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Biological Perspectives Electroconvulsive Therapy

2009; Wiley; Volume: 45; Issue: 1 Linguagem: Inglês

10.1111/j.1744-6163.2009.00203.x

1744-6163

Norman L. Keltner, Deborah J. Boschini,

Neurology and Historical Studies

Perhaps the best example of science purposely driving psychiatric treatment can be found in the development of electroconvulsive therapy (ECT). Thinkers from at least the 17th century suggested the potential therapeutic benefits of induced seizures. Although known to be erroneous today, multiple reports suggested the mutual exclusivity of schizophrenia and epilepsy. Based on this faulty thinking, the hunt began for a seizure-inducing mechanism in order to introduce iatrogenic "epilepsy" into those with severe mental health problems. If seizures and mental illness could not coexist, then those demons of thought would be exorcised by an externally imposed ictal state. The various intermediary steps between hypothesis development and Cerletti and Bini's 1938 discovery of electrical-caused seizures (Lebensohn, 1999) will not be reviewed here, although elegant historical descriptions can be found elsewhere. This brief contribution proposes to simply provide an update on this much-maligned procedure and herald its survival despite suffering malicious public relations attacks over the years. As noted, the discovery of electrical-induced seizures exemplifies psychiatric science at its best. Theory development drove the search engine to find a mechanism for treating schizophrenia. The irony, though, overwhelms the result: epilepsy and schizophrenia are not mutually exclusive brain phenomena after all, and it is not schizophrenia that is best treated by ECT, but rather depression. Yet when held against the serendipitous discovery of lithium, antipsychotics, and antidepressants, one must give a nod to the early somatic therapists. McDonald and Walter (2001) in a review of American movies touching on ECT found an overwhelmingly negative depiction. Pejorative views of ECT were perhaps best captured by Jack Nicholson's famous portrayal of a man subjected to the dark intentions of psychiatric professionals via ECT and psychosurgery. In One Flew Over the Cuckoo's Nest, the American public was propagandized into believing ECT to be barbaric (McFarquhar & Thompson, 2008), punitive, and void of therapeutic value (see Real Reels this issue). While the procedure as portrayed would have been basically accurate a decade sooner, by 1975 when the film was released, the grand mal convulsions produced by the treatment had been subdued with a dose of intravenous succinylcholine. Of course, the American public did not know this, so the film and the book of the same name almost eliminated the use of ECT. Case no. 1: "I am a university professor, aged 56." This beginning to an anonymous story, tells a first hand account of the benefits of ECT. The university professor describes his misery and the near breakup of his family related to bipolar disorder. He recounts the many medications he was prescribed, including lithium, SSRIs, anticonvulsants, and others which were swallowed to no avail. Finally, and it is remarkable that it is always "finally," his psychiatrist suggested ECT. After another year of misery to "think it over" he was tried on a course. He improved and remains improved, is medication free, and his marriage was restored. He is an ECT advocate. (Anonymous, 2008). Today's use of ECT is precise and safe with about 100,000 Americans receiving ECT each year (Smith, 2001). Treatments are done in a hospital setting, typically with a psychiatrist, anesthesiologist/nurse anesthetist, and nurse present. The patient is provided with a barbiturate to induce sleep, then a depolarizing muscle relaxant such as succinylcholine (Anectine) to prevent physical seizures. Typically, an anticholinergic to prevent aspiration of secretions is given and perhaps a beta blocker to contain sympathetic stimulation. Two electrodes are strapped to the patient's head and a very brief burst of electricity passes between the electrodes bidirectionally. This brief burst causes the seizure and the seizure typically causes symptom remission. The patient, unlike years ago, has both brain (electroencephalogram) and cardiovascular monitors connected during and after the procedure. The brain monitoring enhances the prospect of a desired seizure length of about 30 sec. Seizures lasting less than 20 sec typically warrant another attempt. Most patients receive a treatment two to three times per week until about a dozen or so sessions have occurred. Interestingly, as the treatment regimen advances, the seizure threshold increases, creating the paradoxical notion that ECT is an anticonvulsant of sorts. Posttreatment memory problems are common, as well as generalized confusion after awaking from the treatment. Controversy exists as to whether unilateral electrode placement is as efficacious as bilateral placement or whether memory is permanently altered or altered only for the intratreatment period. Both views have equally staunch proponents. ECT is the most effective antidepressant remedy available (Scott, 2008). That said, because of the perception of the procedure, it is considered a treatment of last resort by most clinicians and patients. But if the oft-quoted statistic that antidepressant medications do not provide relief for up to 50% of individuals taking them is accurate, then ECT is a remarkable intervention (Miller, 2007). Up to 90% of individuals finally agreeing to submit to ECT have their depression lifted (Sadock & Sadock, 2003). However, this 90% statistic requires further interpretation because this effectiveness outcome is based on individuals who had failed several antidepressant medications (i.e., the most depressed of the depressed). ECT is seldom attempted until almost all other avenues have been exhausted. Stated another way the question becomes: "How many different antidepressants would you try before submitting to a muscle-paralyzing agent followed by an electrically induced seizure, which you are told will produce amnesia and confusion?" Well, as blunt as the question is, it captures the dilemma facing patients, families, and clinicians. The predictable answer is: "Just about every antidepressant on the market, including those MAO . . . whatever they are, that are warned against on the back of about every medicinal product I pick up in the drugstore." This reality-based dialogue is offered to emphasize the remarkable effectiveness of ECT; again, up to 90% of desperately ill individuals report relief. This level of efficacy may warrant a lowering of the prevailing threshold for usage. The correct response to the oft-asked query of how ECT works is, simply, no one knows for sure. Miller (2007) and others (Bezchilibnyk-Butler & Jeffries, 2004; Esel et al., 2008; Pierce, Flynn, Caudle, & Garcia, 2008; Sadock & Sadock, 2003) provide a summary of the competing explanations: The slowing of brain waves as the treatment progresses. This might be likened to shutting off a computer to reboot the system. The rebalancing of neurotransmitters: second messenger system changes, e.g., G protein coupling changes, changes in adenylyl cylase and phospholipase C (i.e., the second messengers), and regulation of calcium entry into neurons; downregulation of beta-adrenergic postsynaptic receptors; possible changes in serotonergic receptors; and changes in dopaminergic, GABAergic, and cholinergic systems. The rebalancing of hormones: corticotropin-releasing hormone; adrenocorticotropic hormone; thyrotropin-releasing hormone; prolactin; and vasopressin. The brain-strengthening effect of induced seizures, e.g., increased neuronal sprouting, more brain-derived neurotrophic factor. This might be compared to going to the weight room. Just as weak muscles can be strengthened by lifting heavy weights, perhaps the brain, in its fight against depression or psychosis, is strengthened by induced seizures. Miller concludes by suggesting ECT may work by a variety of mechanisms with one, some, or all benefiting any particular individual. The seizure is induced by electricity flowing between two electrodes, typically placed on each side of the head. The initial electrical dosage is about 50–70 mA (for comparison, defibrillators are operated at about 6 A). This electrical charge disrupts the asynchronous firing of neurons and causes a synchronous firing that leads to a seizure (Sadock & Sadock, 2003). The brain fights to restore itself, and typically within 30 min to an hour postseizure, the patient returns to near his pretreatment cognitive status. Electrode placement, as suggested above, can vary, and each method has support. Bilateral positioning can include bitemporal and bifrontal placements. Unilateral placement—that is, both electrodes over the same nondominant hemisphere—is also utilized and linked to lower levels of cognitive turmoil posttreatment. Although a number of issues surround ECT, perhaps the two most significant are the memory problems associated with treatment and the transient nature of its therapeutic outcome. As anyone who has worked with ECT for any length of time can attest, both retrograde (distant memory) and anterograde (new memory) are affected. While retrograde memory typically returns, for some patients peritreatment memory does not return completely. Historically, the extent of memory loss may have been overestimated by some, while the denial of any memory loss emerged as an overzealous reaction by others. Certainly, preexisting cognitive problems increase the risk of treatment-related memory issues (Pierce et al., 2008). The second major issue associated with this treatment is the transient nature of symptom reduction. When the treatment stops, symptoms return for up to 50% of patients, oftentimes within weeks (Lisanby et al., 2008). Given our inability to explain how the treatment works, our inability to explain why it stops working is understandable. Approaches to remedy this significant problem include prescription of antidepressants posttreatment and continuation ECT. Continuation ECT features "booster" treatments given at scheduled intervals posttreatment to prevent decompensation. Gagne, Furman, Carpenter, and Price (2000) found that continuation ECT, when supported by antidepressant treatment, can reduce relapse into depression. Other issues include risk of death during treatment (equivalent to risk of death from general anesthesia), hypertension, arrhythmias, hyponatremia, and migraine headaches. ECT does not cause brain damage. The primary indication for ECT is intractable depression (see Table 1). Both major depression and bipolar depression respond to ECT and do so faster than to conventional treatment. Psychotic depressions particularly benefit from ECT (Sadock & Sadock, 2003). Other disorders responsive to ECT include mania, catatonic and positive schizophrenia, postpartum psychosis, and various movement disorders. Case no. 2: A 23-year-old woman, 1 month postpartum, arrived at a psychiatric hospital in a state of complete catatonia. After a day of careful observation, the woman was given a single treatment of ECT. Within hours of the treatment, she was talking, eating, and providing other self-care activities. After a few days, she was discharged from the hospital. In the United States, nearly 15 million adults experience major depression each year, and depression has become the leading cause of disability for adults ages 15–44 years (National Institute of Mental Health, 2008). Depression decreases quality of life, while increasing morbidity and mortality. The American Psychiatric Association's (APA, 2001) ECT Task Force Report recognizes ECT as a potentially life-saving treatment for individuals with severe depression (Lisanby, 2007). The APA endorses the use of ECT for severely depressed patients who are unable to tolerate or do not respond to antidepressants, especially in situations in which a rapid therapeutic effect is required (Lisanby, 2007). Continuation ECT is recommended by the APA guidelines to prevent relapse. Although the APA's guidelines are frequently cited, the use of ECT remains mostly unmonitored, unregulated, and unreported. There is no board certification available, and many psychiatrists report receiving little or no training during residency (Fink, 2007). Some states have drafted their own practice guidelines; only a handful of states, including Texas and California, require that facilities report the frequency, circumstances, complications, and therapeutic outcomes of ECT use. These factors combine to create an information void, where neither ECT opponents nor advocates have reliable, current national statistics on which to base their positions. This lack of data, combined with lingering outdated perceptions of ECT, is a barrier to more widespread acceptance of this valuable treatment option. Rates of ECT use appear to be higher in the treatment of patients who are female, affluent, older, and Caucasian. Teaching hospitals and private health organizations are more likely to offer ECT than public facilities (Sackeim, Devanand, & Nobler, 1995). Each ECT session costs approximately $800 to $1,000 (Lisanby, 2007), resulting in a cost of $6,400 to $8,000 for eight sessions. However, most insurance plans that provide coverage for mental health services reimburse at least a portion of this fee, as does Medicare. Just as ECT continues to be a safe and effective treatment approach for individuals refractory to other treatments, it also continues to be a treatment of last resort. Until psychiatric professionals develop a more complete understanding of ECT, patients and families are likely to continue to resist ECT as a viable treatment alternative. Well-informed clinicians should be comfortable presenting ECT as a safe, effective, and potentially life-saving therapy for patients who desperately need relief.