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Indications for electroconvulsive therapy include major depression, and the positive predictors of response are still the classic neurovegetative signs non-chronic depression. For people with this kind of symptom profile, the response rate to electroconvulsive therapy is extremely high. It’s difficult to think of a patient in the last two decades who has not had a good response to ECT in the face of this profile. This is probably one of those rare situations in medicine where a given treatment is approaching 100% effective for a given syndrome. Our precision breaks down a bit when we get into the more diagnostically ambiguous spectrum of symptoms in which we see an overlap between depressive disorders and PTSD or character disorders for an atypical pattern of depressive symptoms, with hypersomnia and increased appetite and so forth. The response rates are quite so predictable, certainly people with very ambiguous symptoms can have a sparkling response to ECT and if anything, we have learned humility in the face of this diagnostic inquisition. We find that patients that we never would have thought would have a good response to ECT sometimes have a electroconvulsive therapy, electroshock treatment, shock treatment, electric shock treatment, electro shock treatment
I would like to point out, on the second page about half way down, the natural history of major depression is really quite important to our decision-making. The most important statistic here is the last one. The 36% mortality at 31 months, half of suicide and half of medical causes. These data were derived during the pre-pharmacologic era but it’s important to keep in mind that if you don’t effectively treat major depression, you are dealing with a disorder that has a higher mortality than most forms of neoplastic disease. All of our decision-making around ECT has to be framed in this basic reality, that we are dealing with a lethal illness if we do not effectively treat it. Although half the deaths are suicide, the cardiovascular deaths also
The issue of the use of ECT in clinical practice and specifically when you judge a patient to be resistant to pharmacologic management. I think this is a situation where you get a different answer from every clinician and you will also get a different answer from every patient. It’s a highly individual thing. The troublesome thing in our practice is that we see too many patients who are manifested herb psychopharmacologists who persist beyond where it’s in the best interests of the patient to be referred to ETC. In some ways I think that the best psychopharmacologists are the ones who have the hardest time shifting gears and acknowledging that pharmacologic treatment is not working. And I feel comfortable saying this because I’ve made this mistake myself. Wherein as a psychopharmacologist I have persisted too long. Every year we see a half dozen people who come in after several years of superb pharmacologic care but they’ve lost their job, they’ve lost their finances, they’ve often lost their family, they’ve lost their social contacts and
Moving on to the risk factors. The central point you should understand, and this is really well accepted in academic psychiatry, is that there are no absolutely contraindications for ETC. There are simply relative risk factors. The most important relative risk factors are for cardiovascular and the commonest ones are listed here. Coronary artery disease is clearly the most common of these. These factors can almost always be safely managed in the context of ETC. And I’ll come back to how we do that. What’s important for you as a clinician is to not be scared away by these. Ten or twenty
There are several risk factors that deserve special mention. Digitalis toxicity results in severe bradycardia after ETC. Aortic stenosis, especially critical aortic stenosis, creates a very high intraventricular pressure during systole. Theophylline is associated with ongoing status epilepticus after ECT and therefore should be discontinued. It lowers the seizure threshold quite dramatically. Increased intracranial pressure is of concern because of the
In our ECT suite and unlike most general hospitals we do ECT in the main recovery room. The reason is that it is a safe, well-equipped, well-staffed area that is usually quiet and underutilized at 8 o’clock in the morning before the surgical cases come in. But most important here, this fellow in blue, our anesthesiologist. Consistency of anesthesiology staffing is absolutely important. This used to be considered a trivial exercise in general anesthesia. Now most hospitals consider it a special exercise and a rather challenging one, because of the unprecedented cardiovascular shifts that occur during the grand mal seizure and because of some of the unusual medication issues that come up around ETC. All of our residents are required to spend a month doing this treatment. We feel that these people are likely to encounter this in practice and we hope that by taking this as a policy we will prevent
Short acting injectable beta blockers lower pressure. This is low dose esmolol and low dose labetalol and the pressure is about half of the untreated control. With high dose esmolol and high dose labetalol the pressure is actually lower than pretreatment. So they are very effective at controlling pressure and also these drugs are very effective at controlling rate. Here’s low dose esmolol and low dose labetalol, high dose esmolol and high dose labetalol. Esmolol appears to be a better drug for controlling rate. I just want you to be aware that we have some terrific drugs to control the sympathetic stress that people experience during ETC. Any patient with any cardiovascular diagnosis whatsoever is beta blocked aggressively in our
Moving on to memory deficit, the most important determinate is the laterality of treatment. These are memory deficits following ECT and both the non-verbal and verbal memory, the amount of deficit that people experience is much greater from before ECT to after ETC. There’s a big drop in memory function with bilateral ETC. For both non-verbal and verbal. With unilateral ECT the drop in memory function is much less and with verbal it barely reaches statistical significance. So unilateral ECT is still the best way to address the issue of cognitive deficit. It sometime produces, as you know, severe memory disturbance and sometimes severe confusion and consequently we have all but abandoned the use of bilateral ECT in
Our own data show with the decrease in the Hamilton Depression Rating Scale is exactly the same for unilateral and bilateral ETC. They both drop 17 points, which was a totally controlled study which we did here some years ago, and this confirmed very much that unilateral is the appropriate way to go. The factors associated with ineffective unilateral ECT are listed here. _ spaced electrodes, benzodiazepines on board, structural brain lesions such as stroke or maybe a malformation, and the use of threshold stimulus intensity. You have to get generously above the seizure threshold in order to get clear of the efficacy problems that have been reported.
The scene of the crime is unknown, but I think that it is in the MDA receptor, the GABA receptor or both and particularly it is tempting to hypothesize that the GABA receptor may be the locus of ECT’s effectiveness. Perhaps we do stabilize in pathways, such as GABA by forcing the brain to shut off the seizure. This then drives chloride into the cell and stabilizes the electrochemical polarity of the cell membrane. Here’s another diagram of the chloride channel with the GABA receptor here. This is, at this point, I think the most attractive and popular hypothesis as to how