Electroconvulsive-therapy-associated neutropenia in treatment-resistant schizophrenia: Three case reports.

Abstract

Electroconvulsive therapy (ECT) is an effective therapy for treatment-resistant schizophrenia. Our report is the first to describe neutropenia that developed and persisted during ECT. Case 1 was a 31-year-old woman with treatment-resistant schizophrenia. The patient was admitted to our psychiatric ward. After 32 days of admission, valproic acid was added to the treatment (800 mg/day). On day 37, the patient developed neutropenia (1290/μL), which improved after discontinuation of the valproic acid (3581/μL). Thereafter, the patient's condition deteriorated, and on day 91, ECT was initiated. The therapy was performed three times per week according to the standard ECT protocol. Rocuronium, propofol and suxamethonium were administered by anesthetists, and the patient's brain was stimulated for 8 s. On day 110, blood tests revealed that the patient once again had a low neutrophil count (1162/μL). ECT was discontinued, and the neutropenia improved. Psychotropic medications around ECT (day 91–day 110) were as follows: paliperidone 12 mg (days 38–94), 6 mg (days 95–102), levomepromazine 25 mg (days 63–94), olanzapine 10 mg (days 103–115), 20 mg (day 116–), eszopiclone 2 mg (day 23–), and lormetazepam 1 mg (day 35–). Case 2 was a 38-year-old woman with treatment-resistant schizophrenia. The patient was admitted to our psychiatric ward. Neutropenia appeared after the clozapine dosage was increased to 200 mg/day (1455/μL). The clozapine was immediately discontinued, and the neutropenia improved. ECT was initiated to treat the vivid hallucinations and psychomotor agitation. Subsequently, the neutropenia developed again (1125/μL). ECT was administered 25 times over 2 months; however, the neutropenia persisted during this period. On day 141, the psychiatric symptoms were considered to have improved. ECT was then discontinued, and neutrophil levels subsequently recovered. Psychotropic medications around ECT (day 91–day 110) were as follows: olanzapine 10 mg (days 130–136), 20 mg (day 137–), and brotizolam 0.25 mg (days 53–144). Case 3 was a 57-year-old woman with treatment-resistant schizophrenia. The patient was admitted to our psychiatric ward. The patient's current therapy included quetiapine, but the effects were insufficient. On day 38, ECT was initiated. On day 58, blood tests revealed that the patient had a low neutrophil count (1129/μL). The patient showed no neutropenia-induced clinical symptoms, and ECT was administered 12 times. On day 67, the psychiatric symptoms were considered to have improved. ECT was then discontinued, and neutrophil levels subsequently recovered. Psychotropic medications around ECT (day 38–day 67) were as follows: risperidone 2 mg (days 34–45), paliperidone 6 mg (days 46–60), and 9 mg (day 61–). We have obtained signed release from the patients or legal guardians authorizing publication. The patients described showed no clinical symptoms associated with neutropenia. There are few previous reports on the relation between ECT and blood systems. Furthermore, to the best of our knowledge, there are no reports on ECT-associated neutropenia. Some reports have indicated that ECT increases the total leukocyte count, lymphocyte percentage and lymphocyte natural killer cell activity within a short period of time.1, 2 In contrast, our report showed that the therapy was actually associated with chronic and persistent neutropenia. It is also believed that neutropenia may be associated with anesthetics, but we were unable to confirm this association in our subjects. Two of three cases had histories of drug-induced neutropenia. This finding suggests that care should be taken when administering ECT to patients who tend to develop neutropenia.