Electroconvulsive therapy: Difference between revisions
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* [[Dick Cavett]], TV host, In 1992 he wrote in People, <i>"In my case, ECT was miraculous. My wife was dubious, but when she came into my room afterward, I sat up and said, `Look who's back among the living.' It was like a magic wand."</i> |
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* [[Thomas Eagleton]], American politician |
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* [[Richard Brautigan]], American writer and poet |
* [[Richard Brautigan]], American writer and poet |
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Electroconvulsive therapy, also known as electroshock or ECT, is a type of psychiatric shock therapy involving the induction of an artificial seizure in a patient by passing electricity through the brain. Researchers do not understand how ECT affects the mental state, though patients with a variety of conditions have shown short-term improvement after the procedure. Large segments of the public came to view ECT in a negative light after several unfavorable depictions in popular books and films, and the treatment remains controversial.
ECT was first introduced as a treatment for schizophrenia in the 1930s, and quickly became adopted as a common treatment method for mood disorders—and as a dreaded mechanism for disciplining unruly psychiatric inpatients. Currently, in most countries, electroshock is administered under anaesthesia and muscle relaxants and continues to be used for the treatment of several, typically severe, psychiatric conditions, occupying a narrow but important niche in modern psychiatry. Electroshock without anaesthesia is referred to as "unmodified ECT" or "direct ECT", and is illegal in most countries.
Current usage
Currently ECT is mainly used to treat severe depression, particularly if complicated by psychosis (NIH & NIMH Consensus Conference, 1985; Depression Guideline Panel, 1993; Potter & Rudorfer, 1993). It is also used in cases of severe depression where antidepressant medication (sometimes in multiple courses), psychotherapy, or both have proven ineffective (refractory depression) (Potter et al., 1991; Depression Guideline Panel, 1993), when medication cannot be taken, or when other treatments would be too slow (for example, in a person with delusional depression and intense, unremitting suicidal tendencies). Specific indications include depression accompanied by a physical illness or pregnancy, which renders the use of the usually preferred antidepressants dangerous to the patient or to a developing fetus. Under such circumstances, carefully weighing risks and benefits, some psychiatrists consider ECT to be the safest treatment option for severe depression. It is also sometimes used to treat the manic phase of bipolar disorder and in the uncommon condition of catatonia.
Recent epidemiological surveys in the United States show that the modern use of ECT is generally limited to evidence-based indications (Hermann et al., 1999). Indeed, concern has been raised that in some settings, particularly in the public sector and outside major metropolitan areas, ECT may be underutilized due to the wide variability in the availability of this treatment across the country (Hermann et al., 1995). Consequently, minority patients tend to be underrepresented among those receiving ECT (Rudorfer et al., 1997).
ECT should be administered under controlled conditions, with appropriate personnel (Rudorfer et al., 1997) and some mental health laws mandate this.
Overview
The aim of ECT is to induce a bilateral grand mal seizure (with contractions and twitching of both sides of the body) which lasts at least 60 seconds.
Before the discovery of muscle relaxants, ECT was given unmodified. The patients were rendered instantly unconscious by the electrical current but the strength of the muscle contractions from the electricity and the subsequent fit at times led to complications such as compression fractures of the spine or damage to the teeth. Muscle relaxants allow a modified fit where the strength of the contractions is minor or even nonexistent. However, the use of muscle relaxants requires that the patient is first given a general anaesthesia to prevent the patient from experiencing the very uncomfortable state of being paralysed. The end result is that the patient drifts off to sleep and wakes up a short time later unable to recall the details of the procedure.
To induce the seizure, short bursts of a fixed current (typically 0.9 A) are passed through electrodes applied to the scalp at specific points using a gel, paste or saline solution to prevent burns to the skin. Modern ECT machines regulate the current to keep it constant and thus the voltage may vary up to a maximum, typically 450 V, but is usually around half that level in most cases. Modern machines are usually set in joules. The ECT therapist tries to keep the total energy as low as possible by restricting the strength and duration of the shock. The existence of the seizure is confirmed by observation or by EEG neuromonitoring[1].
Electrical current flows between two electrodes placed on the scalp, usually from temple to temple in the past, though these days ECT is more commonly applied to the non dominant hemisphere of the brain. Placement of both stimulus electrodes on one side of the head ("unilateral" ECT), over the nondominant (generally right) cerebral hemisphere, results in delivery of the initial electrical stimulation away from the primary learning and memory centers. If unmodified, the resultant seizure is characteristically more severe than a naturally occurring epileptic seizure. The production of an adequate, generalized seizure using the proper amount of electrical stimulation is required for therapeutic efficacy (Sackheim et al 1993).
Following the seizure, there is a short period of time during which cortical electrical activity in the brain ceases and an EEG reading is flat. After treatment, patients have no memory of the seizure or events immediately preceding it.
Therapeutic ECT is usually administered as a course of 6 to 12 treatments, administered at a rate of three times per week, on either an inpatient or outpatient basis. Studies have shown that each fit must be separated by a day at least.
The exact mechanisms by which ECT exerts its effect are not known, but studies show that repeated applications have effects on several kinds of neurotransmitters in the central nervous system. ECT seems to sensitize two subtypes of serotonin receptor (5-HT receptor), thereby strengthening signaling. ECT also decreases the functioning of norepinephrine and dopamine inhibiting auto-receptors in the locus coeruleus and substantia nigra, respectively, causing more of each to be released (Ishihara & Sasa 1999).
One study in The Journal of ECT suggests that "long-term ECS increases the expression of brain-derived neurotrophic factor (BDNF) and its receptor, TrkB, in limbic brain regions." (Duman RS, Vaidya VA., 1998)
Types of ECT
Two basic forms of ECT exist: bilateral and unilateral. The first form can be further subdivided into bitemporal and bifrontal ECT.
In bitemporal ECT, the current is passed across the temporal lobes, with an electrode being placed on either side of the head. With unilateral ECT, the electrodes are only placed on the right side of the head, to pass the current primarily through the right temporal lobe.
According to several controlled trials, unilateral ECT is associated with virtually no detectable, persistent memory loss (Horne et al., 1985; NIH Consensus Conference, 1985; Rudorfer et al., 1997). However, most clinicians find unilateral ECT less potent and more slowly acting an intervention than conventional bilateral ECT, particularly in the most severe cases of depression or mania. One approach that is sometimes used is to begin a trial of ECT with unilateral electrode placement and switch to bilateral treatment after about six treatments if there has been no response.
Research has demonstrated that the relationship of electrical dose to clinical response differs depending on electrode placement; for bilateral ECT, as long as an adequate seizure is obtained, any additional dosage will merely add to the cognitive toxicity, whereas for unilateral electrode placement, a therapeutic effect will not be achieved unless the electrical stimulus is more than minimally above the seizure threshold (Sackeim et al., 1993).
Even a moderately high electrical dosage in unilateral ECT still has fewer cognitive adverse effects than bilateral ECT. On the other hand, high-dose bilateral ECT may be unnecessarily risky and may be a preventable cause of severe memory impairment.
Bifrontal ECT is a modified form of bitemporal ECT in which the electrodes are placed 2 inches above the lateral angle of each orbit. It has been shown to have fewer adverse effects on memory than bitemporal, and to increase blood flow to the prefrontal cortex (Blumenfeld et al 2003).
Side effects and complications
Template:TotallyDisputed-section
Side-effect profile
Much of the accepted risk of electroshock arises from the use of general anesthesia. There is much disagreement over the other risks of electroshock.
The most common adverse effects are confusion and retrograde memory loss for events surrounding the period of ECT treatment. Some of the confusion and disorientation seen upon awakening after ECT clear soon after electroshock.
More persistent memory problems are variable and difficult to quantify. Some studies have shown that up to one third of patients report significant memory loss after treatment. Most typical with standard, bilateral electrode placement (one electrode on each side of the head) has been a pattern of loss of memories for the time of the ECT series and extending back an average of 6 months, combined with impairment with learning new information, which continues for perhaps 2 months following ECT (NIH & NIMH Consensus Conference, 1985). There have been no longterm (six months post-ECT or more) studies of cognition, memory ability, and memory loss done in the past two decades, coinciding with the time period when the available NIMH grant money has been monopolized by those with longstanding financial ties to the device manufacturers, especially Sackeim (Sackeim, March 14, 2004; deposition in the case of Akkerman v. Johnson, in which he states both that he has never followed up patients longer than two months and that he has worked as a consultant for the manufacturers since the mid-1980s). However,every longterm study which has been done has confirmed permanent amnesia (for instance, Janis, 1951; Squire, 1983; Weiner, 1986.) Calev, 1994 (not a study) surveyed the literature and concluded that patients must be warned of possible nonmemory cognitive deficits, since "they are not going to function well on more tasks than they anticipate". At least one-third of ECT patients experience permanent memory loss, according to a systematic review in 2003 (Rose, 2003)[2]. There is no evidence to support the industry's claim that most patients return to full functioning following successful ECT, and considerable evidence that many patients do not (FDA, Docket #82P-0316; Pedler, 2000; SURE (Service User Research Enterprise, 2002)). Formal neuropsychological testing has documented permanent neuropsychological deficits in former ECT patients (FDA, Docket #82P-0316), including an IQ loss of greater than 30 points (Donahue, 1999; Andre, 2001; Cott, 2004). The degree of impairment and resulting impact on functioning are highly variable across individuals (NIH & NIMH Consensus Conference, 1985; CMHS, 1998). Electroshock has a number of critics, including scientists, former psychiatric patients, human rights lawyers and civil libertarians, who are opposed to electroshock on the grounds that there is enough evidence, after 60 years, that patients' memories are permanently and severely damaged by the procedure to justify a moratorium (at least until sound and non-financially conflicted research is done into its effects on the brain).
Dozens of human and animal studies confirm that ECT is associated with a plethora of brain abnormalities (Ebaugh et al, 1942; Gralnick, 1944; Jetter, 1944; Meyer et al, 1945; Sprague and Taylor, 1948; Will and Rehfeldt, 1948; Martin, 1949; Riese and Fultz, 1949; Liban et al, 1951; Corselis and Meyer, 1954; Madow, 1956; Faurbye, 1942; Maclay, 1953; Matthew and Constan, 1964; Barker and Barker 1959; Alpers,1942; Bjerner, 1944; Hartelius, 1957; Ferraro et al, 1946; Ferraro et al, 1949; Heilbrun, 1941; Heilbrunn, 1942, 1943; Neuberger, 1942; Lidbeck, 1944; McKegney and Panzetta, 1963, etc.) ECT proponents such as Sackeim (in a 1994 review article) and Weiner (who wrote his in 1984) ---both of whom work for shock machine company Mecta (see Sackeim's 2004 deposition, Weiner's deposition and testimony in the same case, the testimony of Mecta owners and employees, and the credits given to each in the Mecta manuals) ---dismiss the work done in the 1940s and 1950s, alleging that today's ECT is different. But the differences only make the procedure more brain-toxic, not less. Anesthesia and muscle-paralyzing drugs increase the risks of the procedure and thus its mortality rate (Baker and Baker 1959; Novello, 1974; Impastato, 1957). The industry's claims that oxygenation prevents against brain damage and thus makes the results of some earlier studies irrelevant is specious, because even its most vocal spokesman (Sackeim again, 2004) does not agree with this and does not always oxygenate his own patients: "They don't turn blue". Therefore, some of the earlier studies in which animals are not oxygenated are far from outdated. Also, in the 1940s and 1950s, ECT devices were far less powerful than those in use today (Cameron, 1994), so once again, today's machines would be even more likely to cause brain damage than those shown to do so in the early studies.
Breggin's work includes a useful summary of the animal and human brain studies to 1979 Peter Breggin[3].
More recent work confirming brain atrophy, lesions, and other abnormalities associated with so-called modern ECT includes Templer and Veleber, 1982; Colon and Notermans, 1975; Weinberger et al,1979; Calloway et al, 1981; Templer et al, 1973; Shah et al, 2002; Diehl et al, 1994; Marcheselli et al, 1996; Andreasen et al, 1990; Dolan et al, 1986; and Figiel et al, 1990.
The decision to use ECT must be evaluated by each individual, weighing the potential benefits and known risks of all available and appropriate treatments in the context of informed consent (NIH & NIMH Consensus Conference, 1985), free of coercion and veiled threats (i.e., "If you do not sign the form you will not ever be released.") Studies published in 2004 and 2005 showed that half of ECT patients did not feel they could refuse the treatment (Philpot, 2004; Rose, 2005).
The muscle relaxants used during ECT can produce generalised but mild aches in the muscles after waking.
Contraindications
Some psychiatric researchers contend that there are virtually no absolute health contraindications precluding the use of ECT where warranted (Potter & Rudorfer, 1993; Rudorfer et al., 1997), i.e. where the treating psychiatrist, often at his sole discretion but frequently in consultation with a multidisciplinary team, decides that the benefits outweigh the risks of the procedure.
Use in combination with medications
Some types of medication, such as lithium, can add to confusion and cognitive impairment when given during a course of ECT and are best avoided. Medications that raise the seizure threshold and make it harder to obtain a therapeutic effect from ECT, including anticonvulsants and some minor tranquilizers, may also need to be tapered or discontinued.
Device Risk
The United States Food and Drug Administration has classified the devices used to administer ECT as Class III medical devices[4] (Federal Register, 1979). Class III is the highest-risk class of medical devices. The risks of ECT, according to the FDA, include brain damage and memory loss. (Federal Register, 1978).
Effectiveness
Some studies — later confirmed in controlled clinical trials which included the use of simulated or "sham" ECT as a control (Janicak et al., 1985), have determined ECT to be highly effective against severe depression, some acute psychotic states, and mania (Small et al., 1988).
No controlled study has shown any other treatment to have superior efficacy to ECT in the treatment of depression (Janicak et al., 1985; Rudorfer et al., 1997). ECT has not been demonstrated to be effective in dysthymia, substance abuse, anxiety, or personality disorders. The foregoing conclusions, and many of those discussed below, are the products of review of extensive research conducted over several decades (Depression Guideline Panel, 1993; Rudorfer et al., 1997) as well as by a panel of scientists, practitioners, and consumers (NIH & NIMH Consensus Conference, 1985).
Although the average 60 to 70 percent response rate seen with ECT is comparable to that obtained with pharmacotherapy, there is evidence that the antidepressant effect of ECT occurs faster than that seen with medication, which supports the use of ECT in cases where depression is accompanied by potentially uncontrollable suicidal ideas and actions (Rudorfer et al., 1997). However, ECT does not exert a long-term protection against suicide. Indeed, it is now recognized that a single course of ECT should be regarded as a short-term treatment for an acute episode of illness. To sustain the response to ECT, continuation treatment, often in the form of antidepressant and/or mood stabilizer medication, must be instituted (Sackeim, 1994). "Maintenance ECT" as it is called, refers to indefinite periods of recurring electroshock treatments, usually scheduled a few weeks apart. Critics of electroshock assert that the reason maintenance electroshock is required is because the brain requires approximately four weeks to recover from each closed head injury caused by eletroshock treatment. Thus, when the brain has healed, the temporary euphoric effects are lost and the brain must be electroshocked again and again to attain the previous mood level gain.
Individuals who repeatedly relapse following ECT despite continuation medication may be candidates for maintenance ECT, delivered on an outpatient basis at a rate of one treatment weekly to as infrequently as monthly (Sackeim, 1994; Rudorfer et al., 1997).
Informed consent
Informed consent is an integral part of the ECT process (NIH & NIMH Consensus Conference, 1985). The potential benefits and risks of this treatment, and of available alternative interventions, should be carefully reviewed and discussed with patients and, where appropriate, family or friends. Prospective candidates for ECT should be informed, for example, that its benefits are short-lived without active continuation treatment, and that there may be some risk of permanent severe memory loss after ECT. Active discussion with the treatment team, possibly supplemented by the growing amount of printed and videotaped information for consumers, is thought by some to be advisable in the decision-making process both prior to and throughout a course of ECT. Theoretically, in most jurisdictions, consent may be revoked at any time during a series of ECT sessions.
Involuntary ECT
Procedures for involuntary ECT vary from country to country depending on local mental health laws. Legal proceedings are required in some countries whilst in others ECT is seen as another form of treatment that may be given involuntarily as long as legal conditions are observed.
In the United States, involuntary ECT may not be initiated by a physician or family member without a judicial proceeding. In every state, the administration of ECT on an involuntary basis requires such a judicial proceeding at which patients may be represented by legal counsel. As a rule, such petitions are granted only where the prompt institution of ECT is regarded as potentially lifesaving, as in the case of a person who is in grave danger because of lack of food or fluid intake caused by catatonia.
Australian states take the other approach and the law regards involuntary treatment with ECT in the same light as any other involuntary treatment. There is an appeal process available for patients and relatives. This position facilitates the expedited use of ECT in emergencies.
In England and Wales, in the United Kingdom, the Mental Health Act 1983 allows the use of two electroconvulsive therapies in a life-threatening situation, at the discretion of the treating psychiatrist. This is most commonly invoked in the case of a patient who has stopped drinking fluids whilst suffering from a severe depressive illness. Further ECT, or involuntary ECT in less urgent circumstances, must be authorised by an independent psychiatrist, who, if in agreement, will usually give consent for a total of twelve ECT.
Continuation phase therapy
Successful acute phase antidepressant pharmacotherapy or ECT should almost always be followed by at least 6 months of continued treatment (Prien & Kupfer, 1986; Depression Guideline Panel, 1993; Rudorfer et al., 1997). During this phase, known as the continuation phase, most patients are seen biweekly or monthly.
The primary goal of continuation pharmacotherapy is to prevent relapse (i.e., an exacerbation of symptoms sufficient to meet syndromal criteria). Continuation pharmacotherapy reduces the risk of relapse from 40-60 percent to 10-20 percent (Prien & Kupfer, 1986; Thase, 1993). Relapse despite continuation pharmacotherapy might suggest either nonadherence (Myers & Branthwaithe, 1992) or loss of a placebo response (Quitkin et al., 1993a).
A second goal of continuation pharmacotherapy is consolidation of a response into a complete remission and subsequent recovery (i.e., 6 months of sustained remission). A remission is defined as a complete resolution of affective symptoms to a level similar to healthy people (Frank et al., 1991a). As residual symptoms are associated with increased relapse risk (Keller et al., 1992; Thase et al., 1992), recovery should be achieved before withdrawing antidepressant pharmacotherapy.
Many psychotherapists similarly taper a successful course of treatment by scheduling several sessions (every other week or monthly) prior to termination. There is some evidence, albeit weak, that relapse is less common following successful treatment with one type of psychotherapy—cognitive-behavioral therapy—than with antidepressants (Kovacs et al., 1981; Blackburn et al., 1986; Simons et al., 1986; Evans et al., 1992). If confirmed, this advantage may offset the greater short-term costs of psychotherapy.
Historical usage
ECT was developed in the 1930s by Italian neurologist Ugo Cerletti. Cerletti saw electric shocks given to hogs before slaughter. This rendered them unconscious but did not kill them. Cerletti found such electric shocks caused his obsessive and difficult mental patients to become meek and manageable.
When ECT was first instituted, the procedure was performed on fully conscious patients, without the use of anesthesia or muscle relaxants. The patient lost consciousness during the application of the current, and experienced powerful and violently uncontrolled muscle movement. Patients would often break bones, especially vertebrae, and pull muscles from the violent convulsions induced by the seizure. Patients grew to dread the procedure, and it was commonly employed as a means of punishment and sedation for difficult patients in psychiatric hospitals.
With the development of effective medications for the treatment of major mental disorders a half-century ago, the need for ECT lessened, but did not disappear. Prior to that time, ECT often had been administered for a variety of conditions for which it is now generally regarded as ineffective, for example, the treatment of schizophrenia.
Advances in treatment technique over the past generation have enabled a reduction of adverse cognitive effects of ECT (NIH & NIMH Consensus Conference, 1985; Rudorfer et al., 1997). Nearly all ECT devices deliver a lower current, brief-pulse electrical stimulation, rather than the original sine wave output; with a brief pulse electrical wave, a therapeutic seizure may be induced with as little as one-third the electrical power as with the older method, thereby reducing the potential for confusion and memory disturbance (Andrade et al., 1998). Ultra-brief pulse, higher frequency and longer stimulus duration also contribute to ECT effectiveness while minimizing the adverse cognitive effects.
Controversy
In general, but with a small number of exceptions, there is some degree of consensus within the field of psychiatry as to the benefits of ECT. However, ECT remains a topic that can generate much debate in both the field of psychology and among the general public. While its effectiveness has been demonstrated by numerous controlled trials, a large number of people within and outside the field regard it as inhumane and primitive — even barbaric. Opponents claim that the mechanism through which electroshock creates changes in mental state is nothing more than the destruction of brain cells, and even proponents are not quite sure how it works. Many patients who have undergone ECT claim it caused their subsequent mental state to improve; many others think their ECT treatments did more harm than good, and some actively campaign to have the treatment legally banned.
Antipsychiatry believes that, for the most part, there are no real mental illnesses and that ECT is used to suppress certain behaviors which, although perhaps uncommon, are still within the normal range. (See: Retraumatizing the victim, Alan Turing, Rosemary Kennedy for an example).
Anti-electroshock activists allege that patients are rarely, if ever, told the complete truth about the relative risks and benefits of electroshock[5]. To this end, and to demonstrate what would be required to fully satisfy the legal obligation for 'informed consent', one psychiatrist has formulated his own 'consent form'[6] using the Texas Legislature[7] as a model. Also, consumers should note that printed or videotaped materials regarding ECT may be commissioned for and provided by the manufactures of the equipment used to deliver the treatment, and so the possibility of this information leaning towards confirmation bias should be considered. Some question the effects of drugs on the ability to give informed consent.
The use of ECT has been banned in the Republic of Slovenia.
Cultural Depictions of ECT
Electroconvulsive therapy has been depicted, often in a negative light, in several films, books, and songs since its development.
A great deal of anti-ECT sentiment was generated by its unfavorable depiction in the 1975 movie One Flew Over the Cuckoo's Nest, based on a novel by Ken Kesey, which in turn was based loosely on the author's own experiences in various mental hospitals during the 1960s. In the film, the patient are seen receiving ECT which is unmodified, i.e. given without muscle relaxants or anesthesia, a practice which is now illegal in most countries.
In the film Girl, Interrupted, Angelina Jolie's character runs away from a mental hospital because she is being given what she calls "shocks." Other negative depictions can be found in the books Zen and the Art of Motorcycle Maintenance and The Bell Jar, as well as the films Requiem for a Dream and "The Sleep Room" (a movie based on MK Ultra and Ewan Cameron). An episode of the NBC TV drama Law & Order entitled "Cruel and Unusual" also featured negative depictions of ECT.
The U2 song "Electric Co." from the album Boy is an anti-electroconvulsive therapy anthem. It is about the widespread use of electroconvulsive therapy in Ireland's state hospitals in the 1970s, and was reportedly written in response to the treatment's use on one of their close friends.
Research into treatments
There is current research in using Magnetic stimulation therapy (MST) as an alternative to ECT although presently it seems to be somewhat less effective. Dietary omega-3 fatty acids and sleep deprivation are also being researched. Vagus nerve stimulation therapy is another alternative to ECT.
Famous people who have undergone ECT
- Louis Althusser, French philospher
- Antonin Artaud, French playwriter
- Frances Farmer, American cinema actress
- Ernest Hemingway (committed suicide shortly after ECT treatment at the Mayo Clinic in 1961-- reported to have said to his biographer A.E. Hotchner, "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....")
- Pat Ingoldsby, Irish poet
- Robert Pirsig -- his experiences, somewhat fictionalized, are mentioned in his Zen and the Art of Motorcycle Maintenance: An Inquiry into Values
- Sylvia Plath, American poet
- Dory Previn, American poet, writer and lyricist
- Cole Porter, American composer and musician
- Robert Lowell, American poet and writer
- Paul Robeson, American actor
- Lou Reed, rock musician
- Vivien Leigh, British actress
- Clara Bow, American actress
- Gene Tierney, American actor
- Vladimir Horowitz, pianist
- Oscar Levant, pianist
- Dick Cavett, TV host, In 1992 he wrote in People, "In my case, ECT was miraculous. My wife was dubious, but when she came into my room afterward, I sat up and said, `Look who's back among the living.' It was like a magic wand."
- Thomas Eagleton, American politician
- Richard Brautigan, American writer and poet
Source
- Sections of this article were copied word for word from a public domain document Mental Health: a report of the Surgeon General, online at http://www.surgeongeneral.gov/library/mentalhealth/chapter4/sec3_1.html#treatment
The objectivity and scientific integrity of this Surgeon General's Report have been widely criticized: see for instance http://www.ctvip.org/surgeongeneral.html
Criticisms of the ECT section in particular include the limiting of references to only a few writings of financially conflicted researchers, one of whom was cited fourteen times out of a total of seventeen references, and the fact that the editor of this section, Matthew Rudorfer (a known advocate of ECT) cited to himself twelve times.
References
- ^ Diana Rose, senior researcher, Pete Fleischmann, researcher, Til Wykes, professor, Morven Leese, statistician, Jonathan Bindman, senior lecturer (2003). "Patients' perspectives on electroconvulsive therapy: systematic review". British Medical Journal. 326 (7403): 1363.
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- ^ http://www.capitol.state.tx.us/statutes/docs/HS/content/word/hs.007.00.000578.00.doc.
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- ^ Rose D, Wykes T, Bindman J, Fleischmann P (2005). "Information, consent and perceived coercion: patients' perspectives on electroconvulsive therapy". British Journal of Psychiatry. 186 (1): 54–59.
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- Abrams R, Taylor MA. Anterior bifrontal ECT: a clinical trial. Br J Psychiatry. 1973 May;122(570):587-90. PMID 4717031.
- Blumenfeld H, McNally KA, Ostroff RB, Zubal IG. Targeted prefrontal cortical activation with bifrontal ECT. Psychiatry Res. 2003 Jul 30;123(3):165-70. PMID 12928104.
- Calloway SP, Dolan RJ, Jacoby RJ, Levy R. ECT and cerebral atrophy. Acta Psychiatrica Scandinavica 1981; 64: 442-445. PMID 7347109.
- Cerletti U, Bini L. L'Elettroshock. Arch gen neurol psichiat psicoanal 1938;19:266-268.
- Dolan et al. The cerebral appearance in depressed patients. Psychological Medicine 1986; 16: 775-779. PMID 3823294.
- Freeman CP, Weeks D, Kendell RE. ECT II: Patients who complain. Br J Psychiatry 1980; 137:8-16. PMID 7459536.
- Rose D, Wykes T, Bindman J, Fleischmann P (2005). Information, consent and perceived coercion: patients' perspectives on electroconvulsive therapy. British Journal of Psychiatry 186: 54-59. Fulltext.
- Shah PJ, Glabus MF, Goodwin GM, Embeier KP. Chronic, treatment-resistant depression and right fronto-striatal atrophy. British Journal of Psychiatry 2002; 180: 434-440. Fulltext
- SURE (Service User Research Enterprise). Review of Consumers' Perspectives on Electroconvulsive Therapy. London: Department of Health, January 2002.
Andre L (2001, May 18). Testimony at the public hearing of the New York State (U.S.) Assembly Standing Committee on Mental Health on electroconvulsive therapy.
Andreasen et al. MRI of the brain in schizophrenia. Archives of General Psychiatry 1990; 47: 35-41.
Barker J, Baker A. Deaths associated with electroplexy. Journal of Mental Science 1959; 105: 339-348.
Calev A. Neuropsychology and ECT: past and future research trends. Psychopharmacology Bulletin 1994; 30(3): 461-464. PMID 7878183
Calloway SP, Dolan RJ, Jacoby RJ, Levy R. ECT and cerebral atrophy. Acta Psychiatrica Scandinavica 1981; 64: 442-445 PMID 7347109
Cameron DG. ECT: sham statistics, the myth of convulsive therapy, and the case for consumer misinformation. J of Mind and Behavior 1994; 15(1-2): 177-198.
Colon EJ, Notermans SLH. A long-term study of the effects of electro-convulsions on the structure of the cerebral cortex. Acta Neuropathologica (Berlin)1975; 32: 21-25 PMID 1146505
Corsellis J, Meyer A. Histological changes in the brain after uncomplicated electro-convulsive treatment. Journal of Mental Science 1954; 100: 375-383.
Cott, Jonathan. On the Sea of Memory. New York: Random House, 2004.
Diehl DJ, Keshavan MS, Kanal E, et al Post-ECT increases in T2 relaxation times and their relationship to cognitive side effects: a pilot study. Psychiatry Res 1994 (November); 54(2): 177-184.
Dolan et al. The cerebral appearance in depressed patients. Psychological Medicine 1986; 16: 775-779
Donahue A (1999, March 12). Testimony at the public hearing of the Vermont (U.S.) Health and Welfare Committee on electroconvulsive therapy.
Ebaugh FG, Barnacle CH, Neubuerger KT. Fatalities following electric convulsive therapy. A report of two cases with autopsy findings. Transactions of the American Neurological Association 1942; 36.
Faurbye A. Death under electroshock treatment. Acta Psychiatrica Neurologica 1942; 17: 39.
Federal Register(USA),1978, November 28. Page 55729. 21 CFR Part 882. Classification of Electroconvulsive Therapy Device. Proposed Rule.
Federal Register (USA), 1979, September 4. Page 51776. 21 CFR Part 882. Classification of Electroconvulsive Therapy Device. Final Rule.
Ferraro A, Roizin L, Helfand M. Morphologic changes in the brains of monkeys following convulsions electrically induced. Journal of Neuropathology and Experimental Neurology 1946; 5: 285.
Ferraro A, Roizin L. Cerebral morphologic changes in monkeys subjected to a large number of electrically induced convulsions. American Journal of Psychiatry 1949; 106: 278.
Figiel G, Coffey E, et al. Brain MRI findings in ECT-induced delirium. Journal of Neuropsych and Clin Sci 1990: 2: 53-58
Freeman CP, Weeks D, Kendell RE. ECT II: Patients who complain. Br J Psychiatry 1980; 137:8-16. Peddler M. Shock Treatment: A Survey of People's Experience of Electroconvulsive Therapy (ECT). London: MIND, 2000. PMID 7459536
Food and Drug Administration (USA), Dockets Management Branch, Rockville, Maryland. Docket #82P- 0316: Electroconvulsive Therapy Device; Vols. 1-38, 1982---present.
Gralnick A. Fatalities associated with electric shock treatment of psychoses: report of two cases, with autopsy observations in one of them. Archives of Neurology and Psychiatry 1944; 51: 397.
Hartelius H. Cerebral changes following electrically induced convulsions. Acta Psychiatrica & Neurologica Supplement 1952; 77.
Heilbrunn G, Liebert E. Biopsies on the brain following artificially produced convulsions. Archives of Neurology and Psychiatry 1941; 46: 458-552.
Heilbrunn G, Weil A. Pathologic changes in the central nervous in experimental electric shock. Archives of Neurology and Psychiatry 1942; 47: 918.
Janis IL. Psychologic effects of electric convulsive treatments (I. Post-Treatment Amnesias). Journal of Nervous and Mental Disease 1950(a); 111: 359-381. PMID 15422375
Jeter WW. Fatal circulatory failure caused by electric shock therapy. Archives of Neurology and Psychiatry 1944; 51: 557.
Liban E, Halpen L, Rozanski J. Vascular changes in the brain in a fatality following electroshock. Journal of Neuropathology and Experimental Neurology 1951; 309-318.
Maclay WS. Death due to treatment. Proceedings of the Society of Medicine 1953; 46: 13-20.
Madow L. Brain changes in electroshock therapy. American Journal of Psychiatry 1956; 113: 337-347.
Marcheselli et al. Sustained induction of prostaglandin endoperoxidase synthase-2 by seizures in hippocampus. J Biol Chem 1996; 271: 24794-24799.
Martin PA. Convulsive therapies: review of 511 cases at Pontiac State Hospital. Journal of Nervous and Mental Disease 1949; 109: 142-157.
Matthew JR, Constan E. Complications following ECT over a three-year period in a state institution. American Journal of Psychiatry 1964; 120: 1119-1120.
Meyer A, Teare D. Cerebral fat embolism after electric convulsive therapy. British Medical Journal 1945; 2: 42.
Philpot M, Collins C, Trivedi P, Treloar A, Gallacher S, Rose D (2004). Eliciting users' views of ECT in two mental health trusts with a user-designed questionnaire. Journal of Mental Health 13(4): 403-413. (no hit)
Riese W, Fultz GS. Electric shock treatment succeeded by complete flaccid paralysis, hallucinations, and sudden death.
Rose D, Fleischmann P, Wykes T, Leese M, Bindman J (2003, June 21). Patients' perspectives on electroconvulsive therapy: systematic review. British Medical Journal 2003 (June 21): 326 7403), 1363-1367, 2003
Rose D, Wykes T, Bindman J, Fleischmann P (2005). Information, consent and perceived coercion: patients' perspectives on electroconvulsive therapy. British Journal of Psychiatry 186: 54-59. PMID 15630124
Shah PJ, Glabus MF, Goodwin GM, Embeier KP. Chronic, treatment-resistant depression and right fronto-striatal atrophy. British Journal of Psychiatry 2002; 180: 434-440.
Sprague DW, Taylor RC. The complications of electric shock therapy with a case study. Ohio State Medical Journal 1948; 44: 51-54.
Squire LR, Slater PC (1983). Electroconvulsive therapy and complaints of memory dysfunction: a prospective three-year follow-up study. British Journal of Psychiatry 142: 1-8.
SURE (Service User Research Enterprise). Review of Consumers' Perspectives on Electroconvulsive Therapy. London: Department of Health, January 2002.
Templer DI, Veleber DM. Can ECT permanently harm the brain? Clinical Neuropsychology 1982; 4(2): 62-66
Templer RI, Ruff CF, Armstrong G. Cognitive functioning and degree of psychosis in schizophrenics given many electroconvulsive treatments. British Journal of Psychiatry 1973; 123: 441-443.
Videotape deposition of Harold Sackeim. PhD, Case No. 01069713, Atze Akkerman and Elizabeth Akkerman v. Joseph Johnson, Santa Barbara Cottage Hospital, and Does 1-20, Court of the State of California for the County of Santa Barbara, Anacapa Division, March 14, 2004
Weinberger DR, Torrey EF, Neophytides AN et al. Lateral cerebral ventricular enlargement in chronic schizophrenia. Archives of General Psychiatry 1979; 36: 735-739. PMID 36863
Will OA, Rehfeldt FC. A fatality in electroshock therapy: report of a case and review of certain previously discussed cases. Journal of Nervous and Mental Disease 1048; 107: 105-126.
External links
- CCHR.org - 'Electroshock (ECT) and Psychosurgery', Citizens Commission on Human Rights
- ECT.org - 'Effects of ECT' (criticism site)
- NIH.gov - 'Consensus Development Conference Statement', National Institutes of Health (June 10-12, 1985)
- Psych.org - 'Electroconvulsive Therapy (ECT)', American Psychiatric Association
- Surgeon General.gov - 'Mental Health: a report of the Surgeon General: Treatment of Mood Disorders', Surgeon General of the United States