IN THE EARLY 1930S, the Hungarian psychiatrist Ladislas Meduna began to experiment with a different biological approach to the treatment of schizophrenia. Like Sakel, Meduna was of Jewish descent, and the rising tide of antisemitism eventually forced him to emigrate to the United States. His initial experiments were conducted in his native Hungary.
Trained originally in Budapest in the neuroanatomical tradition of his time by a psychiatrist who hewed closely to the orthodoxy of the age, Meduna was taught that schizophrenia was an endogenous hereditary disease that could not be cured. The very idea, according to his mentor Karl Schaffer, was “nonsensical.” Working full time in the laboratory, Meduna did not encounter his first patient with schizophrenia until the late 1920s. He was put in charge of the outpatient department at the Royal National Mental and Nervous Asylum in Budapest, and those with seizures constituted a large part of his clinical load. Continuing his neuroanatomical work, in 1931 he and a colleague noticed that at autopsy there often appeared to be “tremendous changes in the brain” in cases of epilepsy, changes he did not observe in schizophrenia.1
Wagner-Jauregg’s malaria therapy and Jakov Kläsi’s experiments with deep-sleep therapy had persuaded a number of the rising generation of psychiatrists that a view of mental illness as rooted in the body was not incompatible with an active therapeutics. It was this changed intellectual context that encouraged ambitious young psychiatrists like Sakel and Meduna to launch their own experiments. In 1932, Meduna published his findings of an increased proliferation of glia cells in the brains of those suffering from epilepsy, and much later he claimed that he had simultaneously observed a deficit of glia cells in schizophrenics.2 From the late 1920s onward, a handful of psychiatrists had claimed that epilepsy and schizophrenia rarely occurred together.3 Some contended that if epileptics developed schizophrenia, their seizures diminished; others that epileptic seizures seemed to result in a temporary abatement of schizophrenic symptomatology.4 Modern researchers have shown that the claimed antagonism between schizophrenia and epilepsy is completely spurious: in reality, schizophrenia is associated with a higher risk of seizures, and epilepsy goes hand in hand with an elevated risk of developing schizophrenia—a demonstration of the hazards of relying on anecdote and clinical intuition.5 Yet the clinical observations and speculations of the late 1920s and early 1930s that claimed that one disorder precluded the other would prove to have dramatic consequences for the treatment of psychosis.6
Encountering these claims, Meduna reasoned that there might be a biological antagonism between epilepsy and schizophrenia. From that intellectual leap, he reasoned that if he could somehow induce seizures artificially, he might be able to cure schizophrenics. He first attacked the problem with a series of animal experiments, using a series of alkaloids, including caffeine and strychnine, before settling on injections of camphor dissolved in oil. Having tried this solution on guinea pigs and determined to his satisfaction that it was safe to inject, he moved rapidly to experiment on human subjects.7
ON THE MORNING OF JANUARY 23, 1934, Meduna brought in his first patient, a man diagnosed as suffering from catatonic schizophrenia. The man was injected with camphor. Nothing happened for forty-five minutes, and then, at last, the patient had a major seizure. After a short interval, during which the patient briefly stopped breathing, he recovered consciousness but seemed little changed. The episode left Meduna in considerable distress: “My body began to tremble, a profuse sweat almost drenched me, and, as I later heard, my face was ash gray.”8 He had to be supported by two nurses as he was led back to his room.
The patient subsequently underwent several more injections and convulsions, though Meduna soon switched away from camphor to induce them. Its effects were so unpredictable that clinicians were unable to anticipate the timing of the subsequent convulsions, which might occur fifteen minutes to three hours later, or not at all. It tended to produce nausea and vomiting and abscesses at the site of the injection.9 Instead, he settled on a synthetic drug, pentathylenetetrazol, soon known in the United States as metrazol, as his treatment of choice.10
Perhaps Meduna’s reaction should not occasion surprise, given the scene he had just witnessed and the uncertainty about whether the patient would even survive camphor’s “powerful and brutal effects on the organism.”11 Camphor and metrazol had similarly savage impacts, though the latter had somewhat more predictable consequences. Solomon Katzenelbogen, a Swiss-trained psychiatrist who by 1938 occupied the post of director of research at St. Elizabeths Hospital in Washington, DC, provided a vivid account of the standard procedure in these cases. A syringe with a large-diameter needle was introduced into a vein, and its contents injected as rapidly as possible. Delivering the metrazol quickly was vital if it was to induce a seizure, and if a seizure failed to result, a still larger dose was tried. Katzenelbogen advocated being “generous with the dosage” to obviate the need for a second injection. Some recommended repeating the injections every other day until as many as thirty or more convulsions had been induced. Katzenelbogen preferred no more than two treatments a week, such was “the strain imposed on the organism by the convulsions.”12
Yet far from being deterred by the severity of the response, Meduna was certain it was vital to the success of the treatment. To remove an entrenched psychosis, he was convinced, required even more powerful countermeasures. The use of “brute force” was inescapable: “We act with both [metrazol and insulin] as with dynamite, endeavoring to blow asunder the pathological sequences and restore the diseased organism to normal functioning.… [W]e are undertaking a violent onslaught with either method we choose, because at present nothing less than such a shock to the organism is powerful enough to break the chain of noxious processes that leads to schizophrenia.”13
The treatment was worth the trauma because the results were so spectacular, or so Meduna asserted. His first paper on the new treatment reported on twenty-six patients. He claimed there had been ten long-lasting remissions, three temporary remissions, and thirteen patients who were not improved. Two years later, his monograph on convulsion therapy touted much more impressive figures: of sixty-two patients with a particularly pernicious form of schizophrenia, 80 percent had entered remission.14
With results like these, psychiatrists in Europe and America were quick to adopt the new metrazol treatment. Unlike insulin comas, which required special treatment wards and large amounts of scarce and expensive medical and nursing attention, metrazol injections were quick, easy to administer, and cheap. Or usually easy to administer: once patients had had one such treatment, they were often desperate to avoid a second. The British psychiatrist Henry Rollin recalled “the unseemly and tragic farce of an unwilling patient being pursued by a posse of nurses with me, a fully charged syringe in hand, bringing up the rear.” Others reported that patients were so violently resistive they had to be sedated before the seizure could be induced.15
For the professionals administering the treatment, the procedure was deeply upsetting until it became routine. Once the injection had been given, “color drained from the patient’s face, which became stiff and motionless. Onset of seizure was signaled by a cough or a cry, before tonic contractions began … [followed by] a sudden yawning spasm, at which an attendant inserted a gag to avert dislocated jaw.” As the seizure continued, incontinence was common, and the patient then fell into a coma.16 Katzenelbogen, who by then had administered the treatment to hundreds of patients, added that “the patient’s face shows successively flushing, cyanosis, ashy-white color deepening with the period of apnea and then gradually clearing up.”17 But these events, psychiatrists were assured, were usually not remembered by the patients, who were amnesiac for the period of the seizure itself.
What patients usually did remember was the interval between injection and seizure. “In this pre-paroxysmal phase, the most common and striking observation is the patient’s facial expression of fright, of being tortured, of extreme anxiety.” A number of those given the treatment reported that they felt on the brink of dying, and “one patient was sure that embalming fluid was being injected into his veins.” Patients’ accounts of their terror varied, but “they contain nevertheless one common and outstanding feature, namely the feeling of being tortured, and of intense fear of imminent death.” Making matters worse, “If no convulsion takes place, anxiety, restlessness, and general discomfort may continue for hours.” Not to worry, the author of one of these descriptions hastened to reassure his colleagues, “this extremely drastic therapeutic procedure has proven … to be quite safe from danger to life, the rate of fatalities being less than 1 per cent.”18
The sheer violence of the seizures often produced fractures of the long bones or of hip sockets. In 1939, still another complication was reported, soon confirmed by broader studies.19 X-rays of the backs of patients subjected to metrazol seizures revealed that more than 40 percent of them had suffered compression fractures of their spines—a finding that some attempted to minimize by stressing that these spinal fractures were asymptomatic.
Then there were the murmurings, some private, some public, that the extraordinary results claimed by Meduna for his therapy (and Sakel for his) could not be reproduced. Phyllis Greenacre, who had attempted to expose the fallacies of Henry Cotton’s claims, only to be stymied by the resolute refusal of her superior Adolf Meyer to publish her findings, wrote privately from Cornell to her former chief, professing herself deeply worried “by the present therapeutic enthusiasm about the use of insulin, metrazol, and camphor in the treatment not only of schizophrenia, but of almost anything else in the field of psychiatry.” “The present epidemic,” she continued, “seems to be following quite closely in the lines that the Cotton one went;—with similar premature claims of cures; confusion between therapeutic hopes and results;—the utilization of manic-depressive remissions in the interest of ‘proving’ and demonstrating ‘results’ in schizophrenia, etc., etc.” With considerable understatement, she added that “while one does sympathize with the urge to ‘do something,’ it seems that the landslide which is sometimes set in motion has some dangers too.”20
Meyer professed some sympathy with her letter, adding that “I am not at all surprised that … this work of 1925 looms up in the present situation.” But his sympathy did not extend to sharing her critique of the new shock therapies. “I must confess,” he told her, “that in general I have the impression that these non-bloody assaults upon the person have given some very interesting results.” While they were not the complete answer, “where one is almost powerless with regard to the ability to get out of the day-dreaming or scattering conditions” they were certainly an improvement, however much one might regret “that it is so hard for some patients to get en rapport along less aggressive lines.”21
A SHORT TIME AFTER MEDUNA’S FIRST REPORTS on his shock treatment, the Italian psychiatrist Ugo Cerletti was prompted to find an alternative to metrazol by reports of the existential terror metrazol produced in patients. (He had tried Sakel’s insulin coma treatment as early as 1936 and began using metrazol the following year.) Cerletti had been experimenting with electricity and its effects on animals for several years, as part of his research on epilepsy. His trials with dogs, though, at first produced negative results. He had placed one electrode on the head and the other on the anus, and the electric currents that passed through the thoracic cavity stopped the heart and killed half of the dogs he shocked. But a serendipitous visit to the Rome slaughterhouse provided the solution to this problem. Cerletti discovered that pigs destined for slaughter were first stunned by an electric current passed through their brains via electrodes applied to their temples. “Then the butcher, taking advantage of the unconscious state of the animal, gave its neck a deep slash, thus bleeding it to death. I at once saw that the fits were the same as those I had been producing in dogs.” Further animal experiments assured him that the procedure was safe, but still he hesitated “because of the terror with which the notion of subjecting a man to high tension currents was regarded. The specter of the electric chair was in the minds of all.”22 At length, though, Cerletti and his chief assistant, Lucio Bini, decided to experiment on a human subject.
Fortunately, one soon came to hand. On April 10, 1938, the Rome police arrived with a vagrant they had picked up at the Termini train station. Enrico X was confused and incapable of normal communication. The following day, Cerletti and Bini made repeated attempts to induce a grand mal seizure, with the attendant loss of consciousness and violent muscle contractions, but afraid of a possibly fatal outcome, the doses they used failed to produce one, and after the third attempt they gave up. On April 20, they resumed their efforts. This time, Enrico X, treated with increased voltage, responded with a classic seizure, during which Bini recorded that the patient ceased breathing for 105 seconds—what must have seemed an eternity for those clustered around his bedside. “True it is,” Cerletti remarked some years afterward, “that all had their hearts in their mouths and were truly oppressed during the tonic phase with apnea, ashy paleness, and cadaverous facial cyanosis … until at the first deep, stertorous inhalation and the first clonic shudders, the blood ran more freely in the bystanders’ veins as well.”23
Ten minutes after the convulsion, Enrico X began to return to consciousness and, five minutes later, began to speak a few words. “I asked him,” Cerletti recalled, “ ‘What has been happening to you?’ He answered, ‘I don’t know; perhaps I have been asleep.’ … So electroshock was born, for such was the name I forthwith gave it.”24 Cerletti and Bini subsequently gave him another ten shocks, then presented him before the Royal Academy of Medicine of Rome, where for good measure and, to demonstrate the procedure, they gave him another treatment. The demonstration that electroconvulsive therapy (ECT) could return catatonic patients to temporary contact with reality was greeted with astonishment and, when replicated, did much to advance claims about the procedure’s efficacy.
Enrico X was subsequently discharged as cured, and he returned to his family in Milan. Two years later, his wife reported that he had relapsed and been rehospitalized in Milan’s Mombello Psychiatric Hospital. But his case provided Cerletti’s team with a demonstration that convulsions could be induced electrically without causing death, and that after a number of treatments psychiatric symptoms abated. A previously unreachable patient was once more able to communicate. Over the next six months, twenty more patients were treated with an average of more than twenty-one shocks apiece. Only then did Cerletti venture into print. His account of administering the new form of shock therapy remained the standard one throughout the war years.25
In general medical journals, the advent of ECT was greeted with some circumspection. The Lancet expressed concern that there were as yet no adequate data on either efficacy or safety, adding that psychiatrists, who had previously been accused of being “resigned … and torpid,” now seemed to be seized by a kind of “therapeutic fury.” Still, the editorial professed agnosticism about ECT’s worth: “We must not let unconscious associations with what is done periodically in a room in Sing Sing prejudice us against what may turn out to be a valuable way forward.”26 The Journal of the American Medical Association echoed such concerns: “Sufficient data are apparently not available to determine whether irreversible changes are produced in patients after several shocks.” There was obvious concern among “many physicians and physiologists” about whether “the passing of electric current through the brain is a most hazardous procedure.”27 But it swiftly became apparent that most psychiatrists did not share these doubts.
The Second World War contributed to ECT’s adoption in the United States. Renato Almansi, one of Bini’s assistants, was Jewish and fled to the United States in 1939, bringing with him an Italian-designed ECT machine. The following year, Lothar Kalinowsky, a German psychiatrist present at the first ECT trials who was also Jewish and forced into exile, arrived in New York, having previously stopped in Paris and London, where he had introduced colleagues to Cerletti’s technique. Kalinowsky proved the better publicist of the two, and though Almansi has a stronger claim to have been the first to administer ECT in the United States, it was Kalinowsky who would be its most effective promoter throughout his career until his death in 1992.
By October 1941, ECT was being used for a wide spectrum of patients in 42 percent of American mental hospitals.28 ECT induced seizures more reliably than metrazol, and its effects were almost instantaneous, avoiding the long delay and profound terror that followed injection with the drug. It was cheap, easy to administer, and the technique did not take long to learn—a combination of virtues that, when attached to optimistic claims about its therapeutic efficacy, hastened its adoption.29 By the end of the war ECT had largely, though not completely, replaced metrazol as the convulsion therapy of choice.
In some quarters, however, the use of ECT was controversial. In the quarter century after the Second World War, the most prestigious and profitable branches of American psychiatry came to be dominated by psychoanalysts and their supporters. A handful of psychoanalysts provided fanciful psychodynamic accounts of why ECT might work, but most of their number thought the treatment rested on a category mistake. Mental illness was about memories and meanings, and crude jolts of electricity were hardly the way to deal with people’s psychopathology.
The analysts sneered at what one of their number, the Yale psychiatrist Fritz Redlich, called “directive-organic psychiatry.” Those engaging in such practice were, by their lights, an inferior and misguided lot. In the immediate aftermath of the war, the analysts formed a group within the profession to promote their views, and one of their first acts was to publish a report condemning ECT. The Group for the Advancement of Psychiatry (GAP) issued its Report No. 1 on shock therapy in October 1947. It condemned the “promiscuous and indiscriminate use” of ECT, contended that brain damage was the inevitable consequence of its use, and cast doubt on its therapeutic value, save for possibly shortening episodes of depression. Psychiatrists committed to the treatment immediately fought back fiercely. After three years of behind-the-scenes battles, GAP gave in to pressure from the supporters of the treatment and issued a revised report in August 1950. This time GAP report pronounced ECT safe and effective for a wide range of conditions, even when administered on an outpatient basis.30 Freudian analysts’ control over the profession had, it transpired, its limits.
Most psychoanalysts nonetheless remained vigorously opposed to ECT even as professional politics dictated a retreat from expressing their distaste openly, and their status as the elite portion of the psychiatric profession grew steadily more obvious through the 1950s and 1960s. In the future, one important consequence of this situation was that, as the procedure came under attack in the broader culture during the 1960s, prominent psychiatrists either absented themselves from the fray or expressed their own reservations about ECT.