54.

ELECTROCONVULSIVE THERAPY
Kerry L.Bloomhgdale, M . D
1. Has electroconvulsive therapy (ECT) become a less clinically advantageous psychiatric treatment now that such a wide spectrum of psychoactive medications is available? No, but its role has changed over the years. In fact, ECT dominated somatic treatment of major mental illness until the introduction of the phenothiazines in the 1950s. As neuroleptics, antidepressants, and mood stabilizers were made increasingly available, the market share of ECT naturally diminished. However, since the mid 1970s refinement in awareness of when and how to use ECT safely has given it an established and respected place alongside medications in the armamentarium of somatic treatments for mental illness.
2. True or false: ECT is useful primarily in treating the most severe forms of major depressive disorder. False. It is a misconception that ECT is useful only or primarily in severe and psychotic forms of major depressive disorder. It is highly effective not only in these disease entities, but also in moderate and even mild forms of bona fide major depressive disorder. Confusion sometimes arises because, compared with antidepressants alone (without antipsychotic drugs), ECT is much more effective in treating psychotic depression. Furthermore, many clinicians find ECT easier to use than combinations of antipsychotics and antidepressants. Moreover, whenever significant suicidal ideation, intent, or planning occurs, regardless of the presence or absence of psychotic features, clinicians generally choose the most expeditious treatment. Although ECT does not work immediately, it typically works faster than antidepressants.

3. For what psychiatric conditions other than major depressive disorder is ECT useful? Mania: ECT probably is not used more often for this condition because of the potentially rapid effectiveness of mood stabilizers and antipsychotics. However, ECT has a particularly appropriate role in the treatment of mania when (1) the patient is in the first trimester of pregnancy (because of concerns about the teratogenicity of mood stabilizers) or (2) the patient has a history of neuroleptic
malignant syndrome. Schizophrenic decompensation: Transient benefit can be obtained in treating acute forms with many positive symptoms, such as hallucinations, delusions, or floridly bizarre behavior. It may be particularly appropriate in the context of a time-limited stressor, such as loss of a loved one or disruption of a living situation, because of the possible brevity of the schizophrenic patients response to ECT. Lethal catatonia: This is a final common-pathway disorder probably caused by various affective and psychotic conditions and marked by extreme rigidity. Such rigidity may lead to muscle breakdown, acute renal failure, and death. A variety of other conditions, including Parkinsons disease with significant rigidity and neuroleptic malignant syndrome, also can benefit from ECT.
Possible Indicationsfiw ECT

Major depression (unipolar or bipolar) Mania, especially in the context of first-trimesterpregnancy or history of neuroleptic malignant syndrome Schizophrenia, especially in the setting of floridly positive symptoms and/or a time-limited stressor Miscellaneous conditions Lethal catatonia Parkinsons disease Neuroleptic malignant syndrome
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4. Is ECT useful in depressive conditions marked by features of both axis I major depressive disorder and axis I1 personality disorders? To the extent that the clinician can separate the symptoms of major depressive disorder from f a personality disorder, ECT should be useful in treating the depressive symptoms. However, those o such discriminations typically are difficult to make. In practice, the decision of whether to proceed with ECT in the face of this combination often is better made by using your clinical sense of whether an autonomous, somatically treatable depressive syndrome exists than by counting cookbook criteria. Moreover, when considering ECT in patients with symptoms of both major depressive disorder and personality disorder, consider the patients post-treatment subjective sense of well-being as well as the treatment teams objective criteria for response. For instance, even if the major depressive symptoms respond to ECT, the patient may experience almost as much dysphoria after ECT as before because of the relatively refractory problems of personality disorder. 5. Should psychoactivemedications be stopped when ECT is started? The combination of psychoactive drugs with ECT has been the subject of much interest in the recent literature. Whereas there has been no conclusive demonstration that any medication or class of medication consistently adds to the therapeutic effects of ECT, reports have documented patients who seemed to do better clinically with the combination of ECT and a psychoactive medication than with either alone. However, there are reasons to be cautious about the concurrent use of ECT and each class of psychoactive medications. Lithium carbonate, for example, may cause increased neurotoxicity when combined with ECT. Benzodiazepines and anticonvulsant mood-stabilizers, such as carbamazepine and valproic acid, make the elicitation of seizures more difficult. Thus, these medications may be tapered or discontinued (see Question 9). Antidepressants generally lower the seizure threshold, which may increase the duration of seizures or the probability of status epilepticus and spontaneous seizures. Certain antidepressants, such as tricyclics, may increase cardiac irritability when combined with ECT. Antipsychotic medications lower the seizure threshold and, when combined with ECT, may cause greater neurotoxicity.

6. Does ECT cause an excessive cardiovascular response (e.g., hypertension, tachycardia) or a diminished cardiovascular response (e.g., bradycardia)? At different stages in the physiologic response to ECT, the procedure may cause either a heightened or an attenuated cardiovascular reaction. Initially, the ECT stimulus may produce a vagally mediated bradycardia, sometimes associated with a sinus pause. This response is replaced, upon elicitation of the seizure, by a catecholaminergically mediated hypertensive and/or tachycardic reaction. Finally, a compensatory bradycardia may then ensue. Obviously, each of these stages has different treatment implications (see table). If the patient is refractory to the electrical stimulus and does not experience a seizure, he or she will be particularly susceptible to the original sinus pause and/or bradycardia, because the sinus pause or bradycardia will not be counterbalanced by the seizure-induced, catecholaminergically mediated tachycardia.
Cardiovascular Reactions to ECT
STAGE OF ECT CARDIOVASCULAR RESPONSE
~

PRETREATMENT OR ACUTE THERAPY _ _ _ _ _ _ _ _ _____

Electrical stimulus Seizure Postictal

Sinus pause and/or bradycardia Tachycardia and/or hypertension Compensatory bradycardia

Atropine or similar anticholingeric drug Short-acting beta blocker (e.g., esmolol) or alpha and beta blocker (e.g.,labetalol) Atropine or similar anticholinergic drug

7. What are the contraindicationsto ECT? There are no absolute contraindications to ECT.

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Relative Contruindicutions to ECT

SYSTEM

SIGN, FINDING, OR SYMPTOM

POSSIBLE INTERVENTIONS FOR SAFE AND EFFECTIVE ECT

Cardiovascular Ischemic heart disease Tachycardia Hypertension Ventricular ectopy

Pulmonary

Orthopedic Neurologic

Gastroesophageal reflux, surgical history, gastroparesis-all of which may predispose to aspiration Recent fracture, particularly Use of increased dose of muscle relaxant (e.g., succinyl vertebral compression choline) andor curare Space-occupyingintracranial Neurologic and/or neurosurgical consultation indicating that intracranial pressure not likely to rise to dangerous lesion (see Question 8) level during ECT Consider lowering dose of anticonvulsant drug in consulSeizure disorders (see Question 9) tation with neurologist

Reduction in anticipated oxygen consumption by heart (e.g., with preadministration of beta blocker) Reduction of heart rate (e.g., with preadministration of beta blocker) Reduction of blood pressure before and/or during ECT Administration before and/or just after induced seizure of antiarrhythmic agents. Avoid IV lidocaine if possible before seizure because it may raise seizure threshold In addition to standard NPO precaution, preadministration of metoclopramide; intraprocedural pressure on cricoid cartilage; intubation

8. Is a space-occupyingintracranial lesion a contraindication to ECT? Yes, but only relatively, not absolutely. At one time they were considered absolute contraindications, and clinicians avoided ECT because of concern over the sometimes already elevated intracranial pressure. They anticipated that the pressure would go even higher with ECT-induced seizures, putting the patient at risk of complications such as herniation. However, experience has dictated that such lesions can be compatible with safe and effective ECT; clinicians have administered ECT without complications to patients in whom imaging studies subsequently revealed pre-existing space-occupying intracranial lesions. If these lesions are discovered before ECT in patients who are candidates for the procedure (e.g., after work-up for a localizing finding on neurologic examination for ECT), appropriate consultation should be sought. If there is no evidence of a mass effect, such as papilledema on funduscopic examination, or edema and midline shift on imaging studies, and if the lesion appears relatively small, it may be possible to administer ECT safely. In this instance the potential dangers must be balanced carefully against the potential benefits of ECT. 9. Is a patient taking anticonvulsants for seizure disorder a viable candidate for ECT? Yes, in many cases. Consult with a neurologist. The seizure disorder itself is not an absolute contraindication to ECT, although careful consideration should be given to the possibilities that ECT may destabilize an epileptic condition or precipitate status epilepticus. Conversely, of course, ECT may make a patient with epilepsy temporarily more refractory to spontaneous seizures. Anticonvulsants typically do not interfere with ECT, although they may require higher electrical dosing. If it is impossible to elicit adequate seizures in patients taking anticonvulsants for seizure disorder, consult with the patients treating neurologist about cautious titration downward of the anticonvulsant dose. If the patient is taking anticonvulsants purely for their mood-stabilizing effects, the decision to taper them before ECT is less weighty. In addition, before proceeding with ECT, consider tapering and discontinuing drugs such as benzodiazepines that are not used for anticonvulsant purposes, but raise the seizure threshold.
10. Does ECT cause permanent structural or functional brain damage? No compelling evidence indicates that ECT causes structural brain damage. When animals are given electroconvulsive shock usmg parameters analogous to those used in ECT, histopathologic

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studies reveal no structural neuronal damage. Imaging studies before and after patients have received ECT also reveal no structural brain damage. Moreover, autopsies of patients who received ECT do not suggest a pattern of CNS damage caused by ECT. It is more difficult to rule out permanentfunctional CNS damage resulting from ECT. In fact, limited numbers of patients note cognitive changes persisting for extended periods. Studies based on neuropsychological testing of ECT patients show that interference with the ability to form new memories (anterograde amnesia) can persist for at least 3 months after a course of ECT. Patients have difficulty laying down permanent memories of some events that take place just before, during, and immediately after a course of ECT. Neuropsychologically documented retrograde amnesia for events that took place more than several weeks before the start of ECT is rare. In general, then, it is difficult to document ECT interference with memory for events that take place more than a few months before or more than a few months after a course of ECT.

11. Is the suprathreshold approach to dosing in ECT the best way to administer the treatment? Suprathreshold ECT is defined as the use of electrical charge or energy in excess of the amount minimally needed to elicit a seizure. The parameters for suprathreshold ECT are established by first titrating upward to the minimal electrical charge or energy necessary to elicit a seizure; for subsequent seizures that amount is multiplied by a factor greater than 1, such as 1.5. The universal appropriateness of suprathreshold ECT is not fully clear. Clinical research seems to indicate that higher-than-necessary quantities of charge or energy are often more effective than threshold amounts, particularly in unilateral ECT. It has not yet been firmly established whether the cognitive side effects of suprathreshold ECT are greater than those of threshold ECT. 12. Should electrode placement in ECT be unilateral or bilateral? The choice of which electrode placement to use for ECT is controversial. In unilateral ECT, one electrode is placed midline and the other is placed temporally over the nondominant hemisphere (generally presumed to be the right). In bilateral ECT, both electrodes are placed temporally, one over each hemisphere. Bilateral ECT often seems to work more effectively and rapidly than unilateral ECT, but it also may produce more cognitive side effects. Some practitioners believe that bilateral ECT is universally advantageous, if cognitive impairment does not preclude its use. Other clinicians believe that it is appropriate in many cases to initiate ECT treatment with a unilateral approach and then switch to bilateral ECT in patients with poor or sluggish clinical response. 13. What is the optimal number of treatments in a course of ECT? There is no magic number of ECT administrations per course of treatment. In treating patients who manifest a prompt and full response to ECT for major depressive disorder, experienced practitioners may administer 5-10 treatments, generally at the rate of 3 per week. If patients with major depressive disorder do not respond promptly or adequately to ECT, clinicians may give 10-20 treatments, assuming that each treatment results in an adequate seizure. However, in giving such an extended course of treatment, the ECT practitioner also is likely to manipulate key variables such as electrode placement or amount of electrical charge or energy. If the seizure durations are inadequate, the clinician administering the ECT should: ( I ) if possible, make sure that the patient is off all drugs that could raise the seizure threshold; (2) adjust the dose or type of anesthetic agent; (3) hyperventilate the patient; andlor (4) use agents such as intravenous caffeine to lower the seizure threshold. 14. How does the clinician know that a patient is responding to ECT? Generally, objective signs of improvement precede subjective signs. For example, if the patient is treated for major depressive order, other inpatients on the psychiatric unit or, if on an outpatient basis, the family may report that the patient acts more spontaneously, eats more, or sleeps better before doctors or nursing staff observe changes. Clinical staff then may notice similar neurovegetative changes. Finally, the patient may note improved self-esteem, hopefulness, or physical well-being.

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Occasionally, the clinician encounters a difficult and awkward period in his or her alliance with the patient, perhaps between approximately the third and seventh treatments, in which objective signs of improvement are relatively clearcut, but the patient is discouraged about the lack of perceived improvement and wants to stop ECT. At such a time, the ECT practitioners alliance with the patients family or friends may prove critical in ensuring the continuation of treatment.

15. Is the electroencephalograph(EEG) the best way to assess the duration of a seizure in ECT? If accessible, an EEG printout readily provides a way to quantify the duration of the seizure. However, a two-lead EEG produced by an ECT apparatus may be difficult to interpret, especially in documenting an exact seizure duration. Accordingly, the EEG printout should be used in conjunction with visual monitoring of seizure duration, especially if the cuff method is used. This technique consists of inflating a blood pressure cuff to a greater than systolic pressure around an extremity before infusion of the muscle relaxant, to prevent the extremity from being paralyzed during the seizure. The visually monitored duration of the convulsion in the extremity generally provides an accurate measure of seizure length. Another way to corroborate seizure duration is to record the rate of change in heart rate. If IV beta blockers are not used, the heart rate will peak in approximate conjunction with the visually and EEG-monitored durations of the seizure.
16. What are continuation ECT and maintenance ECT? Continuation ECT is administered after a successful, acute course of ECT, but during the interval when the patient would still be suffering from the index episode of illness if the treatment had been unsuccessful. Such a period may be presumed to last for at least several months. Maintenance ECT is administered after the patient is no longer suffering from the underlying episode of illness originally treated acutely with ECT. Continuation and maintenance ECT treatments usually are given less frequently than ECT to treat an acute episode of illness. Preferred schedules of maintenance ECT vary considerably: some experienced clinicians use a fixed schedule, such as weekly, then biweekly, then monthly, assuming that the patient remains symptom-free; others plan follow-up ECT on a less frequent basis, but increase the frequency if symptoms recur.
17. Are continuation and maintenance ECT always indicated when a patient responds acutely to ECT? They are only one follow-up treatment option for the patient who responds acutely to ECT. If the patient was treated for major depressive disorder, antidepressant or mood-stabilizing medications typically are used for follow-up. Some form of supportive or insight-oriented psychotherapy usually should accompany follow-up ECT or medications. The decision about the form of follow-up treatment after a successful acute course of ECT is complicated. It should be made on the basis of anticipated safety and efficacy as well as patient preference. One strategy for patients treated effectively with ECT for an episode of major depressive disorder is to consider medication follow-up after the first episode of illness; if the patient breaks through such follow-up, ECT may be offered again. Follow-up ECT is instituted if the breakthrough, relapse, or recurrence is treated successfully with further acute ECT.

18. Is ECT too complicated from a medical standpoint to be done on an outpatient basis? Except in limited cases, ECT can be done safely and effectively on an outpatient basis. In fact, outpatient ECT may be preferable to inpatient ECT, because the patient is able to remain in his or her home environment and the costs are lower. Obviously, the severity of a patients psychiatric condition may preclude outpatient ECT. Note that the periods of greatest physical risk from ECT are usually the treatment and posttreatment recovery phases. Assuming that the patient is carefully monitored during these phases, outpatient ECT may be considered even for mild-to-moderate medical risk factors. The clinician should give specified pre- and post-treatment suggestions to the patient and responsible family members, such as avoiding oral ingestion before ECT and refraining from activities such as driving, operating machinery, and making major decisions.

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19. True or false: The patients informed consent is unnecessary because most candidates for ECT suffer from diminished cognitive acuity. False! Although the illnesses that respond to ECT commonly affect mental status, it is essential, for legal and ethical reasons, that the patient understand the risks and benefits of ECT before agreeing to the procedure. If the patient is unable to give such informed consent, the clinician should be sure to satisfy the states legal conditions for alternative means of obtaining permission (see Question 20).
20. If a patient is truly unable to give informed consent for ECT, should you obtain the written informed consent of the patients nearest relative? Not necessarily. Inexperienced ECT practitioners may believe that the consent of the nearest relative is automatically an acceptable alternative to informed consent of an incompetent patient. However, the state in which ECT is to be administered may require court appointment of a guardian (who in fact may be the nearest relative) to make treatment decisions for the patient who is unable to do so.

21. Should transcranial magnetic stimulation (TMS), which has few side effects, be used instead of ECT? No. TMS, an electromagnetic technique that stimulates certain areas of the brain in a more specifically targeted fashion than ECT, may be effective for certain psychiatric disorders, including depression. However, its definitive efficacy for psychiatric disorders is still unproven. It remains a significant investigational technique which may help to shed light on important questions about the etiology of depression and the mechanism of action of such treatments as ECT. TMS ultimately may prove to be a useful treatment for psychiatric disorders such as major depression, because TMS does not require general anesthesia and is not intended to induce seizures (although seizures can be a side effect).
BIBLIOGRAPHY
1, American Psychiatric Association: The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. Task Force Report. Washington DC, American Psychiatric Association, 1990. 2. Beyer J, Weiner R, Glenn M: Electroconvulsive Therapy: A Programmed Text. 2nd ed. Washington DC, American Psychiatric Association, 1998. 3. Coffey C (ed): The Clinical Science of Electroconvulsive Therapy. Washington DC, American Psychiatric Association, 1993. 4. Devanand D, Lisanby S, Nobler M, et al: The relative efficiency of altering pulse frequency or train duration when determining seizure threshold. J ECT 14:227-235, 1998. 5. Kellner C, Bourgon L: Combining ECT and antidepressants: Time to reassess. J ECT 14:6547, 1998. 6. Kellner C, Pritchett J, Beale M, et al: Handbook of ECT. Washington DC, American Psychiatric Association, 1998. 7. Post R, Kimbrell T, McCann U, et al: Repetitive transcranial magnetic stimulation as a neuropsychiatric tool: Present status and future potential. J ECT 15:39-59, 1999. 8. Royal College of Psychiatrists: The ECT Handbook. London, Royal College of Psychiatrists, 1995. 9. Sackeim H: The anticonvulsant hypothesis of the mechanisms of action of ECT: Current status. J ECT 15:s-26, 1999. 10. Sackeim H, Prudic J, Devanand D, et al: Effects of stimulus intensity and electrode placement on the effcacy and cognitive effects of electroconvulsive therapy. New Engl J Med 3282339-846, 1993.