A Survey of 1,144 ECT Recipients, Family Members, and Friends: Incidence, Severity, and Duration of Memory Deficits

Evidence‐based electroconvulsive therapy

ELECTROCONVULSIVE THERAPY (ECT) IS ONE OF THE most controversial treatments in all of medicine. There are a number of reasons for this. The discovery in the 1930s that inducing a series of generalized seizures, initially with chemicals, later with electric current, could cause the recovery of patients with severe and previously untreatable mental disorders produced a wave of enthusiasm that eventually led to a period of indiscriminate use and misuse in the middle decades of the 20th century. This period of abuse created, perhaps deservedly at that time, a bad reputation for an effective treatment modality. That reputation was enhanced by the immediate adverse effects of bitten tongues and even fractured bones and teeth caused by the induction of generalized seizures, and the painful effects of electroshocks administered without anesthesia when they did not successfully induce a seizure with loss of consciousness. The 1975 movie One Flew Over the Cuckoo’s Nest contributed to an erroneous view of ECT as a punitive, painful, and assaultive procedure used by authorities to control inconvenient creativity. That view has been associated with attempts to regulate, or even eliminate, the use of ECT through legislation in a number of jurisdictions, and public fears and distrust about the use of ECT have persisted. The best response to such concerns on the part of physicians is to be aware of the facts about current use of ECT, including its efficacy and possible adverse effects, so they can respond to questions from patients, families, and the public. The indications, possible adverse effects, and current recommendations for treatment procedures have been summarized in a task force report just published by the American Psychiatric Association Committee on Electroconvulsive Therapy. An effective and safe treatment for severe major depression, ECT has had response rates reported in the range of 80% to 90% as a first-line treatment, and in the range of 50% to 60% for patients who have not responded to 1 or more trials of treatment with antidepressant drugs. Electroconvulsive therapy may also be seriously considered as treatment for patients with acute mania, and for patients with schizophrenia who have not responded to adequate trials of antipsychotic medications. As currently practiced, ECT involves the use of informed consent, ultra-brief general anesthesia and muscle relaxants (thus attenuating motor seizure activity) with appropriate airway management, and use of ECT devices to provide adequate ictal responses. Most patients in the United States receive 3 treatments per week, and a course of ECT for major depression generally consists of 6 to 12 treatments, with the course ended or tapered as soon as maximum response has been reached. This usually occurs more quickly than the 4 to 6 weeks required for an adequate trial of an antidepressant drug. There continues to be some controversy about the use of right unilateral or bilateral electrode placement, with right unilateral ECT causing less cognitive adverse effects, but bilateral ECT often viewed as being more effective. A recent randomized controlled trial showed that right unilateral ECT at high dosage was as effective as bilateral ECT in many patients and caused less impairment on several measures of anterograde and retrograde memory. The issue of cognitive adverse effects from ECT is central to its reputation for harm and requires careful consideration to separate facts from myths. Studies of this issue have been reviewed and summarized by the American Psychiatric Association Committee on Electroconvulsive Therapy. Patients experience a variable but usually brief period of disorientation (postictal confusion) immediately after seizure induction. Electroconvulsive therapy also typically results in retrograde amnesia, greatest immediately after the course of treatment and for events that occurred temporally close to the treatment. The extent of the retrograde amnesia usually decreases substantially with time, but many patients have persistent loss of memory for some events that occurred in the interval starting several months before and extending to several weeks after their ECT course. Anterograde amnesia, characterized by rapid forgetting of learned information, also may occur during and immediately following ECT but resolves within a few weeks. Importantly, there is no objective evidence that ECT has any long-term effect on the capacity to learn and retain new information. Assessment of cognitive effects from ECT is complicated by the cognitive impairments associated with the mental disorders being treated. For example, patients with severe depression may have substantial impairments in cognitive function, and patients with schizophrenia or other psychotic

The aim of the present study is to investigate the cumulative effects of a clinically determined course of electroconvulsive therapy (ECT) on anterograde and retrograde amnesia. In this study, mood and memory were examined in the context of a protocol driven by therapeutic response, rather than by preordained research criteria. Twenty-two patients with major depressive disorder and 18 nondepressed controls were taught a series of faces and names before the initiation of ECT, and their retention of this information was examined after the end of treatment. Anterograde (ie, new learning) and retrograde memory (ie, recall of information learned before ECT) were assessed. Eleven ECT patients underwent unilateral (UL) stimulation, and 11 had a combination of UL and bilateral stimulation. Major depressive disorder patients and nondepressed controls participants were matched according to baseline memory abilities. Unilateral and unilateral/bilateral (UB) ECT patients were matched according to baseline depression and memory abilities. Treatment with ECT resulted in a dissociation between anterograde and retrograde memory; after treatment, major depressive disorder patients demonstrated significant retrograde amnesia, whereas there was no change in their anterograde memory. Unilateral and UB ECT patients performed equally well on tasks of anterograde memory. Contrary to our expectation, UB ECT was not associated with greater retrograde memory loss than was UL ECT treatment. However, a trend toward a group difference was present on 1 memory measure. Results of the study suggest that a clinical course of ECT is associated with isolated impairment for information learned before treatment (ie, retrograde memory), whereas there was no effect of ECT on posttreatment learning abilities (ie, anterograde memory).

The right to informed consent is a core ethical principle. Recent audits of patient information leaflets about electroconvulsive therapy (ECT), in Australia, England, Northern Ireland, Scotland and Wales, suggest that this principle is often not implemented, with efficacy being exaggerated and risks minimised. In the current study a convenience sample of 858 ECT recipients and 286 family members and friends, from 44 countries, responded to an online survey about their experiences of ECT, including the information they recall being given to them before ECT. Most (59%) of the ECT recipients reported that they had not been given 'adequate information' and a further 17% were 'not sure'. For example, 63% of recipients recall being told that 'ECT can cause temporary memory problems', but only 17% that 'ECT can cause long-term or permanent memory problems, 12% that 'ECT can cause heart problems' and 28% that there are 'Risks from repeated general anaesthesia'. There were higher levels of recalling being told about definite benefits, even though some of these benefits are disputed. When asked to consider a list of items of misinformation, many recipients and relatives reported being told 'Depression is caused by a chemical imbalance in the brain' (58% and 53%, respectively) and 'ECT corrects chemical imbalance or other brain abnormality' (42% and 41%). Study limitations include potential sampling issues (eg, self-selection bias, snowball sampling bias, or other barriers to representativeness due to convenience sampling or network-based recruitment), as well as potential recall bias among survey respondents (last ECT treatment was between 1958 and 2024; average=2012.5). Nevertheless, these findings, in conjunction with previous studies, suggest an urgent need for greater efforts to ensure that patients and families are provided with comprehensive, balanced, evidence-based information when deciding whether to have ECT.

Drugs and human memory (part 1): Clinical, theoretical, and methodologic issues.

Retrograde amnesia is the inability to remember events or information. The successful acquisition and memory of information is required before retrograde amnesia may occur. Often, the trigger for retrograde amnesia is a traumatic event. Loss of memories may be caused in two ways: either by loss/erasure of the memory itself or by the inability to access the memory, which is still present. In general, memories and learning are associated with a positive connotation although the extinction of unpleasant experiences and memories of traumatic events may be highly welcome. In contrast to the many experimental models addressing learning deficits caused by anterograde amnesia, the incapability to acquire new information, retrograde amnesia could so far only be investigated sporadically in human patients and in a limited number of model systems. Apart from models and diseases in which neurodegeneration or dementia like Alzheimer’s disease result in loss of memory, retrograde amnesia can be elicited by various drugs of which alcohol is the most prominent one and exemplifies the non-specific effects and the variable duration. External or internal impacts like traumatic brain injury, stroke, or electroconvulsive treatments may similarly result in variable degrees of retrograde amnesia. In this review, I will discuss a new genetic approach to induce retrograde amnesia in a mouse model and raise the hypothesis that retrograde amnesia is caused by altered intracellular calcium homeostasis. Recently, we observed that neuronal loss of neuroplastin resulted in retrograde amnesia specifically for associative memories. Neuroplastin is tightly linked to the expression of the main Ca2+ extruding pumps, the plasma membrane calcium ATPases (PMCAs). Therefore, neuronal loss of neuroplastin may block the retrieval and storage of associative memories by interference with Ca2+ signaling cascades. The possibility to elicit retrograde amnesia in a controlled manner allows to investigate the underlying mechanisms and may provide a deeper understanding of the molecular and circuit processes of memory.

Objective: Electroconvulsive therapy (ECT) is an effective biological treatment option for severely depressed elderly patients; however, it can cause cognitive side effects, including anterograde and retrograde amnesia. Elderly patients with “cognitive impairment no dementia” (CIND) are reported as being more vulnerable to the cognitive side effects of ECT compared with patients with “no cognitive impairment” (NCI). The few studies that have reached this conclusion can be criticized for using insensitive outcome measures. Method: The present study investigated cognitive side effects using standard neuropsychological tests before and after twice-weekly ECT. Patients were assessed at baseline (T1) and within one week after a course of ECT (consisting of a mean of 10 treatments) (T2), and were followed up for three months after T2 (T3). The sample included 54 patients with NCI (n = 36) or CIND (n = 18). For a control group, we recruited 17 healthy elderly persons. Tests of anterograde memory, information-processing speed, executive function, and retrograde memory were administered. We computed reliable change indices using simple regression methods. Results: Short-term side effects were detected at T2 in a large minority of patients, with no significant differences between NCI and CIND patients. Considerable improvement in global cognitive function from T1 to T3 was observed in 44% of the CIND patients. At the group level, information-processing speed improved significantly in CIND vs. NCI patients. Conclusions: CIND patients were not more vulnerable to amnesia than were NCI patients. Long-term cognitive side effects of ECT were not detected.

Electroconvulsive therapy (ECT) is the gold standard for treatment-resistant depression (TRD). However, cognitive side effects, mainly anterograde and retrograde amnesia, frequently occur. Magnetic seizure therapy (MST) is tested using more focal seizure induction. However, the suggestion MST may be more beneficial than ECT because it causes fewer amnesia have not yet been comprehensively investigated using common neuropsychological testing specifically for ECT. We aimed to examine whether MST causes anterograde and retrograde amnesia. Ten patients with TRD were treated with MST (8.9 [2] treatments) at 100% machine output, a frequency of 100 Hz and 657.4 (62) pulses per train. The short form of the Autobiographical Memory Inventory was administered to test retrograde amnesia. Furthermore, an extended neuropsychological test battery, including verbal and nonverbal recall as well as recognition tasks, was used. We observed changes in retrograde amnesia, although they were not clinically relevant (mean: -0.42 ± 0.14). Furthermore, no anterograde amnesia as well as no effects on global cognitive status, attention, language, and executive functions after MST were measured. The cognitive safety and efficacy of MST in patients with TRD were indicated. However, the main limitations of the present study were the small sample and as a consequence, the low statistical power to detect changes after treatment. Therefore, our findings require replication in further studies. In addition, a direct comparison between MST and ECT in a larger sample should be performed before MST can be discussed as an alternative treatment approach to ECT in clinical practice.

WHAT IS KNOWN ON THE SUBJECT?: Electroconvulsive therapy (ECT) has existed worldwide for nearly 80years. ECT is a fast-working and potentially life-saving treatment, but it is considered controversial. Although frequently mentioned, stigmatization in relation to ECT has not been systematically explored so far. WHAT THIS PAPER ADDS TO EXISTING KNOWLEDGE?: This paper provides new insight into both recipient and expert perspectives on ECT. It identifies several issues of stigmatization related to ECT and suggests that full recovery following ECT might be jeopardized due to both stigmatization and self-stigmatization. The study suggests that most of the stigmatizing behaviors can be ascribed to (a lack of) available knowledge of and experience with ECT. WHAT ARE THE IMPLICATIONS FOR PRACTICE?: Being aware of and listening to the needs of former ECT-recipients seems essential to increase their treatment options and support care as well as a will to prioritize this patient group. For example, by addressing the potential stigma issues in follow-up groups and helping to distribute sober, factual information about ECT in society. Providing written information and psychoeducation for patients and relatives before, during, and after ECT, in addition to supporting active use of diaries, might be valuable remedies for helping patients feel adequately informed and able to accept the pros and cons of ECT during and after treatment period. ABSTRACT: Introduction Electroconvulsive therapy (ECT) has existed worldwide for nearly 80years. Although fast-working and potentially life-saving treatment, ECT is regarded as a strongly controversial treatment and stigmatization is frequently mentioned in relation to it. However, no systematic research in this area has taken place so far. Aim The aim of this qualitative study was to explore the experiences and attitudes of former recipients of ECT and of experts professionally involved with ECT to identify potential stigmatization. Method Two focus groups, one comprising four recipients of ECT and the other seven professional experts, were conducted. Data from each focus group were analyzed separately using a framework-analysis. Results The analysis yielded three major themes for the first focus group interview: ambivalent attitudes, discrediting and exclusion, and survival strategies and three major themes for the second focus group interview: dramatic depictions of ECT, an overlooked and rare treatment, and anti-stigmatization strategies. Discussion and implications for practice Stigmatizing attitudes and behaviors in relation to ECT are closely related to one's personal and factual knowledge, and there is a great need for multi-facetted approaches if social acceptance and recognition are to be achieved. This study provides new knowledge on a scarcely examined area while also introducing suitable methods for anti-stigmatization and empowerment.

Anesthesia for electroconvulsive therapy.

Psychiatric Readmissions Lower Among Patients Receiving ECT

The psychiatry service was called to evaluate a patient in the outpatient procedure unit who could not remember who she was or why she was there. “Ms. R” was a 36-yearold Hispanic woman with a history of morbid obesity who underwent an upper endoscopy for evaluation of nausea and inability to tolerate oral intake 1 month after a Roux-en-Y gastric bypass for her obesity. The endoscopy demonstrated moderate stenosis at the gastrojejunal anastomosis, which did not account for the severity of her nausea. The stenosis was dilated without incident. For the procedure, Ms. R received a total of 420 mg i.v. of propofol, 100 mg i.v. of lidocaine, and 0.2 mg i.v. of glycopyrrolate. She also received a total of 200 μg i.v. of phenylephrine for a transient decrease in blood pressure to 81/45. In the recovery room, when Ms. R awoke from her conscious sedation, she had no recollection of why she was in the hospital, was disoriented to place, and, most significantly, was unable to recall her identity. She was agitated, prompting the psychiatric consultation. Ms. R was visibly frightened when any person tried to approach her, including her boyfriend of 5 years. She repeatedly asked why she was there but was unable to retain the information received. She was given 2 mg of midazolam for agitation, after which a minor improvement in behavior was observed. A repeat dose of midazolam was administered, without further improvement. Forty-five minutes after the procedure, Ms. R was still unable to recall her date of birth. Her vital signs and general physical and neurological examination were within normal limits. Her mental status examination was significant for agitation, disorientation to person and place, and extensive memory loss, which continued for the rest of the day. She repeatedly expressed the delusion that the baby she had just delivered was taken from her. She had no evidence of hallucinations. A preprocedure pregnancy test was negative. Ms. R was on a liquid diet and taking a multivitamin once daily, 1,000 μg of vitamin B12 three times a week sublingually, and calcium citrate daily. Ms. R’s past medical history included a history of gallstones as well as the Roux-en-Y gastric bypass surgery 1 month earlier, at which time her body mass index (BMI) was 47. Ms. R had received 200 mg of propofol as part of the anesthesia during the 3-hour bariatric surgery without incident. Ursodiol was begun 3 weeks before the endoscopy for nausea that developed while she was consuming a postoperative liquid diet. When her diet was advanced to soft foods, she began vomiting. She returned to a liquid diet, and the endoscopy was scheduled. Ms. R’s past psychiatric history was significant for a dissociative fugue, which occurred at the same time as her divorce 7 years earlier and for which she was psychiatrically hospitalized. She continued in individual and group treatment for 2 years after that hospitalization. She had no history of traumatic events. Because of Ms. R’s persistent amnesia and agitation, she was admitted to amedical unit for further evaluation. Results of all testing, routine laboratory tests, urine drug screen, head CT, head MRI, and EEG were normal except for ketones in the urine. Ms. R’s BMI had decreased to 40.5. She was started on a clear liquid diet and had no further nausea. The neurology consultant agreed with the psychiatrist’s diagnosis of dissociative amnesia. During her hospitalization, Ms. R slowly regained some of her memory. She vaguely remembered that she had an adult son living in another state. Ms. R could not remember how to use her cell phone. She was afraid to take a shower without supervision as she was not sure she would know what to do. She also could not recall important historical events, such as the September 2001 attacks on the World Trade Center. There was no evidence of anterograde amnesia after the first hospital day. After showing some improvement over her 6-day hospitalization, she was discharged home with her boyfriend. Two weeks after hospital discharge, Ms. R continued to recover some of her memories and to increase her activities. It was unclear, however, whether her retrograde amnesia was improving or whether she was only retaining newly learned information. She began to cook on her own and reported increased comfort around her boyfriend and her family. Ms. R was afraid to return to work because she was concerned that she would not remember how to do her job. Within 2 months of the episode, Ms. R was retrained by her employer and successfully resumed her work as a secretary. Six months after the procedure, Ms. R’s retrograde amnesia had significantly improved and she continued to form new memories without difficulty.

Byline: M. Reddy Electro-convulsive therapy (ECT) was introduced in 1938 and has been in continuous use since then as a tool for therapeutic neuromodulation in the treatment of various psychiatric disorders. ECT celebrates its 74th birthday this year and is neither tired nor retired as a treatment modality. It remains an important component in the armamentarium of biological therapeutic tools in psychiatry. ECT remains invaluable, and can be termed life saving, in the management of patients with acute suicidal risk, severely retarded depression, catatonia, etc. ECT differs from psychopharmacology in several clinically relevant aspects: action on electrical depolarization and not at receptors at synapses, independent of renal clearance, hepatic metabolism, compliance of patient, drug interactions, etc. [sup][1] As of today there is no single unifying explanation how ECT works so well in a variety of conditions. Since its introduction in 1938 there were several advances in the practice of ECT with introduction of modified ECT, brief pulse and ultrabrief pulse current, unilateral electrode placement, seizure threshold titration, etc. with the goal to increase efficacy and minimize the risk, special focus being on minimizing cognitive side effects. Risk of death with ECT is relatively low at 1 in 10,000 patients. At Asha hospital, Hyderabad, about 30,000 patients received ECT in the last 8 years, mostly modified, without any mortality (oral communication). Amnesia, both anterograde and retrograde, remains a significant troublesome side effect. Generally it is transient but some reports comment on many patients having incomplete recovery in retrograde amnesia. [sup][2] The reasonable safety of unmodified ECT has been well described. [sup][3],[4],[5],[6],[7] The safety profile of ECT remains neighbors's (other biological treatments) envy. Scalia et al. [sup][8] reported the case of a 92-year-old woman who had received 91 ECTs in her lifetime and showed no pathological effects at postmortem examination of her brain when she died of other causes. Dwork et al. [sup][9] reported no evidence of any significant neuro-pathological lesions in nonhuman primates after receiving multiple ECTs. Broadly ECT can be categorized based on the phase of treatment: *Acute (phase) ECT - till response/remission *Continuation (phase) ECT (C - ECT) - few weeks/months after remission to prevent relapse *Maintenance (phase) ECT (M - ECT) - few months or longer to prevent recurrence ECT is used in the management of depression and every psychotic disorder in psychiatry, though depression remains the most common indication. The Consortium for esearch in ECT (CORE) reported a 75% remission in depression [sup][10] which is supported by the UK ECT Review group. [sup][11] Patients with psychotic subtype of depression respond much higher. [sup][12] But there are reports that success rates in community hospital settings have been less at 30-45% as reported by Prudic et al. . [sup][13] There was another report by Sackeim et al. [sup][14] that documented remission rates in depression with ECT at 54%. Another interesting component of this study was that without any form of maintenance treatment 84% of patients relapsed at the end of 6-month follow-up. The CORE group also reported 46% relapse at the end of 6 months. One of their recommendations underscores the need to treat to wellness and not prematurely terminate the acute course of ECT. The clinical utility of continuation ECT and maintenance ECT was well discussed by Andrade et al. [sup][15] and Kellner et al. [sup][16] Most guidelines recommend ECT only for resistant depression and at a much later stage in the treatment process. The National Institute for Clinical Excellence (NICE) guidelines recommend restriction of ECT only for patients with severe depression and state that ECT is not recommended as maintenance therapy. [sup][17] ECT is underutilized as a treatment modality by some psychiatrists, at some institutions and in some geographical locations of the world. …

Over the past two decades, the number of somatic treatments for psychiatric disorders has expanded, leading to new insights into the complex relationship between chemical and electric transmission of signals in the brain. In this article, the authors discuss the different device-based treatments currently available in psychiatry. They review clinical indications; putative mechanism of action; efficacy and adverse effects; the results and limitations of salient clinical trials; and active areas of research into the neurobiology of device-based stimuli.

The fear of adverse cognitive effects remains the biggest impediment to the appropriate prescription of electroconvulsive therapy (ECT) worldwide. The recent study by Biedermann et al. 1 in this issue reminds us that depression itself affects cognition and that ECT may have beneficial, as well as adverse, cognitive effects. The discussion of ECT's effects on cognition, mainly memory, has a long and often fraught history in the psychiatric literature 2. What remains to be said? We feel that more needs to be said about putting the cognitive and other adverse effects of ECT in the proper context and perspective. Also, it needs to be said that resources should be directed toward research that will further minimize the side-effect profile of ECT. It is time to optimize ECT, the only brain stimulation technique with a proven record of safety and efficacy for severe and treatment-resistant depression. The as-yet-unmet promise of other brain stimulation techniques for this population argues strongly for refining, rather than abandoning, ECT. Memory function in the brain is complex and not fully understood. In simple terms, ECT has three main distinct effects on human cognition: It induces a brief confusional state upon awakening; it causes temporary anterograde amnesia; and it causes a variable degree of retrograde amnesia, some of which may be long-lasting. The latter effect is the most feared and hardest to evaluate. Most patients will have some degree of retrograde amnesia, in proportion to the 'intensity' of the ECT that they have received, but it is impossible to accurately predict the amount for a given individual. Some data suggest that the degree of confusion upon awakening from the initial treatment may be a proxy for the eventual degree of retrograde amnesia from the entire course of ECT 3. The study of memory loss from ECT is further complicated by the phenomenon of attribution bias. Once patients have had ECT, they typically attribute any subsequent forgetfulness to the treatment, while overlooking or discounting other possibilities, such as normal forgetfulness, dementia, or medications. The inter-individual variability makes it difficult to tell a patient 'how much' memory loss to expect from a course of ECT. Given this uncertainty, it seems reasonable to prepare a patient for a moderate amount of memory loss and explain to them that the most recent memories are most vulnerable to erasure. To the question, 'Do these memories come back?' extensive clinical experience supports the answer that most do, a few do not. The patient can be confidently assured that his/her memory function will return to normal within a few weeks of stopping ECT, but that a few pieces of content will be missing. There is also good evidence to support the contention that, because the treatments are widely dispersed in time, maintenance ECT causes little cumulative cognitive impairment 4, 5. Many investigators have studied compounds that might mitigate the adverse cognitive effects of ECT, but even the most promising results [including with thyroid hormone 6, galantamine 7, and memantine 8] have not been adequately followed up and replicated. Novel compounds have been suggested, but not studied 9. This is clearly an area where additional targeted research might lead to improved tolerability of ECT. We believe that the adverse cognitive effects of ECT should be considered a tolerability and not a safety issue. In medicine, safety refers to the risk of physical injury or death. To elevate cognitive adverse effects to this level perpetuates the stigma surrounding ECT. In medicine, treatment decisions always involve a risk–benefit calculation. The risks of the condition are weighed against the risks of the treatment or no treatment. It is imperative that the dangers of mood disorders are understood when considering the side-effect profile of ECT or any other antidepressant treatment. Depression can result in disability and exacerbation of medical comorbidities. In rare cases, depressive loss of appetite may lead to serious medical consequences; catatonia, a complication of mood disorder, may be a life-threatening medical emergency. Moreover, untreated or inadequately treated depression may be lethal due to suicide. The most apt analogy to properly contextualize the seriousness of depressive illness weighed against the risks of ECT is cancer and chemotherapy. Many cancers are lethal, life-threatening illnesses for which treatments (surgery, chemotherapy, and radiation) carry considerable risks. Patients rarely categorically refuse cancer treatments because of concerns about adverse effects, yet this happens frequently with ECT. Our contention is that refusing ECT because of concerns about memory loss is equivalent to refusing cancer chemotherapy because of concerns about hair loss. These effects are unpleasant and upsetting, but not worth risking one's life over. Just as the side-effects of chemotherapy abate, so too do those of ECT; most of the hair grows back, most of the memories return, and the patient's life is saved. Practitioners are charged with providing their patients the safest, most tolerable, and effective treatments. For ECT, this means using the most appropriate technique (optimizing electrode placement, stimulus dosing, and anesthesia technique) and fully informing patients about treatment options and potential risks. It can be explained to patients that convalescence from a serious episode of depression, as well as from the effects of the treatment, will take time and patience. Most patients will have been sick in their depressive episode for a very long time; full recovery will take some time as well. Biedermann et al. replicate the known finding of baseline cognitive impairment in severely depressed patients and demonstrate improvement in a specific cognitive domain, verbal memory, after successful ECT. Although limited by a small follow-up sample size, their results help assure depressed patients that ECT's negative cognitive effects are likely transient and some positive cognitive effects may accrue. Just as current chemotherapies will surely be replaced by more targeted therapies, so will ECT likely be replaced by more targeted brain stimulation techniques. Until that time, however, it behooves us to optimize the technique and maximize the use of ECT for those seriously ill patients who need it. It does little good to have a perfect memory of the past if the present is intolerable.