That's a shame. How can we get him back, we need him!

Mary

Then how do you explain the dementia (mainly loss of memory) which
consistently occurs after ECT and sometimes persists indefinitely?

A peer-reviewed published paper with its references:

------------------------------------------------------------------------------------

Shock Treatment, Brain Damage, and
 Memory Loss: A Neurological Perspective

                        John M. Friedberg, M.D.

American Journal of Psychiatry 134:9, September 1977. pp: 1010-1013.

    The author reviews reports of neuropathology resulting from
    electroconvulsive therapy in experimental animals and humans.
    Although findings of petechial hemorrhage. gliosis. and neuronal
loss
    were well established in the decade following the introduction of
    ECT. they have been generally ignored since then. ECT produces
    characteristic EEG changes and severe retrograde amnesia. as well
as
    other more subtle effects on memory and learning. The author
    concludes that ECT results in brain disease and questions whether
    doctors should offer brain damage to their patients.

A 32 year old woman who had received 21 ECT treatments stated 5 years
later.

    One of the results of the whole thing is that I have no memory of
    what happened in the year to year and a half prior to my shock
    treatments. The doctor assured me that it was going to come back
and
    it never has. I don't remember a bloody thing. I couldn't even
find
    my way around the town I lived in for three years. If I walked
into a
    building I didn't even know where I was. I could barely find my
way
    around my own house. I could sew and knit before. but afterward I
    could no more comprehend a pattern to sew than the man in the
moon.
    (1. p. 22)

By 1928, 10 years before the introduction of electroconvulsive
therapy, it was known that accidental death by cardiac arrest could
result from as little as 70 to 80 milliamperes in the human (2). it
was also known in this early period that voltage applied to the head,
as
in legal electrocution, produced hemorrhage and rupture of cranial
contents. Ugo Cerletti (3) demonstrated that electricity in the range
of
100 volts and 200 milliamperes is rarely fatal when the current path
is
confined to the head. but does evoke a grand mal seizure marked by a
stereotyped succession of events. A tetanic muscular contraction, the
"electric spasm,'' is followed after a latency of seconds by
unconsciousness. a high voltage paroxysmal spike and sharp-wave
discharge,
and a clonic convulsion. Upon recovery of consciousness the subject is
left with a transient acute brain syndrome. a high likelihood of
permanent
brain damage, and greater retrograde amnesia than is seen in any other
form of head injury.

   BRAIN DAMAGE IN EXPERIMENTAL ANIMALS

Before examining the premise that ECT damages human brains. a brief
discussion of the lesions produced in animals by electrically induced
convulsions is worthwhile. The many reports on this subject indicate
that
petechial hemorrhages scattered throughout both white and gray matter
and
concentrated in the path of the current are the most consistent
finding.
If animals are sacrificed after a delay of days or weeks following a
convulsive series, hemosiderin pigment in phagocytes remains as
evidence
of vascular insult. Proliferation of glial cells. neuronal changes.
and
drop-out are also commonly reported.

In 1938, the year of the first use of ECT on a human being, Lucio
Bini. Cerletti's collaborator. reported "widespread and severe ' brain
damage in dogs with mouth to rectum electrode placement (4). At least
seven subsequent animal studies employing conventional cranial
electrodes
supported his findings (5-11). These culminated in the exhaustive
controlled experiment by Hans Hartelius in 1952 ( 12). This researcher
found discernible vascular, glial. and neuronal changes in cats
subjected
to a maximum of 16 shocks. The animals were not paralyzed but were
protected from physical injury during the seizure. Damage was slight
but
consistent. and the author concluded:

"The question of whether or not irreversible damage to the nerve cells
may
occur in association with ECT must therefore be answered in the
affirmative.''

Furthermore, by examination of unlabeled slides alone Hartelius was
able to correctly recognize 8 of 8 slides from shocked animals as well
as
8 of 8 controls. Although he considered many of the vascular and glial
changes to be reversible, there was no mistaking the brain of a
shocked
animal for that of a control.

Since that time, ECT in humans has been modified through the use of
oxygen and muscle paralysis to reduce the incidence of bone fractures.
Although it is believed that these modifications also reduce brain
damage.
there are no animal studies to support this idea. On the contrary
recent
work in England by Meldrum and associates (13. 14) on status
epilepticus
in pnmates suggests that the overexcited neuron by itself may be an
important factor in seizure damage, especially in the hippocampus.

                  HUMAN BRAIN DAMAGE

Let us turn now to the neuropathological findings in humans who died
during or shortly after ECT. As in lower animals. bleeding is the most
frequent non- specific tissue response to injury and the one seen most
often after electric shock. The first autopsy study in this country
revealed brain damage identical to that seen in experimental animals.
Alpers and Hughes (15) described the brains of 2 women who had
received 62
and 6 shocks, respectively. The first woman's seizures had been
suppressed
by curare. Both brains showed hemorrhagic lesions around small blood
vessels, rare- faction of tissue, and gliosis.

Throughout the 1940s similar reports continued to call attention to
brain changes after ECT. including cases in which oxygen and curare
had been administered (16). In 1948 Riese (17) added 2 more autopsy
studies to the growing list and commented, "In all observations of
sudden death after electric shock reported so far. petechial
hemorrhages, cellular changes and some glial proliferation stand out
prominently. as an almost constant whole."

Pathologists were especially interested in cases that discriminated
between the direct effect of electricity and the mechanical and
hypoxia effects secondary to convulsive motor activity. In 1953 Larsen
reported on a 45-year old man who had been given 4 electroshocks in
the
course of 5 days. The ECT did not induce any convulsions. The subject
died
from pneumonia 36 hours after the fourth electroshock. At autopsy
fresh
subarachnoid hemorrhage was found in the upper part of the left motor
region...."at the site where an electrode had been applied."(18)

In 1957 Impastato summarized 254 electroshock fatalities. Brain damage
was
the leading cause of death in persons under 40 years of age, and
nearly
one-fifth of all cerebral deaths were hemorrhagic (19).

some physicians were alarmed by the evidence of human brain damage. In
1959 Allen reported 18 cases in which he had found signs and symptoms
of
neurological sequelae following ECT. He concluded, "It is probable
that
some damage, which may be reversible but is often irreversible, is
inseparable from this form of treatment," and called for "more serious
consideration of the entire procedure."(20)

In 1963, McKegney and associates (21) reported the case of a 23 year
old man who became comatose 15 minutes after a single shock. The
significance of this case was twofold: first, a complete physical and
neurolgical examination was reportedly normal pnor to ECT, and
seconded
the ECT technique was contemporary and impeccable. The patient had
received .6 mg of atropine, 16 mg of succinylcholine (Anectine), and
forced oxygenation pre- and post-shock. ECT parameters were
conventional.
i.e.. 130 volts for .3 seconds. Four days later a brain biopsy showed
diffuse degeneration of neurons with hyperplasia of astrocytes. The
young
man never regained consciousness and at autopsy 2 months later
evidence of
old hemorrhage was found in the brain. This was the last detailed
report
in the English-language literature.

The damaging effects of ECT on the brain are thoroughly documented.
All told. there have been 21 reports of neuropathology in humans
(22-36). it is interesting that. despite the importance of a negative
finding there has not been a single detailed report of a normal human
brain after shock.

ELECTROENCEPHALOGRAPHIC EFFECTS OF ECT

Like other insults to the brain, ECT produces EEG abnormalities.
Diffuse slowing in the delta and theta range, increased voltage. and
dysrhythmic activity are seen in all patients immediately following a
series of bilateral ECT and, according to Blaurock and associates
(37),
may persist more than 6 months in 30 per cent of the cases. Such
slowing
suggests damage to the thalamus.

Sutherland and associates (38) showed that the side of the brain
shocked with unilateral ECT could be predicted by double-blind
assessment of EEG tracings.

The seizure thresholds of the hippocampus and other temporal lobe
structures are the lowest in the brain; considerable interest has
centered recently around "kindling, ' or seizure induction by
subthreshold stimulation of these areas in animals (39). The induction
of
a permanent epileptic disorder following ECT in humans was first
reported
in 1942 and other reports followed (40).

                         MEMORY LOSS

ECT is a common cause of severe retrograde amnesia, i.e.. destruction
of
memories of events prior to an injury. The potency of ECT as an
amnestic
exceeds that of severe closed head injury with coma. It is surpassed
only
by prolonged deficiency of thiamine pyrophosphate. bilateral temporal
lobectomy, and the accelerated dementias, such as Alzheimer's.

After ECT it takes 5 to 10 minutes just to remember who you are. where
you
are. and what day it is. In the first weeks after a full course,
retrograde and, to a lesser extent, anterograde amnesia are evident to
the
casual observer. But as time passes compensation occurs. As in other
forms
of brain injury. the subject is often oblivious to the residual
deficit.
Unless specific memories essential to daily living are discovered to
be
unavailable the victim may never know for sure the extent of memory
loss.
Unless sensitive tests for spontaneous recall of personal preshock
data
are employed no one else will know either.

The memory loss following ECT generally follows Ribot's law for all
pathological amnesias: the new dies before the old. This, of course,
is the opposite of normal forgetting. Squire, however, has shown that
the
loss may extend to items learned more than 30 years before (41).

The effect of ECT on memory was common knowledge within a few years of
its
introduction. There were reports of persons who forgot they had
children
(42. 43), although most amnesias involved humbler matters. such as the
woman who forgot how to cook familiar dishes (44) and another who
couldn't
remember her own clothing and demanded to know who had put the
unfamiliar
dresses in her closet (45). Some doctors dismissed these sequelae as
trivial or transient, although one psychiatrist remarked that
psychotherapy was useless in patients undergoing ECT because they
couldn't
remember "'either the analyst or the content of the analytic sessions
from
one day to the next.'' (46).

Numerous such case reports finally led to a definitive study of the
effects of ECT on memory by Irving Janis in 1950 (47). He found that
all 19 subjects in a controlled prospective investigation had
significant memory loss 4 weeks after ECT, compared to negligible
losses among control subjects. He also noted that these losses may
involve events of early childhood dating back 20 to 40 years, with the
more recently en- coded memories being the most vulnerable. Patient E.
for
example. a 38-year-old woman, had told Janis in an interview prior to
ECT
that thyroid medication had caused heart palpitations and panic which
led
to her admission to the psychiatric hospital. When asked after a
course of
10 shocks if she had ever taken thyroid she responded: "I don't think
so."

In the late 1940s. when the enthusiasm for ECT seemed to have passed
its peak (48). Lancaster and associates (49) advocated the use of
unilateral non-dominant ECT in treating patients who earn their
livelihood with retained knowledge. In this variant the current path
and most of the damage is confined to the nonverbal side of the brain,
usually the right hemisphere. This exploits the well-known
neurological
phenomenon of anosognosia. or denial. that is associated with
right-hemisphere lesions - victims can't verbalize their difficulties.
They complain less. Cohen and associates (50). however. using
design-completion tests. proved that shock to the right hemisphere
produces its own kind of memory loss: visual and spatial. Inglis found
in
1970 (51) that the effects of unilateral ECT were comparable to those
of
right and left temporal lobectomy, with identical impairment of memory
and
learning.

Recently there has been a good deal of human experimentation in a
futile effort to find electrode placements that eliminate amnesia. As
the
use of ECT has shifted from state hospitals to private practice, the
literature has focused more and more on memory loss.

Although some studies have purported to show provement of learning
ability after ECT, not one u sham ECT as a control and few used any
controls at all.(1)

In regard to more general intellectual ability, a study in 1973 (54)
showed that the performance on the Bender Gestalt perceptual motor
test of 20 institutionalized subjects who had received 50 or more ECT
treatments 10 to 15 years before testing was significantly impaired
compared to the performance of 20 carefully matched control subjects
who
had not received ECT. The authors inferred that ECT had caused
permanent
be damage.

            MECHANISM OF ACTION OF ECT

The mechanism of action of ECT can now be summarized on the basis of
evidence accumulated since introduction. Penfield and Perot showed in
the
1950's that memory traces may be evoked by direct electrical
stimulation
of the temporal lobe cortex. and nowhere else (55). Scoville and
Milner
(56) discovered that bilateral hippocampal resection utterly abolished
ability to remember any new material. resulting in a catastrophic
inability to learn. From numerous studies of the neuropathology of the
amnestic-confabulatory syndrome of Korsakoff it is known that the
mammillary bodies. the dorsal median nuclei of the thalamus and the
gray
matter surrounding the third ventricle a aqueduct are essential to the
general memory process. All of these critical brain structures are
just
beneath the thin squamous plate of the temporal bone. with seven
centimeters of the electrodes. in the direct path and highest density
of
the current during ECT.

                          CONCLUSIONS

From a neurological point of view ECT is a method of producing amnesia
by
selectively damaging the temporal lobes and the structures within
them.
When it was first introduced it was only one of several methods of
producing brain damage employed in psychiatry, including insulin coma
(1927)* camphor and Pentylenetetrazol (Metrazol) injections (1933).
and
prefrontal lobotomy (1935), it is the only such method from that era
still
used on a large scale. It is highly unlikely that ECT, if critically
examined, would be found acceptable by today's standards of safety.

From a neurological point of view ECT produces form of brain disease.
with
an estimated incidence new cases in the range of 100.000 per year
(57).
Many psychiatrists are unaware that ECT causes brain damage and memory
loss because numerous authorities and a leading psychiatric textbook
(58)
deny these facts.

Others, who know of its effects argue that the interruption of
unpleasant states of mind is worth the damage. Some are beginning to
give the client a truly informed choice, although state laws still
allow ECT to be imposed if the doctor feels that ''good cause''
exists.

Assuming free and fully informed Consent, it is well to reaffirm the
individual's right to pursue happiness through brain damage if he or
she so chooses. But we might ask ourselves whether we, as doctors
sworn to the Hippocratic Oath, should be offering it.

                             REFERENCES

1. Friedberg J: Shock Treatment is Not Good For Your Brain. San
Francisco. Glide Publications. 1976

2. Jaffe R: Electropatholohy: a review of the pathologic changes
produced by electric current. Arch Neurol Psychiatry 5:838- 864. 1928

3. Cerletti U: Electroshock therapy. in The Great Physiodynamic
Therapies in Psychiatry. Edited by Sackler A. Sackler R. Sackler M. et
al.
New York. Hoeber-Harper. t956, pp 91-120

4. Bini L: Experimental researches on epileptic attacks induced by the
electric current. Am J Psychiatry 94:172-174. 1938

5. Heilbrunn G. Lieben E: Biopsies on the brain following artificially
produced convulsions. Arch Neuroi Psychiatry 46:548-552, 1941

6. Neubuerger KT. Whitehead RW. Rutledge RK. et al: Pathologic changes
in
the brains of dogs given repeated electric shocks. Am J Med Sci
204:381-387. 1942

7.. Heilbrunn G. Weil A: Pathologic changes in the central nervous
system in experimental electric shock. Arch Neurol Psychiatry 47:918,
1942

8. Alpers 8J. Hughes J: Changes in the brain after electrically in-
duced convulsions in cats. Arch Neurol Psychiatry 47:385. 1942

9. Alexander L, Lowenbach H: Experimental studies on electroshock
treatment: the intracerebral vascular reaction as an indicator of the
path
of the current and the threshold of early changes within the brain
tissue.
J Neuropathot Exp Neurol 3:139, 1944

10. Ferraro A. Roizin L. Helfand M: Morphologic changes in the brain
of monkeys following convulsions electrically induced. J Neuropathol
Exp Neurol 5:285. 1946

11. Ferraro A. Roizin L: Cerebral morphologic changes in monkeys
subjected to a large number of electrically induced convulsions
(32-100). Am J Psychiatry 06:278. 1949

12. Hanelius H: Cerebral changes following electrically induced
convulsions. Acta Psychiat et Neurol Scand Supplement 77. I 952

13. Meldrum B. Roger V, 8riericy J: Systemic factors and epileptic
brain damage. Arch Neurol 29:82-87. 1973

14. Meldrum B. Honon R. 8rierley J: Epileptic brain damage in
adolescent baboons following seizures induced by allylglycine. Brain
97:407-418. 1974

15. Alpers BJ. Hughes J: The brain changes in electrically induced
convulsions in the human. J Neuropathol Exp Neurol 1:173. 1942

16. Ebaugh FG. Barnacle CH. Neubuerger KT: Fatalities following
electric convulsive therapy: report of two cases. with autopsy. Arch
Neurol Psychiatry 49:107. 1943

17. Riese W: Report of two new cases of sudden death after electric
shock treatment with histopathological findings in the central nervous
system. J Neuropathol Exp Neurol 7:98-100. 1948

18. Larsen EG. Vna-Jansen G: Ischaemic changes in the brain following
electroshock therapy. Acta Psychiat et Neurol Scand 28:75-80. 1953

19. Impastato D: Prevention of fatalities in electroshock therapy. Dis
Nerv Syst 18:34-75, 1957. (author's comment: Impastato, himself a
shock
doctor, estimated a DEATH RATE of 1/200 in this paper. Dr. Max Fink
has
recently alchemized this figure into 1/200 memory loss but the state
of
Texas in 1994 reported almost exactly the same rate as Impastato 37
years
before: 1/200. Not surprising - if anything the energy administered
hasn't
changed or is greater; the target population is older. Memory loss is
always present.)

20. Allen 1: Cerebral lesions from electric shock treatment. NZ Med J
58:369. 1959

21. MclCegney FP. Panzetta AF: An unusual fatal outcome of
electro-convulsive therapy. Am 1 Psychiatry 120:398-400. 1963

22. Ebaugh FG. Barnacle CH. Neubuerger KT: Fatalities following
electric convulsive therapy. A report of 2 cases with autopsy
findings. Trans Am Neurol Assoc. June 1942. p 36

23. Gralnick A: Fatalities associated with electric shock treatment of
psychoses: report of two cases with autopsy observations in one of
them.
Arch Neurol Psychiatry 51:397. 1944

24 Jetter WW: Fatal circulatory failure caused by electric shock
therapy. Arch Neurol Psychiatry 51:57. 1944

25. Meyer A. Teare D: Cerebral fat embolism after electrical con-
vulsion therapy. Br Med J 2:42. 1945

26. Sprague DW. Taylor RC: The complications of electric shock therapy
with a case study. Ohio State Med J 44:51-54. 1948

27.Will OA Jr. Rehfeidt FC: A fatality in electroshock therapy: report
of
a case and review of certain previously described cases. J Nerv Ment
Dis
107:105-126. 1948

28.Martin PA: Convulsive therapies: review of 511 cases at Pontiac
State Hospital. J Nerv Ment Dis 109:142-157. 1949

29. Riese W. Fultz GS: Electric shock treatment succeeded by complete
flaccid paralysis. hallucinations. and sudden death: case report with
anatomical findings in the central nervous system Am J Psychiatry
106:206-211. 1949

30. Liban E. Halpern L. Rozanski J: Vascular changes in the brain in a
fatality following electroshock. J Neuropathol Exp Neurol 10:30W318.
1951

31. Corsellis J. Meyer A: Histological changes in the brain after
uncomplicated electro-convulsive treatment. J Ment Sci 100.375- 383.
1954

32. Madow L: Brain changes in electroshock therapy. Am I Psychiatry
113:337-347. 1956

33. Faurbye A: Death under electroshock treatment. Acta Psychiatrica
et Neurologica 17:39.1942

34. Maclay WS: Death due to treatment. Proc Soc Med 46:13-20 1953

35. Matthew JR. Constan E: Complications following ECT over a
three-year period in a state institution. Am J Psychiatry 120:1 1 19-1
120. 1964

36. Barker J. Baker A: Deaths associated with electroplexy. J Ment Sci
105:339-34S 1959

37. Blaurock M. Lorimer F. Segal M. et al.: Focal
electroencephalographic changes in unilateral electric convulsion
therapy. Arch Neurol Psychiatry 64:220-226. 1950

38. Sutherland E. Oliver J. Knighl D: EEG. memory and confusion in
dominant. non-dominant and bi-temporal ECT. Br J Psychiatry:1059-1064.
1969

39. Wada J. Osawa T: Spontaneous recurrent seizure state induced by
daily electric amygdaloid stimulation in senegalese baboons (papio
papioh Neurology 26:273-286. 1976

40. Parfitt D: Persisting epilepsy following shock therapy. Br Med
2:514. 1942

41. Squire L: A thirty-year retrograde amnesia following
electroconvulsive therapy in depressed patients. Presented at the 3rd
annual meeting of the Society for Neuroscience. San Diego.1973

42. Tyler B. Lowenbach H: Polydiurnal electric shock treatment in
mental disorders. NC Med J 8:577-582. 1947

43. Medlicott R: Convulsive therapy. Results and complications in four
hundred cases. NZ Med J 47:338. 1948

44. Brody M: Prolonged memory defects following electrotherapy. J Ment
Sci
90 779. 1944

45. Zubin J: Objective studies of disordered persons. in Methods of
Psychology. Edited by Andrews T. New York. John Wiley and Sons. 1948.
pp
595-623

46. Stainbrook E: Shock therapy: psychologic theory and research.
Psychol Bull 43:21-60. 1956

47. Janis 1: Psychologic effects of electric convulsive treatments.
Part 1: post-treatment amnesias. J Nerv Ment Dis 3:359-382. 1950

48. Spiegel E (ed): Progress in Neurology and Psychiatry: An Annual
Review. New York. Grune h Stratton. 1957

49. Lancaster N. Steinen R. Frost 1: Unilateral electro-convulsive
therapy. J Ment Sci 104:221-227. 1958

*Sham ECT, an essential control technique due to the high drama of the
procedure, has been employed in only two studies. which were tests of
efficacy, not tests of memory. Neither study showed any superiority of
ECT
over controls.

Revised version of a paper presented at the 129th annual meeting of
the American Psychiatric Association, Miami Beach. Fla. May 1W 14.
1976.

================================================

Best,

Bob

Robert A. Fink, M.D., FACS, P. C.
2500 Milvia Street   Suite 222
Berkeley, California  94704-2636  USA


Telephone:  510-849-2555
FAX:  510-849-2557
<http://www.rafink.com>

"Ex Tristitia Virtus"

--------------------------------------
NOTE:  The above message is not to be considered as
"medical advice".  Medical advice can be given only  
after a "hands-on" examination of the patient by a
physician.

========================================

Please find enclosed a post I made to another group some time ago
concerning my new GP:

It seems that not all GPs are aware that ECT is not in common use any
more. I've not been back to see him and am managing my own med reduction
scheme. I am now down to 200mg Tegretol from an initial 1200, with no
ill effects. Going down to 150 at end of month, aiming for zero by end
of July, and am looking forward to remembering where I put my front door
keys :)