Publication
Article
Psychiatric Times
ECT and Catatonia: Out of the Shadows
Author(s):
Catatonia-a syndrome of disturbed motor, mood, and systemic signs (eg, rigidity, immobility, mutism, staring, posturing, waxy flexibility, echopraxia, echolalia, and stereotypies)-has led to the clarification of its appropriate treatment.
[[{"type":"media","view_mode":"media_crop","fid":"21726","attributes":{"alt":"","class":"media-image media-image-right","id":"media_crop_9160446239298","media_crop_h":"0","media_crop_image_style":"-1","media_crop_instance":"1529","media_crop_rotate":"0","media_crop_scale_h":"150","media_crop_scale_w":"200","media_crop_w":"0","media_crop_x":"0","media_crop_y":"0","style":"float: right; margin: 2px;","title":" ","typeof":"foaf:Image"}}]]The syndrome of catatonia is being increasingly recognized, both academically and clinically, and it is pulling ECT into the spotlight along with it.1 Twenty years ago, one would have said that catatonia was extinct, except perhaps for the rare patient with the catatonic subtype of schizophrenia. Now catatonia is front and center, claiming our attention in emergency departments and hospitals and in a burgeoning number of academic reports. It is even updated in DSM-5.
Catatonia is defined as a syndrome of disturbed motor, mood, and systemic signs, including rigidity, immobility, mutism, staring, posturing, waxy flexibility, echopraxia, echolalia, and stereotypies, among others. It is often accompanied by autonomic disturbances and fever. It occurs across the entire age spectrum and its onset may be acute. Severe forms, or “malignant catatonia,” may be fatal. Delirious mania and neuroleptic malignant syndrome are considered variants of catatonia.2,3 The recently popularized diagnosis of anti–N-methyl-D-aspartate receptor encephalitis (limbic encephalitis) is considered yet another variant.4
Whereas previously catatonia was considered to be associated almost exclusively with schizophrenia, the newer conceptualization recognizes that it most commonly occurs in the context of mood disorders, but it also occurs in medically ill patients and children with severe forms of autism. This newer understanding of the wider clinical context of catatonia is reflected in the changes categorizing it in DSM-5.
The revised DSM-5 classification deletes 295.2, the catatonic type of schizophrenia, adds a new class of “Catatonia Not Elsewhere Classified” (299.89), retains the medical disease association of catatonia (293.89), and accepts catatonia as a specifier of 10 psychiatric diagnoses. While recognizing these changes as an improvement over the old classification, catatonia scholars suggest that the diagnosis be given even more independent status: “Catatonia warrants the proposed separation from schizophrenia and establishment as an independent syndrome in the classification of psychiatric illnesses with a single numeric code.”2
A remarkable number of new publications about catatonia have appeared on PubMed. More than 150 of the nearly 2500 total citations for “catatonia” have been added since the beginning of 2012. A subset of this literature deals with the description and treatment of catatonia in children, some of whom have severe autism and exhibit self-injurious behavior. Self-injurious behavior is hypothesized to be an analogue of the repetitive motor behaviors seen in catatonia in adults.5
Children with autistic catatonia are often critically ill. Their self-injurious behavior, which may be life-threatening, makes it impossible for them to be cared for by their families at home. They are typically treated over the years with every known behavioral and pharmacological intervention, including typical and atypical antipsychotics (often clozapine), with limited success and a high adverse-effect burden.
Case reports in the literature attest to the acute success of ECT in these children, sometimes with dramatic resolution of the most problematic symptoms, including self-injurious behavior.6 However, maintaining the acute improvement is often a challenge, and maintenance ECT, among other comprehensive treatment regimens, is being tried empirically.7
The renewed recognition of catatonia has led to the clarification of its appropriate treatment. Benzodiazepines are key to both the diagnosis (the benzodiazepine challenge test) and the initial treatment (with an intravenous or an oral benzodiazepine) of the syndrome, along with proper medical management of any associated illness.8 Not all patients respond to benzodiazepines, and even those who do, may not have a sustained response.
ECT has long been recognized as the definitive treatment for catatonia, but because of the rarity of the syndrome until its recent increased recognition, this indication was never more than an afterthought in a list of indications for ECT. Even with this resurgence of diagnosis and treatment of catatonia, it remains a tiny fraction of the broader application of ECT. ECT is primarily used for the treatment of severe depression, in the context of both unipolar and bipolar disorder, as well as for certain clinical presentations of psychotic disorders.9
Seeing the dramatic response of desperately ill catatonic patients to ECT is one of the most gratifying clinical experiences for ECT practitioners, referring physicians, and trainees who care for such patients. To have a mute, rigid, febrile, malnourished patient return to normal functioning, behavior, and health is not something one sees often in medical practice, and it is something one never forgets.
Some of the long-held assumptions of ECT treatment of catatonia are now being challenged. Whereas it has been standard practice to use the most potent forms of ECT (bilateral electrode placement with high-dose stimuli), a recent report of a case series of catatonic patients suggests that right unilateral electrode placement ECT may be effective and possibly better-tolerated.10 However tempting these data may be, prudence dictates that for urgently ill patients, the most rapidly acting, and potent, forms of ECT still be used.11
For patients who are acutely ill with neuroleptic malignant syndrome or delirious mania, ECT is often given on a more intensive schedule (eg, daily for 2 to 4 days), especially when patients are febrile.12 Because there are insufficient numbers of catatonic patients to study systematically in randomized clinical trials, we will likely need to continue to rely on accumulating case material and clinical judgment to determine optimal ECT technique in this patient population.
In the FDA panel hearing on ECT device classification in 2011, the only diagnostic category for which there was unequivocal support for unhindered future ECT device availability was catatonia, because catatonic patients are often critically ill. The unfortunate misinterpretation by the panel of the voluminous evidence base for the safety and efficacy of ECT for depression has already been widely reported, but the recognition of catatonia at the FDA meeting remains noteworthy.13
Catatonia is out of the shadows; that is very good for patients suffering from this uncommon, but no longer rare, clinical entity. It is also good for ECT in general: shining light on a less common indication also shines light on ECT as a standard and vital treatment for severe depression. The few may protect ECT for the many.
Disclosures:
Dr Kellner is Professor in the department of psychiatry at Mount Sinai School of Medicine in New York.
References:
1. Aloysi AS, Popeo DM, Kellner CH. Cases of catatonia on an academic electroconvulsive therapy service: lessons to learn. J ECT. 2011;27:259-261.
2. Fink M. Catatonia from its creation to DSM-V: considerations for ICD. Indian J Psychiatry. 2011;53:214-217.
3. Luchini F, Lattanzi L, Bartolommei N, et al. Catatonia and neuroleptic malignant syndrome: two disorders on a same spectrum? Four case reports. J Nerv Ment Dis. 2013;201:36-42.
4. Wilson JE, Shuster J, Fuchs C. Anti-NMDA receptor encephalitis in a 14-year-old female presenting as malignant catatonia: medical and psychiatric approach to treatment. Psychosomatics. 2013 Jul 9; [Epub ahead of print].
5. Wachtel LE, Dhossche DM. Self-injury in autism as an alternate sign of catatonia: implications for electroconvulsive therapy. Med Hypotheses. 2010;75:111-114.
6. Wachtel LE, Contrucci-Kuhn SA, Griffin M, et al. ECT for self-injury in an autistic boy. Eur Child Adolesc Psychiatry. 2009;18:458-463.
7. Wachtel LE, Hermida A, Dhossche DM. Maintenance electroconvulsive therapy in autistic catatonia: a case series review. Prog Neuropsychopharmacol Biol Psychiatry. 2010;34:581-587.
8. Bush G, Fink M, Petrides G, et al. Catatonia. II: treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand. 1996;93:137-143.
9. Weiner RD, Coffey CE. The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. A Task Force Report of the American Psychiatric Association. 2nd ed. Washington, DC: American Psychiatric Association; 2001.
10. Cristancho P, Jewkes D, Mon T, Conway C. Successful use of right unilateral ECT for catatonia: a case series. J ECT. 2013 Jul 15; [Epub ahead of print].
11. Kellner CH, Popeo DM, Aloysi AS. Electroconvulsive therapy for catatonia. Am J Psychiatry. 2010;167:1127-1128.
12. Fink M, Taylor MA. Catatonia: A Clinician’s Guide to Diagnosis and Treatment. New York: Cambridge University Press; 2003.
13. Goodman WK. Electroconvulsive therapy in the spotlight. N Engl J Med. 2011;364:1785-1787.
