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SEIZING UPON ECT'S OPPORTUNITIES

March 1, 2006
by STEPHEN M. SOREFF, MD and PATRICIA H. BAZEMORE, MD
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Despite its reputation, ECT is still being used today—and the science behind it is stimulating similar techniques

In Europe and America during the first half of the 20th century, before the dawn of the psychopharmacologic revolution, thousands of patients languished in hundreds of psychiatric hospitals. Physicians and scientists desperately sought effective treatments.

Their search resulted in four physiologic shock therapies:

  • malaria-induced fever (in 1917)

  • insulin coma and convulsions (1927) (See Behavioral Healthcare, February 2006, p. 9)

  • metrazol convulsions (1934)

  • electric shock therapy (EST) (1938), currently known as electroconvulsive therapy (ECT)

Physicians also tried one surgical approach, prefrontal lobotomy (1936) (See Behavioral Health Management, May/June 2004, p. 14). Of these five therapies, only ECT remains in use today.

This article explores ECT's discovery, mechanism of action, and controversies. We also examine current indications and administration protocols. Finally, we identify ECT's place among modern psychiatric treatments.

ECT's Discovery

The road to ECT began with the work of Ladislaus Joseph von Meduna, the superintendent of Budapest's Royal State Mental Hospital in 1933. He observed, based on tissue samples, that patients with epilepsy had thickened glial tissue in the cortex in comparison with patients with schizophrenia.1 He concluded that there was a “biological antagonism” between epilepsy and schizophrenia and that seizures might be used to cure schizophrenia.2 With this in mind, Meduna set out to find a chemical method of inducing seizures, first using camphor and later metrazol. Meduna reported improvement in 50% of patients who received metrazol at seizure-producing doses.

Ugo Cerletti, a neurologist at the Neuropsychiatric Clinic in Genoa, believed that metrazol's side effects (including severe vomiting and confusion) were unacceptable despite its efficacy. Cerletti thought that electricity might be a more consistent stimulus than metrazol for seizure induction, and he began its use on a trial basis. Although he had some success using electrical current for seizure induction in dogs, he sought another animal model before using it on humans.

Cerletti serendipitously discovered that slaughterhouses in Rome employed electricity to convulse pigs into submission before killing them. Cerletti started electrically inducing seizures in pigs and noted that the swine recovered from the convulsions without obvious sequelae.3

Having perfected the technique, Cerletti and his colleague Lucino Bini were the first to actually administer ECT to a human. The first subject was a man in his 40s presumed to have schizophrenia. This individual had been found speaking gibberish upon his arrival in Rome from Milan by train, and Rome's police commissioner referred him to Cerletti and Bini.

4 As a result of this single treatment, the patient became more coherent, to the satisfaction of the two researchers.



Cerletti (image courtesy of the american psychiatric association library and archives)


Cerletti

(Image courtesy of the American Psychiatric Association Library and Archives)


How ECT Works

Although ECT's efficacy for treating severe depression, catatonia, mania, and some forms of schizophrenia has been documented in many clinical studies, its mechanism of action remains elusive.5 Frequent psychological and physiologic explanations advanced over the years have failed to produce a definitive consensus as to how ECT works.

Among the early psychological theories is the hypothesis that ECT is perceived as punishment for personal guilt. ECT, therefore, addressed guilt in two ways: (1) It induced amnesia surrounding the event that triggered the depression, and (2) the actual fear of ECT as a form of punishment was a way of addressing the guilt. Unsurprisingly, this theory has not been substantiated.6

Physiologic mechanisms of action suggested over the years have included neurotransmitter, neurologic, endocrine, vascular, genetic, and electrical explanations.7,8 Some have reported alterations in serotonergic transmission as a result of ECT.9 Others have reported generations of new neurons and endocrine changes following treatment.9 Fink argues that the lack of the moodaltering peptide antidepressin is the cause of depression, and that ECT stimulates its production.10

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