When is ECT indicated in psychiatric disorders?

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When is ECT indicated in psychiatric disorders?

Although numerous psychotropic agents in multiple classes have emerged over the past few decades, electroconvulsive therapy (ECT) still represents an essential treatment in modern psychiatry. Its record of safety and efficacy is virtually unparalleled vis a vis pharmacological agents.

Advances in anesthetic technique, electrode placement, and electrical stimulus dosing allow ECT to be administered safely to even the most medically ill patients without excessive effects on memory, with excellent clinical benefits (Box 1). A typical course of ECT consists of 8 to 10 treatments administered 2 to 3 times per week.

The medical complications of ECT are rare, and good pre-treatment medical assessment helps ensure its safety.1 Include at minimum a medical history, physical exam, and basic laboratory tests. Specialist consultations are sometimes necessary when patients have comorbid neurologic or cardiologic illnesses (Box 2).

The most bothersome side effect of ECT is memory disturbance. This takes 3 forms: post-treatment confusion and anterograde or retrograde amnesia (Box 3). Less serious side effects include headaches, muscle soreness, and nausea. These are easily treated symptomatically with analgesics or antiemetics.

Box 1

THE TECHNICAL FACTORS OF ECT AFFECTING EFFICACY AND SIDE EFFECTS

Electroconvulsive therapy (ECT) has been in use since 1938.6 It consists of the application of an electric current to the head, which causes a seizure.

Modern ECT technique involves the use of general anesthesia, usually with a barbiturate anesthetic such as methohexital, and muscular paralysis, usually with the depolarizing neuromuscular blocking agent succinylcholine. Continuous oxygenation with positive pressure ventilation, measuring of blood pressure, and monitoring with an electrocardiogram and pulse oximetry make the procedure exceedingly safe.

Efficacy and cognitive side effects may be affected by how ECT is administered. The two treatment electrodes that are placed on the head can be located on either side of the temporal fossa (the bitemporal position), on either side of the forehead (the bifrontal position), or on the right temporal fossa and just to the right of the vertex of the skull (the d’Elia unilateral position). Generally, unilateral electrode placement causes less memory impairment but has been believed to be less effective than bilateral electrode positions.6

Another technical factor receiving attention from researchers is the amount of electricity, or electrical dose, used to elicit the seizure. Generally, especially for unilateral ECT, high electrical doses are needed to attain acceptable treatment efficacy. In fact, one study indicates that if 6 times the minimum electrical seizure threshold is used for unilateral ECT, efficacy for depression is equal to that of bilateral ECT with less memory disturbance.23

Finally, treatment frequency affects ECT outcome: twice-weekly treatment schedules are associated with less memory disturbance—and only slightly slower clinical response—than thrice-weekly schedules.24

The most common indication for ECT is major depression. Using modern diagnostic criteria, most depressed patients respond to ECT. Some features that presage a particularly robust response include psychomotor retardation, psychosis, catatonia, and advanced age. Patients who have medication-resistant depression may require particularly potent forms of treatment, such as bilateral electrode placement and/or higher than usual electrical doses.

Patients with mania respond particularly well to ECT but, because of excellent responses with modern pharmacological agents, rarely need it. For patients with mania who are agitated and noncompliant, ECT may represent a life-saving option for stabilizing an acute episode. Finally, ECT may help yield stability for an acute exacerbation of schizophrenia or may extend the benefits of antipsychotic medication for those with chronic schizophrenia, in which case continuation of ECT is usually advisable.

When ECT is indicated for depression

Typical depressed patients receiving ECT have experienced functional decline and have resisted, or have not tolerated, antidepressant medication. Several specific factors affect whether ECT will help particular depressed patients:

Melancholic features From the earliest use of ECT, it seemed apparent that patients with melancholic depression respond better to ECT than do patients with atypical or mood-reactive depression. Early research seems to have borne this out. Roberts2 found that melancholic features such as psychomotor retardation and guilty ideations strongly and favorably predicted ECT response. More recent research, however, generally fails to find predictive value in ECT response in patients based on presence of melancholia.3

Box 2

WHEN MEDICAL ILLNESS REQUIRES A CONSULTATION BEFORE ECT

The medical and neurologic illnesses that place prospective ECT patients at higher than usual risk of complications include a brain tumor or other intracranial space-occupying lesion, increased intracranial pressure, unstable cardiac function, or high anesthetic risk.25

Patients with severe cardiac disease, such as congestive heart failure, coronary artery disease, or cardiac dysrhythmia, can almost always be treated with ECT safely with adequate attention to pretreatment medical stabilization and use of antihypertensive medications during the treatment to blunt the increase in myocardial oxygen demand during the seizures.

 

 

Why is this? Several factors likely explain this rather dramatic difference. First, the patients given ECT in the early decades of its use most likely suffered with a diverse range of dysphoric states (e.g., patients with “neurotic” depression, dysthymia, or personality disorders), while modern research has been limited to relatively homogeneous samples of patients with major depression defined according to strict research criteria.3 When you try to correlate a putative predictive variable such as presence vs. absence of melancholia with an outcome variable such as reduction in depression ratings, the less variability there is on the predictive variable, the less strong the correlation will be.

Another possible factor accounting for the lack of predictability is a broadened concept of melancholia. According to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV),4 it is possible to have melancholic depression without having weight loss, psychomotor retardation, or excessive guilt—3 signs classically thought to be inherent in the melancholic syndrome. If melancholia is defined more narrowly, to include requirements for weight loss and psychomotor change, then it is probably more likely to correlate with ECT response.

A final potential reason for lack of predictability is the method of ascertaining melancholia. In modern samples, usually the Hamilton Rating Scale for Depression is used.5 Such a scale is administered in a brief interview by a research clinician not familiar with any other aspects of the patient’s mental status. In contrast, in some early studies,2 melancholic signs were ascertained by complete psychiatric history and evaluations as done in clinical practice. Such methods are likely to yield more reliable data on weight loss, guilty ideations, psychomotor activity, and other signs than is a 15-to 20-minute interview conducted by a research technician.

Along these lines, Hickie et al,6 utilizing a thorough evaluation of psychomotor activity before ECT, found that psychomotor retardation robustly predicted positive ECT response. Their scale utilized numerous items assessing agitation and retardation, and required a longer period of assessment than did the Hamilton scale; the latter scale has only 2 items for psychomotor activity, each one a global assessment of agitation or retardation.

So do you consider ECT for patients with melancholic features? Yes. Patients with classic melancholic features such as weight loss, pronounced guilt, and especially psychomotor retardation stand an excellent chance of substantial relief with a course of ECT. Additionally, patients with nonmelancholic depression have good response rates with ECT.

Box 3

WHAT TO TELL YOUR ECT PATIENTS ABOUT MEMORY DISTURBANCE

Patients and their families are frequently concerned about the effects of ECT on memory. The 3 types of memory disturbances to discuss are:

  1. Post-treatment confusion and disorientation. This state usually lasts from a few minutes to several hours or, in the case of some elderly patients after receiving numerous treatments, several days. This state is always reversible.
  2. Anterograde amnesia. This is the inability to recall newly learned information during and up to a few weeks after the course of treatments. During this time, any information given to the ECT patient may not be remembered. Important strategies are to write down instructions and make sure that family members are informed of the need to repeat things and monitor the patient if an outpatient. Fortunately, antero-grade amnesia is also reversible.
  3. Retrograde amnesia. This refers to the forgetting of personal life events and general knowledge about the world. Usually, the events and knowledge that are “wiped out” by the treatments are those from up to a few months before the treatments begin to about a month after the treatments are done. Even more remote memories may be forgotten as well. Unlike the other types of ECT-induced memory impairment, retrograde amnesia may be permanent.

Catatonic features It has been known for decades that catatonic features, regardless of etiology, respond robustly and often quickly to a course of ECT.1,7 But in recent years, the literature has documented the high rates of efficacy of benzodiazepines, usually lorazepam, in the initial treatment of catatonic signs such as mutism, stupor, waxy flexibility, posturing, stereotypies, and rigidity.

Bush et al8 treated 21 acutely catatonic patients, who were so diagnosed according to a standardized catatonia rating scale, with parenteral and oral lorazepam at doses up to 8 mg/d. Sixteen responded dramatically, usually within a day or so. Four of the lorazepam nonresponders were given ECT with excellent results, not only for the catatonic signs but also for other underlying psychopathological features.

Ungvari et al9 treated 18 catatonic patients with either lorazepam or diazepam; all patients had some degree of improvement after several days, but 9 of the 18 exhibited insufficient response. For these, ECT was administered with excellent resolution of the psychopathology, including catatonia.

 

 

A reasonable conclusion from these studies is that acutely catatonic patients should be treated first with a benzodiazepine such as parenteral and/or oral lorazepam, perhaps for up to 3 days, and then given ECT if response is insufficient. For patients with malignant catatonia—a particularly severe and life-threatening form of catatonia—ECT may need to be instituted sooner.10

Psychotic features Though the literature has been mixed on this subject, patients with psychotic depression have high response rates to an adequate course of ECT treatments. Hickie et al6 treated 81 depressed patients with ECT and performed in-depth analyses of a variety of clinical variables, including the presence of psychosis. Patients with psychotic depression were found to have a significantly higher rate of ECT response than those with nonpsychotic depression, though the latter still had high response rates.

ECT is considered a primary indication for patients with psychotic depression1,7 for two reasons:

  1. Response rates are uniformly high.
  2. If such patients were to receive pharmacotherapy, a neuroleptic with all the potential neurologic side effects inherent in such medication would be needed.

Further, clinical experience reveals that psychotically depressed patients tend to be particularly nonfunctional, to have lost weight, and to be suicidal. Thus, the rapid, definitive benefits of ECT are necessary as first-line therapy.

Age Age has been positively correlated with ECT outcome. Black et al,11 in an analysis of clinical predictors of ECT in several hundred patients, found that older patients responded more favorably to ECT than did younger ones. The study included careful assessments of pre- and post-ECT clinical status.

Tew et al,12 in a well-designed prospective study of several hundred ECT patients, found that those older than age 65 responded to ECT more favorably than those younger than 65. Possible mitigating factors in the younger group were greater medication nonresponsivity prior to ECT and longer illness severity. In another prospective study, Wilkinson et al13 also found superior response rates in patients older than 75.

At minimum, a consensus emerges from the literature that ECT response rates are at least as good in the elderly as in younger patients, an important finding given the often debilitating effects of depressive illness in this population and the high rates of medication nonresponse.

Potential for self-harm ECT is highly effective for suicidal or cachectic individuals. Decades of clinical practice have clearly established that acutely suicidal, depressed patients and those whose poor food and fluid intake has caused nutritional compromise represent urgent indications for ECT.1,7 In particular, recent research suggests that ECT response may be especially rapid in bipolar depressed patients.14

Medication resistance It is common practice for depressed patients to be given ECT after resistance to one or more medications is established. But recent research indicates that patients with medication-refractory depression respond to ECT at roughly half the rate of those who have not had an adequate antidepressant trial.15 Medication-resistant patients also have higher relapse rates post-ECT, even when they do initially respond.

Thus, particularly aggressive treatment regimens may be necessary for medication-refractory patients, including use of bilateral electrode placement and/or higher than usual electrical doses.

Another strategy would be to combine medications with ECT during the index course. While not studied prospectively, one retrospective comparison of ECT patients who were either given or not given concomitant nortriptyline suggests that such a strategy may enhance ECT efficacy.16

Personality factors Over the past few decades, patients with nonmelancholic depression have been variably referred to as neurotic, mood-reactive, hysterical, or personality-disordered. The difficulties inherent in precisely defining and measuring these variables make them difficult to apply to day-to-day practice. The more chaotic and unpredictable the patient’s emotional life, and the more mood-reactive the patient is to life events, the less the chance of substantial ECT benefit. In fact, a recent study indicates that depressed patients with personality disorders, especially from DSM-IV cluster B,4 have lower acute ECT response rates and higher post-ECT relapse rates than do depressed ECT patients without personality disorders.17

ECT: first choice for highly agitated manic patients

From the early days of ECT, it rapidly became the mainstay for treating severe, life-threatening manic states until the advent of neuroleptic drugs in the late 1950s. Large, retrospective studies have shown ECT to be highly effective for manic states.18

Two prospective, random assignment trials in particular document the modality’s efficacy. Small et al19 randomly assigned manic patients to either lithium treatment or ECT. While patients in both groups responded well, response was faster in the ECT group. Sikdar et al20 administered chlorpromazine and either real or sham ECT to manic patients and found that adding ECT to neuroleptic patients’ treatments substantially improved outcomes.

 

 

In modern practice, various anticonvulsants have become common for treating mania, and no comparative data between such agents and ECT are available. ECT is reserved for highly agitated, medication-refractory patients. The typical scenario entails a patient who does not respond to high doses of parenteral sedatives or antipsychotics, is in restraints much of the time, and is not cooperating with orally administered medications. In such circumstances, court-ordered approval for ECT is usually needed. Fortunately, in my experience bilateral ECT is almost universally effective for such patients, who are often grateful for their treatment once they achieve euthymia.

Rare uses of ECT in schizophrenia

ECT was commonly used for schizophrenia as well as mania before the advent of neuroleptics7 but is only rarely used for this indication in modern times. Here are the exceptions:1

  1. For acute exacerbations, especially with florid-positive symptoms such as delusions, hallucinations, disorganized thoughts and behavior, or catatonia. ECT can be remarkably effective in rendering patients compliant with oral medication. From there, patients can be discharged and can proceed with outpatient therapy.
  2. For the chronically ill patient, if multiple medication trials fail to achieve optimum results. When administered in combination with antipsychotic medication, a trial of ECT may extend whatever benefits accrue from medication.7 In particular, the combination of ECT and neuroleptic medication may be more effective in such cases than either ECT or medication alone.21

Especially for chronically ill patients with schizophrenia, any benefits of an acute course of ECT will likely be short-lived unless maintenance ECT is instituted. In a well-designed study of schizophrenic patients stabilized with a combination of neuroleptic medication and an acute course of ECT, Chanpattana et al22 found that those maintained for 6 months with combination continuation ECT and pharmacotherapy did much better than did those randomly assigned to either modality alone.

Related resources

  • Abrams R. Electroconvulsive Therapy. 3rd ed. New York: Oxford University Press; 1997.
  • American Psychiatric Association. Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 2nd ed. Washington, D.C.:American Psychiatric Association; 2001.
  • Mukherjee S, Sackeim HA, Schnur DB. Electroconvulsive therapy of acute manic episodes: a review of 50 years’ experience. Am J Psychiatry. 1994;151:169-176.

Drug brand names

  • Methohexital • Amidate, Brevital, Diprivan, Ethrane
  • Succinylcholine • Anectine

Disclosure

The author reports no affiliation or financial arrangement with any of the companies whose products are mentioned in this article.

References

1. American Psychiatric Association. Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 2nd ed. Washington, D.C.: American Psychiatric Association; 2001.

2. Roberts JM. Prognostic factors in the electroshock treatment of depressive states I. Clinical features from history and examination. J Ment Sci. 1959;105:693-702.

3. Sackeim HA, Rush AJ. Melancholia and response to ECT (letter). Am J Psychiatry. 1995;152(8):1242-1243.

4. American Psychiatric Association. Diagniositc and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994.

5. Sobin C, Prudic J, Devanand DP, Nobler MS, Sackeim HA. Who responds to electroconvulsive therapy? Br J Psychiatry. 1996;169:322-328.

6. Hickie I, Mason C, et al. Prediction of ECT response: validation of a refined sign-based (CORE) system for defining melancholia. Br J Psychiatry. 1996;169(1):68-74.

7. Abrams R. Electroconvulsive Therapy. 3rd ed. New York: Oxford University Press; 1997.

8. Bush G, Fink M, Petrides G, et al. Treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand. 1996;93:137-143.

9. Ungvari GA, Leung CM, Wong MK, Lau J. Benzodiazepines in the treatment of catatonic syndrome. Acta Psychiatr Scand. 1994;89:285-288.

10. Philbrick KL, Rummans TA. Malignant catatonia. J Neuropsychiatry and Clinical Neurosciences. 1994;6:1-13.

11. Black DW, Winokur G, Nasrallah A. A multivariate analysis of the experience of 423 depressed inpatients treated with electroconvulsive therapy. Convulsive Ther. 1993;9:112-120.

12. Tew JD, Jr, Mulsant BH, Haskett RF, et al. Acute efficacy of ECT in the treatment of major depression in the old. Am J Psychiatry. 1999;156:1865-1870.

13. Wilkinson AM, Anderson DN, Peters S. Age and the effects of ECT. Int J Geriatr Psychiatry. 1993;8:401-406.

14. Daly JJ, Prudic J, Devanand DP, et al. ECT in bipolar and unipolar depression: differences in speed of response. Bipolar Disorders. 2001;3(2):95-104.

15. Prudic J, Haskett RF, Mulsant B, et al. Resistance to antidepressant medications and short-term clinical response to ECT. Am J Psychiatry. 1996;153(8):985-992.

16. Nelson JP, Benjamin L. Efficacy and safety of combined ECT and tricyclic antidepressant therapy in the treatment of depressed geriatric patients. Convulsive Ther. 1989;5:321-329.

17. Sareen J, Enns MW, Guertin JE. The impact of clinically diagnosed personality disorders on acute and one-year outcomes of electroconvulsive therapy. J ECT. 2000;16(1):43-51.

18. Mukherjee S, Sackeim HA, Schnur DB. Electroconvulsive therapy of acute manic episodes: a review of 50 years’ experience. Am J Psychiatry. 1994;151:169-176.

19. Small JG, Klapper MH, et al. Electroconvulsive treatment compared with lithium in the management of manic states. Arch Gen Psychiatry. 1988;45:727-732.

20. Sikdar S, Kulhara P, Avasthi A, Singh H. Combined chlorpromazine and electroconvulsive therapy in mania. Br J Psychiatry. 1994;164:806-810.

21. Krueger RB, Sackeim HA. Electroconvulsive therapy and schizophrenia. In Schizophrenia. SR Hirsch and D Weinberger, eds. Oxford, England: Blackwell Scientific, 1995;503-545.

22. Chanpattana W, Chakrabhand ML, Sackeim HA, et al. Continuation ECT in treatment-resistant schizophrenia: a controlled study. J ECT. 1999;15:178-192.

23. Sackeim HA, Prudic J, Devanand DP, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral ECT at different stimulus intensities. Arch Gen Psychiatry. 2000;57:425-434.

24. Shapira B, Tubi N, Drexler H, Lidsky D, Calev A, Lerer B. Cost and benefit in the choice of ECT schedule. Twice versus three times weekly ECT. Br J Psychiatry. 1998;172:44-48.

25. Rasmussen KG, Richardson JR, Rummans TA. ECT in the medically ill. Psychiatric Clin North Amer (in press).

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Although numerous psychotropic agents in multiple classes have emerged over the past few decades, electroconvulsive therapy (ECT) still represents an essential treatment in modern psychiatry. Its record of safety and efficacy is virtually unparalleled vis a vis pharmacological agents.

Advances in anesthetic technique, electrode placement, and electrical stimulus dosing allow ECT to be administered safely to even the most medically ill patients without excessive effects on memory, with excellent clinical benefits (Box 1). A typical course of ECT consists of 8 to 10 treatments administered 2 to 3 times per week.

The medical complications of ECT are rare, and good pre-treatment medical assessment helps ensure its safety.1 Include at minimum a medical history, physical exam, and basic laboratory tests. Specialist consultations are sometimes necessary when patients have comorbid neurologic or cardiologic illnesses (Box 2).

The most bothersome side effect of ECT is memory disturbance. This takes 3 forms: post-treatment confusion and anterograde or retrograde amnesia (Box 3). Less serious side effects include headaches, muscle soreness, and nausea. These are easily treated symptomatically with analgesics or antiemetics.

Box 1

THE TECHNICAL FACTORS OF ECT AFFECTING EFFICACY AND SIDE EFFECTS

Electroconvulsive therapy (ECT) has been in use since 1938.6 It consists of the application of an electric current to the head, which causes a seizure.

Modern ECT technique involves the use of general anesthesia, usually with a barbiturate anesthetic such as methohexital, and muscular paralysis, usually with the depolarizing neuromuscular blocking agent succinylcholine. Continuous oxygenation with positive pressure ventilation, measuring of blood pressure, and monitoring with an electrocardiogram and pulse oximetry make the procedure exceedingly safe.

Efficacy and cognitive side effects may be affected by how ECT is administered. The two treatment electrodes that are placed on the head can be located on either side of the temporal fossa (the bitemporal position), on either side of the forehead (the bifrontal position), or on the right temporal fossa and just to the right of the vertex of the skull (the d’Elia unilateral position). Generally, unilateral electrode placement causes less memory impairment but has been believed to be less effective than bilateral electrode positions.6

Another technical factor receiving attention from researchers is the amount of electricity, or electrical dose, used to elicit the seizure. Generally, especially for unilateral ECT, high electrical doses are needed to attain acceptable treatment efficacy. In fact, one study indicates that if 6 times the minimum electrical seizure threshold is used for unilateral ECT, efficacy for depression is equal to that of bilateral ECT with less memory disturbance.23

Finally, treatment frequency affects ECT outcome: twice-weekly treatment schedules are associated with less memory disturbance—and only slightly slower clinical response—than thrice-weekly schedules.24

The most common indication for ECT is major depression. Using modern diagnostic criteria, most depressed patients respond to ECT. Some features that presage a particularly robust response include psychomotor retardation, psychosis, catatonia, and advanced age. Patients who have medication-resistant depression may require particularly potent forms of treatment, such as bilateral electrode placement and/or higher than usual electrical doses.

Patients with mania respond particularly well to ECT but, because of excellent responses with modern pharmacological agents, rarely need it. For patients with mania who are agitated and noncompliant, ECT may represent a life-saving option for stabilizing an acute episode. Finally, ECT may help yield stability for an acute exacerbation of schizophrenia or may extend the benefits of antipsychotic medication for those with chronic schizophrenia, in which case continuation of ECT is usually advisable.

When ECT is indicated for depression

Typical depressed patients receiving ECT have experienced functional decline and have resisted, or have not tolerated, antidepressant medication. Several specific factors affect whether ECT will help particular depressed patients:

Melancholic features From the earliest use of ECT, it seemed apparent that patients with melancholic depression respond better to ECT than do patients with atypical or mood-reactive depression. Early research seems to have borne this out. Roberts2 found that melancholic features such as psychomotor retardation and guilty ideations strongly and favorably predicted ECT response. More recent research, however, generally fails to find predictive value in ECT response in patients based on presence of melancholia.3

Box 2

WHEN MEDICAL ILLNESS REQUIRES A CONSULTATION BEFORE ECT

The medical and neurologic illnesses that place prospective ECT patients at higher than usual risk of complications include a brain tumor or other intracranial space-occupying lesion, increased intracranial pressure, unstable cardiac function, or high anesthetic risk.25

Patients with severe cardiac disease, such as congestive heart failure, coronary artery disease, or cardiac dysrhythmia, can almost always be treated with ECT safely with adequate attention to pretreatment medical stabilization and use of antihypertensive medications during the treatment to blunt the increase in myocardial oxygen demand during the seizures.

 

 

Why is this? Several factors likely explain this rather dramatic difference. First, the patients given ECT in the early decades of its use most likely suffered with a diverse range of dysphoric states (e.g., patients with “neurotic” depression, dysthymia, or personality disorders), while modern research has been limited to relatively homogeneous samples of patients with major depression defined according to strict research criteria.3 When you try to correlate a putative predictive variable such as presence vs. absence of melancholia with an outcome variable such as reduction in depression ratings, the less variability there is on the predictive variable, the less strong the correlation will be.

Another possible factor accounting for the lack of predictability is a broadened concept of melancholia. According to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV),4 it is possible to have melancholic depression without having weight loss, psychomotor retardation, or excessive guilt—3 signs classically thought to be inherent in the melancholic syndrome. If melancholia is defined more narrowly, to include requirements for weight loss and psychomotor change, then it is probably more likely to correlate with ECT response.

A final potential reason for lack of predictability is the method of ascertaining melancholia. In modern samples, usually the Hamilton Rating Scale for Depression is used.5 Such a scale is administered in a brief interview by a research clinician not familiar with any other aspects of the patient’s mental status. In contrast, in some early studies,2 melancholic signs were ascertained by complete psychiatric history and evaluations as done in clinical practice. Such methods are likely to yield more reliable data on weight loss, guilty ideations, psychomotor activity, and other signs than is a 15-to 20-minute interview conducted by a research technician.

Along these lines, Hickie et al,6 utilizing a thorough evaluation of psychomotor activity before ECT, found that psychomotor retardation robustly predicted positive ECT response. Their scale utilized numerous items assessing agitation and retardation, and required a longer period of assessment than did the Hamilton scale; the latter scale has only 2 items for psychomotor activity, each one a global assessment of agitation or retardation.

So do you consider ECT for patients with melancholic features? Yes. Patients with classic melancholic features such as weight loss, pronounced guilt, and especially psychomotor retardation stand an excellent chance of substantial relief with a course of ECT. Additionally, patients with nonmelancholic depression have good response rates with ECT.

Box 3

WHAT TO TELL YOUR ECT PATIENTS ABOUT MEMORY DISTURBANCE

Patients and their families are frequently concerned about the effects of ECT on memory. The 3 types of memory disturbances to discuss are:

  1. Post-treatment confusion and disorientation. This state usually lasts from a few minutes to several hours or, in the case of some elderly patients after receiving numerous treatments, several days. This state is always reversible.
  2. Anterograde amnesia. This is the inability to recall newly learned information during and up to a few weeks after the course of treatments. During this time, any information given to the ECT patient may not be remembered. Important strategies are to write down instructions and make sure that family members are informed of the need to repeat things and monitor the patient if an outpatient. Fortunately, antero-grade amnesia is also reversible.
  3. Retrograde amnesia. This refers to the forgetting of personal life events and general knowledge about the world. Usually, the events and knowledge that are “wiped out” by the treatments are those from up to a few months before the treatments begin to about a month after the treatments are done. Even more remote memories may be forgotten as well. Unlike the other types of ECT-induced memory impairment, retrograde amnesia may be permanent.

Catatonic features It has been known for decades that catatonic features, regardless of etiology, respond robustly and often quickly to a course of ECT.1,7 But in recent years, the literature has documented the high rates of efficacy of benzodiazepines, usually lorazepam, in the initial treatment of catatonic signs such as mutism, stupor, waxy flexibility, posturing, stereotypies, and rigidity.

Bush et al8 treated 21 acutely catatonic patients, who were so diagnosed according to a standardized catatonia rating scale, with parenteral and oral lorazepam at doses up to 8 mg/d. Sixteen responded dramatically, usually within a day or so. Four of the lorazepam nonresponders were given ECT with excellent results, not only for the catatonic signs but also for other underlying psychopathological features.

Ungvari et al9 treated 18 catatonic patients with either lorazepam or diazepam; all patients had some degree of improvement after several days, but 9 of the 18 exhibited insufficient response. For these, ECT was administered with excellent resolution of the psychopathology, including catatonia.

 

 

A reasonable conclusion from these studies is that acutely catatonic patients should be treated first with a benzodiazepine such as parenteral and/or oral lorazepam, perhaps for up to 3 days, and then given ECT if response is insufficient. For patients with malignant catatonia—a particularly severe and life-threatening form of catatonia—ECT may need to be instituted sooner.10

Psychotic features Though the literature has been mixed on this subject, patients with psychotic depression have high response rates to an adequate course of ECT treatments. Hickie et al6 treated 81 depressed patients with ECT and performed in-depth analyses of a variety of clinical variables, including the presence of psychosis. Patients with psychotic depression were found to have a significantly higher rate of ECT response than those with nonpsychotic depression, though the latter still had high response rates.

ECT is considered a primary indication for patients with psychotic depression1,7 for two reasons:

  1. Response rates are uniformly high.
  2. If such patients were to receive pharmacotherapy, a neuroleptic with all the potential neurologic side effects inherent in such medication would be needed.

Further, clinical experience reveals that psychotically depressed patients tend to be particularly nonfunctional, to have lost weight, and to be suicidal. Thus, the rapid, definitive benefits of ECT are necessary as first-line therapy.

Age Age has been positively correlated with ECT outcome. Black et al,11 in an analysis of clinical predictors of ECT in several hundred patients, found that older patients responded more favorably to ECT than did younger ones. The study included careful assessments of pre- and post-ECT clinical status.

Tew et al,12 in a well-designed prospective study of several hundred ECT patients, found that those older than age 65 responded to ECT more favorably than those younger than 65. Possible mitigating factors in the younger group were greater medication nonresponsivity prior to ECT and longer illness severity. In another prospective study, Wilkinson et al13 also found superior response rates in patients older than 75.

At minimum, a consensus emerges from the literature that ECT response rates are at least as good in the elderly as in younger patients, an important finding given the often debilitating effects of depressive illness in this population and the high rates of medication nonresponse.

Potential for self-harm ECT is highly effective for suicidal or cachectic individuals. Decades of clinical practice have clearly established that acutely suicidal, depressed patients and those whose poor food and fluid intake has caused nutritional compromise represent urgent indications for ECT.1,7 In particular, recent research suggests that ECT response may be especially rapid in bipolar depressed patients.14

Medication resistance It is common practice for depressed patients to be given ECT after resistance to one or more medications is established. But recent research indicates that patients with medication-refractory depression respond to ECT at roughly half the rate of those who have not had an adequate antidepressant trial.15 Medication-resistant patients also have higher relapse rates post-ECT, even when they do initially respond.

Thus, particularly aggressive treatment regimens may be necessary for medication-refractory patients, including use of bilateral electrode placement and/or higher than usual electrical doses.

Another strategy would be to combine medications with ECT during the index course. While not studied prospectively, one retrospective comparison of ECT patients who were either given or not given concomitant nortriptyline suggests that such a strategy may enhance ECT efficacy.16

Personality factors Over the past few decades, patients with nonmelancholic depression have been variably referred to as neurotic, mood-reactive, hysterical, or personality-disordered. The difficulties inherent in precisely defining and measuring these variables make them difficult to apply to day-to-day practice. The more chaotic and unpredictable the patient’s emotional life, and the more mood-reactive the patient is to life events, the less the chance of substantial ECT benefit. In fact, a recent study indicates that depressed patients with personality disorders, especially from DSM-IV cluster B,4 have lower acute ECT response rates and higher post-ECT relapse rates than do depressed ECT patients without personality disorders.17

ECT: first choice for highly agitated manic patients

From the early days of ECT, it rapidly became the mainstay for treating severe, life-threatening manic states until the advent of neuroleptic drugs in the late 1950s. Large, retrospective studies have shown ECT to be highly effective for manic states.18

Two prospective, random assignment trials in particular document the modality’s efficacy. Small et al19 randomly assigned manic patients to either lithium treatment or ECT. While patients in both groups responded well, response was faster in the ECT group. Sikdar et al20 administered chlorpromazine and either real or sham ECT to manic patients and found that adding ECT to neuroleptic patients’ treatments substantially improved outcomes.

 

 

In modern practice, various anticonvulsants have become common for treating mania, and no comparative data between such agents and ECT are available. ECT is reserved for highly agitated, medication-refractory patients. The typical scenario entails a patient who does not respond to high doses of parenteral sedatives or antipsychotics, is in restraints much of the time, and is not cooperating with orally administered medications. In such circumstances, court-ordered approval for ECT is usually needed. Fortunately, in my experience bilateral ECT is almost universally effective for such patients, who are often grateful for their treatment once they achieve euthymia.

Rare uses of ECT in schizophrenia

ECT was commonly used for schizophrenia as well as mania before the advent of neuroleptics7 but is only rarely used for this indication in modern times. Here are the exceptions:1

  1. For acute exacerbations, especially with florid-positive symptoms such as delusions, hallucinations, disorganized thoughts and behavior, or catatonia. ECT can be remarkably effective in rendering patients compliant with oral medication. From there, patients can be discharged and can proceed with outpatient therapy.
  2. For the chronically ill patient, if multiple medication trials fail to achieve optimum results. When administered in combination with antipsychotic medication, a trial of ECT may extend whatever benefits accrue from medication.7 In particular, the combination of ECT and neuroleptic medication may be more effective in such cases than either ECT or medication alone.21

Especially for chronically ill patients with schizophrenia, any benefits of an acute course of ECT will likely be short-lived unless maintenance ECT is instituted. In a well-designed study of schizophrenic patients stabilized with a combination of neuroleptic medication and an acute course of ECT, Chanpattana et al22 found that those maintained for 6 months with combination continuation ECT and pharmacotherapy did much better than did those randomly assigned to either modality alone.

Related resources

  • Abrams R. Electroconvulsive Therapy. 3rd ed. New York: Oxford University Press; 1997.
  • American Psychiatric Association. Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 2nd ed. Washington, D.C.:American Psychiatric Association; 2001.
  • Mukherjee S, Sackeim HA, Schnur DB. Electroconvulsive therapy of acute manic episodes: a review of 50 years’ experience. Am J Psychiatry. 1994;151:169-176.

Drug brand names

  • Methohexital • Amidate, Brevital, Diprivan, Ethrane
  • Succinylcholine • Anectine

Disclosure

The author reports no affiliation or financial arrangement with any of the companies whose products are mentioned in this article.

Although numerous psychotropic agents in multiple classes have emerged over the past few decades, electroconvulsive therapy (ECT) still represents an essential treatment in modern psychiatry. Its record of safety and efficacy is virtually unparalleled vis a vis pharmacological agents.

Advances in anesthetic technique, electrode placement, and electrical stimulus dosing allow ECT to be administered safely to even the most medically ill patients without excessive effects on memory, with excellent clinical benefits (Box 1). A typical course of ECT consists of 8 to 10 treatments administered 2 to 3 times per week.

The medical complications of ECT are rare, and good pre-treatment medical assessment helps ensure its safety.1 Include at minimum a medical history, physical exam, and basic laboratory tests. Specialist consultations are sometimes necessary when patients have comorbid neurologic or cardiologic illnesses (Box 2).

The most bothersome side effect of ECT is memory disturbance. This takes 3 forms: post-treatment confusion and anterograde or retrograde amnesia (Box 3). Less serious side effects include headaches, muscle soreness, and nausea. These are easily treated symptomatically with analgesics or antiemetics.

Box 1

THE TECHNICAL FACTORS OF ECT AFFECTING EFFICACY AND SIDE EFFECTS

Electroconvulsive therapy (ECT) has been in use since 1938.6 It consists of the application of an electric current to the head, which causes a seizure.

Modern ECT technique involves the use of general anesthesia, usually with a barbiturate anesthetic such as methohexital, and muscular paralysis, usually with the depolarizing neuromuscular blocking agent succinylcholine. Continuous oxygenation with positive pressure ventilation, measuring of blood pressure, and monitoring with an electrocardiogram and pulse oximetry make the procedure exceedingly safe.

Efficacy and cognitive side effects may be affected by how ECT is administered. The two treatment electrodes that are placed on the head can be located on either side of the temporal fossa (the bitemporal position), on either side of the forehead (the bifrontal position), or on the right temporal fossa and just to the right of the vertex of the skull (the d’Elia unilateral position). Generally, unilateral electrode placement causes less memory impairment but has been believed to be less effective than bilateral electrode positions.6

Another technical factor receiving attention from researchers is the amount of electricity, or electrical dose, used to elicit the seizure. Generally, especially for unilateral ECT, high electrical doses are needed to attain acceptable treatment efficacy. In fact, one study indicates that if 6 times the minimum electrical seizure threshold is used for unilateral ECT, efficacy for depression is equal to that of bilateral ECT with less memory disturbance.23

Finally, treatment frequency affects ECT outcome: twice-weekly treatment schedules are associated with less memory disturbance—and only slightly slower clinical response—than thrice-weekly schedules.24

The most common indication for ECT is major depression. Using modern diagnostic criteria, most depressed patients respond to ECT. Some features that presage a particularly robust response include psychomotor retardation, psychosis, catatonia, and advanced age. Patients who have medication-resistant depression may require particularly potent forms of treatment, such as bilateral electrode placement and/or higher than usual electrical doses.

Patients with mania respond particularly well to ECT but, because of excellent responses with modern pharmacological agents, rarely need it. For patients with mania who are agitated and noncompliant, ECT may represent a life-saving option for stabilizing an acute episode. Finally, ECT may help yield stability for an acute exacerbation of schizophrenia or may extend the benefits of antipsychotic medication for those with chronic schizophrenia, in which case continuation of ECT is usually advisable.

When ECT is indicated for depression

Typical depressed patients receiving ECT have experienced functional decline and have resisted, or have not tolerated, antidepressant medication. Several specific factors affect whether ECT will help particular depressed patients:

Melancholic features From the earliest use of ECT, it seemed apparent that patients with melancholic depression respond better to ECT than do patients with atypical or mood-reactive depression. Early research seems to have borne this out. Roberts2 found that melancholic features such as psychomotor retardation and guilty ideations strongly and favorably predicted ECT response. More recent research, however, generally fails to find predictive value in ECT response in patients based on presence of melancholia.3

Box 2

WHEN MEDICAL ILLNESS REQUIRES A CONSULTATION BEFORE ECT

The medical and neurologic illnesses that place prospective ECT patients at higher than usual risk of complications include a brain tumor or other intracranial space-occupying lesion, increased intracranial pressure, unstable cardiac function, or high anesthetic risk.25

Patients with severe cardiac disease, such as congestive heart failure, coronary artery disease, or cardiac dysrhythmia, can almost always be treated with ECT safely with adequate attention to pretreatment medical stabilization and use of antihypertensive medications during the treatment to blunt the increase in myocardial oxygen demand during the seizures.

 

 

Why is this? Several factors likely explain this rather dramatic difference. First, the patients given ECT in the early decades of its use most likely suffered with a diverse range of dysphoric states (e.g., patients with “neurotic” depression, dysthymia, or personality disorders), while modern research has been limited to relatively homogeneous samples of patients with major depression defined according to strict research criteria.3 When you try to correlate a putative predictive variable such as presence vs. absence of melancholia with an outcome variable such as reduction in depression ratings, the less variability there is on the predictive variable, the less strong the correlation will be.

Another possible factor accounting for the lack of predictability is a broadened concept of melancholia. According to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV),4 it is possible to have melancholic depression without having weight loss, psychomotor retardation, or excessive guilt—3 signs classically thought to be inherent in the melancholic syndrome. If melancholia is defined more narrowly, to include requirements for weight loss and psychomotor change, then it is probably more likely to correlate with ECT response.

A final potential reason for lack of predictability is the method of ascertaining melancholia. In modern samples, usually the Hamilton Rating Scale for Depression is used.5 Such a scale is administered in a brief interview by a research clinician not familiar with any other aspects of the patient’s mental status. In contrast, in some early studies,2 melancholic signs were ascertained by complete psychiatric history and evaluations as done in clinical practice. Such methods are likely to yield more reliable data on weight loss, guilty ideations, psychomotor activity, and other signs than is a 15-to 20-minute interview conducted by a research technician.

Along these lines, Hickie et al,6 utilizing a thorough evaluation of psychomotor activity before ECT, found that psychomotor retardation robustly predicted positive ECT response. Their scale utilized numerous items assessing agitation and retardation, and required a longer period of assessment than did the Hamilton scale; the latter scale has only 2 items for psychomotor activity, each one a global assessment of agitation or retardation.

So do you consider ECT for patients with melancholic features? Yes. Patients with classic melancholic features such as weight loss, pronounced guilt, and especially psychomotor retardation stand an excellent chance of substantial relief with a course of ECT. Additionally, patients with nonmelancholic depression have good response rates with ECT.

Box 3

WHAT TO TELL YOUR ECT PATIENTS ABOUT MEMORY DISTURBANCE

Patients and their families are frequently concerned about the effects of ECT on memory. The 3 types of memory disturbances to discuss are:

  1. Post-treatment confusion and disorientation. This state usually lasts from a few minutes to several hours or, in the case of some elderly patients after receiving numerous treatments, several days. This state is always reversible.
  2. Anterograde amnesia. This is the inability to recall newly learned information during and up to a few weeks after the course of treatments. During this time, any information given to the ECT patient may not be remembered. Important strategies are to write down instructions and make sure that family members are informed of the need to repeat things and monitor the patient if an outpatient. Fortunately, antero-grade amnesia is also reversible.
  3. Retrograde amnesia. This refers to the forgetting of personal life events and general knowledge about the world. Usually, the events and knowledge that are “wiped out” by the treatments are those from up to a few months before the treatments begin to about a month after the treatments are done. Even more remote memories may be forgotten as well. Unlike the other types of ECT-induced memory impairment, retrograde amnesia may be permanent.

Catatonic features It has been known for decades that catatonic features, regardless of etiology, respond robustly and often quickly to a course of ECT.1,7 But in recent years, the literature has documented the high rates of efficacy of benzodiazepines, usually lorazepam, in the initial treatment of catatonic signs such as mutism, stupor, waxy flexibility, posturing, stereotypies, and rigidity.

Bush et al8 treated 21 acutely catatonic patients, who were so diagnosed according to a standardized catatonia rating scale, with parenteral and oral lorazepam at doses up to 8 mg/d. Sixteen responded dramatically, usually within a day or so. Four of the lorazepam nonresponders were given ECT with excellent results, not only for the catatonic signs but also for other underlying psychopathological features.

Ungvari et al9 treated 18 catatonic patients with either lorazepam or diazepam; all patients had some degree of improvement after several days, but 9 of the 18 exhibited insufficient response. For these, ECT was administered with excellent resolution of the psychopathology, including catatonia.

 

 

A reasonable conclusion from these studies is that acutely catatonic patients should be treated first with a benzodiazepine such as parenteral and/or oral lorazepam, perhaps for up to 3 days, and then given ECT if response is insufficient. For patients with malignant catatonia—a particularly severe and life-threatening form of catatonia—ECT may need to be instituted sooner.10

Psychotic features Though the literature has been mixed on this subject, patients with psychotic depression have high response rates to an adequate course of ECT treatments. Hickie et al6 treated 81 depressed patients with ECT and performed in-depth analyses of a variety of clinical variables, including the presence of psychosis. Patients with psychotic depression were found to have a significantly higher rate of ECT response than those with nonpsychotic depression, though the latter still had high response rates.

ECT is considered a primary indication for patients with psychotic depression1,7 for two reasons:

  1. Response rates are uniformly high.
  2. If such patients were to receive pharmacotherapy, a neuroleptic with all the potential neurologic side effects inherent in such medication would be needed.

Further, clinical experience reveals that psychotically depressed patients tend to be particularly nonfunctional, to have lost weight, and to be suicidal. Thus, the rapid, definitive benefits of ECT are necessary as first-line therapy.

Age Age has been positively correlated with ECT outcome. Black et al,11 in an analysis of clinical predictors of ECT in several hundred patients, found that older patients responded more favorably to ECT than did younger ones. The study included careful assessments of pre- and post-ECT clinical status.

Tew et al,12 in a well-designed prospective study of several hundred ECT patients, found that those older than age 65 responded to ECT more favorably than those younger than 65. Possible mitigating factors in the younger group were greater medication nonresponsivity prior to ECT and longer illness severity. In another prospective study, Wilkinson et al13 also found superior response rates in patients older than 75.

At minimum, a consensus emerges from the literature that ECT response rates are at least as good in the elderly as in younger patients, an important finding given the often debilitating effects of depressive illness in this population and the high rates of medication nonresponse.

Potential for self-harm ECT is highly effective for suicidal or cachectic individuals. Decades of clinical practice have clearly established that acutely suicidal, depressed patients and those whose poor food and fluid intake has caused nutritional compromise represent urgent indications for ECT.1,7 In particular, recent research suggests that ECT response may be especially rapid in bipolar depressed patients.14

Medication resistance It is common practice for depressed patients to be given ECT after resistance to one or more medications is established. But recent research indicates that patients with medication-refractory depression respond to ECT at roughly half the rate of those who have not had an adequate antidepressant trial.15 Medication-resistant patients also have higher relapse rates post-ECT, even when they do initially respond.

Thus, particularly aggressive treatment regimens may be necessary for medication-refractory patients, including use of bilateral electrode placement and/or higher than usual electrical doses.

Another strategy would be to combine medications with ECT during the index course. While not studied prospectively, one retrospective comparison of ECT patients who were either given or not given concomitant nortriptyline suggests that such a strategy may enhance ECT efficacy.16

Personality factors Over the past few decades, patients with nonmelancholic depression have been variably referred to as neurotic, mood-reactive, hysterical, or personality-disordered. The difficulties inherent in precisely defining and measuring these variables make them difficult to apply to day-to-day practice. The more chaotic and unpredictable the patient’s emotional life, and the more mood-reactive the patient is to life events, the less the chance of substantial ECT benefit. In fact, a recent study indicates that depressed patients with personality disorders, especially from DSM-IV cluster B,4 have lower acute ECT response rates and higher post-ECT relapse rates than do depressed ECT patients without personality disorders.17

ECT: first choice for highly agitated manic patients

From the early days of ECT, it rapidly became the mainstay for treating severe, life-threatening manic states until the advent of neuroleptic drugs in the late 1950s. Large, retrospective studies have shown ECT to be highly effective for manic states.18

Two prospective, random assignment trials in particular document the modality’s efficacy. Small et al19 randomly assigned manic patients to either lithium treatment or ECT. While patients in both groups responded well, response was faster in the ECT group. Sikdar et al20 administered chlorpromazine and either real or sham ECT to manic patients and found that adding ECT to neuroleptic patients’ treatments substantially improved outcomes.

 

 

In modern practice, various anticonvulsants have become common for treating mania, and no comparative data between such agents and ECT are available. ECT is reserved for highly agitated, medication-refractory patients. The typical scenario entails a patient who does not respond to high doses of parenteral sedatives or antipsychotics, is in restraints much of the time, and is not cooperating with orally administered medications. In such circumstances, court-ordered approval for ECT is usually needed. Fortunately, in my experience bilateral ECT is almost universally effective for such patients, who are often grateful for their treatment once they achieve euthymia.

Rare uses of ECT in schizophrenia

ECT was commonly used for schizophrenia as well as mania before the advent of neuroleptics7 but is only rarely used for this indication in modern times. Here are the exceptions:1

  1. For acute exacerbations, especially with florid-positive symptoms such as delusions, hallucinations, disorganized thoughts and behavior, or catatonia. ECT can be remarkably effective in rendering patients compliant with oral medication. From there, patients can be discharged and can proceed with outpatient therapy.
  2. For the chronically ill patient, if multiple medication trials fail to achieve optimum results. When administered in combination with antipsychotic medication, a trial of ECT may extend whatever benefits accrue from medication.7 In particular, the combination of ECT and neuroleptic medication may be more effective in such cases than either ECT or medication alone.21

Especially for chronically ill patients with schizophrenia, any benefits of an acute course of ECT will likely be short-lived unless maintenance ECT is instituted. In a well-designed study of schizophrenic patients stabilized with a combination of neuroleptic medication and an acute course of ECT, Chanpattana et al22 found that those maintained for 6 months with combination continuation ECT and pharmacotherapy did much better than did those randomly assigned to either modality alone.

Related resources

  • Abrams R. Electroconvulsive Therapy. 3rd ed. New York: Oxford University Press; 1997.
  • American Psychiatric Association. Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 2nd ed. Washington, D.C.:American Psychiatric Association; 2001.
  • Mukherjee S, Sackeim HA, Schnur DB. Electroconvulsive therapy of acute manic episodes: a review of 50 years’ experience. Am J Psychiatry. 1994;151:169-176.

Drug brand names

  • Methohexital • Amidate, Brevital, Diprivan, Ethrane
  • Succinylcholine • Anectine

Disclosure

The author reports no affiliation or financial arrangement with any of the companies whose products are mentioned in this article.

References

1. American Psychiatric Association. Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 2nd ed. Washington, D.C.: American Psychiatric Association; 2001.

2. Roberts JM. Prognostic factors in the electroshock treatment of depressive states I. Clinical features from history and examination. J Ment Sci. 1959;105:693-702.

3. Sackeim HA, Rush AJ. Melancholia and response to ECT (letter). Am J Psychiatry. 1995;152(8):1242-1243.

4. American Psychiatric Association. Diagniositc and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994.

5. Sobin C, Prudic J, Devanand DP, Nobler MS, Sackeim HA. Who responds to electroconvulsive therapy? Br J Psychiatry. 1996;169:322-328.

6. Hickie I, Mason C, et al. Prediction of ECT response: validation of a refined sign-based (CORE) system for defining melancholia. Br J Psychiatry. 1996;169(1):68-74.

7. Abrams R. Electroconvulsive Therapy. 3rd ed. New York: Oxford University Press; 1997.

8. Bush G, Fink M, Petrides G, et al. Treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand. 1996;93:137-143.

9. Ungvari GA, Leung CM, Wong MK, Lau J. Benzodiazepines in the treatment of catatonic syndrome. Acta Psychiatr Scand. 1994;89:285-288.

10. Philbrick KL, Rummans TA. Malignant catatonia. J Neuropsychiatry and Clinical Neurosciences. 1994;6:1-13.

11. Black DW, Winokur G, Nasrallah A. A multivariate analysis of the experience of 423 depressed inpatients treated with electroconvulsive therapy. Convulsive Ther. 1993;9:112-120.

12. Tew JD, Jr, Mulsant BH, Haskett RF, et al. Acute efficacy of ECT in the treatment of major depression in the old. Am J Psychiatry. 1999;156:1865-1870.

13. Wilkinson AM, Anderson DN, Peters S. Age and the effects of ECT. Int J Geriatr Psychiatry. 1993;8:401-406.

14. Daly JJ, Prudic J, Devanand DP, et al. ECT in bipolar and unipolar depression: differences in speed of response. Bipolar Disorders. 2001;3(2):95-104.

15. Prudic J, Haskett RF, Mulsant B, et al. Resistance to antidepressant medications and short-term clinical response to ECT. Am J Psychiatry. 1996;153(8):985-992.

16. Nelson JP, Benjamin L. Efficacy and safety of combined ECT and tricyclic antidepressant therapy in the treatment of depressed geriatric patients. Convulsive Ther. 1989;5:321-329.

17. Sareen J, Enns MW, Guertin JE. The impact of clinically diagnosed personality disorders on acute and one-year outcomes of electroconvulsive therapy. J ECT. 2000;16(1):43-51.

18. Mukherjee S, Sackeim HA, Schnur DB. Electroconvulsive therapy of acute manic episodes: a review of 50 years’ experience. Am J Psychiatry. 1994;151:169-176.

19. Small JG, Klapper MH, et al. Electroconvulsive treatment compared with lithium in the management of manic states. Arch Gen Psychiatry. 1988;45:727-732.

20. Sikdar S, Kulhara P, Avasthi A, Singh H. Combined chlorpromazine and electroconvulsive therapy in mania. Br J Psychiatry. 1994;164:806-810.

21. Krueger RB, Sackeim HA. Electroconvulsive therapy and schizophrenia. In Schizophrenia. SR Hirsch and D Weinberger, eds. Oxford, England: Blackwell Scientific, 1995;503-545.

22. Chanpattana W, Chakrabhand ML, Sackeim HA, et al. Continuation ECT in treatment-resistant schizophrenia: a controlled study. J ECT. 1999;15:178-192.

23. Sackeim HA, Prudic J, Devanand DP, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral ECT at different stimulus intensities. Arch Gen Psychiatry. 2000;57:425-434.

24. Shapira B, Tubi N, Drexler H, Lidsky D, Calev A, Lerer B. Cost and benefit in the choice of ECT schedule. Twice versus three times weekly ECT. Br J Psychiatry. 1998;172:44-48.

25. Rasmussen KG, Richardson JR, Rummans TA. ECT in the medically ill. Psychiatric Clin North Amer (in press).

References

1. American Psychiatric Association. Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 2nd ed. Washington, D.C.: American Psychiatric Association; 2001.

2. Roberts JM. Prognostic factors in the electroshock treatment of depressive states I. Clinical features from history and examination. J Ment Sci. 1959;105:693-702.

3. Sackeim HA, Rush AJ. Melancholia and response to ECT (letter). Am J Psychiatry. 1995;152(8):1242-1243.

4. American Psychiatric Association. Diagniositc and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994.

5. Sobin C, Prudic J, Devanand DP, Nobler MS, Sackeim HA. Who responds to electroconvulsive therapy? Br J Psychiatry. 1996;169:322-328.

6. Hickie I, Mason C, et al. Prediction of ECT response: validation of a refined sign-based (CORE) system for defining melancholia. Br J Psychiatry. 1996;169(1):68-74.

7. Abrams R. Electroconvulsive Therapy. 3rd ed. New York: Oxford University Press; 1997.

8. Bush G, Fink M, Petrides G, et al. Treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand. 1996;93:137-143.

9. Ungvari GA, Leung CM, Wong MK, Lau J. Benzodiazepines in the treatment of catatonic syndrome. Acta Psychiatr Scand. 1994;89:285-288.

10. Philbrick KL, Rummans TA. Malignant catatonia. J Neuropsychiatry and Clinical Neurosciences. 1994;6:1-13.

11. Black DW, Winokur G, Nasrallah A. A multivariate analysis of the experience of 423 depressed inpatients treated with electroconvulsive therapy. Convulsive Ther. 1993;9:112-120.

12. Tew JD, Jr, Mulsant BH, Haskett RF, et al. Acute efficacy of ECT in the treatment of major depression in the old. Am J Psychiatry. 1999;156:1865-1870.

13. Wilkinson AM, Anderson DN, Peters S. Age and the effects of ECT. Int J Geriatr Psychiatry. 1993;8:401-406.

14. Daly JJ, Prudic J, Devanand DP, et al. ECT in bipolar and unipolar depression: differences in speed of response. Bipolar Disorders. 2001;3(2):95-104.

15. Prudic J, Haskett RF, Mulsant B, et al. Resistance to antidepressant medications and short-term clinical response to ECT. Am J Psychiatry. 1996;153(8):985-992.

16. Nelson JP, Benjamin L. Efficacy and safety of combined ECT and tricyclic antidepressant therapy in the treatment of depressed geriatric patients. Convulsive Ther. 1989;5:321-329.

17. Sareen J, Enns MW, Guertin JE. The impact of clinically diagnosed personality disorders on acute and one-year outcomes of electroconvulsive therapy. J ECT. 2000;16(1):43-51.

18. Mukherjee S, Sackeim HA, Schnur DB. Electroconvulsive therapy of acute manic episodes: a review of 50 years’ experience. Am J Psychiatry. 1994;151:169-176.

19. Small JG, Klapper MH, et al. Electroconvulsive treatment compared with lithium in the management of manic states. Arch Gen Psychiatry. 1988;45:727-732.

20. Sikdar S, Kulhara P, Avasthi A, Singh H. Combined chlorpromazine and electroconvulsive therapy in mania. Br J Psychiatry. 1994;164:806-810.

21. Krueger RB, Sackeim HA. Electroconvulsive therapy and schizophrenia. In Schizophrenia. SR Hirsch and D Weinberger, eds. Oxford, England: Blackwell Scientific, 1995;503-545.

22. Chanpattana W, Chakrabhand ML, Sackeim HA, et al. Continuation ECT in treatment-resistant schizophrenia: a controlled study. J ECT. 1999;15:178-192.

23. Sackeim HA, Prudic J, Devanand DP, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral ECT at different stimulus intensities. Arch Gen Psychiatry. 2000;57:425-434.

24. Shapira B, Tubi N, Drexler H, Lidsky D, Calev A, Lerer B. Cost and benefit in the choice of ECT schedule. Twice versus three times weekly ECT. Br J Psychiatry. 1998;172:44-48.

25. Rasmussen KG, Richardson JR, Rummans TA. ECT in the medically ill. Psychiatric Clin North Amer (in press).

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Although numerous psychotropic agents in multiple classes have emerged over the past few decades, electroconvulsive therapy (ECT) still represents an essential treatment in modern psychiatry. Its record of safety and efficacy is virtually unparalleled vis a vis pharmacological agents.

Advances in anesthetic technique, electrode placement, and electrical stimulus dosing allow ECT to be administered safely to even the most medically ill patients without excessive effects on memory, with excellent clinical benefits (Box 1). A typical course of ECT consists of 8 to 10 treatments administered 2 to 3 times per week.

The medical complications of ECT are rare, and good pre-treatment medical assessment helps ensure its safety.1 Include at minimum a medical history, physical exam, and basic laboratory tests. Specialist consultations are sometimes necessary when patients have comorbid neurologic or cardiologic illnesses (Box 2).

The most bothersome side effect of ECT is memory disturbance. This takes 3 forms: post-treatment confusion and anterograde or retrograde amnesia (Box 3). Less serious side effects include headaches, muscle soreness, and nausea. These are easily treated symptomatically with analgesics or antiemetics.

Box 1

THE TECHNICAL FACTORS OF ECT AFFECTING EFFICACY AND SIDE EFFECTS

Electroconvulsive therapy (ECT) has been in use since 1938.6 It consists of the application of an electric current to the head, which causes a seizure.

Modern ECT technique involves the use of general anesthesia, usually with a barbiturate anesthetic such as methohexital, and muscular paralysis, usually with the depolarizing neuromuscular blocking agent succinylcholine. Continuous oxygenation with positive pressure ventilation, measuring of blood pressure, and monitoring with an electrocardiogram and pulse oximetry make the procedure exceedingly safe.

Efficacy and cognitive side effects may be affected by how ECT is administered. The two treatment electrodes that are placed on the head can be located on either side of the temporal fossa (the bitemporal position), on either side of the forehead (the bifrontal position), or on the right temporal fossa and just to the right of the vertex of the skull (the d’Elia unilateral position). Generally, unilateral electrode placement causes less memory impairment but has been believed to be less effective than bilateral electrode positions.6

Another technical factor receiving attention from researchers is the amount of electricity, or electrical dose, used to elicit the seizure. Generally, especially for unilateral ECT, high electrical doses are needed to attain acceptable treatment efficacy. In fact, one study indicates that if 6 times the minimum electrical seizure threshold is used for unilateral ECT, efficacy for depression is equal to that of bilateral ECT with less memory disturbance.23

Finally, treatment frequency affects ECT outcome: twice-weekly treatment schedules are associated with less memory disturbance—and only slightly slower clinical response—than thrice-weekly schedules.24

The most common indication for ECT is major depression. Using modern diagnostic criteria, most depressed patients respond to ECT. Some features that presage a particularly robust response include psychomotor retardation, psychosis, catatonia, and advanced age. Patients who have medication-resistant depression may require particularly potent forms of treatment, such as bilateral electrode placement and/or higher than usual electrical doses.

Patients with mania respond particularly well to ECT but, because of excellent responses with modern pharmacological agents, rarely need it. For patients with mania who are agitated and noncompliant, ECT may represent a life-saving option for stabilizing an acute episode. Finally, ECT may help yield stability for an acute exacerbation of schizophrenia or may extend the benefits of antipsychotic medication for those with chronic schizophrenia, in which case continuation of ECT is usually advisable.

When ECT is indicated for depression

Typical depressed patients receiving ECT have experienced functional decline and have resisted, or have not tolerated, antidepressant medication. Several specific factors affect whether ECT will help particular depressed patients:

Melancholic features From the earliest use of ECT, it seemed apparent that patients with melancholic depression respond better to ECT than do patients with atypical or mood-reactive depression. Early research seems to have borne this out. Roberts2 found that melancholic features such as psychomotor retardation and guilty ideations strongly and favorably predicted ECT response. More recent research, however, generally fails to find predictive value in ECT response in patients based on presence of melancholia.3

Box 2

WHEN MEDICAL ILLNESS REQUIRES A CONSULTATION BEFORE ECT

The medical and neurologic illnesses that place prospective ECT patients at higher than usual risk of complications include a brain tumor or other intracranial space-occupying lesion, increased intracranial pressure, unstable cardiac function, or high anesthetic risk.25

Patients with severe cardiac disease, such as congestive heart failure, coronary artery disease, or cardiac dysrhythmia, can almost always be treated with ECT safely with adequate attention to pretreatment medical stabilization and use of antihypertensive medications during the treatment to blunt the increase in myocardial oxygen demand during the seizures.

 

 

Why is this? Several factors likely explain this rather dramatic difference. First, the patients given ECT in the early decades of its use most likely suffered with a diverse range of dysphoric states (e.g., patients with “neurotic” depression, dysthymia, or personality disorders), while modern research has been limited to relatively homogeneous samples of patients with major depression defined according to strict research criteria.3 When you try to correlate a putative predictive variable such as presence vs. absence of melancholia with an outcome variable such as reduction in depression ratings, the less variability there is on the predictive variable, the less strong the correlation will be.

Another possible factor accounting for the lack of predictability is a broadened concept of melancholia. According to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV),4 it is possible to have melancholic depression without having weight loss, psychomotor retardation, or excessive guilt—3 signs classically thought to be inherent in the melancholic syndrome. If melancholia is defined more narrowly, to include requirements for weight loss and psychomotor change, then it is probably more likely to correlate with ECT response.

A final potential reason for lack of predictability is the method of ascertaining melancholia. In modern samples, usually the Hamilton Rating Scale for Depression is used.5 Such a scale is administered in a brief interview by a research clinician not familiar with any other aspects of the patient’s mental status. In contrast, in some early studies,2 melancholic signs were ascertained by complete psychiatric history and evaluations as done in clinical practice. Such methods are likely to yield more reliable data on weight loss, guilty ideations, psychomotor activity, and other signs than is a 15-to 20-minute interview conducted by a research technician.

Along these lines, Hickie et al,6 utilizing a thorough evaluation of psychomotor activity before ECT, found that psychomotor retardation robustly predicted positive ECT response. Their scale utilized numerous items assessing agitation and retardation, and required a longer period of assessment than did the Hamilton scale; the latter scale has only 2 items for psychomotor activity, each one a global assessment of agitation or retardation.

So do you consider ECT for patients with melancholic features? Yes. Patients with classic melancholic features such as weight loss, pronounced guilt, and especially psychomotor retardation stand an excellent chance of substantial relief with a course of ECT. Additionally, patients with nonmelancholic depression have good response rates with ECT.

Box 3

WHAT TO TELL YOUR ECT PATIENTS ABOUT MEMORY DISTURBANCE

Patients and their families are frequently concerned about the effects of ECT on memory. The 3 types of memory disturbances to discuss are:

  1. Post-treatment confusion and disorientation. This state usually lasts from a few minutes to several hours or, in the case of some elderly patients after receiving numerous treatments, several days. This state is always reversible.
  2. Anterograde amnesia. This is the inability to recall newly learned information during and up to a few weeks after the course of treatments. During this time, any information given to the ECT patient may not be remembered. Important strategies are to write down instructions and make sure that family members are informed of the need to repeat things and monitor the patient if an outpatient. Fortunately, antero-grade amnesia is also reversible.
  3. Retrograde amnesia. This refers to the forgetting of personal life events and general knowledge about the world. Usually, the events and knowledge that are “wiped out” by the treatments are those from up to a few months before the treatments begin to about a month after the treatments are done. Even more remote memories may be forgotten as well. Unlike the other types of ECT-induced memory impairment, retrograde amnesia may be permanent.

Catatonic features It has been known for decades that catatonic features, regardless of etiology, respond robustly and often quickly to a course of ECT.1,7 But in recent years, the literature has documented the high rates of efficacy of benzodiazepines, usually lorazepam, in the initial treatment of catatonic signs such as mutism, stupor, waxy flexibility, posturing, stereotypies, and rigidity.

Bush et al8 treated 21 acutely catatonic patients, who were so diagnosed according to a standardized catatonia rating scale, with parenteral and oral lorazepam at doses up to 8 mg/d. Sixteen responded dramatically, usually within a day or so. Four of the lorazepam nonresponders were given ECT with excellent results, not only for the catatonic signs but also for other underlying psychopathological features.

Ungvari et al9 treated 18 catatonic patients with either lorazepam or diazepam; all patients had some degree of improvement after several days, but 9 of the 18 exhibited insufficient response. For these, ECT was administered with excellent resolution of the psychopathology, including catatonia.

 

 

A reasonable conclusion from these studies is that acutely catatonic patients should be treated first with a benzodiazepine such as parenteral and/or oral lorazepam, perhaps for up to 3 days, and then given ECT if response is insufficient. For patients with malignant catatonia—a particularly severe and life-threatening form of catatonia—ECT may need to be instituted sooner.10

Psychotic features Though the literature has been mixed on this subject, patients with psychotic depression have high response rates to an adequate course of ECT treatments. Hickie et al6 treated 81 depressed patients with ECT and performed in-depth analyses of a variety of clinical variables, including the presence of psychosis. Patients with psychotic depression were found to have a significantly higher rate of ECT response than those with nonpsychotic depression, though the latter still had high response rates.

ECT is considered a primary indication for patients with psychotic depression1,7 for two reasons:

  1. Response rates are uniformly high.
  2. If such patients were to receive pharmacotherapy, a neuroleptic with all the potential neurologic side effects inherent in such medication would be needed.

Further, clinical experience reveals that psychotically depressed patients tend to be particularly nonfunctional, to have lost weight, and to be suicidal. Thus, the rapid, definitive benefits of ECT are necessary as first-line therapy.

Age Age has been positively correlated with ECT outcome. Black et al,11 in an analysis of clinical predictors of ECT in several hundred patients, found that older patients responded more favorably to ECT than did younger ones. The study included careful assessments of pre- and post-ECT clinical status.

Tew et al,12 in a well-designed prospective study of several hundred ECT patients, found that those older than age 65 responded to ECT more favorably than those younger than 65. Possible mitigating factors in the younger group were greater medication nonresponsivity prior to ECT and longer illness severity. In another prospective study, Wilkinson et al13 also found superior response rates in patients older than 75.

At minimum, a consensus emerges from the literature that ECT response rates are at least as good in the elderly as in younger patients, an important finding given the often debilitating effects of depressive illness in this population and the high rates of medication nonresponse.

Potential for self-harm ECT is highly effective for suicidal or cachectic individuals. Decades of clinical practice have clearly established that acutely suicidal, depressed patients and those whose poor food and fluid intake has caused nutritional compromise represent urgent indications for ECT.1,7 In particular, recent research suggests that ECT response may be especially rapid in bipolar depressed patients.14

Medication resistance It is common practice for depressed patients to be given ECT after resistance to one or more medications is established. But recent research indicates that patients with medication-refractory depression respond to ECT at roughly half the rate of those who have not had an adequate antidepressant trial.15 Medication-resistant patients also have higher relapse rates post-ECT, even when they do initially respond.

Thus, particularly aggressive treatment regimens may be necessary for medication-refractory patients, including use of bilateral electrode placement and/or higher than usual electrical doses.

Another strategy would be to combine medications with ECT during the index course. While not studied prospectively, one retrospective comparison of ECT patients who were either given or not given concomitant nortriptyline suggests that such a strategy may enhance ECT efficacy.16

Personality factors Over the past few decades, patients with nonmelancholic depression have been variably referred to as neurotic, mood-reactive, hysterical, or personality-disordered. The difficulties inherent in precisely defining and measuring these variables make them difficult to apply to day-to-day practice. The more chaotic and unpredictable the patient’s emotional life, and the more mood-reactive the patient is to life events, the less the chance of substantial ECT benefit. In fact, a recent study indicates that depressed patients with personality disorders, especially from DSM-IV cluster B,4 have lower acute ECT response rates and higher post-ECT relapse rates than do depressed ECT patients without personality disorders.17

ECT: first choice for highly agitated manic patients

From the early days of ECT, it rapidly became the mainstay for treating severe, life-threatening manic states until the advent of neuroleptic drugs in the late 1950s. Large, retrospective studies have shown ECT to be highly effective for manic states.18

Two prospective, random assignment trials in particular document the modality’s efficacy. Small et al19 randomly assigned manic patients to either lithium treatment or ECT. While patients in both groups responded well, response was faster in the ECT group. Sikdar et al20 administered chlorpromazine and either real or sham ECT to manic patients and found that adding ECT to neuroleptic patients’ treatments substantially improved outcomes.

 

 

In modern practice, various anticonvulsants have become common for treating mania, and no comparative data between such agents and ECT are available. ECT is reserved for highly agitated, medication-refractory patients. The typical scenario entails a patient who does not respond to high doses of parenteral sedatives or antipsychotics, is in restraints much of the time, and is not cooperating with orally administered medications. In such circumstances, court-ordered approval for ECT is usually needed. Fortunately, in my experience bilateral ECT is almost universally effective for such patients, who are often grateful for their treatment once they achieve euthymia.

Rare uses of ECT in schizophrenia

ECT was commonly used for schizophrenia as well as mania before the advent of neuroleptics7 but is only rarely used for this indication in modern times. Here are the exceptions:1

  1. For acute exacerbations, especially with florid-positive symptoms such as delusions, hallucinations, disorganized thoughts and behavior, or catatonia. ECT can be remarkably effective in rendering patients compliant with oral medication. From there, patients can be discharged and can proceed with outpatient therapy.
  2. For the chronically ill patient, if multiple medication trials fail to achieve optimum results. When administered in combination with antipsychotic medication, a trial of ECT may extend whatever benefits accrue from medication.7 In particular, the combination of ECT and neuroleptic medication may be more effective in such cases than either ECT or medication alone.21

Especially for chronically ill patients with schizophrenia, any benefits of an acute course of ECT will likely be short-lived unless maintenance ECT is instituted. In a well-designed study of schizophrenic patients stabilized with a combination of neuroleptic medication and an acute course of ECT, Chanpattana et al22 found that those maintained for 6 months with combination continuation ECT and pharmacotherapy did much better than did those randomly assigned to either modality alone.

Related resources

  • Abrams R. Electroconvulsive Therapy. 3rd ed. New York: Oxford University Press; 1997.
  • American Psychiatric Association. Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 2nd ed. Washington, D.C.:American Psychiatric Association; 2001.
  • Mukherjee S, Sackeim HA, Schnur DB. Electroconvulsive therapy of acute manic episodes: a review of 50 years’ experience. Am J Psychiatry. 1994;151:169-176.

Drug brand names

  • Methohexital • Amidate, Brevital, Diprivan, Ethrane
  • Succinylcholine • Anectine

Disclosure

The author reports no affiliation or financial arrangement with any of the companies whose products are mentioned in this article.

References

1. American Psychiatric Association. Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 2nd ed. Washington, D.C.: American Psychiatric Association; 2001.

2. Roberts JM. Prognostic factors in the electroshock treatment of depressive states I. Clinical features from history and examination. J Ment Sci. 1959;105:693-702.

3. Sackeim HA, Rush AJ. Melancholia and response to ECT (letter). Am J Psychiatry. 1995;152(8):1242-1243.

4. American Psychiatric Association. Diagniositc and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994.

5. Sobin C, Prudic J, Devanand DP, Nobler MS, Sackeim HA. Who responds to electroconvulsive therapy? Br J Psychiatry. 1996;169:322-328.

6. Hickie I, Mason C, et al. Prediction of ECT response: validation of a refined sign-based (CORE) system for defining melancholia. Br J Psychiatry. 1996;169(1):68-74.

7. Abrams R. Electroconvulsive Therapy. 3rd ed. New York: Oxford University Press; 1997.

8. Bush G, Fink M, Petrides G, et al. Treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand. 1996;93:137-143.

9. Ungvari GA, Leung CM, Wong MK, Lau J. Benzodiazepines in the treatment of catatonic syndrome. Acta Psychiatr Scand. 1994;89:285-288.

10. Philbrick KL, Rummans TA. Malignant catatonia. J Neuropsychiatry and Clinical Neurosciences. 1994;6:1-13.

11. Black DW, Winokur G, Nasrallah A. A multivariate analysis of the experience of 423 depressed inpatients treated with electroconvulsive therapy. Convulsive Ther. 1993;9:112-120.

12. Tew JD, Jr, Mulsant BH, Haskett RF, et al. Acute efficacy of ECT in the treatment of major depression in the old. Am J Psychiatry. 1999;156:1865-1870.

13. Wilkinson AM, Anderson DN, Peters S. Age and the effects of ECT. Int J Geriatr Psychiatry. 1993;8:401-406.

14. Daly JJ, Prudic J, Devanand DP, et al. ECT in bipolar and unipolar depression: differences in speed of response. Bipolar Disorders. 2001;3(2):95-104.

15. Prudic J, Haskett RF, Mulsant B, et al. Resistance to antidepressant medications and short-term clinical response to ECT. Am J Psychiatry. 1996;153(8):985-992.

16. Nelson JP, Benjamin L. Efficacy and safety of combined ECT and tricyclic antidepressant therapy in the treatment of depressed geriatric patients. Convulsive Ther. 1989;5:321-329.

17. Sareen J, Enns MW, Guertin JE. The impact of clinically diagnosed personality disorders on acute and one-year outcomes of electroconvulsive therapy. J ECT. 2000;16(1):43-51.

18. Mukherjee S, Sackeim HA, Schnur DB. Electroconvulsive therapy of acute manic episodes: a review of 50 years’ experience. Am J Psychiatry. 1994;151:169-176.

19. Small JG, Klapper MH, et al. Electroconvulsive treatment compared with lithium in the management of manic states. Arch Gen Psychiatry. 1988;45:727-732.

20. Sikdar S, Kulhara P, Avasthi A, Singh H. Combined chlorpromazine and electroconvulsive therapy in mania. Br J Psychiatry. 1994;164:806-810.

21. Krueger RB, Sackeim HA. Electroconvulsive therapy and schizophrenia. In Schizophrenia. SR Hirsch and D Weinberger, eds. Oxford, England: Blackwell Scientific, 1995;503-545.

22. Chanpattana W, Chakrabhand ML, Sackeim HA, et al. Continuation ECT in treatment-resistant schizophrenia: a controlled study. J ECT. 1999;15:178-192.

23. Sackeim HA, Prudic J, Devanand DP, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral ECT at different stimulus intensities. Arch Gen Psychiatry. 2000;57:425-434.

24. Shapira B, Tubi N, Drexler H, Lidsky D, Calev A, Lerer B. Cost and benefit in the choice of ECT schedule. Twice versus three times weekly ECT. Br J Psychiatry. 1998;172:44-48.

25. Rasmussen KG, Richardson JR, Rummans TA. ECT in the medically ill. Psychiatric Clin North Amer (in press).

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Assistant Professor of Psychiatry, Mayo Clinic, Rochester, Minn

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Assistant Professor of Psychiatry, Mayo Clinic, Rochester, Minn

Although numerous psychotropic agents in multiple classes have emerged over the past few decades, electroconvulsive therapy (ECT) still represents an essential treatment in modern psychiatry. Its record of safety and efficacy is virtually unparalleled vis a vis pharmacological agents.

Advances in anesthetic technique, electrode placement, and electrical stimulus dosing allow ECT to be administered safely to even the most medically ill patients without excessive effects on memory, with excellent clinical benefits (Box 1). A typical course of ECT consists of 8 to 10 treatments administered 2 to 3 times per week.

The medical complications of ECT are rare, and good pre-treatment medical assessment helps ensure its safety.1 Include at minimum a medical history, physical exam, and basic laboratory tests. Specialist consultations are sometimes necessary when patients have comorbid neurologic or cardiologic illnesses (Box 2).

The most bothersome side effect of ECT is memory disturbance. This takes 3 forms: post-treatment confusion and anterograde or retrograde amnesia (Box 3). Less serious side effects include headaches, muscle soreness, and nausea. These are easily treated symptomatically with analgesics or antiemetics.

Box 1

THE TECHNICAL FACTORS OF ECT AFFECTING EFFICACY AND SIDE EFFECTS

Electroconvulsive therapy (ECT) has been in use since 1938.6 It consists of the application of an electric current to the head, which causes a seizure.

Modern ECT technique involves the use of general anesthesia, usually with a barbiturate anesthetic such as methohexital, and muscular paralysis, usually with the depolarizing neuromuscular blocking agent succinylcholine. Continuous oxygenation with positive pressure ventilation, measuring of blood pressure, and monitoring with an electrocardiogram and pulse oximetry make the procedure exceedingly safe.

Efficacy and cognitive side effects may be affected by how ECT is administered. The two treatment electrodes that are placed on the head can be located on either side of the temporal fossa (the bitemporal position), on either side of the forehead (the bifrontal position), or on the right temporal fossa and just to the right of the vertex of the skull (the d’Elia unilateral position). Generally, unilateral electrode placement causes less memory impairment but has been believed to be less effective than bilateral electrode positions.6

Another technical factor receiving attention from researchers is the amount of electricity, or electrical dose, used to elicit the seizure. Generally, especially for unilateral ECT, high electrical doses are needed to attain acceptable treatment efficacy. In fact, one study indicates that if 6 times the minimum electrical seizure threshold is used for unilateral ECT, efficacy for depression is equal to that of bilateral ECT with less memory disturbance.23

Finally, treatment frequency affects ECT outcome: twice-weekly treatment schedules are associated with less memory disturbance—and only slightly slower clinical response—than thrice-weekly schedules.24

The most common indication for ECT is major depression. Using modern diagnostic criteria, most depressed patients respond to ECT. Some features that presage a particularly robust response include psychomotor retardation, psychosis, catatonia, and advanced age. Patients who have medication-resistant depression may require particularly potent forms of treatment, such as bilateral electrode placement and/or higher than usual electrical doses.

Patients with mania respond particularly well to ECT but, because of excellent responses with modern pharmacological agents, rarely need it. For patients with mania who are agitated and noncompliant, ECT may represent a life-saving option for stabilizing an acute episode. Finally, ECT may help yield stability for an acute exacerbation of schizophrenia or may extend the benefits of antipsychotic medication for those with chronic schizophrenia, in which case continuation of ECT is usually advisable.

When ECT is indicated for depression

Typical depressed patients receiving ECT have experienced functional decline and have resisted, or have not tolerated, antidepressant medication. Several specific factors affect whether ECT will help particular depressed patients:

Melancholic features From the earliest use of ECT, it seemed apparent that patients with melancholic depression respond better to ECT than do patients with atypical or mood-reactive depression. Early research seems to have borne this out. Roberts2 found that melancholic features such as psychomotor retardation and guilty ideations strongly and favorably predicted ECT response. More recent research, however, generally fails to find predictive value in ECT response in patients based on presence of melancholia.3

Box 2

WHEN MEDICAL ILLNESS REQUIRES A CONSULTATION BEFORE ECT

The medical and neurologic illnesses that place prospective ECT patients at higher than usual risk of complications include a brain tumor or other intracranial space-occupying lesion, increased intracranial pressure, unstable cardiac function, or high anesthetic risk.25

Patients with severe cardiac disease, such as congestive heart failure, coronary artery disease, or cardiac dysrhythmia, can almost always be treated with ECT safely with adequate attention to pretreatment medical stabilization and use of antihypertensive medications during the treatment to blunt the increase in myocardial oxygen demand during the seizures.

 

 

Why is this? Several factors likely explain this rather dramatic difference. First, the patients given ECT in the early decades of its use most likely suffered with a diverse range of dysphoric states (e.g., patients with “neurotic” depression, dysthymia, or personality disorders), while modern research has been limited to relatively homogeneous samples of patients with major depression defined according to strict research criteria.3 When you try to correlate a putative predictive variable such as presence vs. absence of melancholia with an outcome variable such as reduction in depression ratings, the less variability there is on the predictive variable, the less strong the correlation will be.

Another possible factor accounting for the lack of predictability is a broadened concept of melancholia. According to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV),4 it is possible to have melancholic depression without having weight loss, psychomotor retardation, or excessive guilt—3 signs classically thought to be inherent in the melancholic syndrome. If melancholia is defined more narrowly, to include requirements for weight loss and psychomotor change, then it is probably more likely to correlate with ECT response.

A final potential reason for lack of predictability is the method of ascertaining melancholia. In modern samples, usually the Hamilton Rating Scale for Depression is used.5 Such a scale is administered in a brief interview by a research clinician not familiar with any other aspects of the patient’s mental status. In contrast, in some early studies,2 melancholic signs were ascertained by complete psychiatric history and evaluations as done in clinical practice. Such methods are likely to yield more reliable data on weight loss, guilty ideations, psychomotor activity, and other signs than is a 15-to 20-minute interview conducted by a research technician.

Along these lines, Hickie et al,6 utilizing a thorough evaluation of psychomotor activity before ECT, found that psychomotor retardation robustly predicted positive ECT response. Their scale utilized numerous items assessing agitation and retardation, and required a longer period of assessment than did the Hamilton scale; the latter scale has only 2 items for psychomotor activity, each one a global assessment of agitation or retardation.

So do you consider ECT for patients with melancholic features? Yes. Patients with classic melancholic features such as weight loss, pronounced guilt, and especially psychomotor retardation stand an excellent chance of substantial relief with a course of ECT. Additionally, patients with nonmelancholic depression have good response rates with ECT.

Box 3

WHAT TO TELL YOUR ECT PATIENTS ABOUT MEMORY DISTURBANCE

Patients and their families are frequently concerned about the effects of ECT on memory. The 3 types of memory disturbances to discuss are:

  1. Post-treatment confusion and disorientation. This state usually lasts from a few minutes to several hours or, in the case of some elderly patients after receiving numerous treatments, several days. This state is always reversible.
  2. Anterograde amnesia. This is the inability to recall newly learned information during and up to a few weeks after the course of treatments. During this time, any information given to the ECT patient may not be remembered. Important strategies are to write down instructions and make sure that family members are informed of the need to repeat things and monitor the patient if an outpatient. Fortunately, antero-grade amnesia is also reversible.
  3. Retrograde amnesia. This refers to the forgetting of personal life events and general knowledge about the world. Usually, the events and knowledge that are “wiped out” by the treatments are those from up to a few months before the treatments begin to about a month after the treatments are done. Even more remote memories may be forgotten as well. Unlike the other types of ECT-induced memory impairment, retrograde amnesia may be permanent.

Catatonic features It has been known for decades that catatonic features, regardless of etiology, respond robustly and often quickly to a course of ECT.1,7 But in recent years, the literature has documented the high rates of efficacy of benzodiazepines, usually lorazepam, in the initial treatment of catatonic signs such as mutism, stupor, waxy flexibility, posturing, stereotypies, and rigidity.

Bush et al8 treated 21 acutely catatonic patients, who were so diagnosed according to a standardized catatonia rating scale, with parenteral and oral lorazepam at doses up to 8 mg/d. Sixteen responded dramatically, usually within a day or so. Four of the lorazepam nonresponders were given ECT with excellent results, not only for the catatonic signs but also for other underlying psychopathological features.

Ungvari et al9 treated 18 catatonic patients with either lorazepam or diazepam; all patients had some degree of improvement after several days, but 9 of the 18 exhibited insufficient response. For these, ECT was administered with excellent resolution of the psychopathology, including catatonia.

 

 

A reasonable conclusion from these studies is that acutely catatonic patients should be treated first with a benzodiazepine such as parenteral and/or oral lorazepam, perhaps for up to 3 days, and then given ECT if response is insufficient. For patients with malignant catatonia—a particularly severe and life-threatening form of catatonia—ECT may need to be instituted sooner.10

Psychotic features Though the literature has been mixed on this subject, patients with psychotic depression have high response rates to an adequate course of ECT treatments. Hickie et al6 treated 81 depressed patients with ECT and performed in-depth analyses of a variety of clinical variables, including the presence of psychosis. Patients with psychotic depression were found to have a significantly higher rate of ECT response than those with nonpsychotic depression, though the latter still had high response rates.

ECT is considered a primary indication for patients with psychotic depression1,7 for two reasons:

  1. Response rates are uniformly high.
  2. If such patients were to receive pharmacotherapy, a neuroleptic with all the potential neurologic side effects inherent in such medication would be needed.

Further, clinical experience reveals that psychotically depressed patients tend to be particularly nonfunctional, to have lost weight, and to be suicidal. Thus, the rapid, definitive benefits of ECT are necessary as first-line therapy.

Age Age has been positively correlated with ECT outcome. Black et al,11 in an analysis of clinical predictors of ECT in several hundred patients, found that older patients responded more favorably to ECT than did younger ones. The study included careful assessments of pre- and post-ECT clinical status.

Tew et al,12 in a well-designed prospective study of several hundred ECT patients, found that those older than age 65 responded to ECT more favorably than those younger than 65. Possible mitigating factors in the younger group were greater medication nonresponsivity prior to ECT and longer illness severity. In another prospective study, Wilkinson et al13 also found superior response rates in patients older than 75.

At minimum, a consensus emerges from the literature that ECT response rates are at least as good in the elderly as in younger patients, an important finding given the often debilitating effects of depressive illness in this population and the high rates of medication nonresponse.

Potential for self-harm ECT is highly effective for suicidal or cachectic individuals. Decades of clinical practice have clearly established that acutely suicidal, depressed patients and those whose poor food and fluid intake has caused nutritional compromise represent urgent indications for ECT.1,7 In particular, recent research suggests that ECT response may be especially rapid in bipolar depressed patients.14

Medication resistance It is common practice for depressed patients to be given ECT after resistance to one or more medications is established. But recent research indicates that patients with medication-refractory depression respond to ECT at roughly half the rate of those who have not had an adequate antidepressant trial.15 Medication-resistant patients also have higher relapse rates post-ECT, even when they do initially respond.

Thus, particularly aggressive treatment regimens may be necessary for medication-refractory patients, including use of bilateral electrode placement and/or higher than usual electrical doses.

Another strategy would be to combine medications with ECT during the index course. While not studied prospectively, one retrospective comparison of ECT patients who were either given or not given concomitant nortriptyline suggests that such a strategy may enhance ECT efficacy.16

Personality factors Over the past few decades, patients with nonmelancholic depression have been variably referred to as neurotic, mood-reactive, hysterical, or personality-disordered. The difficulties inherent in precisely defining and measuring these variables make them difficult to apply to day-to-day practice. The more chaotic and unpredictable the patient’s emotional life, and the more mood-reactive the patient is to life events, the less the chance of substantial ECT benefit. In fact, a recent study indicates that depressed patients with personality disorders, especially from DSM-IV cluster B,4 have lower acute ECT response rates and higher post-ECT relapse rates than do depressed ECT patients without personality disorders.17

ECT: first choice for highly agitated manic patients

From the early days of ECT, it rapidly became the mainstay for treating severe, life-threatening manic states until the advent of neuroleptic drugs in the late 1950s. Large, retrospective studies have shown ECT to be highly effective for manic states.18

Two prospective, random assignment trials in particular document the modality’s efficacy. Small et al19 randomly assigned manic patients to either lithium treatment or ECT. While patients in both groups responded well, response was faster in the ECT group. Sikdar et al20 administered chlorpromazine and either real or sham ECT to manic patients and found that adding ECT to neuroleptic patients’ treatments substantially improved outcomes.

 

 

In modern practice, various anticonvulsants have become common for treating mania, and no comparative data between such agents and ECT are available. ECT is reserved for highly agitated, medication-refractory patients. The typical scenario entails a patient who does not respond to high doses of parenteral sedatives or antipsychotics, is in restraints much of the time, and is not cooperating with orally administered medications. In such circumstances, court-ordered approval for ECT is usually needed. Fortunately, in my experience bilateral ECT is almost universally effective for such patients, who are often grateful for their treatment once they achieve euthymia.

Rare uses of ECT in schizophrenia

ECT was commonly used for schizophrenia as well as mania before the advent of neuroleptics7 but is only rarely used for this indication in modern times. Here are the exceptions:1

  1. For acute exacerbations, especially with florid-positive symptoms such as delusions, hallucinations, disorganized thoughts and behavior, or catatonia. ECT can be remarkably effective in rendering patients compliant with oral medication. From there, patients can be discharged and can proceed with outpatient therapy.
  2. For the chronically ill patient, if multiple medication trials fail to achieve optimum results. When administered in combination with antipsychotic medication, a trial of ECT may extend whatever benefits accrue from medication.7 In particular, the combination of ECT and neuroleptic medication may be more effective in such cases than either ECT or medication alone.21

Especially for chronically ill patients with schizophrenia, any benefits of an acute course of ECT will likely be short-lived unless maintenance ECT is instituted. In a well-designed study of schizophrenic patients stabilized with a combination of neuroleptic medication and an acute course of ECT, Chanpattana et al22 found that those maintained for 6 months with combination continuation ECT and pharmacotherapy did much better than did those randomly assigned to either modality alone.

Related resources

  • Abrams R. Electroconvulsive Therapy. 3rd ed. New York: Oxford University Press; 1997.
  • American Psychiatric Association. Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 2nd ed. Washington, D.C.:American Psychiatric Association; 2001.
  • Mukherjee S, Sackeim HA, Schnur DB. Electroconvulsive therapy of acute manic episodes: a review of 50 years’ experience. Am J Psychiatry. 1994;151:169-176.

Drug brand names

  • Methohexital • Amidate, Brevital, Diprivan, Ethrane
  • Succinylcholine • Anectine

Disclosure

The author reports no affiliation or financial arrangement with any of the companies whose products are mentioned in this article.

Although numerous psychotropic agents in multiple classes have emerged over the past few decades, electroconvulsive therapy (ECT) still represents an essential treatment in modern psychiatry. Its record of safety and efficacy is virtually unparalleled vis a vis pharmacological agents.

Advances in anesthetic technique, electrode placement, and electrical stimulus dosing allow ECT to be administered safely to even the most medically ill patients without excessive effects on memory, with excellent clinical benefits (Box 1). A typical course of ECT consists of 8 to 10 treatments administered 2 to 3 times per week.

The medical complications of ECT are rare, and good pre-treatment medical assessment helps ensure its safety.1 Include at minimum a medical history, physical exam, and basic laboratory tests. Specialist consultations are sometimes necessary when patients have comorbid neurologic or cardiologic illnesses (Box 2).

The most bothersome side effect of ECT is memory disturbance. This takes 3 forms: post-treatment confusion and anterograde or retrograde amnesia (Box 3). Less serious side effects include headaches, muscle soreness, and nausea. These are easily treated symptomatically with analgesics or antiemetics.

Box 1

THE TECHNICAL FACTORS OF ECT AFFECTING EFFICACY AND SIDE EFFECTS

Electroconvulsive therapy (ECT) has been in use since 1938.6 It consists of the application of an electric current to the head, which causes a seizure.

Modern ECT technique involves the use of general anesthesia, usually with a barbiturate anesthetic such as methohexital, and muscular paralysis, usually with the depolarizing neuromuscular blocking agent succinylcholine. Continuous oxygenation with positive pressure ventilation, measuring of blood pressure, and monitoring with an electrocardiogram and pulse oximetry make the procedure exceedingly safe.

Efficacy and cognitive side effects may be affected by how ECT is administered. The two treatment electrodes that are placed on the head can be located on either side of the temporal fossa (the bitemporal position), on either side of the forehead (the bifrontal position), or on the right temporal fossa and just to the right of the vertex of the skull (the d’Elia unilateral position). Generally, unilateral electrode placement causes less memory impairment but has been believed to be less effective than bilateral electrode positions.6

Another technical factor receiving attention from researchers is the amount of electricity, or electrical dose, used to elicit the seizure. Generally, especially for unilateral ECT, high electrical doses are needed to attain acceptable treatment efficacy. In fact, one study indicates that if 6 times the minimum electrical seizure threshold is used for unilateral ECT, efficacy for depression is equal to that of bilateral ECT with less memory disturbance.23

Finally, treatment frequency affects ECT outcome: twice-weekly treatment schedules are associated with less memory disturbance—and only slightly slower clinical response—than thrice-weekly schedules.24

The most common indication for ECT is major depression. Using modern diagnostic criteria, most depressed patients respond to ECT. Some features that presage a particularly robust response include psychomotor retardation, psychosis, catatonia, and advanced age. Patients who have medication-resistant depression may require particularly potent forms of treatment, such as bilateral electrode placement and/or higher than usual electrical doses.

Patients with mania respond particularly well to ECT but, because of excellent responses with modern pharmacological agents, rarely need it. For patients with mania who are agitated and noncompliant, ECT may represent a life-saving option for stabilizing an acute episode. Finally, ECT may help yield stability for an acute exacerbation of schizophrenia or may extend the benefits of antipsychotic medication for those with chronic schizophrenia, in which case continuation of ECT is usually advisable.

When ECT is indicated for depression

Typical depressed patients receiving ECT have experienced functional decline and have resisted, or have not tolerated, antidepressant medication. Several specific factors affect whether ECT will help particular depressed patients:

Melancholic features From the earliest use of ECT, it seemed apparent that patients with melancholic depression respond better to ECT than do patients with atypical or mood-reactive depression. Early research seems to have borne this out. Roberts2 found that melancholic features such as psychomotor retardation and guilty ideations strongly and favorably predicted ECT response. More recent research, however, generally fails to find predictive value in ECT response in patients based on presence of melancholia.3

Box 2

WHEN MEDICAL ILLNESS REQUIRES A CONSULTATION BEFORE ECT

The medical and neurologic illnesses that place prospective ECT patients at higher than usual risk of complications include a brain tumor or other intracranial space-occupying lesion, increased intracranial pressure, unstable cardiac function, or high anesthetic risk.25

Patients with severe cardiac disease, such as congestive heart failure, coronary artery disease, or cardiac dysrhythmia, can almost always be treated with ECT safely with adequate attention to pretreatment medical stabilization and use of antihypertensive medications during the treatment to blunt the increase in myocardial oxygen demand during the seizures.

 

 

Why is this? Several factors likely explain this rather dramatic difference. First, the patients given ECT in the early decades of its use most likely suffered with a diverse range of dysphoric states (e.g., patients with “neurotic” depression, dysthymia, or personality disorders), while modern research has been limited to relatively homogeneous samples of patients with major depression defined according to strict research criteria.3 When you try to correlate a putative predictive variable such as presence vs. absence of melancholia with an outcome variable such as reduction in depression ratings, the less variability there is on the predictive variable, the less strong the correlation will be.

Another possible factor accounting for the lack of predictability is a broadened concept of melancholia. According to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV),4 it is possible to have melancholic depression without having weight loss, psychomotor retardation, or excessive guilt—3 signs classically thought to be inherent in the melancholic syndrome. If melancholia is defined more narrowly, to include requirements for weight loss and psychomotor change, then it is probably more likely to correlate with ECT response.

A final potential reason for lack of predictability is the method of ascertaining melancholia. In modern samples, usually the Hamilton Rating Scale for Depression is used.5 Such a scale is administered in a brief interview by a research clinician not familiar with any other aspects of the patient’s mental status. In contrast, in some early studies,2 melancholic signs were ascertained by complete psychiatric history and evaluations as done in clinical practice. Such methods are likely to yield more reliable data on weight loss, guilty ideations, psychomotor activity, and other signs than is a 15-to 20-minute interview conducted by a research technician.

Along these lines, Hickie et al,6 utilizing a thorough evaluation of psychomotor activity before ECT, found that psychomotor retardation robustly predicted positive ECT response. Their scale utilized numerous items assessing agitation and retardation, and required a longer period of assessment than did the Hamilton scale; the latter scale has only 2 items for psychomotor activity, each one a global assessment of agitation or retardation.

So do you consider ECT for patients with melancholic features? Yes. Patients with classic melancholic features such as weight loss, pronounced guilt, and especially psychomotor retardation stand an excellent chance of substantial relief with a course of ECT. Additionally, patients with nonmelancholic depression have good response rates with ECT.

Box 3

WHAT TO TELL YOUR ECT PATIENTS ABOUT MEMORY DISTURBANCE

Patients and their families are frequently concerned about the effects of ECT on memory. The 3 types of memory disturbances to discuss are:

  1. Post-treatment confusion and disorientation. This state usually lasts from a few minutes to several hours or, in the case of some elderly patients after receiving numerous treatments, several days. This state is always reversible.
  2. Anterograde amnesia. This is the inability to recall newly learned information during and up to a few weeks after the course of treatments. During this time, any information given to the ECT patient may not be remembered. Important strategies are to write down instructions and make sure that family members are informed of the need to repeat things and monitor the patient if an outpatient. Fortunately, antero-grade amnesia is also reversible.
  3. Retrograde amnesia. This refers to the forgetting of personal life events and general knowledge about the world. Usually, the events and knowledge that are “wiped out” by the treatments are those from up to a few months before the treatments begin to about a month after the treatments are done. Even more remote memories may be forgotten as well. Unlike the other types of ECT-induced memory impairment, retrograde amnesia may be permanent.

Catatonic features It has been known for decades that catatonic features, regardless of etiology, respond robustly and often quickly to a course of ECT.1,7 But in recent years, the literature has documented the high rates of efficacy of benzodiazepines, usually lorazepam, in the initial treatment of catatonic signs such as mutism, stupor, waxy flexibility, posturing, stereotypies, and rigidity.

Bush et al8 treated 21 acutely catatonic patients, who were so diagnosed according to a standardized catatonia rating scale, with parenteral and oral lorazepam at doses up to 8 mg/d. Sixteen responded dramatically, usually within a day or so. Four of the lorazepam nonresponders were given ECT with excellent results, not only for the catatonic signs but also for other underlying psychopathological features.

Ungvari et al9 treated 18 catatonic patients with either lorazepam or diazepam; all patients had some degree of improvement after several days, but 9 of the 18 exhibited insufficient response. For these, ECT was administered with excellent resolution of the psychopathology, including catatonia.

 

 

A reasonable conclusion from these studies is that acutely catatonic patients should be treated first with a benzodiazepine such as parenteral and/or oral lorazepam, perhaps for up to 3 days, and then given ECT if response is insufficient. For patients with malignant catatonia—a particularly severe and life-threatening form of catatonia—ECT may need to be instituted sooner.10

Psychotic features Though the literature has been mixed on this subject, patients with psychotic depression have high response rates to an adequate course of ECT treatments. Hickie et al6 treated 81 depressed patients with ECT and performed in-depth analyses of a variety of clinical variables, including the presence of psychosis. Patients with psychotic depression were found to have a significantly higher rate of ECT response than those with nonpsychotic depression, though the latter still had high response rates.

ECT is considered a primary indication for patients with psychotic depression1,7 for two reasons:

  1. Response rates are uniformly high.
  2. If such patients were to receive pharmacotherapy, a neuroleptic with all the potential neurologic side effects inherent in such medication would be needed.

Further, clinical experience reveals that psychotically depressed patients tend to be particularly nonfunctional, to have lost weight, and to be suicidal. Thus, the rapid, definitive benefits of ECT are necessary as first-line therapy.

Age Age has been positively correlated with ECT outcome. Black et al,11 in an analysis of clinical predictors of ECT in several hundred patients, found that older patients responded more favorably to ECT than did younger ones. The study included careful assessments of pre- and post-ECT clinical status.

Tew et al,12 in a well-designed prospective study of several hundred ECT patients, found that those older than age 65 responded to ECT more favorably than those younger than 65. Possible mitigating factors in the younger group were greater medication nonresponsivity prior to ECT and longer illness severity. In another prospective study, Wilkinson et al13 also found superior response rates in patients older than 75.

At minimum, a consensus emerges from the literature that ECT response rates are at least as good in the elderly as in younger patients, an important finding given the often debilitating effects of depressive illness in this population and the high rates of medication nonresponse.

Potential for self-harm ECT is highly effective for suicidal or cachectic individuals. Decades of clinical practice have clearly established that acutely suicidal, depressed patients and those whose poor food and fluid intake has caused nutritional compromise represent urgent indications for ECT.1,7 In particular, recent research suggests that ECT response may be especially rapid in bipolar depressed patients.14

Medication resistance It is common practice for depressed patients to be given ECT after resistance to one or more medications is established. But recent research indicates that patients with medication-refractory depression respond to ECT at roughly half the rate of those who have not had an adequate antidepressant trial.15 Medication-resistant patients also have higher relapse rates post-ECT, even when they do initially respond.

Thus, particularly aggressive treatment regimens may be necessary for medication-refractory patients, including use of bilateral electrode placement and/or higher than usual electrical doses.

Another strategy would be to combine medications with ECT during the index course. While not studied prospectively, one retrospective comparison of ECT patients who were either given or not given concomitant nortriptyline suggests that such a strategy may enhance ECT efficacy.16

Personality factors Over the past few decades, patients with nonmelancholic depression have been variably referred to as neurotic, mood-reactive, hysterical, or personality-disordered. The difficulties inherent in precisely defining and measuring these variables make them difficult to apply to day-to-day practice. The more chaotic and unpredictable the patient’s emotional life, and the more mood-reactive the patient is to life events, the less the chance of substantial ECT benefit. In fact, a recent study indicates that depressed patients with personality disorders, especially from DSM-IV cluster B,4 have lower acute ECT response rates and higher post-ECT relapse rates than do depressed ECT patients without personality disorders.17

ECT: first choice for highly agitated manic patients

From the early days of ECT, it rapidly became the mainstay for treating severe, life-threatening manic states until the advent of neuroleptic drugs in the late 1950s. Large, retrospective studies have shown ECT to be highly effective for manic states.18

Two prospective, random assignment trials in particular document the modality’s efficacy. Small et al19 randomly assigned manic patients to either lithium treatment or ECT. While patients in both groups responded well, response was faster in the ECT group. Sikdar et al20 administered chlorpromazine and either real or sham ECT to manic patients and found that adding ECT to neuroleptic patients’ treatments substantially improved outcomes.

 

 

In modern practice, various anticonvulsants have become common for treating mania, and no comparative data between such agents and ECT are available. ECT is reserved for highly agitated, medication-refractory patients. The typical scenario entails a patient who does not respond to high doses of parenteral sedatives or antipsychotics, is in restraints much of the time, and is not cooperating with orally administered medications. In such circumstances, court-ordered approval for ECT is usually needed. Fortunately, in my experience bilateral ECT is almost universally effective for such patients, who are often grateful for their treatment once they achieve euthymia.

Rare uses of ECT in schizophrenia

ECT was commonly used for schizophrenia as well as mania before the advent of neuroleptics7 but is only rarely used for this indication in modern times. Here are the exceptions:1

  1. For acute exacerbations, especially with florid-positive symptoms such as delusions, hallucinations, disorganized thoughts and behavior, or catatonia. ECT can be remarkably effective in rendering patients compliant with oral medication. From there, patients can be discharged and can proceed with outpatient therapy.
  2. For the chronically ill patient, if multiple medication trials fail to achieve optimum results. When administered in combination with antipsychotic medication, a trial of ECT may extend whatever benefits accrue from medication.7 In particular, the combination of ECT and neuroleptic medication may be more effective in such cases than either ECT or medication alone.21

Especially for chronically ill patients with schizophrenia, any benefits of an acute course of ECT will likely be short-lived unless maintenance ECT is instituted. In a well-designed study of schizophrenic patients stabilized with a combination of neuroleptic medication and an acute course of ECT, Chanpattana et al22 found that those maintained for 6 months with combination continuation ECT and pharmacotherapy did much better than did those randomly assigned to either modality alone.

Related resources

  • Abrams R. Electroconvulsive Therapy. 3rd ed. New York: Oxford University Press; 1997.
  • American Psychiatric Association. Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 2nd ed. Washington, D.C.:American Psychiatric Association; 2001.
  • Mukherjee S, Sackeim HA, Schnur DB. Electroconvulsive therapy of acute manic episodes: a review of 50 years’ experience. Am J Psychiatry. 1994;151:169-176.

Drug brand names

  • Methohexital • Amidate, Brevital, Diprivan, Ethrane
  • Succinylcholine • Anectine

Disclosure

The author reports no affiliation or financial arrangement with any of the companies whose products are mentioned in this article.

References

1. American Psychiatric Association. Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 2nd ed. Washington, D.C.: American Psychiatric Association; 2001.

2. Roberts JM. Prognostic factors in the electroshock treatment of depressive states I. Clinical features from history and examination. J Ment Sci. 1959;105:693-702.

3. Sackeim HA, Rush AJ. Melancholia and response to ECT (letter). Am J Psychiatry. 1995;152(8):1242-1243.

4. American Psychiatric Association. Diagniositc and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994.

5. Sobin C, Prudic J, Devanand DP, Nobler MS, Sackeim HA. Who responds to electroconvulsive therapy? Br J Psychiatry. 1996;169:322-328.

6. Hickie I, Mason C, et al. Prediction of ECT response: validation of a refined sign-based (CORE) system for defining melancholia. Br J Psychiatry. 1996;169(1):68-74.

7. Abrams R. Electroconvulsive Therapy. 3rd ed. New York: Oxford University Press; 1997.

8. Bush G, Fink M, Petrides G, et al. Treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand. 1996;93:137-143.

9. Ungvari GA, Leung CM, Wong MK, Lau J. Benzodiazepines in the treatment of catatonic syndrome. Acta Psychiatr Scand. 1994;89:285-288.

10. Philbrick KL, Rummans TA. Malignant catatonia. J Neuropsychiatry and Clinical Neurosciences. 1994;6:1-13.

11. Black DW, Winokur G, Nasrallah A. A multivariate analysis of the experience of 423 depressed inpatients treated with electroconvulsive therapy. Convulsive Ther. 1993;9:112-120.

12. Tew JD, Jr, Mulsant BH, Haskett RF, et al. Acute efficacy of ECT in the treatment of major depression in the old. Am J Psychiatry. 1999;156:1865-1870.

13. Wilkinson AM, Anderson DN, Peters S. Age and the effects of ECT. Int J Geriatr Psychiatry. 1993;8:401-406.

14. Daly JJ, Prudic J, Devanand DP, et al. ECT in bipolar and unipolar depression: differences in speed of response. Bipolar Disorders. 2001;3(2):95-104.

15. Prudic J, Haskett RF, Mulsant B, et al. Resistance to antidepressant medications and short-term clinical response to ECT. Am J Psychiatry. 1996;153(8):985-992.

16. Nelson JP, Benjamin L. Efficacy and safety of combined ECT and tricyclic antidepressant therapy in the treatment of depressed geriatric patients. Convulsive Ther. 1989;5:321-329.

17. Sareen J, Enns MW, Guertin JE. The impact of clinically diagnosed personality disorders on acute and one-year outcomes of electroconvulsive therapy. J ECT. 2000;16(1):43-51.

18. Mukherjee S, Sackeim HA, Schnur DB. Electroconvulsive therapy of acute manic episodes: a review of 50 years’ experience. Am J Psychiatry. 1994;151:169-176.

19. Small JG, Klapper MH, et al. Electroconvulsive treatment compared with lithium in the management of manic states. Arch Gen Psychiatry. 1988;45:727-732.

20. Sikdar S, Kulhara P, Avasthi A, Singh H. Combined chlorpromazine and electroconvulsive therapy in mania. Br J Psychiatry. 1994;164:806-810.

21. Krueger RB, Sackeim HA. Electroconvulsive therapy and schizophrenia. In Schizophrenia. SR Hirsch and D Weinberger, eds. Oxford, England: Blackwell Scientific, 1995;503-545.

22. Chanpattana W, Chakrabhand ML, Sackeim HA, et al. Continuation ECT in treatment-resistant schizophrenia: a controlled study. J ECT. 1999;15:178-192.

23. Sackeim HA, Prudic J, Devanand DP, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral ECT at different stimulus intensities. Arch Gen Psychiatry. 2000;57:425-434.

24. Shapira B, Tubi N, Drexler H, Lidsky D, Calev A, Lerer B. Cost and benefit in the choice of ECT schedule. Twice versus three times weekly ECT. Br J Psychiatry. 1998;172:44-48.

25. Rasmussen KG, Richardson JR, Rummans TA. ECT in the medically ill. Psychiatric Clin North Amer (in press).

References

1. American Psychiatric Association. Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 2nd ed. Washington, D.C.: American Psychiatric Association; 2001.

2. Roberts JM. Prognostic factors in the electroshock treatment of depressive states I. Clinical features from history and examination. J Ment Sci. 1959;105:693-702.

3. Sackeim HA, Rush AJ. Melancholia and response to ECT (letter). Am J Psychiatry. 1995;152(8):1242-1243.

4. American Psychiatric Association. Diagniositc and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994.

5. Sobin C, Prudic J, Devanand DP, Nobler MS, Sackeim HA. Who responds to electroconvulsive therapy? Br J Psychiatry. 1996;169:322-328.

6. Hickie I, Mason C, et al. Prediction of ECT response: validation of a refined sign-based (CORE) system for defining melancholia. Br J Psychiatry. 1996;169(1):68-74.

7. Abrams R. Electroconvulsive Therapy. 3rd ed. New York: Oxford University Press; 1997.

8. Bush G, Fink M, Petrides G, et al. Treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand. 1996;93:137-143.

9. Ungvari GA, Leung CM, Wong MK, Lau J. Benzodiazepines in the treatment of catatonic syndrome. Acta Psychiatr Scand. 1994;89:285-288.

10. Philbrick KL, Rummans TA. Malignant catatonia. J Neuropsychiatry and Clinical Neurosciences. 1994;6:1-13.

11. Black DW, Winokur G, Nasrallah A. A multivariate analysis of the experience of 423 depressed inpatients treated with electroconvulsive therapy. Convulsive Ther. 1993;9:112-120.

12. Tew JD, Jr, Mulsant BH, Haskett RF, et al. Acute efficacy of ECT in the treatment of major depression in the old. Am J Psychiatry. 1999;156:1865-1870.

13. Wilkinson AM, Anderson DN, Peters S. Age and the effects of ECT. Int J Geriatr Psychiatry. 1993;8:401-406.

14. Daly JJ, Prudic J, Devanand DP, et al. ECT in bipolar and unipolar depression: differences in speed of response. Bipolar Disorders. 2001;3(2):95-104.

15. Prudic J, Haskett RF, Mulsant B, et al. Resistance to antidepressant medications and short-term clinical response to ECT. Am J Psychiatry. 1996;153(8):985-992.

16. Nelson JP, Benjamin L. Efficacy and safety of combined ECT and tricyclic antidepressant therapy in the treatment of depressed geriatric patients. Convulsive Ther. 1989;5:321-329.

17. Sareen J, Enns MW, Guertin JE. The impact of clinically diagnosed personality disorders on acute and one-year outcomes of electroconvulsive therapy. J ECT. 2000;16(1):43-51.

18. Mukherjee S, Sackeim HA, Schnur DB. Electroconvulsive therapy of acute manic episodes: a review of 50 years’ experience. Am J Psychiatry. 1994;151:169-176.

19. Small JG, Klapper MH, et al. Electroconvulsive treatment compared with lithium in the management of manic states. Arch Gen Psychiatry. 1988;45:727-732.

20. Sikdar S, Kulhara P, Avasthi A, Singh H. Combined chlorpromazine and electroconvulsive therapy in mania. Br J Psychiatry. 1994;164:806-810.

21. Krueger RB, Sackeim HA. Electroconvulsive therapy and schizophrenia. In Schizophrenia. SR Hirsch and D Weinberger, eds. Oxford, England: Blackwell Scientific, 1995;503-545.

22. Chanpattana W, Chakrabhand ML, Sackeim HA, et al. Continuation ECT in treatment-resistant schizophrenia: a controlled study. J ECT. 1999;15:178-192.

23. Sackeim HA, Prudic J, Devanand DP, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral ECT at different stimulus intensities. Arch Gen Psychiatry. 2000;57:425-434.

24. Shapira B, Tubi N, Drexler H, Lidsky D, Calev A, Lerer B. Cost and benefit in the choice of ECT schedule. Twice versus three times weekly ECT. Br J Psychiatry. 1998;172:44-48.

25. Rasmussen KG, Richardson JR, Rummans TA. ECT in the medically ill. Psychiatric Clin North Amer (in press).

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