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For ethical and economic reasons, when patients are acutely ill with catatonia and melancholia, ECT is best considered sooner rather than later.
ECT remains a standard treatment in modern psychiatric medicine for a range of severe psychiatric illnesses because of its unmatched efficacy and speed of response. Recent changes in psychiatric nosology and practice clarify the role of ECT for catatonia and melancholia-2 syndromes for which ECT is a most effective and often lifesaving treatment. For these syndromes, optimally administered ECT typically provides relief within 1 to 3 weeks.
Catatonic patients, especially those with febrile malignant catatonia or the neuroleptic malignant syndrome and those who refuse feeding, should be treated without delay. Unfortunately, antidepressant medications are prescribed for many melancholic patients-often multiple trials of up to 6 weeks each-before ECT is recommended. More severely depressed patients, who are agitated, suicidal, and losing weight, should be referred for ECT as a primary treatment.
Indeed, the remarkable, well-replicated efficacy of ECT for these 2 syndromes raises questions about accepted treatment algorithms that call for 2 or more medication trials, often with multiple medications combined with psychotherapy. Many clinicians question the ethics of such treatment algorithms that ask patients to suffer weeks, even months, of trials before the effective treatment of ECT is prescribed. For both ethical and economic reasons, when patients are acutely ill with catatonia and melancholia, ECT is best considered sooner rather than later.
A century ago, following the images created by Emil Kraepelin, catatonia was seen as a marker of schizophrenia and classified as one of its recognized types. By the 1990s, DSM-IV recognized catatonia as secondary to a medical condition; in the latest iteration, DSM-5 discarded the class of catatonia as a type of schizophrenia and retained it mainly as a systemic medical condition. Much has been learned.
Catatonia rating scales identify more than 20 motor behaviors, including posturing, rigidity, staring, mutism, and repetitive thoughts and acts that mark the stuporous form. Two or more signs that last for 24 hours suggest the presence of the syndrome. The diagnosis can be verified by rapid relief, a 50% reduction in the rating scale scores, with the intravenous administration of 1 to 2 mg of lorazepam. Catatonia is first treated with increasing doses of a benzodiazepine; for lorazepam, often up to 30 mg/d. Up to 80% of patients respond to high-dose lorazepam treatment.1
For those who do not respond or for those with a malignant form of catatonia-with fever, autonomic dysfunction, and stupor-ECT is the primary treatment. ECT can be optimized in several ways. For febrile patients, daily treatment may be necessary.
High-dose benzodiazepines can raise seizure thresholds and interfere with the efficacy of ECT seizures. The most effective ECT uses bilateral electrode placement, and for those who have received benzodiazepines, the protocol may include the benzodiazepine antagonist flumazenil, administered in the sequence of oxygenation, anesthetic, flumazenil, and succinylcholine. Effective seizures are those that are of adequate duration, allowing the full sequence of buildup in the recorded EEG of slow waves, slow waves and spikes, followed by a definable sharp endpoint. Evidence on the use of right unilateral electrode placement to treat seriously ill patients with catatonia, while intriguing, is not compelling enough to change standard practice.
Catatonia is also recognized in an excited, delirious manic form. These patients are often febrile, medically ill, and behaviorally difficult to manage. An intramuscular ketamine injection may be a safe initial sedating agent, allowing placement of the intravenous line and the subsequent administration of the standard sequence of ECT medications. Daily ECT until the condition is stabilized is necessary and often lifesaving. The benefits are best sustained by continuation of ECT over weeks or months. In some instances, continued high-dose benzodiazepine treatment has been useful.
Before 1980 and the adoption of DSM-III, 2 depressive mood disorders were commonly identified: a severe life-threatening psychotic depression, “melancholia,” and the more commonly recognized “psychoneurotic” form. Melancholia was recognized by mood severity, acute onset, suicide risk, psychosis, and vegetative signs such as insomnia and weight loss. Psychoneurotic depression was marked by anxiety, fears, phobias, and obsessive thoughts. Since DSM-III, these conditions have been lumped together as “major depressive disorder.” Melancholia has been of limited interest, classified as a specifier for mood disorders (“with melancholic features”) and no longer recognized as a distinct illness.
Clinical scientists in the 1970s and 1980s reported that hypothalamic-pituitary-adrenal axis function, measurable by serum cortisol levels, was abnormal in melancholia and offered the dexamethasone suppression test as an index to identify and measure the severity of the syndrome.2 The loss of interest in melancholia resulted in the abandonment of cortisol measurement, including the dexamethasone suppression test, in the clinic.
Definitions of melancholia have varied over decades, and this is likely the reason that the evidence for its utility as a predictor of ECT response has been inconsistent. For the purposes of this article, melancholia refers to a severe primary mood disorder, usually episodic, with anhedonia, psychomotor disturbance, impaired concentration, disrupted sleep, poor appetite with weight loss, and often with psychotic thinking (guilty delusions) as well as suicidal ideation and intent.
Patients with melancholia often score in the “severe” range on depression rating scales such as the Hamilton (HAM-D) or Montgomery-Asberg (MADRS). Because the dexamethasone suppression test is no longer used, the diagnosis is made solely on the basis of clinical features, that is, by the severity of symptoms, progressive course, and presence of suicidal intent and psychosis, along with the other mood and motor features of the syndrome.
Effective ECT for severe melancholia, like that for catatonia, is based on optimizing ECT treatment parameters, which favor bilateral electrode placement, 3-times-per-week treatments, and monitored EEG seizures for duration and pattern. To sustain the benefits, continuation treatments over weeks or months are often required. Alternative strategies, of continuation treatment with pharmacotherapy combinations (eg, lithium plus nortriptyline or venlafaxine) or pharmacotherapy combinations along with continuation/maintenance ECT, have also been reported as effective in sustaining remission.3
A recent study in JAMA Psychiatry that documents the efficacy of ECT in reducing hospital readmission rates adds to our understanding of the public health benefits of ECT.4 An accompanying editorial forcefully makes the argument that modern ECT is a safe and well-tolerated treatment that is underutilized in American psychiatry.5 We agree-and hope that highlighting the appropriate place of ECT in treatment algorithms for catatonia and melancholia helps practitioners to consider ECT for their most seriously ill patients.
Dr. Kellner is Chief of Electroconvulsive Therapy, New York Community Hospital, Brooklyn, NY. Dr. Fink is Professor Emeritus, Departments of Psychiatry and Neurology, Stony Brook University, Stony Brook, NY.
1. Sienaert P, Dhossche DM, Vancampfort D, et al. A clinical review of the treatment of catatonia. Front Psychiatry. 2014;5:181.
2. Albala AA, Greden JF, Tarika J, Carroll BJ. Changes in serial dexamethasone suppression tests among unipolar depressive receiving electroconvulsive treatment. Biol Psychiatry. 1981;16:551-560.
3. Kellner CH, Husain MM, Knapp RG, et al. A novel strategy for continuation ECT in geriatric depression: phase 2 of the PRIDE study. Am J Psychiatry. 2016;173:1110-1118.
4. Slade EP, Jahn DR, Regenold WT, Case BG. Association of electroconvulsive therapy with psychiatric readmissions in US hospitals. JAMA Psychiatry. June 28, 2017; Epub ahead of print.
5. Sackeim HA. Modern electroconvulsive therapy: vastly improved yet greatly underused. JAMA Psychiatry. June 28, 2017; Epub ahead of print.
Fink M, Kellner CH, McCall WV. Optimizing ECT technique in treating catatonia. J ECT. 2016;32:149-150.
Krystal AD, Watts BV, Weiner RD, et al. The use of flumazenil in the anxious and benzodiazepine-dependent ECT patient. J ECT. 1998;14:5-14.
Luchini F, Medda P, Mariani MG, et al. Electroconvulsive therapy in catatonic patients: efficacy and predictors of response. World J Psychiatry. 2015;5:182-192.