ECT Anonymous - Research Information - May 1999

Research in psychiatry clearly demonstrates that ECT is far from "safe and effective" - a phrase improperly applied as ECT, unlike a vaccine, carries no requirement that safety and efficacy is proven. Paternalistic dictum, not rational scientific basis, establishes ECT as a medical treatment; the real reason ECT is given is because doctors think it should be. All areas are controversial - knowledge lacunae psychiatry actively encourages. Clinical indications - to say nothing of a considerable non-clinical component - contra-indications, therapeutic aim and agent, the necessity (or otherwise) for a convulsion, method of application, mode of action, stimulus dose, side-effects, efficacy, consent... and so on, are each disputed by clinicians. Bar two from newspapers, the following quotations by mainly pro-ECT authors are taken from the professional journals and books. They're damning, yet won't damn, for psychiatry has imbued ECT with shape-changing properties.

Do you realise that ECT has been linked with brain atrophy?

"A history of electroshock therapy (EST) is associated with larger ventricles. The 16 patients who had received EST had larger ventricles than the 57 patients who had not." (Weinberger et al., 'Lateral Cerebral Ventricular Enlargement in Chronic Schizophrenia, Arch. Gen. Psychiat., Vol. 36, July 1979)

"Among the subset of patients who had received electroconvulsive therapy in the past, a significant correlation was observed between number of electroconvulsive treatments and lateral ventricle volume." (Andreason et al, 'Magnetic Resonance Imaging of the Brain in Schizophrenia: The Pathophysiologic Significance of Structural Abnormalities,' Arch. Gen. Psychiat., Vol. 47, January 1990)

Pro-ECT psychiatrists rely heavily on the absence of uniform scan evidence of damage to insist that ECT doesn't cause brain damage. ECT affects people in different ways, apart from which it is the abnormal brainwave patterns, indicative of epilepsy, that offer vital clues. Hughlings Jackson proposed that the understanding of epilepsy was the key to insanity. It is certainly an important key to somatic, mental and personality degeneration CAUSED by ECT - as epilepsy, with or without clinical seizures, provides a physical mechanism by which many of the diseases of ECT are explicable.

"[Psychiatric] patients with a wide variety of episodic behavioural disturbances ranging from depersonalisation, free floating anxiety, depression to impulsive behaviour, destructive rages, and catatonic-like states show abnormal EEG activity in temporal lobes... Patients with EEG abnormality of temporal lobes... show an unusually high incidence of personality disorder." (Slater, Beard and Glithero, 'Schizophrenia-like Psychoses of Epilepsy,' International J. Psychiat., Vol. 1, 1965)

It isn't disputed that epilepsy can occur as a result of ECT:

"...Small and associates reported the occurrence of a right temporal lobe epileptic focus in a patient receiving a combination of lithium and right unilateral nondominant ECT." (Weiner et al.,'Prolonged Confusional State and EEG Seizure Activity Following Concurrent ECT and Lithium Use,' Am. J. Psychiat., 1980)

Psychiatrists say that, following the introduction of anaesthesia, ECT creates epilepsy only rarely - but is this entirely accurate?

"The term status epilepticus (SE) denotes protracted or repetitive seizures that result in a "fixed epileptic condition." Typically, SE occurs in two primary clinical forms - convulsive and nonconvulsive. ... Nonconvulsive SE is often more difficult to detect clinically and is either absence (petit mal) or partial complex (temporal lobe) in nature. A recent study found a high incidence of patients with psychiatric disorders...among those who have nonconvulsive SE. This type of SE often requires an EEG to confirm the diagnosis." (Daniel J. Lacey, 'Status Epilepticus in Children and Adults,' J. Clin. Psychiat. 49:12 (Suppl), 1988)

Although an EEG is NOT administered by way of a routine check prior to ECT, interestingly, where it is:

"Our patient had been healthy and the EEG prior to the ECT was normal. We presume that this disorder [epilepsy] was caused by a lesion in the brain-stem caused by the ECT." ('Electroencephalography and Clinical Neurophysiology,' 23, p. 195, 1967)

Attribution of alleged seizure disorder disappearance to anaesthetic modifications of convulsive treatment might mislead:

"Our study...does not indicate that modern ECT has eliminated iatrogenic epileptogenesis. Seizures may actually be significantly underreported in the recent literature. (Devinsky and Duchowny, 'Seizures after convulsive therapy: A retrospective case study,' Neurology 33, 1983)

The undoubted similarities between epilepsy and ECT should be remarked. With epilepsy proposed as the key to insanity, it goes without saying that researchers in psychiatry and neurology have been keen to study the connections between spontaneous and induced fits.

"When first introduced it was hoped that it [ECT] would throw some light on epilepsy, with which its convulsive effect is related, but beyond the confirmation of certain therapeutic aspects of epilepsy...it has not yet brought any major revelation such as those obtained by non-clinical techniques. It is essential, however, that research should continue to follow this..." (W. Grey Walter, 'The Living Brain,' Penguin, 1961)

"The need to determine the distinct and precise cut-off point of convulsive activity...does raise a number of questions about the basic physiology of convulsive seizures. The mechanism which would provide such a precise endpoint to electroencephalographic grand mal convulsive activity is not known at this time.... We feel that this phenomenon alone warrants further investigation. Perhaps this technique [Multiple Monitored Electroconvulsive Treatment]...could...provide an opportunity for study by a variety of investigators since the EEG activity can be recorded and since the convulsive activity is predictably produced as a part of the clinical treatment of the psychiatrically ill patient." (White, Shea and Jonas, 'Multiple Monitored Electroconvulsive Treatment,' Am. J. Psychiat. 125:5, 1968)

"ECT is part of the history of epileptic studies, and its understanding and that of epilepsy march together." (John C. Cranmer (Institute of Psychiatry), 'The Truth About ECT,' Brit. J. Psychiat. (1988), 153 (Correspondence))

Some of those Jack Straw has expressed himself keen to lock away - namely the personality disordered - will undoubtedly have temporal lobe damage. We are unlikely to learn what caused it.

"From a neurological point of view, ECT is a method of producing amnesia by selectively damaging the temporal lobes and the structures within them." (John Friedberg, 'Shock Treatment, Brain Damage, and Memory Loss: A Neurological Perspective,' paper for the 129th meeting of the American Psychiatric Assoc., 1976)

"Both bilateral and unilateral ECT...usually seem to be applied over or near the temporal lobes of the brain. ... ...it would appear that there is at least an overlap between the actual physical sites of action involved in both ECT and temporal lobectomy. There are, in addition, other grounds for the belief that ECT may affect in particular, critical structures within the region of the temporal lobes. ... There is, however, also evidence that there may be a local action of electroshock on brain areas underlying electrode placement that is independent of the general...activity and may indeed be in some respects deleterious. Given, then, the physical position of the electrodes over the temporal lobes, and given the differential sensitivity to shock of some associated substructures, it would seem likely that these brain areas are the ones to bear the main brunt of any local effects of shock under the usual conditions of...ECT. (James Inglis, 'Shock, Surgery and Cerebral Asymmetry,' Brit. J. Psychiat. (1970), 117)

Although after 61 years in use, disagreement on the subject of brain damage (as in other areas) is as fierce as ever, some psychiatrists suggest (and even state) that ECT does result in brain damage.

"ECT patients' inferior Bender-Gestalt performance does suggest that ECT causes permanent brain damage." (Templer et al., 'Cognitive Functioning and Degree of Psychosis in Schizophrenics given many Electroconvulsive Treatments,' Brit. J. Psychiat., 1973)

"Thus a patient who chose to undergo some mild brain damage, which would result in mild persistent memory deficits, in order to escape from severe psychic pain that could not be relieved in any other way would not be making an inherently irrational decision." (Culver, Ferrell and Green, 'ECT and Special Problems of Informed Consent,' Am J. Psychiat 137:5, 1980)

"...prolonged administration of psychotropic drugs that cause neurological side effects carries the risk of structural damage to the nervous system, characterized by irreversible mouth-face dyskinesias. This risk is increased by the presence of brain damage or disease whether due to ECT, leucotomy or senile degenerative changes with or without cerebrovascular disease. ... ECT induced brain dysfunction, with cerebrovascular permeability changes as the underlying pathogenic substrate, appears to lower the threshold of resistance to extrapyramidal side effects. ... Neuronal dysfunction...tends to diminish the reparative processes against the neurotoxicity of phenothiazenes." (Elmar G. Lutz, 'Shortlasting Akathisia During Combined Electro-convulsive and Phenothiazine Therapy,' Diseases of the Nervous System, April 1968)

Are you aware that the president of the RCP, Dr. Robert Kendell, and his associates, confirmed the cerebrovascular permeability changes identified by Lutz?

"It is known that ECT produces a temporary breakdown of the blood-brain barrier (BBB) and this is probably due to the concomitant increase in blood pressure and cerebral blood flow. It is also known that repeated convulsions at short intervals produce cerebral oedema. It has been shown that macromolecules leak into cerebral tissue during the temporary breakdown of the BBB induced by ECT. This would cause an increase in the relative osmotic pressure of the brain." (J. Mander, A. Whitfield, D. M. Kean, M. A. Smith, R. H. B. Douglas, and R. E. Kendell, 'Cerebral and Brain Stem Changes After ECT Revealed by Nuclear Magnetic Resonance Imaging,' Brit. J. Psychiat. (1987), 151)

Do you know that cerebrovascular damage is a trigger for paranoid psychosis, which if ECT-created, is iatrogenic psychosis?

"A high prevalence of impairment of the BBB was found. The condition was detected in a quarter of the total patients, but in the younger ones, the prevalence was still higher. No reference material is available, since impairment of the BBB has not previously been studied in psychiatric patients. The high prevalence of impairment of the BBB found in this material rules out any suspicion of a chance coincidence between such impairment and paranoid psychosis. ... ...we cannot exclude the possibility of a common aetiological agent, with psychosis and impairment of the BBB as parallel effects. Several circumstances contradict the assumption that impairment of the BBB is an effect of psychosis.... ... Impairment of the BBB is more probably a cause than an effect of the psychotic disorder...; it might generate, precipitate, or trigger the psychotic disorder. The impaired BBB might, for example, allow entry of substances with effects toxic to the brain which, at least in predisposed individuals, would cause psychosis. ... The highly significant difference in age at onset of psychosis was the one variable investigated that clearly separated the patients with impairment of the BBB from those without." (Axelsson, Martensson and Alling, 'Impairment of the Blood-Brain Barrier as an Aetiological Factor in Paranoid Psychosis,' Brit. J. Psychiat., 1982)

It isn't beyond the bounds of feasibility that the cerebrovascular damage acknowledged to occur with ECT is the source of a range of physical illnesses afterwards complained of, and that ECT results in a weakened immunological defence system.

"It is known that a toxin...or a virus might cause autoimmune reactions to occur. Changes produced in brain cells may cause the body's immune system to think that foreign cells are present and marshal a "self-against-self" reaction against the damaged nerve fibres, similar to what happens in an allergic reaction elsewhere in the body. Brain autoantibodies have been found circulating in old...animals and may represent a breakdown in the membrane that normally separates the blood and body. This membrane normally keeps the antibodies separate from the brain antigens. The level of brain antibodies in the blood of patients with dementia is significantly higher than in age-matched controls without dementia." (Michael A. Weiner, 'Reducing The Risk of Alzheimers,' Gateway Books, 1987.

Obviously, it isn't good for one to have an immune system that has been impaired. It can even be downright dangerous:

"Life table analysis of time patterns of deaths of ECT recipients and depressed nonrecipients for all causes of death showed that ECT recipients died sooner after first hospitalization than patients not receiving ECT. ... The tendency for deaths to occur in ECT recipients earlier than in nonrecipients does not become pronounced until five to ten years following first hospitalization." (Babigian and Guttmacher, 'Epidemiologic Considerations in Electroconvulsive Therapy,' Arch. Gen. Psychiat., Vol. 41, March 1984)

Of course, by no means all recipients of ECT live long enough to worry about long-term mortality:

"Twenty-five per cent of respondents [Consultant Psychiatrists] had experience of death or major medical complication occurring during ECT and 9% had had personal experience of a defibrillator being used, although only 3% had seen it save a patient's life." (Benbow, Tench and Darvill, 'Electroconvulsive therapy practice in north-west England,' Psychiatric Bulletin (1998), 22)

A possibility exists that the increased mortality risk over time might be linked to dysregulation of homeostasis caused by ECT:

"Some of the most characteristic changes [with ECT] ...are the rapid alteration in sleep rhythm, appetite, weight, water metabolism and the menstrual cycle." (Martin Roth, 'A Theory of E.C.T. Action and Its Bearing on the Biological Significance of Epilepsy,' J. Ment. Sci., Jan '52)

A hypothalamic region compromised by ECT would provide a physical basis for the morbidity that dogs survivors. The hypothalamus is integral to the sympathetic nervous system and the most important brain centre dealing with homeostasis.

"The evidence that E.C.T. affects the hypothalamus is mostly indirect, though the uniformity with which the hypothalamus reacts to almost every form of stress leaves little doubt that E.C.T. will act similarly." (W. Ross Ashby, 'The Mode of Action of Electro-Convulsive Therapy,' J. Ment. Sci., 1953)

A critical outcome of disruption to homeostasis is hypothermia. Although hypothermia has been causally linked to chlorpromazine, psychiatry has long known that ECT is similarly associated with hypothermia. Actually hypothermia occurs naturally only in extreme conditions, so it would certainly be fascinating to ascertain how many of the apparently fit elderly who succumb received ECT at some time in their lives, with the hypothalamus remaining enduringly compromised.

"[Delay et al.] pointed out that this therapy [chlorpromazine] is "related to artificial hibernation [a.k.a. hypothermia] in that it makes use of a new, central-action sympathicolytic, administered to achieve a continuous effect, which seems to play an essential part in hibernotherapy..." It is of much interest that one of the previously referred to physiologic common denominators of ECT, insulin coma, and histamine, namely antisympatheticoadrenal action, is here pinpointed...." (M. Sackler, R. R. Sackler, F. Marti-Ibanez and M. D. Sackler, 'The Great Psysiodynamic Therapies,' in 'Psychiatry: an historical reappraisal, Hoeber-Harper, 1956)

Agreed to be related, homeostatic disruption and epileptogenesis from ECT were legitimated as therapeutic brain re-regulators:

"The [delta] rhythm can be induced in young patients by many electric fits repeated without due intervals between them. ... the failure of homeostasis as a result of which delta rhythm appears in the EEG have been the subject of investigation by many workers, but notably by Darrow et al. [J. Neurophysiol., 4, 1944, 217-226] and Gibbs et al. [Arch. Neurol. Psychiat., 47,1942, 879-889]." (Denis Hill, 'The Relationship of Electroencephalography to Psychiatry,' J. Ment. Sci. (91), 1945)

"The fit may, of course, result from a general breakdown of homeostasis. ... There is also the therapeutic action of E.C.T. in a variety of mental states to raise the possibility that the fit might have some part to play in the mechanisms mobilized during metabolic stresses for the restoration of equilibrium." (Martin Roth, 'A Theory of E.C.T. Action and Its Bearing on the Biological Significance of Epilepsy,' J. Ment. Sci., 1952)

Yet delta rhythm is linked not to ECT as treatment for 'illness' but with ECT used to induce submission or 'manageability':

"...the common factor related statistically to delta rhythms is a comparatively docile attitude to suggestions from others. The terms 'malleable', 'easily helped', 'easily led' were used and the word that seems most apt...is 'ductile.' (W. Grey Walter, 'The Living Brain,' Penguin, 1961)

"On a few occasions we have administered MMECT [Multiple Monitored Electroconvulsive Treatment; i.e. intensified ECT with EEG and ECG monitoring] on an emergency basis, within an hour after admission, to patients who were extremely upset and not controlled with heavy sedation. Each time we have found that the patient is much more at ease and tractable on awakening from treatment and no longer presents problems in hospital management." (White, Shea and Jonas, 'Multiple Monitored Electroconvulsive Treatment,' Am. J. Psychiat. 125:5, 1968)

Pathological ductility is a known and well understood property of extensive ECT. It puts people at risk of violations:

"Two senior psychiatrists are being investigated on suspicion of raping or sexually assaulting dozens of female patients. ... One alleged victim... claimed [the accused psychiatrist] ensured her compliance with repeated sex attacks by subjecting her to excessive amounts of electro-convulsive therapy...." ('Psychiatrists accused of serial rapes,' Lois Rogers, The Sunday Times, 24.1.'99)

It has been acknowledged that no sound clinical justification for ECT used either too frequently or extensively exists:

"The results of the studies which gave the longest courses of ECT, twelve or more ECTs, did not indicate that their patients showed a greater responsiveness to real ECT than the patients in the remaining nine studies which gave less than twelve treatments. Frequency of ECT administration does not seem to alter responsiveness to ECT. Strongren (1975) has shown that patients' response to ECT is the same whether it is given two or four times per week." (Dr. Graham Sheppard (Ticehurst House Hospital), 'A Critical Review of the Controlled Real versus Sham ECT Studies in Depressive Illness,' 1988)

It must be stressed that even more so than the standard version, Intensive ECT (a.k.a. 'the Page-Russell Method') was based on experimental work and was not of proven validity. Of this form of ECT Page and Russell stated, "We believe its greater effectiveness over ordinary electroconvulsant therapy is due to the fact that larger stimuli are given in a shorter time." Hence, the use of Intensive ECT was founded on belief i.e. on personal opinion and unsubstantiated polemic.

"In the five years since two of us described intensified electroconvulsant therapy (Page and Russell 1948) we have treated more than 3500 further cases involving more than 15,000 treatments. Many critics seem to have a wrong conception of the method, and believe that the patient receives ten separate treatments in one day. We therefore emphasise that the course normally consists of one treatment daily, and is not given twice a day except in the severest cases. The method originally consisted in giving an initial stimulus of 150V for one second. This stimulus was immediately followed by seven further stimuli of one second each at 150V at intervals of half a second. The number of extra stimuli was increased by one at subsequent daily treatments, up to ten on the fourth day. More recently we have increased the number of extra stimuli, and aim to give sufficient in each case to maintain the tonic phase long enough to take the place of, and eliminate, the clonic phase of the fit. The number required varies with different patients, and is usually between eight and fifteen. The lower number is sufficient in an elderly patient, whereas a young schizophrenic may require fifteen or more. The elimination of the clonic phase may also be achieved with a continuous stimulus of from ten to fifteen seconds." (R. J. Russell, L. G. M. Page & R. L. Jillett, 'Intensified Electroconvulsant Therapy,' The Lancet, 5.12.'53)

"The general conclusion from this survey...is that irreversible sequelae of electrically provoked convulsions are infrequent.... Their occasional occurrence cannot be denied, however, particularly if the number of electric shocks had been very large or shocks had been given (as is done in the so-called intensive treatment) in rapid succession, thus approximating to the events of status epilepticus which is well known to cause more severe sequelae than single seizures. Since frequency and intensity were both marked in our two cases the occurrence of a mild marginal gliosis and patchy astrocytosis of the white matter should not cause surprise. This view is in complete agreement with that of Scholz (1951) who saw no reason why electrically induced convulsions, particularly if they were frequent, should not cause the same type of histological sequelae as is observed after spontaneous epileptic convulsions." (J. A. N. Corsellis and A Meyer, 'Histological Changes in the Brain After Uncomplicated Electro-Convulsant Treatment,' J. Ment. Sci. (1954), 100)

Increases in frequency could also be achieved by giving several convulsions per day over several days, a variation of ECT known as "Regressive." It leaves the person helpless, confused, apathetic, mute, incontinent and unable to eat without assistance.

"Regressive" electroplexy had no lasting beneficial effect on eighteen schizophrenic cases treated. ... This form of physical treatment is not only difficult to carry out, but also involves considerable risks. In the light of our experiences we have discontinued the use of "regressive" electroplexy." (Paul L. Weil, '"Regressive" Electroplexy in Schizophrenics,' J. Ment. Sci. (1950), 96)

Despite lack of verification for the effectiveness of variants of conventional ECT involving increases in the temporal frequency of treatments, it remains available as 'Multiple Monitored Electroconvulsive Therapy' (MMECT).

"Despite the fact that prolonged seizures represent a potential risk for the development of neurologic sequelae and are not associated with increased therapeutic benefits, this phenomenon has not been adequately dealt with in the psychiatric literature, and many practitioners are not aware of its significance, detection, and management. ...
In the more recent technique of multiple monitored ECT, in which two or more EEG-monitored seizures are evoked during a single period of anesthesia, prolonged seizures occur on a much more frequent basis, lasting as long as an hour" (Weiner, Volow, Gianturco and Cavenar, 'Seizures Terminable and Interminable with ECT,' Am. J. Psychiat. 137:11, 1980)

It is surely necessary to wonder what anyone ever was or is doing utilising techniques of ECT in such a way as to induce the brain rhythm of pathological states linked to disequilibrium, through creating a breakdown of the controlling mechanisms of homeostasis normally so carefully preserved by the autonomic nervous system, especially given the supposed mental illnesses that ECT supposedly treats are NOT accompanied by changes in the EEG

"...in what may be called "the problems of function" provided by the main psychiatric reactions...and in relation to individual differences of temperament, intelligence and personality, in all these the EEG has so far proved of little value." (Denis Hill, 'The Relationship of Electroencephalography to Psychiatry,' J. Ment. Sci. (91), 1945)

"Occasionally disorders of thought are found associated with wildly exaggerated alpha characteristics, but mental illness is usually accompanied only by the most subtle and evanescent changes in the EEG." (W. Grey Walter, 'The Living Brain,' Penguin, 1961)

Make no mistake, it is ECT that causes abnormal alterations in the EEG associated with pathological ductility, compromised homeostatic functioning and epilepsy and, through induced epileptogenesis, with behavioural and personality disorders. Clearly, the EEG plays a pivotal role in any exploration of ECT.

"...slow delta rhythms are rarely recorded in normal, awake adults. The do appear, however, in various pathological states and are interpreted as evidence of pathology. ... EEG studies spanning a 28 year period show that ECT alters brain physiology from normal to abnormal. These changes, principally a slowing of the EEG waves, are similar to those found in epilepsy, mental deficiency, and other neuropathologies. The EEG changes associated with ECT appear to be extremely long-lasting; very possibly they are permanent. They do not tell us whether a patient has lost his memory, for that you have to ask the patient. They do tell us that ECT can cause profound alterations in brain function." (Prof. Peter Sterling (Neurobiology), in his testimony for the Standing Committee on Mental Health of the Assembly of the State of New York, 5.10.'78)

"There are now [in 1970] available over twenty studies of the effects of unilateral ECT.... Of these, a few have looked at subsequent EEG records, and most have found evidence of electrical disturbance (e.g. slow waves) ipsilateral to the side of electrode placement." (James Inglis, 'Shock, Surgery and Cerebral Asymmetry,' Brit. J. Psychiat. (1970), 117)

Variables are related in a complex pattern and metabolic impact is also reported, often agreed to be devastating:

"The failure to find evidence of cerebral hypoxia, anaerobic metabolism, or electrolyte shifts does not imply that cerebral metabolism is normal during seizures. In our patients...there was a rise in venous PCO2 [carbon dioxide tension] without a concomitant fall in oxygen, indicating that the cerebral RQ [respiratory quotient] increased. ... Such findings suggest either that substances other than glucose are being metabolized (e.g. pyruvate) or that substances such as amino acids and proteins are being decarboxylated without being oxidized for energy. Geiger demonstrated a shift in metabolism away from exogenous glucose to endogenous cerebral substances in the perfused cat brain during electrically or chemically induced seizures. He demonstrated a shift to oxidation of nonglucose substances during the seizure and a period of increased glucose uptake postictally, the latter suggesting that endogenous substrates were being replaced. If endogenous substances essential to normal cerebral metabolism are depleted during seizures, one might expect postictal brain dysfunction until repletion even without hypoxia. At some point during repeated seizures, depletion of cerebral substances might become irreversible and permanent brain damage ensue. Thus postictal EEG flattening and coma need not imply cerebral hypoxia." (Posner et al., 'Cerebral Metabolism During Electrically Induced Seizures in Man,' Arch. Neurol., Vol. 20, April 1969)

"ECT causes extracellular retention of sodium and water according to Altschule and Tillotson. This may be responsible for the facial coarsening often noted during ECT. Further, significant changes in sodium and potassium concentrations as well as the resultant shift in water balance would affect neuronal function and personality." (A. M. Sackler, R. R. Sackler, F. Marti-Ibanez and M. D. Sackler, 'The Great Psysiodynamic Therapies,' in 'Psychiatry: an historical reappraisal, Hoeber-Harper, 1956)

Are psychiatrists always careful in their administration of ECT?

"I would like first of all to ask why their electrodes are soaked for 30 seconds? I suggest that they would have fewer failures if they ensured soakings of at least 30 minutes." (L. Rose,'Failure to Convulse With ECT' (Correspondence) Brit. J. Psychiat. (1988), 153)

In fact, although throughout the foregoing the assumption is that ECT is properly administered and monitored, with the welfare and safety of patients the principal concern, this has frequently not been the case.

"...a seizure of only 6-10 minutes' duration can be associated with both metabolic insufficiency and delayed return to baseline neurologic function, even in the presence of apparently adequate oxygenation. ... ...in the more recent technique of multiple monitored ECT, in which two or more EEG-monitored seizures are evoked...prolonged seizures occur on a...frequent basis, lasting as long as an hour. ... The fact that prolonged seizures have been reported only in the presence of EEG monitoring raises the question of whether this phenomenon actually occurs on a more frequent basis." (Richard D. Weiner et al, 'Seizures Terminable and Interminable with ECT,' Am. J. Psychiat., 137:11, November 1980)

"Ectron equipment has not been designed for use with EEG because there has been no demand. EEG monitoring has rarely been used in the UK, unless for research." (John Pippard, 'Audit of Electroconvulsive Treatment in two National Health Service Regions,' Brit. J. Psychiat. (1992), 160

"As early as 1950, Bankhead and colleagues suggested that cardiac ectopic phenomena occur during the 'deepest cyanosis following the convulsion', but the use of oxygen during ECT did not then become routine. In a description of ECT in 1968 the shock was delivered 50 seconds after the relaxant and, following the clonic phase, three hand ventilations were delivered using, 'room air...and never oxygen' (Pitts et al., 1968). As recently as 1979 it has been claimed that oxygenation during ECT is unnecessary (Joshi, 1979), although apnoea after the shock can last for a few minutes, and will cause significant hypoxia if untreated. The present study was designed to monitor oxygenation in the clinical situation during routine anaesthesia and ECT. Significant hypoxia was demonstrated.... ...
As...over 50% of the anaesthesia for ECT is performed by anaesthetists in training, teaching should emphasise the need for adequate oxygenation." (Steven R. Swindells and Karen H. Simpson, 'Oxygen Saturation during Electroconvulsive Therapy,' Brit. J. Psychiat. (1987), 150)

Do the psychiatrists who administer ECT have under control even such variables as the current waveforms and frequency or the voltage and energy involved in delivering electricity to the brain? Seemingly not:

"Electronarcosis is more scientific, because a current of known intensity is passed through the patient. In electric convulsion therapy, on the other hand, the actual current passed through the patient is not known, as the patient's resistance drops during the passage of the current, and these changes are not compensated for as in electronarcosis." (Paterson and Milligan, 'Electronarcosis: a new treatment of schizophrenia,' The Lancet, August, 1947)

"The actual impedance of the skull cannot be measured and the amount of electricity passing through the brain cannot be known for any given setting of the ECT apparatus." (John Pippard, 'Audit of Electroconvulsive Treatment in two National Health Service Regions,' Brit. J. Psychiat. (1992), 160)

"Drs Pippard & Russell [Brit. J. Psychiat. (1988), 152, 712-713] are correct in stating that "the optimum parameter levels for ECT are still uncertain". Indeed, it has been argued that the exact effects, if any, of each parameter are either unknown or, at best, ill understood. This need not be so, however. No other medical treatment is administered "blindly", to use the term of Drs Pippard & Russell, and it would appear that remaining uncertainties in ECT are due more to the inability to fully control dosage.... Now that treatment can proceed in a controlled and repeatable fashion, thanks to computer technology, one can hopefully expect the publication of research results providing more and more information on the effects of duration, frequency, pulse width, potential, current, and energy on the effectiveness of ECT." (Ivan G. Schick, 'Failure to Convulse with ECT,' Brit. J. Psychiat. (1989), 154 (correspondence))

"Shocks higher than the threshold dose will cause cognitive impairment in proportion to the overshock. ... This threshold dose varies 1 to 40 from one patient to the next and clinics have no way of determining this dosage. ... The dose of electricity is given by habit rather than by rational strategy and routine settings vary fourfold between clinics." (extracts from the Pippard Report on ECT)

"There is also anecdotal (non-controlled) evidence that a greater incidence of ECT side effects might affect therapeutic response; e.g. in a circular distributed by Ectron, the largest UK manufacturer of ECT machines to psychiatric hospitals throughout the UK in December 1985, it is stated that Ectron's 'early generation' of 'constant current' ECT machines, which were designed to 'achieve minimal side effects,' had achieved 'inadequate clinical response' despite the fact that convulsions had been induced. They went on to say that their next generation of constant current machines, which would be designed to deliver more electrical energy (and therefore increase the risk of side effects) should 'ensure a good clinical response.' ...
...one study (Warren & Groome, 1984) which compared high energy pulse current and low energy pulse current with high energy sinusoidal current did not find any significant difference between the different waveforms in one aspect of memory function: 'acute general memory.'" (Dr. Graham Sheppard (Ticehurst House Hospital), 'A Critical Review of the Controlled real versus Sham ECT Studies in Depressive Illness,' 1988)

"An unjustified outcry concerning "side-effects" of ECT...arose, leading to a concentration on reducing "side-effects" which was at the expense of clinical effectiveness. Unfortunately, the development of constant current pulse-type stimuli...enhanced the problem, since they were more efficient in producing seizures with a much lower dosage and also reduced the side-effects. It was firmly believed that the clinical effect would always be present provided that a seizure was produced. It is now clear that a larger stimulus is necessary to ensure a good clinical response. (R. J. Russell (originator of 'Ectron'), 'Inadequate Seizures in ECT,' Brit J. Psychiat. (1988), 153)

Clearly ECT has dual features: shock and convulsions. A long running dispute exists about which of these should be claimed as the therapeutic agent, and also about which one causes the greatest cerebral damage:

"These cases show that irreversible cerebral damage can be caused by E.C.T. but leave unanswered the question of how much of the damage is due to the current and how much to the effect of the convulsion." (Maclay, 'Death Due to Treatment,' Proceedings of the Royal Society of Medicine, Vol. 46, Jan-Dec '53)

"[In the Forties] Wilcox discovered that the strength of an electrically induced grand mal seizure did not depend upon any more electricity than that required to induce the seizure. This meant that "adequate" convulsions could be induced with much lower dosages of electricity than had previously been used, and that the Cerletti-Bini devices were utilizing much more electricity than needed to induce such convulsions. Cerletti and Bini's device, then, was not an electroconvulsive device, but an electroshock device. ...
It remained only for the investigator to report that there was no possibility of administering EST without the damaging effects, as both the damage and the "therapeutic" effect appeared to be the result of suprathreshold dosages of electricity. But neither Wilcox, Freidman, nor Reiter made any such announcements. Rather than challenge colleagues who were damaging the brains of thousands of persons yearly, Wilcox and Reiter...allowed Impastato and colleagues to introduce the...Molac II, a Cerletti-Bini style SW AC device, capable of administering convulsions many times over seizure threshold. This was, in effect, the first deliberately designed...EST apparatus." (Douglas G. Cameron (World Association of Electroshock Survivors), 'ECT: Sham Statistics, the Myth of Convulsive Therapy, and the Case for Consumer Misinformation,' The Journal of Mind and Behaviour, 1994)

"Heath and Norman (1946) had suggested that a convulsion was not essential in order to gain benefit from electric therapy and that the benefits derived were due to hypothalamic stimulation." (Myre Sim (ed.), 'Guide to Psychiatry,' Churchill Livingstone, 1981)

Whatever the reasons, psychiatrists have been loath to admit it's the electricity that both 'works' and causes 'side effects':

"ECT is in no sense electrical treatment..., but only the use of an electrical stimulus...to set off an epileptiform disturbance in the brain; it is this disturbance which is therapeutic. ... We do not pit the mysterious force of electricity against (mysterious) mental illness, as a hostile lay public may believe.... So electroconvulsive therapy as a name has all the wrong associations and helps to perpetuate the bad image of the treatment. A more accurate name would be relaxant ictal therapy (RIT), which would be better for public relations." (John C. Cranmer (Institute of Psychiatry), 'The Truth About ECT,' Brit. J. Psychiat. (1988), 153 (Correspondence))

"After Ottosson's (1960) work, cognitive impairment was generally regarded as an effect of the electricity mainly, and the therapeutic benefit of ECT was attributed to the seizure. ... [However] many long-held assumptions were false and there is increasing evidence that...the degree to which electrical dose exceeds seizure threshold, and not the absolute dose administered, determines dosing effects on clinical outcome and the magnitude of cognitive deficits." (John Pippard, 'Audit of Electroconvulsive Treatment in two National Health Service Regions,' Brit. J. Psychiat. (1992), 160)

ECT is allegedly used primarily to treat depression … ¡ but the issue isn't as clear-cut as it might seem:

"...sham ECT involves all the procedures associated with real ECT except the passage of electricity through the head. ... ...the reported data at the end of the controlled phase of the [thirteen published] studies [reviewed] and subsequent follow-up data, as a body of evidence, does not...significantly indicate that real ECT is more effective than sham ECT in treating depressive illness." (Dr. Graham Sheppard, 'A Critical Review of the Controlled real versus Sham ECT Studies in Depressive Illness')

Perhaps a bit of a con is being perpetrated. Strangely, the authors of a study involving more than 2,500 first recipients of ECT inadvertently remark over-diagnosis of 'depression' in those patients sent for ECT:

"...depression (endogenous and neurotic) was heavily overrepresented in the ECT groups. ... The most striking difference between ECT and non-ECT first-hospitalization groups was the preponderance of depressed patients among the ECT population." (Babigian & Guttmacher, 'Epidemiologic Considerations in Electroconvulsive Therapy,' Arch. Gen. Psychiat., Vol. 41, March 1984)

"It is worth noticing that the action of E.C.T. cannot be purely on the factors, whatever they are, that are responsible for depression; for several patients in this series showed distinct improvement though they showed previously no trace of depression." (H. Collins and M. Bassett, 'The Effect of Electro-Convulsive Therapy on Initiative,' J. Ment. Sci., 1959)

If ECT works in depression, let us remember it 'works' even better to modify behaviour - and change the personality:

"Their [i.e. electric shock therapy and leucotomy] main interest to us...is their physical interference with personality... lectric-shock therapy...alters the personality...." (W. Grey Walter, 'The Living Brain, 1961, pp. 82 and 197)

"...the best clinical results are often obtained when the patient is shocked into amentia [i.e. mental deficiency]... "Moderate improvement" means that the patient shows conduct improvement and a general lessening of...symptoms." (Abraham Myerson, 'Further Experience with Electric-Shock Therapy in Mental Disease,' New England. J. Med., 1942)

"Neurosurgery and electroshock are clearly the most controversial and dramatic of mind-control methods and, because of this, warnings were raised within the agency about these methods. In 1952 a C.I.A. document said that "the severity of the treatment, possibility of injury and permanent damage to the subject and the highly experienced personnel required rule these techniques out for the moment."" ('Private Institutions Used in C.I.A. Effort to Control Behaviour,' New York Times, August 2, 1997)

Despite standard denials of any lasting harmful effects, researchers are nonetheless exploring listening tests, in low-key but determined efforts to find the definitive test for cognitive dysfunction from ECT.

"...most studies have either indicated that residual neuropsychological impairment follows ECT, or they have yielded mixed or inconclusive data concerning protracted deficits after ECT. ...It has been found that in dichotic perception tasks [tasks divided into two strongly contrasted groups or classes] normal individuals usually exhibit right-ear superiority in the detection of verbal material and left-ear superiority in the detection of non-verbal material. Trauma to the brain in the vicinity of the temporal lobe in the right hemisphere has been found to result in deficits in the perception of material presented to the left ear." ('Dichotic Perception and Memory following Electroconvulsive Treatment for Depression,' Williams, Iacono, Remick and Greenwood, Brit. J. Psychiat. (1990))

The nature of the covert attempts to discover a test for ECT impairment is particularly striking, since:

"The main result of dominant temporal lobectomy in human patients is to produce a defect of verbal learning, especially of verbal material presented through the auditory modality. It is contended...that there may be a close resemblance between the side effects of various forms of temporal lobectomy and those of the corresponding kinds of ECT. ... The results at the time of the three month follow-up demonstrated that verbal learning impairment was still evident in the patients who had received dominant hemisphere ECT." (James Inglis, 'Shock, Surgery and Cerebral Asymmetry,' Brit. J. Psychiat. (1970), 117)

Which brings us to that old chestnut - memory loss following ECT:

"In the early days of shock therapy, changes in memory were believed to be important to the therapeutic process, and memory impairment was encouraged by allowing the patient to remain apneic and cyanotic until normal breathing occurred after each seizure." (Max Fink, 'Myths of Shock Therapy,' Am. J. Psychiat., 1977)

"...it seems clear that we do not yet know with sufficient precision the frequency of the significant persistent memory loss that does apparently rarely follow ECT, and we do not know anything about patient characteristics (e.g. age, sex, type of lateralization of brain functions) that may increase its likelihood. Many more studies...are needed." (Culver, Ferrell and Green, 'ECT and Special Problems of Informed Consent,' Am J. Psychiat 137:5, 1980)

"Does the sharing of such information [about the risk with ECT of permanent memory loss] constitute a risk in itself? It is hard to imagine that any patient who has been fully informed of the possibility of permanent, near-total memory loss would consent to such a procedure." (Carl Salzman, 'ECT and Ethical Psychiatry,' Am. J. Psychiat., 1977)

Near-total memory loss - surely not? Oh yes - sometimes deliberately createdMemory in man "is the bastion of his being. Without memory, there is no personal identity." The psychiatrist who declared this in the course of the 37th Maudsley Lecture (who just happens to be the same doctor who administered ECT calculatedly to 'de-pattern' so-called schizophrenics of their personality), went on to state:

"In the electro-shock procedure, we have a means of producing graduated amnesia, and it is of interest to note that there is a proportional relationship between the number of electroshocks given within a period of time and the extent of the amnesias. It is quite possible, for instance, to produce a long-lasting, probably permanent, amnesia by setting the number of electroshock treatments to be given within a predetermined period." Ewen Cameron, 'The Process of Remembering,' Brit. J. Psychiat. (1963), 109)

There is no mystery concerning how ECT achieves the memory impairment complained of (i.e. an amnesic disorder), accompanied by reduced ability to learn and retain new material. It does so through a local effect on limited brain areas, especially the particularly sensitive structures of the temporal lobes, which include the hippocampus:

"...intervention in certain areas of the temporal lobes has been shown to produce automatism with associated amnesia... it has been found that '...the area of the temporal lobe in which epileptic discharge might produce automatism was the peri-amygdaloid area and the hippocampal zone....' Recent reviews...have strongly suggested that in many human disorders in which learning dysfunction appears as a significant element there is often also to be found evidence to indict malfunctioning of the temporal lobes and their adjacent structures, particularly the hippocampal region. ... The areas most likely to be affected by ECT lie within the temporal lobes and the most probable result of their disturbance is some form of amnesic disorder. The psychological evidence points to close similarities between the behavioural effects of shock and surgery. Both kinds of interference on the dominant side of the brain produce defects of verbal learning; on the non-dominant side they produce defects of non-verbal learning. These parallels imply a pressing need for the systematic study of other modes of ECT that would interfere as little as possible with the normal activity of those parts of the human brain that are essential for adequate learning and memory function." (James Inglis, 'Shock, Surgery and Cerebral Asymmetry,' Brit. J. Psychiat. (1970), 117)

As with the hypothalamus, when ECT is administered involvement of the hippocampus is inevitable:

"Whatever the part of the hippocampus may be in the total picture of electroshock, it must be involved in the highest degree because of its low epileptogenic threshold." (W. T. Liberson and J. G Cadilhac, 'Electroshock and rhinencephalic seizure states,' Confinia neurol., 13, 1953)

What IS going on? Guarding against potential medicolegal exposure is an important consideration. [Note: Although the plaintiff in the first of the following cases lost his case, psychiatry subsequently changed the practice which caused his injuries, with ECT modified by anaesthesia and muscle relaxants afterwards becoming standard practice]:

"Summing up, the Judge stated that "a professional man was not guilty of negligence if he acted in accordance with a practice which was accepted by a competent body of men skilled in that particular art, merely because there was a body of opinion which took the opposite view". He emphasized that the use of E.C.T. was progressive and that "the jury must not look with 1957 spectacles at what happened in 1954", suggesting that failure to use relaxants might now be considered negligent." (J. C. Barker, 'Electroplexy (E.C.T.) Techniques in Current Use,' J. Ment. Sci. (1958), 100)

"Occasionally, doctors have covered up the TD problem: In the important Rennie v. Klein right-to-refuse treatment case, psychiatrists were found to have failed to record evidence of TD, to have denied the prevalence of the syndrome and to have disciplined staff members who persisted in noting dyskinetic symptoms on patient charts. One of the hospitals under litigation had previously told accrediting officials that no patients suffered TD, but a court-ordered study found that 25% to 40% of the patients had TD (Brooks, 1980).

The largest award yet, over $3 million, was made in 1984 in Hedin and Hedin v. United States of America, based on overprescribing and lack of monitoring by a V. A. hospital (Gualtieri et al., 1985). ... The APA [American Psychiatric Association] believes that the lawsuits would have failed if psychiatrists had documented in medical records their monitoring for TD symptoms and their discussions of risks with patients and families. ... [The possibility exists] that TD malpractice may become more likely to be determined by "strict liability" than by "community standards of professional care." The strict liability approach...holds that the product or treatment is so inherently dangerous that the defendant bears a type of automatic responsibility for the detrimental outcome." (Phil Brown and Steven Funk, 'Tardive Dyskinesia: Barriers to the Professional Recognition of an Iatrogenic Disease,' J. Health & Social Behav., 27, 1986)

As well, resistance to recognition plays a part, as was found with Tardive Dyskinesia (TD), now publicly acknowledged as a movement disorder - induced by the neuroleptic drugs extensively used in psychiatry, although listed as a 'mental disorder':

"Psychiatrists often held that symptoms were due to other pathological conditions. For example, many early reports cited the presence of brain damage as evidence for dismissing the existence of persistent TD. ... Subsequent failure to accept evidence of TD or to take adequate measures must be seen as stemming from a desire to protect the pharmacological advances from criticism." (Phil Brown and Steven Funk, 'Tardive Dyskinesia: Barriers to the Professional Recognition of an Iatrogenic Disease,' J. Health & Social Behav., 27, 1986)

"It is suggested by the literature and by observation that ECT-damaged patients exhibit unique behaviour disorders which should not be diagnosed as schizophrenic, psychoneurotic, etc. ... Observers often view these patients as flighty, undependable and angry without apparent reason. It is suggested here that ECT damage be investigated and treated in its own right as an important mental impairment." (R. F. Morgan, 'Electroshock: The Case Against,' IPI Publishing Ltd., 1991)

Once one reads what individual psychiatrists actually say, the level of intellectual and scientific dishonesty - especially official denial of precise knowledge that permits ECT to remain forever a speculative or "progressive" treatment - beggars belief.

"ECT has been held by some to be an intrusive physical technique with inherently unacceptable risks and hence beyond the range of rational choice... We hope the day will soon arrive when we can be more precise in communicating the magnitude of the risks involved.... ... We do not believe that our current lack of precise knowledge makes the patient's decision inordinately difficult; many treatments for which we ask consent in medicine contain a much greater zone of uncertainty about outcome than does ECT." (Culver, Ferrell and Green, 'ECT and Special Problems of Informed Consent,' Am J. Psychiat 137:5, 1980)

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