Electroconvulsive therapy
Electroconvulsive therapy (ECT) is a controversial psychiatric shock therapy involving the induction of a seizure in a patient by passing electricity through the brain. Patients with any of several conditions sometimes show dramatic short-term improvement after the procedure. While many psychiatrists believe that properly administered ECT is a safe and effective treatment for some conditions, a vocal minority of psychiatrists, former patients, antipsychiatry activists, and others strongly criticize the procedure as harmful to patients' subsequent mental state.[1]
ECT was introduced as a treatment for schizophrenia in the 1930s, and soon became a common treatment for mood disorders. In its early days, ECT was administered without anaesthesia or muscle relaxants. Patients were frequently injured as a side effect of the induced seizure. Currently, ECT is administered under anaesthesia and muscle relaxants, which limit the effects of the procedure to the brain itself. ECT without anaesthesia is referred to as "unmodified ECT", or "direct ECT", and is illegal in most countries.
ECT was a common psychiatric treatment until the late 20th century, when it fell into disuse as better drug therapies became available for more conditions. It is now reserved for severe cases of clinical depression and bipolar disorder that do not respond to other forms of therapy. When still in common use, ECT was sometimes abused by unethical mental health professionals as a means of punishing and controlling unruly or uncooperative patients. Many people came to view ECT unfavorably after negative depictions of it in several books and films, and the treatment is still controversial.
Current use
Currently, ECT is mainly used to treat severe depression, particularly if complicated by psychosis.[2][3] It is also used in cases of severe depression where antidepressant medication (sometimes in multiple courses), psychotherapy, or both, have been ineffective (refractory depression),[4] 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, after carefully weighing the risks and benefits, some psychiatrists consider ECT to be the safest treatment option. It is also sometimes used to treat the manic phase of bipolar disorder and the rare condition of catatonia.
Recent epidemiological surveys in the United States show that modern use of ECT is generally limited to evidence-based indications.[5] Indeed, concern has been raised that, in some settings, particularly in the public sector and outside major metropolitan areas, ECT may be underutilized.[6] In particular, minority patients tend to be underrepresented among those receiving ECT.[7] Accurate statistics about the frequency, context and circumstances of ECT in the United States are difficult to obtain because only a few states have reporting laws that require the treating facility to supply state authorities with this information. [8]
Overview
The aim of ECT is to induce a bilateral tonic clonic seizure (a seizure where the person loses consciousness and has convulsions) which lasts for at least 60 seconds. Before the discovery of muscle relaxants, ECT was given unmodified. Patients were rendered instantly unconscious by the electrical current, but the strength of the muscle contractions and the subsequent fit sometimes led to complications, such as compression fractures of the spine or damage to the teeth. Muscle relaxants allow a modified fit, where contractions are weak or nonexistent. However, before using muscle relaxants, the patient must be given a general anaesthetic 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 about half that in most cases. The ECT therapist tries to minimize the total energy by restricting the strength and duration of the current. 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, although now ECT is more often applied to the non-dominant brain hemisphere. Placing both electrodes on one side of the head over the nondominant (generally right) cerebral hemisphere, results in delivery of the initial stimulation away from the primary learning and memory centers. With unmodified ECT, the seizure is characteristically more severe than a naturally occurring epileptic seizure. The production of an adequate, generalized seizure using the proper amount of stimulation is required for therapeutic efficacy.[9] Therapeutic ECT is usually given three times per week for 6 to 12 treatments, on either an inpatient or outpatient basis. Studies have shown that each fit must be separated by at least a day.
After the seizure, cortical electrical activity ceases for a short time, during which an EEG reading is 'flat'. After treatment, patients do not remember the seizure or the events immediately before it.
Exactly how ECT exerts its effects is not known, but repeated applications affects 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.[10] One study suggests that long-term ECT increases the expression of brain-derived neurotrophic factor (BDNF) and its receptor, TrkB, in limbic brain regions.[11]
Types of ECT
There are two basic forms of ECT: bilateral and unilateral, and bilateral ECT can be subdivided into bitemporal and bifrontal ECT. In bitemporal ECT, current is passed across the temporal lobes, between electrodes placed on either side of the head. With unilateral, the electrodes are only on the right side, and pass current mainly through the right temporal lobe.
According to several controlled trials, unilateral ECT is associated with almost no detectable, persistent memory loss.[12][13] However, most clinicians find that unilateral ECT is less potent and acts more slowly 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 unilateral ECT and switch to bilateral ECT after about six treatments if there is no response.
The relationship of electrical dose to clinical response depends on the electrode placement; for bilateral ECT, as long as an adequate seizure is obtained, any higher dose will merely add to the cognitive toxicity, whereas for unilateral ECT, a therapeutic effect will not be achieved unless the electrical stimulus is more than minimally above the seizure threshold.[9]
Even a moderately high electrical dosage in unilateral ECT has fewer cognitive adverse effects than bilateral ECT. On the other hand, high-dose bilateral ECT might be unnecessarily risky and might be an avoidable cause of severe memory impairment.
Bifrontal ECT is a modified form of bitemporal ECT in which electrodes are placed 2 inches above the lateral angle of each orbit. It has fewer adverse effects on memory than bitemporal ECT, and it increases the blood flow to the prefrontal cortex.[14]
Side effects and complications
Side-effect profile
Much of the accepted risk of ECT arises from the use of general anesthesia; there is considerable disagreement about other risks. The most common adverse effects are confusion and retrograde memory loss for events surrounding the period of ECT treatment, and generalised but mild muscle aches after waking. Some of the confusion and disorientation seen on awakening after ECT clears soon after. More persistent memory problems are variable and difficult to quantify. Most typical with standard, bilateral ECT has been a loss of memories for the time of the ECT series and extending back for an average of 6 months, combined with impairment in learning new information, which continues for perhaps 2 months after ECT.[15] No long-term (six months post-ECT or more) studies of cognition, memory ability, and memory loss have been done in the past two decades, but some long-term studies before this reported permanent amnesia,[16][17] although others found problems were gone by seven months after ECT.[18] Calev (1994) surveyed the literature and concluded that patients must be warned of possible non-memory cognitive deficits, as "they are not going to function well on more tasks than they anticipate".[19] At least a third of ECT patients have some permanent memory loss, according to a systematic review in 2003.[20] Formal neuropsychological testing has documented permanent neuropsychological deficits in ECT patients,[21] including an IQ loss of more than 30 points in one.[22] The degree of impairment and resulting impact on functioning vary between individuals.[23] Critics of ECT believe that there is enough evidence that patients' memories can be permanently and severely damaged to justify a moratorium, at least until more research has been done into its effects on the brain.
Many early studies from the 1940s, 1950s, and early 1960s indicated that ECT was associated with brain abnormalities However, other authors point out that today's ECT is different. The recent work assessing the consequences of seizures has found no evidence that they cause brain damage,[24] with prospective studies appearing to confirm this[25].
There is more recent work noting brain abnormalities in those who have had ECT. Colon & Notermans found changes in nuclear volume in the cortex, but without loss of neurons.[26] Calloway et al. found an association with frontal lobe atrophy and ECT on a retrospective review of scans[27] , and accordingly did not claim these were caused by ECT (many schizophrenics, for instance, have abnormal brain anatomy as part of their condition,[28][29] [30][31] and brain changes have also been found in depressive patients[32] ). Diehl et al. in a study of six patients found significant post-ECT T2 increases in the right and left thalamus consistent with a post-ECT increase in brain water content.[33]
ECT may have adverse psychological effects. John Breeding, a psychologist at the University of Texas, has highlighted what he regards as the psychological effects of ECT, particularly: "1) Suppression of emerging distress material 2) Suppression of ability to heal by emotional release; 3) Creation of emotional distress, including deep feelings of terror and powerlessness; 4) Promotion of human beings in the roles of victims and passive dependents of medical professionals; 5) Confirmation of patients' belief that there is something really wrong with them (shame)." [34] Breeding regards psychiatric illness as the product of unresolved psychic conflict, often due to abuse, and feels that the correct treatment for such problems is to bring out this underlying conflict, and has compared the experience of those who have undergone ECT to that of Holocaust survivors.
The decision to use ECT must be evaluated by each individual, weighing the potential benefits and known risks of all available, appropriate treatments in the context of informed consent,[35] free of coercion and veiled threats. Studies in 2004 and 2005 showed that half of ECT patients did not feel that they could refuse the treatment.[36]
Contraindications
Some psychiatric researchers contend that there are virtually no absolute health contraindications that preclude the use of ECT where warranted,[37] i.e. where the treating psychiatrist, often at his sole discretion but frequently in consultation with a multidisciplinary team, decides that the likely benefits outweigh the possible risks. The only major contraindication is increased intracranial pressure, as in cases of recent cerebrovascular accident or known space-occupying lesion such as meningioma, because of the danger of herniation due to transient further increase in intracranial pressure during the procedure.
Device risk
ECT should be administered under controlled conditions, with appropriate personnel.[38] Some mental health laws mandate this.Template:Fact
The United States Food and Drug Administration has classified the devices used to administer ECT as Class III medical devices.[39] Class III is the highest-risk class of medical devices. The risks of ECT, according to the FDA, include brain damage and memory loss.[40]
Effectiveness
Some studies — later confirmed in controlled clinical trials which included the use of simulated (placebo) ECT as a control,[41] have shown that ECT is very effective against severe depression, some acute psychotic states, and mania.[42] No controlled study has shown that any other treatment for depression is more effective than ECT.[43] ECT has not been shown to be effective in dysthymia, substance abuse, anxiety, or personality disorders. These conclusions, and many of those discussed below, are the product of review of extensive research over several decades[44] as well as by a panel of scientists, practitioners, and consumers.[45]
Although the average 60-70% response rate[46] seen with ECT is similar to that seen with pharmacotherapy, there is evidence that the antidepressant effect of ECT occurs faster than with medication, which supports the use of ECT when depression is accompanied by potentially uncontrollable suicidal ideas and actions.[47] However, ECT does not provide long-term protection against suicide; it is now recognized that a single course of ECT should be regarded as a short-term treatment for acute illness. To sustain the response to ECT, continuation treatment, often in the form of antidepressant and/or mood stabilizer medication, is needed. [48] "Maintenance ECT" refers to indefinite periods of repeated ECT, usually scheduled a few weeks apart. Critics of ECT assert that maintenance ECT is needed because the brain requires approximately four weeks to recover from each closed head injury caused by ECT; thus, when the brain has healed, the temporary euphoric effects are lost and ECT must be given again to attain the previous mood gain. Individuals who repeatedly relapse after 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 [49]
Informed consent
Informed consent is an integral part of the ECT process.[50] 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 advisable in the decision-making process both prior to and throughout a course of ECT. Care ought to be taken that the informed consent materials originate from objective sources and not, for example, from the manufacturer of ECT devices. 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, while in others ECT is seen as another form of treatment that may be given involuntarily as long as legal conditions are observed.
The World Health Organization, in its 2005 publication "Human Rights and Legislation WHO Resource Book on Mental Health," specifically states, "ECT should be administered only after obtaining informed consent."
In nearly all states in the USA, involuntary ECT may not be initiated by a physician or family member without a judicial proceeding. In nearly 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, the law requires that such petitions are granted only where the prompt institution of ECT is regarded as potentially lifesaving, as in the case of a person in grave danger because of lack of food or fluid intake caused by catatonia. In Oregon, an institution may administer involuntary ECT without any judicial proceeding at all through the use of an administrative override that requires, among other things, the review of the case by a physician unaffiliated with the treating facility.
Australian states regard 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, the Mental Health Act 1983 allows the use of ECT on detained patients (with and without capacity), if the treatment is authorised by a psychiatrist from the Mental Health Act Commission's panel. If the treating psychiatrist thinks the need for treatment is urgent they may start a course of ECT before authorisation. About 2,000 people a year are treated without their consent under the Mental Health Act.[51] A small number of informal patients are treated without their consent under common law. In Scotland the Mental Health (Care and Treatment) (Scotland) Act 2003 gives patients with capacity the right to refuse ECT.
In 2006, the organization Mental Disability Rights International published the results of a two-year investigation in Turkey that found what MDRI termed "widespread" involuntary ECT administered without anesthesia.Template:Fact
Continuation phase therapy
Successful acute phase antidepressant pharmacotherapy or ECT is generally followed by at least 6 months of continued treatment.[52] During this phase, the continuation phase, most patients are seen biweekly or monthly. The main goal of continuation pharmacotherapy is to prevent relapse (i.e. exacerbation of symptoms). Continuation pharmacotherapy reduces the risk of relapse from 40-60% to 10-20%.[53] Relapse despite continuation pharmacotherapy might suggest either nonadherence[54] or loss of a placebo response.[55]
A second goal of continuation pharmacotherapy is to consolidate a response into complete remission(i.e. a 'complete resolution of affective symptoms to a level similar to healthy people').[56] Residual symptoms are associated with increased risk of relapse.[57] Many psychotherapists taper a successful course of treatment by scheduling several sessions (every other week or monthly) before termination. There is evidence that relapse is less common following successful treatment with one type of psychotherapy—cognitive-behavioral therapy—than with antidepressants.[58]
History
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 that such electric shocks caused his obsessive and difficult mental patients to become meek and manageable. At first, ECT 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 sometimes break bones, especially vertebrae, and pull muscles from the violent convulsions induced by the seizure. Patients came to fear the procedure, and it was sometimes used to punish or sedate difficult patients in psychiatric hospitals.
With the development of effective medications for major mental disorders, the need for ECT lessened, but did not disappear. Until then, ECT often had been administered for several conditions for which it is now generally regarded as ineffective, for example, for treating schizophrenia.
Advances in treatment technique over the past generation have led to fewer adverse cognitive effects of ECT.[59] 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 can be induced with as little as one-third of the electrical power used by the older method, reducing the risk of confusion and memory disturbance.[60] Ultra-brief pulse, higher frequency and longer stimulus duration also contribute to ECT effectiveness while minimizing adverse cognitive effects.
Controversy
As of 2006, most psychiatrists believe that ECT can be beneficial in some circumstances. However, ECT remains controversial, and a vocal minority of psychiatrists oppose it; some regard it as inhumane and primitive. Opponents claim that the mechanism through which ECT changes mental state is nothing more than the destruction of brain cells, and even proponents are unsure how it works. Many patients who have had ECT claim it caused their mental state to improve; many others think their ECT did more harm than good, and some campaign to have the treatment banned, as it is in the Republic of Slovenia. 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.
Anti-ECT activists allege that patients are rarely told the complete truth about the risks and benefits of ECT.[61] To demonstrate what would be required to fully satisfy the legal obligation for 'informed consent', one psychiatrist has formulated his own 'consent form'[62] using the Texas Legislature[63] as a model. It should be noted that printed or videotaped materials regarding ECT might be commissioned by the manufacturers of the equipment used, 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.
Even the term "electroconvulsive therapy" is contested, with many opponents of the procedure instead using the term "electroshock."
Fictional and semi-fictional depictions of ECT
Electroconvulsive therapy has been depicted in several fictional and semi-fictional films, books, and songs, almost always in an extremely negative light. A great deal of anti-ECT sentiment was generated by its 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 experiences in various mental hospitals during the 1960s. It is implied in the film that the hospital staff use ECT to punish uncooperative patients.
ECT has occasionally been portrayed in a positive light, however. In Elizabeth Flock's novel But Inside I'm Screaming, the main character, Isabel, is initally reluctant to undergo ECT for her severe depression, but the ECT is a major factor in her recovery.
Famous people who have undergone ECT
- Louis Althusser, French philosopher
- Peter Green, British blues guitarist
- Antonin Artaud, French playwriter
- Clara Bow, American actress
- Richard Brautigan, American writer and poet
- 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."
- Kitty Dukakis, wife of former Massachusetts governor and 1988 Democratic presidential nominee Michael Dukakis and author of Shock, a book chronicling her experiences with ECT.
- Thomas Eagleton, American vice-presidential hopeful who lost the nomination in 1972 when it was discovered he had undergone ECT
- Frances Farmer, American cinema actress
- Janet Frame, New Zealand writer who was wrongly diagnosed with schizophrenia. Many of her works contain semi-autobiographical accounts of her treatment
- Judy Garland, American film actress and singer
- David Helfgott, Australian pianist
- Ernest Hemingway, American author, committed suicide shortly after ECT treatment at the Mayo Clinic in 1961. He is 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...."
- Vladimir Horowitz, pianist
- Pat Ingoldsby, Irish poet
- Ken Kesey, American author
- Vivien Leigh, British actress
- Oscar Levant, pianist
- Robert Lowell, American poet and writer
- Mervyn Peake, English artist and writer
- 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
- Cole Porter, American composer and musician
- Dory Previn, American poet, writer and lyricist
- Paul Robeson, American actor
- Lou Reed, rock musician
- Yves Saint Laurent, French fashion designer. He underwent treatment after serving in the French military.
- Gene Tierney, American actor
Source note
Sections of this article were copied word for word from the public-domain document Mental Health: a report of the Surgeon General.
Footnotes
- ↑ For many statements from the latter group, see Frank (2006).
- ↑ NIH & NIMH Consensus Conference, 1985; Depression Guideline Panel (1993)
- ↑ Potter & Rudorfer (1993)
- ↑ Potter et al. (1991); Depression Guideline Panel (1993)
- ↑ Hermann R, Ettner S, Dorwart R, Langman-Dorwart N, Kleinman S (1999). "Diagnoses of patients treated with ECT: a comparison of evidence-based standards with reported use.". Psychiatr Serv 50 (8): 1059-65. PMID 10445655.
- ↑ Hermann R, Dorwart R, Hoover C, Brody J (1995). "Variation in ECT use in the United States.". Am J Psychiatry 152 (6): 869-75. PMID 7755116.
- ↑ Rudorfer et al. (1997)
- ↑ Cauchon, Dennis. "Controversy and Questions Shock Therapy: Patients often aren't informed of full danger", USA Today, 1995-12-06. (in English)
- ↑ 9.0 9.1 Sackeim H, Prudic J, Devanand D, Kiersky J, Fitzsimons L, Moody B, McElhiney M, Coleman E, Settembrino J (1993). "Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy.". N Engl J Med 328 (12): 839-46. PMID 8441428.
- ↑ Ishihara & Sasa (1999)
- ↑ Duman R, Vaidya V (1998). "Molecular and cellular actions of chronic electroconvulsive seizures.". J ECT 14 (3): 181-93. PMID 9773357.
- ↑ Horne R, Pettinati H, Sugerman A, Varga E (1985). "Comparing bilateral to unilateral electroconvulsive therapy in a randomized study with EEG monitoring.". Arch Gen Psychiatry 42 (11): 1087-92. PMID 3901956.
- ↑ NIH Consensus Conference (1985); Rudorfer et al. (1997)
- ↑ Blumenfeld et al. (2003)
- ↑ NIH & NIMH Consensus Conference, 1985
- ↑ Janis IL, Astrachan M. The effects of electroconvulsive treatments on memory efficiency. J Abnorm Soc Psychol. 1951 Oct;46(4):501-11 [PMID 14880367]
- ↑ Squire L, Slater P (1993). "Electroconvulsive therapy and complaints of memory dysfunction: a prospective three-year follow-up study.". Br J Psychiatry 142: 1-8. PMID 6831121.
- ↑ Squire L, Slater P, Miller P (1981). "Retrograde amnesia and bilateral electroconvulsive therapy. Long-term follow-up.". Arch Gen Psychiatry 38 (1): 89-95. PMID 7458573.
- ↑ Calev A (1994). "Neuropsychology and ECT: past and future research trends.". Psychopharmacol Bull 30 (3): 461-9. PMID 7878183.
- ↑ Rose (2003)
- ↑ FDA, Docket #82P-0316
- ↑ Donahue (1999); Andre (2001); Cott (2004)
- ↑ NIH & NIMH Consensus Conference (1985); CMHS (1998)
- ↑ Meldrum B (1986). "Neuropathological consequences of chemically and electrically induced seizures.". Ann N Y Acad Sci 462: 186-93. PMID 3085568.
Dwork A et al. (2004). "Absence of histological lesions in primate models of ECT and magnetic seizure therapy.". Am J Psychiatry 161 (3): 576-8. PMID 14992989. - ↑ Coffey C, et al. (1991). "Brain anatomic effects of electroconvulsive therapy. A prospective magnetic resonance imaging study.". Arch Gen Psychiatry 48 (11): 1013-21. PMID 1747016.
- ↑ Colon EJ, Notermans SLH (1975) A long-term study of the effects of electro-convulsions on the structure of the cerebral cortex. Acta Neuropathologica (Berlin) 32:21-5 [PMID 1146505]
- ↑ Colon E, Notermans S (1975). "A long-term study of the effects of electro-convulsions on the structure of the cerebral cortex.". Acta Neuropathol (Berl) 32 (1): 21-5. PMID 1146505.
- ↑ Turner J, Smyth P, Macciardi F, Fallon J, Kennedy J, Potkin S (2006). "Imaging phenotypes and genotypes in schizophrenia.". Neuroinformatics 4 (1): 21-49. PMID 16595857.
- ↑ Honea R, Crow T, Passingham D, Mackay C (2005). "Regional deficits in brain volume in schizophrenia: a meta-analysis of voxel-based morphometry studies.". Am J Psychiatry 162 (12): 2233-45. PMID 16330585.
- ↑ Keshavan M, Diwadkar V, Montrose D, Rajarethinam R, Sweeney J (2005). "Premorbid indicators and risk for schizophrenia: a selective review and update.". Schizophr Res 79 (1): 45-57. PMID 16139479.
- ↑ Tanskanen P, Veijola J, Piippo U, Haapea M, Miettunen J, Pyhtinen J, Bullmore E, Jones P, Isohanni M (2005). "Hippocampus and amygdala volumes in schizophrenia and other psychoses in the Northern Finland 1966 birth cohort.". Schizophr Res 75 (2-3): 283-94. PMID 15885519.
- ↑ Dolan R, Calloway S, Thacker P, Mann A (1986). "The cerebral cortical appearance in depressed subjects.". Psychol Med 16 (4): 775-9. PMID 3823294.
- ↑ Diehl DJ, et al. (1994) Post-ECT increases in MRI regional T2 relaxation times and their relationship to cognitive side effects: a pilot study. Psychiatry Res 54:177-84 [PMID 7761551]
- ↑ Breeding, John (2003). The Necessity of Madness: Explaining How Psychiatry Is a Clinical Construct and Madness Is a Metaphor. Chipmunkapublishing, 460. DOI:2003-01-03. 0954221877.
- ↑ NIH & NIMH Consensus Conference, 1985
- ↑ Philpot (2004); Rose (2005)
- ↑ Potter & Rudorfer (1993); Rudorfer et al. (1997)
- ↑ Rudorfer et al. (1997)
- ↑ Federal Register (1979), p. 51776
- ↑ Federal Register (1978), p. 55729
- ↑ Janicak et al. (1985)
- ↑ Small et al. (1988)
- ↑ Janicak et al. (1985); Rudorfer et al. (1997)
- ↑ Depression Guideline Panel (1993); Rudorfer et al. (1997)
- ↑ NIH & NIMH Consensus Conference (1985)
- ↑ Higher response rates have been reported, e.g. 85-90% in Whybrow PC. 'A Mood Apart: Depression, Mania, and Other Afflictions of the Self'. New York: Basic Books, 1997. and in excess of 90% in Mondimore FM 'Depression: The Mood Disease'. Baltimore: Johns Hopkins University Press, 1995.
- ↑ Rudorfer et al. (1997)
- ↑ Sackeim (1994)
- ↑ Rudorfer et al. (1997)
- ↑ NIH & NIMH Consensus Conference (1985)
- ↑ The Mental Health Act Commission: "In Place of Fear? eleventh biennial report, 2003-2005.", page 236. The Stationery Office, 2005.
- ↑ Prien & Kupfer (1986); Depression Guideline Panel (1993); Rudorfer et al. (1997)
- ↑ Prien & Kupfer (1986); Thase (1993)
- ↑ Myers & Branthwaithe (1992)
- ↑ Quitkin et al. (1993a)
- ↑ Frank et al. (1991a)
- ↑ Keller et al. (1992); Thase et al. (1992)
- ↑ Kovacs et al. (1981); Blackburn et al. (1986); Simons et al. (1986); Evans et al. (1992)
- ↑ NIH & NIMH Consensus Conference (1985); Rudorfer et al. (1997)
- ↑ Andrade et al. (1998)
- ↑ Rose (2005)
- ↑ Johnson (2003)
- ↑ Texas Legislature (2004)
References
Template:Col-2- Abrams R, Taylor MA (1973). "Anterior bifrontal ECT: a clinical trial". Br J Psychiatry 122: 587–90. PMID 4717031.
- Andre L (2001). Testimony at the public hearing of the New York State (U.S.) Assembly Standing Committee on Mental Health on electroconvulsive therapy.
- Andreasen et al. (1990). "MRI of the brain in schizophrenia". Arch Gen Psychiatry 47: 35–41.. PMID 2294854.
- Barker J, Baker A (1959). "Deaths associated with electroplexy". J Mental Sci 105: 339–48.
- Blumenfeld H et al. (2003). "Targeted prefrontal cortical activation with bifrontal ECT". Psychiatry Res 123: 165–70. PMID 12928104.
- Calloway SP et al. (1981). "ECT and cerebral atrophy". Acta Psychiatrica Scand 64: 442–45. PMID 7347109.
- Cameron DG (1994). "ECT: sham statistics, the myth of convulsive therapy, and the case for consumer misinformation". J Mind Behav 15: 177–98.
- Cerletti U, Bini L (1938). "L'Elettroshock". Arch Gen Neurol Psychiat Psycoanal 19: 266–8.
- Clemedson C, Hartelius H, Holmberg G (1957). "The effect of high explosive blast on the cerebral vascular permeability". Acta Pathol Microbiol Scand 40 (2): 89-95. PMID 13424280.
- Corsellis J, Meyer A (1954). "Histological changes in the brain after uncomplicated electro-convulsive treatment". J Mental Sci 100: 375–83.
- Cott, Jonathan (2004). On the sea of memory. New York: Random House.
- Diehl DJ et al. (1994). "Post-ECT increases in T2 relaxation times and their relationship to cognitive side effects: a pilot study". Psychiatry Res 54. PMID 7761551.
- Donahue A (1999, March 12). Testimony at the public hearing of the Vermont (U.S.) Health and Welfare Committee on electroconvulsive therapy.
- Dukakis, K; Tye L (2006). Shock: The healing power of electroconvulsive therapy. Avery/Penguin.
- Ebaugh FG, Barnacle CH, Neubuerger KT (1942). "Fatalities following electric convulsive therapy. A report of two cases with autopsy findings". Trans Am Neurol Assoc: 36.
- Faurbye A (1942). "Death under electroshock treatment". Acta Psychiatrica Neurologica 17: 39.
- Federal Register (USA) (1978, November 28). "21 CFR Part 882. Classification of Electroconvulsive Therapy Device. Proposed Rule": 55729.
- Federal Register (USA) (1979, September 4). "21 CFR Part 882. Classification of Electroconvulsive Therapy Device. Final Rule": 51776.
- Ferraro A, Roizin L, Helfand M (1946). "Morphologic changes in the brains of monkeys following convulsions electrically induced". J Neuropathol Exp Neurol 5: 285.
- Ferraro A, Roizin L (1949). "Cerebral morphologic changes in monkeys subjected to a large number of electrically induced convulsions". Am J Psychiatry 106: 278.
- Figiel G et al. (1990). "Brain MRI findings in ECT-induced delirium". J Neuropsych Clin Sci 2: 53–58. PMID 2136061.
- Food and Drug Administration (USA), Dockets Management Branch, Rockville, Maryland. Docket #82P-0316 (1982). Electroconvulsive Therapy Device; Vols. 1–38.
- Frank, Leonard Roy (ed.) (June 2006). The Electroshock Quotationary (PDF). Campaign for the Abolition of Electroshock in Texas. Retrieved on 2006-07-24.
- Freeman CP, Weeks D, Kendell RE (1980). "ECT II: Patients who complain". Br J Psychiatry 137: 8–16. PMID 7459536.
- Gralnick A (1944). "Fatalities associated with electric shock treatment of psychoses: report of two cases, with autopsy observations in one of them". Arch Neurol Psychiatry 51: 397.
- Hartelius H (1952). "Cerebral changes following electrically induced convulsions". Acta Psychiatrica Neurologica Suppl 77: 128.
- Heilbrunn G, Liebert E (1941). "Biopsies on the brain following artificially produced convulsions". Arch Neurol Psychiatry 46: 458–552.
- Heilbrunn G, Weil A (1942). "Pathologic changes in the central nervous in experimental electric shock". Arch Neurol Psychiatry 47: 918.
- Janis IL (1950). "Psychologic effects of electric convulsive treatments I Post-treatment amnesias". J Nervous Mental Dis 111: 359–81. PMID 1542237.
- Jeter WW (1944). "Fatal circulatory failure caused by electric shock therapy". Arch Neurol Psychiatry 51: 557.
- Johnson B (2003). An Informed Consent Form For Electro Convulsive Therapy (ECT). Draft 1.
- Liban E, Halpen L, Rozanski J (1951). "Vascular changes in the brain in a fatality following electroshock". J Neuropathol Exp Neurol: 309–18. PMID 14861666.
- Maclay WS. "Death due to treatment". Proc Soc Med 1953 46: 13–20. PMID 13027286.
- Madow L (1956). "Brain changes in electroshock therapy". Am J Psychiatry 113: 337–47. PMID 13362628.
- Marcheselli et al. (1996). "Sustained induction of prostaglandin endoperoxidase synthase-2 by seizures in hippocampus". J Biol Chem 271: 24794–9. PMID 8798751.
- Martin PA (1949). "Convulsive therapies: review of 511 cases at Pontiac State Hospital". J Nervous Mental Dis 109: 142–57.
- Matthew JR, Constan E (1964). "Complications following ECT over a three-year period in a state institution". Am J Psychiatry 120: 1119–20. PMID 14144443.
- McKegney FP, Panzetta AF. "An unusual fatal outcome of electro-convulsive therapy". Am J Psychiatry 120: 398-400. PMID 14069472.
- Meyer A, Teare D (1945). "Cerebral fat embolism after electric convulsive therapy". Br Med J 2: 42.
- Mondimore, FM (1995). Depression: The mood disease. Baltimore: Johns Hopkins University Press.
- Peddler M (2000). "Shock treatment: a survey of people's experience of electroconvulsive therapy (ECT)". London: MIND. PMID 7459536.
- Philpot M et al. (2004). "Eliciting users' views of ECT in two mental health trusts with a user-designed questionnaire". J Mental Health 14: 403–13.
- Potter WZ, Rudorfer MV (1993). "Electroconvulsive therapy--a modern medical procedure". N Engl J Med 328 (12): 839–46. PMID 8441434.
- Riese W, Fultz GS. "Electric shock treatment succeeded by complete flaccid paralysis, hallucinations, and sudden death".
- Rose D, Wykes T, Bindman J, Fleischmann P (2005)). "Information, consent and perceived coercion: patients' perspectives on electroconvulsive therapy". Br J Psychiatry 186: 54–59.
- Rose D et al. (2003). "Patients' perspectives on electroconvulsive therapy: systematic review". Br Med J 326: 1323–67. PMID 12816822.
- Rudorfer MV; Henry ME, Sackheim HA (1997). “Electroconvulsive therapy”, A Tasman, J Kay, & JA Lieberman (eds.),: Psychiatry. Philadelphia: W.B. Saunders, 1535–56.
- Shah PJ, Glabus MF, Goodwin GM, Embeier KP (2002). "Chronic, treatment-resistant depression and right fronto-striatal atrophy". Br J Psychiatry 180: 434–40.
- Sprague DW, Taylor RC. "The complications of electric shock therapy with a case study". Ohio State Med J 1948 44: 51–54.
- SURE (Service User Research Enterprise). Review of Consumers' Perspectives on Electroconvulsive Therapy. London: Department of Health, January 2002. Retrieved on 2006-04-21.
- Templer DI, Veleber DM (1982). "Can ECT permanently harm the brain?". Clin Neuropsychol 4: 62–66.
- Templer RI, Ruff CF, Armstrong G (1973). "Cognitive functioning and degree of psychosis in schizophrenics given many electroconvulsive treatments". Br J Psychiatry 123: 441–3. PMID 4147890.
- Texas Legislature (2004). Health & safety code Chapter 578. Electroconvulsive and other therapies Sec.578.001.
- Videotape deposition of Harold Sackeim PhD, Case No. 01069713, Atze Akkerman and Elizabeth Akkerman vs 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 et al. (1979). "Lateral cerebral ventricular enlargement in chronic schizophrenia". Arch Gen Psychiatry 36: 735–9. PMID 36863.
- Whybrow, PC (1997). A mood apart: Depression, mania, and other afflictions of the self. New York: Basic Books.
- Will OA, Rehfeldt FC. "A fatality in electroshock therapy: report of a case and review of certain previously discussed cases". J Nervous Mental Dis 107: 105–26.
External links
- Consensus Development Conference Statement - National Institutes of Health (June 10-12, 1985)
- Surgeon General.gov - Mental Health: a report of the Surgeon General: Treatment of Mood Disorders, Surgeon General of the United States
- Psych.org - Electroconvulsive Therapy (ECT), American Psychiatric Association
- ECT.org - Effects of ECT (criticism)
- CCHR.org - Electroshock (ECT) and Psychosurgery, by Citizens Commission on Human Rights (a Scientology-controlled group)
- Frank, Leonard R. (June 2006). Electroshock Quotationary. Retrieved July 23, 2006, from The Coalition for the Abolition of Electroshock in Texas website.
da:ECT de:Elektrokrampftherapie fr:Sismothérapie he:נזעי חשמל it:Terapia elettroconvulsivante nl:Elektroconvulsietherapie no:Elektrokonvulsiv terapi pl:Terapia elektrowstrząsowa fi:Sähköhoito sv:ECT