{"title":"A Woman With Catatonia, What To Do After ECT Fails: A Case Report.","authors":"Afra van der Markt, H. Heller, E. van Exel","doi":"10.1097/YCT.0000000000000290","DOIUrl":null,"url":null,"abstract":"To the Editor: W e present a 46-year-old woman, with a history of bipolar I disorder, who developed catatonia during a depressive episode. Initial treatment with 8 mg lorazepam per day proved to be ineffective, as was ECT. Therefore, the lorazepam dosage was increased up to 28 mg/d, which finally led to a remission of catatonia. Before admission, our patient had been treated with lithium as a mood stabilizer for 7 years. In this period, she had 1 manic episode, during which olanzapine was added to the lithium. Twomonths before presentation, our patient experienced stress due to several life events. This led to a hypomanic episode, directly followed by a depressive episode, resulting in admission to a psychiatric hospital. On day 1, the first day of admission, the patient developed a motor rigidity, characteristic of catatonia. She presented with rigidity of the legs and confused speech. Lorazepam was started orally in a dose of 8 mg/d, as is advised in the treatment protocol described by Tuerlings et al and endorsed by several other studies. Lithium and olanzapine were discontinued; plasma medication levels were checked for lithium andwere found to be below toxic.Malignant neuroleptic syndrome and malignant catatonia were strongly suspected but were ruled out because there was no increase of serum creatine kinase and no autonomic instability. On day 8, the catatonia had fully developed, with negativism, mutism, posturing, rigidity of the legs, and confused speech. Treatment with electroconvulsive therapy (ECT) was started, which was administered bilaterally. An electroencephalography (EEG) that was performed during ECT showed these seizures were of adequate quality (either a motor seizure of 20 seconds or more or a seizure detected with the EEG of 25 seconds or more). Lorazepam was discontinued because it is known to lower the quality of seizures during ECT. Unfortunately, no clinical improvement was observed after subsequent ECT sessions. It was decided to continue ECT because several sessions may be required before the effect can be measured. Because no clinical improvement had been observed after 5 ECT sessions by day","PeriodicalId":287576,"journal":{"name":"The Journal of ECT","volume":"42 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Journal of ECT","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1097/YCT.0000000000000290","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
To the Editor: W e present a 46-year-old woman, with a history of bipolar I disorder, who developed catatonia during a depressive episode. Initial treatment with 8 mg lorazepam per day proved to be ineffective, as was ECT. Therefore, the lorazepam dosage was increased up to 28 mg/d, which finally led to a remission of catatonia. Before admission, our patient had been treated with lithium as a mood stabilizer for 7 years. In this period, she had 1 manic episode, during which olanzapine was added to the lithium. Twomonths before presentation, our patient experienced stress due to several life events. This led to a hypomanic episode, directly followed by a depressive episode, resulting in admission to a psychiatric hospital. On day 1, the first day of admission, the patient developed a motor rigidity, characteristic of catatonia. She presented with rigidity of the legs and confused speech. Lorazepam was started orally in a dose of 8 mg/d, as is advised in the treatment protocol described by Tuerlings et al and endorsed by several other studies. Lithium and olanzapine were discontinued; plasma medication levels were checked for lithium andwere found to be below toxic.Malignant neuroleptic syndrome and malignant catatonia were strongly suspected but were ruled out because there was no increase of serum creatine kinase and no autonomic instability. On day 8, the catatonia had fully developed, with negativism, mutism, posturing, rigidity of the legs, and confused speech. Treatment with electroconvulsive therapy (ECT) was started, which was administered bilaterally. An electroencephalography (EEG) that was performed during ECT showed these seizures were of adequate quality (either a motor seizure of 20 seconds or more or a seizure detected with the EEG of 25 seconds or more). Lorazepam was discontinued because it is known to lower the quality of seizures during ECT. Unfortunately, no clinical improvement was observed after subsequent ECT sessions. It was decided to continue ECT because several sessions may be required before the effect can be measured. Because no clinical improvement had been observed after 5 ECT sessions by day