Brain Damage and Memory Loss from ECT

Testimony Prepared for the Standing Committee on Mental Health of the Assembly of the State of New York.
October 5, 1978.
by Dr. Peter Sterling, Ph.D.
Associate Professor of Neurobiology
Department of Anatomy
School of Medicine
University of Pennsylvania

Scope and Complexity of the Brain

The brain is the controlling organ of the body. It receives information from the outside world through the 5 senses. It also receives information from the inside of the body regarding all the body’s internal functions: heart rate, blood pressure, amount of glucose (sugar), oxygen, carbon dioxide, hormones, etc., in the blood. It also contains information, coded originally in the genes, regarding the needs that all humans share: the drives for hunger, thirst, sex, and so on. As particular kinds of information is taken into the brain by the various sensors, it is stored. Old information, when needed, is retrieved for comparison with new information so that decisions can be made.

These decisions include the obvious, conscious ones, such as whether we shall get out of bed in the morning, or what clothes we shall wear. They also include decisions of which we are not conscious that have consequences for every cell in the body, such as how high the blood pressure should be, how much of a particular hormone should be secreted, how much blood should be distributed to one organ or another.

The Demands of Complexity

It is a general rule that the more complex a structure is, the more closely regulated its operation must be. In a complex structure, foundations must be firmer and the tolerances closer. The safeguards against disruption must be numerous and of a “fail-safe” variety. A simple hut needs no foundation but there can be no mistakes in the planning or construction of a skyscraper. The simpler the structure, furthermore, the less vulnerable it is to disruption. A hut will most likely survive an earthquake and in any case can be repaired, but a skyscraper, even with all its safeguards, is subject to irreparable collapse. This rule applies to the body as well. Let us compare a relatively simple tissue, the skin, to the most complex organ, the brain.

The skin is exposed directly to the environment and is frequently damaged by mechanical trauma. Its cells have the capacity to divide; new cells easily replace worn or damaged ones. Skin cells must be supplied with nutrients and oxygen from the blood, but their requirements are quite flexible. They can metabolize a variety of substances: fatty acids, glucose, amino acids; they can operate for a while without oxygen and can tolerate wide variations in blood supply. The skin cells are not very sensitive to temperature — that is why we can sit in the sun or plunge into ice water without damage.

The brain is entirely different. Its 10-100 billion neurons are all present at birth. Nerve cells do not divide to replace their losses. Therefore, any loss of cells is permanent. The death of a single neuron represents a loss of up to 100,000 inputs and 100,000 outputs for a total loss of 10 billion connections. Obviously, the brain must be protected from mechanical trauma.

The brain, unlike the skin, has virtually no metabolic flexibility. It can metabolize only glucose and not fatty acids or amino acids. This is one reason why the glucose levels in the blood must be maintained at all times. A sharp fall in blood glucose leads rapidly to failure of brain function and coma. Oxygen supply to the brain must also be maintained for there is hardly any reserve supply. If a pressure cuff is placed around the neck and inflated, a human subject goes blind and loses consciousness in 6 seconds. If he breathes pure nitrogen, consciousness is lost in 17-20 seconds. After 3-4 minutes without oxygen at normal body temperature, there is generalized brain damage; after 4-5 minutes, the damage is irreversible.

Brain temperature must also be closely regulated. Everyone is familiar with their own experience with the deterioration of brain function that occurs in fever where temperature rises only a degree or so above normal. Aspirin, by restoring normal temperature, brings relief. Temperature rises that are only slightly greater than a common fever may cause convulsions and can do permanent damage. Clearly, brain function cannot withstand the extreme changes in blood glucose, oxygen supply, or temperature that bother the skin not at all.

Protective Mechanisms of the Brain

Mechanical protection. The first level of mechanical protection for the brain is the thick bone of the skull. There is an active protection too: because the skull has sensitive nerve endings on the outside, we learn early not to bang it into hard objects. Inside the skull, the brain is protected by 3 separate layers of casings. There is a tough, fibrous outer casing called the “dura” (“hard”). Beneath the dura there is a second, more delicate membrane called the “arachnoid”. This encases the brain in a special fluid called “cerebrospinal fluid” (“cSF”). Thus, the brain is suspended in fluid in the same way the delicate embryo is suspended within the womb. Within limits, mechanical shocks to the head are absorbed by this fluid and are not transmitted to the brain. The third membrane layer is called the “pia”. It is applied directly to the brain’s surface, forming the last major protective barrier. Blood vessels must penetrate the pia to reach neural tissue itself.

Protection of blood supply. Even though the brain is only about 2% of the body’s weight, it uses 20% of the body’s oxygen supply because of its high rate of metabolism. The brain controls its own blood flow and gives itself highest priority along with the heart. If there is not enough blood to go around, the blood supply is shut down to the gut, kidney, skin and muscle — always to preserve flow to brain and heart. If blood pressure falls so low that the heart has difficulty pumping blood to the head, the brain shuts off messages to muscle, causing collapse (fainting). With the head at the same level as the heart as a result of fainting, the crucial blood supply can more easily be maintained. Thus, fainting is an important protective mechanism for the brain.

Blood flow through the brain itself is automatically regulated so that it doesn’t depend on changes in blood pressure for the body as a whole. If the systemic pressure falls, valves in the brain’s vessels open up a bit to maintain flow. Another role for these valves is to protect the delicate brain capillaries from excessively high pressures. This control of blood flow and pressure breaks down during convulsions, a point to which we shall return.

Protecting the brain’s chemical composition: the blood-brain barrier.

In most tissues the blood vessels are somewhat “leaky”. Although red blood cells do not normally escape, some large molecules, such as proteins, and many smaller molecules do escape from vessels into the surrounding tissues. Were this to occur in the brain, it could be disastrous. First, the tiny channels between nerve cells could be plugged by larger molecules and barriers would be established to the normal flow of ions and nutrients. Second, if large molecules leaked from vessels into the brain, water would follow them (to maintain osmotic neutrality). The tissue would then swell. Although most tissues can swell and shrink without causing any difficulty, swelling is a serious matter for the brain because it is encased in bone. If it were to swell, pressure inside the skull would build up. Delicate structures would be squashed against bone, and the blood supply would be cut off by the rise in intracranial pressure. Third, the composition of the blood varies somewhat, even though it is regulated by kidney, liver and other organs. The blood sometimes contains toxic substances that some tissues, such as liver, can handle, but which may damage the brain. In general, the brain’s chemical composition must be regulated far more perfectly than that of any other organ.

Accordingly, there are several lines of defense against changes in the brain’s chemical composition that would result from leaky blood vessels. These defenses are referred to collectively as the “blood-brain barrier First, the vessels are sealed off from the brain by mechanical adhesions between the cells called “tight junctions”. Second, a set of select substances that the brain needs are actively pumped into the brain from the blood. Third, undesirable substances, or those whose concentration must be actively controlled in the brain, are actively pumped out of the brain. You can get some feeling for these processes in slide 1. The brain on the left is from a cat with an intact blood-brain barrier. Blue dye which was injected into the blood was prevented from entering the brain by the blood-brain barrier. All the other tissues, however, are blue. On the right, the blood-brain barrier has been destroyed by irradiation (Klatzo and Seitleberger, 1967). Here, the vessels have become leaky and dye has penetrated the brain. This slide, therefore, has two purposes: to illustrate the existence of the blood-brain barrier and to indicate that it can break down under certain insults. This will be highly relevant when we consider the effects of electrical shock.

Protection of neural stability by inhibition.

One additional protective mechanism must be described before the effects of electrical shocks can be assessed. Nerve cells can either “excite” (turn on) or “inhibit” (turn off) each other. The inhibitory mechanisms are important here for one particular reason, inhibition serves to dampen the excitation, and without it the excitatory tendencies of nerve cells go out of control. All cells tend to be excited simultaneously and tend to re excite each other until massive neural activity swamps out any sensible, coordinated pattern. Such generalized excitation leads to massive, sustained contraction of the musculature, called a “fit”, a convulsion, or a “seizure”. Thus, a fit or seizure is a state in which, for one reason or another, the excitatory processes in the brain temporarily overwhelm the damping, inhibitory processes. A seizure, therefore, is evidence that one of the brain’s protective mechanisms has temporarily been overwhelmed.

To summarize:

1. The brain is an organ of extraordinary complexity and is more complex in man than in lower animals.

2. Its complexity makes it extremely vulnerable to the slightest environmental insults which other tissues of the body could withstand. Neurons once lost as the result of insult are not replaced.

3. To prevent insult, many protective mechanisms, including mechanical, physiological, and behavioral mechanisms have evolved.

Relation Between Observations on Humans and Non-Human Mammals

I have showed a slide from the brain of a cat and will continue to refer to studies on other mammals. It is appropriate to ask, therefore, whether these studies are pertinent to the human brain since there are many differences between human and animal brains. The major difference between humans and animals that is relevant in the present context is that the human brain is a greater and more complex edifice. To return to the earlier analogy, it is more like a skyscraper than a hut. It needs even more protection, not less. All the protections I have discussed so far exist in humans and are, if anything, exaggerated in humans. In the remainder of my testimony, 1 shall refer to animal studies only where we can be reasonably sure that the human tissue would react in the same general way.

Effects of ECT on the Brain

We are now in a position to appreciate some of the effects of electrical shocks to the brain. Let us begin by describing the nature of the shock itself (reviewed by Grahn, et al., 1977). Typically, the electrodes of the ECT instrument are placed on the temples. Such ECT instruments usually contain nothing but a simple transformer that steps up the voltage from the wall outlet from 110V to about 150V. The machine may or may not have an automatic timing device to limit the duration of the shock. The current that passes through the head (between the electrodes) is limited mainly by the electrical resistance of the head. The total power drawn is about 60 watts — enough to light a conventional light bulb. The result is not very different from what would be accomplished by plugging 2 pieces of metal into a wall outlet and placing their other ends on the temples — except that the voltage from the wall outlet is a little lower. The duration of a typical ECT shock is 1/10-3/4 of a second.

Events triggered by electrical shock.

The electricity passing through the brain causes massive, simultaneous excitation of vast numbers of neurons. The inhibitory mechanisms that normally hold neurons in check and shape the normal EEG rhythms are overwhelmed by the excitation. As the excitation builds and swamps the inhibitory mechanisms, it spreads throughout the brain. When the excitation reaches the motoneurons of all the body’s muscles, there is massive, convulsive muscular contraction. The muscles contract so powerfully that tendons may be torn from the bones, the bones themselves may be broken, teeth chipped and broken, and so on. The massive requirements for oxygen and the interruption of breathing caused by the convulsion often causes anoxia. Accompanying the convulsion, there is a tremendous rise in blood pressure: changes in arterial pressure from 80mm Hg to 220mm Hg, or almost 200%, have been recorded (Plum, et al, 1968). This overall response resembles the “grand mal” seizure that occurs in epilepsy.

In recent years some of these consequences of the electrical shock have been ameliorated. The muscle contractions can be prevented by administration of a drug that blocks transmission of impulses from nerve to muscle. The ensuing paralysis protects bone and muscle, and also permits oxygen to be administered by artificial respiration. Under these conditions, the brain is well protected from anoxia. On the other hand, this procedure (paralysis) is frightening. Patients are therefore usually pretreated with barbiturate anesthetics so that their consciousness of their treatment is dulled or lost entirely. The effect of barbiturate anesthetic is to decrease the excitability of neurons in the brain. Larger shocks must, therefore, be employed to evoke a grand mal would be needed without the drugs. Thus, although the patient may gain from the paralysis and the administration of oxygen, he probably also loses by the higher voltage requirement. There is no evidence that these drug treatments substantially alter the electrical and chemical phenomena within the brain that I shall now describe.

Brain changes during ECT.

The massive neural activity evoked by the electrical shock causes and requires major changes in the metabolism and blood supply of the brain.

1. The neurons, because they are so active, require much more oxygen and nutrients. Therefore, with the onset of the seizure, cerebral blood flow rises dramatically — as much as 400%. Cerebral oxygen consumption also rises as much as 400%. In accomplishing such massive increases in blood flow, the automatic mechanisms that normally regulate cerebral blood flow are overwhelmed. For the duration of the seizure and for sometime following it, blood flow to the brain becomes like that of must other tissues in the body — proportional to the arterial pressure forcing the blood through the vessels. These changes accompanying ECT are not modified by the administration of anesthetic, paralytic drugs or oxygen (Plum, et al., 1968; Posner, et al., 1969).

2 The extremely high cerebral blood pressure and the breakdown in auto regulation of cerebral blood flow during the seizure frequently ruptures small, and occasionally large, vessels in the brain. Madow (1956) reviewed 42 cases of autopsy assembled from 26 published reports on patients who had recently received ECT. Twenty-five (60%) had either petechial hemorrhages or large infarcts. About three-quarter of these patients were over forty, but the frequency of hemorrhage in the group under forty was the same as for the older group. There seems every reason to suspect, therefore, that subarachnoid or intracerebral bleeding accompanies ECT about half the time. This is supported by numerous studies in animals autopsied after being subjected to ECT. For example, Alpers and Hughes (1942) found bleeding in 23/30 cats (77%); Heilbrunn(1943) found petechial or larger hemorrhages in all of the rats that convulsed in his experiments to ECT; Heilbrunn and Weil (1942) made similar findings in 17/21 (81%) rabbits. Wherever bleeding occurs in the brain, neurons lose their supply of oxygen and nutrients — and die.

Some studies failed to hemorrhages in animals following ECT, but most of these seem not comparable to the human cases. in two, the voltage applied was far below what is employed on humans (Masserman and Jacques, 1947; Winkleman and Moore, 1944). Others used only a single shock rather than, as is common for humans, a series of treatments (Windle, l948, Alexander and Lowenbach, 1944). Another study with negative findings.(Siekert, et al, 1950) used a small sample (5) of young monkeys (5-7 lbs., corresponding to an age of about one and a half years). Since damage is greater in older animals with less flexible vascular systems (Hartelius, 1952), this negative result on a small sample is not astonishing, nor does it contradict the many positive findings of damage. The positive findings cannot be attributed to poor preservation of the brains after death. While poor preservation makes difficult judging the condition of neurons or glia, it cannot cause bleeding within the brain. Nor can the bleeding be attributed to “old” methods of ECT (no paralysis or oxygen). One would expect under the old conditions the brain to be anoxic, with arrested circulation. This would lead to a lack of blood in the brain, the opposite of what is reported. Thus, the later modifications of ECT can relieve the threat of cerebral anoxia, but not the threat of high pressure, bleeding, loss of blood-brain barrier, or edema

3.The electrical shock causes damage to the blood-brain barrier. Aird, et al., 1956; Angel, et al., 1965; Lee and Olszewski, 1961). This has been shown experimentally in animals, and there is every reason to believe that it happens in humans as well. Whether this is caused by the huge rises cerebral blood pressure is unknown. Whatever the cause, the loss of this protective barrier exposes the brain tissue to components of the blood from. it is normally protected. For example, if a patient has been taking drugs of any kind, the brain may be exposed to much higher levels of the drugs than normally cross the blood-brain barrier.’)

4. The combination of raised cerebral blood pressure and ruptured blood-brain barrier often causes another problem, cerebral edema. The high pressure forces proteins and other substances out of the now “leaky” vessels into the brain tissue. As noted earlier, fluid tends to follow these substances and the tissue begins to swell. This process once started can become disastrous because a “vicious circle” is started. As the pressure inside the skull rises from the swelling, capillaries are closed. Their linings are damaged by anoxia making them even more leaky. This leads to more edema and damage (Fishman, 1975; Klatzo and Seitleberger, 1967). Edema has been noted in the human retina, an easily visible part of the brain, as a consequence of shock (Winnik, et al., 1966). Patients cannot be protected from this process by drugs that lower blood pressure, because the extra pressure is needed to supply the brain’s huge metabolic needs during the seizure. It has been noted in experimental animals and man that rises in blood pressure accelerate the spread of edema (Fishman, 1975; Shutta, et al., 1968; Klatzo and Seitleberger, 1967) and the leakage of trace materials from the blood-brain barrier (Lee and Olszewski, 1961; Klatzo and Seitleberger, 1967). It has also been noted that individuals with high blood pressure “have a significant predisposition to cerebral edema” (Klatzo and Seitleberger, 1967, P.148). Where the swelling is great enough to block the blood supply to neurons .– or even to slow it below the extreme needs of the active tissue — nerve cells will become anoxic and die.

5. Even where there is adequate oxygen, neurons may die because they use up the metabolites that they need to function, It has been demonstrated that during a seizure, the “respiratory quotient” of the brain shifts markedly. This shift indicates a change in cerebral metabolism away from the use of glucose as fuel. Here is what a prominent neurology group had to say about the changes in cerebral metabolism that they measured during ECT-induced seizures in man:

If endogenous substances essential to normal cerebral metabolism are depleted during seizures, one might expect post-ictal brain dysfunction until repletion even without hypoxia. At some point during repeated seizures, depletion of cerebral substances might become irreversible and permanent brain damage ensue. Thus, post ictal EEG flattening and coma need not imply cerebral hypoxia (Posner, et al., 1969, P.394).

Translated into English, this means that even if the brain receives enough oxygen during a seizure. the brain may exhaust its sources of nutrients and be irreversibly damaged. It means that the abolition of electrical activity and the coma that sometimes follows a seizure can occur even though adequate oxygen is supplied.

6. There are changes in a host of brain chemicals as the result of ECT (reviewed by Essman, 1973). Synthesis of protein and RNA are inhibited within five minutes of ECS, with the decrease persisting for a number of hours. The levels of neural transmitters (acetylcholine, norepinephrine, serotonin) and their related enzymes also change. For example, acetylcholine and the enzyme that destroys it, acetyicholinesterase, fall after ECT but rise above normal levels within 2 hours. These changes are reflected in the choline levels in the cerebrospinal fluid, which in man and monkey are increased 24 hours following a single ECT and remain elevated for at least a week after multiple ECT. Changes in serotonin, an important neural transmitter, last up to 5 months. The time courses of these changes are very complex, and their meaning is not yet understood. Nevertheless, each of the chemicals listed has been shown to play some role in memory, and I would anticipate that significant changes in any one of them might contribute to the changes in memory that have been demonstrated to follow ECT.

7. Following ECT, there is a marked rise-in cerebral levels of arachidonic acid (Essman, 1973; Bazan, N.G., 1970, 1971). This compound has been shown to cause aggregation of blood platelets when injected d into the cerebral blood supply, resulting in small “strokes” throughout the brain (Furlow, T.W., Jr. and Bass, N.H., 1975). Conceivably the rise. in arachidonic acid associated with ECT could be a source of the brain damage to be described later.

Changes in the Electroencephalogram (E.E.G.)

The EEG changes markedly during and following ECT. Before describing these changes, it is necessary to explain what the EEG represents. The electrical activity of neurons can be studied in two ways — either by recording the electrical activity of one neuron at a time to see how it responds to particular environmental events — or by recording outside the skull from a large population of neurons and their supporting “glial” cells. It is something like pushing a microphone close to one member of an orchestra (single neuron) and listening to his theme or withdrawing the microphone in order to listen to the whole (EEG). In the first case, one can make out the individual notes; in the second, one hears the overall rhythm, pitch, and loudness, but blended in such a way that the detailed contributions cannot be discerned.. When the rhythms of millions of individual nerve cells are merged in the EEG, the resulting broader rhythms have fairly characteristic features in normal and pathological states. When something is wrong, one cannot identify precisely what it is — especially since glial cells as well as nerve cells contribute to the EEG rhythm — but one can be sure that something is wrong. In awake adults, a beta-rhythm is normally seen with a frequency of about 15-60/ sec. and an amplitude of 5-10uV (low voltage-fast activity). If the person closes his eyes, the rhythms, particularly over the visual area, may slow a little and increase in amplitude, changing to an alpha-rhythm of 8-10 sec., 5OuV. In sleep the rhythm slows to a delta-rhythm, still slower (1-5/sec.) and higher in amplitude (20-200uV).

These slow delta rhythms are rarely recorded in normal, awake adults. They do appear, however, in various pathological states and are interpreted as evidence of pathology such as tumor, epilepsy, raised intracranial pressure, mental deficiency, depression of consciousness by toxic or other factors. For example, lack of oxygen and lack of glucose in the brain both cause the appearance of these large, slow delta waves. Again, we cannot say precisely what these rhythms mean or how they arise from the individual elements, but they do seem to convey the overall “mood” of the brain.

It is not at all surprising that the EEG is altered during the ECT seizures because the seizure itself is an interruption of the normal electrical rhythms. Furthermore, it is to be expected that the EEG would be abnormal for some time after a seizure because of the outpouring of potassium ions from neurons. It is significant, however, that in many patients the EEG remains abnormal for many months. Here, I should like to cite several studies in some detail.

In 1944 Mosovich and Katzenelbogen studied the EEGs of 82 patients before and after ECT. Although the study is old, it is a model of good scientific work, particularly in that it studied patients before treatment and followed them for 10 months afterwards. The currents used were 300-600MA, within the range used today. The study showed that of 42 patients with normal EEGs before ECT, half (21) had abnormal EEGs following treatment. One-third of these abnormalities were severe “cerebral dysrhythmias”. The EEG patterns resembled those commonly seen in epileptic patients in the periods between epileptic seizures. Of 40 patients with moderate EEG abnormalities before ECT, 13 showed cerebral dysrhythmia afterwards. To produce these changes a relatively few sessions sufficed, for they were found in 9/60 patients who had only 3-15 ECT. The frequency of damage increased with increasing number of shocks:. after 16-42 shocks, half the patients (11/22) showed cerebral dysrhythmia… These changes were often extremely long lasting. Thus, 68/82 patients showed the dysrhythmia the day following ECS, and 20 patients still had the pattern 10 months later. For all anyone knows, the changes were permanent (Mosovich and Katzenelbogen, 1944).

These findings have been confirmed in modern studies using anesthesia, oxygen, and muscle paralysis. For example, Abrams, et al. (1972) found significant slow delta waves when either bilateral or unilateral ECS was administered. When the shock was restricted to one side, the EEG changes were found on that side. Volavka, et al., (1972) showed that the amount of delta activity in the EEG was related to the number of shocks administered. These studies had the additional advantage that the EEG expert who read the records did not know how the patients had been treated, i.e., the readings were done “blind”. (Abrams, et al 1., 1972) cite four additional studies done between 1965-1970 with similar EEG findings.

Summary and Conclusions Regarding the Effects of ECT on the Brain

1. During a seizure induced by ECT, there is a tremendous rise in blood pressure and a breakdown of the blood-brain barrier. These two events separately or in combination often cause hemorrhage, edema, and possibly toxic effects because the brain is exposed to chemicals in the blood from which it is normally protected. All of these phenomena cause the irreversible death of neurons in the brain (reviewed by Blackwood and Corsellis, 1976).

2. ECT alters the metabolism of brain proteins, RNA, and neural transmitters whose production is normally regulated carefully. Although the gross metabolism of these substances may later return to normal, their temporary alteration may have permanent effects in the brain. In fact, the very reason that hundreds of scientists around the world are studying the relation between these substances and memory is because small changes in their production might be the way that memories are stored.

3. EEG studies spanning a 28 year period show that ECT alters brain physiology from normal to abnormal. These changes, principally a slowing of the EEG waves, are similar to those found in epilepsy, mental deficiency, and other neuropathologies. The EEG changes associated with ECT appear to be extremely long-lasting very possibly they are permanent. They do not tell us whether a patient has lost his memory — for that you have to ask the patient. They do tell us that ECT can cause profound alterations in brain function.

4. All of the changes that follow ECT vary from animal-to-animal and from person-to-person. Thus, blood pressure rises in one study were small in one case, only 23%, but large in others (up to 400%). Cerebrovascular hemorrhages are found commonly, but not invariably (about 60% of the time); similarly, about half the patients show EEG abnormalities.

Loss of Memory for Past Events Following ECT

Losses of memory for past events commonly occur following insult to the brain, for example, following mechanical injury or from chronic toxic states such as alcoholism (Russell, 1971; Whitty and Zangwill, 1966). It should not be surprising that memory loss also accompanies the damage done to the brain by ECT. Such losses have been documented in numerous case reports dating back to the 1940s (Levy, et al., 1942). In some cases the loss is catastrophically complete: memory is erased for professional skills as well as orientation to places and friends (e.g., Roueche, 1974). More commonly, the loss is “patchy”: some events are lost while others are remembered; recent events are more likely to be lost than those in the distant past, but amnesia can extend backward for several years and can include events of early childhood that date back 20 to 40 years; some memories return while others do not (Janis, l948; A Practicing Psychiatrist, 1965; Brody, 1944; Valentine, et al, 1968; Medlicott, R.W., 1948; Squire, et al, 1975).

One’s confidence that there must be substance to these case reports is strengthened by the hesitations of some physicians experienced in the use of ECT to employ it on patients engaged in intellectual work (e.g., Stromgren, 1973) and in the widespread adoption, especially in Europe, of unilateral ECT. In this method the electrodes are not placed on both temples, but on one side of the head only, in the frontal and parietal regions. The passage of current is therefore largely restricted to one side of the brain. The electrodes are usually placed on the so-called “non-dominant” side, the side concerned with spatial, rather than verbal tasks. With this treatment the EEC changes are limited to the non-dominant hemisphere, and patients, report fewer and less severe losses of memory for past events. Clearly, in order for there to be less memory and loss and less brain damage (EEC changes) with unilateral ECT, there must be substantial amounts of it with bilateral ECT (Abrams, et al., 1972; Stromgren, 1973; Valentine, 1968; Zinkin and Birtchnell, 1968; D’Elia, 1970; Heshe and Roeder, 1976; Lancaster, et al., 1958). Lest it be prematurely concluded that no damage is done by unilateral ECT to the “non-dominant” hemisphere, it is well to realize that the functions of this hemisphere are just beginning to be appreciated and that methods for assessing its function remain primitive (e.g., Ornstein, 1973).

Various objective tests have been used to determine whether memory loss occurs following ECT, including standard IQ. tests, the Benton test, the. Paired Associates test, and tests devised specifically for assessing memory following ECT (e.g., Bender, 1947; Brunschweig, et al., 1971; Dornbush, et al, 1971; Squire and Chace, 1975). Most of the tests require the patient to learn and remember new material of very simple kinds. For example, can a patient memorize a list of words, numbers or faces and recall them after an hour, a day or a few weeks? Others test recognition of remote events that are not intimately connected with the patients’ lives, for example, recognition of the names of old television programs (Squire and Chace, 1975). One of these reports shows that patients have more difficulty recalling their own past than in learning new material and that amnesias recover more slowly than do the processes required for new learning (Brunschweig, et al., 1971). Until recently, such tests revealed very little impairment, and it was common to conclude that patient reports of memory loss are nothing more than complaints associated with their illness or merely an underestimation of their true memory abilities (Squire and Chace, 1975). No study, however, has tried to document this hypothesis, and several solid studies reporting substantial memory losses find no association between the degree of memory loss and the patient’s emotional health. Teuber, et al., (1976) studied 34 patients who had been subjected to cingulotomy (brain surgery) for relief of their mental illness. Many of these patients had been subjected to ECT prior to their surgery. On a battery of nine standardized psychological tests, significant deficits were found correlated not with the surgery but rather with the patients’ history of ECT.

“We found that individuals whose prior treatments had included ECT were inferior to normal control subjects and to patients who had been spared ECT, and this inferiority was apparent on the following measures: verbal and nonverbal fluency, delayed alternation performance, tactual maze learning, continuous recognition of verbal and nonverbal material, delayed recall of a complex drawing, recognition of faces and houses, and identification of famous public figures. In some cases, the degree of deficit was related to the number of ECT received, patients who had been given more than 50 ECT being significantly worse than those who had sustained fewer than 50.” (Teuber, et al., 1976, P. 76).

This study is one of the most thorough applications of objective tests to ECT patients; one would like to see it repeated on patients who had not also sustained surgical brain damage. Yet, it does not tell us what individual patients knew about themselves before and after their ECT. This question received a clear answer in the early 1950s.

The Janis Studies.

One series of studies, those of Dr. Irving Janis of Yale University, stands out in the scientific literature on the effects of ECT on memory for the past (Janis, 1950a; Janis, 1950b; Janis and Astrachan, 1951). Janis, unlike most investigators, studied patients before as well as after ECT and could, therefore, determine whether individual patients showed changes. He studied patients not merely for a few days or weeks following ECT but for up to 3+ months. Janis did not primarily use artificially devised tests but actually asked patients about the details of their lives, covering the following topics: 1) school history, 2) job history, 3) history of the mental disorder, 4) sexual and marital relationships, 5) family relationships, 6) childhood experiences, 7) miscellaneous, e.g., details of the layout and furnishing of the home, 8) outstanding life experiences, e.g., personal failures and troubles, best and worst experiences of one’s life, etc. In these interviews he pressed patients for minute detail. For example, he asked the name, location, years of attendance for each school; reasons for transferring or leaving; names of teachers; subjects failed and reasons for failure; difficulties with school authorities; description of the graduation ceremony on the last day of school. In this way he built up a rich account of personal memories so that he could compare the amount of detail that was supplied following ECT.

The Janis studies were carefully controlled. For patients who were to receive ECT, there was another group who matched the shock patients in age, education, type and degree of illness, and form of psychotherapy. These control patients were interviewed in the same detailed way as the shock patients, both initially and at the same later intervals. In this way Janis could be certain that any losses in memory he might find would be due to the ECT and not to the course of the illness or some other unidentified factor. At the end of the study, Janis asked both the shock and the control patients to state what they thought the purpose of the interviews was. Their replies indicated that none of them suspected that the purpose was to test their memory. They could not have been “faking” responses to determine the outcome of the study because they did not suspect that a study was underway.

The shock patients in this study received standard treatment (60 cycle, AC., 3 times/week). The number of shocks was relatively modest, between 8-27, with an average of 17. No differences were noted between patients who received different numbers of shocks.

The results of Dr. Janis’ study are, in my opinion, conclusive proof that serious losses of personal memories are caused by ECT and that the losses persist. Here is an example of what he found. First, a 38 year old woman before ECT:

Case E. — A 38 year old female schizophrenic (borderline or mixed); 10 electroshocks.

Before ECT. (Q. How did your illness begin?)… .About four years ago, right after I lost my child … I took thyroid then which caused palpitations. I didn’t know , At the time, that that caused it. I felt terrified by them. It was a real panic, as if I were on railroad tracks with a train coming. I was trying to be very brave about the death of my baby, going to work in the hospital where it died, collecting legal papers on it, and so forth, trying to be the super-woman. Then I had the palpitations; a friend told me I should get psychiatric help. I saw my family doctor and he sent for a neurologist. I spent the night at my doctor’s office and then I went to the H Sanitarium for a week. I was hopeful of getting all better. They didn’t feel I was really ill. After that, I began analysis. (Janis, 1950a.)

Note that a single question elicits a long account that is rich in detail. Information flows without prompting by the interviewer. Here is the same woman 3 1/2 weeks after a series of 10 shocks

Three and One-Half Weeks after ECT.

Q.Did you take some medication after the loss of your child? A.I don’t remember. Q.Thyroid? A.I think so. Q.What reaction did you have to it? A.I don’t know. Q.During that period did you have any special symptom -which disturbed you: A.I felt depressed. Q.Anything else? A.l don’t recall. Q.Did you have palpitations? A.I vaguely remember having palpitations now that you mention it. Q.How did you feel about them at the time? A.I don’t recall how I felt. Q.How did you feel at the moment when you had the palpitations? A. Probably not too well. Q.Did you ever go to a sanitarium? A.Yes, I remember going to one. Q.What was the name of it? A.I don’t recall the name. Q.What were the circumstances that led to your going there? A.I don’t remember why I went or what happened, I remember being there though. Q.How long were you there? A.I don’t remember. I don’t think it was for very long. I really can’t reconstruct that-whole period. (Janis, 1950a, pp. 369-370.)

Note I hat the woman has many gaps in her recall and needs specific prompting by the interviewer. Sometimes she recalls facts when prompted (“now that you mention it ….”). Dr. Janis gives several additional detailed examples and summarizes as follows:

…the examples fail to convey the extensiveness and variety of personal experiences subject to amnesia in each individual case. Every one of the 19 patients included in the study showed at least several instances of amnesia and in many cases there were from ten to twenty life experiences which the patient could not recall . (Janis, 1950a.)

In contrast, the control patients were able to reproduce practically all the material they had given in the initial interview, and they recalled it so readily that the examiner rarely needed to resort to raising questions giving specific cues so often required by the ECT patients. In fact, most of the control patients improved between the tests, as one would have expected because of the stimulation of “reliving” old events (Janis and Astrachan, 1951). Janis discovered amnesias in patients diverse in personality type and intellectual status, in patients with different types of mental disorders, in patients who improved psychologically, and in those who did not improve. These amnesias were in some instances for emotionally upsetting material, e.g., related to the illness, but in other instances were for emotionally “neutral” material as well. Furthermore, Janis notes, “many patients were distressed about their failure to recall past experiences and frequently made definite efforts to secure information about the events for which they were amnesic”. He says, “The patients usually expressed little conviction about the occurrence of such experiences and were unable to reconstruct the details beyond what they had been told about it.” (Janis, 1950a, P. 376). Janis notes that there was no tendency for patients to “protect” their amnesias since they sometimes actively sought for cues to help them remember. Therefore, even strong motivation to remember did not help.

A later study employing a somewhat different set of questions revealed “gross amnesic gaps” such as total failures to recall a particular job. Again, there were also more subtle amnesias such as failure to recall details of a specific event. Janis found, in addition to the gross gaps and subtle losses, a slowness and a great effort in recalling details. In some cases, details returned, but only with great effort and with the help of cues provided by the examine, (Janis and Astrachan, 1951). In his published papers, Janis reports following half of the shocked patients for 2 1/2 – 3 1/2 months after the end of ECT. He found that in each case most of the instances of amnesia persisted. Janis continued to follow six of these patients for a full year and found that the amnesias persisted (Janis, 1976).

The Janis studies employed the most sensitive method of any in the literature and the one that most directly addresses the concern of the patients, the loss of their own memories of their pasts. It would seem to me incumbent upon any researcher who fails to find memory loss using an artificially devised test to explain the Janis results. The simplest explanation at present is that the artificial tests are not as sensitive. No author so far has mounted serious criticism of the Janis studies, nor has anyone repeated them. The Janis results fit well with the evidence cited earlier that ECT causes organic brain damage. Overall, the evidence convinces me that ECT is far from benign. If, for others, doubts remain as to whether ECT impairs human memory, the first step toward settling the issue should be a careful and thorough repetition of the Janis studies.


1.Convulsions caused by electrical shocks to the brain are accompanied by alterations within the brain. Many of the brain’s natural protections are broken down. Mentioned in particular are the massive rise in blood pressure, the breakdown of cerebral auto regulation of blood flow, and the breakdown of the blood-brain barrier.

2.Such changes can lead to alterations in brain chemistry and physiology. The change most easily measured in humans is the alteration of the EEG toward a form that is commonly recognized as pathological.

3. Such changes are also associated in many studies with gross pathology such as brain swelling (edema) and particularly brain hemorrhages which lead to the irreversible death of neurons.

4. Such changes are also associated with persisting, probably permanent amnesias for life events and experiences.

5. Such amnesias may only be detected when patients are questioned in detail about their life histories before and following the administration of shocks.

6. At all levels, from changes in blood pressure to losses in memory, there is extreme variability. Losses can, however, be catastrophic after only a few shocks. In general, the younger and healthier the animal or person, the less permanent damage may result.

7. Such losses of memory can and do occur without any necessary changes in overall intelligence as measured by a psychological test and without any other detectable neurological abnormalities. This finding is common not only with ECT but in brain damage accompanying other kinds of insult such as trauma or toxicity.


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Can ECT Permanently Harm the Brain?

Donald I. Templer and David M. Veleber
Clinical Neuropsychology (1982) 4(2): 62-66

Literature relevant to the question of whether ECT permanently injures the brain was reviewed. Similar histological findings of epileptics and patients who had received ECT were discussed. Experimental research with animals seems to have demonstrated both reversible and nonreversible pathology. Psychological test findings, even when attempting to control for possible pre-ECT differences, seem to suggest some permanent cognitive deficit. Reports of spontaneous seizures long after ECT would appear to point to permanent brain changes. Human brain autopsies sometimes indicate and sometimes do not indicate lasting effects. It was concluded that vast individual differences are salient, that massive damage in the typical ECT patient is unlikely, and that irreversible changes probably do occur in some patients.

This review centers around five areas germane to the question of whether electroconvulsive therapy (ECT) causes permanent brain pathology. Relatively indirect evidence is provided by two of these areas, the brain condition of epileptics and the examination of animal brains after experimental ECT. The other three areas are psychological testing findings with history of many ECTs, spontaneous seizures, and autopsy findings. The review does not concern the extensive literature that shows that ECT temporarily impairs cognitive functioning. Such literature eventually shows impairment beginning with the first ECT and becoming progressively worse with succeeding treatments. Improvement occurs following the course of ECT, sometimes with the tested functioning actually being higher than the pretreatment level ­ which is presumed to have been impaired by psychopathology such as thought disorder and depression. Reviews of this literature can be found elsewhere (American Psychiatric Association, 1978; Campbell, 1961; Dornbush, 1972; Dornbush and Williams, 1974; Harper and Wiens, 1975), as can reviews indicating that the unilateral ECT (applied to the right side) in increasing usage in recent years causes less impairment than bilateral ECT (American Psychiatric Association, 1978; d’Elia, 1974; Hurwitz, 1974; Zamora and Kaelbing, 1965). This literature is really not very relevant to the central issue of our review. It has never been disputed that cognitive impairment occurs after ECT. Even the most fervent and excathedra defenders acknowledge that “temporary” impairment occurs. It is the issue of permanency that has been controversial.


It would seem that if an epileptic grand mal seizure produces permanent brain changes, then an electrically induced convulsion should also do so. In fact, inspecting the evidence with respect to epileptics may provide us with a conservative perspective in regard to ECT since the latter could produce damage from the externally applied electrical current as well as from the seizure. Experimental research with animals has shown that the electric shocks (not to the head) produce more deleterious effects in the central nervous system than any other locality or system of the body. More pertinent are the studies of Small (1974) and of Laurell (1970) that found less memory impairment after inhalant induced convulsions than ECT. And, Levy, Serota and Grinker (1942) reported less EEG abnormality and intellectual impairment with pharmacologically induced convulsions. Further argument provided by Friedberg (1977) is the case (Larsen and Vraa-Jensen, l953) of a man who had been given four ECTs, but did not convulse. When he died three days later, a subarachnoid hemorrhage was found in the upper part of the left motor region at the site where an electrode had been applied.

A number of post-mortem reports on epileptics, as reviewed by Meldrum, Horton, and Brierley (1974) have indicated neuronal loss and gliosis, especially in the hippocampus and temporal lobe. However, as Meldrum et al. pointed out, on the basis of these post-mortem reports, one does not know whether the damage was caused by the seizures or whether both were caused by a third factor intrinsic to the epilepsy. To clarify this issue, Meldrum et al. pharmacologically induced seizures in baboons and found cell changes that corresponded to those in human epileptics.

Gastaut and Gastaut (1976) demonstrated through brain scans that in seven of 20 cases status epilepticus produced brain atrophy. They reasoned that “Since the edema and the atrophy were unilateral or bilateral and related to the localization of the convulsions (unilateral or bilateral chronic seizures), the conclusion can be drawn that the atrophic process depends upon the epileptic process and not on the cause of the status.”

A common finding in epileptics and ECT patients is noteworthy. Norman (1964) stated that it is not uncommon to find at autopsy both old and recent lesions in the brains of epileptics. Alpers and Hughes (1942) reported old and recent brain lesions associated with different series of ECT.


There are a number of articles concerning the application of ECT and subsequent brain examination in animals. In the 15 study review of Hartelius (1952), 13 of the 15 reported pathological findings that were vascular, glial or neurocytological, or (as was generally the case) in two or three of these domains. However, as Hartelius pointed out, inferences of these studies tended to be conflicting because of different methods used and because of deficient controls. The research that Hartelius himself carried out was unquestionably the outstanding study in the area with respect to methodological sophistication and rigor. Hartelius employed 47 cats; 31 receiving ECT, and 16 being control animals. To prevent artifacts associated with the sacrificing of the animals, the cerebrums were removed under anesthesia while the animals were still alive. Brain examinations were conducted blindly with respect to ECT vs. control of subject. On a number of different vascular, glial, and neuronal variables, the ECT animals were significantly differentiated from the controls. The animals that had 11-16 ECTs had significantly greater pathology than the animals that had received four ECTs. Most of the significant differences with respect to reversible type changes. However, some of the significant differences pertained to clearly irreversible changes such as shadow cells and neuronophagia.


There have been several studies regarding the administration of psychological tests to patients with a history of many ECTs. Unfortunately, all were not well controlled. Rabin (1948) administered the Rorschach to six chronic schizophrenics with a history of from 110 to 234 ECTs. Three patients had 6, two had 4, and one had 2 Piotrowski signs. (Piotrowski regards five or more as indicating organicity.) However, control subjects were not employed. Perlson (1945) reported the case of a 27-year-old schizophrenic with a history of 152 ECTs and 94 Metrozol convulsions. At age 12 he received an IQ of 130 on the Stanford Achievement Test; at age 14 an IQ of 110 on an unspecified general intelligence test. At the time of the case study, he scored at the 71st percentile on the Otis, at the 65th percentile on the American Council on Educational Psychological Examination, at the 77th percentile on the Ohio State Psychological Examination, at the 95th percentile for engineering freshman on the Bennett Test of Mechanical Comprehension, at the 20th percentile on engineering senior norms and at the 55th percentile on liberal arts students’ norm on a special perception test. These facts led Perlson to conclude that convulsive therapy does not lead to intellectual deterioration. A more appropriate inference would be that, because of the different tests of different types and levels and norms given at different ages in one patient, no inference whatsoever is justified.

There are two studies that provide more methodological sophistication than the above described articles. Goldman, Gomer, and Templer (1972) administered the Bender-Gestalt and the Benton Visual Retention Test to schizophrenics in a VA hospital. Twenty had a past history of from 50 to 219 ECTs and 20 had no history of ECT. The ECT patients did significantly worse on both instruments. Furthermore, within the ECT groups there were significant inverse correlations between performance on these tests and number of ECTs received. However, the authors acknowledged that ECT-caused brain damage could not be conclusively inferred because of the possibility that the ECT patients were more psychiatrically disturbed and for this reason received the treatment. (Schizophrenics tend to do poorly on tests of organicity.) In a subsequent study aimed at ruling out this possibility, Templer, Ruff, and Armstrong (1973) administered the Bender-Gestalt, the Benton, and the Wechsler Adult Intelligence Scale to 22 state hospital schizophrenics who had a past history of from 40 to 263 ECTs and to 22 control schizophrenics. The ECT patients were significantly inferior on all three tests. However, the ECT patients were found to be more psychotic. Nevertheless, with degree of psychosis controlled for, the performance of the ECT patients was still significantly inferior on the Bender-Gestalt, although not significantly so on the other two tests.


It would appear that if seizures that were not previously evidenced appeared after ECT and persisted, permanent brain pathology must be inferred. There have been numerous cases of post-ECT spontaneous seizures reported in the literature and briefly reviewed by Blumenthal (1955, Pacella and Barrera (1945), and Karliner (1956). It appears that in the majority of cases the seizures do not persist indefinitely, although an exact perspective is difficult to obtain because of anticonvulsant medication employed and the limited follow-up information. another difficulty is, in all cases, definitively tracing the etiology to the ECT, since spontaneous seizures develop in only a very small proportion of patients given this treatment. Nevertheless, the composite of relevant literature does indicate that, at least in some patients, no evidence of seizure potential existed before treatment and post-ECT seizures persist for years.

An article that is one of the most systematic and representative in terms of findings is that of Blumenthal (1955) who reported on 12 schizophrenic patients in one hospital who developed post-ECT convulsions. Six of the patients had previous EEGs with four of them being normal, one clearly abnormal, and one mildly abnormal. The patients averaged 72 ECTs and 12 spontaneous seizures. The time from last treatment to first spontaneous seizure ranged from 12 hours to 11 months with an average of 2 and 1/2 months. The total duration of spontaneous seizures in the study period ranged from 1 day to 3 and 1/2 years with an average of 1 year. Following the onset of seizures, 8 of the 12 patients were found to have a clearly abnormal, and 1 a mildly abnormal EEG.

Mosovich and Katzenelbogen (1948) reported that 20 of their 82 patients had convulsive pattern cerebral dysrhythmia 10 months post ECT. None had such in their pre-treatment EEG. Nine (15%) of the 60 patients who had 3 to 15 treatments, and 11(50%) of the 22 patients who had from 16 to 42 treatments had this 10 month posttreatment dysrhythmia.


In the 1940s and 1950s there were a large number of reports concerning the examination of brains of persons who had died following ECT. Madow (1956) reviewed 38 such cases. In 31 of the 38 cases there was vascular pathology. However, much of this could have been of a potentially reversible nature. Such reversibility was much less with the 12 patients who had neuronal and/or glial pathology. The following are the comments pertaining to the neuronal and glial pathology and the amount of time between last treatment and death: “Gliosis and fibrosis” (5 months); “Small areas of cortical devastation, diffuse degeneration of nerve cells”, “Astrocytic proliferation” (1 hour, 35 minutes); “Small areas of recent necrosis in cortex, hippocampus and medulla”, “Astrocytic proliferation” (immediate); “Central chromatolysis, pyknosis, shadow cells (15 to 20 minutes); “Shrinking and swelling. ghost cells”, “Satellitosis and neuronophagia” (7 days); “Chromatolysis, cell shrinkage”. “Diffuse gliosis, glial nodules beneath the ependyma of the third ventricle” (15 days); “Increased Astrocytes” (13 days); “Schemic and pyknotic ganglion cells” (48 hours); “Pigmentation and fatty degeneration, sclerotic and ghost cells”, “Perivascular and pericellular gliosis” (10 minutes); “Decrease in ganglion cells in frontal lobes, lipoid pigment in globus pallidus and medical nucleus of thalamus”, “Moderate glial proliferation” (36 hours); “Glial fibrosis in marginal layer of cortex, gliosis around ventricles and in marginal areas of brain stem, perivascular gliosis in white matter” (immediate); “Marginal proliferation of astrocytes, glial fibrosis around blood vessels of white matter, gliosis of thalamus, brain stem and medulla” (immediate). In one case the author (Riese, 1948), in addition to giving the neuronal and glial changes, reported numerous slits and rents similar to that seen after execution. Needless to say, patients who died following ECT are not representative of patients receiving ECT. They tended to be in inferior physical health. Madow concluded, on the basis of these 38 cases and 5 of his own, “If the individual being treated is well physically, most of the neuropathological changes are reversible. If, on the other hand, the patient has cardiac, vascular, or renal disease, the cerebral changes, chiefly vascular, may be permanent.”


A wide array of research and clinical based facts that provide suggestive to impressive evidence in isolation, provide compelling evidence when viewed in a composite fashion. Some human and animal autopsies reveal permanent brain pathology. Some patients have persisting spontaneous seizures after having received ECT. Patients having received many ECTs score lower than control patients on psychological tests of organicity, even when degree of psychosis is controlled for.

A convergence of evidence indicates the importance of number of ECTs. We have previously referred to the significant inverse correlations between number of ECTs and scores on psychological tests. It is conceivable that this could be a function of the more disturbed patients receiving more ECTs and doing more poorly on tests. However, it would be much more difficult to explain away the relationship between number of ECTs received and EEG convulsive pattern dysrhythmia (Mosovich and Katzenelbogen, 1948). No patients had dysrhythmia prior to ECTs. Also difficult to explain away is that in Table I of Meldrum, Horton and Brierley (1974), the nine baboons who suffered brain damage from experimentally administrated convulsions tended to have received more convulsions than the five that did not incur damage. (According to our calculations, U=9, p Throughout this review the vast individual differences are striking. In the animal and human autopsy studies there is typically a range of findings from no lasting effect to considerable lasting damage with the latter being more of the exception. Most ECT patients don’t have spontaneous seizures but some do. The subjective reports of patients likewise differ from those of no lasting effect to appreciable, although usually not devastating impairment. The fact that many patients and subjects suffer no demonstrable permanent effects has provided rationale for some authorities to commit the non-sequitur that ECT causes no permanent harm.

There is evidence to suggest that pre-ECT physical condition accounts in part for the vast individual differences. Jacobs (1944) determined the cerebrospinal fluid protein and cell content before, during, and after a course of ECT with 21 patients. The one person who developed abnormal protein and cell elevations was a 57-year-old diabetic, hypertensive, arteriosclerotic woman. Jacobs recommended that CSF protein and cell counts be ascertained before and after ECT in patients with significant degree of arteriosclerotic or hypertensive disease. Alpers (1946) reported, “Autopsied cases suggest that brain damage is likely to occur in conditions with pre-existing brain damage, as in cerebral arteriosclerosis.” Wilcox (1944) offered the clinical impression that, in older patients, ECT memory changes continue for a longer time than for younger patients. Hartelius (1952) found significantly more reversible and irreversible brain changes following ECT in older cats than younger cats. Mosovich and Katzenelbogen (1948) found that patients with pretreatment EEG abnormalities are more likely to show marked post-ECT cerebral dysrhythmia and to generally show EEGs more adversely affected by treatment.

In spite of the abundance of evidence that ECT sometimes causes brain damage, the Report of The Task Force on Electroconvulsive Therapy of the American Psychiatric Association (1978) makes a legitimate point in stating that the preponderance of human and animal autopsy studies were carried out prior to the modern era of ECT administration that included anesthesia, muscle relaxants, and hyperoxygenation. In fact, animals which were paralyzed and artificially ventilated on oxygen had brain damage of somewhat lesser magnitude than, although similar patterns as, animals not convulsed without special measures. (Meldrum and Brierley, 1973; Meldrum, Vigourocex, Brierley, 1973). And it could further be maintained that the vast individual differences stressed above argue for the possibility of making ECT very safe for the brain through refinement of procedures and selection of patients. Regardless of such optimistic possibilities, our position remains that ECT has caused and can cause permanent pathology.

Peter Sterling testimony to Texas Legislature

April 17, 1995

Testimony to Texas State Legislature regarding House Bill 2452.
Peter Sterling, Ph.D.

As a neuroscientist I have studied the structure and function of the mammalian brain for more than 30 years. I teach this subject to medical and graduate students at the University of Pennsylvania where I also conduct an active research program on this subject. I became concerned abut the effects of electroconvulsive shock (ECS) on the brain more than 20 years ago after reading in the public press of a bright, professional woman whose memory was destroyed by a series of “therapeutic” ECS treatments. This led me to study the literature on ECS, both the clinical literature regarding possible efficacy and negative side -effects and also the experimental literature – - the application of ECS to animals in order to study the basis for the possible efficacy and side effects. I have continued to follow this literature over several decades and here summarize my main conclusions.
ECS unquestionably damages the brain. The damage is due to a variety of known mechanisms:

1. ECS is designed to evoke a grand mal epileptic seizure involving massive excitation of cortical neurons that also deliver excitation to lower brain structures. The seizure causes an acute rise in blood pressure well into the hypertensive range, and this frequently causes small hemorrhages in the brain. Wherever a hemorrhage occurs in the brain, nerve cells die – and nerve cells are not replaced. 2. ECS ruptures the “blood -brain barrier.” This barrier normally prevents many substances in the blood from reaching the brain. This protects the brain, which is our most chemically sensitive organ, from a variety of potential insults. Where this barrier is breached, nerve cells are exposed to insult and may also die. Rupture of this barrier also leads to brain edema (swelling), which, since the brain is enclosed by the rigid skull, leads to local arrest of blood supply, anoxia and neuron death. 3. Compromised neurons tend to release the neurotransmitter, glutamate, into the surrounding milieu. This chemical excites further neuronal activity which releases more glutamate, leading to “excito-toxicity” – - neurons literally die due to overactivity. Such excito -toxicity has been recognized relatively recently and is now a major topic of research. It is known to accompany seizures and over repeated episodes of ECS may be a significant contributor to accumulated brain damage. The degree of damage consequent to ECS varies between individuals. It can be catastrophic in response to a single series, or it can appear more gradually following repeated series. This is much like the damage to boxers – who may occasionally die in the ring due to massive cerebral hemorrhage, or more commonly accumulate damage until the impairment becomes obvious. Since any positive therapeutic effect of ECS is temporary, the treatment is commonly repeated, so chronic brain damage is inevitable.

The key manifestation of this damage is memory loss. This is disturbing enough, but there are probably other losses as well, such as the ability to think clearly, to learn new facts and so on. It must be particularly incapacitating to individuals who are already impaired by a mental illness. So, one would expect physicians to weigh carefully the possible benefits of the therapy against the cumulative damage that it causes. However, rather than weigh gain vs. loss, psychiatrists deny the obvious, that there is cumulative damage.

The reason that psychiatrists can remain unaware of accumulating memory loss is that they do not routinely test for it. Testing is required when patients take certain drugs, such as lithium. high blood levels of lithium can be toxic; and lithium can damage the blood-forming cells in the bone marrow. Therefore, blood levels of the drug and the state of the bone marrow are monitored. Memory loss could be monitored just as easily, by asking patients before ECS about early events in their lives and then questioning the patients following each series of ECS. When this was done by Janis (almost 50 years ago), losses were marked and prolonged. However, no effort has been made since then to do this simple test.

The physician’s first injunction is “Do no harm.” Because this treatment clearly does harm, I believe it to be misguided. Where the treatment is applied without investigating the degree of harm and monitoring its accumulation, I believe it to be irresponsible and therefore requiring of regulation.


Dr. Peter Sterling is Associate Professor of Neurobiology in the School of Medicine at University of Pennsylvania.

Neurologist’s words on ECT head injury

Update 2006: I have had some very nice emails from Dr. Samant’s child. He has since passed away, but these emails were very touching.


Sydney Samant, M.D.
Clinical Psychiatry News
March 1983

“As a neurologist and electroencephalographer, I have seen many patients after ECT, and I have no doubt that ECT produces effects identical to those of a head injury. After multiple sessions of ECT, a patient has symptoms idenctical to those of a retired, punch-drunk boxer…After a few sessions of ECT the symptoms are those of moderate cerebral contusion, and further enthusiastic use of ECT may result in the patient functioning at a subhuman level. Electroconvulsive therapy in effect may be defined as a controlled type of brain damage produced by electrical means.”

An Introduction to Neuropsychological Assessment

Alan E. Brooker

Clinical neuropsychology is a specialized field of endeavor which seeks to apply the knowledge of human brain-behavior relationships to clinical problems. Human brain-behavior relationships refer to the study of research-derived associations between an individual’s behavior, both normal and abnormal, and the functioning of his or her brain. The clinical neuropsychologist takes extensive measurements of a variety of kinds of human behavior, including receptive and expressive language, problem-solving skills, reasoning and conceptualization abilities, learning, memory, perceptual-motor skills, etc. From this complex and detailed set of behavioral measurements, a variety of inferences can be drawn relating directly to the functioning of an individual’s brain. In clinical neuropsychology, the operation and condition of an individual’s brain is assessed by taking measures of his or her intellectual, emotional and sensory-motor functioning.

In studying brain functioning by measuring behavior, the clinical neuropsychologist makes use of a specialized set of tools which is appropriately labeled the clinical neuropsychological evaluation. This instrument is generally composed of numerous psychological and neuropsychological procedures which measure various abilities and skills. Some of these procedures are drawn from psychology (WAIS-R, Form Board in TPT) and others have been developed specifically from neuropsychological research (Category Test, Speech Sounds Perception Test, etc.). These strictly neuropsychological procedures compose the greater part of the evaluation, especially since they were developed specifically to assess brain functioning by measuring higher mental abilities. Still other procedures in the evaluation were borrowed directly from neurology (certain items on Aphasia Screening; Sensory Perceptual Examination) and were standardized in their administration. Some of the procedures in the evaluation are rather homogeneous in that they depend on mainly one ability or skill for success or failure (Finger Oscillation Test primarily relies on motor tapping speed). Other procedures are more heterogeneous and depend on the organized and complex interaction of several distinct skills or abilities for success (Tactual Performance Test – tactile perceptual ability; appreciation of two-dimensional space; planning and sequencing ability; etc.). In all, the clinical neuropsychological evaluation gives the practitioner in this field a wealth of information about an individual’s unique pattern of skills and abilities.

The clinical neuropsychological evaluation has essentially two main purposes: one involving diagnosis and the other involving behavioral description. The diagnostic power of a neuropsychological instrument, such as the Halstead-Reitan Battery, has been well documented and need not be discussed in detail (Vega and Parsons, 1967; Filskov and Goldstein, 1974; Reitan and Davison, 1974). In neuropsychological diagnosis, the presence or absence of impairments in brain functioning can be determined along with other important factors, such as lateralization, localization, severity, acuteness, chronicity or progressivity, and type of impairment suspected of being present (tumor, stroke, closed head injury, etc.). Four primary methods of inference are utilized in making these determinations, namely, level of performance, pathognomonic sign, comparison of the two sides of the body and specific patterns of test scores.

The level of performance approach primarily involves determining how well or how poorly an individual performs on a certain task, usually by means of a numerical score. Cut-off scores are generally developed for such a task, which allow the practitioner to classify an individual as either impaired or unimpaired with respect to brain functioning, depending upon whether his score falls above or below the cut-off value in use. The Halstead Category Test provides an example of this level of performance approach. On this procedure, a score of 51 errors or above places an individual in the impaired range. Likewise, a score of 50 errors or below places the individual in the normal range generally characteristic of individuals with unimpaired brain functioning. The primary danger of using level of performance measures alone to diagnose brain dysfunction is that of classification errors. In most cases, the cut-off score will not completely separate individuals with brain dysfunction from those without. Therefore, both false-positive and false-negative errors can be expected, depending upon the particular cut-off score established. Such a procedure in fact used in isolation is tantamount to employing single tests to diagnose “brain damage, and this approach has been justly criticized in previous work (Reitan and Davison, 1974). Additional methods of inference are used in neuropsychological assessment in order to sharpen diagnosis and minimize errors.

The pathognomonic sign approach essentially involves identifying certain signs (or specific types of deficient performance) which are always associated with brain dysfunction whenever they occur. An example of such a pathognomonic sign would be an instance of dysnomia on Aphasia Screening made by an individual with a college degree and normal IQ values. Such an individual would not be expected to say “spoon” when shown a picture of a fork and asked to name this object. The appearance of a true pathognomonic sign in a neuropsychological evaluation can always be associated with some sort of impairment in brain functioning. However, the converse is not true. That is, the absence of various pathognomonic signs in a particular individual’s record does not mean that this individual is free of brain dysfunction. Thus, using, the pathognomonic sign approach alone, one runs a considerable risk of making a false-negative error or discounting the presence of brain dysfunction when it in fact does exist. If other methods of inference are employed with this approach, however, then the likelihood is increased that any brain dysfunction present will be identified even in the absence of pathognomonic signs. Therefore, one may again see the value of and necessity for multiple and complimentary methods of inference in clinical neuropsychology.

The third method of inference involves a comparison of the performances of the two sides of the body. This method was borrowed in principle almost directly from clinical neurology but involves measurement of a variety of sensory, motor and perceptual-motor performances on the two sides of the body and comparing these measures with respect to their relative efficiency. Since each cerebral hemisphere governs (more or less) the contralateral side of the body, some idea of the functional condition of each hemisphere relative to the other can be gleaned from measuring the performance efficiency of each side of the body. An example here is the Finger Oscillation Test. Here, tapping speed in the dominant hand is compared with tapping speed in the non-dominant hand. If certain expected relationships are not obtained, then inferences with respect to the functional efficiency of one hemisphere or the other can be made. This inferential approach provides important corroborative and complementary information, especially with respect to lateralization and localization of brain dysfunction.

The final, method of inference to be discussed is that of specific patterns of performance. Certain scores and results may combine into particular patterns of performance which carry important inferential meaning for the clinician. For example, the relative absence of constructional dyspraxia, sensory-perceptual deficits, and aphasic disturbances, together with significant deficits on grip – strength, Finger Oscillation and the Tactual Performance Test, may possibly be associated with brain dysfunction which is more anterior in location than posterior. As another example, severe constructional dyspraxia with an absence of aphasic disturbances, together with severe sensory and motor losses in the left upper extremity, is likely associated with dysfunction in the right hemisphere rather than in the left.

Clinical neuropsychological diagnosis of brain dysfunction is carried out utilizing four primary methods of inference in a complex yet integrated fashion. Each of these methods is dependent upon and complementary to the others. The strength of neuropsychological diagnosis lies in the simultaneous utilization of these four methods of inference. Thus, some particular impairment in brain functioning may yield relatively normal levels of performance but, at the same time, may produce certain pathognomonic signs or yield patterns of performance which are clearly associated with brain dysfunction. The cross-checks and multiple avenues of gaining information, made possible by the simultaneous use of these four methods of inference, allow sound and accurate diagnosis of brain dysfunction by the experienced clinical neuropsychologist.

The second major purpose of clinical neuropsychology, as mentioned above, is behavioral description and delineation of behavioral strengths and weaknesses. This type of formulation can be most essential in making recommendations for an individual’s treatment, disposition and management. This, in fact, is considered by some practitioners to be the most important function of the clinical neuropsychological evaluation. Behavioral description is the clinical neuropsychologist’s unique input into a patient’s total medical workup. Other specialists, notably the neurologist and neurosurgeon, are excellent neurological diagnosticians, and it is not the purpose of clinical neuropsychology to compete with these individuals or attempt to take their place. Thus, neuropsychological diagnosis can be considered an additional avenue of diagnostic input into a patient’s workup. Behavioral description, on the other hand, is the clinical neuropsychologist’s unique domain. Here, this practitioner can provide input into a patient’s total medical picture which is not available from any other source.

Behavioral descriptions should start out with a thorough understanding of the patient’s background, his educational level, his occupation, his age, his likes, dislikes, future plans, etc. This information is usually brought into play subsequent to a blind analysis of the patient’s neuropsychological evaluation and a preliminary diagnosis and behavioral description based on this analysis. Before the final behavioral description and recommendations are given, however, the patient’s background information is integrated into the formulation. Here, the clinical neuropsychologist can look at the particular patient’s pattern of intellectual and adaptive strengths and weaknesses shown on the neuropsychological evaluation and integrate these findings with the patient’s individual situation. This can be considered to be a very important process in terms of formulating specific, meaningful and directly applicable recommendations for the particular individual under study.

Specific issues which often warrant coverage in neuropsychological behavior description involve a variety of areas. From the clinical neuropsychological evaluation, specific areas in need of rehabilitation can be identified, as well as areas of behavioral strength which warrant the individual’s awareness. Advice on coping with environmental demands in the face of particular behavioral deficits is often necessary, as well as some realistic prediction of future change in neuropsychological status. The degree of behavioral deficit in various areas can often be specified and questions with respect to a patient’s ability to manage himself and behave adaptively in society can be answered directly. Forensic issues can often be dealt with in terms of providing direct, clear information with respect to a patient’s judgment, competence, degree of intellectual and adaptive loss following brain disease or trauma, etc. Other specific areas in which the clinical neuropsychological evaluation can provide input include educational potential, occupational potential, the effects of brain dysfunction on social adjustment, etc. The importance of the behavioral picture of a patient obtained from the neuropsychological evaluation is immense.

As mentioned above, the clinical neuropsychological evaluation is not meant to compete with or take the place of more traditional medical procedures. In fact, certain important differences exist between the clinical neuropsychological evaluation and these procedures. First of all, the neuropsychological evaluation is primarily concerned with higher mental abilities, such as language, reasoning, judgment, etc. Traditional neurology, on the other hand, emphasizes assessment of sensory and motor functions and reflexes. Thus, although the neurologist and neuropsychologist study the same general phenomenon, that is, nervous system function and dysfunction, these practitioners nevertheless emphasize different aspects of this phenomenon. The clinical neuropsychologist takes precise and specific measurements of a variety of aspects of higher cortical functioning. The neurologist, on the other hand, primarily concentrates on lower-level phenomena of nervous system functioning. The results of these two types of evaluation may not always agree, given the different aspects of the central nervous system emphasized and the different methods and procedures used by each of these practitioners. Logically, the clinical neuropsychological assessment and the neurological evaluation should be considered complementary to each other. Certainly, neither one is a substitute for the other. Where possible, both of these procedures should be employed in order to obtain a full and detailed picture of an individual’s central nervous system functioning.

Traditional psychological assessment procedures and the clinical neuropsychological evaluation also have a number of differences worth noting. In traditional psychological assessment, for example, an individual’s average or modal performance is usually desired. On the neuropsychological evaluation, however, the examiner strives to obtain an individual’s best or optimal performance. Considerable encouragement and positive support is given to the patient during a neuropsychological evaluation to perform as well as possible. Such encouragement is generally not given under traditional psychological assessment conditions. Additionally, psychological procedures, such as the Rorschach, MMPI, Wechsler Intelligence Scales, Draw-A-Person, etc., have traditionally been used by psychologists who diagnose brain damage and disease. Although each of these procedures may contribute significant information about a person’s behavior, their validity in detecting the presence or absence of brain dysfunction and determining the nature and location of the dysfunction is rather limited. These assessment procedures have not been developed specifically for the purpose of identifying and describing brain damage and disease. The clinical neuropsychological evaluation, on the other hand, has been developed specifically for this purpose and has been validated against stringent medical criteria, such as surgical findings and autopsy reports. In addition, traditional psychological assessment procedures generally do not make use of the multiple inferential methods employed by the clinical neuropsychological evaluation. Oftentimes, only one or at most two inferential methods are used with traditional psychological assessment procedures in making determinations of the presence or absence of brain dysfunction. Thus, the comprehensive approach to making inferences and drawing conclusions used by the clinical neuropsychologist is felt to be superior to more traditional psychological methods in the diagnosis and description of brain dysfunction.


Filskov, S. & Goldstein, 5. (1974). Diagnostic validity of the Halstead-Reitan Neuropsychological Battery. Journal of Consulting and Clinical Psychology, 42(3), 382-388.

Lezak, M.D. (1983). Neuropsychological Assessment. New York: Oxford University Press.

Reitan, R.M. & Davidson, L..A. (1974). Clinical Neuropsychology: Current Status and Applications Washington: VJ-I. Winston & Sons.

Vega, A., & Parsons, 0. (1967). Cross-validation of the Halstead-Reitan Tests for brain damage. Journal of Consulting Psychology, 3 1(6), 6 19-625.


Dr. Alan E. Brooker is a clinical neuropsychologist with the Department of Mental Health at the David Grant USAF Medical Center. Travis Air Force Base, CA. 94535.

Brain scans and Charles Kellner

Dr. Kellner says “There are now important carefully controlled studies with MRI brain scans before and after ECT showing conclusively that there is absolutely no structural brain damage.” Click here to view the video of him saying this.

These are the studies. Judge for yourself. Are THESE conclusive evidence?

Title Year No. of patients What was tested?

Definitions at bottom
Cerebral and brain stem changes 1987 14 T1 yes, temp
Effects of ECT on brain structure 1988 9 cortical atrophy/

global comparisons
no acute change
Time course of cerebra 1990 20

(only 13 were fully tested)
T1 yes, temp
Brain anatomic effects 1991 35 brain volume/

global comparison
some, but explained as cerebrovascular disease
Post-ECT increases 1994 6 T2 yes, “significant”

Br J Psychiatry 1987 Jul;151:69-71

Cerebral and brain stem changes after ECT revealed by nuclear magnetic resonance imaging.

Mander AJ, Whitfield A, Kean DM, Smith MA, Douglas RH, Kendell RE

Nuclear magnetic resonance images of the brain were obtained in fourteen patients with major depression during a course of ECT. The T1 relaxation time rose immediately after the fit, reaching a maximum 4-6 h later. The T1 values then returned to their original level; no long-term increase occurred over the course of treatment. These results are consistent with an extensive but temporary breakdown of the blood-brain barrier during ECT.


Am J Psychiatry 1988 Jun;145(6):701-6

Effects of ECT on brain structure: a pilot prospective magnetic resonance imaging study.

Coffey CE, Figiel GS, Djang WT, Sullivan DC, Herfkens RJ, Weiner RD

The authors describe a pilot prospective investigation of the effects of ECT on brain structure using magnetic resonance imaging (MRI). In nine patients with major depression, a course of ECT produced no acute changes in brain structure according to blind raters’ assessments of cortical atrophy and global comparison of pre- and post-ECT studies. There were also no significant changes in the ventricle-brain ratios. Pre-ECT brain abnormalities were common in these patients yet were also unaffected by ECT. Future MRI studies of ECT should include more subjects and should address long-term changes and subtle brain abnormalities.


Br J Psychiatry 1990 Apr;156:551-3

Time course of cerebra; magnetic resonance changes after electroconvulsive therapy.

Scott AI, Douglas RH, Whitfield A, Kendell RE

Nuclear magnetic resonance images of the non-dominant cerebral hemisphere were obtained in 20 unipolar depressed patients immediately before and 25 minutes after electroconvulsive therapy (ECT). T1 values rose about 1%. Repeated scanning up to 24 hours after ECT was carried out in 13 of these patients. The greatest change in magnetic resonance images was two hours after ECT, and thereafter images gradually returned to baseline values. There was no correlation between magnetic resonance changes and the time taken to become reorientated after ECT.


Arch Gen Psychiatry 1991 Nov;48(11):1013-21

Brain anatomic effects of electroconvulsive therapy. A prospective magnetic resonance imaging study.

Coffey CE, Weiner RD, Djang WT, Figiel GS, Soady SA, Patterson LJ, Holt PD, Spritzer CE, Wilkinson WE

To determine prospectively whether electroconvulsive therapy (ECT) produces structural brain changes, 35 inpatients with depression underwent magnetic resonance imaging before and twice after (at 2 to 3 days and at 6 months) completion of a course of brief-pulse, bilateral ECT. The magnetic resonance images were analyzed blindly for evidence of changes in brain structure using two approaches: measurement of regional brain volumes and a pairwise global comparison. Structural brain abnormalities were present in many patients before ECT. The course of ECT produced no acute or delayed (6-month) change in brain structure as measured by alterations of the total volumes of the lateral ventricles, the third ventricle, the frontal lobes, the temporal lobes, or the amygdala-hippocampal complex. In five subjects, the pairwise global comparisons revealed an apparent increase in subcortical hyperintensity, most likely secondary to progression of ongoing cerebrovascular disease during follow-up. Our results confirm and extend previous imaging studies that also found no relationship between ECT and brain damage.


Psychiatry Res 1994 Nov;54(2):177-84

Post-ECT increases in MRI regional T2 relaxation times and their relationship to cognitive side effects: a pilot study.

Diehl DJ, Keshavan MS, Kanal E, Nebes RD, Nichols TE, Gillen JS

This pilot study examined the hypothesis that magnetic resonance imaging T2 relaxation times of specific brain regions increase after electroconvulsive therapy (ECT) and that these increases are related to the cognitive side effects of ECT. Six depressed patients undergoing unilateral ECT were studied. The results demonstrate significant post-ECT T2 increases in the right and left thalamus, and suggest a correlation between regional T2 increase and anterograde memory impairment following ECT. These findings are consistent with a post-ECT increase in brain water content (perhaps secondary to a breakdown of the blood-brain barrier) and suggest that this process may be related to the memory impairment following ECT.


T1: In magnetic resonance, the time for 63% of longitudinal relaxation to occur; the value is a function of magnetic field strength and the chemical environment of the hydrogen nucleus; for protons in fat and in water, in a 1.5T magnet, about 250 msec and 3000 msec respectively. A T1-weighted image will have a bright fat signal.

T2: In magnetic resonance, the time for 63% of transverse relaxation to occur; the value is a function of magnetic field strength and the chemical environment of the hydrogen nucleus; for protons in fat and in water, in a 1.5T magnet, about 60 msec and 250 msec respectively. A T2-weighted image will have a bright water signal.

global: The complete, generalized, overall, or total aspect.

atrophy: A wasting of tissues, organs, or the entire body, as from death and reabsorption of cells, diminished cellular proliferation, decreased cellular volume, pressure, ischemia, malnutrition, lessened function, or hormonal changes. Syn: atrophia.

Now Where Did I Put Those Keys?

The World & I, 11-01-1998
Norbert R. Myslinski

As researchers unravel the brain’s inner workings during the formation and loss of memories, we may find new ways to prevent serious memory lapses.

Along with ordering their first pair of bifocals and starting to feel the pains of arthritis, baby boomers are now worrying about their memory remember seems to be going in the opposite direction as their need to remember. Are these memory lapses a normal part of growing old, or are they the beginnings of Alzheimer’s disease? How can we tell the difference? Is there anything we can do to improve our memory?

Our understanding of the neurobiology of memory has taken gigantic strides in the last five years. We have discovered genes involved in controlling memory. We are testing drugs that may enhance memory. We have scanning technology that enables us to visualize the flow of brain activity at the same time as the subject searches for a memory. And we have even seen changes in nerve cell connections (synapses) in response to learning and experience. These and other recent discoveries promise future treatments to help those having trouble with memory lapses, whether as a result of a degenerative brain disease or just normal aging.

Memories, memories

Memory is not a singular brain function. Rather, the brain processes, stores, and retrieves information in many distinct ways and in many different places. Memories have been classified according to the type of information or the time of retention.

Type of information. Memories categorized by type of information can be either declarative, procedural, or emotional. Declarative memory is the ability to remember names, faces, telephone numbers, or important events. It is material available to the conscious mind, encoded in the cerebral cortex, and expressed by language.

Procedural memory refers to motor activity and skills acquired and retrieved on a subconscious level. We utilize procedural memory during such activities as piano playing, knot tying, and bike riding, when we do not consciously direct our detailed movements. In fact, thinking about the movements may inhibit our ability to perform them. Procedural memories are stored in parts of the brain known as the basal ganglia, the cerebellum, and the premotor cortex.

Emotional memory re-creates our original emotional response. A sight, a sound, or even a smell can bring back the joy, fear, love, or hate that we once associated with it. A buzzing bee or an attractive face may mean little emotionally, until we create memories of being stung or falling in love. The anatomical correlate of emotional memory is the amygdala, located in the temporal lobes on each side of the brain. Destroying the amygdala destroys emotional memory.

If left unchecked, emotional memory can lead to chronic fear, forming the basis of anxiety disorders such as phobias, panic attacks, and post-traumatic stress disorder (PTSD). Normally, the prefrontal cortex dampens the amygdala’s response and calms the fear. But for most PTSD sufferers, their prefrontal cortex does not send this message. About 25 percent of Americans have a diagnosable anxiety disorder at some point in their lives, and the collective bill for treating these disorders amounts to about $45 billion per year.

Time of retention. When viewed from the perspective of time of retention, memories may be classified as being part of either working memory or long-term memory. Working memory is the “blackboard” of the brain. It is the capacity to keep information in the conscious mind while performing tasks using that information. It maintains images “on-line” long enough to manipulate them for problem solving and planning. It is similar to a computer’s RAM (random access memory). Long-term memory is filed away, stored over extended periods of time, to be retrieved later. It is similar to memory stored on a hard disk drive.

Contrary to popular belief, our brains do not record everything that happens to us. More than 99 percent of the sensory information that enters our bodies is filtered out and does not even reach our consciousness. Most of what does reach consciousness hovers briefly in working memory and then evaporates. Only meaningful experiences are preserved in long-term memory. If we were aware of every sensory message and stored every thought, there would be no room for analyzing, creating, and enjoying.

Losing our memories

Memory loss that accompanies normal aging is primarily a deficit in working memory, due to changes in the prefrontal cortex. It includes absent-mindedness, a shortened attention span, and a decreased ability to hold a thought. This slower, less-precise working memory is a nuisance, but by itself it does not signal the beginning of a degenerative disease, and it is not inevitable. Although memory generally declines with age, some octogenarians retain better working memories than people in their twenties.

Pathological amnesias, on the other hand, differ from regular, age- related memory loss. They occur in either of two main forms: retrograde and anterograde. Retrograde amnesia is the loss of memories of the past. A person who experiences physical trauma to the brain or an electroconvulsive shock may forget his past while retaining the ability to create new memories.

Most of us and Hollywood associate the term amnesia with this form, although its occurrence is rare. When it does happen, memories of the recent past are more likely to be lost than older ones. The extent of the loss varies from events that happened just some seconds back to those that occurred several years ago, depending on the strength of the learning and the severity of the disruption.

Anterograde amnesia is the inability to create new memories. The patient is trapped in an ever-present “now”–whether meeting with the same people or experiencing a recurrent event, he regards them as being new and novel, over and over again. He still has memories from before onset of the amnesia, but he cannot add to them. Common causes of this kind of memory loss include trauma, stroke, viral encephalitis, and Alzheimer’s disease. All of them damage the hippocampus, which lies deep on both sides of the brain. Thiamine deficiency experienced by some chronic alcoholics also produces anterograde amnesia, by creating lesions in parts of the brain known as the mammillary bodies and the medial thalamus.

Every time we perceive something, a unique set of brain cells is activated in a specific sequence. If not pursued, the perception fades and the cells return to their original state. If the thought is entertained, the relationship between these cells is strengthened. The transmission of signals through synapses becomes easier between these cells than between cells that do not have this relationship. The set of cells with facilitated synapses is now the anatomical correlate of the memory and is called a memory engram. Once the engram is formed, anything that activates it will revive the original perception as a memory. If allowed to lie dormant for too long, this relationship dissolves and so does the memory.

Synapses between neurons that produce the neurotransmitter dopamine in the prefrontal cortex are responsible for working memory. The hippocampus of the temporal lobes is responsible for consolidating or solidifying the memory. Every time the memory engram is activated, the hippocampus facilitates the synapses and strengthens the relationship between neurons in the circuit.

Memory consolidation can occur consciously, by repetition, but it usually occurs unconsciously, by the action of the hippocampus. The latter is more likely to happen when the experience is novel, has emotional significance, or relates to something we already know. The more the engram is activated, the stronger the memory. This facilitation involves electrical, biochemical, and anatomical changes.

Most long-term memories are physically consolidated (recorded) somewhere in the 100 billion nerve cells of the brain. Initial facilitation is based on changes in the long-term electrical potentials of cells and modification of preexisting proteins. Important neurotransmitters responsible for these changes include glutamate and nitric oxide.

Stronger facilitation requires the expression (turning on) of certain genes and the synthesis of new proteins. These events produce anatomical changes in cells, including the sprouting of new branches and the creation of new synapses.

Among the substances important for this growth is a peptide called BDNF (brain-derived neurotrophic factor). New research has shown that the brain also grows new cells in response to learning. In other words, our experiences can restructure our brains.

Brain regeneration, memory genes, smart pills

Brain cell growth.For decades it has been considered a fundamental truth that adult brains never grow new cells. But one of the most exciting recent discoveries in memory research is that neurons do multiply. Recent work with monkeys has shown that new cells are constantly being made in the hippocampus, the part of the brain that consolidates long-term memories. Experts believe that this is true for human brains as well.

If we can discover how to control this intrinsic ability of the brain, we would be able to create new cells to replace dead or degenerating ones. This knowledge could lead to new treatments for stroke, trauma, or degenerative brain diseases such as Parkinson’s and Alzheimer’s.

Memory genes. In the 1970s, Seymour Benzer found that a particular genetic mutation in a fruit fly caused it to become a “dunce.” Several years ago, Tim Tully and Jerry Yin at Cold Spring Harbor Laboratory (on Long Island in New York) developed a “smart” fruit fly by stimulating the same gene (CREB) that was mutated in Benzer’s fly. CREB functions as a master switch that unlocks dozens of other genes important for the consolidation of memory. It is like a general contractor, who controls the work crews that actually do the remodeling of the synapses to create memories. Based on past experience, the CREB gene probably occurs in humans, too. But there are at least 23 other genes known to affect memory, and researchers have yet to find ways to turn on these genes selectively in the brain.

Over-the-counter drugs.Many people would like to improve their memory instantly by taking a pill. And many over-the-counter drugs and herbs- -such as choline, St. John’s wort, and ginkgo biloba–are being marketed as having the ability to bolster memory. But they have not been proven to boost raw memory power.

Some of these products contain a stimulant such as caffeine. The stimulant can improve attention, and it may consequently enhance our ability to remember. Other common ingredients are antioxidants. Oxidative changes are thought to enhance the degeneration of brain cells, as seen in the brains of Alzheimer’s disease (AD) patients. It has therefore been speculated that antioxidants such as vitamin E might improve the memory of AD patients and possibly that of normal elderly individuals. Studies support the idea that damage due to oxidation does play a role in AD and that antioxidants improve the independence and behavioral symptoms of AD patients. But while antioxidants may help maintain the viability of brain cells, they probably do not have any specific effect on the memory process.

Prescription drugs.Over 100 cognitive enhancers are currently being tested. Most would be used for AD patients, but some may enhance memory function in normal individuals as well. These drugs would not recover past memories that have been lost, but they would improve our ability to store new information. The tests, however, may take many years. In the case of tacrine (Cognex), the first drug approved to treat AD, it took about 15 years to go from the research lab to the doctor’ s office.

One approach that is being tested is called estrogen-replacement therapy. Early evidence of estrogen’s role in memory came when researchers found that the plasticity of the rat brain varied with the rat’s reproductive cycle. More recently, scientists at Columbia University found that estrogen-replacement therapy was associated with a reduced risk of AD. The study involved more than a thousand women of European, Hispanic, and African ancestry. For women who did not take estrogen, the incidence rate for AD was 8.4 percent; among those who took estrogen, it was 2.7 percent. Some researchers suggest that estrogen exerts its beneficial effects by increasing the number of neuronal projections known as dendritic spines, which enhance communication between neurons. Others say that estrogen works together with compounds called neurotrophins to facilitate communication.

These and other results suggest that estrogen during and after menopause may significantly lower the risk of AD and delay the onset of memory loss. Whether it can delay memory loss due to normal aging has yet to be proven. Additional research is needed to learn the exact mechanism by which estrogen protects against memory loss, before doctors can recommend it for that purpose.

Another set of tests is being carried out with anti-inflammatory drugs. It has long been noticed that AD is less common among people with arthritis. This observation now seems related to their use of anti- inflammatory drugs. In a study by the National Institute of Aging, more than 2,000 men and women were surveyed about their use of medications. Those who regularly used nonsteroidal anti-inflammatory drugs (NSAIDs), other than aspirin, had a lower risk of developing AD than those who did not. This and other pieces of evidence suggest a relationship between brain inflammation and memory loss in cases of both AD and normal aging.

In a 3-year study of over 7,000 normal volunteers, NSAIDs were found to lower the risk of age-related loss of memory and other cognitive functions. Those taking NSAIDs showed cognitive ability equivalent to that of a person 3.5 years younger, and the risk of cognitive decline was reduced by about 20 percent. However, further testing is necessary, and the use of NSAIDs to preserve cognitive function in normal individuals is not yet advised.

In The Milk Train Doesn’t Stop Here Anymore, Tennessee Williams wrote, “Life is all memory except for the one present moment that goes by you so quick you hardly catch it going.” Memories are us. They are a function of our past experiences and a framework for our future selves. And what we individually choose to remember or forget is intrinsic to who we are. As demonstrated by many AD patients, without memories we are stuck in a moment in time.

Research to help prevent such tragic memory losses is praiseworthy, and efforts to enhance normal memory by improving ourselves are admirable as well. But using drugs to tinker with normal memory may not be worth it in the long run. These drugs, like most others, will take as well as give. We must think carefully about what we are giving up before we take them.

Norbert R. Myslinski is associate professor of neuroscience at the University of Maryland, past president of the Baltimore chapter of the Society for Neuroscience, and director of Maryland Brain Awareness Week.

Psychopathology of Frontal Lobe Syndromes

Michael H. Thimble, F.R.C.P., F.R.C. Psych

From Seminars in Neurology
Volume 10, No. 3
September 1990

Although personality and behavior disorders have been described following frontal lobe lesions since the mid part of the last century, it is remarkable how frontal lobe pathologic conditions often go unnoticed clinically, and indeed how the relevance of frontal lobe syndromes in man to an understanding of brain-behavior relationships has been neglected. This is in spite of the pertinent observations of Jacobsen (2) on the effects of frontal lobe lesions in primates, the careful reports of the consequences of head injuries in the World War II, (3) and of patients examined following prefrontal leukotomies, (4) all of which studies lead to the delineation of specific defects in behavior associated with lesions in this part of the brain. Their increasing significance and clinical relevance is noted by the recent publication of several monographs on frontal lobe syndromes (5,6) and the growing literature on various frontal lobe disorders, for example, frontal lobe dementias and frontal lobe epilepsies.


The frontal lobes are anatomically represented by those areas of the cortex anterior to the central sulcus, including the main cortical areas fur the control of motor behavior. The anterior cingulate gyrus can be considered part of the medial frontal lobe. The term “prefrontal cortex” is most appropriately used to designate the main cortical target projections for the mediodorsal nucleus of the thalamus, and this area is also sometimes referred to as frontal granular cortex. It is denoted by Brodmann areas 9-15, 46, and 47.

On the basis of primate data, Nauta and Domesick (7) suggested that the orbital frontal cortex makes connections with the amygdala and related subcortical structures and can be considered an integral part of the limbic system. Other important prefrontal connections are made by the mesocortical dopamine projections from the ventral tegmental area of the midbrain. Unlike subcortical dopamine projections, these neurons lack autoreceptors. (8) Further links from the frontal cortex are to the hypothalamus (the orbital frontal cortex alone in the neocortex projects to the hypothalamus), the hippocampus, and the retrosplenial and entorhinal cortices. It should further be noted that the prefrontal cortex sends projections to, but does not receive projections from, the striatum, notably the caudate nucleus, globus pallidus, putamen, and substantia nigra. A final point is that the area of the prefrontal cortex that receives the dominant dorsomedial thalamic nucleus overlaps with that from the dopaminergic ventral tegmental area.

From the neuropsychiatric point of view, therefore, the most relevant anatomic connections would appear to be frontothalamic, frontostriatal, frontolimbic, and frontocortical, the last deriving from the extensive reciprocal connections of the frontal lobes with sensory association areas, most notably the inferior parietal lobule and the anterior temporal cortex.


One of the specific behavior deficits following frontal lobe damage is attention disorder, patients showing distractibility and poor attention. They present with poor memory, sometimes referred to as “forgetting to remember.” The thinking of patients with frontal lobe injury tends to be concrete, and they may show perseveration and stereotypy of their responses. The perseveration, with inability to switch from one line of thinking to another, leads to difficulties with arithmetic calculations, such as serial sevens or carryover subtraction.

An aphasia is sometimes seen, but this is different from both Wernicke’s and Broca’s aphasia. Luria (9) referred to it as dynamic aphasia. Patients have well-preserved motor speech and no anomia. Repetition is intact, but they show difficulty in propositionizing, and active speech is severely disturbed. Luria suggested that this was due to a disturbance in the predictive function of speech, that which takes part in structuring sentences. The syndrome is similar to that form of aphasia referred to as transcortical motor aphasia. Benson (10) also discusses the “verbal dysdecorum” of some frontal lobe patients. Their language lacks coherence, their discourse is socially inappropriate and disinhibited, and they may confabulate.

Other features of frontal lobe syndromes include reduced activity, particularly a diminution of spontaneous activity, lack of drive, inability to plan ahead, and lack of concern. Sometimes associated with this are bouts of restless, aimless uncoordinated behavior. Affect may be disturbed. with apathy, emotional blunting, and the patient showing an indifference to the world around him. Clinically, this picture can resemble a major affective disorder with psychomotor retardation, while the indifference bears occasional similarity to the “belle indifference” noted sometimes with hysteria.

In contrast, on other occasions, euphoria and disinhibition are described. The euphoria is not that of a manic condition, having an empty quality to it. The disinhibition can lead to marked abnormalities of behavior, sometimes associated with outbursts of irritability and aggression. So-called witzelsucht has been described, in which patients show an inappropriate facetiousness and a tendency to pun.

Some authors have distinguished between lesions of the lateral frontal cortex, most closely linked to the motor structures of the brain, which lead to disturbances of movement and action with perseveration and inertia, and lesions of the orbital and medial areas. The latter are interlinked with limbic and reticular systems, damage to which leads to disinhibition and changes of affect. The terms “pseudodepressed” and “pseudopsychopathic” have been used to describe these two syndromes.” A third syndrome, the medial frontal syndrome, is also noted, marked by akinesia, associated with mutism, gait disturbances, and incontinence. The features of these differing clinical pictures have been listed by Cummings, (12) as shown in Table I. In reality, clinically, most patients display a mixture of syndromes.


Table 1. Clinical Characteristics of the Three Principal Frontal Lobe Syndromes

Orbitofrontal syndrome (disinhibited)
Disinhibited, impulsive behavior (pseudopsychopathic)
Inappropriate jocular affect, euphoria
Emotional lability
Poor judgment and insight
Frontal convexity syndrome (apathetic)
Apathy (occasional brief angry or aggressive outbursts common)
Psychomotor retardation
Motor perseveration and impersistence
Loss of self
Stimulus-bound behavior
Discrepant motor and verbal behavior
Motor programming deficits
* Three-step hand sequence
* Alternating programs
* Reciprocal programs
* Rhythm tapping
* Multiple loops

Poor word list generation
Poor abstraction and categorization
Segmented approach to visuospatial analysis
Medial frontal syndrome (akinetic)
Paucity of spontaneous movement and gesture
Sparse verbal output (repetition may be preserved)
Lower extremity weakness and loss of sensation


In some patients, paroxysmal behavior disorders are recorded. These tend to be short-lived, and may include episodes of confusion and, occasionally, hallucinations. They are thought to reflect transient disturbances of the frontolimbic connections. Following massive frontal lobe lesions, the so-called apathetico-akinetico-abulic syndrome may occur. Patients lie around, passive, unaroused, and unable to complete tasks or obey commands.

Further clinical signs associated with frontal lobe damage include sensory inattention in the contralateral sensory field, abnormalities of visual searching, echo phenomena, such as echolalia and echopraxia, confabulation, hyperphagia, and various changes of cognitive function. Lhermitte (13,14) has described utilization behavior and imitation behavior, variants of environmental dependency syndromes. These syndromes are elicited by offering patients objects of everyday use and observing that, without instruction, they will use them appropriately, but often out of context (for example, putting on a second pair of spectacles when one pair is already in place). They will also, without instruction, imitate an examiner’s gestures, no matter how ridiculous.


The importance of making an accurate seizure diagnosis in patients with epilepsy has been accelerated in recent years by the use of advanced monitoring techniques such as videotelemetry. The more recent classification schemes of the International League Against Epilepsy recognize a major distinction between partial and generalized seizures (20) and between localization-related and generalized epilepsies. (21) In the latest classification (22) the localization-related epilepsies include frontal lobe epilepsies, in several different patterns. The general characteristics of these are shown in Table 2 and their subcategories in Table 3.


Table 2. International Classification of Epilepsies and Epileptic Syndromes

1. Localization-related (focal, local, partial) epilepsies and syndromes.
* 1.1 Idiopathic (with age-related onset)
* 1.2 Symptomatic
* 1.3 Cryptogenic
2. Generalized epilepsies and syndromes
* 2.1 Idiopathic (with age-related onset–listed in order of age)
* 2.2 Cryptogenic or symptomatic (in order of age)
* 2.3 Symptomatic
3. Epilepsies and syndromes undetermined as to whether they are focal or generalized.


Table 3. Localization-Related (Focal, Local, Partial) Epilepsies and Syndromes

1.2 Symptomatic
* Chronic progressive epilepsia partialis continua of childhood (Kojewnikow’s syndrome)

* Syndromes characterized by seizures with specific modes of precipitation

* Temporal lobe

* Frontal lobe
o Supplementary motor seizures
o Cingulate
o Anterior frontopolar region
o Orbitofrontal
o Dorsolateral
o Opercular
o Motor cortex

* Parietal lobe

* Occipital lobe


They may be anatomically categorized, for example, into seizures arising from the rolandic area, the supplementary motor area (SMA). from polar areas (Brodmann areas 10, 11, 12, and 47), the dorsolateral area, the opercular area, the orbital region, and the cingulate gyrus. Rolandic seizures are typical jacksonian simple partial attacks, while SMA-derived attacks often lead to adversion with posturing and autonomic changes. Characteristic features of complex partial seizures arising from frontal areas include frequent clustering of brief seizures, with sudden onset and cessation. Often, the accompanying motor behavior may be bizarre; and, since the surface electroencephalogram (EEG) may be normal, these attacks may readily be diagnosed as hysterical pseudoseizures.


That neurologic abnormalities underlie the clinical condition schizophrenia is now secure knowledge (see Hyde and Weinberger in this issue of Seminars). However, the precise pathologic lesions and the localization of the abnormalities continue to arouse interest and controversy. Much recent work has highlighted abnormalities of frontal lobe function in this condition. Several authors have drawn attention to the likeness of some schizophrenic symptoms to frontal lobe disorder, in particular that involving dorsolateral prefrontal cortex. Symptoms included are those of the affective changes, impaired motivation, poor insight. and other “defect symptoms.” Evidence for frontal lobe dysfunction in schizophrenic patients has been noted in neuropathologic studies, (23) in EEG studies, (24) in radiologic studies using CT measures, (25) with MRI, (26) and in cerebral blood flow (CBF) studies. (27) The last have been replicated by findings of hypofrontality in several studies using positron emission tomography (PET). (28) These findings emphasize the importance of neurologic and neuropsychologic investigation of patients with schizophrenia, using methods that may uncover underlying frontal lobe disturbances, and the important role that frontal lobe dysfunction may play in the development of schizophrenic symptoms. (23)


The dementias are assuming increasing importance in psychiatric practice, and progress has been made with regard to classifying them and to discovering their underlying neuropathologic and neurochemical basis. While many forms of dementia involve frontal lobe changes, it is now clear that several types of dementia more selectively affect frontal lobe function, particularly early in the disease. The paradigm of frontal lobe dementia is that described by Pick in 1892, which was associated with circumscribed atrophy of both the frontal and temporal lobes. This form of dementia is much less common than Alzheimer’s disease. It is more frequent in females. It may be inherited through a single autosomal dominant gene, although most cases are sporadic.

There are distinguishing features that reflect the underlying pathologic changes of Pick’s disease and separate it from Alzheimer’s disease. In particular, abnormalities of behavior, emotional changes, and aphasia are frequent presenting features. Some authors have noted elements of the Kluver-Bucy syndrome at one stage or another in the disease. (29) Interpersonal relationships deteriorate, insight is lost early, and the jocularity of frontal lobe damage may even suggest a manic picture. The aphasia is reflected in word-finding difficulties, empty, flat, nonfluent speech, and aphasia. With progression, the cognitive changes become apparent: these include memory disturbance but also impairment on frontal lobe tasks (see later). Ultimately, extrapyramidal signs, incontinence, and widespread cognitive decline are seen.

The EEG tends to remain normal in this disease, although CT or MRI will provide confirmatory evidence of lobar atrophy. The PET picture confirms diminished metabolism in frontal and temporal areas. Pathologically, the brunt of the changes is borne by these areas of the brain and mainly consists of neuron loss with gliosis. The characteristic change is the “balloon cell” which contains disordered neurofilaments and neurotubules, and Pick bodies, which are silver-staining and are also composed of neurofilaments and tubules.

Recently, Neary and colleagues (30) have drawn attention to a group of patients with non-Alzheimer’s dementia who typically present with changes of personality and social conduct and with atypical Pick’s changes in the brain. They note that this form of dementia may be more common than previously thought.

Another form of dementia that primarily affects frontal lobe function is that of normal pressure hydrocephalus. This may be related to several underlying causes, including cerebral trauma, previous meningitis, neoplasia, or subarachnoid hemorrhage, or it may occur idiopathically. Essentially, there is a communicating hydrocephalus with failure of absorption of cerebrospinal fluid (CSF) via the sagittal sinus through blockage, the CSF being unable to reach the convexity of the brain or be absorbed through the arachnoid villi. The characteristic clinical features of normal pressure hydrocephalus include gait disturbance and incontinence, with normal CSF pressure. The dementia is of recent onset and has characteristics of a subcortical dementia with psychomotor slowing and dilapidation of cognitive performance, in contrast to more discrete memory abnormalities that may herald the onset of Alzheimer’s disease. Patients lose initiative and become apathetic; in some cases the presentation may resemble an affective disorder. In reality the clinical picture can be varied, but frontal lobe signs are a common feature and, especially when combined with incontinence and ataxia, should alert the physician to the possibility of this diagnosis.

Other causes of dementia that may present with an apparently focalized frontal picture include tumors, especially meningiomas, and rare conditions such as Kufs’ disease and corticobasal degeneration.


Detection of frontal lobe damage can be difficult, especially if only traditional methods of neurologic testing are carried out. Indeed, this point cannot be overemphasized, since it reflects one of the main differences between traditional neurologic syndromes, which affect only elements of a person’s behavior – for example, paralysis following destruction of the contralateral motor cortex -and limbic system disorders generally. In the latter it is the whole of the patient’s motoric and psychic life that is influenced, and the behavior disturbance itself reflects the pathologic state. Often, changes can be discerned only with reference to the previous personality and behavior of that patient, and not with regard to standardized and validated behavioral norms based on population studies. A further complication is that these abnormal behaviors may fluctuate from one testing occasion to another. Therefore the standard neurologic examination will often be normal, as may the results of psychological tests such as the Wechsler Adult Intelligence Scale. Special techniques are required to examine frontal lobe function, and care finding out how the patient now behaves and how this compares with his premorbid performance.

Orbitofrontal lesions may be associated with anosmia, and the more the lesions extend posteriorly, the more neurologic signs such as aphasia (with dominant lesions), paralysis, grasp reflexes, and oculomotor abnormalities become apparent. Of the various tasks that can be used clinically to detect frontal pathologic conditions, those given in Table 4 are of value. However, not all patients with frontal damage show abnormalities on testing, and not all tests are found to be abnormal in frontal lobe pathologic states exclusively.

Table 4. Some Useful Tests at Frontal Lobe Function

Word fluency
Abstract thinking (if I have 18 books and two bookshelves, and I want twice as many books on one shelf as the other. how many books on each shelf?)
Proverb and metaphor interpretation
Wisconsin Card Sorting Test
Other sorting tasks
Block design
Maze lest
Hand position test (three-step hand sequence)
Copying tasks (multiple loops)
Rhythm tapping tasks

Cognitive tasks include the word fluency test, in which a patient is asked to generate, in 1 minute, as many words as possible beginning with a given letter. (The normal is around 15.)
Proverb or metaphor interpretation can be remarkably concrete.
Problem-solving, for example carry-over additions and subtractions, can be tested by a simple question (see Table 4). Patients with frontal lobe abnormalities often find serial sevens difficult to perform.

Laboratory-based tests of abstract reasoning include the Wisconsin Card Sort Test (WCST) and other object-sorting tasks. The subject must arrange a variety of objects into groups depending on one common abstract property, for example color. In the WCST, the patient is given a pack of cards with symbols on them that differ in form, color, and number. Four stimulus cards are available, and the patient has to place each response card in front of one of the four stimulus cards. The tester tells the patient if he is right or wrong, and the patient has to use that information to place the next card in front of the next stimulus card. The sorting is done arbitrarily into color, form, or number, and the patient’s task is to shift the set from one type of stimulus response to another based on the information provided. Frontal patients cannot overcome previously established responses, and show a high frequency of preseverative errors. These deficits are more likely with lateral lesions of the dominant hemisphere.

Patients with frontal lobe lesions also do badly on maze learning tasks, the Stroop test, and block design; they show perseveration of motor tasks and difficulty carrying out sequences of motor actions. Skilled movements are no longer performed smoothly, and previously automated actions such as writing or playing a musical instrument are often impaired. Performance on tests such as following a succession of hand positions (with the hand first placed flat, then on one side, and then as a fist, on a flat surface) or tapping a complex rhythm (for example two loud and three soft beats) is impaired. Following nondominant hemisphere lesions, singing is poor, as is recognition of melody and emotional tone, the patient being aprosodic. Perseveration (especially prominent with deeper lesions in which the modulating function of the premotor cortex on the motor structures of the basal ganglia is lost (9)) may be tested by asking the patient to draw, for example, a circle or to copy a complex diagram with recurring shapes in it that alternate one with another. The patient may continue to draw circle after circle, not stopping after one revolution, or miss the pattern of recurring shapes (Fig. 2). Imitation and utilization behavior can also be tested for.

In many of these tests there is a clear discrepancy between the patient’s knowing what to do and being able to verbalize the instructions, and his failure to undertake the motor tasks. In everyday life this can be extremely deceptive and lead the unwary observer to consider the patient to be either unhelpful and obstructive or (for example, in a medicolegal setting) to be a malingerer.

Some of these tasks, for example the word-fluency task, or inability to make melodic patterns, are more likely to be related to lateralized dysfunction, and the inhibition of motoric tasks relates to the dorsolateral syndrome.


Several authors have put forward explanations for frontal lobe syndromes. (6,9) The posterolateral areas of the frontal cortex are most closely linked to motor structures of the anterior part of the brain, thus leading to the motor inertias and the perseverations seen with lesions here. They are more pronounced after dominant hemisphere lesions, when the speech-related disorders become manifest. More posterior lesions appear to link with difficulties in organizing movement; anterior lesions result in difficulties in motor planning and a dissociation between behavior and language. Elementary motor perseverations probably require lesions that are deep enough to involve the basal ganglia. Disturbances of attention are related to the brainstem-thalamic-frontal system, and the basal (orbital) syndromes are due to disruption of frontal-limbic links. Loss of inhibitory function over the parietal lobes, with release of their activity, increases the subject’s dependence on external visual and tactile information, leading to echo phenomena and the environmental dependency syndrome.

Teuber (31) suggested that the frontal lobes “anticipate” sensory stimuli that result from behavior, thus preparing the brain for events about to occur. The expected results are compared with actual experience, and thus smooth regulation of activity results. More recently, Fuster (5) has proposed that the prefrontal cortex plays a role in the temporal structuring of behavior, synthesizing cognitive and motor acts into purposeful sequences. Stuss and Benson (6) put forward a hierarchical concept for the regulation of behavior by the frontal lobes. They referred to fixed functional systems, including a number of recognized neural activities, such as memory, language, emotion, and attention. which are modulated by “posterior” areas of the brain in contrast to the frontal cortex. Two anterior counterparts are proposed, namely, the ability of the frontal cortex to sequence, change set, and integrate information, and to modulate drive, motivation, and will (the former are most strongly dependent on intact lateral, dorsal and orbital frontal convexity regions; the latter are related more to medial frontal structures). A further independent level is that of executive function of the human frontal lobes (anticipation, goal selection, preplanning, monitoring), which is superordinate to drive and sequencing, but may be subordinate to the role of the prefrontal cortex in self-awareness.


In this review, some basic aspects of frontal lobe functioning have been discussed and methods of testing for frontal lobe abnormalities outlined. It has been emphasized that the frontal lobes are affected in a number of diseases, which cover a broad spectrum of neuropsychiatric problems. Furthermore, it is suggested that the frontal lobes are involved in syndromes not traditionally thought to be related to frontal lobe dysfunction, for example, schizophrenia, and rarer presentations such as misidentification syndromes, Frontal lobe dysfunction often goes unrecognized, especially in patients who have normal neurologic testing and apparently intact IQ when routine methods of investigation are employed. Although marked disturbances of behavior following frontal lobe dysfunction have now been described for well over 120 years, these large areas of the human brain, and their links with some of the highest attributes of mankind, have been relatively neglected and are worthy of much further exploration by those interested in neuropsychiatric problems.


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Report prepared for the National Head Injury Foundation
September 1991

by Linda Andre

Committee for Truth in Psychiatry


Electroshock, variously known as electroconvulsive therapy, ECT, shock treatment, or simply shock, is the practice of applying 70 to 150 volts of household electric current to the human brain in order to produce a grand mal, or generalized, seizure. A course of ECT usually consists of 8 to 15 shocks, administered every other day, although the number is determined by the individual psychiatrist and many patients receive 20, 30, 40 or more.

Psychiatrists use ECT on persons with a wide range of psychiatric labels, from depression to mania, and have recently begun to use it on persons without psychiatric labels who have medical diseases such as Parkinson’s disease.

A conservative estimate is that at least 100,000 persons receive ECT each year, and by all accounts this number is growing. Two-thirds of those being shocked are women, and more than half of ECT patients are over the age of 65, although it has been given to children as young as three. ECT is not given at all in most state hospitals. It is concentrated in private, for-profit hospitals.

ECT drastically changes behavior and mood, which is construed
as improvement of psychiatric symptoms. However, since psychiatric symptoms usually recur, often after as little as one month, psychiatrists are now promoting “maintenance” ECT—one electrical grand mal seizure every few weeks, given indefinitely or until the patient or family refuses to continue.


There are now five decades of evidence for ECT brain damage and memory loss. The evidence is of four types: animal studies, human autopsy studies, human in vivo studies which use either modern brain-imaging techniques or neuropsychological testing to assess damage, and survivor self-reports or narrative interviews.

Most of the studies of the effects of ECT on animals were done in the 1940s and ’50s. There are at least seven studies documenting brain damage in shocked animals (cited by Friedberg in Morgan, 1991, p. 29). The best known study is that of Hans Hartelius (1952), in which brain damage was consistently found in cats given a relatively short course of ECT. He 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.”

Human autopsy studies were done on persons who died during or shortly after ECT (some died as a result of massive brain damage). There are more than twenty reports of neuropathology in human autopsies, dating from to 1940s to 1978 (Morgan, 1991, p. 30; Breggin, 1985, p.4). Many of these patients had what is called modern or “modified” ECT.

It is necessary to clarify briefly here what is meant by “modified” ECT. News and magazine articles about ECT commonly claim that ECT as it has been given for the past thirty years (that is, using general anesthesia and muscle-paralyzing drugs to prevent bone fractures) is “new and improved”, “safer” (i.e. less brain-damaging) than it was in the 1940s and ’50s.

Although this claim is made for public relations purposes, it is flatly denied by doctors when the media is not listening. For example, Dr. Edward Coffey, head of the ECT department at Duke University Medical Center and a well-known advocate of ECT, tells his students in the training seminar “Practical Advances in ECT: 1991″:

The indication for anesthetic is simply that it reduces the anxiety and the fear and the panic that are associated or that could be associated with the treatment. OK? It doesn’t do anything else beyond that…There are, however, significant disadvantages in
using an anesthetic during ECT…The anesthetic elevates seizure threshold… Very, very critical…

So it is necessary to use more electricity to the brain, not less, with “modified” ECT, hardly making for a safer procedure. In addition, the muscle-paralyzing drugs used in modified ECT amplify the risks. They make the patient unable to breathe independently, and as Coffey points out this means risks of paralysis and prolonged apnea.

Another common claim of shock doctors and publicists, that ECT “saves lives” or somehow prevents suicide, can be quickly disposed of. There is simply no evidence in the literature to support this claim. The one study on ECT and suicide (Avery and Winokur, 1976) shows that ECT has no effect on the suicide rate.

Case studies, neuroanatomical testing, neuropsychological testing, and self-reports that remain strikingly similar over 50 years testify to the devastating effects of ECT on memory, identity, and cognition.

Recent CAT scan studies showing a relationship between ECT and brain atrophy or abnormality include Calloway (1981); Weinberger et al (1979a and 1979b); and Dolan, Calloway et al (1986).

The vast majority of ECT research has focused and continues to focus on the effects of ECT on memory, for good reason. Memory loss is a symptom of brain damage and, as neurologist John Friedberg (quoted in Bielski, 1990) points out, ECT causes more permanent memory loss than any severe closed-head injury with coma or almost any other insult to or disease of the brain.

Reports of catastrophic memory loss date to the very beginning of ECT. The definitive study of ECT’s memory effects remains that of Irving Janis (1950). Janis conducted detailed and exhaustive autobiographical interviews with 19 patients before ECT and then attempted to elicit the same information four weeks afterwards. Controls who did not have ECT were given the same interviews. He found that “Every one of the 19 patients in the study showed at least several life instances of amnesia and in many cases there were from ten to twenty life experiences which the patient could not recall.” Controls’ memories were normal. And when he followed up half of the 19 patients one year after ECT, there had been no return of memory (Janis, 1975).

Studies in the 70s and 80s confirm Janis’ findings. Squire (1974) found that the amnesic effects of ECT can extend to remote memory. In 1973 he documented a 30-year retrograde amnesia following ECT. Freeman and Kendell (1980) report that 74% of patients questioned years after ECT had memory impairment. Taylor et al (1982) found methodological flaws in studies that purport to show no memory loss and documented deficits in autobiographical memory several months after ECT. Fronin-Auch (1982) found impairment of both verbal and nonverbal memory. Squire and Slater (1983) found that three years after shock the majority of survivors report poor memory.

The highest governmental authority on medical matters in the United States, the Food and Drug Administration (FDA), agrees that ECT is not good for your health. It names brain damage and memory loss as two of the risks of ECT. The FDA is responsible for regulating medical devices such as the machines used to administer ECT. Each device is assigned a risk classification: Class I for devices that are basically safe; Class II for devices whose safety can be assured by standardization, labeling, etc.; and Class III for devices which pose “a potential unreasonable risk of injury or illness under all circumstances. As a result of a public hearing in 1979, at which survivors and professionals testified, the ECT machine was assigned to Class III. There it remains today, despite a well-organized lobbying campaign by the American Psychiatric Association. In the files of the FDA in Rockville, Maryland, are at least 1000 letters from survivors testifying to the damage that was done to them by ECT. In 1984 some of these survivors organized as the Committee for Truth in Psychiatry to lobby for informed consent as a way of protecting future patients from permanent brain damage. Their statements challenge the assumption that survivors “recover” from ECT:

Most of my life from 1975-1987 is a fog. I remember some things when reminded by friends, but other reminders remain a mystery. My best friend since high school in the 1960s died recently and with her went a big part of my life because she knew all about me and used to help me out with the parts I couldn’t remember. (Frend, 1990)

I haven’t had a shock for over ten years now but I still feel
sad that I can’t remember most of my late childhood or any of my high school days. I can’t even remember my first intimate experience. What I know of my life is second hand. My family has told me bits and pieces and I have my high school yearbooks. But my family generally remembers the “bad” times, usually how I screwed up the family life and the faces in the yearbook are all total strangers. (Calvert, 1990)

As a result of these “treatments” the years 1966-1969 are almost a total blank in my mind. In addition, the five years preceding 1966 are severely fragmented and blurred. My entire college education
has been wiped out. I have no recollection of ever being at the University of Hartford. I know that I graduated from the institution because of a diploma I have which bears my name, but I do
not remember receiving it. It has been ten years since I received electroshock and my memory is still as blank as it was the day I left the hospital. There is nothing temporary about the nature of memory loss due to electroshock. It is permanent, devastating, and irreparable. (Patel, 1978)


Both psychiatrist Peter Breggin (Breggin,, 1991, p. 196) and
ECT survivor Marilyn Rice, founder of the Committee for Truth in Psychiatry, have pointed out that minor head injury as a result of trauma often occurs without loss of consciousness, seizures, disorientation, or confusion, and is thus much less traumatic than a series of electroshocks. A better analogy would be that each individual shock is the equivalent of one moderate to severe head injury. The typical ECT patient, then, receives at least ten head injuries in rapid succession.

Proponents as well as opponents of ECT have long recognized it as a form of head injury.

As a neurologist and electroencephalographer, I have seen many patients after ECT, and I have no doubt that ECT produces effects identical to those of a head injury. After multiple sessions of ECT, a patient has symptoms identical :o those of a retired, punch-drunk boxer.. .After a few sessions of ECT, the symptoms are those of moderate cerebral contusion, and further enthusiastic use of ECT may result in the patient functioning at a subhuman level. Electroconvulsive therapy in effect may be defined as a controlled type of brain damage produced by electrical means. (Sament, 1983)

What shock does is throw a blanket over people’s problems. It would be no different than if you were troubled about something in your life and you got into a car accident and had a concussion. For a while you wouldn’t worry about what was bothering you because you would be so disoriented. That’s exactly what shock therapy does. But in a few weeks when the shock wears off, your problems come back. (Coleman, quoted in Bielski, 1990)

We don’t have a treatment. What we do is inflict a closed-head injury on people in spiritual crisis.. .closed-head injury! And we have a vast literature on closed-head injury. My colleagues are not eager to have literature on electroshock closed-head injury; but we have it in every other field. And we have considerably more than people are allowing for here today. It is electrical closed-head injury. (Breggin, 1990)

There has never been any debate about the immediate effects of a shock: it produces an acute organic brain syndrome which becomes more pronounced as shocks continue. Harold Sackeim, the ECT establishment’s premier publicist (anyone who has occasion to write about or refer to ECT, from Ann Landers to a medical columnist, is referred by the APA to Dr. Sackeim) states succinctly:

The ECT-induced seizure, like spontaneous generalized seizures in epileptics and most acute brain injury and head trauma, results in
a variable period of disorientation. Patients may not know their names, their ages, etc. When the disorientation is prolonged, it is generally referred to as an organic brain syndrome. (Sackeim, 1986)

This is so expected and routine on ECT wards that hospital staff become inured to making chart notations like “Marked organicity” or “Pt. extremely organic” without thinking anything of it. A nurse who has worked for years on an ECT ward says:

Some people seem to undergo drastic personality changes.
They come in the hospital as organized, thoughtful people who
have a good sense of what their problems are. Weeks later I see
them wandering around the halls, disorganized and dependent. They
become so scrambled they can’t even have a conversation. Then
they leave the hospital in worse shape than they came in.
(Anonymous psychiatric nurse, quoted in Bielski, 1990)

A standard information sheet for ECT patients calls the period
of most acute organic brain syndrome a “convalescence period” and warns patients not to drive, work, or drink for three weeks (New York Hospital-Cornell Medical Center, undated). Coincidentally, four weeks is the maximum time period for which proponents of ECT can claim alleviation of psychiatric symptoms (Opton, 1985), substantiating the statement made by Breggin (1991, pp. 198-99) and throughout the ECT literature that the organic brain syndrome and the “therapeutic” effect are the same phenomenon.

The information sheet states as well that after each shock the patient “may experience transitory confusion similar to that seen in patients emerging from any type of brief anesthesia.” This misleading characterization is belied by two doctors’ published observations of patients after ECT.(Lowenbach and Stainbrook, 1942). The article begins by stating “A generalized convulsion leaves a human being in a state where all that is called the personality has been extinguished.”

A compliance with simple commands like opening and closing the eyes and the appearance of speech usually coincide. The first utterances are usually incomprehensible, but soon it is possible to recognize first the words and then sentences, although they may have to be guessed at rather than directly understood…

If at this time patients were given a written order to write their name, they would not ordinarily follow the command…if then the request was repeated orally, the patient would take the pencil and write his name. At first the patient produces only scribbling and has to be constantly urged to continue. He may even drop back into sleep. But soon the initial of the first name may be clearly discernible…Usually 20 to 30 minutes after a full-fledged convulsion the writing of the name was again normal…

The return of the talking function goes hand in hand with the writing ability and follows similar lines. The muttered and seemingly senseless words and maybe the silent tongue movements are the equivalent of scribbling.. .But as time goes on it “is possible to establish question and answer sessions.. .From now on, the perplexity of the patient arising from his inability to grasp the situation pervades his statements.

He may ask if this is a jail. ..and if he has committed a crime.. The efforts of the patient to re-establish their orientation almost always follow the same line: “Where am I.”… know you” (pointing to the nurse)… to the question “What is my name?” “I do not know”…

The patient’s behavior when asked to perform a task such as to get up from the bed where he lies demonstrates another aspect of the process of recovery.. .he does not act according to voiced intentions. Sometimes urgent repetition of the command would set off the proper movements; in other cases beckoning had to be initiated by pulling the patient from the sitting position or removing one leg from the bed.. .But the patient then frequently stopped doing things and the next series of actions, putting on his shoes, tying the laces, leaving the room, had each time to be expressly commanded, pointed out, or the situation had to be actively forced. This behavior indicates lack of initiative…

It is possible, indeed likely, that a patient and her family could read the entire information sheet mentioned earlier and have
no idea that ECT involves convulsions. The words “convulsion” or “seizure” appear not at all. The sheet states that the patient will have “generalized muscular contractions of a convulsive nature”.

Recently Dr. Max Fink, the country’s best-known shock doctor, offered to let the media interview a patient right after a course of electroshock… for a fee of $40,000 (Breggin, 1991, p. 188).

It is common for persons who have received ECT to report being “in a fog”, without any of the judgment, affect, or initiative of their former selves, for a period of up to one year post-ECT. Afterwards they may have little or no memory of what happened during this period.

I experienced the explosion in my brain. When I woke up from the blessed unconsciousness I did not know who I was, where I was, nor why. I could not process language. I pretended everything because I was afraid. I did not know what a husband was. I did not know anything. My mind was a vacuum. (Faeder, 1986)

I just completed a series of 11 treatments and am in worse shape than when I started. After about 8 treatments I thought I had improved from my depression.. . I continued and my effects worsened. I began experiencing dizziness and my memory loss increased. Now that I had the 11th my memory and thinking abilities are so bad I wake up in the morning empty-headed. I don’t remember many past events in
my life or doing things with the various people in my family. It is hard to think and I don’t enjoy things. I can’t think about anything else. I can’t understand why everyone told me this procedure was so safe. I want my brain back. (Johnson, 1990)


The loss of one’s life history–that is, loss of part of the self–is in itself a devastating handicap; but added to this unique quality of ECT head injury are the cognitive deficits associated with other types of traumatic brain injury.

There is not now nearly enough research on the nature of ECT cognitive deficits, or of the impact of these deficits on social roles, employment, self-esteem, identity, and long-term quality of life for survivors. There is only one study which examines how ECT (negatively) affects family dynamics (Warren, 1988). Warren found that ECT survivors “commonly” forgot the very existence of their husbands and children! For example, one woman who had forgotten she had five children was furious when she found out her husband had lied to her, telling her the children belonged to a neighbor. Husbands frequently used their wives’ amnesia as an opportunity to reconstruct marital and family history, to the husbands’ advantage. Clearly, Warren’s study suggests there is much to explore in this area.

There is currently no research which addresses the question of how best to meet the rehabilitative and vocational needs of ECT survivors. One such study, proposed but not implemented in the 1960s, is described in Morgan (1991, pp. 14-19). Its hopeful conclusion that “with enough data, it may some day be possible to deal therapeutically with ECT-damaged patients, perhaps with some radically new approach to psychotherapy, or direct re-education or modification of behavior” has, a generation later, not come to pass. Funding sources such as the National Institute on Disability and Rehabilitation Research must be encouraged to sponsor such research.

The research which exists shows that sensitive psychometric testing always reveals cognitive deficits in ECT survivors. Even given the differences in available testing methods, the nature of these deficits has remained stable over 50 years. Scherer (1951) gave tests of memory function, abstraction, and concept formation to a group of survivors who had received an average of 20 shocks (using brief-pulse or square wave current, the type that is standard today) and to a control group of patients who did not receive ECT. He found that “lack of improvement as between pre- and post-shock results may indicate that shock has injured the patient to the extent that he is unable to achieve his premorbid intellectual potentialities, even though he can shake off the intellectually debilitating effects of the psychosis.” He concluded that “harmful organic results in areas of intellectual function.. .may nullify the partial benefits of the treatment.”

Templer, Ruff and Armstrong (1973) found that performance on
the Bender Gestalt test was significantly worse for persons who had received ECT than for carefully matched controls who had not.

Freeman, Weeks and Kendell (1980) matched a group of 26 ECT survivors with controls on a battery of 19 cognitive tests; all of the survivors were found to be significantly cognitively impaired. The researchers attempted to attribute the impairment to drugs or mental illness, but could not do so. They concluded that “our results are compatible” with the statement that ECT causes permanent mental impairment. The interviews with survivors revealed almost identical deficits:

Forgetful of names, gets easily sidetracked and forgets what he was going to do.

Forgets where she puts things, can’t remember names.

Memory poor and gets confused, to such an extent that he loses jobs.

Difficult to remember messages. Gets mixed up when people tell her things.

Said she was known in her bridge club as the “computer because of her good memory. Now has to write things down, and misplaces keys and jewelry.

Can’t retain things, has to make lists.

Templer and Veleber (1982) found permanent irreversible cognitive deficits in ECT survivors given neuropsychological testing. Taylor, Kuhlengel and Dean (1985) found significant cognitive impairment after only five shocks. “Since cognitive impairment is such an important side effect of bilateral ECT, it seems important to define as carefully as possible which aspects of the treatment are responsible for the deficit,” they concluded. Although they did not prove their hypothesis about the role of an elevation in blood pressure, “It is important to continue to search for the cause or causes of this impairment. If this important side effect could be eliminated or even modified, it could only be a service to patients…” But there is no separating the so-called therapeutic effects from the disabling cognitive effects.

A study-in-progress designed and implemented by members of the National Head Injury Foundation (SUNY Stony Brook, unpublished thesis project) with the same size sample as the Freeman et al study uses a simple self-scoring questionnaire to evaluate cognitive deficits in both the acute and chronic organic brain syndrome stages. The study also elicits information about coping strategies (self-rehabilitation) and about the amount of time it takes to accommodate to deficits.

All respondents in the study indicated they suffered from common symptoms of head injury both during the year after ECT and many,
many years afterwards. The average number of years since ECT for
the respondents was twenty-three. 80% had never heard of cognitive rehabilitation.

Only one-fourth felt they had been able to adjust to or compensate for their deficits by their own efforts. Most indicated they were still struggling with this process. Of those few who felt they had adjusted or compensated, the average number of years to reach this stage was fifteen. When those who had adjusted or compensated were asked how they did it, the most frequently cited answer was “hard work on my own.”

Respondents were asked if they would have liked acknowledgment of or help with their cognitive problems during the year after ECT, and whether they would still like help regardless of how long ago they had been shocked. All but one of the respondents said they would have wanted help in the post-ECT year, and 90% said they still wanted help.

In the last several years with the increased availability of neuropsychological testing, increasing numbers of ECT survivors have taken the initiative where researchers have failed, and have had testing done. In every known case, testing has shown unmistakable brain dysfunction.

Patients’ accounts of cognitive deficits from diverse sources
and across continents remain constant from the 1940s to the 1990s. If these people are imagining their deficits, as some shock doctors like to claim, it is unthinkable that patients over five decades should all imagine exactly the same deficits. One cannot read these accounts without calling to mind the description of minor head injury in the National Head Injury Foundation brochure “The Unseen Injury: Minor Head Trauma”:

Memory problems are common.. .You may be more forgetful of names, where you put things, appointments, etc. It may be harder to learn new information or routines. Your attention may be shorter, you may be easily distracted, or forget things or lose your place when you have to shift back and forth between two things. You may find it harder to concentrate for long periods of time, and become mentally confused, e.g. when reading. You may find it harder to find the right word or express exactly what you are thinking. You may think and respond more slowly, and it may take more effort to do the things you used to do automatically. You may not have the same insights or spontaneous ideas as you did before.. .You may find it more difficult to make plans, get organized, and set and carry out realistic goals…

I have trouble remembering what I did earlier this week. When I talk, my mind wanders. Sometimes I can’t remember the right word to say, or a co-worker’s name, or I forget what I wanted to say. I have been to movies that I can’t remember going to. (Frend, 1990)

I was an organized, methodical person. I knew where everything was. I’m different now. I often can’t find things. I’ve become very scattered and forgetful. (Bennett, quoted in Bielski, 1990)

These words eerily echo those of the ECT survivors described by Dr. M.B. Brody in 1944:

(18 months after 4 shocks) One day three things were missing, the poker, the paper, and something else I cannot remember. I found the poker in the dustbin; I must have put it there without remembering. We never found the paper and I am always very careful of the paper. I want to go and do things and find I have already done it. I have to think about what I am doing so that I know I have done it.. .it is uncanny when you do things and find you cannot remember them.

(One year after 7 shocks) The following are some of the things I forget: the names of people and places. When the title of a book is mentioned I may have a vague idea that I have read it, but cannot remember what it is about. The same applies to films. My family tells me the outlines and I am able to remember other things at the same time.

I forget to post letters and to buy small things, such as mending and toothpaste. I put things away in such safe places that when they are needed it takes hours to find them. It did seem that after the electric treatment there was only the present, and the past had to be recalled a little at a time.

All of Brody’s survivors had incidents of not recognizing familiar people:

(One year after 14 shocks) There are many faces I see that I
know I should know quite a lot about, but only in a few cases can I recall incidents connected with them. I find I can adjust myself to these circumstances by being very careful in making strong denials, as fresh personal incidents constantly crop up.

38 years later, a woman who had 7 shocks wrote:

I was shopping in a department store when a woman came over to me, said hello and asked me how I was. I had no idea who she was or how she knew me.. .1 couldn’t help feeling embarrassed and helpless, as if I were no longer in control of my faculties. This experience was to be the first of many encounters in which I would be unable to recall people’s names and the context in which I knew them. (Heim, 1986)

The deficits in storing and retrieving new information associated with ECT may severely and permanently impair learning ability. And, just as the NHIF brochure states, “Often these problems are not encountered until a person returns to the demands or work, school, or home.” Attempting to go or return to school especially overwhelms and commonly defeats ECT survivors:

When I returned to classes I found I couldn’t remember material I had learned earlier, and that I was totally unable to concentrate… My only choice was to withdraw from university. If there was one area in which I had always excelled, it was in school. I now felt like a complete failure and that I’d never be able to return to university. (Heim, 1986)

Some of the things I tried to study was like trying to read a book written in Russian—no matter how hard I tried I could not get the sense of what the words and diagrams meant. I forced myself to concentrate but it continued to appear gibberish. (Calvert, 1990)

In addition to destruction of entire blocks of pre-ECT memories I have continued to have considerable difficulty in memory with regard to academic pursuits. To date, of embarrassing necessity I have been forced to tape-record all education materials that require memorization. This has included basic classes in accounting and word-processing materials. I was forced to retake accounting in 1983. Now, I am again forced to retake a basic one-semester course in computerized word processing. Currently, I am finding it extremely embarrassing and hurtful when fellow classmates (however innocently) refer to my struggles in grasping my study materials, thusly: “You are an AIR-BRAIN!” How can I explain that my struggles are due to ECT? (Winter, 1988)

I started school full time and found I did much better than
I could imagine remembering information on field placement and classes—but I couldn’t understand what I read or put ideas together—analyze, draw conclusions, make comparisons. It was a shock. I was at last taking courses on theory.. .and ideas just didn’t remain with me. I finally accepted the fact that it was just going to be too much torture for me to continue so I quit my field placement, two courses, and attended only one discussion course until the end of the semester when I withdrew. (Maccabee, 1989)

It is often the case that the ECT survivor is disabled from
her or his previous work. Whether or not a survivor returns to work depends on the type of work previously done and the demands it makes on intellectual functioning. The statistics on employment of ECT survivors would seem to be just as dismal as statistics on employment of head-injured persons in general. In the SUNY survey, two-thirds of the respondents were unemployed. Most indicated that they had been employed prior to ECT and unemployed since. One elaborated:

At the age of 23 my life was changed because after ECT I experienced disabling difficulty understanding, recalling, organizing and applying new information and also problems with distractibility and concentration. I had ECT while I was teaching and because my level of functioning had changed so dramatically I quit my job. My abilities have never returned to pre-ECT quality. Pre-ECT I’d been able to function in a totally individualized sixth-grade classroom where I designed and wrote much of the curriculum myself. Due to the problems I had after ECT I never returned to teaching. (Maccabee, 1990)

A nurse writes of a friend at one year post-ECT:

A friend of mine had 12 ECT treatments in September-October 1989. As a result, he has retrograde and anterograde amnesia and is unable to perform his work as a master plumber, cannot remember his childhood and cannot remember how to get around the city where he has lived all his life. You can imagine his anger and frustration.

The psychiatrists have been insisting that his problem is not ECT-related but is a side effect of his depression. I have yet
to see a severely depressed person fight so hard to regain their ability to think clearly and be able to go back to work again. (Gordon, 1990)

She has stated clearly the impossible situation of ECT survivors. There can be no help for them until there is recognition of the traumatic brain injury they have sustained and its disabling effects.


ECT survivors have the same needs for understanding, support,
and rehabilitation as other head injury survivors. If anything, it could be said that their needs may be greater, since the massive retrograde amnesia unique to ECT can precipitate an even greater crisis of identity than occurs with other head injuries.

Neuropsychologist Thomas Kay, in his paper Minor Head Injury: An Introduction for Professionals, identifies four necessary elements in successful treatment of head injury: identification of the problem, family/social support, neuropsychological rehabilitation, and accommodation; Identification of the problem, he says, is the most crucial element since it must precede the others. Tragically at this time it is the rule rather than the exception that for ECT survivors none of these elements come into play.

This is not to say that ECT survivors never successfully build a new self and a new life. Many courageous and hardworking survivors have—but they have until now always had to do it alone, without any help, and it has taken a sizable chunk of their lifetimes to do it.

As time goes on, I have made a great effort to regain the maximum use of my brain by forcing it to concentrate and to try to remember what I hear and read. It has been a struggle… I feel like I have been able to maximize the undamaged parts of my brain.. .I still mourn the loss of a life that I didn’t have. (Calvert, 1990)

Survivors are beginning to share their hard-won strategies with other survivors, professionals who would help them would do well to listen to those whose daily business, even decades after ECT, is surviving.

I tried a course in general psychology, which I’d had As on in college. I quickly discovered that I couldn’t remember anything if I just read the text.. .even if I read it several times (like four or five). So I programmed my materials by writing out questions for each sentence and writing the answers on the back of the cards. I then quizzed myself until the material was memorized. I have all the cards from two courses. What a stack… I memorized the book, practically… and worked five to six hours a day on weekends and three or four during the work week… It was quite different from when I was in college. Then, I read things and remembered them. (Maccabee, 1989)

She also describes her own cognitive retraining exercise:

The main exercise consists primarily of counting from 1-10 while visualizing, as steadily as possible, some image (object, person, etc.) I thought of this exercise because I wanted to see if I could practice using the right and left sides of my brain. Since I began this I think I read that that isn’t what I was doing. But, it seemed to work. When I first started the exercise I could hardly hold an image in mind, much less count at the same time. But I have become quite good at it and I relate it to an improved ability to deal with distractions and interruptions.

Similar exercises, in fact, are practiced in formal cognitive rehabilitation programs.

Often self-rehabilitation is a desperate, trial-and-error process that takes many lonely, frustrating years. A woman describes how she taught herself to read again after ECT, at age 50:

I could process language only with difficulty. I knew the words, how they sounded, but I had no comprehension.

I did not literally start at “scratch”, as a preschooler, because I had some memory, some understanding of letters and sounds—words—but I had no comprehension.

I used TV for newscasts, the same item in the newspaper, and tried to match these together to make sense. Only one item, one line. Try to write it in a sentence. Over and over, again and again.

After about six months (this was daily for hours), I tried Reader’s Digest. It took me a very long time to conquer this–no pictures, new concepts, no voice telling me the news item. Extremely frustrating, hard, hard, hard. Then magazine articles. I did it! I went on to “For Whom the Bell Tolls” because I vaguely remembered I had read it in college and had seen the movie. But it had many difficult words and my vocabulary was not yet at the college level, so I probably spent two years on it. It was 1975 when I felt I had reached the college level in reading.(I started in 1970.) (Faeder, 1986)

One survivor for whom the slow process of rehabilitation has taken two decades expresses the hope of many others that the process might be made easier for those being shocked in the ’90s:

I might never have thought that rehabilitation was something that ECT patients could benefit from until I was examined in 1987, at my request, at a local psychogeriatric center because I worried that perhaps I had Alzheimer’s disease because my intellectual functioning still caused me problems. During the psychological testing, which extended over a period of two months due to scheduling problems, I observed that my concentration improved and I functioned better at work. I reasoned that the “time-encapsulated” efforts to concentrate and focus my attention carried over. The tests were not meant to be rehabilitative, but they somewhat served this purpose—and convinced me that sequential retraining or practicing of cognitive skills could be beneficial to ECT patients. Of course, this was almost 20 years after ECT…

I hold a responsible, though poorly paying, job as an administrative assistant for a professional organization—performing at tasks that I never thought I would be able to do again. I might have been able to do them earlier if I’d had rehabilitation training. At this time I am concerned about the plight of ECT patients who are still struggling. While these ECT “complainers” are at risk of becoming increasingly depressed—and perhaps suicidal—because
of their disabilities, professionals continue to argue about whether or not ECT causes brain damage using insufficient and in some cases outdated data.

I wish that some brain trauma research and rehabilitation
center would accept a few ECT patients and at least see if practicing or “reprogramming” of cognitive skills could result
in improved performance. (Maccabee, 1990)

In 1990, three ECT survivors were treated in the cognitive rehabilitation program of a New York City hospital. Slowly, attitudes and preconceived ideas are changing.


ECT has gone in and out of fashion during its 53-year history; now on the wane, now making a comeback. Whatever happens in this decade (ironically designated by President Bush the Decade of the Brain), ECT survivors cannot afford to wait until a favorable political climate allows them the help they need. They need it now.

There are some hopeful signs. The 1980s saw an unprecedented boom in ECT (medical malpractice) lawsuits citing brain damage and memory loss, to the point where settlements are steadily increasing for those with the stamina and resources to pursue legal redress. The ECT machine remains in Class III at the FDA. ECT survivors are joining head injury support groups and organizations in record numbers.

State legislatures are toughening ECT laws, and city councils
are taking courageous stands against ECT. On February 21, 1991, after well-publicized hearings at which survivors and professionals testified, the Board of supervisors of the City of San Francisco adopted a resolution opposing the use of ECT. A bill pending in the New York State Assembly (AB6455) would require the state to keep statistics on how much ECT is done, but its accompanying strongly worded memorandum opens the door for stricter measures in the future. In July 1991 the Madison, Wisconsin city council proposed a resolution to recommend a ban on the use of ECT. (Shock was banned in Berkeley, California in 1982 until the local psychiatrists’ organization overturned the ban on a technicality.) The council’s Public Health Committee unanimously agreed that accurate information about the effects of ECT on memory must be presented to patients, and they are writing a resolution to contain full and accurate information. And in August 1991 ECT survivors testified, and a manuscript containing accounts of memory loss by 100 survivors was presented, at hearings in Austin, Texas, before the Texas Department of Mental Health. Subsequently the Department’s regulations were revised to contain a stronger warning about permanent mental dysfunction.


It is difficult, even in so many pages, to paint a full picture of the suffering of ECT survivors and the devastation experienced not only by the survivors but by their families and friends. And so the last words, chosen because they echo the words of so many others over the years, belong to a former nurse estranged from her husband and living on Social Security Disability, fighting in the legal system for redress and working with an advocacy group.

What they took from me was my “self”. When they can put a dollar value on theft of self and theft of a mother I would like
to know what the figure is. Had they just killed me instantly the kids would at least have had the memory of their mother as she
had been most of their lives. I feel it has been more cruel, to
my children as well as myself, to allow what they have left to breathe, walk, and talk.. .now the memory my kids will have is of this “someone else” who looks (but not really) like their mother. I haven’t been able to live with this “someone else” and the life I’ve lived for the past two years has not been a life by any stretch of the imagination. It has been a hell in the truest sense of the word.

I want my words said, even if they fall on deaf ears. It’s not likely, but perhaps when they are said, someone may hear them and at least try to prevent this from happening again. (Cody, 1985)


Avery, D. and Winokur, G. (1976). Mortality in depressed patients treated with electroconvulsive therapy and antidepressants. Archives of General Psychiatry, 33, 1029-1037.

Bennett, Fancher. Quoted in Bielski (1990).

Bielski, Vince (1990). Electroshock’s Quiet Comeback. The San Francisco Bay Guardian, April 18, 1990.

Breggin, Peter (1985). Neuropathology and Cognitive Dysfunction from ECT. Paper with accompanying bibliography presented at the National Institutes of Health Consensus Development Conference on ECT, Bethesda, MD., June 10.

Breggin, Peter (1990). Testimony before the Board of Supervisors of the City of San Francisco, November 27.

Breggin, Peter (1991). Toxic Psychiatry. New York: St. Martins Press.

Brody, M.B. (1944). Prolonged memory deficits following electrotherapy. Journal of Mental Science, 90 (July), 777-779.

Calloway, S.P., Dolan, R.J., Jacoby, R.J., Levy, R.(1981). ECT and cerebral atrophy: a computed tomographic study. Acta Psychiatric Scandinavia, 64, 442-445.

Calvert, Nancy (1990). Letter of August 1.

Cody, Barbara (1985). Journal entry, July 5.

Coleman, Lee. Quoted in Bielski (1990).

Details of Electrotherapy (undated). New York Hospital/Cornell Medical Center.

Dolan, R.J., Calloway, S.P., Thacker, P.F., Mann, A.H.(1986). The cerebral cortical appearance in depressed subjects. Psychological Medicine,16, 775-779.

Faeder, Marjorie (1986). Letter of February 12.

Fink, Max (1978). Efficacy and safety of induced seizures (EST) in man. Comprehensive Psychiatry, 19 (January/February), 1-18.

Freeman, C.P.L., and Kendell, R.E. (1980). ECT I: Patients’ experiences and attitudes. British Journal of Psychiatry, 137, 8-16.

Freeman, C.P.L., Weeks, D., Kendell, R.E. (1980). ECT II: Patients who complain. British Journal of Psychiatry, 137, 17-25.

Friedberg, John. Shock Treatment II: Resistance in the 70s. In Morgan (1991) pp. 27-37.

Frend, Lucinda (1990). Letter of August 4.

Fromm-Auch, D. (1982). Comparison of unilateral and bilateral ECT: evidence for selective memory impairment. British Journal of Psychiatry, 141, 608-613.

Gordon, Carol (1990). Letter of December 2.

Hartelius, Hans (1952). Cerebral changes following electrically induced convulsions. Acta Psychiatrica et Neurologica Scandinavica, Supplement 77.

Heim, Sharon (1986). Unpublished manuscript.

Janis, Irving (1950). Psychologic effects of electric convulsive treatments (I. Post-treatment amnesias). Journal of Nervous and Mental Disease, III, 359-381.

Johnson, Mary (1990). Letter of December 17.

Lowenbach, H. and Stainbrook, E.J. (1942). Observations of mental patients after electroshock. American Journal of Psychiatry, 98, 828-833.

Maccabee, Pam (1989). Letter of May 11.

Maccabee, Pam (1990). Letter to Rusk Institute of Rehabilitation Medicine, February 27.

Morgan, Robert, ed. (1991). Electroshock: The Case Against. Toronto: IPI Publishing Ltd.

Opton, Edward (1985). Letter to the members of the panel, NIH Consensus Development Conference on Electroconvulsive Therapy, June 4.

Patel, Jeanne (1978). Affidavit of July 20.

Rice, Marilyn (1975). Personal communication with Irving Janis, Ph.D., May 29.

Sackeim, H.A. (l986). Acute cognitive side effects of ECT. Psychopharmacology Bulletin, 22, 482-484.

Sament, Sidney (1983). Letter. Clinical Psychiatry News, March, p. 11.

Scherer, Isidore (1951). The effect of brief stimulus electroconvulsive therapy upon psychological test performances. Journal of Consulting Psychology, 15, 430-435.

Squire, Larry (1973). A thirty year retrograde amnesia following electroconvulsive therapy in depressed patients. Presented at the third annual meeting of the Society for Neuroscience, San Diego, CA.

Squire, Larry (1974). Amnesia for remote events following electroconvulsive therapy. Behavioral Biology, 12(1), 119-125.

Squire, Larry and Slater, Pamela (1983). Electroconvulsive therapy and complaints of memory dysfunction: a prospective three-year follow-up study. British Journal of Psychiatry, 142, 1-8.

SUNY (State University of New York) at Stony Brook (1990- ) Dept. of Social Work. Unpublished masters’ thesis project.

Taylor, John, Tompkins, Rachel, Demers, Renee, Anderson, Dale (1982). Electroconvulsive therapy and memory dysfunction: is there evidence for prolonged deficits? Biological Psychiatry, 17 (October), 1169-1189.

Taylor, John, Kuhlengel, Barbara, and Dean, Raymond (1985). ECT, blood pressure changes and neuropsychological deficit. British Journal of Psychiatry, 147, 36-38.

Templer, D.I., Veleber, D.M. (1982). Can ECT permanently harm the brain? Clinical Neuropsychology, 4, 61-66.

Templer, D.I., Ruff, C., Armstrong, G. (1973). Cognitive functioning and degree in psychosis in schizophrenics given many electroconvulsive treatments. British Journal of Psychiatry, 123, 441-443.

Warren, Carol A.B. (1988). Electroconvulsive therapy, the family, and the self. Research in the Sociology of Health Care, 7, 283-300.

Weinberger, D., Torrey, E.F., Neophytides, A., Wyatt, R.J. (1979a). Lateral cerebral ventricular enlargement in chronic schizophrenia. Archives of General Psychiatry, 36, 735-739.

Weinberger, D., Torrey, E.F., Neopyhtides, A., Wyatt, R.J. (1979b). Structural abnormalities in the cerebral cortex of chronic schizophrenic patients. Archives of General Psychiatry, 36, 935-939.

Winter, Felicia McCarty (1988). Letter to the Food and Drug Administration, May 23.

For copyright information, contact Linda Andre, (212) NO-JOLTS.

Psychiatrists’ private views on ECT

Although publicly few psychiatrists speak out against ECT, privately some have views that stray from the party line.

In a survey from the APA task force on ECT, psychiatrists were asked,

“Is it likely that ECT produces slight or subtle brain damage?”

41 percent voted yes, with only 26 percent voting no.


Spring 2002 (pp.63-71)
Ethical Human Sciences and Services: An International Journal of Critical Inquiry

This is another exquisite article by my friend Leonard Roy Frank.


Voices From Within: A Study of ECT and Patient Perceptions

By Juli Lawrence


This study examines ECT (electroconvulsive therapy) patients’ own perceptions concerning their treatment and after effects. Research concerning memory loss and cognitive problems as a result of ECT has focused on researchers’ ideas about what is important in assessing memory loss and cognitive damage. This study is an attempt to give ECT patients and survivors a voice of their own, from the perspective of those who have experienced the treatment.


Review of the Literature
Background, Research Methods


This study resulted from repeated patient complaints that memory deficits and cognitive disturbances following ECT are not being acknowledged by doctors and researchers. The study contains the viewpoints of 41 subjects who have undergone ECT treatments.

Failure to record patient views is a fundamental flaw in all previous research. Patient views are dismissed by many practitioners, who contend the patients themselves do not understand true memory deficits, or by claiming that the memory problems result from underlying depression, and not ECT. From the perspective of many patients, it is those experts who do not fully understand memory and how severely it can be affected by ECT.

This study demands attention by those experts who use ECT in their psychiatric practice. One of the most important findings in this study is that patients who feel they have been damaged by ECT do not return to the doctor who performed ECT and discuss the problem. Instead, feeling that they have suffered side effects that were unanticipated, they simply go on to another doctor, or leave psychiatric treatment altogether. This is not to be seen as an indictment of the patient. It’s quite normal that someone who feels s/he has been misled or even lied to would not return to the offending doctor, particularly when the patient feels s/he’s been abused.

Thus, when ECT practitioners claim their patients don’t complain, they may be telling the truth, based on their lack of follow-up with patients who have left their care. The patients who have had disastrous experiences never return to inform them, and therefore, they never know.

Additionally, when patients do try to discuss these problems with the doctor, their feelings are often dismissed as being mistaken or a misunderstanding.

This study is an attempt to identify areas of concern among ECT patients, and to give previously unheard voices a chance to speak out. It is also intended to make clear that there are effects that the established ECT community does not want to acknowledge.

Review of the Literature

The literature concerning effects of ECT, including possible brain damage, is biased in favor of ECT. At a recent conference comprised of mental health researchers (45th National Conference on Mental Health Statistics, held in May 1996 in Washington, DC), this concern was posed to researchers in the field. Researchers from universities and the National Institute for Mental Health acknowledged the lack of unbiased research in the field of electroconvulsive therapy, and stressed the need for future independent research.

A full listing, with abstracts, of the literature reviewed is available upon request.

The author reviewed over 500 articles and abstracts from 1966 to present on ECT using Medline.

A current trend in ECT research is evaluating the use of various drugs and herbal substances along with ECT, in attempts to reduce memory loss.

Of 50 articles on ECT since 1986 that discussed memory and cognitive deficits, only eight actually addressed the issue of memory loss. One article reviewed the benefits on memory of unilateral vs. bilateral techniques. Six discussed the varying brain and chemical changes that occur during ECT. Four evaluated trends in ECT over the past decades. The remaining 62 percent (31 articles) focused on using different chemicals (caffeine, calcium channel blockers, ginseng, and so on) during the treatment to reduce memory loss and other negative side effects. Additionally, of those 50 journal articles, 15 were rat and mice studies.

Of those eight that reviewed memory loss and cognitive deficits, only one was based on the presumption that such problems do, in fact, exist. (Durr, 1995) This was from a nursing journal, suggesting that those who deal the most with patients on a continued basis accept that disturbances do occur, despite practitioners’ continued assertions to the contrary.

Two of the articles concluded that ECT treatments actually improved memory and cognitive functioning by eliminating the underlying depression (Frith, et al, 1987; Reid, 1993) The remaining articles tested ECT recipients against normal controls and depressed patients, concluding that any memory and cognitive problems were temporary. One study compared 15 depressed patients, 17 in remission from depression, 20 normal control subjects and 15 in remission as a result of ECT. Although this study showed impairment two weeks after ECT, at six months, no problems were reported. (Williams, et al, 1990)

Finally, one article did discuss the more severe problems associated with bilateral versus unilateral treatment and urged clinicians to take into account the non-memory cognitive effects of bilateral treatment, and to inform patients of these problems prior to consent. (Calev, et al, 1995)

In a 1983 study (Squire et al, 1983), researchers examined self reports of memory problems in patients receiving both unilateral and bilateral ECT, and among patients with depression who received other treatments. The patients who did not receive ECT did not report any memory problems seven months after hospitalization. Compared with bilateral ECT, those who received unilateral ECT reported minor memory complaints. Half of the patients who received bilateral ECT reported poor memory three years after their treatments.

An extensive search of the literature conducted by the author revealed little information on patient views. One study compared 26 patients who complained of permanent, unwanted effects against two control groups. Subjects were given a battery of 19 cognitive tests. The significant differences among the complainers were mostly attributed to depression and medication, not to the ECT treatments. However, some impaired cognitive functioning was seen as a result of ECT. (Freeman et al, 1980)

Background, Research Methods

This study arose from concern that the voices of ECT patients were not being heard. The common complaints of sustained memory loss, cognitive learning difficulties and other effects after a series of ECT, are often met with contempt from the psychiatric community. The medical establishment contends that such effects simply do not occur; they are the result of the underlying depression, or are simply “misunderstandings” by the patients.

In January, the author sent out surveys asking questions about individuals’ experiences with ECT. The survey was posted across the Internet in newsgroups, mailing lists, on-line services, bulletin boards and by word of mouth. In addition to posting the survey in mental health related areas, it was sent to several non-mental health newsgroups and mailing lists. (The original survey is available upon request.)

Problems in sampling methods

Obviously, a perfect sampling of ECT recipients is not possible. Confidentiality prevents the non-medical researcher from access to lists of patients, and this was one way of securing responses.

In true representative sampling, the sample must be representative of the target population in order for any inferences to be valid across the entire population. Past ECT studies are no different than this study in that respect. Researchers make claims that ECT causes no permanent damage, based on a sample of perhaps 10 or 20 subjects. These subjects are treated at the same time, in the same hospital, by the same doctor. And because they have continued treatment with the same treatment team, one would assume that they were satisfied with treatment.

The Voices study does not investigate any one patient from a particular doctor, a particular area of the world, or one moment in time. Rather, it looks at a variety of patients who have had ECT treatment in a variety of locations, different doctors, and different time periods. Surveys were received from patients who had undergone ECT in the last four decades, and from the United States, New Zealand, Australia, Canada and the UK.

A study that would truly reflect the honest experiences of ECT patients would involve interviewing thousands of patients across the world. Other research that is desperately needed is a before and after-ECT study of the brain. The American Psychiatric Association is on record as saying it opposes such a study.

A large-scale study of ECT recipients’ perceptions about their treatment would be a good use of NIMH funds, and something that should be considered by researchers in future studies.

The actual survey was conducted via the Internet and regular mail between the months of January and April, 1996, with a period of follow-up questions in May and June. Participants were given not only an electronic mail address, but a post office box if they had no access to computers or wanted more anonymity. Additionally, anyone could use one of the anonymous servers on the Internet if confidentiality were crucial. Those servers provide an anonymous identification so that the reviewer could follow up with additional questions, yet not know the identity of the responder.


41 replies were received. 23 from females and 18 from males. The average age at time of ECT treatment was 37. For females, the average age was 38.39, for males, 35.22.

75% of the respondents had their ECT treatment in this decade. The remainder had their treatments in the 60s (2%), 70s (12%) and 80s (9.7%).

Among all respondents, 70% felt it had no effect on their depression (or whatever symptoms were being treated). 12% said it had some, or temporary effect on their symptoms. Among females, 65.2% felt it had no positive effect, and among males, 77.7% felt it did no good.

Of all respondents, 17% reported that they felt their ECT treatments helped them. Among females, 21.7% felt it helped them and 11% of males felt it helped.

Memory loss is a major concern among those who have undergone ECT. 83 percent felt that their long-term memory had been affected . This ranged from loss of certain events in their lives, to the inability to remember family members, and in some cases, up to 20 years of memories were erased. Only 17% felt that their long-term memory had not been adversely affected.

“The worst thing that ever happened to me…”
“ECT destroyed my family…”
“Doctor claimed memory problems would vanish in two weeks…”

Of females, 82.6% said long-term memory was affected, and among males, 83.3% reported problems.

“I can’t remember my 20-year Marine Corps career…or daughter’s birth or childhood…”

Short-term memory appears to have been affected slightly less, or the effects were temporary. In all, 63.4% reported problems with short-term memory loss. 12% said they had no problems at all with short-term memory loss. And 22% said that short-term memory loss was either temporary or minor.

“I couldn’t remember people’s names, but it gradually came back…with some prompting…”

Half of all respondents reported that they were given no information about ECT and its effects, other than to be told it was effective. The other half were given information in the way of video tapes, pamphlets, books, and detailed discussions with their physician or nurse. Of those, however, several reported that they wish they’d been given more accurate information concerning memory loss and other adverse effects.

“I did have detailed discussions with my doctors before the treatment, but I just couldn’t realize how bad the memory loss was going to be. If I had, I’m not sure I would have taken the treatments…”

Informed consent is a crucial issue among ECT survivors, many of whom feel they were lied to. And being given accurate information prior to ECT may have a bearing on the aftermath. Among those who reported they had been given information prior to ECT, 30% said ECT helped them, and another 25% felt it had provided some or temporary relief. And among that same group, 45% said they would consider ECT again if other treatments failed. 35% said they would absolutely not have it again, with the remainder reporting that they might consider it, but were not sure.

“My doctor told me nothing except how great it was supposed to be…”
“I was told there would be no permanent damage and memory would return in six weeks. I am still waiting—it’s 11 years and six weeks…”
“Doctor stopped returning my phone calls when I said ‘memory’s not returning…’”
“I was certainly not exposed to any information about the possibility of the type of damage I have suffered…”

Among all respondents who answered the question (6 provided no answer to this question), 42.85% said they felt ECT had caused definite changes in cognitive abilities. This included being able to do mathematics, balance checkbooks, use their technical skills, write, and use their creativity. 40% said that ECT had caused no cognitive damage, with the rest either unsure or feeling the damage was minimal.

“Brain damage has been documented by testing (3 times)…”
“The neuropsychiatrist admitted that impairment was probable, although difficult or impossible to test for conclusively…”
“Turned me into a walking zombie, killing all emotions and feelings for several months…”
“It’s like a bomb being set off inside your head…literally a mind-blowing torture…”

The majority, 85%, had ECT to treat major depression. The remaining 15% had rapid cycling, mania, mixed states, and one person reported he was given ECT because of juvenile delinquency.

30% of the respondents were unsure of whether they had unilateral or bilateral treatments. Of the remaining , 63% reported they had bilateral, with 7% reporting unilateral ECT treatments. One person had both unilateral and bilateral during different series of treatments.

The smallest number of ECT treatments reported was three, after the patient refused to have another. The highest was greater than 100. (This number is not figured into the following average.) Of those who knew the number of treatments they had, the average number was 12.6.

The following question was asked in the form of a follow-up question: “If you felt ECT harmed your memory seriously or caused other adverse side effects, did you discuss this with your doctor following treatment?”

The answer to this question is the most important finding in the study, in the author’s opinion. Two respondents said they discussed this with their doctor afterwards, and were treated with kindness, sympathy and respect. Eight said they attempted to discuss the problem, but their feelings were dismissed by the doctor. The doctors said they mis-remembered, or the problems were from the underlying depression or medications, or they simply were mistaken. These eight people reported that they felt the doctor did not believe them, or did not care.

Of those who answered the follow-up question, 24, or 75%, said they never returned to the doctor who performed the ECT. Therefore, the doctor never knew the problems that ECT caused the patients…and thus, when doctors claim they have few to no patients who complain, they may be telling the truth.

This kind of finding should astonish doctors who perform ECT, and should cause them to follow up on patients who leave their care after the treatment, as well as reconsider their opinions on patient complaints.

While this study is not meant to be the last word on patient views of ECT, it should be carefully studied by those who perform the treatment. The alarming rate of those patients who feel damaged by ECT and never return should open the eyes of the medical community and help them understand some of the reasons they feel their patients do not suffer any negative side effects.


Critical to the understanding of ECT and its outcome is to give a strong voice to those who have undergone this treatment. True informed consent is crucial in order to give patients the chance to make an educated decision about the treatment of their illnesses. Many patients continue to express their dismay in learning that they have suffered more severe side effects than doctors prepared them for.

It is hoped that this study will act as a catalyst to further research, one which will continue to listen to the patients of ECT.


Durr AL, Golden RN (1995) Cognitive effects of electroconvulsive therapy: a clinical review for nurses. Convulsive Therapy 11(3):192-201.

Reid WH (1993) Electroconvulsive therapy. Tex Med 89:58-62.

Frith CD, Stevens M, Johnstone EC, Deakin JF, Lawler P, Crow TJ (1987) A comparison of some retrograde and anterograde effects of electroconvulsive shock in patients with severe depression. Br J Psychol 78 ( Pt 1):53-63.

Williams KM, Iacono WG, Remick RA, Greenwood P (1990) Dichotic perception and memory following electroconvulsive treatment for depression. Br J Psychiatry 157:366-72.

Calev A, Gaudino EA, Squires NK, Zervas IM, Fink M (1995) ECT and non-memory cognition: a review. Br J Clin Psychol 34: 505-515.

Squire LR, Slater PC. (1983) Electroconvulsive therapy and complaints of memory dysfunction: a prospective three-year follow-up study. Br J Psychiatry 142:1-8.

Freeman CP, Weeks D, Kendell RE. (1980) ECT: II: patients who complain.
Br J Psychiatry 137:17-25.


About the author

Juli Lawrence, MA, BS, BA, is a freelance journalist, specializing in health-related topics. Her educational background includes degrees in journalism and Russian language/literature, and a Master’s in cultural anthropology. She received bilateral ECT in 1994.

She worked for several years in social services, primarily in public relations, but also did prevention work among adolescents. She is the co-author of a manual for prevention workers on combating substance abuse during adolescent pregnancy. Prior to her work in social services, she worked as reporter/editor for several newspapers and wires.

She recently presented a paper at the 45th National Conference on Mental Health Statistics in Washington, D.C and served on the Federal Task Force on ECT.

She may be reached at emailgraphic.jpg

Hormone link to ECT side effects

BBC News
20 September, 2001

Measuring the levels of a hormone could help doctors decide whether it is safe to give a patient electro-convulsive therapy (ECT).

ECT is a controversial treatment used to relieve the symptoms of severe depression.

There is evidence that it is effective at relieving these symptoms in many cases.

But some of those who have undergone the treatment claim they have suffered long-lasting cognitive side effects including memory loss, mood swings and recurrent head-aches.

Now, a team of scientists, led by Thomas Neylan, from the University of California in San Francisco, has found that levels of the stress hormone cortisol might indicate which patients will suffer most from these side-effects.

Serious consequences

ECT is carried out under anaesthetic and a muscle relaxant is administered to patients to prevent the muscle spasms that the treatment would otherwise cause.

If susceptibility to these side effects can be predicted it is important to know

Alison Cobb, Mind
Dr Neylan said: “Most people, if not all, will have short-term cognitive side effects following ECT, but in some people these effects can last much longer with serious consequences.”

In his study, Dr Neylan took saliva samples from 16 patients, all of whom had consented to ECT, before treatment to test levels of the hormone cortisol.

The patients also underwent tests to assess their mood, cognitive functioning and memory before and after the treatment.

The results found that the higher the base level of cortisol in each patient, the higher the cognitive impairment after ECT.

These preliminary results, although only based on a small study, could provide doctors with valuable information when deciding whether or not a patient suffering from severe depression should undergo electro-convulsive therapy.

Alison Cobb, from Mind, told BBC News Online: “Memory loss is one of the main side effects that people can have from ECT and it can be permanent.

“In a recent survey carried out by Mind, 42% of respondents reported loss of past memories as a permanent side effect, 36 per cent difficulty in concentrating and 27 per cent inability to remember new information.

“If susceptibility to these side effects can be predicted it is important to know.”

She added that the patient’s own opinion should be one of the most important issues when decisions about ECT are made.

No-one, she said, should be forced to undergo ECT against their will.

Herbal treatments for ECT Memory Loss

Herbal Treatments for ECS-Induced Memory Deficits: A Review of Research and a Discussion on Animal Models

Chittaranjan Andrade, M.D., S. Sudha, Ph.D., and B. V. Venkataraman, Ph.D.

The Journal of ECT
16(2):144-156 0 2000

Summary: During the last decade the use of herbal medicinal substances in the attenuation of anterograde and retrograde amnesia induced by electroconvulsive shock (ECS) has been studied using animal research. We will discuss the background of herbal medicine in India, review the research findings on herbal medicines for ECS-induced amnestic deficits, and examine the applications and limitations of animal models in this context. We will focus on our own research and insights, with particular emphasis on practical issues.

Electroconvulsive therapy (ECT) is associated with anterograde and retrograde amnestic deficits that can, in certain cases, be severe, persistent, or both (Abrams, 1997). Several pharmacological treatments have been suggested to reduce such deficits, but in general the results have been disappointing (Andrade, 1990; Krueger et al., 1992; Nobler and Sackeim, 1993). In recent years, studies have explored the antiamnestic efficacy of herbal medicines in the context of animal models of ECT (Andrade, 1995). This paper will briefly introduce the practice of herbal medicine in India, summarize the studies that have examined herbal attenuation of amnestic deficits induced by electroconvulsive shocks (ECS), and discuss the application and limitations of animal models in the context of such research.


Systems of herbal medicine are practiced in traditional societies in many parts of the world; allopathic science may gain much from the study of such systems. Several important allopathic drugs, such as digitalis, quinine, and atropine, originated from plant sources; psychiatrists need no reminding that over half a century ago, the (Indian) herbal pharmacopoeia contributed reserpine to modern medicine. The need to study the psychotropic properties of herbal drugs is recognized even in developed societies; for example, clinical research on St. John’s Wort was recently reviewed in the British Medical Journal (Linde et al., 1996), and a multicenter study on the efficacy of an extract of Gingko biloba in patients with dementia was recently published in the Journal of the American Medical Association (JAMA) (Le Bars et al., 1997). During November 1998, an entire issue of JAMA was devoted to articles on alternative systems of medicine, including herbal treatments.

American laboratories are already screening individual herbs for psychotropic potential; the United States’ efforts in this regard have been summarized by Cott (1995). By way of example, Cott et al. (1994) reported that extracts from Withania somnifera show high affinity for GABA receptors, and that extracts from Centella asiatica show affinity for CCK receptors. Withania somnifera and Centella asiatica are known as Ashwagandha and Mandookaparni (respectively) in Ayurveda, which is a traditional system of medicine in India. Since GABA agonism and CCK antagonism have been linked to anxiolysis, these findings support the recommendation in Ayurveda that Ashwagandha and Mandookaparni be used as sedatives (Handa, 1995).

The discipline of Ayurveda has existed in India for millennia. One of the practices of Ayurveda is to treat poor health with medicines obtained from herbs. These medicines are prepared from the leaves, roots, or other parts of certain plants. The medicines are most commonly dispensed in the form of a powder or as a water-based extract that is prepared as a decoction, much as tea is brewed. Indian herbal substances with psychotropic properties have been described by Iyengar (1981), Satyavati (1995), Dhawan (1995), and Handa (1995).

Ayurvedic medicine is widely practiced in India to this day. Students receive their training in Ayurvedic medical colleges, and are subsequently licensed by the state to practice their art. Their training and licensing is independent of and parallel to the training and licensing of allopathic practitioners.

The Indian government as a policy encourages Ayurvedic and other forms of indigenous medicine (such as Unani and Sidda). One of the forms of encouragement is to permit the marketing and prescribing of herbal medicinal substances with no prior requirement that these substances be demonstrated to be effective and safe. All that the Drug Controller of India requires, in fact, is evidence that the substances in question have been recorded to have medicinal properties in the ancient Indian literature. In contrast, allopathic drugs introduced into the country must pass through clinical trials before their marketing is permitted; this requirement is not relaxed even if the drug has been approved of for marketing in the developed world.

Ayurvedic clinicians classify and diagnose illness in a manner that is radically different from that followed in allopathy; concepts in the field of mental health have been described by Ramachandra (1990). Furthermore, Ayurvedic clinicians do not have adequate training in the design, conduct, and analysis of clinical trials. As a result, they do not engage themselves in research that is of a nature that allopathic medical journals will find acceptable. In consequence of this, and in consequence of the policy of the Drug Controller of India, a very large number of herbal medicines and formulations thereof are commercially marketed and prescribed in the country without evidence of efficacy and safety. In general, however, experience suggests that adverse effects are not an issue because patients hardly ever experience ill effects when receiving herbal medicines; what remains in question is whether these medicines are effective at all.

The study of the Indian herbal pharmacopoeia through clinical trials is an expensive, laborious, and time-consuming option. The logistics of conducting clinical trials on herbal medicines are further complicated by two factors: most herbal pharmaceutical companies are too small to be able to afford to commission clinical trials, and the larger companies are not interested in clinical trials because their products have already been licensed for sale. Interested scientists are therefore compelled to resort to animal models for the efficacy screening.


Where Should One Begin?

Our interest in the herbal attenuation of ECT-induced cognitive impairment arose in the early 1990s. We were faced with a wide choice of individual substances, all of which were described in Ayurveda to enhance central nervous system functioning; these substances included Shankapushpi, Brahmi, Ashwagandha, Mandookaparni, and others (for review, see Iyengar, 1981; Dhawan, 1995; Handa, 1995; Satyavati, 1995). We were also faced with a wide choice of commercial formulations comprising combinations of various substances in various proportions; these formulations were marketed with the assertion that individual ingredients complement each other in efficacy and cancel out each other in adverse effects (this assertion is a common philosophy underlying Ayurvedic medical practice).

We considered it appropriate to commence our studies with a formulation rather than with an individual herb because a formulation, comprising several ingredients, is more likely to contain a biologically useful chemical, and is therefore more likely to yield positive results. As the starting point for our research, we selected the most popular procognitive formulation (Mentat) marketed by the largest herbal pharmaceutical company (Himalaya Drug Company) in the country.


Mentat is also known as BR-16A. It contains over 20 different ingredients; the exact formulation differs between pediatric and adult presentations of the composite. Important ingredients of BR-16A, suggested to improve memory function, include the following: Jal-brahmi (Bacopa monnieri), Mandookaparni (Centella asiatica), Ashwagandha (Withania somnifera), Shankapushpi (Evolvulus alsinoides), Jatamansi (Nardostachys jatamansi), Vach (Acorus calamus), Malkangni (Celastrus paniculatus), and Sonth (Zingiber officinale). Other ingredients of BR-16A, claimed to be “nerve tonics,” include Tagar (Valeriana wallachii), Badam (Prunus amygdalus), Salap (Orchis mascula), Lavang (Syzygium aromaticum), and Pearl (Mukta pishti). The remaining ingredients are putative general tonics and vitalizers (Himalaya Drug Company, 1991).

We examined the cognitive benefits with Mentat (200 mg/kg/day) using a food-motivated paradigm in food-deprived rats studied in the Hebb-Williams complex maze and in the T maze. In the former task, each rat was trained to leave a start chamber, traverse corridors in the maze, and locate the reward chamber; the learning score was the time taken by the rat to reach the reward chamber. In the latter task, each rat was taught to leave the stem of the T maze, choose between correct and wrong arms of the maze, and locate the reward chamber at the end of the correct arm; the learning indices were the number of trials taken by the rat to achieve a criterion that defined satisfactory learning, and the number of wrong arm entries during this period.

The results were encouraging. We found that 3 weeks of administration of Mentat significantly improved Hebb-Williams maze learning in rats (Joseph et al., 1994). This established the potential of Mentat as a procognitive formulation worthy of examination in the context of ECT-induced cognitive dysfunction. We next showed that in an identical experimental design, Mentat attenuated anterograde amnestic deficits induced by six once-daily ECS (Joseph et al., 1994). In a second study, we found that rats that were pretrained in the Hebb-Williams and the T maze tasks, and which received six once-daily ECS, learned better during post-ECS reexposure to the same tasks if they had received Mentat for 2 weeks than if they had received placebo (Andrade et al., 1994a). It is uncertain, however, whether Mentat improved renewed learning, or enhanced retention of learning during the first (pre-ECS) exposure to the tasks, or both. In a third study, we found that the administration of Mentat for approximately I week to rats pretrained in the T maze resulted in an attenuation of the retrograde amnestic deficits induced by two ECS administered on the same day, 5 hours apart (Andrade et al., 1995). In the most elaborate study of all, we employed the Hebb-Williams maze to confirm that approximately 2 weeks of treatment with Mentat enhances the ability of rats to learn the task as well as attenuates both retrograde and anterograde amnesia induced by two once-daily ECS (Faruqi et al., 1995).

Results in healthy rats may not be generalizable to dysfunctional humans. In an attempt to make the animal model more representative of situations of clinical impairment, we preselected rats for poor learning on the Hebb-Williams maze and examined whether the administration of Mentat for 3 weeks could attenuate the anterograde amnestic effects of six once-daily ECS; the results again supported the use of Mentat (Ramteke et al., 1995).

We have not been able to offer any convincing explanation for the mechanism of procognitive action of Mentat. In only one of the studies described, we found that Mentat produced a small but statistically significant abbreviation of the ECS seizure duration (Faruqi et al., 1995). This finding was in line with unpublished data furnished by the drug company that Mentat shortens chemically induced seizures, and abbreviates breakthrough seizure duration in epileptic patients on antiepileptic medication. In this study, however, seizure duration showed no statistical relationship to the learning performance of the rats, suggesting that the mild anticonvulsant effect of Mentat did not directly or indirectly mediate its antiamnestic effects.

In another study, we used in vivo chemical challenges in rats to demonstrate that Mentat enhances dopamine postsynaptic receptor functioning, but does not influence the activity of dopamine autoreceptors or alpha-2 noradrenergic receptors (Andrade et al., 1994b). The relevance of these findings to the procognitive effects of Mentat requires further study.


As already described, Mentat is a complex herbal formulation. With the expectation that not all of its contained ingredients are relevant to its procognitive actions, we searched for simpler formulations to study, and finally chose Memorin (Phyto-Pharma). This formulation is derived from Mandookaparni (Centella asiatica, Jatamansi (Nardostachys jatamansi), Yashtimadhu (Glycyrrhyza glabra), Shankapushpi (Evolvulus alsinoides), and a subformulation, Smruti Sagar. While Memorin is not exactly a subset of Mentat, there is considerable overlap in the contained ingredients.

We examined the cognitive benefits with Memorin (200 mg/kg/day), using the T maze as in the Mentat studies and using a passive avoidance paradigm. In the latter experiment, each rat was trained to remain in the bright chamber of a shuttle box to avoid receiving an electric shock in the dark chamber; the duration for which the rat remained in the bright chamber was its recall score.

As with Mentat, the results with Memorin were encouraging. The administration of Memorin for 2 weeks attenuated retrograde amnesia, measured using the passive avoidance paradigm, in rats that received two ECS on the same day, spaced 5 hours apart (Vinekar et al., 1998). Likewise, 2 weeks of Memorin attenuated the anterograde amnesia induced by two ECS (again administered on the same day, 5 hours apart) and measured in the T maze (Andrade et al., 1999). In neither study did Memorin influence the ECS seizure duration. As with Mentat, we were unable to suggest any mechanism for the procognitive action of Memorin.

Our experience with Memorin in elderly subjects diagnosed with age-related cognitive decline (DSM-IV) has been very encouraging. Memorin capsules administered four per day in two divided doses produced significant improvements in several measures of memory relative to placebo (Andrade et al., 1998). A small pilot study comparing Memorin and placebo in patients receiving ECT has recently been completed, and the data are presently under analysis.


Shankapushpi (Evolvulus alsinoides) is an ingredient of both Mentat and Memorin. Shankapushpi is highly rated in Ayurveda as a treatment for impairments related to the central nervous system. Accordingly, we examined the ability of an aqueous extract of Shankapushpi to promote learning, and to attenuate ECS-induced anterograde and retrograde amnesia studied using the T maze and the Hebb-Williams maze.

The results were altogether disappointing. Shankapushpi did not enhance learning performance on either task, nor did it attenuate either anterograde or retrograde amnesia induced by various schedules of ECS in rats (abstracted in Andrade et al., 1996). It is of course conceivable that Shankapushpi may contain a procognitive ingredient that does not emerge in an aqueous extract; if so, an alcoholic extract of Shankapushpi, or extracts obtained by some other process, may yield more encouraging results; this issue will require evaluation in future experiments.


Herbal medicines are prepared from the leaves, roots, and other parts of specific plants. The biology of these plant parts varies as a function of their location on the plant, the time of day, the season of the year, the cultivation process, variations in weather and soil, and other factors. Accordingly, standardization of an herbal pharmaceutical product requires much care.

Today, the principal chemical ingredients of most of the important herbal source materials are known and have been published (e.g., Kirtikar and Basu, 1993; 1994). What is uncertain, however, is the identity of the chemical that is biologically relevant in a particular herb. Most herbal pharmaceutical companies therefore obtain a chromatographic “fingerprint” of a gold standard of their herbs, and endeavor to ensure that all subsequent batches of their products match this fingerprint. The shortcoming of this procedure is that the standardization process may be based upon irrelevant ingredients.


Animal models of cognition are well described in the literature and will not be reviewed here. Instead, we present certain theoretical and practical issues that arise from the conduct and interpretation of research based on such models. We focus on our own experiences in this regard, derived from the studies described in the earlier section.

General Limitations of Animal Models

Conducting research on human subjects may yield the most reliable results, but is expensive, time-consuming, and fraught with ethical difficulties. The use of animal models of physiological or psychological function or dysfunction is therefore helpful during the early stages of hypothesis generation, during drug development, and in other contexts of explorative research. The utility of animal models notwithstanding, it must be remembered that resulting findings are generalized to human contexts; this exposes the limitations of such models. Consider the following issues:

1. A rat is far removed from a human; the validity with which comparisons can be drawn between rodent and human research is therefore uncertain. For example, the complex processes described under registration, retention, recall, and recognition under short- and long-term storage conditions in humans may not apply to the same extent in rats. The neurophysiology and neurochemistry of a rat may be simpler than that of a human, making it easier for a drug to have a demonstrable procognitive effect in the former than in the latter situation. A contrary view is also conceivable: A complex human system may have more sites at which a multiingredient herbal compound could act, making the compound more likely to be effective in the human context than in the laboratory context.

2. A healthy rat is far removed from a dysfunctional human. For example, even if memory processes are identical in rats and humans, it is uncertain whether memory processes in healthy rats are similar to memory processes in humans who are modified by conditions such as depression and schizophrenia. It is likewise uncertain whether a drug that has procognitive effects in a healthy rat will have procognitive effects in a human whose biology is compromised by the neurophysiological, neurochemical, and neuroendocrine changes associated with psychiatric illness.

3. Even if healthy rats can be equated with dysfunctional humans, animal models of psychological states are still remote approximations of what they are clinically considered to represent. For example, the processes that delay a rat’s ability to locate the reward chamber in the Hebb-Williams maze are likely to be much different from the processes that underlie ECT-induced autobiographical memory impairment, if only because maze learning is a spatial task while autobiographical memory is nonspatial. A drug that is effective in one context may therefore not be effective in the other context.

4. Even if animal models correspond perfectly with the human processes that they are desired to represent, the absence of internal and external “noise” in laboratory contexts prejudices the generalizability of animal studies. For example, laboratory animal~ used in research usually belong to the same age, sex, and inbred strain; they therefore closely resemble each other in behavior. Furthermore, the laboratory environments in which the animals are housed and the experiments conducted are both carefully controlled, and are kept constant all through the experiment. All these factors reduce the variance of the results in animal experiments. In contrast, in human contexts interpersonal and environmental differences across subjects are multiple and are very difficult to control. These factors increase the variance of results in clinical research. The consequence of low variances in animal research and high variances in clinical research is that statistical significance is far more easily attained in the laboratory than in the clinic. Thus, for example, a drug that has a small procognitive effect may produce statistically significant results in the laboratory and insignificant results in the real world. In other words, the small positive effect of the drug is, in human research, drowned out by the background noise. This may be one of the reasons why many procognitive treatments that have been shown to be effective in animal models prove to be ineffective in clinical trials. A point worth noting is that small positive effects, if they exist, can be demonstrated in clinical contexts if a sufficiently large sample is studied; however, it is uncertain whether the statistically significant results so obtained would be clinically meaningful.

Thus, it is necessary to generalize with caution between animal and clinical research; when such generalizations are made, the limitations of animal models must be kept in mind.

General Biases That Operate in Animal Models of Cognition

Measures of cognition in animal models may be influenced by biasing factors that are unrelated to cognition. Such factors include motivation, motility, and left-right preferences.

An animal must be adequately motivated to attempt a cognitive task and to do well on it. In other words, performances that are deemed to represent learning efforts must be driven by motivation to learn rather than by random, exploratory behavior. Motivation is generally ensured through reward (e.g., a food pellet) or punishment (e.g., a footpad electric shock). Food-motivated tasks may require the rat to be on I hour/day restricted feeds for 2-3 days prior to the learning experiments; feeding on the days on which learning is assessed is permitted after the learning tasks for the day have been completed.

(If the learning tasks span several days, it may be advisable to permit feeding only when several hours have elapsed after exposure to the task; otherwise, the rat may show poor motivation to attempt the task, having already learned that food will be provided after exposure to the task.)

A problem with such food deprivation is that the rat may become sluggish; as a result, the rat may not attempt the task at all. For example, we have observed that rats on restricted feeds sometimes do not move out of the stem of the T maze. The learning of these rats cannot be assessed, and the results of the experiment may consequently suffer bias. Rats that are sluggish but that do attempt the task may show biased performances on time-based variables. Another problem with food deprivation is that hypoglycemia can itself compromise learning. The interaction between this variable and the experimental variable cannot be estimated. These limitations of food-motivated tasks with rats on restricted diets must be kept in mind when conducting and interpreting research based on such paradigms.

Learning tasks that are time dependent are biased by variations in basal animal motility. For example, in the Hebb-Williams maze, the dependent variable that estimates learning performance is the speed by which the rat reaches the reward chamber. This variable is influenced by the rat’s basal motility: a sluggish rat will “learn” more slowly while a restless rat will “learn” more quickly. Hence, a treatment that alters basal motility will produce spurious changes in teaming performance. The direction of the error will depend on the nature of the task and the effect that the treatment has on motility. A treatment that decreases motility will falsely enhance learning performances and will fail to adequately identify amnestic effects in learning tasks, such as passive avoidance paradigms, in which an absence of response from the animal indicates learning. Such a treatment will fail to adequately identify learning, and will falsely inflate amnestic effects in learning tasks such as the Hebb-Williams maze and active avoidance paradigms, in which an active response from the animal indicates learning. Treatments that increase motility will produce errors in the opposite direction. For example, Posluns and Vanderwolf (1970) found that retrograde amnesia in passive avoidance tests after ECS may be partly due to a deficit in the ability to suppress motor activity.

Possible solutions to motility-related problems in time-based learning tasks are either to previously study and rule out an effect of the treatment upon basal motility before proceeding with the task or to use a task such as the T maze, the results of which are not influenced by motility factors. Another possibility is to deliberately use a learning task that predisposes to a false negative error when studying a putatively procognitive drug that affects basal motility. The logic here is that it may be better to err on the side of caution during screening. While including a sham treatment control group by itself will not help, the use of a factorial experimental design can reduce (but not necessarily eliminate) motility related errors. In a study intended to test the antiamnestic effects of a drug in ECT-treated animals, the experiment would include drug/ECT, sham drug/ECT, drug/ sham ECT, and sham drug/sham ECT groups. The last two groups serve as internal controls to the main experimental and main control groups. In the analysis of results, the interaction effect between the drug and ECT would indicate the antiamnestic action of the drug.

Many of the ingredients of the herbal formulations that we studied are claimed to have tranquilizing properties and would consequently be expected to reduce motility. We therefore focused on T maze paradigms in our recent research and used factorial designs in all our studies to minimize motility-related errors.

For over two decades it has been recognized that rats show clear left-right preferences, and it has recently been recognized that these preferences influence rats’ choices on spatial tasks such as the T maze. Very recently (Andrade et al., unpublished observations), we showed that the bias in T maze arm preference was substantial: 22.2% of the rats that we studied showed a left preference, and 52.8% showed a right preference. This bias was spontaneous and was consistent over two testing sessions 30 days apart. Left- and right-biased rats learned rapidly when trained to enter the arm ipsilateral to the bias; learning was significantly poorer or did not occur contralaterally. This contralateral learning difficulty was particularly evident when transfer of learning was assessed, especially with right-biased rats. Interestingly, unbiased rats (25%) also showed some difficulties in attaining the criterion for learning in one or the other arm of the T maze. This finding is probably a result of the broad definition that we used for absence of bias in contrast with the strict definition used for the presence of bias. Actually, some of the unbiased rats also showed bias albeit to a lesser extent, and this bias may have been responsible for the learning confusion observed. Our findings suggest that unless spontaneous laterality preferences are taken into consideration, spurious results may be obtained in spatial learning tasks.

In our own research, described in an earlier section, we attempted to ensure validity of results by screening all rats for the ability to learn in both arms of the T maze, and by randomizing rats into groups based on their learning performances. We consider that there are three prerequisites for valid use of the T maze in cognitive research: Animals should be preselected for capacity to learn in both arms, randomization into experimental and control groups should be stratified for spontaneous arm bias, and original learning should be directed towards the arm contralateral to the bias while transfer of learning, if required, can be directed into the ipsilateral arm. These prerequisites are unfortunately likely to make T maze research time-consuming and unattractive.

General Precautions Necessary in Animal Models of Cognition

Many obvious precautions are described to ensure that performances on learning tasks are not biased. For example, studies are best conducted on young adult male rats. Rats that are not adults have immature nervous systems and may not learn consistently. Rats that are too old have age-related impairments that compromise their learning performances. Female rats experience estrus every 5 days, and their learning behavior may be influenced as a function of their hormonal status.

Rats should be obtained from the same batch for the entire study, otherwise heterogeneity across batches may confuse results. While the use of an inbred strain may to some extent ensure uniformity, there is no assurance that ever, within an inbred strain rats will be uniform in their behavior on a particular task (Pradhan et al., 1990). Only naive rats should be selected for experiments; rats that have been used in an earlier experiment are likely to show biases in behavior. The rats must be uniformly treated in matters ranging from housing to handling and feeding. If rats belonging to different experimental groups are treated differently, differing performances may be attributable to such differences in treatment rather than to differences in learning. The rats should be housed and maintained in reasonable comfort. Rats that are isolated one per cage, or that are otherwise stressed may perform poorly as a function of such stresses.

Rats should be handled regularly so that their responses to a learning task are not biased by the stress of the handling during the experiment. Rats should be familiarized with the experimental apparatus prior to the actual experiment so that their performances are not biased by exploratory behavior. The experiment must be conducted in an environment that is relatively sound proof and free from other distractions. The researcher must be seated such that his or her presence does not distract the rat. External stimuli, including lighting, should not cue the rat. Lighting in particular should be kept constant all through the study, because rats are very light sensitive, and become less or more motile with more and less environmental brightness, respectively. The apparatus must be cleaned after every rat has completed its task, otherwise the scent markings of the rat will bias the performances of future rats exposed to the apparatus. Learning assessments must be conducted at the same time of day lest circadian rhythm variations bias results. These and other precautions are well described in most textbooks on laboratory procedures (Bures et al., 1976; Joseph and Waddington, 1986; Van Ree and de Wied, 1988).

One further precaution deserves special mention. In animal research, rats are frequently assigned to one of several different groups. It is generally not feasible to complete an entire experiment in a single day; therefore, for convenience researchers sometimes execute their study by testing one group at a time. The fallacy of this procedure is that it permits the entry of sampling, handling, environmental, and other biases into the study. A more appropriate way of conducting the experiment is to ensure that each group is proportionately represented in each session of work.


Models of ECS-Induced Amnesia

The literature on ECS and learning in animal models has been reviewed by Krueger et al. (1992) and Fochtmann (1994). This section will therefore provide only a brief summary. Retrograde amnesia associated with ECS has been studied most commonly using the passive avoidance paradigm (e.g., Alpern and McGaugh, 1968). Conditioned taste aversion has also been employed as a model (e.g., Shaw, 1986). Active avoidance, appetitive or aversive water reinforcement, bar pressing, conditioned emotional responses, T- and Y-maze learning, brightness discrimination, and hunger-fear conflict responses are some of the other paradigms that have been used to assess retrograde amnesia after single or repeated ECS (Fochtmann, 1994).

Anterograde amnesia with single or multiple ECS has been less extensively studied. Again, the most common method employed has been the passive avoidance paradigm (e.g., Gardner et al., 1972). Several other models of learning have also been described. Not all have succeeded in eliciting amnesia (Fochtmann, 1994). A general observation has been that the ability of ECS to prevent an association from occurring initially is more pronounced than its ability to disrupt an already formed association (Kral and Beggerly, 1973).

The method of ECS administration has been shown to affect the degree of memory impairment. Corneal electrode placement is associated with greater amnestic effects than transauricular electrode placement (Dorfman and Jarvik, 1968). Brief-pulse ECS is associated with less severe memory impairment as compared with sine wave stimuli (Docter, 1957). Altering the convulsion with the use of either anesthesia or nonconvulsive stimulation has variable effects on ECS-induced memory deficits. Increasing the number, frequency, intensity, or duration of ECS, or the proximity of the ECS to the time of training or testing, is associated with a greater degree of memory impairment (Fochtmann, 1994). These issues need to be kept in mind when choosing a model.

Practical Issues

Genetic differences influence task learning, and both good- and poor-learning strains have been discussed (Roullet and Lassalle, 1995; Van Buskirk and McGaugh, 1973). For example, C57BL/61bg mice are good learners in conditional spatial alternation tasks, while DBA/21bg mice are poor learners and require at least twice the number of training trials (Paylor, 1993). When an inbred strain of rats is unavailable, there is variation in learning behavior across batches of rats as well. Thus, previous experiences and textbook descriptions of animal models of cognition notwithstanding, prior to each experiment each laboratory may need to restandardize the model of learning and ECS-induced amnesia, readjusting variables ranging from the extent of pre-ECS training and the magnitude of aversive shocks to the strength, number, and frequency of ECS stimuli.

Administration of unmodified ECS may lead to spinal fracture and paraplegia in a small percentage of rats. In our experience, the risk is greater in very young animals and when higher stimulus doses are used; however, old animals and those with greater muscle mass are also at risk. Administration of modified ECS is difficult. Ventilating a paralyzed rat before and after the ECS poses problems, and the use of anesthesia may enhance the ECS-induced cognitive deficits (Miller et al., 1985). While the latter may be desirable because it makes the model more representative of clinical contexts, results may actually be inconsistent. Some studies have reported less amnesia with the use of anesthesia, and even the elimination of convulsion (Fochtmann, 1994).

Making an ECS schedule representative of clinical contexts is not easy. We have observed that the administration of alternate-day ECS does not reliably induce amnesia with the models of cognition that we have studied. In this regard, models of retrograde amnesia pose particular problems. The number and frequency of the ECS administered must ideally mimic a clinical course of treatments; however, employing such a schedule of ECS risks introducing time-dependent forgetting of pre-ECS learning. We have therefore administered daily ECS, and sometimes even twice daily ECS, with the (unproven) assumption that the mechanisms of ECS-induced amnesia are similar, provided that the number and frequency of ECS do not differ too widely from clinical norms.

Care must be taken to ensure that the interval between the administration of ECS and subsequent exposure of the rat to the learning task is consonant with the aspect of memory that is being studied. Early exposure to the task is relevant to the transient, postictal cognitive effects of ECT while later exposure is relevant to the more enduring deficits.

Finally, just as learning assessments are best conducted at a fixed time of day, ECS should ideally be administered at a fixed time. This is because variations in ECS-induced seizures have been noted at various points in the diurnal cycle. These variations have been attributed to endogenous opioid levels (Oliverio et al., 1985).


In this article, we have briefly introduced the practice of herbal medicine in India, summarized the studies that have examined the herbal attenuation of amnestic deficits induced by ECS, and discussed the application and limitations of animal models in the context of such research. We have primarily focused on our own work and insights, and have also examined practical issues that are involved in studies of this nature. For a comprehensive review of the effects of ECS on memory and cognition, the effects of pharmacological agents on ECS-induced memory deficits, and the effect of coadministered drugs on ECS seizure properties, the reader is referred to Krueger et al. (1992) and Fochtmann (1994).

Acknowledgment: This article was supported in part by a grant from the Council for Scientific and Industrial Research (CSIR), New Delhi, India.


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Testimony of Anne Krauss to NY Assembly

Hello. My name is Anne Krauss. I’m presently employed as the Administrator for the National Association for Rights Protection and Advocacy, although I am here today as a private citizen, not as a representative for that organization. Up until March 21 this year, I worked for the New York State Office of Mental Health as Recipient Affairs Specialist for Long Island. On March 9, I received a call from John Tauriello, Deputy Commissioner and Counsel of the New York State Office of Mental Health (NYS OMH) and Robert Meyers, NYS OMH Deputy Director of the Division of Community Care Systems Management. They informed me that if I continued to actively advocate on behalf of Paul Thomas in his efforts to prevent Pilgrim Psychiatric Center from shocking him, OMH would view this as a conflict of interest with my employment. I explained that I was engaged in this activity on my own time and at my own expense. However, they insisted that, since Mr. Thomas is engaged in a legal battle with the organization for which I worked, that it would be unethical for me to advocate for Mr. Thomas while working for OMH. On March 21, I submitted my letter of resignation, which was accepted on March 22.

Up until December, 2000, electroshock had not been an issue to which I had devoted much attention. I would have been surprised to learn that less than four months later, electroshock would be the issue which would lead me to resign. When I learned in December that Pilgrim Psychiatric Center was seeking to treat a patient with electroshock against his family’s wishes, I began to seriously educate myself about this complicated issue. When I learned that Paul Thomas, whom I first met in 1998, had received over 50 shock treatments in less than two years despite his objections, I felt compelled to act.

I am a person who firmly believes that it is important to gain a scientific understanding of a problem before reaching any decisions about a course of action. I come from a family of scientists. Both my father and my brother were educated at the California Institute of Technology. I was a physics major at Harvard University when I married and dropped out to raise a family. My husband received a Ph.D. at Cal Tech in biochemistry after receiving a medical degree at Cornell College of Medicine. I eventually finished my undergraduate education at Empire State College, then entered a Ph.D. program in experimental psychology and cognitive neuroscience at Syracuse University. Once again, family obligations cut short my educational pursuits, but my devotion to scientific approaches remains unwavering.

Proponents of ECT claim that research overwhelmingly supports the hypothesis that electroshock is safe and effective. A cursory glance at the research literature would appear to support this claim. However, I would caution the members of this Assembly Committee to look very closely and critically at the scientific evidence which is currently available. In ten minutes, there is not time to adequately examine what research has been done, or, more importantly, what research has not been done. Even if this whole day were devoted to understanding the research picture, we could only scratch the surface. However, let me share some information which I hope will pique your curiosity, as it did mine, so that you will withhold judgment until you have time to thoroughly investigate the evidence.

Electroshock devices are classified by the Food and Drug Administration as Class III medical devices. Class III is the most stringent regulatory category for medical devices. Electroshock devices were placed in this category because of their potential to cause unreasonable risk of illness or injury. These devices can be marketed under current regulations only because they have been “grandfathered” in by virtue of being marketed prior to 1976, when the medical device classification and regulation system was put into place. The manufacturers of these devices have never submitted the evidence which the premarket approval process requires of all devices introduced after 1976. Premarket approval is a process of scientific and regulatory review to ensure the safety and effectiveness of class III devices. Keep this in mind if you hear that older reports of neuropathology resulting from electroconvulsive therapy in experimental animals and humans are “outdated”. Similar studies have not been conducted using contemporary shock techniques and devices. Such studies have not been required for marketing, since these new devices are accepted by the FDA to be “as safe and as effective or substantially equivalent” to the older devices. Until such studies are conducted, there is a lack of scientific evidence that these newer devices actually are safer, as claimed.

You may have noticed that I prefer the term “electroshock” rather than “ECT” or “electroconvulsive therapy”. The term ECT implies that the effectiveness of the treatment depends upon the production of a convulsion, or seizure. If this were indeed the case, the safest device would use the minimum dosage of electricity necessary to induce a convulsion. Such a device was developed, and, indeed, the memory changes, confusion, and agitation observed in people shocked with this device were not as large as observed in association with higher dose machines. However, use of low dose machines was abandoned, because psychiatrists found them considerably less effective. This suggests that the size of the electric shock, rather than simply the length of the convulsion, plays an important role in this treatment. It also suggests that negative side effects are inseparable from what psychiatrists perceive as the therapeutic effect. It is also interesting to note that even proponents of electroshock do not claim a therapeutic effect lasting longer than a few weeks, which coincidentally is the same length of time required for the most obvious of the memory disruptions to clear.

In considering the evidence, I also caution you to distinguish between solid research evidence and mainstream medical opinion. Remember that Moniz was awarded a Nobel prize for the lobotomy, which was considered a major medical breakthrough in its day. Remember also that tardive diskenesia was recognized by critical researchers and, yes, anecdotally by patients, for well over a decade before the medical establishment was willing to admit the true dimensions of this serious problem associated with pharmaceutical treatment of psychosis. Remember this before you hastily marginalize researchers and patients who are critical of electroshock.

During these past five months I have learned that, despite rhetoric which pays lip service to a concept of recovery from psychiatric disability based on self-help and empowerment, in practice OMH acts as though the only legitimate treatments are pharmaceuticals or electroshock. Twelve years ago I was hospitalized with what was diagnosed as a schizophreniform psychosis, and I had experienced considerable psychiatric disability even prior to my hospitalization. Symptoms of neuroleptic malignant syndrome, a life-threatening side-effect of medication, abruptly ended the pharmaceutical treatment I had been receiving. Since that time, a combination of psychotherapy and self-help through peer support have helped me to recover to a point that I no longer consider myself to have a psychiatric disability.

I realize that my story can be criticized as anecdotal, however, a careful review of the literature will reveal considerable evidence that, even for people experiencing extreme psychiatric states, effective alternatives exist other than drugs and shock. Dr. Bertram Karon conducted a study in which psychotherapeutic treatment of people diagnosed with schizophrenia was compared to pharmaceutical treatment. This study, which was funded by NIMH, provided evidence that the outcomes for the group treated with psychotherapy were superior to those of the drug treated group.

In his book, Recovery from Schizophrenia, Richard Warner compares conditions in non-industrialized countries to those in the West, in an effort to explain why, although the appearance of altered state is relatively constant across cultures, recovery rates seem to be much higher in the non-industrialized world. The factors he identifies which appear to promote recovery in non-western cultures are remarkably similar to those present in the self-help community which I found helpful in my recovery.

Both of the people I know for whom OMH is seeking court ordered shock have not been given adequate access to psychotherapy. Limitations on visitation have also seriously curtailed their access to peer support. One person is still not permitted to receive visitors other than immediate family members. The ward environment in which he must live would be stressful for anyone, and certainly has not been designed to effectively promote recovery in a person who is experiencing an altered state. Yet OMH claims that electroshock is the only available option for both of these individuals, because of dangerous effects each has experienced from drug treatment.


At a minimum, a moratorium on forced electroshock treatment should be sought in New York State until FDA premarket approval requirements are met. No person should be involuntarily subjected to treatment with a Class III device for which the FDA has not yet received reasonable assurance of both safety and effectiveness. Acceptance by the medical community is not a substitute for rigorous testing.

Reporting requirements for basic information on each procedure administered in New York should be instituted, including patient age, location of treatment, status as voluntary or involuntary patient, and any death of a patient occurring within two weeks of the procedure. Similar reporting requirements in Texas indicate that a person receiving 60 treatments, the number Mr. Thomas has undergone in the past two years, faces a risk of death of approximately 2%. A retrospective study of electroshock in New York would also be illuminating.

Capacity determinations should be made by psychologists, not by psychiatrists, and certainly not by the same psychiatrists whom have determined that a particular treatment is the best or only treatment option. Under the present system, disagreement with the psychiatrist’s opinion is considered evidence of “lack of insight”, which in turn is viewed as a symptom of mental illness. Separating the issue of capacity to make a reasoned treatment decision, which is more of a psychological than a psychiatric question, from the question of agreement or disagreement with the proposed treatment, could effectively address this problem. Legislators could gain a better understanding of this issue if they read the transcript of Mr. Thomas’ hearing.

It is very difficult to devise a legislative approach to guaranteeing that patients will have access to alternatives to electroshock. Increased funding and continued support for psychotherapy and self-help, including research in these areas, is important. However, as long as mental health treatment is ultimately under the control of psychiatrists, it is likely that alternatives to somatic treatments will not be viewed as legitimate. Psychiatry tends to view all mental difficulties as resulting from physical abnormalities in the brain. At the risk of oversimplification to make a point, I’ll claim that in many cases this makes about as much sense as blaming the Intel Pentium processor for Microsoft’s buggy software. Perhaps psychiatry’s “hardware” bias could be offset through giving greater power to both psychologists, who by analogy are “software” experts, and to those of us who have experienced altered state, and know in the most intimate and direct way how somatic treatments and human relationships impact upon us.