The Journal of Mind and Behaviour, Winter and Spring 1994, Volume 15, Numbers I and 2 Pages
177-198
ECT: Sham Statistics, the Myth of
Convulsive Therapy, and the Case for Consumer Misinformation
Douglas G. Cameron
World
Association of Electroshock Survivors
Abstract
This paper emphasizes that,
contrary to the claims of ECT experts and the ECT industry, a majority, not
"a small minority," of ECT recipients sustain permanent memory
dysfunction each year as a result of ECT. The paper exposes the convulsion
hypothesis, upon which ECT is allegedly based, as mythological. Finally,
through hidden and comparative electrical parameters, it exposes the extreme
destructive power of today's "new and improved" ECT devices.
Introduction
The purpose of this paper is
threefold: to identify misleading or false information on memory damage
disseminated by electroconvulsive/electroshock therapy (ECT/EST) device
manufacturers as well as by the American Psychiatric Association (APA); to
provide historical and mathematical proof that convulsive therapy is a myth;
and to show that modern ECT/EST devices are much more powerful, not less
powerful, than ECT/EST devices of the past.
ECT is the passage (for 0,1
up to 6 seconds), usually from temple to temple through the frontal lobes, of
electric current, for the purpose of inducing "therapeutic" grand mal
convulsions. Follow-up studies about the effects of ECT in which recipients
themselves evaluate the procedure are both rare and embarrassing to the ECT
industry. The outcomes of these studies directly contradict propaganda
regarding permanent memory loss put forth by the four manufacturers of ECT devices
in the United States (Somatics, MECTA, Elcot, and Medcraft), upon whom
physicians and the public rely for information, much as the public relies upon
pharmaceutical companies for information on drugs.
One of the first and best
prospective follow-up studies on ECT recipients was conducted over 40 years ago
by Irving Janis (1950). He merely asked ECT recipients personal, mainly
biographical questions before they underwent ECT, then again several weeks and
months later. In all cases, whether or not the recipients themselves recognized
memory loss, they had forgotten much of their personal history. Unpublished
conversations with many of Janis' patients six months
or one year later (Davies, Detre, and Egger, 1971)
led him to conclude the memory loss was long-term, perhaps permanent. (l) (2).
This is just as the majority of patients have claimed since ECTs inception in
1938 (Brody, 1944; Brunschwig, Strain, and Bidder,
1971; Squire and Slater, 1983).
Few other similar studies
were performed until Freeman and Kendell's (1980)
investigation. In the meantime, doctors (not patients) concluded that ECT was
"successful" and provided "marked improvement" with
"minimal side-effects" (Bender, 1947; Chabasinski,
1978). Freeman and Kendell's study was prompted by
patients who, on BBC radio, described ECT as the most fearful and terrifying
experience of their lives. Freeman and Kendell set out to prove that patients
were "unafraid" of the treatment. They recounted the following:
"We were surprised by
the large number who complained of memory impairment (74%). Many of them did so
spontaneously, without being prompted, and a striking 30 percent felt that
their memory had been permanently affected." (1980, p. 16, italics added)
In this study, shock
survivors were "invited" back to the same hospital where they had
been shocked and many were interviewed by the same doctor who had shocked them.
Some of these persons, when asked if they were afraid of the treatment, might
have been reticent to admit the treatment was indeed frightening. Even the
authors acknowledge this intimidation factor: "It is obviously going to be
difficult to come back to a hospital where you have been treated and criticize
the treatment that you were given in a face-to-face meeting with a doctor. . .
. What is less certain is whether there was a significant number of people in
the mid ground who felt more upset by ECT than they were prepared to tell
us" (1980, p. 16). In any case, almost a full third did complain of
permanent memory loss: an astonishing number considering the circumstances.
Squire and his colleagues
conducted what are perhaps the best-known studies on ECT and memory loss.
Squire and Slater (1983) report that "55% felt that their memories were
not as good as those of other people of the same age and that this was related
to their having received ECT" (p. 5). The average reported memory loss was
27 months' duration for the entire group, and for the
55% who felt they had sustained injury, it was 60 months. Using various
cognitive tests, Squire and Slater could not "find" evidence for the
latter figure, but they estimated an "authentic" average eight-month
gap in memory even after three years. Squire (1986, p. 312) also conceded that
his tests may not have been sensitive enough.
Both Janis and Squire
concluded that 100% of ECT recipients they tested sustained at least some
permanent memory loss, even though some patients denied such loss. Squire's
"authentic eight month gap" after three years was that reported by
the 55% in their study who felt ECT had damaged their memory. Interestingly,
after three years, the 45% who felt ECT had not injured their memories reported
an even larger average persistent gap, of 10.9 months (Squire and Slater,
1983). A control group of depressed patients reported a five-month gap as a
result of depression alone. None was administered ECT, and no one in the group
reported any gap in memory three years later (in fact, control subjects'
memories had cleared only a few months into the experiment). Consequently,
Squire and Slater concluded that there existed some actual permanent memory gap
as a result of ECT, even for ECT recipients denying such an effect. (3)
The Committee For Truth In Psychiatry, founded by Marilyn Rice in 1984,
includes approximately 500 ECT survivors in the United States, who suffer from
permanent memory loss as a direct result of ECT. The Committee has the sole aim
of convincing or forcing mental health authorities to give truthful informed
consent regarding ECT. (4)
Misinformation from the ECT
Manufacturers
An insidious source of
misinformation about ECT's effects on memory are videotapes marketed by some of
the ECT device manufacturers (Somatics, MECTA) and
made available to patients, family members, and shock facility professionals in
the United States and Canada. There are no disclosures in these videos
identifying either Somatics or MECTA as manufacturers
of ECT devices (Fink, 1986; Grunhaus, 1988).
MECTA's (1987) video for
professionals, Health Information Network, features a panel of "experts,"
Richard Weiner of Duke University, Harold Sackheim of
New York State Psychiatric Institute, and Charles Welch of Harvard Medical
School, each interviewed in turn. Welch says: "I tell my patients they may
experience a temporary loss of memory during the time they're having the
treatments and for several weeks after that."' In another MECTA video
designed for individuals and family members, the narrator is slightly more
honest: "[W]e know that 80 to 90 percent of the patients who received bilateral
ECT will report that their memory has recovered within 3 to 6 months after the
treatment, while 10 to 20 per cent may report a change in the quality of the
memory" (Grunhaus, 1988).
Another educational video
prepared by Somatics features Max Fink (1986), leading
proponent of ECT in the United States. Fink states:
"The usual thing that
patients complain about and the family complains [about] is the patient has a
loss of memory and that occurs in every patient, Every
patient has a loss of memory for the treatment itself. . . . Now when we give a
patient treatment over three or four weeks they tend to have a fuzzy idea of
what happened in the hospital But [other than] the treatments themselves, the
patients do not forget what happened in their early life, they don't forget
what happened in their childhood, they don't forget the telephone, they don't
forget the names of their children, they don't forget their work, and they have
no difficulty in learning these things after the treatment is over when they're
better. . . . Now some doctors and some people have said "Well,
electroshock erases the mind and it's like erasing a blackboard." That's
nonsense. If there is any erasure, it is for the events during the hospital. In
many ways we're very grateful that patients forget that. After all, it's not a
pleasant time of your life. For a depressed patient to be in the hospital, it's
not pleasant and if they forget that, that's fine."
Misinformation
from the American Psychiatric Association
In 1990, the APA published recommendations
from an ECT Task Force aimed at specifying the
"standard of care" regarding the administration of ECT throughout the
United States (APA Task Force, 1990). Weiner, Fink, and Sackheim,
who appear on the previously mentioned MECTA and Somatics
videos, are three of the six members of the Task Force. Fink has admitted in a
court deposition to receiving royalties from videos created and marketed by Somatics (Aubrey vs. Johns Hopkins Hospital, 1991).
Psychiatrist Richard Abrams, the most frequently referenced author in the Task
Force Report, owns Somatics (Breggin,
1992, p. 13). Psychiatrist Barry Maletzky, one of the
authors cited in the Report, is viewed in one MECTA
video "pitching" that company's device to potential purchasers (Maletzky, 1987). Numerous videos, books and brochures
created or marketed by these companies are mentioned in the appendix of the
Task Force Report. The names and addresses of all four ECT device manufacturers
are also listed. The APA Task Force Report on ECT might more appropriately be
deemed The Manufacturers' Task Force Report on ECT. (5)
In a sample informed consent
form appended to the Task Force Report, the following statement (which has
appeared in numerous scientific and professional articles) appears: " A small minority of patients, perhaps 1 in 200,
report severe problems in memory that remain for months or even years"
(APA, 1990, p. 158; Foderaro, 1993, p. A16). The
number, however, has unclear origins. This author located only two "one in
200" estimates in the ECT literature. One mention comes from a book by
Fink (1979, p. 52), who states:
"Spontaneous seizures
are a rare manifestation and may be considered evidence of persistent altered
brain function. From a review of various reports, I estimate that post ECT
organic syndrome, including amnesia and tardive
seizures to persist in one in 200 cases."
Fink provides no specific
references or data for his estimate. (6) Even so, the figure again appears in
the appendix of his book, in a sample of informed consent (p. 221). The other
"one in 200" estimate this author located comes from an Impastato (1957) study, but rather than citing cases of
permanent memory loss, Impastato is citing the death
rate for ECT recipients over 60 years of age. Another inaccurate statement in
the Task Force Report was noted by Breggin (1992, p.
14). Citing the Freeman and Kendell (1980) study, the Report states that
"a small minority of patients" report persistent deficits. Unless 30%
is a small minority, the APA is misinforming the public.
One finding stands out from
follow-up studies, including those without conspicuous intimidation factors (Brunschwig, Strain, and Bidder, 1971; Janis, 1950; Small,
1974; Squire, 1986; Squire and Chace, 1975; Squire
and Slater, 1983): a majority of subjects continue to believe they were
permanently injured due to ECT. The "small minority" statistic put
out by the ECT industry, by the APA, and further emulated by the FDA, has no
factual basis.
Patients' claims of years of
permanent memory erasure as a result of ECT, then, are invalidated by
"cognitive tests." Squire and Slater's (1983) estimate of an
"authentic" eight month memory gap is transformed by manufacturers
into "memory changes of events prior to, during, and immediately following
the treatment" (MECTA Corporation, 1993, p. 84). Unfortunately, phrases
similar to these by the manufacturers, which suggest that memory loss is
narrowly restricted, have come to be regarded as sufficient by numerous state
Medical Disclosure Panels. Consequently, potential patients clearly receive
inadequate information regarding memory loss and ECT as part of informed
consent (see, for example, Texas Department, 1993, p. 2; Texas Medical
Disclosure Panel, 1993, p. 14). As has been shown, more persons (the majority
of ECT recipients) are convinced they are suffering permanent memory
dysfunction as a result of ECT, and the memory gap is much wider (at least 8
months) than is currently reported or implied within their various informed
consent protocols by the manufacturers of ECT devices, the APA, and various
mental health authorities. Past and potential ECT recipients were and are being
grossly misinformed.
The
Myth of Convulsive Therapy
It has now become
fashionable to declare brain damage from ECT a thing of the past because of "new refinements" in the procedure and
in the machines (Coffey, 1993; Daniel, Weiner, and Crovitz,
1983; Foderaro, 1993; Kellner, 1994; Weiner, Rogers,
and Davidson, 1986a). Breggin (1979, 1991) has
debunked these "new and improved" claims, yet it appears that the
strongest arguments in favour of ECT are the "new and improved" brief
pulse machines. The implication that the sine wave device of old has been
replaced by the brief pulse device of present lurks behind much of the
continued use of ECT. The remainder of this paper shall examine the "new
and improved" brief pulse device in light of the original aim and purpose
of ECT.
Von Meduna
introduced the concept of convulsive therapy in the 1930s (see von Meduna, 1938; Mowbray, 1959). He
believed that a "therapeutic" or "anti-schizophrenic"
effect could be obtained from the chemical induction of grand mal seizures. In
1938, Cerletti and Bini
introduced electroshock treatment (EST), or convulsions induced without
chemicals. The convulsion appeared to be eliciting what later came to be
described as an "anti-depressant effect" (Alexander, 1953, p. 61).
While "patients" were at first intimidated and terrified, after a
series of ECT they appeared more co-operative, docile, apathetic, or 'in some
cases even cheerier toward their physician. These
"improvements" (as short-lived then as now), appeared to validate von
Meduna's convulsion theory.
From the onset, the
treatment also produced severe memory problems, openly acknowledged as brain
damaging effects by any of a myriad of published papers during that era (Brody,
1944; Ebaugh, Barnacle, and Neuburger,
1942; Sakel, 1956; Salzman, 1947). At the time, both
the "anti-depressant" effect and the memory dysfunction were
attributed to the convulsion. Gaining almost instant popularity among European
psychiatrists, the machine was soon introduced into the United States, and by
1950 as many as 175,000 people annually may have been administered enforced ECT
(Cohen, 1988; Robie, 1955).
A handful of professionals
rejected the idea of brain damage as treatment (Oelmas-Marsalet,
1942; Liberson, 1946; Wilcox, 1946; Will, Rehfeldt, and Newmann, 1948). One
of them was Paul H. Wilcox, who by 1941 had concluded that the
"therapeutic" effect of EST could be successfully separated from its
brain damaging effects (Alexander, 1953, pp. 61-62; Friedman, Wilcox, and
Reiter, 1942, pp. 56-63). Wilcox's own theory of electro-stimulation challenged
Meduna's theory. According to Wilcox (1946,1972), perhaps it was simply electric stimulation of the
brain which created the anti-depressant effect. Providing the correct dosage of
non-convulsive electrical stimulation to the brain might elicit the therapeutic
effects without the brain-damaging convulsion.
This "non-convulsive
therapy" failed to elicit the "therapeutic" effect (Impastato, 1952). However, in his quest to determine the
ideal electrical dosage, 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 (Alexander, 1953, p. 64; Sulzbach,
Tillotson, Guillemin, and Sutherland, 1943, p. 521).
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 (Friedman, 1942, p. 218). Cerletti and Bini's device, then,
was not an electroconvulsive device, but an electroshock device.
Wilcox reasoned that even if
convulsions were necessary for the "antidepressant" effect, by
inducing convulsions with the least electricity dosage possible, side effects
might be reduced or eliminated (Friedman et al., 1942; Impastato,
Frosh, and Robertiello, 1951). Wilcox set out to build
the first "true" ECT machine, which he completed in 1942 (see
Friedman, 1942). By ECT Wilcox meant electrically induced "adequate"
grand mal convulsions, utilizing electrical dosage minimally above seizure
threshold. (7)
To build his machine, Wilcox
collaborated with an electrical engineer named Reuben Reiter. Following
Wilcox's instructions, Reiter first operationalised
Wilcox's minimal dosage concept into a direct current (DC) device, as opposed
to the Cerletti-Bini alternating current (AC) device.
The power of the new Wilcox-Reiter machine was thus immediately reduced by
half. Wilcox was able to induce equal or "adequate" grand mal
convulsions (of at least 25 seconds' duration) with his new machine, showing
the Cerletti-Bini EST apparatus culpable of
electrical overkill (Friedman, 1942, p. 218). The Wilcox-Reiter machine
approached the challenge of threshold convulsions differently than other
devices: from below rather than above threshold (Impastato,
Berg, and Gabriel, 1957). The machine depended upon the cumulative effect of
the electricity in order to induce a convulsion, at the first indications of
which the current was immediately abated. Wilcox, Friedman, and Reiter turned
the switch on and off manually as fast as possible during an application, (8)
which further reduced the current (Friedman, 1942, p. 219; Weiner, 1988, p. 57,
Figure 3). Finally, in 1942, Wilcox and Friedman developed unilateral ECT
(Alexander, 1953, p. 62; Friedman, 1942, p. 218), a method to reduce seizure
threshold, allowing even more reductions in electrical dosage. That usually
consists of placing one electrode on the temple and the other on top of the
head so that a single frontal lobe of the brain is shocked. Unilateral ECT is
often touted today as a "new and improved" methodology (Weiner, 1988,
p. 59).
These methods and
refinements greatly reduced the dosage of electricity required to induce an
"adequate" convulsion. Wilcox now attributed memory loss and brain
damage to such excess electricity (Alexander, 1953, p. 62). The Cerletti-Bini EST device utilized up to 125 volts of
electricity and up to 625 milliamperes of current,
compared to between 20 and 40 volts and an average of 40 milliamperes
for the Wilcox-Reiter ECT device (Alexander, 1953, p. 62; Impastato
et al., 1951, p. 5).
Correspondingly, the
Wilcox-Reiter device greatly reduced, but did not eliminate, side effects. This
was shown in EEG studies comparing the Wilcox-Reiter with the Cerletti-Bini. For example, Wilcox (1946)
and others (Liberson, 1949; Proctor and Goodwin,
1943) found a positive relationship between electrical dosage and abnormal or
slow brain wave activity and memory dysfunction. Brain damage and memory
dysfunction did indeed appear to be more a product of electricity than of
convulsion.
Weiner (1988) criticizes the
early comparative EEG studies as compromised by the possible use of unilateral
ECT and other variations. Still, the relationship between memory impairment,
brain damage and electrical dosage has been corroborated by various early and more
recent studies (Alexander and Lowenbach, 1944; Cronholm and Ottosson, 1963;
Dunn, Giuditta, Wilson, and Glassman, 1974; Echlin,
1942; Essman, 1968; Gordon, 1982; Liberson,
1945a; Malitz, Sackheim,
and Decina, 1979; McGaugh
and Alpern, 1966; Reed, 1988; Squire and Zouzounis, 1986). Many of these studies compared the
effects of electricity to those of other convulsive stimuli on brain tissue.
The results implicated the electricity much more than the convulsion. Specific
observations as a result of applying even sub-convulsive dosages of electricity
to the brain include retrograde amnesia in animals (McGaugh
and Alpern, 1966); constriction of arteries,
arterioles, and capillaries passing through the meninges
of the brain (Echlin, 1942); metabolic changes in the brain chemistry of
animals (Dunn et al., 1974); permeability of the blood brain barrier (Aird, Strait, and Pace, 1956); and other evidence of brain
damage or its effects. According to an APA Fact Sheet (1992) on ECT,
spontaneous seizures, even lasting up to 90 minutes, do not cause brain damage.
Breggin (1979, p. 118) also notes, in his review on
electrical damage to the brain, that "although convulsions of all kinds
can cause biochemical disturbances in the brain, experienced researchers in the
field believe that a case has been made for the electrical current as the main
culprit."
First
Brief Pulse
Also in the early 1940s,
another psychiatrist, W. T. Liberson, who accepted
von Meduna's theory, was inspired by the Wilcox
discoveries to devise yet another method by which to reduce electrical dosage. Liberson (1945b, 1946, p. 755) is credited with producing
the first "brief pulse" (BP) ECT device, using a systematically and
continuously interrupted current. Because of the interruptions, each pulse of electricity
becomes briefer than standard sine wave (SW) or relatively non-interrupted
"wall" current. A single standard SW is 8.33 milliseconds (msec) long, compared to 1.0 msec
for a single standard BP. The Wilcox-Reiter DC device cut the number of waves
in half compared to the Cerletti-Bini AC device. Liberson adopted Wilcox's previous modifications and
introduced electronically systematic continuous interruptions in the current as
well (not merely the less efficient manual interruptions introduced by Wilcox),
so that each individual pulse now became briefer.
For a time, Liberson's BP device was the one using the least electrical
dosage and thus causing the least amount of memory damage (Alexander, 1953, p.
62; Liberson, 1945b, 1946, p. 755; Liberson and Wilcox, 1945). Both Wilcox's and Liberson's devices were ECT machines, in that their purpose
and successful function was to induce constant strength grand mal convulsions
with minimal dosages of electricity (Alexander, 1953, p. 64). However, could
these new machines produce the same therapeutic or anti-depressant effect as
the Cerletti-Bini devices? Did adequate convulsions
without the higher electrical dosages still "work"? Would von Meduna's convulsion theory prove correct?
Brief
Pulse Fails
Despite the advantages of
the Liberson ECT device, physicians in clinical
practice did not use it widely.
Brief pulse devices may have been slightly more expensive to build. Also, the
earliest BP device emitted such low electrical dosage that unconsciousness was sometimes
induced by the convulsion rather than by the electricity. In these instances
the ECT recipient remained conscious until the convulsion, resulting in even
more apprehension than in unmodified (without anaesthesia)
high dosage SW EST (Liberson, 1948, p. 30). The
problem was corrected by a slight increase in the pulse width or by the
utilization of sodium pentothal or both (Liberson,
1948, pp. 30,35). (9) Some psychiatrists believed fear
to be a necessary dimension of the procedure and so increased apprehension may
not have been a negative factor for physicians in using the device (Cook, 1940;
Liberson, 1948, p. 37). However, most clinicians
complained that the same anti-depressant effect attainable with high dosage EST
devices could not be achieved with Liberson's
low-current BP ECT device (Impastato et al., 1957, p.
381). Many psychiatrists were not convinced the treatment worked without the
higher dosage of electricity and its accompanying side effects. In fact, since the treatment appeared less effective with reduced
side effects, many practitioners held side effects to be desirable, an integral
part of the treatment itself (Alexander, 1955).
Although Liberson
claimed complete therapeutic success with his device, he soon began proposing
more treatments per series - in fact, as many as thirty (Liberson,
1948, p. 38). Rationalizing, Liberson proposed
"a relatively great number of BST (brief stimulus) treatments in order to
'consolidate' the therapeutic results. . . . As [BP] treatments are not followed
by as much organic disturbance as with the classical ones, one should be
particularly eager not to stop the treatments too early" (Liberson, 1948, p. 36). Liberson
failed to explain why, if the "anti-depressant" effect was a product
of the adequate convulsion, a greater number of individual treatments would be
required.
As early as 1948 then, it
was known that, even with potent seizures, the "anti-depressant"
effect at low electrical dosages was simply not satisfactory. (10) Liberson (1946, p. 755) must have understood that
electricity was the true "therapeutic" agent, but rather than publish
findings showing von Meduna's convulsion theory
weakened considerably, he focused instead on making his BP ECT device
"work." After calling for more and more treatments, he recommended
longer doses of BP ECT (Liberson, 1945b), eventually
marketing a machine which allowed the current to flow between the temples for a
full five seconds (compared to between 0.5 and one second previously) [see
Weiner, 1988, p. 59, Figure 6]. The Liberson device
could no longer be called an ECT, but was now an EST device. Next,
although Liberson had already increased the
wavelength duration from 0.3 to between 0.5 and one millisecond. (11)
(Weiner, 1988, p. 57), his newer BP model offered adjustable wavelengths from
between 1.5 to two milliseconds. The current was eventually stepped up to
between 200 and 300 milliamps and, finally, Liberson
returned to AC - doubling the original power.
All these modifications, of
course, defeated the original purpose of the BP experiment: to induce adequate
seizures at just above threshold electrical dosage. But even as Liberson continued increasing the
"anti-depressant" effect of his BP machines by augmenting the dosage
of electricity in various ways, the machines still lacked the power of the
original or newer Cerletti-Bini style EST devices.
Physicians everywhere seemed to prefer the higher dosage machines for their
greater effectiveness (Cronholm and Ottosson, 1963; Page and Russell, 1948). Eventually, Liberson stopped increasing the power of his own device any
further.
No one, including Liberson, mentioned that the convulsion theory might have
been shown false, that adequate convulsions by themselves did not appear to
produce a "therapeutic" effect. Nor did anyone suggest that it was
electroshock that psychiatrists preferred, not minimal dosage electroconvulsion at all. By the mid-1950s, the Liberson BP ECT series disappeared forever from the
marketplace.
The
Wilcox-Reiter Device
Just as Liberson
originally adopted the Wilcox-Reiter modification of DC in lieu of AC, Wilcox
and Reiter soon incorporated Liberson's electronic BP
principle into their own device. Wilcox and Reiter held one additional
advantage: a cumulative sub-convulsive technique culminating in just above
threshold seizures. This allowed the Wilcox-Reiter devices to surpass even Liberson's BP in ability to induce grand mal convulsions
with the least electricity possible. The Reuben Reiter Company (producer of the
Wilcox-Reiter machine) continued to produce such ECT devices into the 1950s.
Even so, by 1953, it was
apparent that the Wilcox-Reiter ECT "electro-stimulators" also began
to decline in popularity and could not compete with the more powerful Cerletti-Bini style American EST machines (i.e., Radha, Lectra, and Medcraft). In December 1956, at the Second Divisional
Meeting of the APA in Montreal, Canada, psychiatrist David Impastato
(12) and his colleagues made this announcement:
"These currents
(unilateral currents of the previous Reiter machines) evoke convulsions after
three to five or more seconds of stimulation. In view of this, we may call such
convulsions threshold convulsions. The fracture rate is moderately reduced when
these currents ate used, but apnea, post-convulsive confusion and agitation and
subsequent memory changes are greatly reduced. In spite of these advantages,
the use of unidirectional currents has not found favour in all quarters because
a number of observers feel that with these currents more treatments than with
AC currents are needed to effectuate a remission or to quickly bring under
control such abnormal behaviour as unmanageable agitation and suicidal drives.
The psychiatrist of this faith therefore continues to use the old AC current
machines and makes the best of the undesirable side actions." (Impastato et al., 1957, p. 381)
This announcement was, in
effect, the unprecedented concession that the Wilcox-Reiter experiment with ECT
had failed; that adequate convulsion alone had not, according to clinicians
everywhere, created the desired antidepressant effect Wilcox, Friedman, Reiter,
and Liberson had hoped for, 15 years earlier. ECT had
failed and EST had emerged victorious. Almost all manufacturers of the popular
SW devices recognized the "adequate dosage" precept. The more
powerful their machines became, the more "effective," and
commercially successful.
There was at this time no FDA, no physician adverse effect reporting system, no
psychiatric survivor led civil rights movement, no informed consent
requirements. In short, there was no one but the ECT investigator him/herself
to announce that ECT had failed and that EST was producing the desired effects.
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, Friedman, nor
Reiter made any such announcement. Rather than challenge colleagues who
were damaging the brains of thousands of persons yearly, Wilcox and Reiter,
after voicing half-hidden resentment through Impastato's
announcement and publication (Impastato et al., 1957)
[see footnote 12] against those who failed to use the safer unidirectional
minimal current ECT devices, then allowed Impastato
and colleagues to introduce the newest Wilcox-Reiter machine, 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 Wilcox-Reiter
EST apparatus.
The Molac
II was announced as having a superior feature over "old" Cerletti-Bini style machines, a millisecond of high voltage
current (around 190 volts) in order to render the person unconscious before
delivering two to three seconds of AC current at around 100 initial volts.
Ironically, Impastato and colleagues, just before the
announcement of the new Molac II, had railed against
the side effects of the "classic Cerletti-Bini
EST machine," attributing them to "excessive current used" (Impastato et al., 1957, p. 381). There was no reason to
believe the current intensity of the new device was any lower and whereas the
original Cerletti-Bini machine could administer
current up to five tenths of a second, the new Molac
II had no timer at all. The recommended duration of each treatment was between
two and three seconds, but this was left completely up to the doctor's
discretion. The black button could be held down indefinitely!
After designing the least
dangerous machine in history, Wilcox and Reiter had now designed the most
dangerous EST machine in history, completely discarding their minimal dosage,
adequate convulsion precept of ECT. Ironically, the Impastato
et al. (1957) paper ended by claiming that Molac II
recipients tested on the "Proteus Maze" did no worse than those who
had been treated with previous minimal dosage machines, a contradiction of
everything Wilcox, Friedman, and Reiter stood for and had maintained for the
previous 17 years. Since December, 1956, there have been no ECT devices
produced in America. The same experiment ended similarly in Europe (see
footnote 7).
The
Case for Consumer Misinformation
In 1976, due to the actions
of a California group of psychiatric survivors, Network Against
Psychiatric Assault (NAPA), the psychiatric survivor movement scored a major
victory (Hudson, 1978, p. 146). NAPA had attained for the state of California
the first semblance of informed consent for EST in the United States (perhaps
the first semblance of informed consent anywhere for persons labelled "mentally ill"). At least 30 other
states enacted similar rule changes within the next few years. Psychiatrists in
state institutions had to begin asking patients if they wanted EST. In these
institutions, where EST had been predominantly administered up to this time,
shock .was, for a period at least, largely abandoned. At about this time too,
shock devices came under the scrutiny of the FDA. It was time for the shock
industry to take a different approach.
Also in 1976, psychiatrist
Paul Blachley helped launch an attempt to make shock
respectable again in America. A major part of a campaign to alter and improve
the now very negative image of shock came in the form of "new and
improved" EST devices, specifically the resurgence of Liberson's
BP machine. Blachley's new company, Monitored Electro
Convulsive Therapy Apparatus (MECTA), was soon followed by Somatics,
Elcot, and Medcraft in
producing the "safer wave form," or BP ECT, devices.13 With these
newer devices, hospitals began, as standard procedure, to anaesthetize
patients, the great majority of whom were now private hospital patients with
insurance.
A recent New York Times
article lauded the "modern" brief pulse models as
"improved," and having modifications "like reduced doses of
electricity" (Foderaro, 1993, p. A16). Recently,
the television show 48 Hours featured psychiatrist Charles Kellner of the
Medical University of South Carolina, who regularly administers electric shock.
Kellner (1994) stated: "Well, it's such a different treatment now that
there's almost no comparison. . . . It really is a different treatment now. . .
. Having the seizure is the therapeutic part of ECT; probably about one fifth
of the electricity that was used in the old days. . . ." Such claims are
false or misleading: the new BP devices are neither lower stimulus nor lower
current devices than the older, or even the newer, SW models.
All other electrical
components being equal, simple unmitigated BP (systematic interruptions of SW
current) does in fact lead to reduced electrical dosages. However, aware that
convulsions alone, induced by simple BP, are ineffective, manufacturers of
modern BP devices amplify all other electrical components in order to compensate
for the interruptions. Therefore, modern "souped
up" BP apparatuses re-equal the cumulative electrical charges of the Cerletti-Bini style SW in every respect. For instance, 100
percent power of standard SW will emit the same 500 millicoulombs
of electrical charge as 100 percent power of a modern BP machine such as Somatic's Thymatron DG. While one
would expect reduced charges with BP, in fact, the old standard SW, i.e., Medcraft's 1950 model, emits slightly less charge than the
modern day BP Thymatron DG. This would not be
possible without electrical compensation of BP devices.
This compensation is
accomplished in the following ways:
(a) The frequency is
increased. Frequency is the number of pulses of electricity per second flowing
past a given point. Although sine waves are "wider" than brief
pulses, they are emitted at a constant rate of 120 per second. In comparison,
modern 8P devices can emit up to 180 pulses per second of electricity (e.g.,
MECTA's SR-2 and JR-2), or up to 200 pulses (e.g., Elcot's
MF-l000).
(b) The current is
increased. Current can be defined as electron flow per second and is measured
in amperes or milliamperes (mA).
'The "old" SW devices deliver between 500 and 600 mA
of current. The "new" BP Thymatron DG by Somatics delivers 900 mA constant
current, the MECTA SR/JR devices, 800 mA, and the Medcraft 8-25 BP up to 1000 mA or
one full ampere.
(c) Duration is increased.
Duration is the amount of time the current flows through the brain. Maximum
duration of modern BP machines is four to six times the maximum duration of the
older SW models.
(d) Wave lengths can be
increased in most modern BP devices. The Elcot
MF-1000, for instance, has adjustable brief pulses from a typical one msec up to an atypical two msec. A standard SW is 8.33
msec.
(e) Alternating current is
used. In spite of the fact that both Liberson and
Wilcox utilized DC successfully to induce adequate grand mal convulsions,
modern BP devices utilize AC.
Thus modern BP devices are
made to equal the charge (14) of SW devices in every consideration with respect
to percent of energy utilized. In addition, they surpass the "older"
SW machines in energy output (joules), or actual power emitted. (15) The
following electrical features account for this increase:
(a) Much higher voltages are
utilized. For example, the Thymatron DG utilizes up
to 500 volts; the MECTA SR/JR, up to 444 volts; the new Medcraft
up to 325 volts; and the Elcot MF-1000 up to 500
volts. Compare this to between 120 volts maximum for the oldest sine wave
models and 170 volts maximum for modern SW devices.
(b) Constant current and
continually increasing voltages are properties of all modern BP devices.
Constant current means that the current never fluctuates or descends. This
unique feature of BP devices is accomplished by higher and increasing voltages,
a characteristic not found in SW devices. The constant lower
voltage in the latter results in gradually decreasing currents. Just as
the resistance of a wooden wall can eventually slow down and overpower an
electric drill, so the human skull gradually slows down current. Modern BP
devices maintain a constant current of about one ampere throughout the full
four to six seconds it is emitted, making these devices the most powerful in
ECT/EST history.
The tremendous energy output
of modern BP devices (see footnote 15), the best measure of the machine's
potential destructiveness, is a well-kept manufacturer's secret. The modern day
BP devices are more than four times as powerful as the older SW devices, and
about two and a half times as powerful as modern day SW devices. In fact,
today's "new and improved" BP device is over eight times more
powerful than the original Cerletti-Bini device
renowned for permanent memory loss and upon which Wilcox and Liberson attempted to improve. Modern day BP devices have
not been shown to be cognitively advantageous to SW devices in any modern
study, and the few studies which have claimed cognitive advantages with modern
day BP could not be replicated by other researchers (see Squire and Zouzounis, 1986; Weiner, Rogers, and Davidson, 1986a,
1986b).
Conclusion
Contrary to the claims put
forth by the four manufacturers of EST devices, the evidence
reviewed in this paper clearly shows that the majority of EST recipients report
damage as a result of EST. EST recipients - whether or not they report memory
loss - do, in fact, sustain actual permanent memory loss, averaging at least
eight months, as a result of the procedure.
Modern day BP devices are
not "lower current" machines, as most proponents claim. Through
electrical compensation, they equal SW devices in every respect, and emit far
greater energy. The results of studies claiming cognitive advantages using
modern day BP over SW have not been replicated. Any advantage of the original
BP device has been attenuated in modern day devices.
Hundreds of studies
conducted between 1940 and 1965 (Corsellis and Meyer,
1954; Hartelius, 1952; Heilbrunn
and Weil, 1942; McKegney and Panzetta,
1963; Quandt and Sommer,
1966) demonstrating brain damage have been criticized as "old."
However, since that time, the machines have only become more powerful. Thus few
studies are "old" or irrelevant.
Most experts agree that
current, and not convulsion (APA, 1992; Breggin,
1979, pp. 114, 122; Dunn et al., 1974; Sutherland et al., 1974) is responsible
for long-term memory loss and severe cognitive dysfunction. Yon Meduna's "therapeutic convulsion" is a myth,
convincingly disconfirmed by early minimal stimulus convulsion experiments.
Memory dysfunction and the "therapeutic" effect - which appear to be
products of electricity - may well be inextricably related.
All four manufacturers
continue to claim their devices are convulsive therapy devices. Nevertheless,
because some of the Wilcoxian principles of the past
are being rediscovered today, and because the efficacy of threshold convulsions
is questionable (APA Task Force, 1990, pp. 28, 86, 94), a few BP manufacturers
and researchers who collaborate with the manufacturers have gained enough
confidence to call for even more powerful electrical devices - under the
unsubstantiated claim that BP supra threshold dosages of electricity are safer
than SW supra threshold dosages (Glenn and Weiner, 1983, pp. 33-34; MECTA,
1993, pp. 13, 14; Sackheim, 1991). For instance,
Gordon (1980) rediscovered the adequateness of grand mal convulsions
administered at low electrical dosages. Gordon (1982) later reiterated that
high doses of electricity cause irreversible brain damage. Unaware of the lost
history, Gordon suggested using minimal stimulus machines to induce
convulsions. Deakin (1983) responded that minimal
stimulus machines would be misguided, alluding to
Robin and De Tissera's (1982) important double-blind
study which demonstrated that current is the factor in ECT efficacy - not
convulsions. (16) Sackheim, Decina,
Prohovnik, Portnoy, Kanzler, and Malitz (1986) and Sackheim (1987) published studies corroborating the
relevancy of electrical dosage to efficacy, and Sackheim
restated this theme in a lecture delivered in New York in 1992 (Sackheim, 1992). Today's manufacturers are quietly leaning
away from von Meduna's convulsion theory, away from
the concept of adequate convulsions at minimal dosage and toward an unobtrusive
attempt to legitimise adequate or supra threshold
electrical dosages. (17) These tendencies, coupled with the power of modern BP
devices, should lead to re-appraisal of the devices worldwide.
Manufacturers may have
parted from the convulsion theory exemplified by just above seizure threshold
devices of the past, to what might be just above damage threshold devices of
the present, and if not forced to stop and prove the safety of their devices
(allowing for even more powerful machines), might be embarking upon just above agnosognosic threshold apparatuses of the future.
In summary, modern electric
shock machine companies are attempting to redefine safety from the original
convulsion concept of "just above seizure threshold" to "safer
wave form." The Food and Drug Administration must rescrutinise
today's SW and BP devices, withdrawing their "grandfathered in"
status under convulsive therapy devices. Because they utilize an entirely
different principle, and because they are suprathreshold
devices rather than convulsion-dependent devices, all modern day BP and SW EST
device manufacturers must be required to prove machine safety to the Food and
Drug Administration, prior to further utilization of new machines. All modern
day SW and BP EST devices are more powerful than early instruments. Modern day
BP suprathreshold devices have not proved safer than
SW suprathreshold devices. Side effects have been
convincingly identified as products of electricity. These facts warrant the
elimination of all EST machines from the marketplace.
References
Abrams,
R., and Swartz, C. (1988). ECT
instruction manual. Lake Bluff, Illinois: Somatics,
Inc. Abrams, R., and Swartz, C. (1990). The technique of ECT
[video]. Lake Bluff, Illinois: Somatics, Inc.
Aird,
R.B., Strait, L.A., and Pace, J.W. (1956). Current
pathway and neurophysiologic effects of electrically induced convulsions.
Journal of Nervous and Mental Disease, 123, 505-512.
Alexander, L. (1953).'Treatment of mental disorder. Philadelphia: W.B. Saunders.
Alexander, L. (1955). Modified electroconvulsive therapy with unidirectional current.
Diseases of the Nervous System, 16, 1-4.
Alexander,
L., and Lowenbach, H. (1944).
Experimental studies on electro-shock treatment. Journal of Neuropathology and
Experimental Neurology, 3, 139-171.
American
Psychiatric Association. (1990). The
practice of electroconvulsive therapy: Recommendations for treatment, training,
and privileging. Task Force on ECT. Washington, D.C.:
American Psychiatric Association.
American
Psychiatric Association. (1992). American Psychiatric Association
fact sheet: Electroconvulsive therapy (ECT) [three page flyer]. Washington,
D.C.: American Psychiatric Association.
Aubrey, K. vs. Johns Hopkins
Hospital. (1991). Health Claims Arbitration Office, Dec. 3, 1991, Rockville
Maryland, p. 140.
Bender,
L. (1947). One hundred cases of childhood schizophrenia
treated with electric shock. Transactions of the American Neurological
Association, 762, 165-168.
Breggin,
P.R. (1979). Electroshock: Its brain disabling effects. New York: Springer.
Breggin,
P.R. (1990). Brain damage, dementia and persistent cognitive dysfunction
associated with neuroleptic drugs. Journal of Mind
and Behaviour, 11, 425-463.
Breggin,
P.R. (1991). Toxic psychiatry: Why therapy, empathy, and love must replace the
drugs, electroshock, and biochemical theories of the "new psychiatry. " New York: Sr. Martin's Press.
Breggin,
P.R. (1992). The return of ECT. Readings: A Journal of
the American Orthopsychiatric Association, 7, 12-17.
Brody, M.P. (1944).
Prolonged memory defects following electrotherapy. Journal of Mental Science,
90, 777-779.
Brunschwig,
L., Strain J., and Bidder, T.G. (1971). Issues in the
assessment of post-ECT memory changes. British Journal of Psychiatry,
119,73-74.
Cameron, D.G. (1979). How to survive being committed to a mental hospital. New
York: Vantage Press.
Cameron, D.G. (1991). (Ed.).
Electroshock treatment: 100 cases of permanent memory loss, Vol. I. Unpublished
manuscript, World Association of Electroshock Survivors, P.O. Box 343, San
Marcos, Texas 78667.
Cameron, D.G. (1994).
Passage of the strictest ECT legislation in America: The story behind it and
how it was accomplished. Unpublished manuscript, World
Association of Electroshock Survivors, P.O. Box 343, San Marcos, Texas 78667.
Chabasinski,
T. (1978). The other half. In
L. Frank (Ed.), The history of shock treatment (pp.
26-27). San Francisco: Frank.
Coffey,
C.E. (1993). Structural brain imaging
and ECT. In C.E. Coffey (Ed.), The clinical
science of electroconvulsive therapy (pp. 73-92). Washington, D.C.: American
Psychiatric Press.
Cohen, D. (1988). Social work and psychotropic drug treatments. Social Service
Review, 62, 576-599.
Cook, L.C. (1940). Has fear
any therapeutic significance in convulsion? Journal of Mental
Science, 40, 414.
Corsellis,
J.M., and Meyer, A. (1954). Histological changes in the
brain after uncomplicated electroconvulsant
treatments. Journal of Mental Science, 100, 375-383.
Cronholm,
B., and Ottosson, J.O. (1963). Ultrabrief
stimulus techniques in ECT. II: Comparative studies of therapeutic
effects and memory disturbances in treatment of endogenous depression with the Elther ES apparatus and Siemens konvulsator
III. Journal of Nervous and Mental Diseases, 137, 268-276.
Daniel, W.F., Weiner. R.D., and Crovitz, H.F. (1983).
Autobiographical amnesia with ECT: An analysis of the role of stimulus
waveform, electrode placement, stimulus energy, and seizure length. Biological
Psychiatry, 18, 121-126.
Deakin. J.F. W. (1983). Antidepressant effects of electroconvulsive
therapy: Current or seizure? British Medical Journal, 286,
1083.
Davies. R.K.,
Detre T.P., and Egger, M.D. (1971).
Electroconvulsive therapy instruments: Should they be re-evaluated? Archives of
General Psychiatry, 25, 97-99.
Delmas-Marsalet, P.L.
(1942). L'electro-choc par courant continu. Comptes rendus des Seances. Socieli de Biologie et de ses Filiales
el Associees (Paris), 136, 551-553.
Dunn, A., Giuditta A., Wilson. J.E., and Glassman,
E. (1974). The effect of electroshock on brain RNA and
protein synthesis and its possible relationship to behavioural effects. In M. Fink, S. Kety, and J. McGaugh (Eds.). Psychobiology of
convulsive therapy (pp. 185-197). New York: Wiley.
Ebaugh. F., Barnacle. C., and Neuburger. K. (1943). Fatalities following electroconvulsive therapy. Archives of
Neurological Psychiatry, 49, 107-117.
Echlin, F.A. (1942).
Vasospasm and forced cerebral ischemia. Archives of Neurological Psychiatry,
47, 77-96.
Essman,
W.B. (1968). Electroshock-induced retrograde amnesia in
seizure-protracted mice. Psychological Reports, 22, 929-935.
Fink. M. (1979). Convulsive therapy: Theory and practice .New
York: Raven Press.
Fink. M. (1986). Informed ECT for health
professionals [video]. Lake Bluff. Illinois: Somatics. Inc. Foderaro.
L. (1993. July 19). With reforms in treatment, shock
therapy loses shock. New York Times, p. A16.
Food
and Drug Administration. (1990. September 5). Neurological
devices: Proposed rule to reclassify the electroconvulsive therapy device for
use in treating severe depression. Federal Register, Part
III. 21 CFR Part 882.
Fox, H.A. (1993). Patients' fear of and objection to electroconvulsive therapy.
Hospital and Community Psychiatry, 44, 357-360.
Frank, L.R. (1978). (Ed.). The history of shock treatment. San Francisco: Frank.
Freeman, C.P.L..
and Kendell, R.E. (1980). ECT; I.
Patients' experiences and attitudes. British Journal of Psychiatry, 137,
8-16.
Friedman. E.
(1942). Unidirectional electrostimulated
convulsive therapy. American Journal of Psychiatry, 99, 218-223.
Friedman. E., Wilcox. P.H., and Reiter, R.M. (1942). Electrostimulated convulsive doses
in intact humans by means of unidirectional currents. Journal of Nervous
and Mental Disease, 96, 56-63.
Geyer. H. (1960). Evaluation of hydroxyzine prior to electroshock therapy. Diseases
of the Nervous System, 21, 1-4.
Glenn. M.,
and Weiner. R. (1983). Electroconvulsive
therapy, a programmed text (pp. 33-34). Washington. D.C.: American
Psychiatric Press.
Gordon. D.
(1980). Ruptured spleen in electric convulsive
therapy. British Medical Journal, 280, 1426.
Gordon. D.
(1982). Electroconvulsive therapy with minimal hazard.
British Journal of Psychiatry, 141, 12-18. .
Grunhaus. L. (1988). Electroconvulsive therapy; ECT: The treatment,
the questions, the answers [video]. Ann Arbor. Michigan: University of Michigan
Medical Centre. [Distributed through Lake Oswego, Oregon:
MECTA Corporation).
Hartelius. H. (1952). Cerebral changes following electrically induced
convulsions: An experimental study on cats. Acta Psychiatrica and Neurologica Scandinavica, 77, 1-128.
Heilbrunn. G., and Weil. A. (1942). Pathologic
changes in the central nervous system in experimental electric shock. Archives
of Neurological Psychiatry, 47, 918-927.
Hirsch. C.S., and Martin, D.L. (1971). Unexpected
death in young epileptics. Neurology, 21, 682-690.
Hudson. W.
(1978). NAPA battles shock. In L. Frank (Ed.). The history of shock treatment (pp. 146-152). San Francisco:
Frank.
Impastato. D. (1952). Electrically produced
unilateral convulsions. Diseases of the Nervous
System, 13, pages unavailable.
Impastato, D.
(1957). Prevention of fatalities in electroshock therapy.
Diseases of the Nervous System, 18, 34-75.
Impastato,
D., Berg, S., and Gabriel, A.R. (1957). The Molac-11 - an
alternating current electroshock therapy machine incorporating a new principle.
Journal of Nervous and Mental Disease, 125, 380-384.
Impastato,
D., Frosh, J., and Robertiello, R. (1951). Improved electro-convulsive therapy with low amperage
unidirectional currents. Diseases of the Nervous
System, 12, pages unavailable.
Janis, I. (1950). Psychologic
effects of electric convulsive treatments (I, II, III, post treatment amnesia).
The Journal of Nervous and Mental Disease, 3, 360-397; 469-489.
Kellner, C.H. (1994,
February 2). Electroshock with Susan Spencer [television interview]. In C. Lasiewicz [Producer], 48 Hours.
New York: CBS.
Liberson,
W.T. (1945a). Study of word association processes, part II: Reactions to
"average emotional" and "average neutral" words in normal
and abnormal populations. Effect of electric convulsive
therapy. Digest of Neurology and Psychiatry, 13, pages
unknown.
Liberson,
W.T. (1945b). Time factors in electric convulsive therapy. Yale Journal of
Biology and Medicine, 17, 571-578.
Liberson,
W.T. (1946). Physiological basis of electric convulsive
therapy. Connecticut State Medical Journal, 10, 754-756.
Liberson,
W.T. (1948). Brief stimulus therapy. American Journal
of Psychiatry, 105, 28-39. Liberson, W.T. (1949).
Review of psychiatric progress, 1948. Electroencephalography.
American Journal of Psychiatry, 105, 503-505.
Liberson,
W.T., and Wilcox, P.H. (1945). Comparison
of "brief pulse" technique with Friedman-Wilcox-Reiter technique.
Digest of Neurology and Psychiatry, 8, 292-302.
Maletzky, B.
(1987). Dual channel-JR/SR models [video]. Lake Oswego, Oregon: MECTA
Corporation.
Malitz,
S., Sackheim, H.A., and Decina,
P. (1979). ECT in the clinical treatment of major
affective disorders: Clinical and basic research issues. Psychiatric Journal of
the University of Ottawa, 7, 126-134.
McGaugh,
J.L., and Alpern, H.P. (1966).
Effects of electroshock on memory: Amnesia without convulsions. Science, 152,
665-666.
McKegney,
F.P., and Panzetta, A.F. (1963). An unusual fatal outcome of electro-convulsive therapy.
American Journal of Psychiatry, 120, 398-400.
MECTA Corporation. (1987). Health information network for hospitals and professionals
[video]. Lake Oswego, Oregon: MECTA Corporation.
MECTA Corporation. (1993). MECTA Instruction Manual, SR and JR Models. Lake
Oswego, Oregon: MECTA Corporation.
Medcraft
Corporation. (1984). Medcraft
B24III, Electroconvulsive Therapy Instrument [flyer]. Darien,
Connecticut: Medcraft Corporation.
Mowbray,
R.M. (1959). Historical aspects of electric convulsant therapy. Scottish Medical Journal, 4,
375,
Page,
L.G.M., and Russell, R.J. (1948). Intensified
electrical convulsion therapy in the treatment of mental disorder.
Lancet, 1 597-598.
Proctor,
L.D., and Goodwin, B.A. (1943). Comparative
electroencephalographic observations following electroshock therapy using raw
60 cycle alternating and unidirectional fluctuating current EEG. American
Journal of Psychiatry, 99, 525-530.
Quandt,
J., and Sommer, H. (1966). Zur frage der himgewebsschadigungen nach electtischer krampfbehandlung. Zeitschrift
fur Neurologie und Psychiatrie, 34, 513.
Reed, K. (1988).
Electroconvulsive therapy: A clinical discussion. Psychiatric
Medicine, 6, 29. Robie, T. (1955). Safe electric treatment of
melancholia. The Journal of the Medical Society of
New Jersey, 52, 82-87.
Robin, A., and De Tissera, S. (1982). A double blind controlled comparison of
[he therapeutic effects of low and high-energy electro-convulsive therapies.
British Journal of Psychiatry, 141, 357-366.
Sackheim,
H.A. (1987). Seizure threshold in electroconvulsive therapy.
Archives of General Psychiatry, 44, 355-360.
Sackheim,
H.A. (1991). Are ECT devices underpowered? Convulsive Therapy, 1, 233-236.
Sackheim,
H.A. (1992). An adequate treatment [audio tape].
(Lecture delivered in April, Marriott Marquis Hotel, New York City, Advanced
Clinical Issues in ECT, The Certificate Course.)
Sackheim,
H.A., Decina, P., Prohovnik,
I., Portnoy S., Kanzler,
M., and Malitz, S. (1986). Dosage, seizure threshold, and the antidepressant efficacy of
electroconvulsive therapy. In S. Malitz and
H.A. Sackheim (Eds.), Electroconvulsive therapy:
Clinical and basic research (pp. 398-410). New York: New York Academy of
Sciences.
Sakel,
M. (1956). Sakel shock treatment. In A. Sackler
(Ed.), The great physiodynamic therapies in
psychiatry: An historical perspective (pp. 13-14). New York: Hoeber-Harper.
Salzman, L. (1947). An evaluation of shock therapy. American
Journal of Psychiatry, 103, 676. Small, I.E (1974).
Inhalant convulsive therapy. In M. Fink, S. Kety, and J.L. McGaugh (Eds.),
Psychobiology
of convulsive therapy (pp. 65-77). New York: Wiley.
Somatics,
Inc. (1993). Caution [flyer]. Lake Bluff, Illinois: Somatics,
Inc.
Squire,
L. (1986). Memory functions as affected by
electroconvulsive therapy. Annals of the New York Academy of Sciences, 462,
307-313.
Squire,
L.R., and Chace, P.M. (1975).
Memory functions six to nine months after electroconvulsive therapy. Archives
of General Psychiatry, 32, 1557-1564.
Squire,
L., and Slater, P.C. (1983). Electroconvulsive therapy
and complaints of memory dysfunction: A prospective three-year follow-up study.
British Journal of Psychiatry, 142, 1-8.
Squire,
L., Slater, P.C., and Miller, P.L. (1981). Retrograde amnesia
and bilateral electroconvulsive therapy: Long-term follow-up. Archives of
General Psychiatry, 38, 89-95.
Squire,
L., and Zouzounis, J.A. (1986). ECT
and memory: Brief pulse versus sine wave. American Journal of Psychiatry, 143,
596-601.
Sulzbach,
W., Tillotson, K.J., Guillemin, V., and Sutherland,
G.E (1943). A consideration of some experiences with
electric shock treatment in mental diseases, with special regard to various
psychosomatic phenomena and to certain electrotechnical
factors. American Journal of Psychiatry, 99, 519-524.
Sutherland,
J.M., Tait, H., and Eadie,
M.J. (1974). The epilepsies.
London: Churchill Livingston. Texas Department of Mental
Health and Mental Retardation. (1993). Texas informed consent form for
ECT requiring a signature for each individual treatment. Disclosure and Consent
for Electroconvulsive Therapy. Austin, Texas: Texas Department of Mental Health
and Mental Retardation.
Texas
Medical Disclosure Panel. (1993). Informed consent,
medical treatment and surgical procedure established by the Texas Medical
Disclosure Panel, 601.1; Procedures Requiring Full Disclosure (List A), Section
13; Nervous System Treatments and Procedures.
von Meduna, L. (1938). General discussion of
the cardiazol therapy. American
Journal of Psychiatry, 94, 46.
Weiner, R.D. (1988). The first ECT devices. In M. Fink (Ed.),
Convulsive Therapy (pp. 50-61). New York: Raven Press, Ltd.
Weiner, R.D., Rogers, H.J.,
and Davidson, J.R.T. (1986a). Effects of stimulus parameters
on cognitive side effects, in electroconvulsive therapy. In S. Malitz and H.A. Sackheim
(Eds.), ECT. Clinical and basic research issues (pp. 315-325). New York:
Annals of the New York Academy of Sciences.
Weiner, R.D., Rogers, H.J.,
and Davidson, J.R.T. (1986b). Effects of ECT upon brain
electrical activity, in electroconvulsive therapy. In S. Malitz and H.A. Sackheim (Eds.),
ECT: Clinical and basic research issues (pp. 270-281). New York: Annals of the
New York Academy of Sciences.
Wilcox, P.H. (1946). Brain facilitation, not brain destruction, the aim in electroshock
therapy. Diseases of the Nervous System, 7, 201-204.
Wilcox, P.H. (1972). Electro-stimulation for promoting brain reorganization.
Diseases of the Nervous System, 33, 326-327.
Will, O.A., Rehfeldt, F.L., and Newmann, M.H.
(1948). A fatality in electroshock therapy: Report of a case and review of
certain previously described cases. Journal of Nervous and Mental Disease, 107,
105-126.
Requests for reprints should
be sent to Douglas G. Cameron, World Association of Electroshock Survivors, PO. Box 343. San Marcos. Texas 78667
1, Years after Janis' 1950
study, Marilyn Rice (see below) contacted Irving Janis, and in a personal
telephone interview, Janis explained how, one year later, he had followed up
his 1950 study (unpublished) and how its results appeared reliable.
2, Only Squire, Slater, and
Miller (1981, p. 95) have repeated the Janis prospective study. Even after two
years, and even with reminder cues, 50% of the ECT recipients in this study
still could not recall specific autobiographical events spontaneously recalled
before ECT. This does not preclude the possibility that autobiographical events
which could be "remembered" after two years,
might simply have been re-learned rather than recalled.
3, That
Squire and Slater selected the permanent gap to be the smaller one may indicate
bias. Also, after three years, the larger gaps originally reported may only
have appeared reduced (e.g., to eight and 10.9 months). Squire and Slater's
conclusion that 100% of their subjects suffered an ECT induced average eight
month permanent gap in memory is unquestionably the most conservative
conclusion one may draw from their data. In any case, both studies indicate
that patients under-report rather than over-report
treatment induced permanent memory loss.
4, Larry Squire himself
administered Marilyn Rice a battery of cognitive tests as part of a malpractice
suit she brought, in which she charged that years of her memory were
permanently erased by ECT (Squire was hired by the defence).
In a personal interview with the author, she related that she passed all of
Squire's tests easily and in fact, regarded them as absurd. Throughout her
lifetime, Marilyn contended that eight shock treatments had eliminated, in
addition to treasured personal memories, all the mathematical and cumulative
knowledge of her twenty years with the Department of Commerce in Washington
D.C., where she co-ordinated vital statistics and
activities concerning the National Budget (Frank, 1978). In spite of her
claims, the results of Squire's tests were successfully used in court to prove
her memory.'intact" and she lost her malpractice
suit. Rice, who died in 1992, lobbied the Food and Drug Administration (FDA)
and state legislatures to mandate warnings of permanent memory loss and brain
damage. Her influence on state legislatures may have been demonstrated by the
recent 1993 Texas legislation, S.B. 205, which mandates a fresh signature by
the patient and a fresh discussion with the patient on the "possibility of
permanent irrevocable memory loss" before each individual treatment (not
series) [see Cameron, 1994].
5, The APA apparently
gathered most of its facts from the device manufacturers or those closely
connected with the products; in turn, the FDA obtained most of its information
from the APA (APA, 1990; FDA 1990).
6, Fink's unsubstantiated
statistic was brought to my attention by shock survivor Linda Andre, Director
of Committee For Truth In Psychiatry.
7, Thus, the Americans Wilcox
and Friedman, not the Italians Cerletti and Bini, produced the world's first ECT device. The experiment
with reduced electrical current was repeated in France that same year (Delmas-Marsalet, 1942).
8, In
that sense, the Wilcox-Reiter ECT device should also be credited with being the
first brief pulse device (see below).
9, Eventually, with the
introduction of informed consent, all unmodified EST (without exception
terrifying to recipients) was replaced with anaesthetized EST. Fear associated
even with modified EST continues to baffle practitioners today (Fox, 1993).
10, One
might argue that barbiturates prompted Liberson to
enhance electrical components as seizure threshold increases with barbiturate
use. While this might explain some increases in electrical parameters, it does
not explain increased numbers of treatment nor does it explain the eventual
abandonment of minimal stimulus devices both here and abroad (see below).
11, This
initial increase in wave length was developed to induce unconsciousness in the
"patient" through electricity rather than convulsion (Liberson, 1948, p. 30).
12, Impastato
had introduced several of the earlier Wilcox-Reiter models and was probably an
undeclared paid consultant to Reiter.
13, Two
companies (Medcraft and Elcot)
continue to manufacture the older Cerletti-Bini style
SW devices, both more powerful than Cerletti and Bini's original SW device renowned for brain damage and
memory loss (Impastato et al., 1957) and upon which
Wilcox and Liberson attempted to improve. Cerletti and Bini's original
device emitted a maximum 120 volts for a maximum of 0.5 seconds. Medcraft's "modern" SW device, unchanged since
its 1953 model, the BS 24 (now the BS 24 111), has a maximum potential of 170
volts and emits a current for up to one full second (Weiner, 1988, p. 56; Medcraft Corporation, 1984). Today's SW devices, as well as
modern day BP devices, are EST devices.
14. By charge is meant the
cumulative amount of electricity which has flowed past a given point at the end
of an electron transaction.
15, Using a straightforward
mathematical formula, the power of the new brief pulse devices can be verified
by calculating joules (or the more familiar "watts" as in a light
bulb), the measure of actual energy emitted (voltage is potential energy or
power). All four companies (e.g. MECTA. 1993. p. 13)
do list their devices as 100-joule maximums in all 4 brochures, but the
manufacturers' calculations are based on a typical resistance of 220 ohms (ohms
are the measure of resistance, here, of the skull and brain. to current flow).
However, the true maximum joules or watts for all modern day
BP devices is much higher than the estimate reported by the
manufacturers. For SW devices, the formula is: joules = volts x current x
duration, or joules = current squared x impedance x duration. For BP devices,
the formula is: joules = volts x current x (hz x 2) x wavelength x duration, or joules = current
squared x impedance x (hz x 2) x wavelength x
duration. All four manufacturers utilize the latter in lieu of the former
formulas, deriving the 100-joule maximums for their BP machines. Utilizing the
former formulas, however, which give us non-theoretical amounts, we find that
the Thymatron DG BP is capable of emitting 250 joules
or watts of electricity; the MECTA SR/JR BP models, 256 joules; the Medcraft 8-25 BP, 273 joules; and the Elcot
device even more. Compare these energy emissions with the following typical
analogy: the standard SW device can light up a 60 watt light bulb for up to one
second. (Modern SW devices can light up a 100-watt light bulb for up to one
second.) Modern BP devices can light up the same 60-watt tight
bulb for up to four seconds.
16, Ex-lobbyist Dianna Loper, who suffers from severe grand mal epilepsy as a
result of EST, worked on the passage of S.B. 205 in Texas. Her neurologist John
Friedberg called Dianna's seizures the worst he had witnessed. Even so, I noted
Dianna never suffered extensive long-term memory loss as a result of her
seizures, but she had side effects exactly like those described by the
manufacturers - temporary confusion, headache, temporary memory loss, and
sometimes permanent loss of an event immediately surrounding (within minutes -
not months) the seizure. On the other hand, as a result of EST, Dianna has
memory loss spanning years, as well as permanent memory retention problems. (My
own experience with EST, resulting in permanent loss of both my high school and
college educations, parallels Diann'a's and many
thousands like us [Cameron, 1991]). Manufacturers typically describe the less
egregious effects of epilepsy or convulsions when describing "side
effects" of EST, characteristically ignoring the effects of the one factor
not present in spontaneous seizures -the electricity. Dianna (along with the
author) is Director of World Association of Electroshock Survivors (WAES),
which seeks to prohibit EST worldwide.
17, This
is best exemplified through unilateral ECT. Originally utilized by Wilcox and
Friedman to induce the most minimal stimulus threshold seizures possible
(Alexander, 1953, p. 62; Liberson, 1948, p. 32),
unilateral ECT is used by modern manufacturers to induce the highest electrical
dosages possible (Abrams and Swartz, 1988, pp. 28-29) in order to achieve
efficacy.