By ANDREW BRIDGES
The Associated Press
Friday, January 26, 2007
WASHINGTON — A novel machine designed to treat depression by zapping the brain with magnetic pulses shows no clear evidence of working, federal health advisers concluded Friday.
The device is called the Neurostar TMS, or transcranial magnetic stimulation, system. It uses magnetic energy to induce electrical currents in the region of the brain associated with mood.
Neuronetics Inc. believes those currents stimulate neurons in the region and relieve the symptoms of depression. The Malvern, Pa., company seeks clearance from the Food and Drug Administration to market the machine _ something the panel’s lukewarm reception may make less likely. The FDA isn’t required to follow the advice of its outside experts, but it usually does.
A clinical trial of the device provided results that, in one analysis, suggested it’s no better than sham treatment, according to FDA documents. Still, the FDA asked its neurological devices panel to review the overall safety and efficacy of the device.
Panelists said there was some suggestion the Neurostar works, but they called the effect marginal, borderline and questionable, an FDA spokeswoman said.
The company intends the device to be used by psychiatrists on an outpatient basis as an alternative to electroconvulsive therapy, or shock treatment, for the treatment of major depression. It would be used on depressed patients for whom therapy and antidepressants have not worked.
To gain federal approval, the FDA told Neuronetics that its device doesn’t necessarily have to be as effective as shock treatment if it can be shown to be a safer treatment option. Shock therapy can cause memory and cognitive changes, as well as headaches and burns.
Panelists said there were no important safety issues with the Neurostar. But none of the experts said the device works as substantially well as does shock therapy.
Company spokesman Peter Anastasiou said the company was confident in its efficacy data.
“In our view, we showed efficacy in a very tough to treat patient population,” Anastasiou said.
Added: January 26, 2007 |
Dec 6 2006
Reuters Health Information
NEW YORK (Reuters Health) Dec 06 – Electroconvulsive therapy (ECT) is comparable to pharmacologic treatment in preventing relapse of depression, but both approaches have limited efficacy, investigators report in the December Archives of General Psychiatry.
While electroconvulsive therapy is extremely effective for acute treatment of major depression, ECT is also being used as continuation or maintenance treatment (C-ECT) to prevent relapse. However, there are few data to support such use, note Dr. Charles H. Kellner and colleagues at five different academic clinical centers.
Dr. Kellner, from the UMDNJ New Jersey Medical School in Newark, and members of the CORE group (Consortium for Research in ECT) conducted a two-phase trial with 531 patients with primary major depressive disorder.
The first phase involved a course of bilateral ECT delivered three times per week for all the subjects until their illness went into remission. Participants who maintained remission at 1 week were then randomly assigned in the second phase to continuation ECT or a combination of nortriptyline and lithium.
ECT was administered weekly for 4 weeks, every other week for 8 weeks, and monthly for 2 months.
Relapse rates were 37.1% for C-ECT and 31.6% for medication treatment. In the two arms, 46.1% and 46.3% remained in remission, respectively, while 16.8% and 22.1% dropped out.
Subjects in both groups who remained in remission showed similarly improved cognitive abilities during the course of the trial, as assessed by the modified MMSE.
“An important interpretation of these data is that relapse or treatment discontinuation rates after successful ECT remain unacceptably high with standard treatment regimens,” Dr. Kellner and his team write, although they acknowledge that both types of treatment were “modestly effective in preventing depressive relapse.”
However, they caution that failure to detect significant differences between groups “cannot be taken to mean that the outcomes in the two groups are equal.” Instead, their advice is to decide treatment options “based on judgments about tolerability for the individual patient and patient preference.”
They hope that further research will turn up biomarkers to predict which patients will respond better to one or the other treatment. They also suggest that better remission rates might be achieved by combining C-ECT and medication therapy.
Arch Gen Psychiatry 2006;63:1337-1344.
Added: December 22, 2006 |
Archives of General Psychiatry
A Multisite Study From the Consortium for Research in Electroconvulsive Therapy (CORE)
Charles H. Kellner, MD; Rebecca G. Knapp, PhD; Georgios Petrides, MD; Teresa A. Rummans, MD; Mustafa M. Husain, MD; Keith Rasmussen, MD; Martina Mueller, PhD; Hilary J. Bernstein, DHA; Kevin O’Connor, MD; Glenn Smith, PhD; Melanie Biggs, PhD; Samuel H. Bailine, MD; Chitra Malur, MD; Eunsil Yim, MS; Shawn McClintock, MS; Shirlene Sampson, MD; Max Fink, MD
Arch Gen Psychiatry. 2006;63:1337-1344.
Background Although electroconvulsive therapy (ECT) has been shown to be extremely effective for the acute treatment of major depression, it has never been systematically assessed as a strategy for relapse prevention.
Objective To evaluate the comparative efficacy of continuation ECT (C-ECT) and the combination of lithium carbonate plus nortriptyline hydrochloride (C-Pharm) in the prevention of depressive relapse.
Design Multisite, randomized, parallel design, 6-month trial performed from 1997 to 2004.
Setting Five academic medical centers and their outpatient psychiatry clinics.
Patients Two hundred one patients with Structured Clinical Interview for DSM-IV–diagnosed unipolar depression who had remitted with a course of bilateral ECT.
Interventions Random assignment to 2 treatment groups receiving either C-ECT (10 treatments) or C-Pharm for 6 months.
Main Outcome Measure Relapse of depression, compared between the C-ECT and C-Pharm groups.
Results In the C-ECT group, 37.1% experienced disease relapse, 46.1% continued to have disease remission at the study end, and 16.8% dropped out of the study. In the C-Pharm group, 31.6% experienced disease relapse, 46.3% continued to have disease remission, and 22.1% dropped out of the study. Both Kaplan-Meier and Cox proportional hazards regression analyses indicated no statistically significant differences in overall survival curves and time to relapse for the groups. Mean ± SD time to relapse for the C-ECT group was 9.1 ± 7.0 weeks compared with 6.7 ± 4.6 weeks for the C-Pharm group (P = .13). Both groups had relapse proportions significantly lower than a historical placebo control from a similarly designed study.
Conclusions Both C-ECT and C-Pharm were shown to be superior to a historical placebo control, but both had limited efficacy, with more than half of patients either experiencing disease relapse or dropping out of the study. Even more effective strategies for relapse prevention in mood disorders are urgently needed.
Author Affiliations: Department of Psychiatry, University of Medicine and Dentistry of New Jersey–New Jersey Medical School, Newark (Drs Kellner, Petrides, and O’Connor); Departments of Psychiatry and Behavioral Sciences (Dr Kellner) and Biostatistics, Bioinformatics, and Epidemiology (Drs Knapp and Mueller and Mss Bernstein and Yim), Medical University of South Carolina, Charleston; Department of Psychiatry, The Zucker Hillside Hospital, North Shore–Long Island Health System, Glen Oaks, NY (Drs Petrides, Bailine, Malur, and Fink); Department of Psychiatry and Psychology, Mayo Foundation, Rochester, Minn (Drs Rummans, Rasmussen, Smith, and Sampson); and Department of Psychiatry, University of Texas Southwestern Medical Center at Dallas (Drs Husain and Biggs and Mr McClintock).
Added: December 12, 2006 |
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
Added: September 26, 2006 |
September 19, 2006
New York Times
By JANE E. BRODY
For an older woman I know who was suffering from “implacable depression” that refused to yield to any medications, electroconvulsive therapy — popularly called shock therapy — was a lifesaver. And Kitty Dukakis, wife of the former governor of Massachusetts and 1988 Democratic presidential nominee, says ECT, as doctors call it, gave her back her life, which had been rendered nearly unlivable by unrelenting despair and the alcohol she used to assuage it.Neither woman has experienced the most common side effect of ECT: memory disruption, though Mrs. Dukakis recalls nothing of a five-day trip to Paris she took after her treatment.
The television host Dick Cavett, who also had the treatment, wrote in People magazine, “In my case, ECT was miraculous.”
Mr. Cavett added, “It was like a magic wand.”
But for a man I know who was suicidally depressed and given ECT as a last resort, it did nothing to relieve his depression but destroyed some of his long-term memory.
Such differences in effectiveness and side effects are not unusual in medicine and psychiatry, and they are not played down in a new book called “Shock,” which Mrs. Dukakis wrote with Larry Tye, a former Boston Globe reporter. The book, in which Mrs. Dukakis details her experience with depression and ECT, explores the history, effectiveness and downsides of this nearly 70-year-old treatment, a remedy that has been repeatedly portrayed in film and literature as barbaric, inhuman, even torturous.
Few people seem to know that ECT has undergone significant changes in recent decades, placing it more in line with widely accepted treatments like those used to restart a stopped heart or to correct an abnormal heart rhythm. After a rather precipitous decline in the 1960’s when effective antidepressant drugs became available, ECT since the 1980’s has experienced something of a comeback, and is used primarily in these circumstances:
• When rapid reversal of a severe or suicidal depression is needed.
• When depression is complicated by psychosis or catatonia.
• When antidepressants and psychotherapy fail to alleviate a crippling depression.
• When antidepressants cannot safely be used, such as during pregnancy.
• When mania or bipolar disorder do not respond to drug therapy.
Though there is no official count, experts estimate that more than 100,000 patients undergo ECT each year in the United States.
ECT was developed in the 1930’s by an Italian neurologist, Ugo Cerletti, who “tamed” difficult mental patients with electric shocks to the brain after noting that such shocks given to hogs before slaughter rendered them unconscious but did not kill them. In its first decades of use, ECT was administered to fully conscious patients, causing them to lose consciousness and experience violent seizures and uncontrolled muscle movements that sometimes broke bones. It was sometimes used in patients without their consent, or at least without informed consent.
And while evidence for its effectiveness did not extend much beyond depression, for a time ECT was applied to patients with all kinds of emotional disturbances, including schizophrenia. It was also widely used in mental hospitals to punish or sedate difficult patients, as was graphically depicted by Jack Nicholson in the movie “One Flew Over the Cuckoo’s Nest.”
Some people may also recall that Ernest Hemingway, who suffered from life-long and often self-medicated depression, committed suicide in 1961 shortly after undergoing ECT. He had told his biographer: “Well, what is the sense of ruining my head and erasing my memory, which is my capital, and putting me out of business? It was a brilliant cure, but we lost the patient.”
A Modified Treatment
Though the impression of ECT left in the public mind by such films and writings persists, ECT today is a far more refined and limited therapy. Most important, perhaps, is the use of anesthesia and muscle relaxants before administering the shock, which causes a 30-second convulsion in the brain without the accompanying movements. Thus, there is no physical damage. The pretreatment also leaves no memory of the therapy itself.
The amount of current used today is lower and the pulse of electricity much shorter — about two seconds — reducing the risk of post-treatment confusion and memory disruption. While memory losses still occur in some patients, now the most serious risk associated with ECT is that of anesthesia.
Most patients require a series of six to eight treatments, delivered over several weeks. As my friend discovered, however, it is not universally effective. About three-fourths of patients are relieved of their debilitating symptoms at least temporarily. The remaining one-quarter are not helped, and some may be harmed.
Despite its long history, no one knows how ECT works to ease depression and mania. There is some evidence that it reorders the release of neurotransmitters, favoring an increase of substances like serotonin, which counters depression. Some experts view it as a pacemaker for the brain that disrupts negative circuitry.
The beauty of ECT is the speed with which it works. Antidepressants can take as long as six weeks to relieve serious depression. Mrs. Dukakis reported that she had begun to feel better after the first in an initial series of five outpatient ECT treatments given over a two-week period.
A Stopgap Measure
But — and this is a big but — ECT is not a cure for depression. It is more like a stopgap measure that brings patients to a point where other approaches, including antidepressants and cognitive behavioral therapy, can work to stave off relapses. Although some ECT patients never relapse, most are like Mrs. Dukakis, who over the course of four years has come back for seven more rounds of ECT. She explained that while she used to deny the early signs of a recurring depression, she now calls her doctor “as soon as I spot the gathering clouds.”
“ECT has wiped away that foreboding,” she wrote, and “given me a sense of control, of hope.” It has also helped her get off antidepressants, which had side effects like bowel, sexual and sleep disturbances and an inability to experience “the full range of my feelings.”
ECT should not be administered without the patient’s (or the patient’s surrogate’s) fully informed consent, which includes consideration of all possible side effects. The most common side effects are headache, muscle soreness and confusion shortly after the procedure, as well as short-term memory loss, which usually improves over a period of days to months.
But according to the American Psychiatric Association, there is no evidence that ECT causes brain damage. Abuse of the procedure has declined strikingly. Today fewer than 2 percent of patients hospitalized in psychiatric facilities in New York State receive ECT. Properly used, it can be lifesaving.
Though there is not nearly the money to be made from ECT that there is in selling antidepressants, work on improvements continues. Modern ECT is sometimes delivered to only one side of the brain, reducing the chances of memory deficits.
Another new approach uses a magnetically induced current that can be aimed at specific regions of the brain, possibly altering them permanently. An advantage of this treatment, however, is that it does not require the use of anesthesia.
Added: September 18, 2006 |
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.
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: email@example.com
Running title: Cognitive Effects of ECT
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
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.
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.
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.
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.
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.
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.
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.
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Tables and Figures-ECT Cognitive Effects
Added: August 6, 2006 |
ECT (ELECTRO CONVULSIVE THERAPY): NEED FOR DEBATE
Center for Advocacy in Mental Health
A research center of Bapu Trust, Pune, India
The World Health Report, 2001 of the WHO is the most recent among a line of reports and documents suggesting the tremendous increase in the burden of mental disorders in developing regions. Several researchers (for example Patel, 1999) have underscored the “social determinants model” of mental health, where poor social and economic development is linked with increased risk for mental ill health. The poor and vulnerable groups are seen as being at high risk for common mental disorders (CMD). The research of the last decade on gender and mental health has also shown the greater vulnerability of men and women to substance abuse and depression respectively (Davar, 1999; 2001).
Incommensurate with the emerging epidemiological and social science data bases in mental health today, and the increasing awareness in society about mental disorder, there is a large gap in service provision and quality of care research or advocacy. When it comes to service provision, “cost effectiveness”, “risk benefit analysis”, etc. has led to some questionable arguments and conclusions, because of the lack of public debate. Only partisan views prevail in this area and the debate is polarized between medical professionals and human rights groups in mental health.
Two significant arguments made on the basis of cost effectiveness are the following:
(1) That direct ECT (Electro Convulsive Therapy) is the cheapest and most effective form of treatment (Andrade, 2003a, b; Tharyan, et. al. 1993) and
(2) That anti-depressants are better (cheaper and more effective) than placebo or psychological counseling in the treatment of depression (Patel et al 2003).
Both these arguments boost the prominent bio-medical profile and future of mental health provision in India. With a view to starting a public debate on community alternatives and quality of care in mental health service provision, in this paper, we take a position regarding the recent advocacy promoting the use of direct ECT (i.e. shock treatment without anesthesia), as the cheapest, and most effective form of treatment for mental disorders (Andrade, 2003a, b; Tharyan, et. al. 1993).
We argue that direct ECT is a controversial, hazardous and traumatizing procedure. There is no contemporary evidence base for the use of the procedure. There is an uncommon degree of death, injury, terror and trauma caused by the procedure. And finally, there is a high potential for abusing it as a form of punishment. These factors, we conclude, makes direct ECT an instrument of torture, rather than of treatment. The use of the procedure must be brought within human rights jurisprudence and should be the subject of consumer action and litigation. Regulatory bodies such as the IECs, Medical Research Council and the Psychiatric Society should stop further research on direct ECT.
We do admit that families may have obtained beneficial results from use of the ECT when administered well. However, we agree with Pathare (2003) who writes that people friendly, psychotherapeutic and community-based options must be developed instead of routinely prescribing ECT on the basis of the “poor country” argument. The topic of ECT in general and its relevance in community mental health must be more widely debated.
1. ELECTRO-CONVULSIVE THERAPY (ECT): OUT OF THE CLOSET
Finally, the subject is out of the closet. Shock treatment has always been a taboo subject in India. It has been an esoteric topic discussed in medical forums, but never brought up before for public debate. Recently, in the wake of the Supreme Court approval of the procedure, a prominent psychiatrist has written making a case for direct ECT (Andrade, 2003a, b). This article follows in a line of other articles advocating direct ECT in recent times (Tharyan, et al 1993). This resurgence of direct ECT is risky in mental health service provision in India.
1.1 What is ECT?
In ECT, an electrical current of between 70 to 170 volts is passed for between 0.5 and 1.5 seconds. In direct ECT, the body is thrown into frank epilepsy like seizures. While the patient is conscious in the beginning, he or she is rendered unconscious when the grand mal seizure starts. He is held down physically by staff to prevent fractures and internal injuries. The risk of injury is high. As the procedure is usually given in series, this hazard is experienced again and again. In an ideal text book situation, the procedure is repeated between 6 to 10 times. But continuous dosing of up to 20 times or more is neither unknown nor uncommon in India.
In its “modern” or “modified” form (Modified ECT), text book practice suggests that the patient should not eat or drink for four hours or more before the procedure, to reduce the risk of vomiting and incontinence. Medication may be given to reduce the mouth secretions. Muscle relaxants and anesthesia are given to reduce the overt epileptic / muscular convulsions. The muscle relaxant paralyzes all the muscles of the body, including those of the respiratory system. Anxiety may be caused to the patient due to a sense of suffocation and anesthesia is given to prevent the anxiety. General anesthesia is given intravenously to make the patient unconscious. A “crash cart” is kept nearby, with a variety of life-saving devices and medications, including a defibrillator for kick starting the heart in case of a cardiac arrest. The brain is subjected to seizure activity induced by the electrical current, as it is believed that seizure is the essentially curative. The causal mechanism by which the treatment works is not known. Endocrinological, neurotransmitter and other changes have drawn a blank (Kiloh, et al 1988). It is believed that electricity itself and the seizure activity it produces is the curing element.
To get a picture of the procedure, read below, a full narrative of the experience of modified ECT, reported by doctors in 1988:
“In a generalized seizure (grand mal) the patient loses consciousness immediately and the whole musculature goes into a powerful tonic spasm. The upper limbs are held close to the body with flexion of the wrists and fingers, while the lower limbs extend with inversion of the feet and flexion of the toes. The trunk muscles contract and as the extensor muscles are the more powerful the spine tends to become hyperextended. The respiratory muscles are involved so that respiration ceases. The pupils dilate and become inactive and the eyes are insensitive to touch. There is an increase in heart rate and a rise in both systolic and diastolic blood pressure. If the bladder or bowel are distended at the time of the fit, either or both may be evacuated. The tonic phase usually lasts some 10-30 s followed by a partial, brief relaxation of muscles and a swift return of the spasm. Violent jerks then convulse the body in rapid succession and blood-stained froth may exude from the mouth. The clonic jerkings continue, the intervals between them lengthening, until with a final jerk the clonic stage terminates. At this point a degree of cyanosis is usual but after a brief period of flaccidity breathing is re-established. Often as consciousness begins to return, the patient passes into a deep sleep. If this does not occur the patient shows evidence of confusion with disorientation and may talk in a rambling and disjointed manner sometimes with paraphasias. The patient is likely to be restless and may show excited behaviour perhaps becoming irritable, angry and even violent” (Kiloh, et. al. 1988: p. 189).
1.2 Use of ECT in India
Only a few scattered articles exist in India, mostly published in the official journal of the Indian Psychiatric Society (Indian Journal of Psychiatry), on direct ECT practice. Vahia et al’s early study (1974) reported that in Bombay, 10580 patients out of 12,540 were given direct ECT, a large proportion of the help seeking population. Davar (1999) reviewing secondary literature wrote that, unlike the trend in the west, the use of ECT increased 20-fold in a hospital in Mumbai over a decade. Agarwal, Andrade and Reddy (1992) reported that direct ECT is widely practiced in India as a form of psychiatric treatment. Sharma and Chadda’s (1990) review of hospital facilities also showed that a majority of Indian mental hospitals used direct ECT.
Agarwal and Andrade (1997) studied the attitudes of psychiatrists towards ECT. Of 263 respondents 2.7% strongly objected to the procedure and another 9.5% generally opposed. Another 5.3% had no feelings one way or another. 64.3% were generally favourable, another 12.5% were decidedly favourable. 80% of doctors felt that ECT is the safest, cheapest and most effective form of treatment. A fair majority disagreed that ECT should be used when all else failed. The researchers are “reassured that most felt positive towards ECT”.
Professionals claim that patients are overwhelmingly happy about the effects of ECT (Andrade, 2003b). However, there is no experiential or quantified consumer satisfaction research to back this up. Not surprisingly, patient views on ECT are completely missing in the literature. Experiential accounts of staff or doctors, who have administered the procedure, are not available. There are problems, as we will see, about doing such studies. One study done during the direct ECT era (Verghese, Gupta & Prabhu, 1968) reported that not a single patient out of 36, voluntarily opted for ECT. 26 passively submitted, 8 had apprehensions and 2 strongly objected. This study reported memory loss and marked disorientation following the treatment. This is the only consent study we have found reported in literature.
1.3 SC interest in direct ECT
As readers of EPW may be aware, direct ECT has been placed as a controversial and contested issue before the Supreme Court recently. In the month of August, 2001, 28 people labeled with mental illness perished in a fire tragedy in Ramanathapuram district of Tamil Nadu. The manager of the private shelter in Erwadi had kept them tied to their cots, and so, escape was impossible. The SC took suo moto action and ordered all State Governments to file affidavits on a continuing basis, tabling information on the following topics: the availability of services within the state for mental disorders; whether the Mental Health Act has been implemented; the functioning of the State Mental Health Authority (SMHA); information on religious healing sites and whether mentally ill persons have been kept in chains in any part of the state. The SC appointed an amicus curiae to make recommendations, to field relevant information to the court and to process related petitions that may be filed by the public.
Direct ECT is considered a most contested and controversial procedure in the treatment of mental disorders. Saarthak, an NGO working for persons with mental illness in New Delhi, filed a petition before the SC appealing mainly the following: limitations on physical restraint, an unconditional ban on direct ECT and removal of Section (81.2) of the Mental Health Act, which allows proxy consent for research on persons with mental illness (Writ Petition No. 562/2001 in Saarthak vs. Union of India). While noting that ECT is not the top question for discussion in mental health today, Pathare (2003) has written responding to the Saarthak petition: “This debate [direct vs. modified] is a non-starter: it is accepted the world over that ECT must be administered in a modified form. It has been argued that there is a special case for permitting direct ECT in India because of the lack of facilities for anesthesia and to reduce the costs of treatment. Both these arguments are spurious. ECT is a major procedure and must be carried out under reasonably safe medical conditions” (p. 11). Not many professionals have written in response to the SC intervention.
The response of the state and the judiciary to use of direct ECT has however been ambivalent. In response to the SC orders, many states have reported that direct ECT is being phased out and that as per modern practice, only modified ECT is being used. Some states have given a justification for continuing the use of direct ECT, while also certifying that in their State this practice is not being followed.
In their final judgment, the apex court noted that “ECT remains effective in several major mental disorders”. It is “life saving” and reduces the “risk of suicide”. It further states, notoriously, that direct ECT is safer than modified ECT, as in the latter the risk of use of anesthesia and muscle relaxants is added. Dr. D. Mohan, Psychiatrist, AIIMS advised the apex court, in this instance. The doctor observes a mortality rate of “only 0.03%” in direct ECT, considered clinically insignificant, where as with modified ECT risks of use of anesthesia are to be added. Dr Gauri Devi, erstwhile director of NIMHANS, wrote observing mainly that modified ECT is a non-issue in the treatment of certain mental disorders. But she did not frontally address the issue of direct ECT, the central topic of the Saarthak litigation.
The Supreme Court judgment in this regard raises several questions about the interphase between law and science, the responsibility of medical professionals when giving testimony or scientific evidence, and the collective responsibility of the sciences and the judiciary, towards establishing certain standards of quality health care. The AIIMS professional did not give the background database about direct ECT, or explore the controversy surrounding it, even as a matter of informing the court. Instead of treating this as a quality of care issue and as an investigative matter, he “certified” the procedure as safe, raising the concern about questionable authorisation. The court, on its part, considered the certification given by a couple of psychiatrists as sufficient for making a decision. The Saarthak petition with respect to ECT was not treated with the respect that it deserved by the judiciary or by the professional community.
Around the world, in well-developed legal or policy formulations on involuntary commitments for mental illness, there are provisions and sanctions on the use of (modified) ECT. In India, legal or policy instruments in mental health do not address the procedure of ECT. The Mental Health Act, 1987, is about the institutionalization of persons with mental illness through commitment procedures. The Act was formulated in the context of involuntary commitment of persons labelled with mental illness – a reality in mental health care. Involuntary commitment ill automatically cancels the constitutional right of liberty (Dhanda, 2001) and a further law was required to allow this to happen within the law. However, the Act makes no mention at all of ECT, the top notch instrument of involuntary treatment in mental health care.
A few premier mental health institutions in the country have internal guidelines for the practice of ECT within their institution. At a National workshop on ECT in NIMHANS in 1990, members of the Indian Psychiatric Society recommended the use of modified ECT, in the presence of a qualified anesthetist as the norm for clinical practice. In a meeting of the State Health Secretaries in Bangalore in June, 1999, organized by NIMHANS, modified ECT has been recommended. Regulation of direct ECT has happened in some states of India mainly by High Court interventions. The Bombay High Court recommended against the use of direct ECT way back in 1989, following the Mahajan Committee Recommendations. In Goa too, due to legal advocacy and the proactive role of psychiatrists there, direct ECT has been banned (WP (Civil) No. 257, 1998, Collossa vs. State of Goa in the High Court of Mumbai). In Japan, ECT is used, just as in India, without anesthesia (Minkowitz, 2002), often as a type of punishment for political prisoners. Some countries in the Central and South of America continue to use direct ECT, and international human rights organizations are involved in challenging and reforming the practice.
1.4 Status of Direct ECT in the developed world
If we were to ask, “what is the evidence base which will validate the use of direct ECT” it is difficult to find the answer. It is difficult to find materials on direct ECT in world academic journals of the last 30 years. The only “evidence base” cited is the one or two studies done in India itself, Tharyan, et. al.’s eleven year study (1993) being a very significant one. Indian professionals advocating direct ECT will not find international academic journals, which will publish their articles, and so such articles are published in the obscure Indian Journal of Psychiatry. The world professional community considers the procedure of shock treatment without anesthesia, as barbaric and obsolete.
Many European countries including Holland have phased out even modified ECT, with other countries drastically reducing usage. In the US, use of ECT came down by 46% following consumer action between 1975 and 1980. As awareness about quality care and patient self-determination grows in mental health, every “forced ECT” (i.e. modified ECT where patient has not consented) in any part of the US elicits immediate activism, direct consumer action and patient litigation. In the words of LR Frank, who is called the “Gandhi” of mental health activism in the US, “ECT is a brutal, dehumanizing, memory-destroying, intelligence-lowering, brain-damaging, brain-washing, life threatening technique. ECT robs people of their memories, their personality and their humanity. It is a method for gutting the brain in order to control and punish people who fall or step out of line, and intimate others who are on the verge of doing so” (Frank, 2003: p. 17). Several efforts are on to ban the use of even modified ECT, some of them with partial success. The American Psychiatric Association survey of 1978 showed that only 16% of psychiatrists in the US gave ECT. Consumer groups in mental health maintain “Shock Doctor Rosters”, registering and shaming in public all doctors who indiscriminately prescribe shock treatments, and who do not offer a whole range of other psychotherapeutic opportunities.
This is why Dr Andrade’s recent article (2203a), which has set off a recent controversy in Issues in Medical Ethics, is incredibly astonishing and terribly disappointing. The paper does not even place an exclamation mark in making a case for direct ECT. To make a case for direct ECT in today’s context establishes a fresh, new low for psychiatric ethics in India. So, instead of debating the issue of ‘whether or not ECT at all’, and what other people and user-friendly alternatives we can create in mental health, we are placed in this ridiculous situation of debating direct ECT.
2. IMPACT OF DIRECT ECT
Any discussion on direct ECT, as mentioned above, has to draw from literature that is dated by atleast three decades. It is important to ask, why did the developed world ban the practice? Two major effects of direct ECT led to the phasing out of this procedure in the west– One, relating to the death and injury, and second, relating to the terror and the trauma, caused by the procedure on patients. We discuss these two aspects in this section and the next.
2.1 Injury caused by direct ECT
Direct ECT was invented in curious circumstances. The Italian, Ugo Cerletti, was inspired by the fact that electricity was used in preparing pigs for slaughter in an abattoir. They were rendered unconscious by bilateral placement of electrodes and passing current. Convulsions preceded the loss of consciousness. Following much experimentation on the pigs, he and his colleague, Lucio Bini invented the ECT procedure in 1938 when they first induced an artificial convulsion in a man (Kiloh, et. al., 1988). The man in question was a wandering mentally ill person. In 1940s and 1950s ECT use greatly increased, with experimental research on direct ECT holding sway.
Soon the data on death and injury, which started emerging on direct ECT, was alarming enough to lead to a ban on the procedure. 0.5% to 20% reportedly experienced vertebral fractures in use of direct ECT (Wiseman, pp. 118-119). In the UK, what stopped direct ECT was a well-known case, Bolam v. Friern Barnet Hospital Management Committee, when the patient sustained pelvic fracture. The US army forbade use of ECT during World War II in the early days, but with the increasing role of psychiatrists in the military during this time, it was reintroduced in 1943. The “Young Turks” of the nascent American Psychiatric Society railed against the “promiscuous and indiscriminate use of ECT” in 1947.
Professionals claim (Andrade 2000; 2003a; Tharyan et al 1993) that direct ECT is risk free. Infact, the world experience shows that direct ECT is not safe. As Andrade (2003a) himself mentions, reviewing previous research done in the 40s and 50s, direct ECT is associated with risk of vertebral / thoracic fractures, dislocation of various joints, muscle or ligament tears, cardiac arrhythmias, fluid secretion into the respiratory tract, internal tears, haemorrhages and blood letting, other than fear and anxiety. Risks are greater in males, older subjects, pregnant women and those with osteoporosis. Their own study (Andrade et al 2000) had found that “only 2%” of patients (i.e. 1 out of every 50 patients) experienced “an adverse musculoskeletal event with unmodified ECT”. Tharyan, et al (1993) enlist the risks involved in direct ECT: fractures of the spine, femur, humerus, acetabulum, scapula; dislocations of the arm, jaw and hip; rupture of abdominal muscles; fat embolism; rupture or bleeding of internal organs or viscera and increased apprehension. They do not mention cardiac complications and death, both of which their own study reported.
For “evidence base”, Andrade (2003a) cites the earlier study by Tharyan, et al. (1993), advocating direct ECT. First, a single study is not “an evidence base”. Secondly, this study itself needs careful examination. Andrade writes that in this study, only 12 patients experienced fractures out of a total of 1835 patients receiving 13,597 treatments. In the way the data from this study has been re-presented, it sounds as if a few of the patients walked out of the ECT table with a slight twisting of the middle finger. Andrade fails to mention all the relevant data from this study. The fractures that patients had during this study were thoracic / vertebral fractures involving almost a third of the body vertebrae. The sudden onset of convulsions has a crushing impact on the bones. The neurological disabilities and other orthopaedic consequences of these spinal injuries are unknown. Andrade also fails to mention that in this study, there was one reported death due to cardiac arrest (i.e. one patient out of 1835 died), a good percentage experienced body aches, both local and generalised, and another one percent of the patients had cardiac complications. These data, especially the high rate of spinal injury and mortality rate, which from the patient point of view seem horrific, are not considered “clinically significant” by the authors of this study. Absent, the professional standards for refusing any practice in psychiatry, there does not seem any other way of contesting this data except by throwing up your hands in horror.
Table 1: Complications. Click for larger view.
Source: Kiloh, et. al. (1988: pp.254-266) “True side effects” refers to inevitable events that always accompany ECT; “Complications” refers to infrequent but not rare events accompanying ECT; “risks” refers to unlikely events accompanying ECT; and “complaints” refers to the physical or somatic complaints associated with ECT. It must be highlighted that with modified ECT, such events are “less likely” but not completely ruled out.
2.2 Death due to ECT
The recent APA Task Force on ECT (2001) notes that contrary to earlier evidence, they have to now acknowledge that mortality rates with ECT (modified) may be as high as 1 in 10,000 patients. Consumers (Frank, 2002) say that mortality rates may be as high as 1% with modified ECT. The mortality rates are probably higher among the elderly. The Task Force report also notes that 1 in 200 will experience irretrievable memory loss, a fact hitherto dismissed as irrelevant by the medical fraternity.
Death in the case of ECT is usually due to cardio-vascular or cerebral-vascular complications, followed by respiratory failure. Shukla (1985), in discussing a case report of death following modified ECT, reviews the mortality data associated with the procedure. Rates between 0.8% and 0.003% have been reported in the western literature. Shukla, finding it a curious fact that deaths have not been reported at all in the Indian professional literature, observes that fatalities are not always publicly reported, particularly in India, but every psychiatrist would have experienced such cases in his practice.
3. DIRECT ECT AS TRAUMA
Leo Frank, an ex-patient subjected to many years of insulin treatment and direct ECT, says, “Why is it that 10v of electricity applied to a political prisoner’s private parts is seen as torture, while 10 or 15 times that amount applied to the brain is called “treatment”?” (2002, p. 19). Many human rights instruments around the world cover the area of the psychiatric system also, as medical coercion and violence, the loss of liberty, political abuse and being incarcerated through misuse of the criminal justice system is high in this health care sector. Involuntary commitment, patient consent, restraint and limits to coercive treatment are covered in human rights jurisprudence because of the fact that this constituency is particularly at risk for loss of constitutional rights. The UN Principles of 1991 also enlists fundamental rights and freedoms of psychiatric patients, and right to quality health care, as such explicit protection is seen as necessary for this vulnerable population. The Council of Europe came out with a White Paper (2000) on “protection of rights” of mentally ill patients and the Convention for Prevention of Torture (2002) also covers involuntary commitment. The ICCPR also covers the rights of institutionalized patients. As the label of mental disorder literally deletes personhood, such human rights safe guards are seen as necessary.
In India, we do not have human rights instruments covering the fundamental rights and freedoms of psychiatric patients. (The Mental Health Act, even though it has a human rights chapter, makes some general statements on such rights such as “no cruelty”). Such instruments are necessary because such patients are the most vulnerable within the community and risk abuse and civil rights violation on a daily basis (Dhanda, 2001).
In developing this instrument, use of direct ECT must be enlisted as a type of torture and as a human rights violation, as found in other world conventions. The European CPT (Convention for the Prevention of Torture) 2002 prohibits the use of direct ECT as a form of torture. The Convention says: “The CPT is particularly concerned when it encounters the administration of ECT in its unmodified form; this method can no longer be considered as acceptable in modern psychiatric practice. ECT should always be administered in a modified form” (Chapter VI, Section 39). One of the reasons cited by the CPT for prohibition on direct ECT is the terror experienced by patients during and after the procedure. The White paper (2000) on the “Protection of the human rights and dignity of people suffering from mental disorder, especially those placed in a psychiatric establishment” drafted by the Working Party of the Steering Committee on Bio Ethics (CDBI), Council of Europe, also prohibits the use of direct ECT.
3.1 Mental effects of direct ECT
Nearly all patients suffer amnesia about the period around which they were given ECT. People given ECT do not remember the experience itself and are not able to report on what it felt like to be given an ECT. In fact, this is a good reason why getting patient experiences of ECT is near impossible: As in trauma, the memories about the experience itself are not available to the conscious mind. Why does memory get wiped out, is a question that all concerned people have been grappling with for a long time. Earlier, professionals used to actually believe that brain damage is curative. We have also heard the clich? that “why would patients want to remember painful memories about mental disorder”, mistakenly suggesting that such memories were wiped out selectively. Advocates against the procedure argue that since it traumatizes the brain, memories are wiped out.
Direct ECT, as a treatment procedure, causes several disruptive psychological effects (Wiseman, 1995). Patient stories show that loss of memory and concentration are common. This affects personal lives (loss of cherished memories), and job performance (technical or mathematical memory, which can be the basic skill for engineers, lawyers or accountants can be lost). Artistic abilities can be lost. Because of this, there is the risk of having to do mechanical unskilled jobs, be unemployed, lose relationships, etc. Confusion, self-doubt due to the loss of memory, uncertainty, increased helplessness, loss of ability to learn and unlearn, lethargy, loss of ability in cognitive subjects will be experienced by many. Suicide and increased violence has also been associated following the use of ECT.
It is common experience in India, too, that patients are terrified of ECT. Within institutional settings, taking someone for ECT is experienced as a punishment by the patients. There is an undercurrent of humilation, shaming and punitive action in the use of the procedure within institutional contexts. Few patients, even those who actually find it beneficial, escape the sense of rage and humiliation that the procedure evokes. As direct ECT is very much like what is crudely shown on bollywood films, the fear and apprehension is quite understandable.
Direct ECT, in the medical narratives, comes across as any other stimulus, which freezes a person in terror, fear and pain. The terror associated with the procedure is a sign of trauma, and not a sign of insanity. As Breggin writes, ECT evokes raw survival fears to the fore. Even the highest experts on ECT (Abrams, et al pp. 130-131) have written that organic brain syndrome to varying degrees is common following all ECTs. ECT may affect all aspects of the brain system including thoughts, feelings and behaviours. EEG abnormalities may not go away for several months or years following ECT, indicating continuing brain seizure activities and possible brain damage. Other psychiatric experts write: “What cannot be denied is that transient forms of brain dysfunction, sometimes of considerable severity, occur with the Cerletti-Bini technique [direct ECT] particularly in elderly patients” (Kiloh, et. al., 1988: p. 190). The most evident effect of ECT on the brain was the vegetativeness of the patient, and reduction in his motor abilities. In fact, psychiatrists of yore believed that temporary brain damage effects the “cure” of mental illness (p. 213).
Direct ECT was described even in doctor’s narratives as somewhat close to lobotomy, the surgical removal of a portion of the frontal brain. Early doctors who gave direct ECT expected “regression”, a state when the patient was meek and submissive, wetting or soiling themselves, whimpering and crying easily, like a child. A writer in the Diseases of the Nervous System wrote, in 1951: “By the end of this intensive course of treatment practically all 52 patients showed profound disturbances. All showed incontinence of urine, and incontinence of feces was not uncommon. Most of them were underactive and did not talk spontaneously. Many failed to respond to questions but a few patients would obey simple requests. They appeared prostrated and apathetic. At the same time, most of them whined, whimpered and cried readily, and some were resistant and petulant in a child like way” (Wiseman, pp.118-119). The suggestion in literature is that ECT affects the limbic system of the brain, the same system that is affected by deep trauma.
In the UK, following the famous case against direct ECT, there was also a general consensus among professionals and policy makers that its unpleasant effects gave more scope for it to be used as a punishing tool, and several such stories did emerge until the 1980s. Case after case indicates that ECT is made as a choice of treatment in the case of “unmanageable” patients. ECT quiets the patients and remits agitation immediately, for unknown reasons. Within institutional contexts, therefore, the risk of abuse of the procedure is high. In India, although there is negligible documentation, direct ECT has been used as a punishment by families in collusion with psychiatrists against errant daughters and given to cure “naxalism” (Ramaswamy, 1999). For many years, the writer has suffered irretrievable memory loss. ECT has been given in India for all and sundry problems, including “curing” homosexuality. The use of direct ECT for dealing with political prisoners in Japan is also known (Minkowitz, 2002).
3.2 Use of sedation to allay fear
The fear associated with direct ECT is equal to the fear caused by any instrument of punishment and torture, and it is not a sign of insanity. It is the prejudicial attitude of professionals towards persons with mental illness, which allows them to interpret every response to their treatment as a symptom warranting further abusive treatment. With this logic, it will never be possible for a patient diagnosed with mental illness, to ever raise a question about the treatment they receive, for all such questions will risk being interpreted as a “psychiatric symptom”. Infact, Peter Breggin (1993), an erstwhile psychiatrist who gave up the profession in disgust over its abusive practices, and joined the mental health consumer movement as a researcher and a social scientist, wrote that the most dangerous impact of ECT was that the patient is no longer in a position to protest the damage done to him (p. 240). This strategy of seeing patient refusal of a particular treatment, as symptomatic behaviour, is evident in Tharyan et al’s study as well, which we discuss below. Such attitudes diminish the self determination of the patient in his or her own care.
In Tharyan et al’s opinion fuelling study, too, a high percentage of patients (7.5%) reported fear and apprehension of the procedure, and 50 patients actually refused the treatment. On ordinary ethical conditions of doing human behavioural research, we assume that such subjects would have been allowed to drop out of the study. How did the researchers proceed with this frightened sample of 150 patients?
Well, they did so, by actually sedating them and getting them to comply. Quoting them in full: “A fifty of them [patients] refused further ECT due to this fear while in the remainder (100 patients) the fear was reduced by sedative premeditation enabling them to complete the course of ECT. In the earlier half of the decade under review, barbiturates, oral diazepam, parenteral haloperidol and even thiopentone were used to allay anxiety; in recent years, this has been effectively managed by pretreatment with 1 to 4 mg of lorazepam given orally”. Further, it was interesting for these authors to observe that those who refused ECT were not among those who were sedated, that is, most of those sedated complied.
Such is the prejudicial approach to mentally ill patients, that refusal of a hazardous and life-threatening procedure is considered as a mere symptom, and further treated with sedatives to obtain patient compliance. We are of course aware of other power situations, such as rape or wife battery, when refusal is treated as consent. Tharyan et al’s study also suggests that it is common practice to sedate patients who refuse ECT. Amazingly, in their list of recommendations, they recommend the use of sedatives to minimize the fear of ECT among the patients. Their political message seems to be that, if people refuse a hazardous treatment, or if they will not participate in research that involves study of such a treatment, then it is okay sedate them. Patient ethics fundamentally rests on the principle of autonomy, which is seriously violated with this approach.
The world data of three decades already exists to rule out the procedure as barbaric. No further research is necessary on direct ECT. And if over six decades of ECT research has come up with little hard data on the causal effects of its beneficence, except the vague claim that electricity itself causes the cure, then perhaps it is time to question the assumption of its value in mental health service provision. Andrade recommends systematic sampling and interviewing of patients who have received ECT, as “dissatisfied patients can be found for all treatments?” (pp. 44-45). This call for quantified survey data on patient experience of direct ECT is against the very basis of human rights jurisprudence, where a single case of violation is indeed representative.
Because of the physical and mental trauma caused by the procedure, patients given direct ECT must be considered as victims of torture and the perpetrators of this form of torture must be brought within human rights jurisprudence. Direct ECT research should not be allowed to happen in future, as this would be a clear human rights violation. Statutory authorities, institutional ethics committees and consumer bodies must ask explanations regarding the recent highly objectionable research done on direct ECT.
4. WHY DIRECT ECT
The main argument used by Tharyan, et al (1993), Andrade (2003) and others is that direct ECT is “cost-effective”. The dogma among professionals is that direct ECT is the cheapest and safest form of treatment for mental disorder, as it does not require medical facilities and an anesthetist. It is argued that in a resource poor setting, we have to compare “existing alternatives”, use the cheapest means available for cure, and not go for the most ideal (modified ECT). If the choice were between no ECT and direct ECT, then direct ECT is considered to be the more “ethical” alternative in the treatment of mental disorders. We question these arguments in this last section.
4.1 ECT is not a cure
Andrade (2003b) argues that:
“From an emotional perspective, a seizure-inducing treatment could certainly seem barbaric. However, if ECT is barbaric or unattractive, so too are cardioversions, abortions, Caesarean sections, radical mastectomies, open heart surgeries, orthopaedic and neurosurgical interventions, and so where does one draw the line?” (p. 44)
It is misleading to compare ECT with major surgery in justifying usage. Surgery intends to cure. But ECT is palliative, not curative. This means that in practice, professionals use it repeatedly as and when they like as, palliative care being an ongoing need, unlike curative care. Infact, relapse rate has been reportedly high in the use of ECT for schizophrenia and patients have to go for ECT “like an addiction”, in the words of someone who has experienced the treatment. Within the span of a week or two, mastectomies or open heart surgeries are not prescribed in series. It would incredibly impoverish families and patients, if this were so. The text book prescribes 6 to 10 sessions of ECT, unlike the case of surgery. If we wish to adopt the surgery metaphor, then, ideally, the procedure would be used as a last resort. However, ECT is used often as the first line of treatment for dealing with mental disorders in India. Over-prescription is the rule rather than the exception. In the cost-effectiveness argument, are such realities of practice taken into account?
Finally, the stout evidence base underlying surgery is simply not comparable to the very weak epistemological foundations of ECT. Mental sciences in general suffer from weak epistemologies (Davar and Bhat, 1995) when compared to the natural sciences. Professionals cannot say how ECT works. Neurotransmitter and endocrinological studies have drawn a blank (Kiloh, et al 1988), and all that can be said is that electricity itself cures.
4.2 Training for direct ECT
Tharyan, et al’s study (1993) reassures the reader that in giving direct ECT, “trained” professionals were used to give direct ECT. What does “training” mean in the context of giving direct ECT? You just need some physically very strong people to tie down the patient in strategic points and to keep the jaw and joint areas from major injury. [If we were to include direct ECT in our community mental health, NGO training or volunteer training programs, what kind of programs will we have to run? Training Programs on "Accident management during ECT", "Bone setting and suturing course for ECT managers", "Martial arts and body techniques for CHWs giving direct ECTs", etc. seem appropriate titles.]
However that may be, in Tharyan et al’s study (1993), the composition of the full “trained team” used to prevent injury were the following: four orderlies, three nurses, two postgraduate trainees and a consultant psychiatrist, that is, a total of 10 “trained” people! If cost-effectiveness is our preferred parameter for “ethically” choosing a particular option, wouldn’t it be just cheaper to hire an anesthetist? It is unrealistic that in the actual settings where direct ECTs are going to be used, for example, the district hospital or the private clinic, there would be so many “trained” people to audit the ECT procedure. The research situation was an ideal situation, unlike the practice situation. Even here, with a full load of 10 people tying down a patient from the convulsions, the reported injury rate was not insignificant.
Another aspect of cost is highlighted by Kiloh, et. al. (1988) (who in general approve of ECT as a sound treatment in some cases). They cite studies of patients wherein, following ECT, the depressive symptoms remitted immediately, but they had to stay in the hospital for a week to clear their “confusion, memory loss, euphoria, lability of mood and affect, and impaired judgement” (p. 251). In the case of direct ECT, we can expect that the costs of injury, illhealth and disability are higher. We wonder if these costs have been factored into the dogma about the cost-effectiveness of direct ECT.
4.3 ECT is lucrative
While we question the faith that direct ECT is cost effective for the patient, we suspect that it is lucrative for the doctor. In the US (Wiseman, 1995; Kiloh et al 1988), ECT research is conducted by very few organizations. Large research, medical foundations and psychiatric learned societies do not fund ECT research. The medical fraternity looks down upon the procedure. The government does not fund ECT research, and it is not often used in the federal, and state hospitals. However, this trend may be changing with the recent American Psychiatric Association’s approval of the procedure.
In India, ECT is lucrative business. It falls within specialist practice. In nearly every city in India, a majority of psychiatrists practice privately and give ECT in their private clinics. In Pune city for example, nearly 90% of psychiatrists are in private practice, with the public mental health system having become literally dysfunctional. They cater mainly to the middle class with fees ranging between 100 rupees to 500 rupees per consultation. A recent survey in western India showed that nearly 80% of private psychiatrists give ECT, costing anywhere between 500 to 1000 rupees per dosage. If we set the dosage at textbook level (i.e. 6 to 10 ECTs), the total cost would be anywhere between 3,000/= to 10,000/= rupees per series. Direct ECT is a money-spinner for many psychiatrists in the business. There are unscrupulous psychiatrists who ask the patient to first take an ECT before even consultation (Bapu workshop, 2002)!
4.4 Policy regulation absent
In India, ECT is given without restriction for anything and everything, often as first line of treatment, for even “curing” homosexuality. Andrade (2003a) writes that ECT is given to catatonic, suicidal, or otherwise “highly disturbed” patients. To say that “highly disturbed” patients can be given ECT allows too much ambiguity and scope for abuse of the procedure. In the direct ECT era, Shukla (1974) recommended use of direct ECT as a solution for passing a nasal tube to catatonic patients who refuse food: “At times it is very difficult to pass a tube even under sedation. I have tried the following in such patients with a 100% success: I give the patient direct ECT. (There are no problems as these patients are usually fasting and their stomach, bowel and bladder are empty). As soon as the convulsions stop and the patient is in a flaccid state, I pass the tube and it goes in very easily” (p. 95).
Policy guidelines and evidence base repeatedly comes up with only one diagnosis where ECT may be tried if other treatments fail- that is in the case of endogenous depression. Some documents do say that in this case, modified ECT can also be tried as first line of treatment, but enlist further conditions, including patient consent, an active audit program in each ECT department. The CPT 2002 also talks about patient consent and ECT audit, including a registry of ECT.
Reviews of research on the use of ECT in the case of schizophrenia upto the mid ’80s, when ECT research was at its peak, shows that
1. It is not possible to be emphatic about the value of ECT in patients diagnosed with schizophrenia
2. ECT and neuroleptic drugs have the same outcomes statistically
3. The relapse rate is high in use of ECT, showing that it probably has short term benefits
On the basis of the review, Kiloh et al (1988) observe that “the question whether the long-term effects of neuroleptic drugs, notably tardive dyskinesia, are more or less disabling than the possible ill effects of long term ECT cannot be answered” (p. 244).
ECT guidelines do not exist in India, making it a huge ethical issue among patients and consumers. Indian psychiatrists recognize the cavalier use of ECT. Agarwal (1990) in his editorial notes remarkable deficiencies in the administration of ECT even in the West, writing, “the situation in India is bound to be more disappointing”. ECT in India is often prescribed in series, without any review, the conditions for safe use and correct use are not specified, the staff giving ECT are often untrained, and physical pre-exam is often not done, as it is felt that ECT is safe for anyone and everyone (“virtually no contradictions”, according to the psychiatric dogma).
The community mental health program in India (NMHP, 1982) promises to take mental health services to the community. Unfortunately, in most parts of India, it has remained a drug and ECT dispensing service, with minimal understanding or engagement with the community. The advocacy for direct ECT is likely to increase misuse of ECT in private practice and in the community mental health programs. Lack of awareness among communities about this procedure is likely to be harvested by unscrupulous professionals. As people with mental illness are not considered fit to give consent, patient consent is rarely addressed. In many hospitals, patients and their families are only told that they are receiving an “injection”, as it is argued that patients will not understand the procedure. Consent letters, if used at all, are signed on that basis. See, for example, the narrative below.
“In the beginning my husband did not benefit from the medicine, so he had to be given shots. And while giving shots also they take [the patient] with great love and affection, not that they tied and took him. They will lure you and take you. There are two or three employees. Those who try to run, they have to be stern with them. Even for shots? because there is a danger that perhaps they may die? attention has to be paid even to their teeth that they should not dislocate or fall. When shots are administered the teeth is clenched and it clatters? the entire jaw may even come out, so they put a big bandage inside. If it moves, the entire set both can come out in that bandage. They would tell you before hand that you keep either milk or tea ready.”
Quality of care
The research cited in this paper advocating direct ECT was done under ideal treatment conditions. The institutions where the research was conducted (NIMHANS, CMC) were well funded public health institutions, with a promise of high quality care. Adequate staff were allocated for the research. Under ideal conditions, the injury rate is not insignificant, as we have argued above. What can we expect from less than ideal conditions? We give a case study below:
“Meena” was imprisoned in a Maharashtra jail for killing her sister. She suffered from “voices in the head” for several years. After the accident, she was arrested and then taken for treatment. Here we present a portion of her experiences with shock treatment without anesthesia:
“I was totally maddened by this time. The police arrested me and kept me in the lock-up. I felt very remorseful after that. They later took me to a nearby famous hospital. There they gave me shock treatments. 4 shocks they gave me with anaesthesia and three shocks they gave me without anaesthesia. I remember feeling those three shocks while I was awake. I had not fainted, and could feel the shocks. It was extremely painful. They used not to give me any tea in the morning either. I would not allow them to put the cloth in my mouth. It was extremely painful. I suffered an enormous amount. It was the most horrible pain in my head. I don’t remember anything else about the time. I was also very rude with the doctors. The voices in my head stopped after that. I kept feeling remorseful about how I had killed my auntie’s only child. My aunty came to visit me in hospital also. I asked her whether she had told the doctors to give me shocks. She didn’t know anything about it. I was unconscious for 3 days after the shocks. It was very traumatic.”
We have all experienced the mundane pain of needles poking at our elbow because the poorly trained staffer “could not find a vein”. What are the effects of poorly administered direct ECT? The patient is rendered unconscious only when the grand mal seizure starts at a particular electrical threshold. Meena was probably given ECT without anesthesia at infra-threshold, so she did not become unconscious.
4.5 Other guidelines
Recently, in Utah, an ECT Bill passed by the House is being considered by the Senate in which consumer groups have had a large role to play. The proposed bill (www.le.state.ut.us/-2003/htmdoc/hbillhtm/HBO109S1.htm) does the following: It prohibits shock for children under the age of 14. It prohibits shock for individuals who are committed against their will. It prohibits a legal guardian to consent to shock for someone else. It requires a second medical opinion to shock someone over the age of 65. It requires that informed consent mentions that possible side effects of shock may include permanent memory loss, cardiac arrest and death. It requires a reporting system to show how many are shocked every year and if they suffer from any side effects within a certain amount of time. It requires that an autopsy be done if someone dies after shock, and that the autopsy look for brain damage by searching for destroyed small blood vessels. It allows free individuals over the age of 18 to receive shock after they get full informed consent.
The Royal College of Psychiatrists Commission Guidelines give conditions for anesthetic equipment, the ECT machine, staff requirements and treatment protocols. As direct ECT machines are obsolete, such machines would be ruled out by international standards. The FDA considers ECT machines as “Class III” devices, that is “hazardous”.
There is a need to investigate the condition and commerce of existing ECT machines in India, who makes these machines, who approves them, what are the standards for the machines. In UK, an internationally recognized advocate of ECT, Dr Abrams, who wrote the very popular reference book, Electroconvulsive Therapy, was found to be one of the two member Board of Directors of Somatics, a commercial venture involving ECT machine manufacture and sale. Half his yearly income was drawn from Somatics. While not making allusions to possibility or ethics of the commercial interests of any professional in the practice, we are indeed suggesting that the commerce of ECT needs to be more thoroughly investigated.
The National Mental Health Association, the largest non-profit mental health organization in the US, issued a public statement on the 11th of June, 2000. The statement says that the NMHA recognizes that ECT is a controversial procedure and that although it may have beneficial results, it also involves serious risks. It has urged the increased, rigorous and objective research, as well as dissemination of such research, on ECT especially from the safety point of view. The organization also supported the position that ECT recipients must be informed of all the pros and cons and have access to all kinds of information to be able to make fully informed decisions. NMHA further recommends that “ECT be presented as an alternative with extreme caution, only after all other treatment approaches have either failed or have been seriously and thoroughly evaluated and rejected” (www.nmha.org/position/ps31.crm).
CONCLUSION: THE NEED FOR PUBLIC DEBATE
There must be a public debate on the issue of the use of ECT in India. Most world data bases of the last decade, culminating in WHO’s World Health Report, 2001, have highlighted the phenomenal “increase” in the “burden” of mental disorders in developing countries. The spin-offs of globalisation and economic reform, (including debts, ethnic violence, poverty, homelessness, displacement and cultural loss) have resulted in the greater mental ill health of vulnerable groups. Poverty and mental disorder are being linked in a significant way in the literature. Meanwhile, there has been little challenge to the privatization of mental health and little is known about the influence of drug companies on the development of research, technology and service within the sector.
Advocating direct ECT against the background of the Indian reality of a questionable mental health care quality can be risky. Andrade writes that “if the risk-benefit ratio favours the treatment, and if the treatment is better than existing alternatives, in the interest of the patient the treatment must survive” and that “unmodified ECT may be preferable to no ECT” (2000b:p.44). The fact of not having created interesting and humane alternatives in mental health has been the pathos of the Indian mental health service system. It is disappointing that this fact should lead to advocacy of direct ECT, instead of fuelling the creation of imaginative psycho-therapeutic and community models. On the basis of the argument that India is a “poor” country and the poor need quick alternatives, justifications have also existed for various invasive and undignified “treatments”, such as mass sterilization, and hysterectomies, in the case of the mentally challenged girls.
Background to the paper
The ideas presented here are the result of several discussions in our Center by Aparna Waikar, Bhargavi Davar, Chandra Karhadkar, Darshana Bansode, Deepra Dandekar, Seema Kakade, Sonali Wayal, and Yogita Kulkarni. Bhargavi Davar did the research for this paper. Deepra Dandekar and Darshana Bansode submitted a case study from the “Archives” team of our Center, from their documentation of the plight of mentally ill women prisoners in Maharashtra. The community narrative on ECT as “injections” came from our “Needs Assessment Study of NGOs in mental health”. Fieldwork was done by Lalita Joshi and Seema Kakade for this study. Our activities are funded by Sir Dorabji Trust and Action Aid India.
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Added: July 29, 2006 |
The Journal of ECT 2002; 18(2):90-94
Efficacy of Electroconvulsive Therapy Combined with Antipsychotic Medication
in Treatment-Resistant Schizophrenia
Wai Kwong Tang, M.D.; Gabor S. Ungvari, M.D., Ph.D.
This study examined the short-term efficacy of electroconvulsive therapy
(ECT) combined with antipsychotic medication in treatment-resistant
schizophrenia (TRS). Fifteen patients with TRS from an in-patient psychiatric
rehabilitation unit participated. Patients completed a course of ECT
consisting of 8 to 20 sessions, while their antipsychotic medications were
continued throughout the study. Patients were assessed at baseline, 1 week, 1
month, and 2 months after their last ECT session. Assessment instruments
included the Brief Psychiatric Rating Scale (BPRS), Hamilton Depression
Rating Scale, Scale for the Assessment of Negative Symptoms (SANS), Global
Assessment Scale (GAS), Clinical Global Impression (CGI), Nurses’ Observation
Scale for In-Patient Evaluation, and occupational therapists’ rating of the
patients’ functioning with respect to work, social, and leisure activities.
Compared with the baseline assessment, at each posttreatment evaluation,
patients showed statistically significant improvement in the GAS and CGI. In
addition, they were significantly better in terms of BPRS and SANS scores, as
well as work performance and social functioning at the 2-month post-ECT
Key Words: Electroconvulsive therapy; Schizophrenia; Clozapine; Treatment
resistance; Electroconvulsive therapy, continuation and maintenance
Department of Psychiatry, Chinese University of Hong Kong, Hong Kong SAR,
Accepted June 4, 2002.
Address correspondence and reprint requests to Dr. W. K. Tang, Department of
Psychiatry, 11/F, Prince of Wales Hospital, Shatin, N.T., Hong Kong SAR,
China. E-mail: firstname.lastname@example.org
The Journal of ECT 2002; 18(2):90-94
Copyright © 2002 Lippincott Williams & Wilkins
All rights reserved
Depending on the definition of antipsychotic treatment resistance, sample
selection, assessment tools, and other methodological aspects of the inquiry,
25-60% of patients with schizophrenia are regarded as treatment resistant (
1, 2). For the purpose of this study, treatment resistance is defined as the
failure to respond to at least two courses of antipsychotic drugs belonging
to different chemical classes, in doses no less than 600 mg chlorpromazine
equivalent given for at least 6 weeks, coupled with a failure to respond to
clozapine in doses of at least 300 mg/d administered for at least 8 weeks, or
refusal to take clozapine. While a number of adjunct treatments for
treatment-resistant schizophrenia (TRS) have been suggested, including
lithium, anticonvulsants, benzodiazepines, and cognitive behavior therapy,
none have proven effective for the majority of patients, a substantial
proportion of whom also fails to show improvement to atypical antipsychotic
drugs ( 3-6).
Patients who are resistant to even repeated trials of atypical antipsychotic
drugs pose a real challenge, as they usually require long periods of
hospitalization, are frequently tormented by positive symptoms, and/or became
extremely withdrawn. Their quality of life is very low by any standard.
Electroconvulsive therapy (ECT), either alone or in combination with
conventional antipsychotic drugs, has been shown to be effective in a certain
percentage of patients with acute schizophrenia ( 7), particularly in the
catatonic subtype and also in schizoaffective disorder ( 8). The use and
efficacy of ECT in chronic schizophrenia is a more controversial topic. Some
authors ( 9) opined that ECT is ineffective in chronic schizophrenia, while
others ( 7) concluded that its efficacy depends on the length of illness and
the frequency and total number of ECT sessions applied.
Lately ECT has come to be regarded as the last resort in patients with
chronic TRS ( 10), although its efficacy has not been systematically
investigated. Anecdotal evidence in the form of case reports ( 11) and case
series ( 12) suggests that ECT combined with conventional antipsychotic drugs
might be effective in TRS. Similarly, ECT combined with clozapine has been
reported effective in several cases of clozapine-resistant schizophrenia
(CRS) ( 13-16). An extensive manual and computer-assisted search including
MEDLINE, EMBASE, and PSYCHINFO databases between 1990 and May 2001 failed to
locate any prospective, open, or controlled study employing a range of
standardized assessment on the use of ECT in TRS in general or CRS in
particular except for one study ( 17) on maintenance ECT in TRS.
We have also noted favorable response to ECT in Chinese patients with acute
episodes of schizophrenia in Hong Kong. According to an unpublished survey
conducted by the principal author, 252 courses of ECT were performed in the
period between July 1997 and July 1998 in our acute psychiatric unit. (A
course is defined as ECT sessions given in consecutive weeks.) Fifty-seven
courses, 23% of all courses of ECT administered during the above-mentioned
period, were administered to patients with schizophrenia or schizoaffective
disorder. The proportion of patients with TRS was unknown. Patients were
given ECT three times a week. The mean number of ECT sessions was 8 (range:
1-21). Based on clinical judgment, varying degree of improvement was noted in
45 (79%) of 57 courses of ECT administered to patients with schizophrenia.
Over the past 3 years, we also have used ECT in combination with traditional
and atypical antipsychotic drugs in a few chronically ill patients with
treatment-resistant schizophrenia (TRS) ( 18). Encouraged by case reports and
our own promising clinical experience, we set out to examine the short-term
therapeutic efficacy of ECT in a prospective study using standardized
assessment in Chinese patients diagnosed with schizophrenia who met criteria
for treatment resistance to traditional antipsychotic drugs ( 19) and either
failed to respond to clozapine and/or other atypical antipsychotic
medications, or refused to take clozapine.
In our clinical practice, ECT-responder TRS patients are offered continuation
and maintenance ECT (ECT-C and ECT-M, respectively) ( 18). In this study, we
also planned to identify those patients who would benefit from ECT-C and
MATERIALS AND METHODS
Setting and Patients
The study was conducted in a 166-bed psychiatric rehabilitation and extended
care unit in Hong Kong from February 1999 to March 2000. The mean age of the
whole patient population in this facility was 47 ± 14 years, and 67% of them
were male. Prior to the study, all patients who met DSM-IV criteria for
schizophrenia were reassessed for confirmation of their diagnosis and for
criteria of TRS (see below). Patients with the diagnosis of DSM-IV
schizophrenia who fulfilled the criteria of TRS were offered a trial of
clozapine if not previously given. Patients who had proved to be resistant to
clozapine and those who refused clozapine were invited to participate in the
ECT trial. Inclusion criteria were as follows: 1. Age 18-65 years; 2. Both
sexes; 3. Diagnosis of schizophrenia according to DSM-IV criteria; 4. Length
of illness >3 years; 5. At least 6 months of continuous hospitalization; 6.
Resistance to at least two courses of antipsychotic drugs belonging to
different chemical classes, in doses no less than 600 mg chlorpromazine
equivalent, for at least 6 weeks; 7. Refusal to take clozapine or failure to
respond to doses of at least 300 mg/d given for at least 8 weeks; 8. Ability
and willingness to give informed consent. Exclusion criteria were medical
contraindications to ECT and ECT given within the past year.
The Ethics Committee of the Faculty of Medicine, Chinese University of Hong
Kong, granted approval to conduct the study.
Each patient was given ECT three times a week in a nearby acute psychiatric
unit. A brief-pulse machine (MECTA SR-1; MECTA Corporation, Tualatlin, OR,
U.S.A.) was used. Seizure length was monitored by a one-channel, built-in
electroencephalogram (EEG) and the cuff technique. Thiopentone anesthesia and
succinylcholine were the standard premedications; atropine or glycopyrrolate
was not routinely administered. Only bilateral ECT using bitemporal electrode
placement was given. Seizure threshold was determined in the first ECT
session for every patient by a standard titration protocol ( 9). The total
number of ECT sessions for each patient was determined by the authors’
consensus opinion based on clinical improvement and adverse side effects.
Following earlier studies ( 17, 20-22), we aimed to give a total of 20 ECT
sessions unless adverse effects and/or patient’s refusal shortened the course.
Concurrent Antipsychotic Medication
While waiting for ECT treatment, patients were given olanzapine (=20 mg/day)
or risperidone (=14 mg/day) unless they had failed to respond to these drugs
in the past. These drugs were gradually titrated up to their respective
maximum recommended dose unless adverse side effects prevented an increase.
In keeping with our protocol and rational clinical practice, if patients
responded to these atypical antipsychotic drugs, then ECT would be withheld.
If they did not respond, then a course of ECT would be given. Throughout the
course of ECT, the current antipsychotic drugs were continued at the same
dose. If the patients responded to ECT, the same medication would be
continued after ECT; if ECT was ineffective, patients were offered another
atypical antipsychotic drug.
Rating scales to evaluate changes in the patients’ clinical condition
included the Brief Psychiatric Rating Scale (BPRS, 18-item version) ( 23),
Hamilton Depression Rating Scale (HDRS) ( 24), 17-item Chinese language
version, ( 25), Scale for the Assessment of Negative Symptoms (SANS) ( 26),
Global Assessment Scale (GAS) ( 27), Clinical Global Impression (CGI) ( 28),
and the Nurses’ Observation Scale for In-Patient Evaluation (NOSIE-30) ( 29).
The NOSIE-30 was divided into positive (4, 8, 9, 15, 17, 19, and 30) and
negative items (1-3, 5-7, 10-14, 18, and 20-29) as in previous studies ( 30)
and the two groups of items [NOSIE(+) and NOSIE(-)] were entered into the
statistical analysis separately. (For instance, a positive item was #4:
“Shows interest in activities around him” while a negative one was #5: “Sits,
unless directed into activities”.) All ratings were done at baseline and 1,
4, and 8 weeks following the completion of the ECT course.
The principal author, who did not have direct clinical responsibility for the
patients, rated all the clinical scales. Independent from the clinical
ratings, three experienced nurses rated the NOSIE-30. In addition, all
patients were assessed by three occupational therapists 2 months after the
completion of the ECT course or drug treatment with a 5-point scale (from 1 =
very poor to 5 = excellent) on functioning in work (OT-W), social (OT-S), and
leisure (OT-L) activities. No interrater reliability was established for the
ratings made by nurses and occupational therapists.
Descriptive statistics were used to characterize demographic and clinical
data of the study sample. The baseline and posttreatment scores were compared
by repeated measures analysis of variance and within-patient contrast or
Wilcoxon signed ranks test. Statistical significance was set at p < 0.05
level. Ratings of the four patients who were retreated because of a relapse
following an initial response were not separated from the rest of the sample.
One hundred twenty-six patients met DSM-IV criteria for schizophrenia at the
rehabilitation unit, of whom 55 (44%) fulfilled the above criteria for TRS.
Seven patients had ECT in the previous year, thus 48 met the criteria of our
study. Fifteen patients agreed to have ECT, while 24 refused and 9 patients
were unable to comprehend the consent form.
Nine (60%) of the 15 patients consenting to ECT were male. The mean duration
of illness and of lifetime hospitalization was 18.9 ± 5.9 and 9.3 ± 4.5
years, respectively. The mean number of psychiatric admissions was 6.1 ± 4.4.
The mean age of patients and the length of current admission was 40.1 ± 10.5
and 7.2 ± 5.1 years, respectively.
Parameters of ECT
The number of ECT sessions ranged from 8 to 20, with a mean of 15.9 ± 4.2.
ECT was administered three times per week. The mean seizure threshold was
94.9 ± 29.9 mC. The mean maximum stimulus was 318.1 ± 200.7 mC. The mean
seizure duration determined by EEG and the cuff method was 43.0 ± 7.2 and
38.7 ± 5.1 s, respectively.
Past Psychiatric Treatment
Only two patients had received ECT in the past. According to a chart review,
both patients had a good response to past ECT, although the exact magnitude
and length of improvement were not known.
The number of trials with typical antipsychotic medications with a dosage of
at least 600 mg/d chlorpromazine equivalent ranged from 2 to 5. With respect
to atypical antipsychotic drugs, two patients received risperidone, five had
trials of olanzapine and five tried both. Eleven patients were resistant to
clozapine, while clozapine was contraindicated for two patients due to
preexisting neutropenia and atrial flutter; two patients refused to take
clozapine. In the clozapine-resistant group, the maximum dose of drug was 600
mg/d for each patient. The mean length of treatment with maximum clozapine
dose was 11.0 ± 4.2 weeks.
In terms of past adjunct treatment, four patients tried sodium valproate, and
three lithium carbonate. One further patient received both carbamazepine and
Antipsychotic Treatment Following ECT
Following the course of ECT, 2 patients were started on olanzapine (10 and 20
mg/day), and 3 received risperidone (2 to 6 mg/day), while 10 continued their
pre-ECT antipsychotic medication.
The baseline and post-ECT scores for all rating scales are shown in Table 1.
There were statistically significant differences between the baseline scores
and 1-week, 1-month, and 2-month post-ECT assessment scores of GAS, Clinical
Global Impression (Severity of Illness) [CGI (SOI)], and Clinical Global
Impression (Global Improvement) [CGI (GI)] ratings. In addition, the
difference between baseline and post-2-month scores was also significant for
the BPRS, SANS, OT-W, and OT-L.
TABLE 1. Results of baseline and post-ECT assessment
Judged by the CGI, 6 of the 15 patients did not improve at all, 4 patients
relapsed within 3-6 weeks following initial good treatment response, while 5
patients maintained the improvement for at least 2 months following the last
A second course of ECT followed by ECT-C was administered to the four
patients, who, after an initial response, experienced a relapse of symptoms
by 3-6 weeks after the completion of their first ECT course. The number of
ECT sessions in the second course ranged from 6 to 20 for these four patients.
Two of the nine patients who responded to ECT and were offered ECT-C accepted
this treatment option, but only one of them maintained the initial
improvement for 1 year. The second patient’s condition deteriorated within 3
months despite ECT-C.
Adverse Effects of ECT
The only cardiac complication occurred in a previously healthy 41-year-old
male patient who had asymptomatic ST elevation in the V3 and V4 leads of an
electrocardiogram (ECG) following the second ECT session. This ECG
abnormality spontaneously resolved the same day. Cardiological consultation
found no evidence of acute myocardial infarction or any contraindication to
12 further ECT sessions. Postictal confusion was observed in one patient. Two
patients complained of slight, transient memory impairment. Other minor and
transient side effects included headache, dizziness, and pain over the
intravenous site in two patients each.
This study targeted the most severely disabled group of schizophrenia
patients whose illness was resistant to most pharmacotherapeutic and social
interventions available. These patients had been confined to hospital for
several years and ECT was the last available treatment of them. There have
been no randomized, controlled studies on the efficacy of ECT in TRS or CRS.
Conducting such studies is very difficult for obvious ethical as well as
logistical reasons. A small-scale open trial ( 31) and case series ( 32, 33)
have shown that ECT could be effective in CRS.
Our study was an open, nonrandomized, prospective trial using standardized
assessment tools. This investigation was designed to measure the short-term
(2-month) outcome of ECT in patients with treatment-resistant chronic
schizophrenia, the majority of whom were also resistant to clozapine,
risperidone, and olanzapine.
The limitations of the study should be acknowledged. The sample size was
relatively small, and no formal cognitive assessment was carried out. In a
pharmacotherapeutic aspect, the study sample was not entirely homogenous, as
not all patients were tried on every available atypical medication prior to
ECT. In addition, the length of clozapine treatment was relatively short, and
its outcome was not measured by standardized rating scales.
The statistical analysis was somewhat confounded by including the ratings for
the four patients who were retreated for a deterioration in their mental
state shortly after their initial good response to ECT. Their 1-month and
2-month post-ECT scores were those following the second course of ECT. This
arrangement is essentially very close to a real clinical situation whereby a
promising, albeit short-lived, improvement to ECT would warrant a further
course of ECT in patients who otherwise were unresponsive to any other
Our results indicate that ECT significantly enhanced patients’ global
functioning in the short term. It appears that besides clinical rating
scales, functional assessment should also be included in the outcome measures
when evaluating the usefulness of ECT in TRS or CRS.
ECT significantly reduced positive and negative symptoms, although the
posttreatment BPRS and SANS scores were still very high, indicating
considerable residual psychopathology. While improving the patients’ overall
condition, ECT did not produce a real clinical breakthrough in any patient
even in the short term. However, it did show that there is a potential for
improvement even in patients with chronic schizophrenia unresponsive to most
typical and atypical antipsychotic drugs.
The effect of ECT on affective symptoms was very small, suggesting that the
patients’ improvement was not due to a reduction in affective symptoms.
Without a control group, the possibility of a placebo response in our
patients cannot be excluded, particularly in those four patients who had an
early relapse. However, a robust placebo effect is unlikely, as several
patients maintained initial improvement for more than 2 months. Also, the
majority of staff members voiced strong skepticism towards ECT, thus the
patients could hardly sense the atmosphere of heightened expectations.
Patients who had responded well to ECT gradually deteriorated and returned to
their pre-ECT clinical condition, with the exception of one of two patients
who went on to have ECT-C. (A systematic long-term follow-up is currently
being carried out.) This observation is in accordance with that of other
authors ( 34).
Patients with satisfactory short-term response to ECT are potential
candidates for ECT-C or ECT-M. Recent case reports and case series observed
good results with ECT-M in TRS using an interval of 1 week to 1 month between
ECT sessions ( 17, 35-38). Two of our 15 patients had ECT-C but only one of
them maintained the improvement over 1 year, suggesting that ECT-C and ECT-M
might be useful for selected patients with otherwise intractable TRS.
The optimal number of ECT sessions in patients with schizophrenia remains
controversial. Kendell ( 22) noted that “it used to be widely believed that
schizophrenic patients usually needed between 12 to 20 ECT for maximum
improvement,” but he found no convincing evidence to support this belief.
Fink (personal communication, 1999) also suggested administering up to 20 ECT
sessions in case of clozapine-resistant schizophrenia. In our study, we aimed
to give up to 20 sessions of ECT unless there was a significant improvement
in mental state, or clinically noticeable memory impairment or other adverse
side effects. Seven of our 9 patients who eventually improved with ECT showed
at least some degree of improvement after 12 ECTs; 3 patients’ mental state
further improved when ECT was continued up to a maximum of 20 ECTs. Due to
the paucity of data concerning the number of ECTs in TRS and CRS,
psychiatrists have to rely on their clinical judgment, weighing the benefits
against the adverse effects in each individual patient.
Juarez-Reyes MG, Shumway M, Bacchetti P, et al. Effects of stringent
criteria on eligibility for clozapine among public mental health clients.
Psychiatr Serv 1995; 46:801-6.
Essock SM, Hargreaves WA, Dohm F, et al. Clozapine eligibility among state
hospital patients. Schizophr Bull 1996; 22:15-25.
Kane JM, Honigfeld G, Singer J, et al. and the Clozaril Collaborative Study
Group. Clozapine for the treatment-resistant schizophrenic. Arch Gen
Conley RR, Buchanan RW. Evaluation of treatment-resistant schizophrenia.
Schizopr Bull 1997; 23:663-74.
Daniel DG, Whitcomb SR. Treatment of refractory schizophrenic patient. J
Clin Psychiatry 1998; 59 (Suppl 1): 13-19.
Flynn SW, MacEwan GW, Altman S, et al. An open comparison of clozapine and
risperidone in treatment-resistant schizophrenia. Pharmacopsychiatry 1998;
Fink M. Is ECT a useful therapy in schizophrenia?In: Brady JP, Brodie HKH,
eds. Controversy in Psychiatry. Philadelphia, PA: WB Saunders & Co., 1978:
Fink M, Sackeim HA. Convulsive therapy in schizophrenia. Schizophr Bull
Royal College of Psychiatrists. The ECT Handbook. The Second Report of the
Royal College of Psychiatrist’s Special Committee on ECT. Freeman CP, ed.
London: Royal College of Psychiatrists, 1995.
Kuipers E. The management of difficult to treat patients with schizophrenia,
using non-drug therapies. Br J Psychiatry 1996; 169 (suppl 31): 41-51.
Shear MK. Case conferences from Cornell. Psychiatr Q 1978; 50:299-306.
Sajatovic M, Meltzer H. The effect of short term electroconvulsive treatment
plus neuroleptics. Convulsive Ther 1993; 9:167-75.
Green AI, Zalma A, Berman I, et al. Clozapine following ECT: A two-step
treatment. J Clin Psychiatry 1996; 55:388-9.
Benatov R, Sirota P, Megged S. Neuroleptic-resistant schizophrenia treated
with clozapine and ECT. Convulsive Ther 1996; 12:117-21.
Bhatia SC, Bhatia SK, Gupta SG. Concurrent administration of clozapine and
ECT: A successful therapeutic strategy for a patient with treatment-resistant
schizophrenia. J ECT 1998; 14:280-3.
Sharif ZA, Raza A, Ratakonda S, et al. Efficacy and safety of combining ECT
and clozapine in patients with treatment refractory schizophrenia. Schizophr
Res 1998; 29:163.
Chanpattana W, Chakrabhand ML, Sackeim HA, et al. Continuation ECT in
treatment-resistant schizophrenia: a controlled study. J ECT 1999; 15:178-92.
Tang WK, Ungvari GS. Electroconvulsive therapy in rehabilitation: the Hong
Kong experience. Psychiatr Serv 2001; 52:303-6.
Barnes TRE, McEvedy CJB. Pharmacological treatment strategies in the
non-responsive schizophrenic patient. Int Clin Psychopharmacol 1996; 11
(Suppl 2): 67-71.
Danziger L, Kendwall JA. Prediction of the immediate outcome of shock
therapy in dementia praecox. Dis Nerv Sys 1946; 7:229-303.
Baker AA. Bird G. Lavin NI, Thorpe JG. ECT in schizophrenia. J Ment Sci
Kendell RE. The present status of electroconvulsive therapy. Br J Psychiatry
Woerner M, Mannuzza S, Kane JM. Anchoring the BPRS: an aid to improved
reliability. Psychopharmacol Bull 1988; 24:112-17.
Hamilton M. Development of a rating scale for primary depressive illness. Br
J Soc Clin Psychol 1967; 6:278-96.
Zheng Y. Zhao J. Philips M, et al. Validity and reliability of the Chinese
Hamilton Depression Rating Scale. Br J Psychiatry 1988; 152:660-4.
Andreasen NC. The scale for assessment of negative symptoms (SANS). Br J
Psychiatry 1989; 155 (Suppl. 7): 53-8.
Endicott J, Spitzer R, Flies J. The Global Assessment Scale. Arch Gen
Psychiatry 1976; 33:766-71.
Guy W. ECDEU Assessment for Psychopharmacology. Washington, DC: HEW Public
Health Service, 1976:534-7.
Honigfeld G, Gillis RD, Klett CJ. NOSIE-30: a treatment-sensitive ward
behavior scale. Psychol Rep 1966; 19:180-2.
Ungvari GS, Chiu HFK, Lam LCW, et al. Gradual withdrawal of long-term
anticholinergic antiparkinson medication in Chinese patients with chronic
schizophrenia. J Clin Psychopharmacol 1999; 19:141-8.
James DV, Gary NS. Elective combined electroconvulsive and clozapine
therapy. Int Clin Psychopharmacol 1999; 14:69-72.
Kales HC, Dequardo JR, Tandon R. Combined electroconvulsive therapy and
clozapine in treatment-resistant schizophrenia. Prog Neuro-Psychopharmacol
Biol Psychiatry 1999; 23:547-56.
Kupchik M, Spivak B, Mester R, et al. Combined electroconvulsive-clozapine
therapy. Clin Neuropharmacol 2000; 23:14-6.
Frankenburg FR, Suppes T, Mc Lean PE. Combined clozapine and
electroconvulsive therapy. Convulsive Ther 1993; 9:176-80.
Lohr WD. Maintenance electroconvulsive therapy in schizophrenia. J Clin
Psychiatry 1994; 55:217-8.
Hoflich G, Kasper S, Burghof K, Scholl H, Möller H. Maintenance ECT for
treatment of therapy-resistant paranoid schizophrenia and Parkinson’s
disease. Biol Psychiatry 1995; 37:892-4.
Ucok A, Ucok G. Maintenance ECT in a patient with catatonic schizophrenia
and tardive dyskinesia. Convulsive Ther 1996; 12:108-12.
Chanpattana W. Maintenance ECT in schizophrenia: a pilot study. J Med Ass
Thai 1998; 81:17-24.
The Journal of ECT 2002; 18(2):90-94
Added: July 29, 2006 |
Vol 16 No 5
A shocking treatment?
A psychologist recently suggested that commenting on electroconvulsive therapy (ECT) was outside our arena of professional responsibility (Gelsthorpe, 1997). I disagree.
Although clinical psychologists do not prescribe ECT, those who work in adult mental health or with the elderly will inevitably be present at meetings in which ECT is suggested as an intervention, and may have patients who have been given it. ECT may be a factor in an assessment of memory or cognitive impairment. Physical treatments such as ECT convey important messages about the nature and causes of mental distress, which may contradict or undermine our psychological interventions. ECT may be a source of psychological trauma and distress in its own right. And, of course, any of us or our friends and relatives could one day be in the position of deciding whether to have ECT ourselves. We may also, after consideration of the evidence, feel that the administration of ECT involves ethical issues that transcend professional boundaries. For all these reasons, the use of ECT should be a matter of concern to all psychologists.
Still widely practiced
Contrary to popular belief, ECT is still widely practised; it was given to approximately 11,340 patients in England in 1999, compared with a peak of around 28,000 in 1985 (Department of Health, 1999.) Of these, two thirds were women, 41 per cent were over 65, and 15 per cent had ECT under section, or without consenting. It is rarely used in Italy, Japan, Germany, Slovenia, the Netherlands and Austria, and is used much less in many other European countries than in the UK.
A course of ECT consists of four to twelve individual treatments in which an electric current is passed through an anaesthetised patient’s brain, triggering an epileptic seizure (Royal College of Psychiatrists, 1995). ECT was introduced in the 1930s on the basis of an inaccurate belief that epilepsy and schizophrenia were incompatible conditions, and therefore, by a form of backward logic, inducing a seizure might cure psychosis. Ugo Cerletti, the Italian psychiatrist who is credited with the invention of ECT, gave a chilling account of the very first administration to a tramp, who broke out of his habitual incoherence to beg ‘Not another one! It’s murder!’ (Frank, 1978). Before muscle relaxants were used, fractured ribs and limbs were common.
Current psychiatric opinion is represented by the Royal College of Psychiatrist’s ECT Handbook (1995), which states that ‘ECT…is an effective treatment in severe depressive illness’ and occasionally also in other conditions such as psychosis and mania. In contrast, organisations like ECT Anonymous, along with many service users, have campaigned for the abandonment of an intervention that they describe as ‘barbaric and destructive’ (Lawson, 1992).
The use of physical interventions in mental distress is justified, at least partly, by the assumption that mental illnesses have some biological (biochemical or genetic) causal mechanisms. The great majority of ECT research, including the recent health technology appraisal of ECT commissioned by NICE (see weblinks), is situated firmly within this biomedical paradigm. But while it is obviously true that all emotional and psychological states have their physiological correlates, it is important to be clear that no hard evidence for primary causal factors in depression has ever been reliably identified. As David Healy has written, ‘there is no known lowering of serotonin in depression’ (Healy, 1998, p.8).
It is also important to note that no biological mechanisms for the action of ECT have been reliably established, although many have been proposed. Richard Abrams, author of the standard textbook Electroconvulsive Therapy, sums up the situation:
Modern ECT researchers…do not have any more of a clue to the relationship between brain biological events and treatment response in ECT than they did at the time of the first edition of this book – which is to say, none at all. (Abrams, 1997, p.268)
This means that statements such as that found in the Royal College of Psychiatrists (1997) factsheet – ‘Repeated treatments alter chemical messages in the brain and bring them back to normal’ – are, to say the least, purely speculative, and highly misleading when presented to patients (or anyone else) as established facts. We should also be careful about the terms ‘works’ and ‘treatment’. By definition, ECT cannot be a cure if we have not established either the biology of depression or ECT’s mechanism of action. Nor can it be described in any specific sense as a ‘treatment’ for depression, or for any other form of mental distress.
The above considerations also make it especially important to take service-user reports into account, especially if they say (as about one third of them do) that ECT is distressing to receive and has side-effects such as memory loss (Rogers et al., 1993; United Kingdom Advocacy Network, 1996). Unlike the case of, for example, chemotherapy, which also has side-effects and is distressing to receive, ECT cannot be justified on the grounds that it is effective at an underlying biological level. We are dealing here with mental states, not physical ones; and if people say that they feel worse after ECT, we have to accept that they are worse.
Does ECT help?
The use of ECT is justified, if at all, in empirical practice. Many psychiatrists claim that in their clinical experience ECT is effective or even life-saving, especially in severe depression. However, such assertions need to be backed up by research evidence, which is mostly lacking. Much of the research in this area is of very poor quality – failing, for example, to include follow-up periods or control groups (Clare, 1993). The picture is further clouded by the fact that papers are often quoted misleadingly or inaccurately – papers that are commonly quoted as support for ECT’s efficacy repay careful reading. For example, Greenblatt et al. (1964) appears to be the source of the common claim that ECT is effective in 8 out of 10 cases (made, for example, in an unreferenced statement in the Royal College of Psychiatrists’ 1997 factsheet on ECT). In fact, the response to ECT in this study was equalled by that to antidepressants.
The Royal College of Psychiatrists’ ECT Handbook states that it is established as an effective treatment, and quotes Buchan et al. (1992) in support. This careful study (generally considered to be the best set of trials yet) compared sham (that is, the procedure but with no seizure) and real ECT and followed patients up at four weeks and at six months. It concluded:
- ECT did have some beneficial effects, but only on those patients whose depression was accompanied by physical retardation or delusions (a very small minority of those who are diagnosed as depressed). In their words, ‘real ECT does not appear to be effective in non-retarded, non-deluded patients’ (p.359).
- This benefit was apparent at four weeks. At six months there was no difference between treatment and placebo groups.
Other trials (e.g. Gregory et al., 1985) confirm that benefits are short-term. A number of other reviews (e.g. Breggin, 1997; Cauchon, 1995a; Skrabanek, 1986) have generally been unable to find any controlled studies that showed benefits lasting longer than four weeks.
In summary, there is reasonable evidence that ECT can be effective, in the short term and within the provisos about ‘effectiveness’ outlined in the introductory points, for a small subsection of those who are severely depressed. But sound evidence for the effectiveness of ECT in other conditions is lacking. For example, a Cochrane review found only limited evidence to support its use in schizophrenia, the condition for which it was originally indicated (Tharyan & Adams, 2002). It is also widely acknowledged by psychiatrists that the relapse rate is high (Royal College of Psychiatrists, 1995), and there is no evidence that benefits last more than four weeks.
Does ECT prevent suicide, or death through refusal to eat?
ECT is sometimes given in the belief that the risk to the patient’s life will be reduced. There is, however, no hard evidence that ECT prevents suicide. The paper often quoted in support of this view (Avery & Winokur, 1976, p.1033) in fact states: ‘In the present study, treatment was not shown to affect the suicide rate.’Various other studies (Black et al., 1989; Fernando & Storm, 1984; Milstein et al., 1986) have also failed to find any reduction in suicide rates.
The idea that ECT may increase the risk of suicide has never, to my knowledge, been discussed in the literature. However, it must be borne in mind as a possibility. The most famous example is Ernest Hemingway, who told a friend: ‘What is the sense of ruining my head and erasing my memory, which is my capital?… It was a brilliant cure but we lost the patient.’ (quoted in Frank, 1978.) He killed himself a few weeks later. Biographers of Sylvia Plath have argued that fear of being given ECT again was a significant factor in her suicide (Rowley, 1998). The family of Joseph Docherty, who killed himself after warning staff that he did not want any more ECT, was recently awarded a large settlement (Daly, 1999).
The Buchan et al. (1992) study summarised earlier is relevant to the situation where patients are refusing food. They did find, as noted above, that very severely depressed patients had some short- term benefits from ECT. But an earlier version of the trials concluded that ‘many depressive illnesses, even if severe, may have a favourable outcome with intensive nursing and medical care even if physical treatments are not given’ (Johnstone et al., 1980). So it seems reasonable to offer alternatives to ECT even for the small number of people who may show short- term benefits from it – including those who are suicidal or are refusing food.
In any medical treatment the benefits must be weighed against the risks. In the case of ECT this means asking not only ‘Does it help?’ but also ‘Does it do harm?’
Can ECT do harm?
The practice of ECT has long been acknowledged to be unsatisfactory, even by those who see a place for it (Kendell, 1998). In the last 25 years the Royal College of Psychiatrists has carried out three large-scale surveys (Duffett & Lelliott, 1998; Pippard, 1992; Pippard & Ellam, 1981), but even the most recent one found that there were still serious deficits in the administration of ECT, with only one third of clinics meeting RCP guidelines. For example, staff were poorly trained and supervised, and some clinics used machines that did not allow a sufficiently wide range of current to be delivered, so that patients with a low seizure threshold, which can vary up to fortyfold between different people, were at risk of receiving too high a dosage.
This risk is particularly important given Pippard’s (1992) assertion that ‘cognitive function is liable to be more impaired the more the stimulus exceeds threshold’ (p.632). This amounts to an admission that cognitive impairment is currently unavoidable for an unknown number of ECT recipients. A former president of the Royal College of Psychiatrists has warned that this is a scandal waiting to erupt (Kendell, 1998).
The same survey indicates that twice as many ECT treatments are given per head of the population in the North West compared with London, while a previous survey found seventeenfold variations between different hospitals and even greater ones between different consultants (Pippard & Ellam, 1981). This suggests a lack of agreement about good practice with the possibility that many people are receiving ECT unnecessarily.
The issue of possible harm by the very nature of the intervention, even where guidelines are followed, is, of course, highly controversial. Despite the technical problems described above, it is asserted that ‘repeated studies over 50 years have failed to reveal any memory loss beyond the first few weeks’ (Freeman, 1992). The Royal College of Psychiatrists’ factsheet states that it is ‘among the safest medical treatments given under general anaesthesia’ and that ‘as far as we know [italics added] ECT does not have any long term effects on your memory or intelligence’. (The phrase I have italicised was added in the 1997 version.)
Critics of ECT have summarised a large body of evidence which, they say, has been overlooked, misrepresented or ignored (see e.g. Breggin, 1997; Frank, 1990; Friedberg, 1976; Morgan, 1991). They claim that general mental and emotional dysfunction, not just memory loss, is a consequence of ECT, and they cite evidence of abnormalities and brain damage from animal studies, human autopsies, human brainwave studies, MRI scans, case histories, memory tests, and so on. They point out that the idea that ECT causes brain damage was first introduced by its advocates, who considered that this was a price worth paying: ‘The evidence assembled from the various fields of investigation in regard to shock therapy points definitely to damage to the brain.’ (Freeman and Watts, quoted in Frank, 1978, p.17.) Some critics also point out that an accidental shock to the head strong enough to cause a convulsion, perhaps from a faulty domestic appliance, would normally be treated as a medical emergency (Breggin, 1997).
It is also worth noting that several studies have found increased mortality rates in ECT patients compared with patients not receiving ECT (Babigian & Guttmacher, 1984; O’Leary & Lee, 1996; Tsuang et al., 1979). While the precise reasons for this are unclear, it seems that any short-term benefit may be bought at the expense of higher long-term risk of death from various causes.
It is sometimes forgotten that the administration of ECT inevitably carries some risk of mortality if only because of the use of a general anaesthetic. In Texas, which keeps a record of all deaths that occur within 14 days of ECT, the mortality figures for the elderly stand at 1 in 200 (Cauchon, 1995b), mostly due to cardiac problems. These are important facts to set against the argument that ECT can be life- saving in elderly severely depressed patients, who are the largest group receiving it, both with and without consent.
What are the psychological effects of ECT?
Surveys show that 30–43 per cent of people find ECT helpful. However, up to a third of all those who undergo ECT report that it was a very distressing experience (Rogers et al., 1993; United Kingdom Advocacy Network, 1996). Recent research (Johnstone, 1999; MIND, 2001) shows that people may react to ECT with strong and enduring feelings of terror, shame, humiliation, failure, worthlessness and betrayal, and a sense of having been abused and assaulted. Some experience ECT as a damaging repeat of earlier traumas, including physical and sexual abuse. An underlying theme was a profoundly different understanding of depression to the professionals; these people believed that they had broken down for reasons which a physical intervention obviously could not address. They were left with their emotional difficulties compounded, and their trust in mental health professionals undermined.
How does ECT ‘work’?
In the absence of established theories about ECT’s mechanism of action, the question of how it works (in the cases where it does seem effective) becomes particularly important. Peter Breggin, an American psychiatrist and long-time opponent of ECT, has argued that its effects coincide precisely with the known sequelae of any trauma to the brain – the acute stage of confusion, headache and nausea, followed by a period of emotional shallowness, denial and artificial euphoria that usually wears off after four weeks. The loss of painful memories may also be experienced as a relief. He believes that it is this state that is sometimes mistaken, by staff and patients, for improvement. In this view – shared by others who oppose ECT – brain damage is not just a risk at a few clinics with outdated equipment, it is the basic mechanism of action in every case. ‘There can be no real disagreement about its damaging effects. The only legitimate question is: How complete is recovery?’ (Breggin, 1997, p.140.)
If the critics of ECT are right, then the decision to administer it becomes more complex than an evidence-based assessment of the risk–benefit ratio, such as that carried out by NICE. It becomes an ethical issue as well. In the words of neurologist John Friedberg:
Assuming free and fully informed consent, it is well to reaffirm the individual’s right to pursue happiness through brain damage if he or she so chooses. But we might well ask ourselves whether we, as doctors sworn to the Hippocratic Oath, should be offering it. (Friedberg, 1977, p.1013)
These sentiments have been strongly echoed by service users: ‘It is not justifiable to give people something that harms their brains and gives them an epileptic fit on the NHS. It’s just not, in my view, an ethical way to proceed’; ‘It is inhuman and inhumane’ (Johnstone, 1999, p.81).
Equally, if this is an ethical and not just a medical issue, it raises questions for all professionals working in psychiatry and mental health, not just doctors. At the very least we need to inform ourselves about this controversial practice and be willing to enter the debate.
■ Lucy Johnstone is Academic Tutor on the Clinical Psychology Doctorate, University of Bristol. E-mail: L.C.Johnstone@bristol.ac.uk.
Abrams, R. (1997). Electroconvulsive therapy (3rd edn). Oxford/New York: Oxford University Press.
Avery, D. & Winokur, G. (1976). Mortality rates in depressed patients treated with electroconvulsive therapy and anti-depressants. Archives of General Psychiatry, 33, 1029–1037.
Babigian, H.M. & Guttmacher, L.B. (1984). Epidemiological considerations in electroconvulsive therapy. Archives of General Psychiatry, 41, 661–672.
Black, D.W.,Winokur, G., Mohandoss, E., Woolson, R.F. & Nasrallah,A. (1989). Does treatment influence mortality in depressives? Annals of Clinical Psychiatry, 1(3), 166–173.
Breggin, P. (1993). Toxic psychiatry. London: Fontana/Collins.
Breggin, P. (1997). Brain-disabling treatments in psychiatry.NewYork: Springer.
Buchan, H., Johnstone, E., McPherson, K., Palmer, R.L., Crow,T.J. & Brandon, S. (1992).Who benefits from electroconvulsive therapy? British Journal of Psychiatry, 160, 355–349.
Cauchon, D. (1995a, 6 December). Stunningly quick results often fade just as fast. USA Today.
Cauchon, D. (1995b, 7 December). Patients often aren’t informed of full danger. USA Today.
Clare,A. (1993). Psychiatry in dissent: Controversial issues in thought and practice. London: Routledge.
Daly, M. (1999, 27 September). Electric shock victims win historic victory. The Big Issue,p.10.
Department of Health (1999). Electroconvulsive therapy: Survey covering the period from January 1999 to March 1999, England. Statistical Bulletin 1999/22. London: Author.
Duffett, R. & Lelliott, P. (1998).Auditing electroconvulsive therapy:The third cycle. British Journal of Psychiatry, 172, 401–405.
Fernando, S. & Storm,V. (1984). Suicide among psychiatric patients of a district general hospital. Psychological Medicine, 14, 661–672.
Frank, L.R. (Ed.) (1978). The history of shock treatment. San Francisco:Author. Frank, L.R. (1990). Electroshock: Death, brain damage, memory loss, and brainwashing. In D. Cohen (Ed.) Challenging the therapeutic state (pp.489–512). New York: Institute of Mind and Behavior.
Freeman, H. (1992, 14 December). [Letter to the editor]. The Independent.
Friedberg, J.M. (1976). Shock treatment is not good for your brain. San Francisco: Glide.
Friedberg, J.M. (1977). Shock treatment, brain damage, and memory loss:A neurological perspective. American
Journal of Psychiatry, 134, 1010–1014. Gelsthorpe, S. (1997). Conflict, collusion, co-operation and trying to be constructive. Clinical Psychology Forum, 103, 34–38.
Greenblatt, M., Grosser, G.H. & Wechsler, H. (1964). Differential response of hospitalised depressed patients to somatic therapy. American Journal of Psychiatry, 120, 935–943.
Gregory, S., Shawcross, C.R. & Gill, D. (1985).The Nottingham ECT Study. British Journal of Psychiatry, 146, 520–524.
Healy, D. (1998). Gloomy days and sunshine pills. Openmind, 90, 8–9.
Johnstone, E.C., Deakin, J.F.W., Lawler, P., Frith, C.D., Stevens, M., McPherson, K. et al. (1980, 20/27 December).The Northwick Park ECT Trial. The Lancet, pp.1317–1320.
Johnstone, L. (1999).Adverse psychological effects of ECT. Journal of Mental Health, 8(1), 69–85.
Kendell, R.E. (1998).What are royal colleges for? Psychiatric Bulletin, 22, 721–723.
Lawson, M. (1992, 17 December). [Letter to the editor].The Independent.
Milstein,V., Small, J., Small, I.F. & Green, G.E. (1986). Does ECT prevent suicide? Convulsive Therapy, 2, 3–6.
MIND (2001). Shock treatment:A survey of people’s experiences of ECT. London: Author.
Morgan, R.F. (Ed.) (1991). Electroshock:The case against.Toronto: IPI Publishing.
O’Leary, D. & Lee,A.S. (1996). Seven year prognosis in depression. British Journal of Psychiatry, 169, 423–429.
Pippard, J. (1992).Audit of electroconvulsive treatment in two national health service regions. British Journal of Psychiatry, 160, 621–637.
Pippard, J. & Ellam, L. (1981). Electroconvulsive treatment in Great Britain. British Journal of Psychiatry, 139, 563–568.
Rogers,A., Pilgrim, D. & Lacey, R. (1993). Experiencing psychiatry: Users’ views of services. London: Macmillan/MIND.
Rowley, R. (1998, Spring). Electroconvulsive treatment in Sylvia Plath’s life and work. Thumbscrew, 10, pp.1–9.
Royal College of Psychiatrists (1995). The ECT handbook. London:Author.
Royal College of Psychiatrists (1997). ECT (electroconvulsive therapy). Patient Information Factsheet no.7. London: Author.
Skrabanek, P. (1986). Convulsive therapy – A critical appraisal of its origins and value. Irish Medical Journal, 79(6), 157–165.
Tharyan, P. & Adams, C.E. (2002). Electroconvulsive therapy for schizophrenia (Cochrane Review). Cochrane Library issue 4. Retrieved 22 November 2002 from www.cochrane.org/cochrane/ revabstr/ab000076.htm
Tsuang, M.T., Dempsey, G.M. & Fleming, J.A. (1979). Can ECT prevent premature death and suicide in ‘schizoaffective’ patients? Journal of Affective Disorders, 1(3), 167–171.
United Kingdom Advocacy Network (1996, Spring/Summer). ECT survey. The Advocate, 1,p.24–28. References
Added: July 28, 2006 |
Full report from the UK on the usage of ECT. 2003
Note that the use of ECT in schizophrenia, based on the evidence, is not recommended. Someone might want to send the clue train to New York state hospitals.
Added: July 27, 2006 |
PR Newswire; 11/5/2004
NEW YORK, and WINSTON-SALEM, N.C., Nov. 5 /PRNewswire/ — The Committee for Truth in Psychiatry (CTIP) – a national organization of recipients of electroconvulsive therapy (ECT) – has challenged a new study from Wake Forest University, calling it scientifically worthless. The study claims that treatment with ECT improves patients’ quality of life and functioning.
“The author, W. Vaughn McCall, did not disclose that he is president of the ECT industry trade organization, the Association for Convulsive Therapy, which could bias his research towards minimizing the risks of ECT,” says CTIP director Linda Andre. McCall undertook his study after the British government recommended that ECT be used with caution because there is not enough good research on its effects on memory and quality of life. In a systematic review of existing research published in the British Medical Journal in 2003, England’s equivalent of the National Institute of Mental Health found that at least one out of three ECT patients suffers significant permanent memory loss.
CTIP says that financial and career conflicts of ECT researchers like McCall are behind the lack of quality research. “The real story, which you can’t get unless you read the study, is how they got those results; they asked about whether patients could function at the lowest levels imaginable,” says Andre. “It is not quality of life in any meaningful way.” Patients earn the highest possible scores on the questionnaires as long as they can get out of bed, feed and dress themselves, and use a toilet unaided instead of having bowel and bladder accidents.
But these are not the abilities affected by ECT. Rather, a significant number of ECT patients report permanent loss of memories of up to 20 years of their lives. They also report loss of skills and knowledge acquired prior to ECT, and permanent deficits in memory ability and cognitive function. Though the ECT industry has long claimed these deficits are imaginary, the British researchers disagreed.
“The McCall study compares apples to oranges,” says Andre. “I myself forgot my entire college education, and lost my ability to do graduate work and my career to ECT. But I can feed myself and even my cat, wipe my own behind, and get on a bus. By the standards of this study, my quality of life couldn’t be better.”
Added: July 26, 2006 |
Last Resort Therapy
The Record (Bergen County, NJ)
CORRECTION: An article about electroshock treatments that appeared in the Oct. 25 Health section incorrectly reported the name of the founder of the Committee for Truth in Psychiatry. The group was founded by Marilyn Rice. (PUBLISHED THURSDAY, NOVEMBER 10, 2005, PAGE A02.)
When most people think of electroshock therapy, they picture Jack Nicholson writhing in agony on a gurney in “One Flew Over the Cuckoo’s Nest,” but “Jane” has never seen the film.
The 52-year-old doctor from Morris County, reluctantly agreed to ECT (the procedure is now called electroconvulsive therapy) in February after her 30-year battle with manic depression had reached its terrible crescendo.
Medications no longer worked and the cocktail of drugs brought nighttime insomnia and daytime drowsiness. Tremors shook her hands, she gained 50 pounds, and her sex life evaporated.
“I don’t like to think about it, but I was really suicidal,” said Jane, whose mother is institutionalized with severe depression. Since then, she has had 16 treatments at University Hospital in Newark and said her lifelong depression has lifted.
“It basically saved my life,” she said.
ECT, which causes a grand mal seizure, has changed since its early days, when even proponents agree it was used on too many patients, in painful procedures. Now, patients who receive ECT are given anesthesia and muscle relaxants, which prevent broken bones and muscle injuries. The amount of electricity in most ECT treatments is about 800 milliamps, about one-fifth the power you would feel if you were shocked through your wall socket, doctors said.
Many psychiatrists admit memory loss is a serious potential side effect of ECT, but the treatment is often the last resort, when medications don’t work, for people who are severely depressed.
“ECT is the gold standard by which all anti-depression treatments are judged,” said Dr. Charles Kellner, who treated Jane. “It works better and faster than any other treatment.”
At Englewood Hospital and Medical Center, Dr. Charles Blackinton said those referred for ECT often can’t take drugs because of medical conditions or can’t tolerate the side effects.
“People are no longer willing to put up with partially remitted depression,” said Blackinton, who has been doing ECT at the hospital since 1964.
But while ads for anti-depressants are commonplace on TV, ECT has not escaped its association with psychiatry’s dark ages. Jane asked to remain anonymous because of the stigma.
ECT also has not shed its vocal critics, who insist success rates are overblown, that memory loss from ECT is more widespread than reported and that it is often irreversible.
“Neurologists are trying to prevent seizures because of the bad things that they do to the brain, while psychiatrists go out of their way to produce seizures,” said Dr. Peter Sterling, professor of neuroscience at the University of Pennsylvania School of Medicine. “It doesn’t make any sense to me.”
Despite the fact that ECT has been used in the United States for more than 50 years, no one knows exactly how it works or how many patients receive it each year.
The American Psychiatric Association estimates 100,000 patients get ECT annually – but doctors admit the figure is merely a guess because no government agency or outside group monitors or tracks ECT nationwide.
Englewood Hospital has seen a rise in ECT patients; from 142 in 2003 to 168 for the first eight months of 2005. At the University Hospital, which has had an ECT program for 2 1/2 years, about 26 patients have undergone ECT each year, including some who came from as far away as California.
While several states have laws that require reporting information on ECT patients, New Jersey does not.
Linda Andre, a freelance writer in New York City, founded the Committee for Truth in Psychiatry in 1984 to cope with her negative reaction to ECT.
She said she was coerced into ECT by family members. She said she has no memory of ever being depressed and that the treatment wiped out five years of memories.
“Your life is erased like it never happened. … It can be very difficult to live your life after that,” she said. Andre said her group has about 500 members nationwide, and all of them have experienced severe side effects from ECT.
She said she often hears former patients say doctors don’t adequately explain side effects and push people into the treatment.
One of the biggest hurdles Jane had to overcome before she agreed to ECT was the fact that her doctor couldn’t explain how it worked.
“I’m a scientist,” she said. “That was very hard for me to accept.”
It is not the electricity but rather the seizure caused by ECT’s current that is believed to be the key, said Kellner. One theory is that when the body releases neurotransmitters to “turn off” the seizure, those are the same brain chemicals that naturally help alleviate depression.
Backing up that theory is the fact that many of the most recent and most effective anti-depression drugs were first developed as anti-convulsants, Kellner said.
Dozens of studies have been done on ECT’s effectiveness with a wide range of success rates.
* In a 2005 study, 85 percent of patients reported a remission in their depression during ECT treatments and within a week of the course’s conclusion.
* Another study, from 2004, reported between 30 and 46 percent of patients interviewed within days of ECT reported that their depression had lifted.
* A 2001 study found that without follow-up medication, depression returned in 85 percent of patients within six months. Only 39 percent reported a relapse if they had medications.
ECT is a short-term solution, said researcher Dr. Vaughn McCall, editor of the Journal of ECT and the president of the Association for Convulsive Therapy, which has about 400 members worldwide.
“The first thing you have to do with a patient is disabuse them of the idea that this is a cure,” McCall said.
Just because ECT helps only in the short term does not mean it should be discounted, argued Kellner.
“If someone kills themselves because they couldn’t get well in the short term, then it doesn’t matter what would have worked in the long term,” he said.
ECT can pull a patient from the depths of a life-threatening depression quickly and long enough to allow time for medications to work, to find a proper cocktail, or to allow for a natural lifting of depression, McCall said. In some cases, patients rely on a “maintenance” ECT – having the treatments spread out for years.
“There’s no good answer for why drugs sometimes work after ECT when they didn’t work before,” said Englewood’s Blackinton.
Dr. Peter Breggin, author of the book “Toxic Psychiatry,” is likely the most well-known critic of ECT. He said the reason some patients show an improvement after ECT is precisely because of the damage caused to the brain.
“Patients are too numb, bewildered and confused to be anything, let alone depressed,” he said.
The other major hot button issue of ECT is memory loss. Supporters of ECT say memory loss is usually not permanent or extensive and generally involves impersonal memories like names of places.
“There are some reports of people with much more profound memory loss … we don’t understand why this happens, but it is quite rare,” said Kellner.
Critics say studies are tailored to weed out severe cases, and there is not enough follow-up on patients to give a real understanding of effects.
“All the studies are done by shock docs,” said Breggin. “I’d discount anything they have to say.”
In one study from 1986, patients wrote down an inventory of personal information and memories before ECT treatment and were asked the same questions again post-ECT.
Those with bilateral ECT – when electrodes are placed on both sides of the head – had forgotten about 30 to 40 percent of the information. Patients in a control group who did not have ECT forgot about 15 to 20 percent of the information.
Because of the problems with memory loss, researchers are looking for ways to induce seizures, or create similar brain chemistry, without electricity.
One way is through magnetic stimulation, which produces seizures in a more localized, specific part of the brain, said Dr. Sarah Lisanby, a researcher and practicing physician at Columbia University. Another technique is called Vargus Nerve Stimulation, which uses a small device implanted in the body that stimulates a nerve running through the neck to the brain.
One of Sterling’s arguments against ECT comes from how researchers are trying to promote these new treatments.
“In order to promote them, they’re pointing out the damage caused by ECT, the fact that it is safer than ECT, even though they had denied for years that ECT caused damage,” he said.
Lisanby noted that while ECT can have serious side effects, so do psychiatric medications.
“I’d like to see us as a field do a better job of communicating more accurate information about the benefits and risks of ECT as compared to other treatments,” she said. “I think that could help combat some of the stigma and lack of information on what ECT is.”
(SIDEBAR, page F01)
What the procedure entails
Most patients who have ECT have a course of therapy that includes six to 12 treatments, starting with three times a week.
* A patient who is referred for ECT undergoes a physical exam to ensure there is no neurological problem that could be causing depressive symptoms. Blood tests and spinal X-rays are taken to ensure the patient can tolerate the anesthesia and seizure caused by ECT.
* Doctors explain to the patient and family members side effects, including memory loss and cognitive difficulties. They are advised to have someone help at home after treatments, to refrain from driving, and to avoid major decisions.
* At the hospital, monitors are placed on the patient to track blood pressure, heart rate, oxygen content and brain waves. Gauze is inserted into the person’s mouth to prevent tooth damage. A general anesthetic is administered, and the ECT electrodes are placed on the scalp. In bilateral ECT, one is placed on each temple; in unilateral ECT, the electrode is placed on the top of the head near the right side.
* The electrical pulse lasts from half a second to eight seconds, and the patient undergoes a grand mal seizure, which can last from 25 seconds to 90 seconds. In many cases, because of the muscle relaxant given, the patient’s body barely moves.
* Once the patients awaken, usually after less than 10 minutes, they remain in a recovery area until they can be driven home or return to a psychiatric unit of a hospital.
Source: Dr. Charles Blackinton, Englewood Hospital
Added: July 26, 2006 |
LOS ANGELES: As of April 1, 2003, Medicare will cease all national coverage of “multiple seizure” electroshock treatments, after an investigation revealed the practice is unworkable and places patients at risk. The Center for Medicare and Medicaid Services (CMS) conducted the investigation after a December 2001 report by the Office of the Inspector General (OIG) found multiple seizure electroshock had “none of the claimed benefits and many risks,” including “profound confusional states.”
Also known as multiple monitored ECT (MMECT), Medicare has been paying out $500,000 a year for its use. On February 24 this year, CMS said that Medicare would no longer cover this practice, stating, “The clinical effectiveness of multiple-seizure electroconvulsive therapy [ECT] has not been verified by scientifically controlled studies…studies have demonstrated an increased risk of adverse effect….”
CMS also found that in the elderly population, the risk may be “several fold higher” than for “younger patients for severe confusion, falls, and cardiorespiratory complications.” The elderly are a key market for ECT. In Texas, one of the few states that keeps track of shock statistics, 65-year-olds get 360 percent more ECT than 64-year-olds because Medicare coverage takes effect at sixty-five.
In the 1960s, psychiatrists added muscle relaxants to modify the assault on the body. Today, the administration of ECT is a $3-5 billion a year industry in the United States with more than 100,000 Americans undergoing it, many involuntarily. Yet, a 2001 Colombia University study found ECT is so ineffective at ridding patients of their depression that nearly all of those who receive it relapse within six months of stopping treatment.
Added: July 25, 2006 |
This is an outline of a paper I gave at the 2001 Mental Health Statistics Conference (SAMHSA) in Washington, DC.
ECT Reporting – The Statistical Gap
Shortly before she left office as SAMHSA Director, Dr. Nelba Chavez spoke of the pockets of mental health research that existed. These were pockets of good, solid research, but she encouraged those in the field to push on and to try to close the enormous gaps that exist in research today.
The field of electroconvulsive therapy, or ECT, is littered with chasms where research simply does not exist. This paper will highlight those gaps, as well as propose new directions for ECT research.
The most basic question, how many people have ECT each year in the US, is not answerable. Researchers can estimate, and these estimates generally range from 100,000 to 200,000 persons per year. But precise numbers continue to evade us, and the last major study to undertake the question of how many patients in the US receive ECT annually was published in 1994. This study, “The Use of ECT in the United States” by JW Thompson et al, used estimates from the NIMH Sample Survey Program for 1975, 1980 and 1986 to conclude that ECT use dropped dramatically from more than 58,000 in 1975, to an estimated 36,558 patients in 1986.
A study in 1995 by Hermann used data from the American Psychiatric Association’s 1988-1989 Professional Activities Survey to estimate ECT use in 317 metropolitan statistical areas. Annual ECT use varied from 0.4 to 81.2 patients per 10,000 population.
While this was a engaging study, it relied entirely upon those APA members who responded to the survey, and their 4,398 patients treated with ECT. The authors concluded that the estimated national rate of ECT utilization would be 4.9 patients per 10,000 population, resulting in an estimate of 100,000 US patients treated with ECT in the year studied, 1988-89. So the first study concluded 36,500 patients were treated with ECT in 1986, and the second study estimated 100,000 patients treated two years later. It seems unlikely that the use of ECT in the United States would nearly triple in two years.
Thus, we come back to the question, just how many persons are treated with ECT each year? The answer is we don’t know.
This illustrates what many consider to be the biggest problem in contemporary ECT research – the lack of real data. There is no lack of research on ECT, with two professional journals devoted entirely to the subject. But as Dr. Chavez pointed out, the research exists in pockets. One of the biggest areas of research involves the continuing quest to prove the mechanism of action, just how ECT works. Despite millions of dollars and countless hours of research, a definite answer continues to elude scientists.
A few states have enacted legislation to help answer this question – and others. Those states include Massachusetts, Illinois, Vermont, Colorado, California and most notably, Texas. Two weeks ago, the Missouri State Senate rejected a statewide ECT reporting bill, calling it too controversial.
Indeed, the legislation passed in Texas has seen opposition along the way. The statute in Texas goes beyond mere reporting to include restrictions on the use of ECT on anyone under age 16, as well as limiting the number of treatments per patient, requiring a second opinion when used on the elderly and tighter control of involuntary ECT.
Many ECT practitioners and proponents fought the reporting law, but a report written by three prominent Texas psychiatrists last year called it source of valuable data and recommend a continuation of the reporting requirement. And, they call for additional rating instruments, including a patient self-report rating scale for symptom severity and memory impairment, as well as a longer follow-up period. Currently, Texas only requires a four-week post ECT follow-up.
How many people die annually from ECT? The American Psychiatric Association reports a figure of 1 in 10,000. While the Texas statistics don’t show a clear number since cause of death isn’t listed, a review of autopsy reports indicates a rate of closer to 1 in 450. Of course the state of Texas is not representative of the rest of the country because of its tighter regulations. Researchers should have better data than this. Having no way of knowing accurate numbers of patients treated each year, or the number of complications – this is unacceptable from a scientific standpoint.
There are several other areas of interest that arise from an analysis of the Texas data, including the high use of bilateral ECT, approximately 82 percent. This number conflicts with the widely-touted viewpoint that unilateral is used more often today because it causes fewer side effects.
We come back to the idea of pockets of great research, with enormous gaps we need to fill.
The wealth of data gathered in Texas over the last several years should be a model for a federal reporting system of ECT. Last summer, the National Mental Health Association announced in its policy statement that it advocates the establishment of a national data bank, operated under the oversight of the Center for Mental Health Services, requiring the scrupulous recording of all ECT given, with documentation and dissemination of results.
So the first order of business must be such a database and a federal ECT reporting law.
A second area of research that must be addressed is the area of memory research. There exist a variety of studies that examine memory issues in ECT patients. However, critics insist that the measures of memory loss are superficial and ignore major components of the system of memory.
Writing in Nature last year, neuroscientist Peter Sterling says: “Memory loss could be monitored by questioning patients before ECT about early events in their lives and then re-questioning them following each series of ECT. When this was done 50 years ago, memory losses were marked and prolonged. However, no effort has been made since to routinely perform this simple test.”
That study fifty years ago was done by Irving Janis, and remains the definitive study of the effects of ECT on memory. Janis interviewed 19 patients at length, and then interviewed them four weeks after ECT, attempting to obtain the same information. He gave the same interviews to controls who did not have ECT. Janis wrote “Every one of the 19 patients in the study showed at least several life instances of amnesia and in many cases there were from ten to twenty life experiences which the patient could not recall.”
Studies undertaken in the 70s and 80s added to Janis’ findings that ECT does, in fact, produce memory loss.
But contemporary researchers continue to maintain that ECT does not produce permanent memory loss and that such reports are either the result of patient misunderstanding, or the effects of the depression and not the ECT.
This has caused a great chasm between researchers and persons who identify themselves as ECT consumers and survivors. Even those who say they were glad they had ECT complain of memory loss and say they wish they had been told of the risks upfront.
Since the beginnings of ECT use, patients have complained of cognitive impairment and those complaints have remained consistent through present time. ECT patients and survivors alike have asked researchers to focus more upon these issues, but are told “it’s all in your head” and their complaints dismissed.
Anecdotal reports of success are welcomed and even published, yet the large body of anecdotal reports that focus upon the negative side of ECT are discarded, saying that anecdotal reports are not valid.
One of the biggest problems with the memory studies as performed today is that they do not use sensitive and elaborate testing, such as those used by de Mille to differentiate matched subgroups of fifty patients who were lobotomized in the 60s. Many so-called memory tests today simply use the Mini Mental State Exam to prove that no deficits occur. Critical researchers say it’s not difficult to find, but you must test for it, and they continue to say that contemporary studies are deliberately not testing for deficits they know will appear. In the study of permanent effects of ECT, testing such as that of de Mille should be made at intervals of a day, a week, a month and a year post-ECT.
Let’s return again to the Texas data.
I’d like to hand out the actual reporting form that is used in Texas.
There have been two major journal articles that have analyzed the data, one in the Journal of Forensic Sciences November 2000; the other in Journal of Clinical Psychiatry in 1998.
This does illustrate the problems associated with the treating ECT physician deciding for the patient and often not hearing any complaints. As you can see from the form, the doctor simply chooses a number from one to five. One of the journal authors does go on to suggest a patient self reporting form, and this would be a strong addition to the current collection of data.
(subjective nature of severity and memory impairment)
A federal database of these kinds of data would be extraordinarily valuable in providing tools with which researchers could evaluate ECT, and examine trends.
Consumer/survivor input into research studies is needed so that the issues that are important are no longer ignored. A research panel that is made up of consumer/survivors should be established, and it should direct some of the research. It should go beyond an advisory capacity and encourage consumer/survivors to lead the way and begin to research the issues that concern them.
As the saying goes, nothing about us without us and that saying applies to research. More than sixty years of being told “it’s all in your head” must change and consumer/survivors need access to research funds, as well as the accommodations necessary to give them the tools they need to perform valid, scientific research…concerning the issues that affect them.
Some very strong efforts are being made to include consumer/survivor voices in policy decisions, but an equal effort must be made in the research arena.
Another of the criticisms directed at ECT researchers is that the bulk of the research is conducted by the same group of people. They sit on the editorial boards of the journals and some have financial interests in the manufacturing companies. Allowing consumer/survivors a voice in these research projects, as well as the opportunity to provide some outside direction could help in overcoming some of the criticisms.
However, barring full inclusion into the research process, ECT consumer/survivors should be given the resources to do their own research, on those issues they feel have been continually ignored.
Animal studies are a third area of concern in the realm of ECT research.
The majority of studies on the effects of ECT on animals were done in the 40s and 50s. Numerous authors have called upon these studies as evidence that ECT does cause brain damage. Contemporary researchers dismiss the studies, saying they were done 50-60 years ago and are no longer valid due to problems in methodology and due to claims that the process of ECT is substantially different today. Yet researchers are not attempting to do similar studies using more modern machines and better scientific methods.
A review of Medline citations that involved the study of ECT and animals returned thousands of citations, leading at first glance to the belief that animal studies are being conducted. However, closer examination reveals that the criticisms are valid. The animal studies involve almost exclusively the continuing quest to discover how ECT works.
Surely some of this research money could be used to repeat the studies of earlier decades. Until a major animal study similar to that of Hans Hartelius in 1952 and many others like his, the disagreement will remain and the question never fully answered: Does ECT cause brain damage. Both sides of the controversy remain steadfast in their views, but good, solid animal studies are needed before the truth will ever be known. And to deflect the criticism that will definitely result from both sides, depending on the outcome, I would like to see several large, multi-disciplinary studies involving large animals, bringing in experts from outside the field of ECT.
ECT isn’t the only area where there exist research deficits of course. But it is very illustrative of an area of research that is closed to outsiders and where any criticism is continually deflected, despite six decades of consistent complaints.
And that brings us to the topic of anecdotal reports, a very problematic area for researchers.
When the FDA classified ECT devices in 1979 as the most dangerous and demonstrating an unreasonable risk of illness or injury, the American Psychiatric Association heavily lobbied the FDA to reclassify the machines as safe. The original classification would have required the industry to perform animal testing and prove its safety. However, ECT survivors organized and also lobbied the FDA. This resulted in over 1000 anecdotal reports to the FDA.
Because complaints are not taken seriously by ECT researchers, and never have been, anecdotal reports such as these are disregarded, saying they are not scientific evidence. However, it’s a Catch-22.
Patient complains and the treating physician dismisses the complaints saying the patient is either mistaken or so mentally ill, she doesn’t know what’s going on. In that way, the ECT industry has managed to disregard decades of complaints.
Kalinowsky and Hock wrote in their 1952 textbook that “All patients who remain unimproved after ECT are inclined to complain bitterly about their memory difficulties.”
The trend today has been to accept a few token stories about memory loss, provided the person says ECT saved my life. If the entire report is negative, i.e. it didn’t help and left me with damage, it goes back to the person being too mentally ill to understand what’s going on, or worse, simply a liar and troublemaker.
Additionally, anecdotal reports are acceptable when written as case reports, or when promoting the value of ECT. All of a sudden they count. Yet when ECT survivors try to draw upon their own experiences, you hear “Those are anecdotal and don/t mean anything.”
I’ve lost count of the anecdotal reports that I receive in email via the website I run. Obviously those can’t be said to be representative of the overall population of ECT users, but I do believe there is value in anecdotal reporting, especially when it seems that complaints will be continually ignored. Although I’ve never actually tabulated the emails I’ve gotten over the last few years or tried to count who had what, the majority of them talk openly about the devastating memory loss, the lack of resources for recovery, and dismissal by their doctors – even when they say ECT saved my life.
When I did a small study called Voices a few years ago, I was stunned to find that many patients become frustrated after ECT and their doctor’s rejection of their complaints…so frustrated that 75 percent of those – even those who reported good outcomes with ECT’s relief on depression – have moved on to a new doctor. Some of course left psychiatry altogether, but the majority became so angered that they found new doctors.
So we come back to the issue that there are all of these self reports and very few are listening. The FDA has its collection of reports that resulted when they considered reclassifying the devices. But I’m not sure that the role of the FDA as a regulatory agency is the most appropriate place to collect oral histories and anecdotes.
What I would like to see is a central database where people can share their stories, good and bad. It’s important that all voices be heard and that no one’s story be rejected or ridiculed. It’s an idea I’m considering on my own, simply because it needs to be done….kind of an ethnography of electroconvulsive therapy patients.
Finally, a lack of research in the area of recovery troubles me the most and it should be a priority. The needs of ECT patients are unique – not only do they have to continue the quest to keep depression away, they have needs that are not recognized by most.
The most common complaints after ECT are:
Inability to remember learned materials, and difficulty in relearning, or in learning new skills
Inability to concentrate on the job
There are many anecdotal reports of persons who had thriving careers, but post ECT have forgotten their skills.
There must be recognition from the medical and support communities of these problems, as well as research into recovery methods.
As it is, ECT patients use a system of trial and error, finding techniques that work. Sometimes they connect with others and share ideas.
I compare the recovery process to that of someone who has lost a limb. Once the deficits are recognized and accepted, the person must find ways of coping and find ways of favoring areas of their thinking processes that have not been affected. When a person loses a limb, it takes time to adapt and to find ways of managing without that limb. Eventually, the person learns to work around limitations and to find methods to assist in getting back to everyday life.
There are areas in ECT research where problems are still not recognized, despite 60 years of consistent reports and complaints. We must begin to recognize and accept that these problems do exist before we can take the necessary steps to correct the deficits in research.
As a beginning step towards data collection and better understanding of this complex issue, we need a reporting bill similar to that in the state of Texas, and we need it on a federal level. This is something that both sides of the controversy can sign onto and the very idea of a reporting bill should not be controversial. It should be matter of fact and acceptable to all.
Second, we need to address the gaps in research studies in the area of animal research and the effect of ECT on the brain. These studies should be done by a team of researchers that include scientists from outside the field of ECT, using experts from the field of neuroscience.
Third, we need to do a better job of studying memory deficits, and not limit the research to superficial testing. The testing should be rigorous and should also include researchers from outside the field of ECT who fully understand the complexities of memory.
Fourth, we must find a way to compile anecdotal reports to give credibility to the unheard voices of ECT. Instead of ridicule, ECT consumer/survivors demand respect for their experiences, and they deserve to be heard. This information must be made easily available to those considering ECT so that they’ll have a variety of viewpoints upon which to draw and make a more informed choice.
Fifth, we need to find ways to encourage independent consumer/survivor research, to bring together mentors from the research community and to drive research in areas that reflect consumer/survivor values.
Finally, we need to commit resources to the study of recovery for ECT patients. We must recognize the unique needs and find ways to provide rehabilitation and tools for recovery.
Added: July 24, 2006 |
20+ pages of information concerning Harold Sackeim’s application for continuing grant money for “Continuation Pharmacotherapy Following ECT.” Includes progress notes, statistics.
Want to prove his hypothesis that those who don’t respond well to meds also don’t respond well to ECT. (My comment: if you respond to meds, then why do you need ECT?)
High relapse rate, despite added medications.
Read full application:
Added: July 24, 2006 |