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Published Online: 1 January 2012

Successful Treatment of Benzodiazepine-Resistant Malignant Catatonia With Electroconvulsive Therapy

Publication: The Journal of Neuropsychiatry and Clinical Neurosciences
To the Editor: This report describes the case of a patient who presented with malignant catatonia (MC) that did not respond to benzodiazepine treatment but was treated successfully with ECT.

Case Report

A 20-year-old male patient presented to the emergency department with symptoms of introversion, crying spells, refusal of food, and motor repetitive behaviors. He had a fever of 39.3°C, an elevated heart rate of 120 bpm, leukocytosis with a white blood cell (WBC) count of 18,690/mm3, and an elevated creatine phosphokinase (CPK) level of 2,247 U/liter. Cranial computerized tomography (CT) and lumbar puncture (LP) were normal. The consulting infectious-disease specialist concluded that the symptoms of the patient were not due to an infectious disease of the CNS, but, as he had a cough, and the source of fever could not be identified, a diagnosis of atypical pneumonia could not be excluded. Therefore, levofloxacin, at a dose of 500 mg/day was initiated.
Psychiatric examination revealed agitation, negativism, and mutism. He had repetitive and stereotypic motor behaviors and rigid extremities. Poor hygiene and oral candidiasis were also noted. He was admitted to the psychiatric inpatient unit with a diagnosis of MC. Because assessments to exclude a disease of the CNS were not yet complete, ECT could not be performed as an initial step. Intravenous diazepam treatment, 10 mg/day was initiated. On the 3rd day of treatment, the WBC count of the patient decreased to 8,620/mm3, and CPK levels decreased to 2,230 U/liter. Olanzapine was initiated at a dose of 10 mg/day. The patient was reevaluated by the consulting neurologist, who recommended cranial MRI and thyroid function tests (TFT), to exclude Hashimoto thyroiditis. Both the MRI and TFT were within normal limits. The WBC count and CPK levels decreased over the ensuing days, but the clinical signs and symptoms of catatonia did not change. Olanzapine treatment was ceased at the 5th day of treatment, and diazepam dose was increased gradually to a dose of 20 mg/day on the 7th day of treatment. At this point, as his general-medical condition was stabilized, ECT was initiated. The motor behaviors and mutism improved significantly, and he began to talk after the first session of ECT. After a total of five ECT sessions, his clinical condition was significantly improved. Thereafter, ECT was stopped.

Conclusion

This case adds to other reports of MC that respond less favorably to benzodiazepines but respond to ECT.1,2 Daily ECT was reported as an essential treatment modality for recovery of patients with malignant catatonia.3 However, in our case, as a CNS disease could not be excluded initially, ECT could not be initiated promptly. This led to initial treatment with benzodiazepine, which was also found to be effective in treatment of catatonia.4 Contrasting with a previous report that recommended at least six sessions of ECT for patients responsive to ECT within the first few treatments,5 five ECT sessions were found to be adequate for the treatment of our patient.

Acknowledgments

The authors indicate that they have no conflict of interest relevant to this article to disclose and no support was received from any grant and funding source.

References

1.
Bush G, Fink M, Petrides G, et al.: Catatonia, II: treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand 1996; 93:137–143
2.
Ungvari GS, Leung CM, Wong MK, et al.: Benzodiazepines in the treatment of catatonic syndrome. Acta Psychiatr Scand 1994; 89:285–288
3.
Baker AS, Suh E, Prudic J: Malignant catatonia: role of right unilateral electroconvulsive therapy. J ECT 2008; 24:168–170
4.
Daniels J: Catatonia: clinical aspects and neurobiological correlates. J Neuropsychiatry Clin Neurosci 2009; 21:371–380
5.
Weder ND, Muralee S, Penland H, et al.: Catatonia: a review. Ann Clin Psychiatry 2008; 20:97–107

Information & Authors

Information

Published In

Go to The Journal of Neuropsychiatry and Clinical Neurosciences
Go to The Journal of Neuropsychiatry and Clinical Neurosciences
The Journal of Neuropsychiatry and Clinical Neurosciences
Pages: E48
PubMed: 22450649

History

Published online: 1 January 2012
Published in print: Winter 2012

Authors

Details

Gul Karacetin, M.D.
Dept. of Child and Adolescent PsychiatryCorum State HospitalCorum, Turkey (GK) Cerrahpasa Medical FacultyUniversity of IstanbulIstanbul, Turkey (TD)Dept. Of PsychiatryCerrahpasa Medical FacultyUniversity of IstanbulIstanbul, Turkey (RB)
Reha Bayar, M.D.
Dept. of Child and Adolescent PsychiatryCorum State HospitalCorum, Turkey (GK) Cerrahpasa Medical FacultyUniversity of IstanbulIstanbul, Turkey (TD)Dept. Of PsychiatryCerrahpasa Medical FacultyUniversity of IstanbulIstanbul, Turkey (RB)
Turkay Demir, M.D.
Dept. of Child and Adolescent PsychiatryCorum State HospitalCorum, Turkey (GK) Cerrahpasa Medical FacultyUniversity of IstanbulIstanbul, Turkey (TD)Dept. Of PsychiatryCerrahpasa Medical FacultyUniversity of IstanbulIstanbul, Turkey (RB)

Notes

Correspondence: Gul Karacetin M.D., University of Istanbul, Cerrahpasa Medical Faculty, Department of Child and Adolescent Psychiatry; e-mail: [email protected]

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