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The Intimate Relationship Between Catatonia and Convulsive Therapy

Fink, Max MD

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doi: 10.1097/YCT.0b013e3181feb69f
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The "memory loss, memory loss" mantra that has been the central preoccupation in electroconvulsive therapy (ECT) studies for more than 2 decades focused research on the technical issues of electrode placement, dosing, and energy forms, with the subjects limited to those with "therapy-resistant depression." This population, however, is defined by imprecise and highly subjective criteria leading to very heterogeneous populations in the studies. At the same time, clinicians sought to optimize treatment responsivity by answering the question: "For whom are induced seizures helpful?" The syndromes of catatonia1 and melancholia2 were redefined as distinct clinical syndromes with precise clinical criteria, verifying laboratory tests, and each with a high responsivity to ECT. This issue of J ECT presents 10 reports of experiences with ECT in catatonia. Four case reports describing similar experiences were published earlier in 2010 in this journal3-6 adding to 40 additional articles in the 25 years of publication of J ECT.

Catatonia is a bizarre motor syndrome of acute onset in fully awake but unresponsive subjects with such freakish signs as mutism and staring; sustained peculiar postures; negativism with refusal of food and poor self-care; verbal and motor repetitive behaviors, often self-injurious; excited states; and occasional stupors that are so severe as the subjects appear to be lifeless. A malignant form with high fever and severe vegetative dysfunction leads to death. The syndrome accompanies depressive and manic disorders, psychoses, toxic states secondary to neuroleptic drugs, and systemic medical conditions. It is defined by the presence of 2 or more signs (from lists of approximately 30) for more than 24 hours and is quickly responsive to intravenous barbiturates, benzodiazepines (BZDs), and ECT. Surveys in general medical hospitals find catatonia in 10% of patients.1

An intimate relationship of the treatment and the syndrome began with the very first research trials in 1934. Ladislas Meduna, the Hungarian neuropathologist, had observed paucity in the numbers of glial cells in the patients who died of schizophrenia and abundance in those with seizure disorders.7 At the time, it was thought that it was possible to ameliorate a psychiatric syndrome by inducing a systemic disease (as demonstrated by Wagner-Jauregg's Nobel prize-winning description of malaria therapy for neurosyphilis).8 After identifying intramuscular injections of camphor to be effective seizure-inducing agents in animal trials, Meduna was prepared to treat patients with schizophrenia.

Meduna describes the first patient as Zoltan, a 37-year-old man who "... had been suffering from a catatonic stupor for about four years. He never moved, never ate, never took care of his bodily needs, and had to be tube-fed daily."7 After 9 injections, with 6 induced seizures, he recovered and was discharged to the community; alas, after 3 months, he relapsed and was readmitted to the hospital.

Of the first 11 patients treated by Meduna, 9 evinced mutism, negativism, posturing, and stupors; 6 required daily tube-feeding.9 Although injections of camphor induced full grand mal seizures in less than half the injections, the relief of these symptoms encouraged further clinical trials. Within a few months, Meduna changed the induction method to intravenous pentylenetetrazol (Metrazol), and his 1937 report cited a successful experience in more than half of the 110 patients treated.10

The first patient in whom seizures were induced electrically by Cerletti and his co-workers in Rome also exhibited a form of catatonia. A 39-year-old man was found wandering in the train station delirious and frightened, mumbling neologisms, thoughts of being telepathically influenced, refusing to eat and care for himself.11 This description meets the criteria for delirious mania, a syndrome commonly associated with catatonia.1 He, too, remitted rapidly.

In retrospect, it was fortuitous that Meduna and Cerletti selected patients with catatonia. Patients dominated by signs of hebephrenia or paranoia would not have responded, the clinicians would have been discouraged, and induced seizures as therapy would have been anecdotes among the myriad of proposed therapies that litter the historical medical dustbin.


Karl Kahlbaum identified a motor and vegetative dysregulation syndrome that we now know as catatonia in a diverse group of hospitalized patients in 1874. Two decades later, Emil Kraepelin saw an intimate connection between catatonia and his concept of dementia praecox. Eugen Bleuler next endorsed the connection in his delineation of schizophrenia, and this association was accepted in each Diagnostic and Statistical Manual of Mental Disorders (DSM) classification of psychiatric disorders published by the American Psychiatric Association and each International Classification of Diseases of the World Health Organization. Reports of catatonia among patients with mood disorders, neurotoxic states, and systemic medical conditions in the 1970s led to calls to recognize catatonia as a syndrome distinct from that of schizophrenia, and in 1994, a new class of "catatonic disorder due to a general medical condition" was added in DSM-IV allowing recognition outside the connection to schizophrenia.1

However, this change failed to influence either the broader recognition of catatonia or its treatment, and calls for the establishment of the syndrome as a unique clinical entity filled the literature in the past decade.12-14 Although compelling arguments for this reclassification have been repeatedly made, the DSM-V Psychosis Work Group (responsible for consideration of catatonia) has resisted the change, hewing to the line that the syndrome is best classified as a specifier of mood, psychotic, and medical disorders.15 A specifier in the DSM classification, however, has no notational uniqueness. Lacking a numeric identification makes examination of records impossible, restricting clinical research. More critical for patient care, the lack of an identifiable numeric label limits physician and hospital reimbursement under medical insurance rules. For scientific and practical reasons, catatonia scholars call on the DSM-V commissioners to establish catatonia as a distinct syndrome, akin to that of delirium and dementia, separate from the persistent and limited association with schizophrenia.16 These 35 scholars include all those who have surveyed the incidence of catatonia in psychiatric populations.


In a review of the ECT experience in a large Dutch teaching hospital, van Waarde et al17 identified 27 catatonia patients among the 285 ECT treated patients for an 18-year period. Pharmacotherapy had failed in 85% of the patients; and with ECT, 59% improved. Daily ECT was essential to the recovery of the patients with malignant catatonia, those with severe autonomic dysregulation and highest fevers. The need for daily ECT supports the 1952 classic study by Arnold and Stepan18 who reported that daily ECT avoided fatalities in malignant catatonia.

Better outcomes were also associated with longer duration of electroencephalographic seizure activity. Although catatonia is sensitive to induced seizures, it is essential that the seizure quality be optimized, and this is best done by bilateral electrode placement and more frequent treatments. Furthermore, because the administration of high doses of BZDs is the first intervention for catatonia, the BZD antagonist flumazenil is a useful adjunct in the anesthesia induction.1

In a MEDLINE literature review of ECT in children and adolescents, Consoli et al,19 reporting from the Paris clinic of David Cohen, identify 59 reports with 47% having mood disorders; 27%, schizophrenia; and 23%, brain and pervasive developmental disorders. The diversity of the primary psychiatric diagnoses supports the call for catatonia as a distinct identifiable and treatable syndrome, as favorable outcomes were reported in 76% of the treated patients, with only 1 patient failing to benefit.

Child psychiatrists have long focused on familial and social causes and interventions for childhood disturbances, with minimal interest in ECT. An examination of the ethics of these attitudes find that ECT meets ethical standards of beneficence, nonmaleficence, and autonomy, but the failure to consider ECT, the widespread restriction of its use in children and adolescents, and the lack treatment facilities are unjust. This conclusion was also developed by Ottossson and Fink20 in their consideration of ethics in ECT.

Consoli and coworkers also cite recent studies of parental and patient attitudes to the outcomes of treatment, finding the experiences considered favorably.

Four case reports describe the diversity of systemic illnesses and favorable outcomes among patients with catatonia treated with ECT. Two patients with chronic autism and mental retardation responded favorably,21 as did a man with multiple sclerosis and recurring catatonia.22 Repetitive motor behaviors, as tics and self-injurious behavior, are responsive to ECT.23 The neuroleptic malignant syndrome, a form of malignant catatonia, is responsive to ECT in a patient with postsurgical delirium.24

Unusual syndromes that are responsive to ECT are described. Patients in delirious mania, a syndrome of excitement, delirium, and psychosis, also exhibit posturing, negativism, echolalia, and refusal to eat. The syndrome has been considered a form of catatonia.1 The favorable experience with ECT in 2 cases is described.25

Signs of catatonia are commonly found among patients who have psychotic depression, suggesting that the 2 syndromes have much in common. The delusional syndrome that one is not alive (Cotard syndrome) is responsive to ECT, as exemplified in the report by Grover et al.26


What are we to make of the unique sensitivity of catatonia to induced grand mal seizures? Does this well-documented fact tell us something of the mechanism of ECT? If we understood the pathophysiological features of seizures, would we understand the syndrome of catatonia? (Indeed, considering the equivalent responsivity of melancholia to ECT, what is the relationship of the 2 syndromes?)

It is surprising that neuroscientists dedicate their efforts to the complex mish-mash syndromes of schizophrenia and major depression and ignore catatonia because the syndrome is definable and treatable, developing homogeneous population samples, offering dramatic changes in behavior within a short period after 2 narrowly defined effective treatments, sedative anticonvulsants and ECT. What is common to the pathophysiological features of these interventions? Dirk Dhossche, a student of catatonia trained at Stony Brook University, assays the questions that are at the heart of the pathophysiology literature.27 He is unable to target any brain or body system that offers an explanation of the syndrome's pathological mechanism or the relief afforded by the known treatments. He focuses interest on the neuroleptic malignant syndrome, the Prader-Willi and Kleine-Levin syndromes, and the N-methyl-d-aspartate receptor encephalitis as unique behavior syndromes that offer definable populations for study.

In the 1980s, it was possible for clinicians to ask "where had the catatonics gone?" reflecting the dramatic change in psychiatric venue from the psychiatric hospital to the private office and outpatient clinic.28 Hospital clinicians described the many faces of catatonia and the remarkable sensitivity of the syndrome to induced grand mal seizures.1 They challenged the classification that married catatonia to schizophrenia. The intimate connection of catatonia and ECT should entice neuroscientists and clinicians to examine the relationship to better understand a specific psychiatric pathophysiological feature and the mechanism of action of ECT.


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© 2010 Lippincott Williams & Wilkins, Inc.