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Recognition during electroconvulsive therapy (ECT) is difficult due to postictal physiology, psychotropic polypharmacy, and frequent lack of quantitative neuromuscular monitoring. A 34-year-old woman with treatment-resistant schizophrenia developed consistently prolonged paralysis after succinylcholine during ECT, confirmed by markedly reduced plasma pseudocholinesterase activity. Switching to rocuronium with high-dose sugammadex and continuous quantitative monitoring led to immediate uneventful recovery and supported the need for routine monitoring to detect atypical recovery and reduce missed awareness risk.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/pseudocholinesterase-deficiency-in-a-patient-undergoing-electroconvulsive-therapy-a-case-report/418029/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/pseudocholinesterase-deficiency-in-a-patient-undergoing-electroconvulsive-therapy-a-case-report/418029.png","ImageObject",300,407,{"name":92,"@type":93},"Asher","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-29","2026-09-28",true,{"@type":102,"interactionType":103,"userInteractionCount":14},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"Why is pseudocholinesterase deficiency hard to detect during ECT?","Question",{"text":112,"@type":113},"Postictal physiology, psychotropic polypharmacy, and the frequent absence of quantitative neuromuscular monitoring can make residual paralysis difficult to recognize.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How was pseudocholinesterase deficiency confirmed in the reported case?",{"text":117,"@type":113},"Laboratory testing showed markedly reduced plasma pseudocholinesterase activity (3745 U/L), confirming PD.",{"name":119,"@type":110,"acceptedAnswer":120},"What intervention prevented prolonged paralysis in subsequent ECT sessions?",{"text":121,"@type":113},"Succinylcholine was replaced with rocuronium, and reversal was performed with high-dose sugammadex (960 mg), under continuous quantitative neuromuscular monitoring.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},418029,1792218140,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":14,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":19,"language":139,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":67,"update_tm":143,"read_time":52,"preview_page_count":4},687197207639,"https://ap-avatar.wpscdn.com/davatar_a8503ba1806abce46bf441b54a3ca4cd","Review began 11/16/2025  \nReview ended 11/29/2025  \nPublished 12/02/2025  \n© Copyright 2025  \nLadeira et al. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 4.0. , which permits unrestricted use , distribution , and reproduction in any medium , provided the original author and source are credited.  \nDOI: 10.7759/cureus.98333  \nOpen Access Case Report  \nPseudocholinesterase Deficiency in a Patient Undergoing Electroconvulsive Therapy: A Case Report  \nAntónio C. Ladeira 1 , João Laranjeira 1, Luciana Guariento 1 , Muriel Lérias-Cambeiro 1, Paula Victor 1 1. Anaesthesiology, Unidade Local de Saúde Santa Maria, Lisbon, PRT  \nCorresponding author: António C. Ladeira, [antoniodladeira@gmail.com](antoniodladeira@gmail.com)  \nAbstract  \nPseudocholinesterase deficiency (PD) is a genetic or acquired condition that impairs the metabolism of succinylcholine, leading to unpredictable and potentially prolonged paralysis. Its recognition during electroconvulsive therapy (ECT) is particularly difficult because postictal physiology, psychotropic polypharmacy, and the frequent absence of quantitative neuromuscular monitoring may make residual paralysis difficult to detect. We report a 34-year-old woman with pharmacotherapy-resistant schizophrenia who developed consistently prolonged paralysis after succinylcholine during ECT. In the first session, anaesthesia with propofol (80 mg) and succinylcholine (60 mg) produced an adequate seizure, but recovery of spontaneous ventilation and motor function was delayed by approximately 24 minutes, with only mild tachycardia and hypertension; this was initially attributed to chronic psychotropic treatment. The same pattern recurred during the second session despite adequate hypnotic depth on bispectral index (BIS) monitoring and unreliable neuromuscular monitoring data. Laboratory testing subsequently revealed markedly reduced plasma pseudocholinesterase activity (3745 U/L), confirming PD. Succinylcholine was then replaced with rocuronium (40 mg), and reversal was performed with high-dose sugammadex (960 mg), resulting in immediate and uneventful recovery in all remaining sessions under continuous quantitative neuromuscular monitoring. This case illustrates that PD may go unrecognised in ECT when quantitative neuromuscular monitoring is unavailable or unreliable and reinforces the need for routine monitoring to detect atypical recovery patterns and reduce the risk of unrecognised awareness during anaesthesia.  \nCategories: Psychiatry, Pharmacology, Anesthesiology  \nKeywords: awareness, delayed emergence, electroconvulsive therapy, neuromuscular monitoring, pseudocholinesterase deficiency, rocuronium, succinylcholine, sugammadex  \nIntroduction  \nElectroconvulsive therapy (ECT) is a well-established treatment for severe psychiatric disorders resistant topharmacotherapy, such as major depression and schizophrenia [1-3]. The procedure requires general anaesthesia and the administration of a neuromuscular blocking agent (NMBA) to minimise the risk of musculoskeletal injury during the seizure.  \nSuccinylcholine is the most commonly used NMBA in ECT owing to its rapid onset and brief duration of action [1,3] . Its metabolism depends on plasma pseudocholinesterase (butyrylcholinesterase) activity, and deficiency of this enzyme, whether genetic or acquired, can result in prolonged neuromuscular block [4,5] .  \nPseudocholinesterase deficiency (PD) may be hereditary, following an autosomal recessive pattern, or acquired due to conditions such as liver disease, malnutrition, pregnancy, malignancy, or exposure to drugs including monoamine oxidase (MAO) inhibitors and corticosteroids [6,7] . The prevalence is estimated at approximately one in 3,200 for homozygotes and up to one in 25 for heterozygotes [4,6] .  \nRecognising PD during ECT can be particularly challenging. The procedure is performed rapidly, often outside the operating theatre, and neuromuscular mo","cbCaigJdsT6SaL7I","https://ap.wps.com/l/cbCaigJdsT6SaL7I","pdf",345617,"English","# Abstract\n# Introduction\n# Case Presentation\n# Discussion\n# Conclusion","[{\"question\":\"Why is pseudocholinesterase deficiency hard to detect during ECT?\",\"answer\":\"Postictal physiology, psychotropic polypharmacy, and the frequent absence of quantitative neuromuscular monitoring can make residual paralysis difficult to recognize.\"},{\"question\":\"How was pseudocholinesterase deficiency confirmed in the reported case?\",\"answer\":\"Laboratory testing showed markedly reduced plasma pseudocholinesterase activity (3745 U/L), confirming PD.\"},{\"question\":\"What intervention prevented prolonged paralysis in subsequent ECT sessions?\",\"answer\":\"Succinylcholine was replaced with rocuronium, and reversal was performed with high-dose sugammadex (960 mg), under continuous quantitative neuromuscular monitoring.\"}]","Pseudocholinesterase Deficiency in a Patient Undergoing Electroconvulsive Therapy - A Case Report | PDF",1790611665]