in as much detail as possible, their typical day, yesterday and a day in the previous week, in counterbalanced order (to control for order effects or bias). The interview is scored by focusing on the number of basic activities that are recorded for each of the target days. Discourse analyses of the interview content can also be undertaken to measure the frequency of repetition of events, pragmatic problems and the use of verbal tics.

The merit of both the Mundane Memory Questionnaire and the Everyday Memory Interview is that they measure the ability of patients to recall personally relevant events, are straightforward to administer and are free from practice effects. Modified versions of the tasks could also be completed by patients’ caregivers or spouses, should collateral information be desired.

Semantic and phenomenal characteristics

Although both episodic and autobiographical memory have been widely researched, very few studies have used tasks that are concise, distinguish between semantic and episodic information, and control for emotional valence. Semantic information consists of general knowledge: things we know without any connection to personal experience, whereas episodic information refers to details such as time, person, place and emotions about specific personally experienced events. Levine et al‘s (2002) Autobiographical Memory Interview separates the semantic from episodic details of events. Beatty et al (2006) adapted and extended this measure to show how the recall of specific personally relevant events over the previous 12 months was influenced by whether participants construed the events as positive, negative or neutral. The transcribed interviews were analysed in terms of the number of specific episodic details recalled for each type of event, thereby controlling for the emotional valence of the event. This interview can be extended to include events from the less recent past, in order to gain a thorough appreciation of the extent of a patient’s retrograde amnesia.

Beatty et al (2006) also used the Memory Characteristic Rating Scale (adapted from Johnson et al, 1988) in conjunction with Levine et al‘s (2002) Autobiographical Memory Interview to measure the phenomenal characteristics of the different events. The Memory Characteristic Rating Scale uses a seven-point Likert scale to rate the vividness with which participants can recall specific aspects of an event, such as visual and auditory details. This combination of tasks facilitates examination of the association between the emotional valence of an event and the vividness with which different characteristics can be recalled.

Topographical memory

The effects of ECT on topographical memory, way-finding and spatial representation are largely unknown. We can find only one self-report of such deficits (Anonymous, 1965). Assessments of patients who have received ECT do not appear to consider the possibility of such impairments, despite their impact on everyday life. In our work on temporal lobe epilepsy (Mangaoang et al, 2004; Roche et al, 2005), we developed a number of tasks (the Landmark Location, Landmark Recognition and Virtual Map tasks) to measure the ability of patients with left or right unilateral hippocampal damage to recognise photographs of well-known Dublin landmarks and to accurately name their location on a modified map of the city. Patients also described in writing the routes they would take to get from one landmark to another on a map of a virtual city. These tasks were extremely sensitive to the everyday way-finding problems experienced by many of the patients, particularly those with right-sided hippocampal damage (Mangaoang et al, 2004) and could potentially be used to identify whether patients treated with ECT experience similar difficulties.

Sensitivity to metamemory and mood

In considering metamemory and memory self-efficacy (Box 2), the study team used a simple memory rating scale, asking patients to rate their own perception of their current memory functioning at the time of assessment on a five-point Likert scale (1 = ‘very bad’, 5 = ‘excellent’).

Patients’ self-reported symptoms of depression can be assessed using the Beck Depression Inventory (Beck et al, 1996). Alternatively, McMackin et al (2005) have used a mood rating scale that asks patients to rate their mood state at the time of assessment on a nine-point Likert scale (1 = ‘worst you’ve ever felt’, 9 = ‘best you’ve ever felt’). Either instrument could be easily incorporated into an assessment battery for patients receiving ECT.

Potential role of memory rehabilitation and cognitive retraining

Although reports have claimed that about one-third of people receiving ECT experience persistent memory loss (Service User Research Enterprise, 2002; Rose et al, 2003; Scott, 2005), it is unclear whether patients receive treatment or assistance from psychiatrists or other mental health professionals to deal with this disability. We do know that some patients turn to sources of help outside psychiatry (e.g. self-help groups) for support (Johnstone, 1999). This failure to attempt to rehabilitate patients may reinforce the negative public image of ECT specifically and psychiatry in general.

Adopting extisting techniques: brain trauma

The importance of carrying out detailed neuro-psychological assessments of patients following ECT in order to identify persistent cognitive problems was recognised over a decade ago (Calev, 1994). Unfortunately, however, even when cases of severe and persistent memory loss are highlighted in the literature, no study has recommended or attempted to provide any kind of rehabilitation or follow-up care. Documenting persistent and severe deficits in memory and cognition is not enough; patients need to be helped to adjust to the major effects that such disabilities may have on their everyday lives. Robertson & Pryor (2006) recommend that tests assessing neuropsychological function of brain-injured patients be used for ECT-treated patients. We would argue that the cognitive rehabilitative techniques that are used with brain-injured patients should also be considered for use with patients experiencing memory and/or other cognitive disability following ECT.

During the past 20 years, the course and nature of cognitive difficulties after brain injury and the key components of rehabilitation have become better understood. The significance of personal background, the range of emotional responses to injury and its consequences, and the role of coping skills in long-term adjustment are now more readily accepted (Mateer et al, 2005).

Cognitive rehabilitation therapy

Cognitive rehabilitation therapy is ‘a systematic, functionally oriented service of therapeutic cognitive activities and an understanding of the person’s behavioural deficits’ (Malia et al, 2004). Its aim is to achieve functional changes by reinforcing or strengthening previously learned patterns of behaviour, or establishing new patterns of cognitive activity or mechanisms to compensate for impaired neurological systems (Bergquist & Malec, 1997). Cognitive rehabilitation therapy has a large evidence base and has been widely researched among patients with acquired brain injury.

Memory rehabilitation

Recently, Ponds & Hendriks (2006) have described what appears to be the first formal attempt to offer a rehabilitation programme focusing on memory to patients with epilepsy. However, no attempts have yet been made to extend such treatment to patients who experience memory deficits following ECT.

What rehabilitation could achieve

Designing a rehabilitation programme for patients with memory or other cognitive disability associated with ECT would constitute the first step towards treating these deficits rather than merely reporting them. Such a programme would also acknowledge the individual’s difficulties and the challenges they face in coping with the demands of everyday life.

How it could be done

Baseline and post-treatment neuropsychological assessments could be used to clarify the nature and extent of cognitive difficulties. From there, appropriate steps towards memory rehabilitation and cognitive retraining (see below) could be undertaken in individual and/or group sessions, and could be extended to include the individual’s family or caregivers. Follow-up assessments of progress would allow any changes in cognitive status to be measured and also to monitor the transfer of acquired skills to other areas of functioning such as the social and occupational domains of the individual’s life. In this way it would be possible to determine whether the rehabilitation programme was having a beneficial effect on the patients’ overall quality of life.

Ultimately, successful practical attempts to address the impact of cognitive disabilities on the lives of patients treated with ECT would be welcomed not only by the patients themselves but also by their relatives and caregivers. The provision of such a service might also improve potential patients’ attitudes towards ECT, by reassuring them that, should they develop a persistent cognitive problem following treatment, some form of structured treatment and assistance would be made available to them. This might help the decision-making process for patients who are considering ECT as a treatment option.

Design of a successful rehabilitation programme

There are many factors to consider in the design of a cognitive rehabilitation programme. These include understanding that rehabilitation is a collaborative process, recognising the importance of including family and/or caregivers and being sensitive to the impact that a patient’s level of awareness, meta-memory, mood and motivation can have on their ability to take part in a programme. Premorbid personality and psychological functioning are also extremely important. Therefore, cognitive rehabilitation should involve work on the patient’s psychosocial skills such as coping, anxiety control, self-esteem, self-concept, motivation, locus of control and adjustment (Malia et al, 2004).

Existing programmes

Mateer et al (2005) believe that a combination of neuro-rehabilitation, pharmacotherapy and cognitive-behavioural therapy is often needed. Thus, many programmes incorporate multiple interventions such as attention training, memory compensations, skills training, feedback on performance, psycho-education, stress management, confidence-building and psychotherapy aimed at increasing self-awareness, acceptance and adjustment.

Cognitive rehabilitation programmes that take into account the emotional as well as the cognitive aspects of the injury appear to offer patients the best chance of adapting to their altered situations (Mateer et al, 2005). Being aware of the patient’s emotional well-being is extremely important as it may help identify the development of cognitive distortions such as catastrophic thinking (in which the individual imagines the worst possible outcome of events and situations). Catastrophic thinking can occur when an individual has a distorted belief about the implications of a cognitive error or episode of forgetfulness (Mateer et al, 2005). For example, a patient may interpret normal lapses of memory as confirmation of a memory impairment that will never improve. They may have difficulty in distinguishing between a normal memory lapse and a cognitive error that commonly results from a genuine brain impairment and this may reduce the individual’s ability to cope. Cognitive appraisal and beliefs of self-efficacy are increasingly recognised as being crucial to an individual’s ability to manage stress (Lachman et al, 1992; Mateer et al, 2005).

Recommendations for successful rehabilitation

Approaches to successful cognitive rehabilitation consider both general and specific aspects of the patient’s difficulties (Box 4). The general aspects focus on psychoeducation covering the effects of brain damage and cognitive difficulties, the impact of personality changes and emotional reactions, and the perception of cognitive disorders (Malia & Brannagan, 2004; Ponds & Hendriks, 2006). Aspects specific to memory rehabilitation address the types of memory problem that should be targeted for treatment and the best strategies that could be used (Ponds & Hendriks, 2006). Treatment plans should be given to the patient, caregivers or family members and the appropriate hospital staff. Progress on the treatment plan should be reviewed regularly (Malia et al, 2004).

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Psychoeducation

At the earliest possible stage, patients should be fully informed of their cognitive problems and their likely prognosis in terms of cognitive function (Malia et al, 2004; Mateer et al, 2005). Education should take place both in formal educational groups for patients and their careers/families and during regular individual contact with the patient, and it should be seen as an ongoing process (Malia et al, 2004). Group sessions should focus on understanding specific brain injuries and what rehabilitation is all about, cognitive and emotional problems following brain injury, how to cope with the changes experienced and developing a new sense of self.

The Society for Cognitive Rehabilitation (Malia et al, 2004) states that the aim of psychoeducation is to help the patient develop appropriate self-awareness, self-esteem, confidence, feelings of personal control and a trusting, working relationship with the therapist. It believes that the importance of education cannot be overemphasised: without good awareness, much of what is subsequently offered will have no enduring effects on the individual’s life in the outside world.

At present, very few patients and families are informed about the consequences of acquired cognitive deficits for future life or the possibilities to train or restore memory (Ponds & Hendriks, 2006). Creating a realistic perspective about the impact and possibilities for improvement of memory problems is the first important step in every memory treatment programme. Mittenberg et al (1996) showed that giving head-trauma patients a booklet on recovering from head injury had a significant positive effect on the number, duration and severity of reported symptoms (headache, memory, fatigue, concentration difficulties, anxiety, depression and dizziness) at 6-month follow-up.

It is crucial to give patients information on ECT during the consent process (Robertson & Pryor, 2006). Moreover, if the results from neuropsychological assessments indicate a need for intervention, patients should also be given psychoeducation or information booklets such as those given to head-injured patients, as these can be extremely beneficial in helping to alleviate the distress experienced by patients with mild brain damage. The information may also help patients adjust to any persistent cognitive difficulties they experience.

Rehabilitation techniques and strategies

The aim of rehabilitation is not restoration but compensation (Malia et al, 2004). This can be achieved through the use of internal or external rehabilitation strategies and modifications to the environment. Strategies adapted for use with people who have epilepsy have been shown to improve many aspects of their lives, including attention and memory, emotional regulation and psychosocial functioning (Ponds & Hendriks, 2006). Cognitive rehabilitation should improve the individual’s ability to function as independently as possible in the least restrictive setting and its end result must be to improve quality of life and real-life skills (Malia et al, 2004).

Studies investigating memory rehabilitation have focused on alleviating many different aspects of memory difficulties. These include both general memory problems such as learning and retrieval, and specific problems with orientation, dates, names, faces, routes or appointments (Wilson et al, 2001; Boman et al, 2004; Avila et al, 2004). Rose & Brooks (2003) have highlighted the potential role of virtual reality paradigms in memory rehabilitation.

According to Ponds & Hendriks (2006), two general approaches are currently used in memory rehabilitation: drill and practice, and compensatory strategies.

Drill and practice

The patient is encouraged to practice repeatedly specific memory tasks. This leads to an improvement on these tasks only; there is no transfer of benefits to general memory.

Compensation

This second approach involves teaching the patient compensatory internal and/or external strategies for coping better with everyday memory problems. Internal memory strategies comprise verbal and visual techniques. These encourage the patient to focus on linking isolated items, via associations, and on enriching the ‘to-be-remembered’ information with additional retrieval cues. The success of internal memory strategies may be due to the deeper level of processing and the elaboration of information that this brings about (Ponds & Hendriks, 2006). External memory strategies include devices that are used to store information (e.g. a calendar, diary, voice recorder or portable electronic organiser) or remind people to perform a particular activity at a specifed time (Wilson et al, 2001; Hart et al, 2004; Kapur et al, 2004; Kirsh et al, 2004).

External strategies also include rearranging or making modifications to the individual’s environment, for example always keeping important items such as keys, wallet or purse and diary together in a labelled drawer in the kitchen (Ponds & Hendriks, 2006). Clearly, internal strategies require greater cognitive capacity and insight than external strategies because the strategy has to be remembered at the very time the individual is becoming overwhelmed with the demands of a task (Malia & Brannagan, 2004).

Process training

Strategy teaching is an integral part of what is known as ‘process training’ in cognitive rehabilitation (Malia et al, 2004). Process training attempts to stimulate poorly functioning neurological pathways in the brain in order to maximise their efficiency and effectiveness. It aims to overcome damage by using both new, undamaged pathways and old partially damaged ones. Process training involves comprehensive assessment and an analysis of the results of this using a practical cognitive model. Regular reassessment should be undertaken to ensure that the patient is moving towards the agreed functional goals, and the results should determine the direction and progress through the process-training exercises.

Evidence shows that the use of process-training materials designed on the basis of neuropsychological theories and arranged into a structured programme can lead to gains in the majority of patients (Boman et al, 2004). Studies have also highlighted the benefits of using computerised assessment and rehabilitation tools in memory process training (Moore et al, 2001; Tarn & Man, 2004; Cappa et al, 2005).

Why is post-ECT rehabilitation so uncommon?

There are many reasons why no one has yet tried to introduce cognitive rehabilitation for patients who report persistent cognitive difficulties after ECT Until recently there appears to have been a general reluctance among psychiatrists to admit that ECT could cause memory or other cognitive problems that are severe, persistent and disabling. Even when patients show significant impairments in memory functioning, there has been considerable debate regarding the extent to which these may be attributable to ECT as opposed to factors such as depression (Robertson & Pryor, 2006). There has also been a failure to acknowledge the effect these consequences on the patient’s sense of self (Johnstone, 1999).

The delay in implementing in routine clinical practice the guidelines and recommendations for the neuropsychological assessment of patients at any stage during programmes of ECT has been a significant contributory factor. Furthermore, when patients receiving ECT have been assessed, the focus has generally been on documenting deficits rather than suggesting how to treat them. It is possible that psychiatrists have limited knowledge about the types of cognitive problem experienced by patients, how they affect their lives and what could be done to facilitate the recovery of cognitive functions or compensate for persistent deficits. They may also be unaware of the potential role of rehabilitation, what it involves and how it may inform the treatment and management of patients under their care.

However, the main reason for the near absence of post-ECT rehabilitation may be the lack of specialist neuropsychological services available to ECT psychiatrists and treatment teams (Robertson & Pryor, 2006). A psychiatrist may well recognise the merit of rehabilitation programmes but have no one to whom the patient can be referred. In Ireland, neuropsychology services are severely underdeveloped, particularly outside of Dublin. Therefore, the lack of suitably qualified personnel with expertise in this area is a significant problem. Multidisciplinary team approaches that include psychiatrists, neuropsychologists, occupational therapists, social workers and community liaison officers may be an integral part of best practice recommendations in cognitive rehabilitation, but in reality such services may not be available.

Conclusions

All patients should undergo cognitive assessment before their first ECT session. Subsequent comprehensive neuropsychological assessments should be routinely undertaken if patients report memory and cognitive disability following ECT. Assessments should take into account baseline (pre-treatment) functioning and should use tasks that are sensitive to the nature of the patient’s everyday problems and that take account of the influence of patient’s current memory, sense of memory self-efficacy and mood. Reassessment should be scheduled after a sufficiently long interval (more than 6 months after treatment) so that persistent cognitive and memory deficits can be identified. Furthermore, patients’ self-reports of adverse side-effects, particularly those concerning deterioration in memory and cognition while undergoing a course of ECT, should be properly investigated by staff in the ECT clinic (NICE, 2003; Benbow & Crentsil, 2004).

It should now be clear that documenting neuropsychological deficits is not enough; a specific programme of cognitive rehabilitation should be designed and made available to all patients with persistent cognitive difficulties following ECT, and details about this treatment should be included with the information that patients receive prior to treatment. This programme should incorporate methods of training and strategy learning of known efficacy that aim to generalise skills to all domains of the patient’s life. Clinicians should be aware cognitive rehabilitation appears to be most successful when patient’s physical, psychological, social and vocational well-being are considered together and when the programme is extended to include the family or caregivers (Mateer et al, 2005).

Cognitive rehabilitation following ECT offers a constructive way of treating and managing the most commonly reported side-effect, which is currently left untreated. Over time, this acknowledgement of the presence and impact of cognitive disability in ECT-treated patients, together with the education of patients, families and mental health professionals about ways to deal with these difficulties, would lead to better overall adjustment by patients and the development of a new sense of self.

Declaration of interest

None.

References

*References of principal interest to clinicians.

*Anonymous (1965) The experience of electro-convulsive therapy by a practising psychiatrist. British Journal of Psychiatry, 111, 365-367.

Ávila, R., Bottino, C. M. C, Carvalho, I. A. M., et al (2004) Neuro- psychological rehabilitation of memory deficits and activities of daily living in patients with Alzheimer’s disease: a pilot study. Brazilian Journal of Medical and Biological Research, 37, 1721-1729.

Beatty S., Mangaoang, M. A. & O’Mara, S. M. (2006) Episodic and recent autobiographical memory in healthy adults: A pilot study. Irish Psychologist, 33, 71-75.

Beck, A. T., Steer, R. A. Q. & Brown, G. K. (1996) Manual for the Beck Depression Inventory – II. Psychological Corporation

*Benbow, S. M. & Crentsil, J. (2004) Subjective experience of electroconvulsive therapy. Psychiatric Bulletin, 28, 289-291.

Bergquist, T. F. & Malec, J. F. (1997) Psychology: current practice and training issues in treatment of cognitive dysfunction. NeuroRehabilitation, 45,112-129.

Boman, I.-L., Lindsted, M., Hemmingsson, H., et al (2004) Cognitive training in home environment. Brain Injury, 18, 985-995.

Broadbent, D. E., Cooper, P. E., FitzGerald, P., et al (1982) The Cognitive Failures Questionnaire (CFQ) and its correlates. British Journal of Clinical Psychology, 21,1-16.

Brodaty PL, Hickie, I., Mason, C, et al (2000) A prospective follow-up of ECT outcome in older depressed patients. Journal of Affective Disorders, 60,101-111.

Calev, A. (1994) Neuropsychology and ECT: past and future research trends. Psychopharmacology Bulletin, 30, A61-46A.

Cappa, S. F, Benke, T, Clarke, S., et al (2005) EFNS guidelines on cognitive rehabilitation: report of an EFNS task force. European Journal of Neurology, 12, 665-680.

Cavanaugh, J. C. & Poon, L. W. (1989) Metamemorial predictors of memory performance in young and older adults. Psychology and Aging, 4,365-368.

Chung, K.-F. (2002) Relationships between seizure duration and seizure threshold and stimulus dosage at electroconvulsive therapy: Implications for electroconvulsive therapy practice. Psychiatry and Clinical Neuroscience, 56, 521-526.

*Coleman, E. Z., Sackeim, H. A., Prudic, J., et al (1996) Subjective memory complaints prior to and following electroconvulsive therapy. Biological Psychiatry, 39,346-356.

Cronholm, B. & Ottosson, J.-O. (1963) The experience of memory function after electroconvulsive therapy. British Journal of Psychiatry, 109, 251-258.

*Donahue, A. (2000) Electroconvulsive therapy and memory loss: a personal journey. Journal of ECT, 16,133-143.

ECT Accreditation Service (2005) Standards for the Administration of ECT (3rd edn). Royal College of Psychiatrists. http:/ /www. rcpsych.ac.uk/pdf/ECTASStandardsDec05.pdf

Eldridge, M., Barnard, P. & Bekerian, D. (1994) Autobiographical memory and daily schemas at work. Memory, 2, 51-74.

Elliot, E. & Lachman, M. E. (1989) Enhancing memory by modifying control beliefs, attributions, and performance goals in the elderly. In Advances in Psychology: Psychological Perspectives of Helplessness and Control in the Elderly (ed. P. S. Fry), pp. 369-367. Elsevier Science Publishers.

*Freeman, C. P., Weeks, D. & Kendell, R. E. (1980) ECT II: Patients who complain. British Journal of Psychiatry, 137, 8-16.

Hart, T, Buchhofer, R. & Vaccaro, M. (2004) Portable electronic devices as memory and organizational aids after traumatic brain injury. A consumer survey study. Journal of Head Trauma Rehabilitation, 19, 351-365.

Hertzog, C, Dixon, R. A. & Hultsch, D. F. (1990) Relationships between metamemory, memory predictions, and memory task performance in adults. Psychology and Aging, 5,215-227.

Johnson, M. K., Foley M. A., Suengas, A. G., et al (1988) Phenomenal characteristics of memories for perceived and imagined autobiographical events. Journal of Experimental Psychology: General, 117,371-376.

*Johnstone, L. (1999) Adverse psychological effects of ECT. Journal of Mental Health, 8, 69-85.

Jonker, C, Smits, C. H. M. & Deeg, D. J. H. (1997) Affect-related metamemory and memory performance in a population-based sample of older adults. Education and Gerontology, 13, 115-128.

Kapur, N., Glisky E. L. & Wilson, B. A. (2004) Technological memory aids for people with memory deficits. Neuropsychological Rehabilitation, 14,41-60.

Kirsch, N. L., Shenton, M. & Rowan, J. (2004) A generic, ‘in-house’ alphanumeric paging system for prospective activity impairments after traumatic brain injury. Brain Injury, 18, 725-734.

*Koopowitz, L. F, Chur-Hansen, A., Reid, S., et al (2003) The subjective experience of patients who received electroconvulsive therapy. Australian and New Zealand Journal of Psychiatry, 37, 49-54.

Lachman, M. E., Weaver, S. L., Bandura, M., et al (1992) Improving memory and control beliefs through cognitive restructuring and self-generated strategies. Journal of Gerontology: Psychological Sciences, 47, P293-P299.

Legendre, S. A., Stern, R. A., Solomon, D. A., et al (2003) The infuence of cognitive reserve on memory functioning following electroconvulsive therapy. Journal of Neuropsychiatry and Clinical Neuroscience, 15, 333-339.

Lemogne, C, Piolion, P., Friszer, S., et al (2005) Episodic autobiographical memory in depression. Specificity, autonoetic consciousness, and self-perspective. Consciousness and Cognition, 15, 258-268.

*Levine, B., Svoboda, E., Hay, J., et al (2002) Aging and autobiographical memory. Dissociating episodic from semantic retrieval. Psychology and Aging, 17, 677-689.

Lisanby S. H, Maddox, J. H, Prudic, J., et al (2000) The effects of electroconvulsive therapy on memory of autobiographical and public events. Archives of General Psychiatry, 57, 581-590.

Malia, K. B. & Brannagan, A. E. (2004) How to Do Cognitive Rehabilitation Therapy: A Guide for All of Us. Brain Tree Training.

Malia, K. B., Law, P., Sidebottom, L., et al (2004) Recommendations in Best Practice in Cognitive Rehabilitation Therapy: Acquired Brain Injury. Society for Cognitive Rehabilitation.

Mangaoang M. A., McMackin D., Quigley J., et al (2004) The effects of left and right selective amygdalohippocampectomy on everyday memory, discourse production and spatial representations. FENS Forum Abstracts, 2, A124.19.

*Mateer, C. A., Sira, C. S. & O’Connell, M. E. (2005) Putting Humpty Dumpty together again: the importance of integrating cognitive and emotional interventions. Journal of Head Trauma and Rehabilitation, 20, 62-75.

McMackin, D., Mangaoang, M. S., Anderson, M., et al (2005) Group cognitive behavioural therapy for major depressive disorder: relationship to neuropsychological function and measures of stress. Acta Neurobiologiae Experimentalis, 65, S64.

Mittenberg, W, Tremont, G, Zielinski, R E., et al (1996) Cognitive-behavioral prevention of postconcussion syndrome. Archives of Clinical Neuropsychology, 11,139-145.

Moore, S., Sandman, C. A., McGrady K., et al (2001) Memory training improves cognitive ability in patients with dementia. Neuropsychological Rehabilitation, 11, 245-261.

National Institute for Clinical Excellence (2003) Guidance on the Use of Electroconvulsive Therapy (Technology Appraisal 59). NICE. http://www.nice.org.uk/pdf/59ectfullguidance.pdf

Parrott, W G & Sabiny J. (1990) Mood and memory under natural conditions: Evidence for incongruent recall. Journal of Personality and Social Psychology, 59, 321-336.

*Peretti, C. S., DAnion, J. M., Grangé, D., et al (1996) Bilateral ECT and autobiographical memory of subjective experiences related to melancholia. A pilot study. Journal of Affective Disorders, 41, 9-15.

*Ponds, R. W H. M. & Hendriks, M. (2006) Memory rehabilitation in epilepsy. Seizure, 16, 267-273.

Prudic, J., Olfson, J., Marcus, S. C, et al (2004) Effectiveness of electroconvulsive therapy in community settings. Biological Psychiatry, 55, 301-312.

*Robertson, H. & Pryor, R. (2006) Memory and cognitive effects of ECT: informing and assessing patients. Advances in Psychiatric Treatment, 12,228-237.

Roche, R. A. P., Mangaoang, M. A., Commins, S., et al (2005) Hippocampal contributions to neurocognitive mapping in humans. A new model. Hippocampus, 15, 622-641.

Rogers, M. A., Bradshaw, J. L., Philips, J. G., et al (2002) Attentional asymmetries following ECT in patients with major depression. Neuropsychologica, 40, 241-244.

Rose, F. D. & Brooks, B. M. (2003) The use of virtual reality in memory rehabilitation: current findings and future directions. NeuroRehabilitation, 18,147-157.

*Rose, D., Fleischmann, P., Wykes, T., et al (2003) Patients’ perspectives on electroconvulsive therapy: systematic review. BMJ, 326,1363-1367.

Royal College of Psychiatrists (1995) The ECT Handbook: The Second Report of the Royal College of Psychiatrists’ Special Committee on ECT (1st edn) (Council Report CR39).

Royal College of Psychiatrists. Royal College of Psychiatrists (1999) Guidelines for Health Care Commissioners for an ECT Service (Council Report CR73).

Royal College of Psychiatrists. Royal College of Psychiatrists (2005) The ECT Handbook: The Third Report of the Royal College of Psychiatrists’ Special Committee on ECT (2nd edn) (Council Report CR128). Royal College of Psychiatrists.

*Salford Community Health Council (1998) Electroconvulsive Therapy, Its Use and Effects. Salford Community Health Council.

Scott, A. I. F. (2005) College guidelines on electroconvulsive therapy: an update for prescribers. Advances in Psychiatric Treatment, 11,150-156.

*Service User Research Enterprise (2002) Review of Consumers’ Perspectives on Electroconvulsive Therapy. Institute of Psychiatry.

Sharma, V. (2001) The effect of electroconvulsive therapy on suicide risk in patients with mood disorders. Canadian Journal of Psychiatry, 46, 704-709.

Smith, G. V., Delia Sala, S., Logie, R. H, et al (2000) Prospective and retrospective memory in normal ageing and dementia. A questionnaire study. Memory, 8,311-321.

Squire, L. R. & Chace, P. M. (1975) Memory functions six to nine months after electroconvulsive therapy. Archives of General Psychiatry, 32,1557-1564.

Squire, L. R. & Slater, P. C. (1983) Electroconvulsive therapy and complaints of memory dysfunction: a prospective three-year follow-up study. British Journal of Psychiatry, 142,1-8.

Squire, L. R., Slater, P. C. & Chace, P. M. (1975) Retrograde amnesia: temporal gradient in very long-term memory following electroconvulsive therapy. Science, 187, 77-79.

Squire, L. R., Slater, P. C. & Miller, P. L. (1981) Retrograde amnesia and bilateral electroconvulsive therapy. Long-term follow-up. Archives of General Psychiatry, 38, 89-95.

Sunderland, A., Harris, J. E. & Gleave, J. (1984) Memory failures in everyday life following severe head injury. Journal of Clinical Neuropsychology, 6,127-142.

Tam, S.-F. & Man, W.-K. (2004) Evaluating computer-assisted memory retraining programmes for people with post-head injury amnesia. Brain Injury, 18, A61-A70.

Teasdale, J. D., Taylor, R. & Fogarty S. J. (1980) Effects of induced elation-depression on the accessibility of memories of happy and unhappy experiences. Behaviour Research and Therapy, 18, 339-340.

Templer, D. I. & Veleber, D. M. (1982) Can ECT permanently harm the brain? Clinical Neuropsychology, 4, 62-66.

UK ECT Review Group (2003) Efficacy and safety of electroconvulsive therapy in depressive disorders: a systematic review and meta-analysis. Lancet, 361, 799-808.

*Weeks, D., Freeman, C. P. L. & Kendell, R. E. (1986) ECT: III: Enduring cognitive deficits? British Journal of Psychiatry, 137, 26-37.

Weiner, R. D., Rogers, H. J., Davidson J. R., et al (1980) Effects of electroconvulsive therapy upon brain electrical activity. Annals of the New York Academy of Sciences, 462, 270-281.

Williams, J. M. G, Watts, F. N., MacLeod, C, et al (1988) Cognitive Psychology and Emotional Disorders. John Wiley & Sons.

Wilson, B. A., Emslic, J. C, Quirk, K., et al (2001) Reducing everyday memory and planning problems by means of a paging system: a randomised control crossover study. Journal of Neurology, Neurosurgery and Psychiatry, 70, 477-^82.

MCQs

1 Patients currently referred for ECT complete routine neuropsychological assessments:

a following the course of ECT treatments
b prior to receiving the first ECT treatment
c 3 months after the last ECT treatment
d 6 months after the last ECT treatment
e patients do not routinely complete neuropsychological assessments at any stage during treatment.

2 The following are not necessary in neuropsychological assessment of patients receiving ECT:

a the Eysenck Personality Inventory
b recommendations for treatment or rehabilitation of
impairments
c tasks measuring ‘real-world’ functioning
d collateral information from the patient’s family or caregivers
e measurement of factors influencing a patient’s ‘cognitive reserve’.

3 Tasks that require patients to self-rate their own memory functioning include:

a the Landmark Recognition Task
b the Mundane Memory Questionnaire
c the Autobiographical Memory Interview
d the Prospective and Retrospective Questionnaire
e the Everyday Memory Interview.

4 Cognitive rehabilitation is least successful when it focuses on:

a compensation for deficit rather than restoration of function
b the cognitive and emotional aspects of brain injury
c including the patient’s family or caregivers in the rehabilitation process
d the drill and practice approach
e the generalisation of acquired skills to the social and vocational domains of the patient’s life.

5 Cognitive rehabilitation techniques have been adapted and used for:

a patients with acquired brain injury
b patients with permanent memory and cognitive disability following ECT
c patients with intellectual (learning) disability
d patients with temporary memory and cognitive problems following ECT
e all of the above.

mcq.jpg

Maeve Mangaoang is a research psychologist at St Patrick’s Hospital (St Patrick’s Hospital, PO Box 136, James’s Street, Dublin 8, Ireland. Email: mangaom@tcd.ie) and a research associate at the Trinity College Institute of Neuroscience. Her interest in cognitive rehabilitation stems from her current research on electroconvulsive therapy (ECT) as a treatment for major depressive disorder and previous work in experimental neuropsychology among patients with temporal lobe epilepsy. Jim Lucey is a consultant psychiatrist and Head of the ECT Department at St Patrick’s Hospital. He also has a special interest in the treatment of obsessive-compulsive disorder.

Little merit in ECT, US study finds

Opponents of electric-shock therapy are calling for a ban on its use in the elderly after a new study shows they are at increased risk of permanent brain damage.

The Press (New Zealand)
Feb 7 2007
By KAMALA HAYMAN

The elderly, women and people with lower IQs are the most vulnerable to brain damage, particularly memory loss, according to the first large-scale study on the long-term effects of electroconvulsive therapy (ECT).

About 300 patients a year are given ECT in New Zealand. Two-thirds are women and about 60 per cent are over the age of 50.

In a report released last year, the Health Ministry said ECT was “a valuable and sometimes life-saving” treatment for depression, mania and catatonia, although its effects were typically short-term.

In the New York study, just published in the Neuropsychopharmacology international journal, researchers followed 347 patients for six months.

The research team, led by Harold Sackeim, said the study provided the evidence that “adverse cognitive effects can persist for an extended period and that they characterise routine treatment with ECT”.

The “more severe and persisting” memory problems were found in those given ECT to both sides of the brain, leading the team to conclude there was “little justification” for such treatment.

Some patients were given ECT to only the right side of the brain, to protect the memory centre in the left.

Auckland clinical psychologist John Read said some New Zealand patients were still being given ECT on both sides of the brain.

Read, a long-standing campaigner against the use of ECT, has sent a second petition to the parliamentary health select committee calling for a ban on the treatment in older people, pregnant women and those under 18.

Read said the beneficial effects of ECT were short-term and there was no evidence it saved lives by preventing suicide.

He said patients given ECT should be told: “It does make some people feel better for a short period of time and it causes permanent brain damage for a significant proportion of people.”

A Christchurch 53-year-old, given ECT for severe depression last year, said she had consented to her 12-dose treatment but did not believe it was informed consent as she was not warned of the risk of permanent memory loss. “I have lost my long-term memory and I have lost totally the ability to administer and organise things,” she said.

Despite the “dreadful” side-effects, the woman, who did not want to be named, said ECT was a valuable treatment. Severe depression was not only life-threatening, it was a horrendous experience. “I was like the walking dead.”

She said her depression returned several months after the ECT, although it had since lifted, possibly due to acupuncture and meditation.

Canterbury psychiatric patients are among the most likely in the country to have ECT. In the year to June 2005, 79 Canterbury patients had a course of ECT, about one-quarter of the 307 treated nationally.

Health select committee chairwoman and Green MP Sue Kedgley said ECT was a “barbaric and old-fashioned technique” used in New Zealand with little regulation, monitoring or evaluation. The number of patients given ECT varied wildly in different parts of the country, as did the length of each course.

Kedgley was concerned that one in five patients had ECT without giving consent, and the rate was above 50% in some districts.

“If it is going to cause the harm that this research shows, then I certainly question why it should be given to people without their consent,” she said.

Canterbury psychiatrist Richard Porter, who oversees ECT use, said one-sided (unilateral) ECT was usually prescribed unless treatment was particularly urgent or there was no response to unilateral ECT.

“The choice is discussed with patients and family and the pros and cons explained before the decision is made,” he said. This particularly applied to the elderly, in whom it had been “known for a long time” that memory loss was more likely, he said.

Electroconvulsive Therapy Causes Permanent Amnesia and Cognitive Deficits

ect.org note: This article is appearing in numerous publications and websites, so to avoid repeating the same information again and again, an ongoing list of publications will be posted below.

———–

Forbes
Electroconvulsive Therapy Causes Permanent Amnesia and Cognitive Deficits, Prominent Researcher Admits
12.21.06, 3:38 PM ET

NEW YORK, Dec. 21 /PRNewswire-USNewswire/ — In a stunning reversal, an article in the journal Neuropsychopharmacology in January 2007 by prominent researcher Harold Sackeim of Columbia University reveals that electroconvulsive therapy (ECT) causes permanent amnesia and permanent deficits in cognitive abilities, which affect individuals’ ability to function.

“[T]his study provides the first evidence in a large, prospective sample that adverse cognitive effects can persist for an extended period, and that they characterize routine treatment with ECT in community settings,” the study notes.

For the past 25 years, ECT patients were told by Sackeim, the nation’s top ECT researcher, that the controversial treatment doesn’t cause permanent amnesia and, in fact, improves memory and increases intelligence. Psychologist Sackeim also taught a generation of ECT practitioners that permanent amnesia from ECT is so rare that it could not be studied. He asserted that most people who said the treatment erased years of memory were mentally ill and thus not credible.

The National Institute of Mental Health (NIMH) estimates that more than 3 million people have received ECT over the past generation. “Those patients who reported permanent adverse effects on cognition have now had their experiences validated,” said Linda Andre, head of the Committee for Truth in Psychiatry, a national organization of ECT recipients.

Since the mid-1980s, Sackeim worked as a consultant to the ECT device manufacturer Mecta Corp. He never revealed his financial interest in ECT to NIMH, as required by federal law, and, until 2002, did not reveal it to New York officials as required by state law. Neuropsychopharmacology has endured negative publicity over its failure to disclose financial conflicts of journal authors, resulting in the editor’s resignation and a promise to disclose such conflicts in the future; yet there is no disclosure of Sackeim’s long-term relationship with Mecta, nor did Sackeim disclose his financial conflict when his NIMH grant was renewed to 2009 at approximately $500,000 per year.

The six-month study followed about 250 patients in New York City hospitals, an unusually large number; most ECT studies are based on 20 to 30 patients. Sackeim’s previously published studies were short term, making it impossible to assess long-term effects. “However, in other contexts over the years — court depositions, communications with mental health officials, and grant protocols — Sackeim has claimed to follow up patients for as long as five years. This raises serious questions as to how long he has actually known of the existence and prevalence of permanent amnesia and why it wasn’t revealed until now,” Andre said.

Besides finding that ECT routinely causes substantial and permanent amnesia, the study contradicts Sackeim’s oft-published statements that ECT increases intelligence and that patients who report permanent adverse effects are mentally ill.

“The study is a stunning self-repudiation of a 25-year career,” Andre said.

———————————————————-

Other publications that have picked up the story:

Dec 22 2006:

Forbes
Medical News Today
Brietbart
Dallas News
Kron.com
MedicalDevices.org
TXCN.com – Healthcare & Hospitals
WFAA
Philadelphia Weekly
Genetic Engineering News
Pharma-Lexicon

Electroconvulsive Therapy Causes Permanent Amnesia And Cognitive Deficits, Prominent Researcher Admits

Electroconvulsive Therapy Causes Permanent Amnesia And Cognitive Deficits, Prominent Researcher Admits

Medical News Today
Dec 22 2006

In a stunning reversal, an article in the journal Neuropsychopharmacology in January 2007 by prominent researcher Harold Sackeim of Columbia University reveals that electroconvulsive therapy (ECT) causes permanent amnesia and permanent deficits in cognitive abilities, which affect individuals’ ability to function.

“This study provides the first evidence in a large, prospective sample that adverse cognitive effects can persist for an extended period, and that they characterize routine treatment with ECT in community settings,” the study notes.

For the past 25 years, ECT patients were told by Sackeim, the nation’s top ECT researcher, that the controversial treatment doesn’t cause permanent amnesia and, in fact, improves memory and increases intelligence. Psychologist Sackeim also taught a generation of ECT practitioners that permanent amnesia from ECT is so rare that it could not be studied. He asserted that most people who said the treatment erased years of memory were mentally ill and thus not credible.

The National Institute of Mental Health (NIMH) estimates that more than 3 million people have received ECT over the past generation. “Those patients who reported permanent adverse effects on cognition have now had their experiences validated,” said Linda Andre, head of the Committee for Truth in Psychiatry, a national organization of ECT recipients.

Since the mid-1980s, Sackeim worked as a consultant to the ECT device manufacturer Mecta Corp. He never revealed his financial interest in ECT to NIMH, as required by federal law, and, until 2002, did not reveal it to New York officials as required by state law. Neuropsychopharmacology has endured negative publicity over its failure to disclose financial conflicts of journal authors, resulting in the editor’s resignation and a promise to disclose such conflicts in the future; yet there is no disclosure of Sackeim’s long-term relationship with Mecta, nor did Sackeim disclose his financial conflict when his NIMH grant was renewed to 2009 at approximately $500,000 per year.

The six-month study followed about 250 patients in New York City hospitals, an unusually large number; most ECT studies are based on 20 to 30 patients. Sackeim’s previously published studies were short term, making it impossible to assess long-term effects. “However, in other contexts over the years — court depositions, communications with mental health officials, and grant protocols — Sackeim has claimed to follow up patients for as long as five years. This raises serious questions as to how long he has actually known of the existence and prevalence of permanent amnesia and why it wasn’t revealed until now,” Andre said.

Besides finding that ECT routinely causes substantial and permanent amnesia, the study contradicts Sackeim’s oft-published statements that ECT increases intelligence and that patients who report permanent adverse effects are mentally ill.

“The study is a stunning self-repudiation of a 25-year career,” Andre said.

Depressed OAP died after electric shock treatment

Dec 7 2006

By Gemma Collins
Berkshire Co UK

A FRAIL pensioner who battled with manic depression for 60 years, died after undergoing electric shock therapy at Reading’s Prospect Park Hospital.

Violet Dixon, 81, who suffered from Bipolar affective disorder was given Electroconvulsive Therapy after becoming so depressed and run down that staff feared she would die.

Mrs Dixon who lived with husband Victor in Compton near Newbury had been suffering from anxiety and depression since the 1940s and in the last three years had received several ECT treatments – which involves passing an electric charge through electrodes on her head to provoke a fit or a seizure.

A Reading inquest heard that in February, while sectioned under the Mental Health Act, Prospect Park staff felt she needed electric shock treatment because she was not responding to medication.

But after a second treatment, Mrs Dixon started vomiting, despite being anaesthetised and not having eaten for 24 hours.

She was rushed to the Royal Berkshire Hospital with Aspiration Pneumonia – caused by inhaling vomit – but died there the next day.

The post-mortem revealed that, unknown to her doctor at Prospect Park Hospital, Mrs Dixon had been suffering from an inflamed gall bladder.

Royal Berks anaesthetist Dr Gillian Harrison, who put Mrs Dixon under before her ECT, said: “These patients are mentally ill and often have other medical problems which are very difficult to tell when they won’t give you any history because they are so ill, and they won’t be compliant to medical tests.

“Mrs Dixon had been carefully examined, it was totally unexpected that she had bowel obstruction.”

Berkshire coroner Peter Bedford, recording a ‘narrative verdict’, said Mrs Dixon had undergone many previous ECT treatments without adverse effects.

He said gall stones had caused an undiagnosed gall bladder infection, and added: “This had caused an obstruction which led to severe gastric delay and in turn led to the sequence of events causing her death.”

Harold Sackeim reverses position in upcoming study

by Linda Andre
Director, CTIP

The Cognitive Effects of Electroconvulsive Therapy in Community Settings

NIMH-funded research study published in the January 2007 issue of Neuropsychopharmacology

Author and primary investigator: Harold Sackeim

Funding: NIMH grants

#35636, Affective and Cognitive Consequences of ECT, funded since 1981 for a total of approximately ten million dollars so far (grant has been renewed through 2009)

#59069, ECT Practices in Community Settings—Evaluating Outcomes, funded since 1999 for a total of approximately 3.5 million dollars so far

Summary: After 25 years and millions of dollars of federal funding to research the adverse cognitive effects of ECT—25 years in which not one single longterm followup study was ever published—self-proclaimed “world expert” on ECT Harold Sackeim has now reversed his position, admitting that ECT routinely causes permanent memory loss and deficits in cognitive abilities. His new study—the first to be published in which he followed patients as long as six months, and one of his only studies to use controls—validates a generation of patient reports of permanent iatrogenic disability, and disproves Sackeim’s previously published claims that these reports were simply symptoms of mental illness. Other findings: there is no evidence that ECT increases intelligence, as Sackeim has previously claimed; and women are much more likely than men to experience severe permanent amnesia.

Significance: Harold Sackeim has been called the Pope of ECT, and for good reason. He’s published more on ECT than anyone in the world, has received more money to research it than anyone in the world, and is the author of the American Psychiatric Association’s patient information statement and consent forms, which are used by most hospitals in America. Through his writing, teaching, testimony—and positions on peer review, editorial, and funding boards, including NIMH grant review panels—he has more influence on what the profession and the public believe about ECT than anyone in the world. What Harold says goes.

Conclusion: This study could have been done at any point in the past 25 years. If it had, a generation of patients could have been warned of the likelihood of permanent significant memory and cognitive deficits before, instead of finding out after, ECT. In fact, there is evidence—from Harold’s own statements—that over the years he has in fact conducted studies following up ECT patients for a long as five years…but never published the results. Why not? Why did it take 25 years and over ten million dollars to validate what patients have been saying all along? In other words: What did Harold know, when did he know it, and why wasn’t it revealed?

Quotable quote from the study: This study provides the first evidence in a large, prospective sample that the adverse cognitive effects can persist for an extended period, and that they characterize routine treatment with ECT in community settings.

For a detailed critique, see below.

For the past 25 years, patients who received electroconvulsive therapy (ECT) have been told by the nation’s top ECT doctor that the controversial treatment doesn’t cause permanent amnesia or cognitive deficits and, in fact, improves memory and increases intelligence. Psychologist Harold Sackeim of Columbia University also taught a generation of ECT practitioners around the world that permanent amnesia is so rare it could never be studied. Sackeim was the popularizer if not originator of the position that former patients who said the treatment erased memory were simply mentally ill and thus not credible.

His newest and perhaps last ECT research study disproves his tenaciously held claims about the treatment’s harmlessness. It is, in effect a stunning self-repudiation of a 25-year research career…one in which he accepted federal research money with one hand and consulting fees from shock machine companies with the other.

See, for instance, the key finding:

This study provides the first evidence in a large, prospective sample that the adverse cognitive effects can persist for an extended period, and that they characterize routine treatment with ECT in community settings.

Similarly, from the abstract:

Despite ongoing controversy, there has never been a large scale, prospective study of the cognitive effects of electroconvulsive therapy

Sounds like the research team is congratulating itself for being “the first,” as if they’d made a discovery before anyone else, doesn’t it? You might think that…if you didn’t know that Sackeim has held the only available NIMH research grant to study ECT’s adverse effects, titled “Affective and Cognitive Consequences of ECT,” continuously since 1981…and if you didn’t know what Sackeim promised the federal government in his original application for grant funding:

“The major objective of the proposed research is to examine the effects of bilateral and right unilateral electroconvulsive therapy on affective and cognitive functioning. The consequences of the two treatment modes will be studied in regard to neuropsychological functions that have previously not been studied…Drug-free inpatients presenting major unipolar depressive disorder will be tested before, during and after treatment and a matched normal control group will be tested at comparably spaced times.”

Instead of doing this, however, he used his grant money largely to compare different types of ECT to each other, not to examine the effects of ECT; and only less than a handful of his 200+ published studies used normal controls, an absolute necessity to isolate the effects of ECT.

Why did it take 25 years to conduct one large, long-term controlled follow-up study? And in the absence on this research, why did Harold so confidently assure professionals, patients, legislators, and the public that ECT was safe?

A closer look at the study shows us that, in fact, Harold and his team are still not being honest with us, still not revealing all they know. They tried their damnedest not to find out what ECT really does…but failed. Here they reveal only the minimum information they had to concede after using every trick in the book to bias their research in favor of not finding negative effects of ECT.

What tricks did they use here?

1) The assumption that ECT does not cause permanent amnesia and cognitive deficits was built into the design of the study. How so? The study allowed subjects who’d had ECT before, as recently as two months prior, to be counted as the “before ECT” patients–meaning before this course of ECT. It assumed that any effects of ECT resolve within two months. 43% of the subjects had had prior ECT, so that at least half of the data involved comparing the effects of ECT to the effects of more ECT–not isolating the effects of ECT.

2) The outcome measures used to measure amnesia and cognitive function are irrelevant and inadequate to measure the known effects of ECT. Yet even deliberately using measures that would result in underestimating deficits, these deficits were still found to be profound and persistent!

For a critique of the tests used by Sackeim, see Robertson and Pryor’s article, Memory and cognitive effects of ECT: informing and assessing patients, in Advances in Psychiatric Treatment (2006), vol. 12, p. 228-238. For example, the Mini Mental Status exam used by Sackeim is a test that screens for dementia, the grossest and most glaring form of cognitive disability, and is useless for detecting the kinds of deficits caused by ECT.

Sackeim uses a memory test he invented himself, the Autobiographical Memory Inventory. This test is unpublished, not publicly available, not validated, and is not used except by ECT advocates. Robertson and Pryor note that the majority of questions are not relevant to the types of information forgotten by ECT survivors, nor can the test detect amnesia beyond a one-year period. A string of references in Sackeim’s new article attempt to provide support for the claim that the AMI “has shown strong reliability and validity as a measure of retrograde amnesia.” Not only do they not show this, but all the referenced articles were written by Sackeim himself!

3) Patient IQs were estimated pre-ECT using a method that underestimates intellectual ability especially with much higher than average IQs; no attempt was made to ascertain actual IQ. No one looked at these patients’ IQs post-shock to see what happened to them; why not?

Sackeim et al. conclude, based on inaccurate assumptions and no data from these or any other patients, that “Individuals with greater premorbid abilities can better compensate for the impact of ECT on cognitive functions” (references claiming to support this point have nothing to do with ECT but are articles about an unproven theory of “cognitive reserve”).

Even if the researchers didn’t choose to seek out survivors of ECT who once had very high IQs, or to respond to the many survivors of formerly superior IQs who have contacted them, there is a substantial record of accounts by persons who had extremely high or genius IQs who have spoken and written publicly of the devastating effects of having those IQs lowered by ECT (Jonathan Cott, Linda Andre, Anne Donahue, and Marilyn Rice are four such individuals.) None of these accounts suggests that people with “greater premorbid abilities” have an easier time after ECT; in fact, they strongly suggest the opposite.

In addition to these tricks, the researchers used one of the most reliable methods of biasing results: concealing data.

1) “A substantial number of secondary cognitive measures” are said to have been administered along with the named tests, yet the researchers nowhere reveal what they were and what the results were.

2) The names of the seven facilities in the New York City metropolitan area are not revealed. While this isn’t necessary for evaluating the results of the study, it means the facilities with the worst outcomes can’t be held publicly accountable, nor can the millions of city residents protect themselves from the worst offenders.

3) The results of the cognitive tests on the 24 control subjects are not revealed, nor is how they compared to the people who had ECT.

It’s a very big deal for the Sackeim team to use matched normal controls; in 25 years and hundreds of studies they have not done so. Normal controls are essential to ethical and valid research. This article states that “The comparison sample completed the same neuropsychological battery at time points corresponding to the assessment period in patients.” But you search in vain to find out how the controls did on the five named tests of memory and cognitive functioning and the unnamed “secondary measures”, and how they compared to the ECT patients immediately and six months after ECT. It’s not in the text, and it’s not in the tables. So why have the controls take the tests at all, if you’re not going to reveal the results?

Only one thing is revealed: The normal controls did much better than the bilateral ECT patients on the (flawed) measure of amnesia:

“The average decrement in AMI-SF scores in patients treated exclusively with BL ECT was 3.4 and 2.8 times the amount of forgetting seen in the healthy comparison groups at the post-ECT and 6-month time periods, respectively, suggesting that the deficits were substantial.”

4) Sackeim does not reveal—has never revealed in hundreds of published articles—his financial ties to the shock machine companies Mecta and Somatics. Yet in sworn testimony, Sackeim admits he has worked for Mecta for at least twenty years. He designs their shock machines for them. Not only is disclosure required by journals such as Neuropsychopharmacology (ironically, the subject of a recent scandal in which authors and even the journal’s editor did not reveal their ties to another company which has hired Sackeim, Cyberonics), it is also required by state law (because Sackeim is an employee of New York State) and federal law (because Sackeim accepts NIMH money).
Sackeim flaunts these laws by not disclosing the money he makes from the shock machine manufacturers.

This article is a damning critique of work done over 25 years (and at the expense of millions of taxpayer dollars) by this very team of researchers.

If you know that Sackeim’s been funded for decades to do this research and chose not to do it, the following statements read very differently than the researchers intended. Instead of self-congratulation, they read as condemnation.

“Empirical information about ECT’s long-term effects derives mainly from small sample studies conducted in research settings, with follow-up intervals limited to two months or less…These studies could not adequately assess the severity and persistence of long-term deficits.”

The use of small samples and short-term follow-up characterizes all of Sackeim’s work until now, and was their choice, deliberately made so as not to know (officially) about “the severity and persistence of long-term deficits.” These researchers single-handedly had the wherewithal to address these belatedly-acknowledged flaws in their own research at any time since 1981.

“We conducted the first large-scale, prospective study of cognitive outcomes following ECT.”

Why the first study only after 25 years? What of the generation of patients—two and a half million people according to their own estimate—who have received shock in those years without knowing the long-term consequences?

“Severity of depressive symptoms showed little relationship with the cognitive measures. At the post-ECT time point, none of the 11 measures were related to concurrent HRSD scores. Findings were also negative for 8 of the 11 measures at the six-month follow-up.”

Translation: patients aren’t just imagining or lying about their cognitive and memory deficits because they’re crazy. Yet in many published articles written on the NIMH dime, and over and over in public testimony and in court, that is exactly what Sackeim and Prudic have claimed. And they have influenced countless others to believe it.

DAMNING FINDING #1: amnesia is substantial and permanent

“The average decrement in AMI-SF scores in patients treated exclusively with BL ECT was 3.4 and 2.8 times the amount of forgetting seen in the healthy comparison groups at the post-ECT and 6-month time periods, respectively, suggesting that the deficits were substantial.”

“At the six-month time point, there continued to be a significant relationship between the number of BL ECT treatments and the extent of retrograde amnesia.”

“Greater amnesia for autobiographical events was significantly correlated with the number of ECT treatments received 6 months earlier.”

DAMNING FINDING #2: cognitive deficits are substantial and permanent

“Compared to baseline performance, at the postECT time point the total patient sample showed deficits in the mMMS, sensitivity of the CPT, delayed recall of the BSRT, delayed reproduction on the CFT…” (All are measures of memory and cognitive ability).

“This study provides the first evidence in a large, prospective sample that the adverse cognitive effects can persist for an extended period, and that they characterize routine treatment with ECT in community settings.”

DAMNING FINDING #3: ECT permanently affects reaction time

“Although psychomotor function is of practical importance with respect to driving and other motor activities, the impact of ECT on this domain has rarely been examined…”

(Once again: Whose fault is that?)

“The fact that relative reaction time deficits were observed at the 6-month follow-up indicates a persistent change in the speed of information processing, motor initiation, or response levels…The findings here raise the concern that this form of stimulation has deleterious long-term effects of elemental aspects of motor performance or information processing.”

DAMNING FINDING #4: Bilateral ECT is no good

“For decades, BL ECT represented the gold standard with respect to ECT efficacy…A majority (of US ECT practitioners) administer mainly or exclusively BL ECT…
There appears to be little justification for the continued first-line use of BL ECT in the treatment of major depression.”

(More than 90% of the ECT given in the U.S., and at least as high a proportion in other countries, is bilateral.)

DAMNING FINDING #5 They lied when they wrote in the APA consent form that ECT improves your memory

What this team has said in numerous published articles—and what Sackeim wrote into the American Psychiatric Association guidelines on ECT, the “bible” used by all rank and file shock doctors—that ECT improves memory and intelligence, is not true.

“It is noteworthy that most cognitive parameters were substantially improved at 6-month follow-up relative to pre-ECT baseline, presumably because of the negative impact of the depressed state on baseline performance…It cannot be concluded, however, that the extent of improvement in any group returned to premorbid levels.”

DAMNING FINDING #6: A much greater percentage of women than men are damaged by ECT than men: 81% vs. 18%.

“There was a gender difference, with a greater preponderance of women (81.6%) compared to men (18.4%) in the persistent deficit group.”

No doubt Sackeim and his handlers will try to “spin” this study as a scientific breakthrough, and hold him up as a reformer and patient advocate. Nothing could be farther from the truth.

Where is the apology to the generation of people who were lied to, who will never regain their memories and their cognitive abilities?

Full study

Shock Treatment: Efficacy, Memory Loss and Brain Damage

Shock Treatment: Efficacy, Memory Loss, and Brain Damage – Psychiatry’s
Don’t Look, Don’t Tell Policy
by Richard A. Warner

This downloadable paper was written by a paralegal in an ECT case that is currently on appeal. He researched the subject for two years, and decided to put that research to use, in this paper.

Shock Treatment: Efficacy, Memory Loss, and Brain Damage

PDF: 300k

Dr. Bonnie Burstow: shock is a form of violence against women

Dr. Bonnie Burstow explores electroshock as a form of violence against women. She is a feminist therapist, an anti-psychiatry and anti-fascist activist. She is also the former co-chiar of the Ontario Coalition Against Electroshock and is the author of Radical Feminist Therapy: Working in the Context of Violence.

Two versions:
An edited version runs just under 30 minutes and the full speech runs just over 60 minutes.

Listen to an edited version (30 min) or full speech (60 min)

ECT cognitive effects: unpublished article reveals damning information

Update: The full article has been published in Nature and may be read here in PDF format.

An unpublished article, send by an insider to ect.org, reveals what ECT activists have been saying for years: ECT does cause cognitive damage. The “running title” of the article is “Cognitive Effects of ECT.”

The article is scheduled to be published in Neuropsychopharmacology in January.

4,247 Words
5 Tables
5 Figures

The Cognitive Effects of Electroconvulsive Therapy in Community Settings

Harold A. Sackeim1,2,3, Joan Prudic1,2, Rice Fuller4, John Keilp2,5, Philip W. Lavori6, and Mark Olfson*,2,7

1 Department of Biological Psychiatry, New York State Psychiatric Institute, New York, NY; 2Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, NY; 3 Department of Radiology, College of Physicians and Surgeons, Columbia University, New York, NY; 4Institute for Health, Health Care Policy, and Aging Research, Rutgers University, New Brunswick, NJ; 5Department of Neuroscience, New York State Psychiatric Institute, New York, NY; 6Department of Veterans Affairs Cooperative Studies Program and the Division of Biostatistics, Department of Health Research and Policy, Stanford University, Palo Alto, CA; 7Department of Clinical and Genetic Epidemiology, New York State Psychiatric Institute, New York, NY.

* Correspondence: Dr Harold A. Sackeim, Department of Biological Psychiatry, New York State Psychiatric Institute, 1051 Riverside Drive, New York, NY 10032 USA. Tel: (212) 543-5855, Fax: (212) 543-5854, E-mail: has1@columbia.edu

Running title: Cognitive Effects of ECT

ABSTRACT

Despite ongoing controversy, there has never been a large scale, prospective study of the cognitive effects of electroconvulsive therapy (ECT). We conducted a prospective, naturalistic, longitudinal study of clinical and cognitive outcomes in patients with major depression treated at 7 facilities in the New York City metropolitan area. Of 751 patients referred for ECT with a provisional diagnosis of a depressive disorder, 347 patients were eligible and participated in at least 1 postECT outcome evaluation. The primary outcome measures, Modified Mini- Mental State exam scores, delayed recall scores from the Buschke Selective Reminding Test, and retrograde amnesia scores from the Columbia University Autobiographical Memory Interview–SF (AMI– SF), were evaluated shortly following the ECT course and 6 months later. A substantial number of secondary cognitive measures were also administered. The 7 sites differed significantly in cognitive outcomes both immediately and 6 months following ECT, even when controlling for patient characteristics. Electrical waveform and electrode placement had marked cognitive effects. Sine wave stimulation resulted in pronounced slowing of reaction time, both immediately and 6 months following ECT. Bilateral ECT resulted in more severe and persisting retrograde amnesia than right unilateral ECT. Advancing age, lower premorbid intellectual function, and female gender were associated with greater cognitive deficits. Thus, adverse cognitive effects were detected 6 months following the acute treatment course. Cognitive outcomes varied across treatment facilities and differences in ECT technique largely accounted for these differences. Sine wave stimulation and bilateral electrode placement resulted in more severe and persistent deficits.

Key words: electroconvulsive therapy, major depression, memory, cognitive side effects, amnesia

INTRODUCTION

Electroconvulsive therapy is widely considered the most effective antidepressant treatment, with medication resistance its leading indication (American Psychiatric Association, 2001). However, critics contend that ECT invariably results in substantial and permanent memory loss (Breggin, 1986; Sterling, 2000), with some patients experiencing a dense retrograde amnesia extending back several years (Donahue, 2000; Sackeim, 2000). In contrast, some authorities have argued that, with the introduction of general anesthesia and more efficient electrical waveforms, ECT’s adverse cognitive effects are short-lived, with no persistent effects on memory (Abrams, 2002; Fink, 2004).

Shortly following the ECT course most patients manifest deficits in retaining newly learned information (anterograde amnesia) and recalling events that occurred in the weeks or months preceding the ECT course (retrograde amnesia) (Sackeim, 1992; Squire, 1986). Randomized controlled trials have shown more severe short-term memory deficits with sine wave compared to brief pulse stimulation (Valentine et al, 1968; Weiner et al, 1986), bilateral (BL) compared to right unilateral (RUL) electrode placement (Lancaster et al, 1958; Sackeim et al, 1986; Sackeim et al, 1993; Sackeim et al, 2000), and higher electrical dosage (McCall et al, 2000; Ottosson, 1960; Sackeim et al, 1993). These adverse effects are reduced by the use of RUL ECT with brief or ultrabrief pulse stimulation and electrical dosage titrated to the needs of the individual patient (Sackeim, 2004b). Nonetheless, a minority of US practitioners still use sine wave stimulation, approximately half do not adjust dosage relative to the patient’s seizure threshold, and a majority administer mainly or exclusively BL ECT (Farah and McCall, 1993; Prudic et al, 2004; Prudic et al, 2001). The continued use of treatment techniques associated with more severe short-term cognitive deficits may reflect the beliefs that the cognitive deficits are transient and that older treatment methods provide greater assurance of efficacy (Scott et al, 1992).

Empirical information about ECT’s long-term effects derives mainly from small sample studies conducted in research settings, with follow-up intervals frequently limited to two months or less. By excluding individuals with significant medical and psychiatric co-morbidities, use of optimized forms of ECT, and limited statistical power, these studies could not adequately assess the severity and persistence of long-term deficits. In a sample treated in community settings, we conducted the first large-scale, prospective long-term study of cognitive outcomes following ECT. We characterized the profile of cognitive change immediately and 6 months following completion of ECT, and examined the relationships of treatment technique and patient characteristics to cognitive outcomes. We also determined whether a patient subgroup had especially marked long-term deficits and whether particular forms of ECT administration were overrepresented among these patients.

PATIENTS AND METHODS
Study Sites and Study Participation

The study was conducted at 7 hospitals in the New York City metropolitan area: 2 private psychiatric hospitals, 3 community general hospitals, and 2 hospitals at university medical centers. A clinical outcomes evaluator was assigned to each hospital and collected all research information. The study was conducted by investigators at the New York State Psychiatric Institute (NYSPI), and patients at this facility did not participate. Institutional Review Boards at NYSPI and each of the 7 hospitals approved the study.

Participants were recruited from the inpatients and outpatients referred for ECT with a clinical diagnosis of a depressive disorder. Over a 26-month period, 751 patients were so referred [see Prudic et al (2004) and Figure 1 for details on sample composition]. Study participants met the Diagnostic and Statistical Manual (DSM-IV) criteria for a major depressive episode (unipolar or bipolar) or schizoaffective disorder, depressed, on the basis of the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I/P) (First et al, 1996a). Patients were excluded if they received ECT in the past 2 months, scored below 15 on the Mini-Mental State Exam (Folstein et al, 1975), or spoke neither English nor Spanish. Patients were at least 18 years of age and provided informed consent after study procedures had been fully explained.

Study Measures

The primary instrument to assess severity of depressive symptoms was the Hamilton Rating Scale for Depression (HRSD, 24- item) (Hamilton, 1967). Comorbid DSM-IV psychiatric Axis I disorders, including substance abuse or dependence, were determined using a full SCID-I/P interview (First et al, 1996a). Medical comorbidity was assessed with the Cumulative Illness Rating Scale (CIRS) (Miller et al, 1992). At preECT baseline the North American Adult Reading Test (NAART) provided an estimate of premorbid intelligence (Johnstone et al, 1996).

An extensive neuropsychological battery was administered at preECT baseline, within days of completing the ECT course, and at 6-month (24-week) follow-up. A description of the battery and the derived outcome measures are presented in Table 1. The modified Mini-Mental State exam (mMMS) (Stern et al, 1987), a measure of global cognitive status and an expanded version (range 0-57) of the original MMS (Folstein et al, 1975), has shown sensitivity to variation in ECT technique (Sackeim et al, 1993; Sackeim et al, 2000). Psychomotor function was assessed with 3 measures of reaction time (RT): Simple (SRT) (Benton, 1977), Choice (CRT) (Benton and Blackburn, 1957), and Stroop RT (MacLeod, 1991). In each task, median RT for correct response was determined. Although psychomotor function is of practical importance with respect to driving and other motor activities, the impact of ECT on this domain has rarely been examined (Calev et al, 1995; Sackeim, 1992). Attention was assessed with the Stroop (MacLeod, 1991) and the Continuous Performance Test (CPT) (Ballard, 1997; Cornblatt et al, 1984). In severe depression, attention is often impaired, but believed to improve with symptomatic remission (Sternberg and Jarvik, 1976; Zakzanis et al, 1998). However, there is virtually no information on the effects of ECT on these classic attentional measures.

Anterograde and retrograde amnesia are the two deficits most characteristic of ECT. Anterograde learning and memory were assessed with the Complex Figure Test (CFT) (Rey, 1941; Spreen and Strauss, 1998) and the Buschke Selective Reminding Test (BSRT) (Buschke, 1973; Hannay and Levin, 1985). Deficits in delayed recall on the BSRT have been repeatedly documented shortly following ECT, and found to be sensitive to variation in treatment technique (Sackeim et al, 1993; Sackeim et al, 2000). Retrograde amnesia for autobiographical information was measured with the Columbia University Autobiographical Memory Interview– Short Form (AMI-SF) (McElhiney et al, 1997; McElhiney et al, 1995). The original version of the AMI, containing 281 items, has shown strong reliability and validity as a measure of retrograde amnesia, and sensitivity to variation in ECT technique (Lisanby et al, 2000; McElhiney et al, 1995; Sackeim et al, 1993; Sackeim et al, 2000; Sobin et al, 1995).

Three alternate versions of the mMMS, CFT, and BSRT were randomized to testing occasion. The order of the stimuli in each of the computerized tasks was newly randomized at each testing occasion. To allow for comparison of scores across tests and time points, the baseline scores on each test were converted to standardized scores, with a mean of 0 (SD = 1) for the total sample. Scores at the two subsequent assessments were standardized in relation to the distribution of scores at baseline. In all cases, higher standardized scores reflected superior performance. The primary cognitive outcome measures were postECT scores on the AMI-SF, mMMS, and delayed recall on the BSRT. The primary measure at the 6-month follow-up was the AMI-SF score. To identify a subgroup with marked and persistent retrograde amnesia, the most common source of complaint regarding long-term deficits, individuals were identified who following both the postECT and 6-month follow-up assessments had decreases of at least –2.0 SD units or greater on the AMI-SF.

Study Procedures

The outcomes evaluators screened all patients scheduled to start ECT at the facility with a provisional clinical diagnosis of a depressive disorder (N = 751; Figure 1). After obtaining consent and determining eligibility, the evaluator administered the clinical assessment and neuropsychological batteries prior to the first ECT treatment (N = 398).

The intent-to-treat sample included those patients who received at least one treatment and participated in a postECT clinical outcome evaluation (N = 347).

Time limitations and other factors resulted in variable rates of completion of the cognitive tasks, especially at the baseline evaluation. For the baseline assessment, the sample size for the cognitive measures ranged from 242 (CPT) to 347 (mMMS). The ranges were 224 to 346 and 202 to 260 at the postECT and 6-month follow-ups. Thus, 99% of the intent-to-treat sample participated in all or part of the cognitive evaluation at postECT and 75% did so at the 6-month follow-up.

The outcomes evaluator attended ECT treatments and documented the type and doses of medications, type of physiological monitoring, ECT device model, electrical waveform, electrode placement, stimulus dosing strategy, and the specific parameters used for stimulation. The duration of the motor convulsion and, when monitored, the EEG seizure were recorded.

When the treating psychiatrist indicated that the acute ECT course was completed, the patient was scheduled for the postECT assessment. The aim was to test patients between 3 and 7 days after ECT. For the 347 patients in the intent-to-treat sample, the average interval to postECT assessment was 4.37 days (SD = 4.19). At the postECT assessment, the Structured Clinical Interview for DSM-IV Axis II Personality Disorders (SCID-II) was administered to derive DSM-IV diagnoses of personality disorders (First et al, 1996b). All consenting patients were clinically monitored for a period of 24 weeks following the acute ECT course. They were administered the HRSD at 4-week intervals and interviewed regarding the treatments received since last contact. At the 6- month time point, the clinical and neuropsychological evaluations were repeated.

A group of 24 healthy comparison participants, with negative lifetime histories of psychiatric illness, were matched to the patient sample in the distributions of age, gender, and education. The comparison sample completed the same neuropsychological battery at time points corresponding to the assessment periods in patients and each test was scored in standardized units relative to the patient distribution at baseline. Only one measure, d’ or sensitivity on the CPT, showed a practice effect, with signficant improvement from baseline to the postECT time point and stable thereafter. The scoring of the AMI-SF necessarily results in higher scores at baseline than follow-up. The CPT and AMI-SF scores in the patient sample were adjusted for the average change seen in the comparison sample, removing the temporal effects on these two measures.

Average raw scores for the patient sample and average raw and standardized scores for the healthy comparison sample are presented for the baseline evaluation in Table 2. Analyses of covariance (ANCOVAs), with age, gender, and education as covariates, indicated that the healthy comparison sample had superior scores on 9 of 11 of the baseline cognitive measures.

Statistical Methods

The pattern of change in neuropsychological scores was determined for the total sample by conducting paired t-tests contrasting scores at postECT and 6-month follow-up with preECT scores. Differences among the sites in cognitive outcomes were tested with analyses of covariance (ANCOVAs). For each measure, an ANCOVA was conducted on the score at postECT with site (7 levels) as a between-subject term and patient age, estimated premorbid IQ (based on the NAART), gender, HRSD score at time of assessment, number of days intervening between the end of ECT and postECT assessment, and preECT baseline cognitive score as covariates. The ANCOVAs conducted on the neuropsychological measures at the 6-month follow-up used the same model except that the number days since end of ECT was dropped and whether or not patients had received further treatment with ECT in the follow-up period was added as a covariate. The covariates in these models were selected a priori based upon reported associations with postECT cognitive measures (Sackeim et al, 1992; Sobin et al, 1995; Zervas et al, 1993). Other potential covariates screened for inclusion in the analyses were cumulative medical burden (CIRS score), other Axis I diagnosis, Axis II diagnosis, psychotic depression subtype, inpatient vs. outpatient treatment setting, history of previous ECT, length of current depressive episode, and number of previous depressive episodes. The criterion for inclusion of a covariate in the final analyses was a significant association (p < 0.05) with at least two of the primary outcome measures. None of the screened variables met this criterion. Post hoc Tukey-Kramer comparisons identified pair- wise differences among the sites.

The associations between treatment technique and cognitive outcomes were first tested in the subgroup of patients who were treated with only one electrode placement, BL or RUL ECT, during acute phase treatment. Patients treated exclusively with bifrontal (BF) ECT (n = 12), a mixture of BL, RUL, and/or BF ECT (n = 75), or exclusively with RUL ECT with sine wave stimulation (n =2) were dropped from these analyses. The ANCOVAs used the same models as the analyses of site differences, except that the site term was deleted and terms for electrode placement, waveform nested within electrode placement, stimulus dosage, and number of treatments were added. Stimulus dosage was computed as the percentage of maximal device output averaged across all treatments. To corroborate findings, a second set of ANCOVAs was conducted in the intent-to-treat sample. In these analyses, the terms for the number of BF, BL, and RUL treatments (3 factors) replaced the categorical classification of electrode placement and the term for the total number of treatments. To determine whether the site differences were attributable to differences in treatment technique, the last set of analyses was repeated adding site as a between-subject factor. A logistic regression analysis was conducted to determine which treatment technique factors were related to likelihood of manifesting especially marked and persistent retrograde amnesia.

RESULTS

Compared to baseline performance, at the postECT time point the total patient sample showed deficits in the mMMS (t(345) = 8.0, p < 0.0001), SRT (t(281) = 4.2, p < 0.0001), sensitivity (d') on the CPT (t(221) = 7.4, p < 0.0001), learning phase of the BSRT (t(314) = 3.5, p < 0.0001), delayed recall on the BSRT (t(301) = 10.5, p < 0.0001), delayed reproduction on the CFT (t(270) = 7.2, p < 0.0001), and in AMI-SF scores (t(328) = 21.7, p < 0.0001) (Figure 2). At this time point, the Stroop interference effect was reduced (t (264) = 5.3, p < 0.0001). The deficits following ECT were greatest for the measures assessing memory for autobiographical events (AMI-SF), retention of newly learned information (delayed performance on the BSRT and CFT), global cognitive status (mMMS), and simple reaction time (SRT). Compared to the preECT baseline, there was significantly improved performance at the 6-month follow- up on all tasks other than the three reaction time measures (SRT, CRT, and Stroop RT) and sensitivity (d') on the CPT. Furthermore, AMI-SF scores remained markedly below baseline values (t(251) = 21.1, p < 0.0001). There were no significant differences among the 7 hospitals in ANCOVAs conducted on the preECT baseline cognitive measures. In contrast, the 7 hospitals differed in mMMS and AMI-SF scores at both the postECT (mMMS: F(6, 333)= 3.25, p = 0.004; AMI–SF: F(6, 313) = 2.70, p = 0.01) and 6-month follow-up (mMMS: F(6, 248) = 3.43, p = 0.003; AMI–SF: F(6, 240) = 2.26, p = 0.04) time points (Figure 3). In addition, there were significant differences among the hospitals at the postECT assessment for 5 other cognitive measures: CRT (F(6, 244) = 3.34, p = 0.004), Stroop RT (F(6, 252) = 3.02, p = 0.007), CPT sensitivity (d') (F(6, 211) = 2.23, p = 0.04), BSRT learning (F(6, 302) = 2.14, p <0.05), and BSRT delayed recall (F(6, 289) = 2.19, p = 0.04). Across these 7 measures and time points, patients at hospital D consistently showed marked deficits, while patients at hospital G showed the least impairment. The site differences in short- and long-term cognitive outcomes persisted following statistical control for the patient features most strongly associated with the cognitive measures.

When the sample was restricted to patients treated with a uniform electrode placement (N = 258), there were marked effects of specific aspects of ECT practice on short- and long-term cognitive measures. At postECT, stimulus waveform had a significant impact on 4 of the 11 cognitive measures (Table 3, Figure 4). In each case, performance was poorer with sine wave compared to brief pulse stimulation. There were robust effects of sine wave stimulation on all three reaction time measures. At postECT, patients treated with BL or RUL ECT differed significantly in 5 of the 11 cognitive measures (Table 3, Figure 4). BL ECT was associated with greater amnesia than RUL ECT on two of the three primary outcome measures, delayed recall on the BSRT and memory for autobiographical events (AMI–SF). The effects of electrode placement and number of ECT treatments were especially marked on the AMI-SF.

At the 6-month follow-up, patients treated with sine wave stimulation continued to have slower reaction time on the SRT and the Stroop RT tasks (Table 4, Figure 4). At this time point, patients treated with BL ECT had inferior performance to patients treated with RUL ECT on the mMMS, SRT, Stroop effect, learning phase of the BSRT and AMI-SF scores. Greater amnesia for autobiographical events (AMI-SF scores) was significantly correlated with the number of ECT treatments received 6-months earlier.

In the confirmatory analyses, there were significant linear relationships between the number of treatments administered and postECT AMI–SF scores for each of the three electrode placements. However, the slope of the decline in AMI–SF scores with increasing treatment number was substantially greater for BL ECT (F(1, 318) = 53.74, slope = -0.14, SE = 0.02, p < 0.0001) than RUL (F(1, 318) = 7.72, slope = -0.06, SE = 0.02; p = 0.005) or bifrontal ECT (F(1, 318) = 8.01, slope = -0.09, SE = 0.03, p = 0.005). At the 6-month time point, there continued to be a significant relationship between the number of BL ECT treatments and the extent of retrograde amnesia (F (1, 240) = 9.61, df = 1, 240, slope = -0.06, SE = 0.02, p = 0.002), while there were no relationships with the RUL or BF placements. Thus, the magnitude of long-term retrograde amnesia linearly increased with longer courses of BL ECT, but was unrelated to the number of RUL or BF treatments administered. Of the 306 patients classified, 38 (12.4%) patients met the a priori criteria for having marked and persistent retrograde amnesia on the AMI-SF. In the logistic regression analysis, number of BL ECT treatments was the only treatment variable that significantly predicted membership in this subgroup, ?2(1, 296) = 14.7, p = 0.0001. There was also a gender difference, ?2(1, 296) = 5.8, p < 0.02, with a greater preponderance of women (81.6%) compared to men (18.4%) in the persistent deficit group. The analyses of study site effects were repeated now including stimulus waveform and number of treatments with each electrode placement as independent variables. The site effects were no longer significant, with the exception of mMMS scores at the 6-month follow-up. Therefore, the site differences in short- and long-term cognitive outcomes were largely attributable to variation in the type of electrical waveform and electrode placement used in ECT administration. As seen in Tables 3 and 4, several of the covariates had powerful relations with cognitive performance at the postECT and 6- month follow-up time points. For every measure and at both time points baseline scores had strong relationships with subsequent assessments, indicating strong reliability. For 8 of the 11 postECT measures, cognitive performance was positively related to the number of days that elapsed from the end of ECT until the cognitive assessment. It is noteworthy that this effect did not occur with the AMI-SF which assessed retrograde amnesia, the deficit thought to be most persistent. Two patient characteristics, age and the estimate of premorbid IQ, had frequent and strong relationships with cognitive outcomes, especially at the postECT assessment. In each instance, older patients and those with lower estimated intellectual function had more severe deficits. The gender differences, including the AMI-SF scores at the two time points, reflected greater deficits in women than men, and women were disproportionately represented in the group with marked and persistent impairment on the AMI-SF. Women have a substantially lower seizure threshold than men (Sackeim et al, 1987) and electrical dosage was not adjusted in most cases relative to the individual patient's seizure threshold. This pattern of gender differences might reflect the fact that electrical dosage was more markedly suprathreshold in women. Severity of depressive symptoms showed little relationship with the cognitive measures.

At the postECT time point, none of the 11 measures were related to concurrent HRSD scores (Table 4). Findings were also negative for 8 of the 11 measures at the 6-month follow-up. At this time point, lesser severity of depressive symptoms was associated with superior mMMS, delayed BSRT, and AMI-SF scores.

DISCUSSION

This was the first large-scale, prospective study of objective cognitive outcomes of patients treated with ECT. The 7 hospitals differed in the magnitude of deficits at the postECT assessment (Figure 2), with significant differences in 7 of the 11 cognitive measures. At the 6-month time point, differences among the hospitals persisted for the measure of global cognitive status (mMMS) and the primary outcome measure that assessed retrograde amnesia for autobiographical events (AMI-SF). In turn, these differences among the hospitals were largely attributable to differences in ECT technique. The use of sine wave stimulation and the BL electrode placement were both associated with greater short- and long-term deficits. In particular, sine wave stimulation had a marked effect on psychomotor response speed. Patients who received this form of stimulation were slowed at the 6-month assessment relative to patients treated with brief pulse stimulation on 2 of the 3 reaction time measures. In contrast, the long-term effects due to electrode placement were expressed in the magnitude of retrograde amnesia. At both the short- and long-term time points, patients treated with BL ECT had greater amnesia for autobiographical events, and the extent of this amnesia was directly related to the number of BL ECT treatments received.

The demonstration of differences in long-term cognitive outcomes as a function of hospital setting and treatment technique supports the conclusion that some forms of ECT have persistent long- term effects on cognitive performance. However, the findings do not indicate that the treatments with more benign outcomes are free of long-term effects. It is noteworthy, for example, that most cognitive parameters were substantially improved at 6-month follow- up relative to preECT baseline, presumably because of the negative impact of the depressed state on baseline performance. Without evaluating a comparable group that did not receive ECT, it cannot be concluded, however, that the extent of improvement in any group returned to premorbid levels.

The finding that sine wave stimulation resulted in slowed reaction time could have reflected a speed/accuracy trade off, with patients receiving sine wave stimulation sacrificing response speed for accuracy. However, the sine wave and brief pulse groups did not differ in accuracy on any of the reaction time tasks where accuracy could be measured (CRT and Stroop). The fact that relative reaction time deficits were observed at the 6-month follow-up indicates a persistent change in the speed of information processing, motor initiation, or response execution. Randomized controlled studies have not found an advantage for sine wave stimulation with respect to efficacy (Andrade et al, 1988; Carney and Sheffield, 1974; Scott et al, 1992; Valentine et al, 1968; Weiner et al, 1986), and the American Psychiatric Association (2001) indicated that there is no justification for its continued use. The findings here raise the concern that this form of stimulation has deleterious long-term effects on elemental aspects of motor performance or information processing.

BL ECT results in broader and more severe short-term cognitive effects than RUL ECT, particularly with respect to retrograde amnesia. With respect to the AMI-SF scores, BL ECT resulted in greater retrograde amnesia than the other electrode placements and, even at the 6-month time point, this effect was linearly related to the number of BL treatments administered during the acute ECT course. The average decrement in AMI-SF scores in patients treated exclusively with BL ECT was 3.4 and 2.8 times the amount of forgetting seen in the healthy comparison groups at the postECT and 6-month time points, respectively, suggesting that the deficits were substantial. Furthermore, of a variety of treatment technique and patient characteristic variables, only receipt of BL treatment distinguished the group with marked and persistent retrograde amnesia. For decades, BL ECT represented the gold standard with respect to ECT efficacy, and the equivalence of RUL ECT was uncertain (Abrams, 1986). Based on accumulating evidence that the efficacy of RUL ECT is strongly influenced by dosage relative to seizure threshold, highly effective forms of RUL ECT are available (McCall et al, 2000; Sackeim et al, 2000). Indeed, recent work suggests that high dosage RUL ECT delivered with an ultrabrief stimulus maintains efficacy and results in minimal retrograde amnesia even in the period immediately following the ECT course (Sackeim, 2004b). Consequently, there appears to be little justification for the continued first-line use of BL ECT in the treatment of major depression.

While there is a large literature on patient characteristics that predict ECT clinical outcome, little is known about the individual difference factors related to cognitive outcomes (Sobin et al, 1995). Age and premorbid estimate of IQ showed robust associations, especially at the postECT time point. In line with prior reports (Sackeim, 2004a), advancing age was associated with greater deficits. The findings regarding premorbid intelligence are novel. This pattern suggests that individuals with greater premorbid abilities can better compensate for the impact of ECT on cognitive functions (Stern, 2002; Stern et al, 1994)

Among the limitations of this study is the fact that differences among patients in the treatment received were not randomized, but determined by the usual practices of the setting in which they were treated and other uncontrolled factors. Thus, in theory it is possible that the associations in this observational study between cognitive outcomes and site and treatment technique factors were due to the effects of other unmeasured variables that covaried with the settings and forms of ECT administration. This concern is mitigated by three considerations. First, the findings were consistent with the results of many randomized controlled trials demonstrating that short-term cognitive outcomes are negatively impacted by receipt of sine wave stimulation or use of the BL electrode placement. The long-term effects observed in this study reflect a lack of resolution of specific deficits observed in the immediate postECT time period (e.g., retrograde amnesia).

Second, there was evidence that the number of treatments administered, an essential characteristic of dosage, linearly covaried with the extent of long-term retrograde amnesia for autobiographical information for patients treated with BL ECT, but not for patients treated with RUL ECT.

This provided internal support for the claim that choice of electrode placement is critical in determining the severity of long-term deficits. Finally, there was considerable variability within some sites in ECT technique, such as choice of waveform and electrode placement. Site differences in cognitive outcomes dissipated when controlling for treatment technique factors. Regardless, this study provides the first evidence in a large, prospective sample that adverse cognitive effects can persist for an extended period, and that they characterize routine treatment with ECT in community settings.

Acknowledgements

Supported in part by grants R01 MH59069, R01 MH35636, R01 MH61609, and R01 MH05148 from the National Institute of Mental Health, Bethesda, MD.

We thank Dr. Bernard Lerer for his comments on this work, and the staff at the 7 hospitals who facilitated the conduct of this study.

REFERENCES

Abrams R (1986). Is unilateral electroconvulsive therapy really
the treatment of choice in endogenous depression? Ann NY Acad
Sci 462: 50-55.

Abrams R (2002). Electroconvulsive Therapy. Oxford University
Press: New York.

American Psychiatric Association (2001). The Practice of ECT:
Recommendations for Treatment, Training and Privileging.
Second Edition. American Psychiatric Press: Washington, D.C.

Andrade C, Gangadhar BN, Subbakrishna DK, Channabasavanna SM,
Pradhan N (1988). A double-blind comparison of sinusoidal wave
and brief-pulse electroconvulsive therapy in endogenous
depression. Convulsive Ther 4: 297-305.

Ballard JC (1997). Computerized assessment of sustained
attention: A review of factors affecting vigilance
performance. J Clin Exp Neuropsychol 18: 843-863.

Benton AL (1977). Interactive effects of age and brain disease
on reaction time. Arch Neurol 34: 369-370.

Benton AL, Blackburn HL (1957). Practice effects in reaction-
time tasks in brain-injured patients. J Abnorm Soc Psychol 54:
109-113.

Breggin PR (1986). Neuropathology and cognitive dysfunction from
ECT. Psychopharm Bull 22: 476-479.

Buschke H (1973). Selective reminding for analysis of memory and
learning. Journal of Verbal Learning and Verbal Behavior 12:
543-550.

Calev A, Gaudino EA, Squires NK, Zervas IM, Fink M (1995). ECT
and non-memory cognition: a review. Br J Clin Psychol 34 (Pt
4): 505-515.

Carney M, Sheffield B (1974). The effects of pulse ECT in
neurotic and endogenous depression. Br J Psychiatry 125: 91-
94.

Cornblatt BA, Lenzenweger MJ, Erlenmeyer-Kimling L (1984). The
continuous performance test, identical pairs version:
Contrasting attentional profiles in schizophrenic and
depressed patients. J Psychiatr Res 29: 66-85.

Donahue AB (2000). Electroconvulsive therapy and memory loss: a
personal journey. J ECT 16: 133-143.

Farah A, McCall WV (1993). Electroconvulsive therapy stimulus
dosing: A survey of contemporary practices. Convulsive Ther
9: 90-94.

Fink M (2004). Electroshock: Healing mental illness. Oxford
University Press: New York.

First MB, Spitzer RL, Gibbon M, Williams JBW (1996a). Structured
Clinical Interview for Axis I DSM-IV Disorders — Patient
Edition (with Psychotic Screen) (SCID-I/P). Biometrics
Research Department, New York State Psychiatric Institute: New
York.

First MB, Spitzer RL, Gibbon M, Williams JBW, Benjamin L
(1996b). Structured Clinical Interview for DSM-IV Axis II
Personality Disorders (SCID-II). Biometrics Research
Department, New York State Psychiatric Institute: New York.
Folstein MF, Folstein SE, McHugh PR (1975). “Mini-Mental State”.
J Psychiatr Res 12: 189-198.

Hamilton M (1967). Development of a rating scale for primary
depressive illness. Br J Soc Clin Psychol 6: 278-296.
Hannay HJ, Levin HS (1985). Selective reminding test: An
examination of the equivalence of four forms. J Clin Exp
Neuropsychol 7: 251-263.

Johnstone B, Callahan CD, Kapila CJ, Bouman DE (1996). The
comparability of the WRAT-R reading test and NAART as
estimates of premoribd intelligence in neurologically impaired
patients. Arch Clin Neuropsychology 11: 513-519.

Lancaster NP, Steinert RR, Frost I (1958). Unilateral
electroconvulsive therapy. J Ment Sci 104: 221-227.
Lisanby SH, Maddox JH, Prudic J, Devanand DP, Sackeim HA (2000).
The effects of electroconvulsive therapy on memory of
autobiographical and public events Arch Gen Psychiatry 57:
581-590.

MacLeod CM (1991). Half a century of research on the Stoop
effect: An integrative review. Psychol Bull 109: 163-203.
McCall WV, Reboussin DM, Weiner RD, Sackeim HA (2000). Titrated
moderately suprathreshold vs fixed high-dose right unilateral
electroconvulsive therapy: acute antidepressant and cognitive
effects. Arch Gen Psychiatry 57: 438-444.

McElhiney M, Moody B, Sackeim H (1997). The Autobiographical
Memory Interview – Short Form. New York State Psychiatric
Institute: New York.

McElhiney MC, Moody BJ, Steif BL, Prudic J, Devanand DP, Nobler
MS, et al (1995). Autobiographical memory and mood: Effects of
electroconvulsive therapy. Neuropsychology 9: 501-517.

Miller MD, Paradis CF, Houck PR, Mazumdar S, Stack J, Rifai AH,
et al (1992). Rating chronic medical illness burden in
geropsychiatric practice and research: application of the
Cumulative Illness Rating Scale (CIRS). Psychiatry Res 41:
237-248.

Ottosson J-O (1960). Experimental studies of the mode of action
of electroconvulsive therapy. Acta Psychiatr Scand [Suppl]
145: 1-141.

Prudic J, Olfson M, Marcus SC, Fuller RB, Sackeim HA (2004).
Effectiveness of electroconvulsive therapy in community
settings. Biol Psychiatry 55: 301-312.

Prudic J, Olfson M, Sackeim HA (2001). Electro-convulsive
therapy practices in the community. Psychol Med 31: 929-934.

Rey A (1941). L’examen psychologique dans les cas
d’encephalopathie traumatique. Archives de Psychologie 28:
286-340.

Sackeim HA (1992). The cognitive effects of electroconvulsive
therapy. In Moos WH, Gamzu ER, Thal LJ eds), Cognitive
Disorders: Pathophysiology and Treatment. Marcel Dekker: New
York, pp 183-228.

Sackeim HA (2000). Memory and ECT: From polarization to
reconciliation. J ECT 16: 87-96.

Sackeim HA (2004a). Electroconvulsive therapy in late-life
depression. In Roose SP, Sackeim HA eds), Late-Life
Depression. Oxford University Press: New York, pp 241-278.

Sackeim HA (2004b). The convulsant and anticonvulsant properties
of electroconvulsive therapy: towards a focal form of brain
stimulation. Clinical Neuroscience Review 4: 39-57.

Sackeim HA, Decina P, Prohovnik I, Malitz S (1987). Seizure
threshold in electroconvulsive therapy. Effects of sex, age,
electrode placement, and number of treatments. Arch Gen
Psychiatry 44: 355-360.

Sackeim HA, Freeman J, McElhiney M, Coleman E, Prudic J,
Devanand DP (1992). Effects of major depression on estimates
of intelligence. J Clin Exp Neuropsychol 14: 268-288.

Sackeim HA, Portnoy S, Neeley P, Steif BL, Decina P, Malitz S
(1986). Cognitive consequences of low-dosage electroconvulsive
therapy. Ann N Y Acad Sci 462: 326-340.

Sackeim HA, Prudic J, Devanand DP, Kiersky JE, Fitzsimons L,
Moody BJ, et al (1993). Effects of stimulus intensity and
electrode placement on the efficacy and cognitive effects of
electroconvulsive therapy. N Engl J Med 328: 839-846.

Sackeim HA, Prudic J, Devanand DP, Nobler MS, Lisanby SH, Peyser
S, et al (2000). A prospective, randomized, double-blind
comparison of bilateral and right unilateral electroconvulsive
therapy at different stimulus intensities. Arch Gen Psychiatry
57: 425-434.

Scott AI, Rodger CR, Stocks RH, Shering AP (1992). Is old-
fashioned electroconvulsive therapy more efficacious? A
randomised comparative study of bilateral brief-pulse and
bilateral sine-wave treatments. Br J Psychiatry 160: 360-364.

Sobin C, Sackeim HA, Prudic J, Devanand DP, Moody BJ, McElhiney
MC (1995). Predictors of retrograde amnesia following ECT. Am
J Psychiatry 152: 995-1001.

Spreen O, Strauss E (1998). A Compendium of Neuropsychological
Tests: Administration, Norms, and Commentary. Oxford
University Press: New York.

Squire L (1986). Memory functions as affected by
electroconvulsive therapy. Ann NY Acad Sci 462: 307-314.

Sterling P (2000). ECT damage is easy to find if you look for
it. Nature 403: 242.

Stern Y (2002). What is cognitive reserve? Theory and research
application of the reserve concept. J Int Neuropsychol Soc 8:
448-460.

Stern Y, Gurland B, Tatemichi TK, Tang MX, Wilder D, Mayeux R
(1994). Influence of education and occupation on the incidence
of Alzheimer’s disease. JAMA 271: 1004-1010.

Stern Y, Sano M, Pauson J, Mayeux R (1987). Modified mini-mental
status examination: validity and reliability. Neurology 37
(suppl 1): 179.

Sternberg DE, Jarvik ME (1976). Memory function in depression:
Improvement with antidepressant medication. Arch Gen
Psychiatry 33: 219-224.

Valentine M, Keddie K, Dunne D (1968). A comparison of
techniques in electro-convulsive therapy. Br J Psychiatry 114:
989-996.

Weiner RD, Rogers HJ, Davidson JR, Squire LR (1986). Effects of
stimulus parameters on cognitive side effects. Ann NY Acad Sci
462: 315-325.

Zakzanis KK, Leach L, Kaplan E (1998). On the nature and pattern
of neurocognitive function in major depressive disorder.
Neuropsychiatry Neuropsychol Behav Neurol 11: 111-119.

Zervas IM, Calev A, Jandorf L, Schwartz J, Gaudino E, Tubi N, et
al (1993). Age-dependent effects of electroconvulsive therapy
on memory. Convulsive Ther 9: 39-42.

Tables and Figures-ECT Cognitive Effects


Harold Sackeim Mecta deposition video clips

Here are a number of clips from the videotaped deposition of Harold Sackeim (2004). Sackeim was the expert witness for Mecta in a lawsuit in California.

You can read most of the deposition here, in PDF format.

I’m splitting the videos into two pages to reduce your load. If the page loads slowly, or the videos don’t load, try again in thirty minutes…it’s likely YouTube is down.

Richard Abrams is defensive, says Harold Sackeim

Harold Sackeim, king of ECT, discusses his complaints about Richard Abrams, president of Somatics, Inc., saying that Abrams is defensive because of the “fascist” groups, and goes too far with his defensiveness by ignoring the “problems” inherent with ECT. Meow!

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Harold Sackeim tells NY Assemblyman Rivera he “discarded” requests

After making a public offer to evaluate individuals with damage after ECT, Sackeim explains that he told the NY Assemblyman Peter Rivera (D-Bronx) he discarded the responses. They “spent the day” together. How cozy. Rivera is head of the New York Committee on Mental Health. Harold has more than one cozy relationship, and it’s paid off in a big way for him.

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Killroy was here

An endorsement? No, but Harold admits he’s been here. Everyone, please, a warm welcome to the Lord of the Dance, Harold Sackeim.

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He’s said it, very clearly

Very emphatically: “I don’t dispute that there are some people who have very severe memory loss. I’ve been the one who’s been saying that very clearly.”

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2 million people?

“Uh, what I do know is that probably about 2 million people are receive ECT each year…” When questioned by the attorney asking if he “knows” that, Harold backpedals and says he said “estimate.” A few years ago he told Extra it was a million. I guess that Cyberonics VNS device isn’t working out so well.

Perhaps saying “I do know” and then claiming he said “estimate” is being a tad picky. But consider that this seems to be a habit with him: reinventing himself, parading himself as the champion of the shock patient by criticizing “Dick” Abrams, and claiming he’s a purist scientist, even when he admits statistics were not genuine statistics as claimed, but merely a guesstimate. Since the long-held guess of how many Americans receive ECT annually is 100,000 to 200,000 (usually quoted as 100,000 in the media), where on earth did he get this 2 million figure for the world?

Oh, it’s an estimate. He made it up.

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Follow the money…

Here’s something he can’t make up, because there’s a paper trail. He billed Mecta for $10,875 for pretrial consulting. And that was *before* the trial, or even this deposition, took place. No telling what the final bill will be! His rate is $500 an hour to help Mecta defend against a lawsuit. Notice how he refuses to say the amount, instead, referring to the “rate that’s there.” For whatever reason, Harold Sackeim cannot say the words “I charge $500 an hour.”

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Part 2 of the video deposition

Harold Sackeim Mecta deposition video clips, page 2

The Awakening

This clip is an interesting explanation of why psychiatrists have apparently been unaware for 70 years that ECT can and does cause profound memory loss and cognitive damage. The reason? Because until a few years ago, the only persons who complained of severe memory loss also said it didn’t help them. It took finding some patients who experienced devastating memory loss who would also proclaim it “saved their life” before Harold Sackeim would listen.

Hey, I’m not the one who said it…Harold is. He’s the champion of the shock patient, at least in his own head. Maybe he needs to revisit the early years of Sackeimology, when his research revolved around self deception, the lies we tell ourselves.

Harold (call him doctor, damn you!) relates an interesting story, if true. He’s been known to make up statistics and a vignette or two. And he questioned whether or not the individuals on ect.org were really ECT patients. That’s called projection, Harold. Or deflection. You should have learned these terms when you studied Sackeimology.

The story takes place at an ECT donut course. (Shock docs and donuts are like cops and donuts.) One of the “very famous people” (that could really only be Abrams, Fink or Kellner, probably the Finkster) announced that profound memory loss just doesn’t happen. But our hero Harold asked the audience – all shock docs – if they’d encountered it. Two-thirds raised their hands. Oops. 70 years of denial down the drain.

It was almost a watershed moment, he says. The only thing missing was the heavens opening and the Angel Gabriel trumpeting the good news: Harold Sackeim is GOD, everyone. He’s your savior.

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FDA and ECT devices

This is the well-known story of how the FDA has been lobbied by the industry to change ECT devices from Class III to Class II. What’s interesting (and keeps popping up in Harold’s testimony) is that apparently the psych rights movement is having an impact on things. Despite his admitting that he speaks with the FDA regularly, and that the industry has lobbied the FDA for the change, Harold says the FDA is afraid to make a move.

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“I DO consider it.”

When asked if he discounts the many personal accounts of memory loss post-ECT, he responds that he does consider it.

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Electrical parameters

Harold discusses the parameters of ECT, cognitive side effects and Mecta machines.

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What they knew, when they knew

Is it necessary to inform patients of the risk of permanent, severe memory loss? Harold says it’s not in dispute…of course you tell them, and he always does. At least in the last three or four years…once they discovered it really happens. Before then, well, they kinda knew, but they just had no scientific evidence that it did, and the wrong kinds of people had been talking about it. So it’s not their fault because they didn’t know. They just didn’t know. Until a few years ago.

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Sackeim: “I got the field to do that”

Harold says the APA Task Force Report now says that ECT can cause profound memory loss. ECT patients have only been saying that for…hmmm, nearly SEVENTY YEARS!

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Memory and cognitive effects of ECT

Memory and cognitive effects of ECT: informing and assessing patients

Advances in Psychiatric Treatment (2006), vol. 12, 228 238

Harold Robertson & Robin Pryor

Abstract:

Over the past few years electroconvulsive therapy (ECT) has come under increased scrutiny in the UK, with the first systematic review of patients’ experiences and new national guidelines. Our aim in this article is to translate recent and sometimes confusing research and policy statements into practical guidance that benefits patients. We examined the evidence on the permanent memory and cognitive effects of ECT, with a focus on delineating their nature, understanding how ECT may cause them, informing prospective patients about them, and assessing their impact on former patients. We describe a simple and effective method for assessing retrograde amnesia. Data do not exist at this time to confirm the mechanisms by which ECT exerts its adverse effects, but clinicians should fully inform patients of the possible permanent adverse effects of the treatment, which include amnesia, memory disability and cognitive disability, and should provide follow-up testing using relevant instruments.

In January 2002, as part of a review of electroconvulsive therapy (ECT) undertaken by the UK’s Department of Health, the Service User Research Enterprise (SURE) published the first-ever systematic review of patients’ views on ECT (Service User Research Institute, 2002). The review encompassed several large-scale surveys by or of people who had received ECT in the UK (United Kingdom Advocacy Network, 1996; ECT Anonymous, 1999; Pedler, 2000). In April 2003, the National Institute for Clinical Excellence (now the National Institute for Health and Clinical Excellence, NICE) issued guidance on the use of ECT, and at the same time, the UK ECT Review Group published a review of its safety and efficacy (National Institute for Health and Clinical Excellence, 2003; UK ECT Review Group, 2003). The Royal College of Psychiatrists has established the ECT Accreditation Service and revised its guidelines for practitioners to take into account the NICE advice (Royal College of Psychiatrists, 2005).

Some of the conclusions to come out of the new work – in particular, that at least one-third of patients experience permanent amnesia (Service User Research Institute, 2002; Rose et al, 2003; Scott, 2005), that half of patients had not received an adequate explanation prior to treatment (Rose et al, 2003, 2005; Philpot et al, 2004) and that newer methods of ECT have not resulted in an appreciable decrease in adverse effects (UK ECT Review Group, 2003) – suggest that changes are overdue in both practice and policy.

The new evidence presents opportunities for improving clinical care in several areas: delineating the nature of ECT’s permanent adverse effects; developing adequate and relevant tools to assess patients; and providing consent that is fully informed.

Defining deficits

It is evident from a close reading of patient reports such as those documented by SURE that ‘memory’ is too simple a term to encompass the range of ECT’s permanent adverse effects, yet there has been almost no work done on improving terminology (Box 1). The confusion goes back to the first instrument specifically designed to assess people given ECT, the Squire Memory Questionnaire (SMQ; Squire et al, 1979). The SMQ was developed to distinguish between the cognitive impairments associated with depression and those caused by ECT. Although Squire and his colleagues believed that they had done this (Squire & Slater, 1983; Squire & Zouzounis, 1988), others have not used the test for its intended purpose, and it is hard to say whether the SMQ has muddied the water more than it has cleared it. Although often spoken of as if it measured a unitary entity ‘memory’, the SMQ actually encompasses multiple dimensions of cognition: attention, alertness, concentration, learning. It does not at all address the most common effect of ECT, which is variously called amnesia, retrograde amnesia or memory loss. By these terms is generally understood the obliteration of a specific time period in a person’s life.

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It is when ‘memory’ is used as a shorthand term for both retrograde amnesia and ongoing difficulties with memory function in the present that confusion ensues, a confusion that intensifies when the latter is sometimes called ‘anterograde amnesia’. Although most will understand anterograde amnesia to mean ongoing memory disability, this is not always the case. The US National Institute of Mental Health has defined anterograde amnesia as the inability to remember events that happened after ECT (National Institutes of Health, 1985) and the College’s new handbook (Royal College of Psychiatrists, 2005) appears to use it in the same way.

To confuse matters further, the term ‘short-term memory loss’ is sometimes used as a synonym for anterograde amnesia. Short term to some will mean temporary, to others it will be seen as a description of the type of memory that is affected – the ability to retain information for a short period, or working memory (Baddeley & Hitch, 1974) – which says nothing about its longevity. The term ‘temporary’ rather than ‘short-term’ should always be used to refer to effects that resolve, but even then it should be used with caution because neuropsychology recognises that transient impairment of cognitive function may have residual permanent effects. ‘Dysfunction’ or ‘disability’ should be used rather than ‘loss’ (which implies a one-time event) to refer to ongoing difficulties with memory ability and cognition.

If the term anterograde amnesia must be used, it should be clearly defined as difficulties with memory in daily life, and examples given (Box 2).

Inevitably, memory overlaps with and subsumes other cognitive functions, such as learning and attention as well as overall intelligence. When individuals who have had ECT report ongoing memory disability, it is necessary for a clinician
trained in neuropsychological evaluation to tease out the roles played by attention, concentration, overall slowed mental processing and deficits of executive function such as inability to shift mental set. The ECT psychiatrist and treatment team may not be trained in neuropsychological evaluation, since outside of research settings it is not routinely performed on people who have had ECT. When it is, it is usually initiated by the patient, not the doctor. Because of this, the treating psychiatrist may fear personal liability and thus be unwilling to attribute deficits to ECT.

It has long been known that ECT can produce deficits in non-memory-related cognitive function (Calev, 1994). However, long-term studies comparing controls and people who have had ECT to determine when and if non-memory cognitive function normalises after ECT have not been done. A comprehensive battery of neuropsychological tests carried out on individuals who had had ECT between 9 months and 30 years previously revealed impairment on a range of measures, even after controlling for the effects of illness and medication (Freeman et al, 1980).

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Despite recommendations that psychiatrists inform patients of non-memory cognitive after- effects (Calev, 1994) and warn them that ‘they are not going to function well on more tasks than they anticipate’ (Calev et al, 1995), patients are still routinely not informed about these effects; there is no mention of them in the recommended consent forms of the American Psychiatric Association (APA; 2001), the Royal College of Psychiatrists (2005: Appendix 1V) or the manufacturers of ECT equipment. This may contribute to the consistent findings (Rose et al, 2003, 2005; Philpot et al, 2004) that half of people given ECT say they did not receive an adequate explanation of the treatment.

The current APA consent forms not only contain no warnings about adverse effects on cognition, but advise that ‘Most patients report that memory is actually improved by ECT’ (American Psychiatric Association, 2001). This statement is contradicted by all service-user research as well as the findings of SURE (2002) and NICE (2003); indeed, Scott (2005) remarked that NICE took ‘special note of the evidence from users that cognitive impairment after ECT often outweighed their perception of any benefit from it’.

Is it depression?

If the task of assessing amnesia, memory disability and cognitive deficits is left to a patient’s treating psychiatrist, there may be a tendency to attribute all deficits, without evaluation, to depression, even when the patient has fully recovered. The APA guidelines state that

‘Patients with the greatest symptomatic benefit from
ECT typically report the greatest improvement in
subjective evaluations of memory. Thus, when patients
report subjective memory impairment after ECT, their
mood as well as their cognition should be assessed’
(American Psychiatric Association, 2001: p. 72).

It seems that this statement is based on SMQ scores from six studies: Pettinati & Rosenberg, 1984; Weiner et al, 1986; Mattes et al, 1990; Sackeim et al, 1993 and Coleman et al, 1996, which involved the same patients; and Sackeim et al, 2000. On average, patients reported improvement in cognitive functions assessed by the SMQ within 1 week of ECT. However, the following should be taken into account: first, the improvement was relative only to immediate pre-ECT status, not baseline, thus in fact reflecting a net impairment; and second, objective testing revealed that the patients were in fact cognitively impaired post-ECT. There are other studies in which patients reported impairment post- ECT on the SMQ (Squire et al, 1979; Squire & Slater, 1983; Squire & Zouzounis, 1988). To the extent that a handful of studies support a claim of correlation between memory and cognitive self-rating and mood during or immediately after ECT, there might be a correlation between relatively improved memory self-rating and improved mood. There is no evidence of a correlation between impaired memory/cognition after ECT and impaired mood, much less a causal relationship. The problem of premature assessment There are many reasons why hospitalised patients who have received ECT might overestimate their abilities. After each treatment they experience acute organic brain syndrome (Sackeim, 1986). In hospital, they are not exposed to even minimally taxing actions such as shopping and driving. There are no environmental cues as to what they are expected to know and remember in their roles outside the hospital. In a few days or even weeks, patients cannot gain enough experience of using their minds and memories to accurately assess their altered capacities (Weiner et al, 1986; Coleman et al, 1996; Donahue, 2000). In the longer term, i.e. 2-6 months, patients who initially rated their memory and cognition as improved, experience and accurately report impairment (Weiner et al, 1986; Coleman et al, 1996).

More recent work using the SMQ suggests that, in the short term as well, patient ratings of memory function are negative and are correlated with the results of objective tests, even when controlling for the level of depression. These researchers say that patient reports of memory impairment ‘must not be dismissed as being depressive complaints only’ (Schulze-Rauschenbach et al, 2005).

Differentiating the effects of ECT

Although terms such as memory loss are often used interchangeably by clinicians to describe the temporary effects of depression on cognition (especially attention) and the long-lasting effects of ECT on a range of cognitive functions, this confusion is unnecessary and could be avoided. The effects of ECT are quantitatively and qualitatively different from those of depression (Squire et al, 1979) and researchers have consistently distinguished between them (Cronholm & Ottoson, 1963; Squire et al, 1979; Squire & Slater, 1983; Pettinati & Rosenberg, 1984; Squire & Zouzounis, 1988). Numerous controlled studies show that individuals who are depressed but have not had ECT do not suffer amnesia (Janis, 1950;

Weiner et all 1986). People who have experienced the effects of both depression and ECT rarely mistake one for the other (Food and Drug Administration, 1982; Donahue, 2000): ECT’s effects are different and worse, they occur only after ECT and they persist in the absence of depression and drugs.

Possible mechanisms of action

How might ECT cause permanent amnesia and memory and cognitive disability? There are several theories (Box 3). One is that memory is affected because the applied electrical current is densest in the medial temporal area structures associated with memory, including the hippocampus; these areas have low seizure thresholds. However, this has not been studied directly (Calev, 1994).

Other theories focus on ECT’s effects on brain metabolism and neurochemistry: breach of the blood-brain barrier and increased cerebral blood pressure (Bolwig et al, 1977; Taylor et al, 1985); regional increases in T2 relaxation times (Diehl et a!, 1994); disturbance of the long-term potentiation mechanism (Sackeim, 2000; Rami-Gonzalez et al, 2001); excessive release of excitatory amino acids and activation of their receptors (Chamberlin & Tsai, 1998; Rami-Gonzalez et all 2001), and decreased cholinergic transmission (Khan et al, 1993; Rami- Gonzalez et al, 2001). Even temporary alterations in any of these may have permanent effects on the brain.

Since ECT affects both temporal and frontal lobes, it is logical that its effects would not be limited to amnesia, but would involve both memory and non-memory neuropsychological functions (Calev et al, 1995). Sackeim (2000) hypothesises that the traditional view that amnesia results from damage to medial temporal lobe structures alone may be wrong, since it is known both that frontal lobe damage can result in amnesia as extensive as that seen after ECT and that ECT exerts its most profound effects on the prefrontal cortex.

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If this hypothesis holds, then frontal functions must be affected as well as memory. Simply because there has been very little investigation of ECT’s effects on these functions, doctors should not be sanguine as to lack of permanent effects. Absence of evidence is not evidence of absence. In particular, Sackeim (2000) points to the lack of formal research on ECT’s effects on the executive functions of the prefrontal cortex: working memory (holding onto information in the service of a range of cognitive functions), logical reasoning and abstraction, shifting of mental set, problem-solving, planning and organising. These are ‘fundamental to organising one’s life and controlling behavior, yet there has been little investigation of the impact of ECT’ (Sackeim, 2000).

Three trials, two controlled and one small and uncontrolled, support the theory of frontal lobe involvement in functional impairment, although assessments were carried out only during or immediately after ECT (Neylan et al, 2001; Rami- Gonzalez et al, 2003; Schulze-Rauschenbach et al, 2005).

A generation ago, one researcher, reviewing the literature on ECT experimentation, wrote that the ease of its administration has resulted in its widespread use

‘without the usual background information customarily thought appropriate for most treatment modalities o this is undoubtedly the case because of the clinically observed changes in affect and behavior that result from such treatment. While such behavioral observations are certainly fruitful, such a model should be reversed to allow behavioral inferences to the possible effects on neocortical structures of such a procedure’ (Goldstein et al, 1977).


The evidence base

In the absence of long-term follow-up studies over the past two decades, the best available evidence for the permanent effects of ECT on memory ability and cognition has been generated by former patients. This has most often taken the form of patient-designed survey instruments, which ask specifically about cognition. Of the groups whose findings were incorporated into the SURE systematic review, one found that 65% of people who had had ECT reported impaired organisational skills (ECT Anonymous, 1999). Another found that one-third had difficulty concentrating, and 15% reported loss of reasoning ability (Pedler, 2001). A third asked people whether they had experienced a loss of intelligence ‘soon after the treatment’, and about 40% answered affirmatively (they were not asked whether the loss persisted) (Philpot et al, 2004). However, former patients have publicly testified that ECT can result in a very significant (>30 point) permanent decrement in IQ score (Food and Drug Administration, 1982; Andre, 2001; Cott, 2005: p. 5) and have documented the claims by extensive neuropsychological evaluation.

Although surveys and case reports are not rigorous controlled trials, in the absence of such trials conducted months or years after ECT, they provide a basis for inferences as to the treatment’s permanent adverse effects and possible mechanisms of action.

What’s wrong with the way patients have been assessed?

Claims that ECT does not have permanent adverse effects on memory and cognitive ability have been based on extremely gross measures of mental function such as the Mini-Mental State Examination (MMSE; Folstein et al, 1975) and other dementia screening scales (Stoudemire et al, 1993; Sackeim, 2000; McCall et al, 2004). But if ECT had produced wholesale dementia on a scale gross enough to be detected by these tests, it would have been abandoned decades ago.

Researchers have used very simple, brief measures to assess patients – typically, highly structured tests of verbal learning involving familiar material. Examples include the Auditory Verbal Learning Test (AVLT; Rey, 1964) and various forms of paired associates, with very short retention intervals. But there is no evidence that ECT interferes with well- established skills such as vocabulary or with short recall periods (Squire & Chace, 1975; Zervas & Jandorf, 1993).

Even people with severe brain injury or lobotomy can perform well on simple tests of overlearned verbal material that require culturally common information, for example the Wechsler Memory Scale. Highly motivated and concerned ECT patients are even more likely to do well on these tests. However, clinicians who conclude from this that there is ‘no memory loss’ have not measured memory loss at all, and certainly not the type of memory and cognitive disability that people can experience after ECT (National Institute for Clinical Excellence, 2003).

Collectively, the comments of people who have had ECT indicate loss of complex skills that underlie real-world roles such as student, professor, nurse or physicist, and often inability to return to those roles post-ECT (Box 4).

The sensitivity of the tests used after ECT depends largely on whether and how well they reflect actual cognitive demands of the type placed on ex-patients. Researchers have assured patients that ECT has no permanent adverse effects on the basis of the assumption that these demands will be minimal (McCall et al, 2004). But this assumption has never been tested, and patient reports warn against it. The ECT patient population includes people who are in the prime of life, highly educated and involved in demanding professions, and who can be very articulate in describing their deficits. If simple standardised tests cannot detect these deficits, the challenge is not to dismiss their comments but to find or devise more appropriate tests.

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The Autobiographical Memory Interview

Weiner et al (1986) and Sackeim and his colleagues (Coleman et al, 1996; Sackeim et al, 2000) have attempted to measure amnesia with an unvalidated instrument of their own design, known as the (Columbia University) Autobiographical Memory Interview. This test is insensitive to ECT-induced amnesia in two related ways: it measures very old information whereas ECT amnesia is known to be densest for more recent memory; and as many as 60% of the 200-300 test items involve overlearned and highly rehearsed facts – grandparents’ names, telephone numbers of close relatives, etc. – which are not likely to be erased by ECT. The overlearned and the old information may overlap (as in questions such as ‘What is your address’) or it may not, but in either case confounding the testing with these factors will unnecessarily result in an underestimate of the extent of retrograde amnesia.

Furthermore, the Autobiographical Memory Interview assumes that amnesia is limited to events that took place within the 12 months prior to ECT and does not attempt to assess amnesia that is not limited to that time period. However, only about 20% of the questions ask specifically about that year; the rest ask about overlearned personal information (What are your parents’ names? What are the rooms in your house?) or about events that have ‘ever’ happened to patients or their families.

Thus, it is remarkable that even as insensitive an instrument as this has shown extensive permanent retrograde amnesia measured at 2 months (Cole- man et al, 1996) and 6 months (Weiner et al, 1986) after ECT.

Assessment of amnesia

Routine neuropsychological tests are unhelpful in attempting to assess retrograde amnesia (Rose et al, 2003). Squire & Slater (1983) attempted to measure amnesia by asking people who had had ECT to make a time line showing the amount of life lost. The accu- racy of this depends, of course, on the patients’ ability to assess the extent of their amnesia, which can take many years, as they can only discover what they have forgotten when prompted by others to remember it. If asked soon after ECT, they are very likely to under- estimate the extent of retrograde amnesia.

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Because the information stored in memory is unique to each individual, standardised questionnaires or checklists may prove insensitive to amnesia even when the patient can describe or demonstrate it. Janis (1950) interviewed patients before and 1 month after ECT. He suggested general topics but let the patients speak at length. After ECT, he attempted to elicit the same information, but could not. For each individual he could count 10-20 significant life experiences that had been erased that were not limited to the period immediately before the treatment. Even when he prompted patients to recount events they had described in great detail before treatment, they could neither recall nor recognise them. One year after ECT, the amnesias remained stable. The same interviews were given to controls matched in all ways: age, gender, education, duration of hospitalisation, type and duration of mental disorder; the controls, who had not had ECT, had no amnesia.

The Janis test (Janis, 1950) can be done easily and cost-effectively even by those with no special research training. SURE (2002) in particular calls for the replication of this study, as have others over the years. But it has not yet been done.

Assessment of memory and cognitive ability

Tests of memory and cognitive ability must assess a range of functions, because ECT impairment may vary not only between individuals (Goldstein et al, 1977) but within individuals when they undergo more than one course of treatment. Simple tests of rote verbal learning or the memory sub-tests of the Wechsler are not sufficient, since ECT (if the amnesia is not catastrophic) spares vocabulary, overall wealth of knowledge and overlearned verbal skills. Patients who have had ECT should be evaluated with the type of neuropsychological batteries that would be used for patients with a known or suspected history of brain injury. These should include tests of non- verbal and visuospatial memory and reasoning such as those listed in Box 5.

If there are constraints of time and finances, tests should be tailored to the individual’s deficits, which can be identified by narrative self-report and by rating scales such as the Cognitive Failures Questionnaire (Broadbent et al, 1982).
When should patients be tested?

If there is to be baseline testing, compensation must be made to account for the difference between the patient’s true memory and cognitive capacity and the performance when preoccupied by depression, medicated or hospitalised. If such compensation is not made, all a return to ‘baseline’ function after ECT would show would be that ECT’s effects are roughly equal to – although not necessarily the same as – those of depression (Calev et al, 1995).

A better estimation of pre-ECT capacity would be the patient’s history and normal functioning at school, work or in some other capacity. Many patients, at least in the USA, will have had an IQ test, which can be used for comparison with post- ECT scores.

Patients cannot be meaningfully evaluated in hospital during or soon after ECT. Neither self- reports nor crude memory tests may be reliable (Cronholm & Ottoson, 1963). A patient may do well on the MMSE or counting serial sevens but may not know that her friend visited her the day before – and will not know she doesn’t know. Having had no reason theretofore not to trust her memory, and not having been warned to expect severe dysfunction, she will adamantly insist that her memory cannot be faulty. It is not the psychological defence mechanism of denial, nor is it only the acute organic brain syndrome which occurs with ECT, that causes this genuine unawareness. Most patients have never before experienced a day in their life when they did not know what they ate for dinner or who they had seen or what they had read the day before. They do not even know that this is possible, let alone that it is happening to them.

The ECT Accreditation Service (2005) recommends that patients should be interviewed 3 and 6 months after ECT. But at 3 months, they may not have recovered the ability to hold on to day-to-day memories (they may still be within the period of anterograde amnesia, estimated by the US National Institutes of Health (1985) to average 2 months). We propose that follow-up should be no sooner than 6 months. One year allows for optimal stabilisation of permanent cognitive deficits and better assessment of retrograde amnesia.

The Service User Research Enterprise (2002) has called for a research study with ‘long followup because losses of memory prior to ECT may only become apparent after a long interval’, as have Greenhalgh et al (2005: p. 78).

What should patients be told?

Amnesia

The clinician who tells her patients that there is a lack of research on the permanent adverse effects of ECT will certainly be on solid ground; however, this is unlikely to help patients in making a potentially life-altering decision. The best she can do is present her patients with what is known (and not known) and encourage them to assess the risk in light of their personal situation.

Thus, patients can be told that permanent amnesia is one of the ‘common’ (Sackeim, 2000) or ‘serious/ frequently occurring’ (Royal College of Psychiatrists, 2005: p. 207) effects of ECT and that it affects at least one-third of patients (Service User Research Institute, 2002; Rose et al, 2003). Such amnesia may be presented as having multiple dimensions: the amount of life lost, the temporal gradient, the nature of what is lost, and the effect of the memory erasure on the individual’s life.

The amount of life lost to amnesia cannot be predicted; patients should be warned that it has been known to extend to 10-20 years (Pedler, 2001; Service User Research Enterprise, 2002). It should be made clear that amnesia is not limited to information about discrete events or to facts that are easily regained, such as dates and telephone numbers, but that it encompasses all thoughts, feelings, personal interactions and relationships, learning and skills associated with the erased time period, and thus there is no simple or easy way to recapture what is lost. Since the temporal gradient of ECT amnesia is the opposite of normal forgetting, patients should be warned that the most recent months or years will be most affected. When amnesia is permanent it has profound, rarely positive, effects on all aspects of the patient’s subsequent life. For many people the effects of permanent amnesia and/or memory and cognitive disability negate any benefit sustained from ECT (National Institute for Clinical Excellence, 2003).

The College now advises psychiatrists to discuss the topic of retrograde amnesia carefully (Royal College of Psychiatrists, 2005: p. 7). But profound and sudden retrograde amnesia has no parallel in ordinary human experience. Doctors cannot be expected to understand the myriad ways in which permanent amnesia can disrupt one’s life. For this reason, prospective patients should be encouraged to speak with, or read accounts written by, people who have experienced amnesia. Such accounts are contained within the above-mentioned reports of SURE, NICE and MIND (Pedler, 2001), and are widely available in print (e.g. Donahue, 2000) and through online forums, e.g. http://www. ect.org) where prospective patients and families can sometimes ask questions directly of former patients.

Cognitive impairment

The Royal College of Psychiatrists (2005: p. 19) and NICE (2003) advise that the potential for cognitive impairment be highlighted during the consent process. Patients should be clearly told that ECT may have serious and permanent effects on both memory ability and non-memory cognition. These are best described in everyday terms: ‘the ability to plan and organise and get things done’ rather than ‘executive function’.

Intact memory and intelligence are highly prized in our culture. The more valuable a possession, the more important it is to know about even a small chance that it might be permanently lost. Even if the answer to how often IQ is permanently lowered is ‘We don’t know’, that is a material fact to be weighed by the patient. As individuals, patients vary greatly in the demands placed on their intellect and the potential consequences of permanent impairment. The decision to agree to ECT is theirs; the duty to inform, their physician’s.

Conclusions

Evaluation and re-evaluation of ECT’s risks and benefits by SURE, NICE and the Royal College of Psychiatrists, and the growing recognition of the extent and importance of research by and involving people who have experienced ECT, as well as increased interest in qualitative data, should lead to improvement in both patient care and research. In light of alarming findings that 50% of patients report receiving inadequate warnings of the potential side- effects of ECT, informed consent practices need to be revised. In particular, prospective patients should be warned of the significant risk of permanent amnesia and the possibility of permanent memory and cognitive disability. Research to adequately assess the nature and longevity of these effects should be undertaken, ‘incorporating patients’ perspectives on the impact of ECT into future RCTs’ (Greenhalgh et al, 2005: p. 78). By all accounts this is long overdue.

Declaration of interest
None.

References
American Psychiatric Association Committee on Electroconvulsive Therapy (2001) The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. Washington, DC: American Psychiatric Association.

Andre, L. (2001) Testimony at the Public Hearing of the New York State (U.S.) Assembly Standing Committee on Mental Health on Electroconvulsive Therapy. Albany, NY: American Orthopsychiatric Association.

Baddeley, A. D. & Hitch, G. J. (1974) Working memory. In Recent Advances in Learning and Motivation (vol. 8 ) (ed. G. A. Bower), pp. 47-90. New York: Academic Press.

Bender, L. (1938) A Visual Motor Gestalt Test and Its Clinical Use.

Research Monographs 3. New York: American Orthopsychiatric Association.

Bolwig, T. G., Hertz, M. M. & Paulson, 0. B. (1977) The permeability of the blood-brain barrier during electrically induced seizures in man. European Journal of Clinical Investigation, 7,87-93.

Broadbent, D. E., Cooper, P. F., FitzGerald, P., et al (1982) The cognitive failures questionnaire (CFQ) and its correlates. British Journal of Clinical Psychology, 21, 1-16.

Brown, L., Sherbenou, L. J. & Johnsen, S. K. (1982) Test of Non- Verbal Intelligence. Austin, TX: Pro-Ed.

Calev, A. (1994) Neuropsychology and ECT: past and future research trends. Psychopharmacology Bulletin, 30, 461-464.

Calev, A., Gaudino, E. A., Squires, N. K., et al (1995) ECT and non-memory cognition: a review. British Journal of Clinical Psychology, 34, 505-515.

Chamberlin, E. & Tsai, G. E. (1998) A glutamatergic model of ECT- induced memory dysfunction. Harvard Review of Psychiatry, 5,307-317.

Coleman, F. Z., Sackeim, H. A., Prudic, J., et al (1996) Subjective memory complaints prior to and following electroconvulsive therapy. Biological Psychiatry, 39, 346-356.

Cott, J. (2005) On the Sea of Memory. New York: Random House.

Cronholm, B. & Ottoson, J.-O. (1963) The experience of memory function after electroconvulsive therapy. British Journal of Psychiatry, 109, 251-258.

Daneman, M. & Green, I. (1986) Individual differences in comprehending and producing words in context. Journal of Memory and Language, 25,1-18.

de Filippis, N. A., McCampbell, E. & Rogers, P. (1979) Development of a booklet form of the Category Test: normative and validatory data. Journal of Clinical Neuropsychology, 1, 339-342.

Diehl, D. J., Keshavan, M. S., Kanal, E., et al (1994) Post-ECT increases in T2 relaxation times and their relationship to cognitive side effects: a pilot study. Psychiatry Research, 54, 177-184.

Donahue, A. (2000) Electroconvulsive therapy and memory loss: a personal journey. Journal of ECT, 16,133-143.

ECT Accreditation Service (2005) Standards for the Administration of ECT (3rd edn). London: Royal College of Psychiatrists’ Research Unit.

ECT Anonymous (UK) (1999) Questionnaire results: March 1999. Riddlesden, Keighsley: ECT Anonymous.

Food and Drug Administration (1982) Docket #82P-0316, Electroconvulsive Therapy Device. Rockville, MD: FDA.

Folstein, M. F, Folstein, S. B. & McHugh, P. R. (1975) “Mini- Mental State”: a practical method for grading the cognitive status of patients for the clinician. Journal of Psychiatric Research,
12,189-198.

Freeman, C. P., Weeks, D. & Kendell, R. B. (1980) ECT II: Patients who complain. British Journal of Psychiatry, 137,8-16.

Goldstein, S. G., Filskov, S. B., Weaver, L. A., et al (1977) Neuropsychological effects of electroconvulsive therapy. Journal of Clinical Psychology, 33, 798-806.

Greenhalgh, J., Knight, C., Hind, D., et al (2005) Clinical and cost-effectiveness of electroconvulsive therapy for depressive illness, schizophrenia, catatonia, and mania: systematic reviews and economic modeling studies. Health Technology Assessment, 9, 1-170.

Heaton, R. K. (1981) Wisconsin Card Sorting Test (WCST). Odessa, FL: Psychological Assessment Resources.

Janis, I. L. (1950) Psychologic effects of electric convulsive treatments (I. Post-treatment amnesias). Journal of Nervous and Mental Disease, 111, 359-381.

Khan, A., Mirolo, M. H., Mirolo, H. A., et al (1993) Can ECT- induced cognitive effects be altered pharmacologically? Progress in Neuropsychopharmacology and Biological Psychiatry, 17,861-873.

Mattes, J. A., Pettinati, H. M., Stephens, S., et al (1990) A placebo- controlled induced memory impairment. Biological Psychiatry, 27,289-303.

McCall, W. V., Dunn, A. & Rosenquist, P. R. (2004) Quality of life and electroconvulsive therapy. British Journal of Psychiatry, 185,405-409.

National Institute for Clinical Excellence (2003) Guidance on the Use of Electroconvulsive Therapy (Technology Appraisal 59, April). London: NICE. http://www.nice.org.uk/pdf/ S9ectfullguidance.pdf

National Institutes of Health (1985) Electroconvulsive therapy. NIH Consensus Statement Online. June 10-12 [cited year month day]; 5 (11),1-23. Bethesda, MD: NIH. http:/ /consensus.nih.gov/1985/l98sElectroconvulsiveTherapyoslhtml.htm

Neylan, T. C., Canick, J. D., Hall, S. B., et al (2001) Cortisol levels predict cognitive impairment induced by electroconvulsive therapy Biological Psychiatry, 50, 331-336.

Pedler, M. (2001) Shock Treatment: A Survey of People’s Experience of Electroconvulsive Therapy (ECT). London: Mind.

Pettinati, H. M. & Rosenberg, J. (1984) Memory self-rating before and after electroconvulsive therapy: depression-versus ECT induced. Biological Psychiatry, 19, 539-548.

Philpot, M., Collins, C., Trivedi, P., et al (2004) Eliciting users’ views of ECT in two mental health trusts with a user-designed questionnaire. Journal of Mental Health, 13, 403- 413.

Rami-Gonzalez, L., Bernardo, M., Beget, T., et al (2001) Subtypes of memory dysfunction associated with electroconvulsive therapy Characteristics and neurobiological bases involved. Journal of ECT, 17,129-135.

Rami-Gonzalez, L., Salamero, M., Beget, T., et al (2003) Pattern of cognitive dysfunction in depressive patients during maintenance electroconvulsive therapy. Psychological Medicine,
33,345-350.

Reitan, R. M. & Wolfson, D. (1993) The Halstead-Reitan Neuropsychological Test Battery: Theory and Clinical Application (2nd edn). Tucson, AZ: Neuropsychology Press.

Rey, A. (1964) L’examen clinique en psychologie. Paris: Presses Universitaires de France.

Rose, D., Fleischmann, P., Wykes, T., et al (2003) Patients’ perspectives on electroconvulsive therapy: systematic review. BMJ, 326,1363-1367.

Rose, D., Wykes, T., Bindman, J., et al (2005) Information, consent and perceived coercion: patients’ perspectives on electro- convulsive therapy. British Journal of Psychiatry, 186, 54-59.

Royal College of Psychiatrists (2005) The ECT Handbook (2nd edn) (Council Report CR128). London: Royal College of Psychiatrists.

Sackeim, H. A. (1986) Acute cognitive side effects of ECT. Psychopharmacology Bulletin, 22,482-484.

Sackeim, H. A. (2000) Memory loss and ECT: from polarization to reconciliation. Journal of ECT, 16, 87-96.

Sackeim, H. A., Devanand, D. P. & Prudic, J. (1993) Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. New England Journal of Medicine, 328, 839-846.

Sackeim, H. A., Prudic, J. & Devanand, D. P. (2000) A prospective, randomized double-blind comparison of bilateral and right unilateral ECT at different stimulus intensities. Archives of General Psychiatry, 57, 425- 434.

Schulze-Rauschenbach, S. C., Harms, U., Schlaepfer, T. B., et al (2005) Distinctive neurocognitive effects of repetitive transcranial magnetic stimulation and electroconvulsive therapy in major depression. British Journal of Psychiatry, 186, 410-416.

Scott, A. I. F. (2005) College guidelines on electroconvulsive therapy: an update for prescribers. Advances in Psychiatric Treatment, 11, 150-156.

Service User Research Enterprise (2002) Review of Consumers’ Perspectives on Electroconvulsive Therapy. London: Institute of Psychiatry.

Sivan, A. B. (1992) Benton Visual Retention Test (5th edn). San Antonio, TX: Psychological Corporation.

Squire, L. R. & Chace, P. M. (1975) Memory functions six to nine months after electroconvulsive therapy. Archives of General Psychiatry, 32, 1557-1564.

Squire, L. R. & Slater, P. C. (1983) Electroconvulsive therapy and complaints of memory dysfunction: a prospective three-year follow-up study. British Journal of Psychiatry, 142, 1-8.

Squire, L. R. & Zouzounis, J. A. (1988) Self-ratings of memory dysfunction: different findings in depression and amnesia. Journal of Clinical and Experimental Neuropsychology, 10, 727-738.

Squire, L. R., Wetzel, C. D. & Slater, P. C. (1979) Memory complaints after electroconvulsive therapy: assessment with a new self-rating instrument. Biological Psychiatry, 14, 791-801.

Stoudemire, A., Hill, C. D., Morris, R., et al (1993) Long-term affective and cognitive outcomes in depressed older adults. American Journal of Psychiatry, 148, 1336-1340.

Taylor, J. R., Kuhlengel, B. G. & Dean, R. 5. (1985) ECT, blood pressure changes and neuropsychological deficits. British Journal of Psychiatry, 147, 36-38.

United Kingdom Advocacy Network (1996) ECT Survey: The National Experience. Sheffield: UKAN.

UK ECT Review Group (2003) Efficacy and safety of electro- convulsive therapy in depressive disorders: a systematic review and meta-analysis. Lancet, 361, 799-808.

Wechsler, D. (1997) Wechsler Adult Intelligence Scale III. San Antonio, CA: Psychological Corporation.

Weiner, R. D., Rogers, H. J., Davidson, J. R., et al (1986) Effects of stimulus parameters on cognitive side effects. Annals of the New York Academy of Sciences, 462, 315-325.

Zervas, I. M. & Jandorf, L. (1993) The Randt memory test in electroconvulsive therapy: relation to illness and treatment parameters. Convulsive Therapy, 9, 28-38.

For a commentary on this article see pp. 237-238, this issue.

Harold Robertson (148 Beach 94th St, Suite 6, 3rd Fl., Queens, NY 11693, USA. Email: robertson.harold@gmail.com) is the director of a not-for-profit charitable foundation in New York focusing on the underserved patient population. His interest in psychiatric research, in particular research into the use of electroconvulsive therapy, has brought him into contact with others with similar interests across the globe for the past 20 years. Robin Pryor is a psychologist who has held a private practice in New York, NY, for 30 years. His particular interests are the history of psychiatry and first-person narratives of mental health service users. He writes and lectures on these topics.

Beyond “anecdotal” evidence: Poster Session at NIMH Conference

This was a poster session presented at the annual NIMH Conference by Linda Andre and Juli Lawrence. Note: graphics are clickable for larger views.

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Beyond “anecdotal” evidence:

The contribution of ECT survivors to research on the permanent effects of ECT on memory, memory ability and cognition

Authors:

Linda Andre
Juli Lawrence

2002

Statement of the Problem:

Evidence from ECT survivors has been dismissed as “anecdotal.”

Such evidence exists in many forums: in the popular press, in literature, in public testimony before legislatures, on the internet, in the archives of the Food and Drug Administration—but almost never in the published medical literature. Thus, this evidence has been almost entirely ignored by paid professional ECT researchers.

The discounting of the writings and testimony of ECT survivors has led to a “knowledge gap” in ECT research. The enormous body of knowledge of those with direct knowledge of the nature and extent of ECT’s permanent effects has been discounted by professional researchers. Professionals have attempted to study these effects without input from those directly affected. They have not been successful.

In an attempt to close this knowledge gap, survivor researchers have designed and instrumented our own research projects to investigate the permanent effects of ECT on memory, memory ability, and cognition.

There is a great disparity between the results obtained by professionals and those obtained by survivors.

Method:

We examine the dominant existing professional published research in comparison with four survivor-designed studies and attempt to account for the disparities.

Though we surveyed research from the 1940s to the present, we focus here on NIMH-funded research of the past 25 years. Although some studies from the 1940s and 50s stand as unsurpassed examples of sound research—especially the famous Janis study which has prompted calls for replication to this day—most of the earlier studies are characterized by the same methods, assumptions, and flaws as the later work.

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Survey of the professional literature:

There have been only two major NIMH grants to study memory.
MH24600: Memory as Affected by Disease, Injury, and ECT
Principal Investigator: Larry Squire

This grant was not primarily or exclusively designed to study the effects of ECT; the topic of study is memory loss in general.

• Used a self-designed instrument, the Squire Memory Questionnaire, designed to distinguish the effects of depression on memory and cognition from the effects of ECT. It was not designed to investigate the permanent effects on ECT on memory and cognition by comparing individuals who had ECT with their own baselines or with normal matched controls. Also, the questionnaire measures multiple aspects of cognition, not only memory or memory ability.

• Used low sensitivity instruments to assess memory ability (i.e., word lists remembered over a very short interval; remembering names of TV shows)

• Findings and conclusions often contradictory.

• A study that followed patients for six to nine months found the majority reported impaired memory ability due to ECT. (Squire and Chace, 1975)

• A study that followed patients for three years found that the majority (58%) reported impaired memory ability due to ECT. Patients also reported an average eight month period of amnesia. (Squire and Slater, 1983)

“Certain empirical questions about ECT that seem at first glance rather simple to answer by experiment are still widely debated. Does ECT permanently impair memory?” (1986)

“Information about recent events can be lost for a long time, possibly permanently, after ECT.” (1986)

“One way of understanding how such complaints could occur long after ECT is to suppose that they are based on the experience of amnesia initially associated with ECT.”

“There is no good evidence that new learning ability is still deficient six months after treatment.” (1986 Consensus)

“The possibility cannot be ruled out that more sensitive testing methods will some day reveal a greater degree of permanent memory loss.”

MH35636: Affective and Cognitive Consequences of ECT
Principal investigator: Harold Sackeim, PhD

• First awarded in 1981; renewed through 2010; funded approximately $300,000 per year for a total of more than six million dollars

• Principal investigator’s longterm financial and career conflict of interest make this work scientifically invalid.

• Beginning around 1982, Sackeim began working for ECT device manufacturer Mecta as a consultant, designing their devices including the SR-1 and SR-2. He also received grant money directly from Mecta. His financial interest in Mecta has never been disclosed to NIMH as required by federal law.

• Instead of studying memory and cognition directly, the work has focused on a comparison of different ECT techniques.
• Most of these studies follow patients no longer than two months. (This research team claims that all patients are followed up at six months and one year, but the results of these followups aren’t published.)

• Amnesia is assessed using a self-designed, unvalidated instrument, the Autobiographical Memory Inventory, designed without input from survivors. Survivor researchers estimate that at least 60% of the items are insensitive to ECT’s stereotypical effects (for example, they measure very old, overlearned information which is almost never forgotten after ECT).

• Cognition is assessed by gross instruments such as the MMSE. Memory ability is assessed by simple tests such as paired words. (This research team claims that more extensive neuropsychological testing—some of which would be relevant to ECT’s effects—is done on all patients before and after ECT, but the results of these tests have not been published.)

• Much of the grant has been spent selectively reviewing existing research rather than doing experiments. For example, rather than directly design an experiment to test whether ECT causes brain damage, the grantees chose to write a review of some of the existing experiments.

CONCLUSIONS:

After more than 20 years and more than ten million dollars spent on one grant alone, basic research on the permanent effects of ECT on memory, memory ability, and cognition is lacking. By the principal investigator’s own admission, there is no data and there are no answers to the most basic questions about ECT’s effects on memory.

“Prospective patients, family members, and the public often want to know the frequency with which patients report substantial memory impairment following ECT. While we believe that such reports are infrequent, there is little objective evidence to support this judgment or even to broadly estimate base rates.” editorial

“There is no evidence that ECT results in impairments of executive functions (e.g. the capacity to shift mental sets), abstract reasoning, creativity, semantic memory, implicit memory, or skill acquisition and retention.” APA

“No study has documented anterograde amnestic effects of ECT more than a few weeks following the ECT course.” APA

“A very rare number of patients may experience marked retrograde amnesia as a result of ECT. There is no firm estimate on this incidence, but my estimate would be on the order of 1 in 500 patients.” (statement—May)

“All of the available information, from scores of studies, indicates that this deficit (anterograde memory loss) disappears within days to a few weeks following the end of ECT.”(statement—May)

“I’ve never seen a case where there has been permanent effect of ECT on anterograde amnesia. And I invite anyone in the country who believes ECT’s had a deleterious effect on their cognition to come in for evaluation.” (May testimony)

Survey of the survivor literature:

Because of the enormous gaps in ECT research, survivors have undertaken research projects on their own to reflect the variety of experiences. The results of these studies widely challenge the results of the professional literature.

The following is a representative, but not exhaustive, listing of survivor-designed and implemented research.

Committee for Truth in Psychiatry ECT Survey, 1990

52 survivors who reported that they had experienced permanent amnesia and reported that they had not been warned about the adverse effects of ECT were asked about the nature of these effects, using a questionnaire adapted from a standard form used to assess brain injury. They were asked about thirteen common symptoms of brain injury, and asked whether they experienced each in the acute period (the first year after ECT) and in the long term.

All respondents indicated suffering from at least some of these symptoms since ECT, both short-term and long-term. Half of the respondents checked nearly all items in both time periods:

  • general loss of memory ability;
  • forgetfulness or absentmindedness
  • language impairment (not being able to think of a word, or forgetting what one intended to say)
  • difficulty in reading comprehension
  • not “getting the point” of jokes, stories, movies, etc.
  • forgetting new information abnormally rapidly
  • impaired sense of direction
  • difficulty concentrating
  • difficulty with spatial relations
  • loss of manual skill
  • other loss of familiar skills

The average number of years since ECT was 23. The average age at ECT was 24.

They were then asked about the degree to which they had been able to compensate for these deficits, and whether they found them disabling.

Only one-fourth of the respondents felt they had been able to compensate. They further reported that it had taken them anywhere from 8 to 43 years to reach the point where they were able to compensate for their deficits..

Two-thirds were unemployed, reporting that they had been employed prior to ECT and unemployed as a result of it.

90% said they still needed help in coping with enduring cognitive deficits.

“I think that the residual effects from ECT certainly slowed my ability to do the thinking, concentration, and memory necessary to do my school work…and thus added years to my achieving graduation from college.”

“There was no acknowledgment of any damage so no help was offered.”

“Neuropsychological evaluation showed low IQ, cognitive difficulties”

“I’m OK with multiple choice tests but can’t remember enough to do essays.”

“Retired on Disability, though an associate professor with lifetime tenure. Was doing PhD in Physics.”

“Before ECT I knew my way around town as well as I knew my way around my own house. Now my sense of direction is horrible. I’m always getting lost.”

“43 years to get back to almost as good as before.”

“I am a great deal brighter than average—so professionals do not believe I suffer any losses from ECT. I was not tested before ECT, only after!”

VOICES, 1996

Questionnaires were distributed via online newsgroups and email lists of psychiatric consumer/survivors. 41 respondents participated in the study. 83 percent reported feeling their long-term memory had been affected. This ranged from loss of certain events in their lives, to the inability to remember family members, and in some cases, up to 20 years of memories were erased. Only 17% felt that their long-term memory had not been adversely affected.

“The worst thing that ever happened to me…”
“ECT destroyed my family…”
“Doctor claimed memory problems would vanish in two weeks…”

Of females, 82.6% said long-term memory was affected, and among males, 83.3% reported problems.

“I can’t remember my 20-year Marine Corps career…or daughter’s birth or childhood…”

Short-term memory appears to have been affected slightly less, or the effects were temporary. 63.4% reported problems with short-term memory loss. 12% said they had no problems at all with short-term memory loss. And 22% said that short-term memory loss was either temporary or minor.

“I couldn’t remember people’s names, but it gradually came back…with some prompting…”

Half of all respondents reported that they were given no information about ECT and its effects, other than to be told it was effective. The other half were given information in the way of video tapes, pamphlets, books, and detailed discussions with their physician or nurse. Of those, however, several reported that they wish they had been given more accurate information concerning memory loss and other adverse effects.

“I did have detailed discussions with my doctors before the treatment, but I just couldn’t realize how bad the memory loss was going to be. If I had, I’m not sure I would have taken the treatments…”

ECT Anonymous, 1999

ECT Anonymous, located in the United Kingdom, surveyed 200 ECT survivors. 82 percent of respondents reported a loss of past memories, ranging from slightly (8 percent), moderately (33 percent) and severely (41 percent). 84 percent said they had impaired present memory ability, and 85 percent reported difficulties with concentration after having ECT.

MIND, 2001

In early 2001, the UK mental health charity MIND sent out over 6,000 copies of its detailed questionnaire regarding ECT use. 418 replies were received.

Key findings:

  • Almost three quarters (73%) of the total sample and almost two thirds (60.5%) of those given ECT most recently were not, as far as they remember, given any information about possible side effects.
  • Of those consenting to treatment in the last two years, 48% received, as far as they remember, no information about how the treatment would work and 44.5% no information about possible side effects.
  • 84% of respondents said that they had experienced unwanted side effects as a result of having ECT.
  • 40.5% reported permanent loss of past memories and 36% permanent difficulty in concentrating.
  • Respondents from black and minority ethnic communities were more likely to be detained under the Mental Health Act and to have received ECT without consent. They reported a more negative view of ECT than the overall sample with 50% finding it unhelpful, damaging or severely damaging in the short-term and 72% in the long-term.

“If I had known I had the right to refuse I would have done so. My understanding was that I had no choice in the matter and that they could do it by force.”

“Was told by consultant ‘best thing since sliced bread’, ‘be well in no time’. When went wrong, ‘this was the first time this had happened’.”

“Possible side effects were downplayed and only lightly touched upon.”

“I was given no information at all”

Published case studies

The individual case study is an important and necessary method of collecting evidence, since it allows the nature and extent of amnesia, memory disability, and memory loss to be described in detail impossible to obtain in-group studies. Consistency in individual case studies illustrates that ECT’s permanent effects have not changed over the years.

As Empty As Eve, by Berton Roueche; first published in the New Yorker, September 9, 1974; reprinted in The Medical Detectives, 1981

“There weren’t just gaps in my memory. There were oceans and oceans of blankness. And yet there seemed to be kind of a pattern. My childhood recollections were as strong as ever. The fog of amnesia increased as I came forward in time. The events of the past several years were the blurriest and the blankest. Another area that didn’t seem to be affected was ingrained habits—repetitive acts and procedures. I mean, I hadn’t lost my command of the English language. I still knew the multiplication tables…But worst of all my problems was that I couldn’t seem to retain. I couldn’t hang on to my relearning. Or only a part of it. The rest kept sliding away again.”

Electroconvulsive Therapy and Memory Loss: A Personal Journey, by Anne Donahue; The Journal of ECT, June 2000.

“My long-term memory deficits far exceed anything my doctors anticipated, I was advised about, or that are validated by research. To the contrary, either I am one in a thousand, a complete anomaly, to be able to document memory loss still remaining after 3 years and extending as far back as occurrences eight to nine years ago, or the profession in general, after all these years of treatment with ECT, has still failed to identify and come to terms with the true potential risks.”

Further evidence for permanent memory and cognitive impairment is found in the neuropsychological evaluations (standardized batteries of tests for brain damage, taking place over two or more days) obtained by individual survivors at their own expense; many of these are collected in the archives of the Food and Drug Administration, Docket #82P-0316.

SUMMARY of survivor findings:

  • Amnesia (retrograde memory loss) occurs in a majority of ECT survivors. Commonly, the loss encompasses years prior to ECT.
  • Memory disability (anterograde memory loss) is common and does not resolve after ECT.
  • When tested long after ECT, survivors experience cognitive deficits.
  • Each survivor has her pre-ECT self as a perfectly matched control subject, eliminating confusion as to etiology of deficits.
  • More research is needed using extensive batteries of neuropsychological tests such as those used to detect brain damage. From the preliminary data gathered by survivors, a characteristic pattern of ECT damage has emerged. While survivors may do well on simple tests such as paired words or the Mini Mental Status Exam, more comprehensive standard neuropsychological batteries reveal deficits in higher mental functions such as flexibility, shifting cognitive set, abstract and analytical thinking, and executive function. Loss of measured general intelligence (IQ) tends to be highly significant—30-40 points.
  • Survivors have absolutely no difficulty distinguishing normal memory failures from those caused by ECT. ECT amnesia and memory disability has little in common with normal memory fallibility, age-related disability, or problems associated with mental illness.

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Discussion

Published medical literature research:

A small and exclusive playing field: a handful of research teams dominate grant funding.

The only available NIMH grant to investigate memory is tarnished by financial and other conflicts of interest; since this grant is renewed indefinitely, there is little opportunity for researchers outside the ECT industry to obtain funding.

Rarely follows patients as long as six months; almost never longer

Most studies look only at the short-term effects (from during ECT to a few days or weeks after)

Sample sizes very small in general (>50)

Self-designed memory instruments designed without input from survivors, largely insensitive to stereotypical ECT amnesia, memory disability, and cognitive disability

Rarely directly study the effects of ECT on memory, memory ability, and cognition. Instead, studies compare persons who had different types of ECT with each other, rather than with their own baselines or normal controls, resulting in an underestimate of memory/cognitive damage.

Often use no or inappropriate controls

Subjects do not reflect true diversity of ECT patient population: all treated at the same hospital, with the same doctor, at the same time, usually with same machine and technique

Because patients interviewed by their own treating doctor and/or institution, and sometimes while still institutionalized, bias is toward underreporting of adverse effects

Ambiguous inquiries about “memory”, without distinguishing between memory, memory ability, and cognitive abilities

Survivor research:

Researchers unpaid; work done at researcher’s own personal financial expense

Self-designed instruments designed by and for survivors to be sensitive to the deficits we commonly experience

Large sample sizes (<50)

Heterogeneous samples more representative of the ECT population as a whole:

Memory, memory ability, and cognition are studied directly, not as a sidebar to research on optimizing technique

Emphasis on describing discrete cognitive deficits rather than lumping them together with amnesia as "memory"

Patients are their own controls

Mostly very long-term follow-ups: patients who had ECT more than one year---and sometimes ten years or more---previously, thus eliminating replacing speculation with evidence as to whether adverse effects ultimately resolve

Because responding ex-patients are self-selecting, those with more severe adverse affects may be overrepresented

Because researchers are strangers and non-professionals, no incentive to underrreport adverse effects

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