{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,21]],"date-time":"2025-11-21T04:21:34Z","timestamp":1763698894702,"version":"3.45.0"},"reference-count":18,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2025,7,9]],"date-time":"2025-07-09T00:00:00Z","timestamp":1752019200000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clinical Case Reports"],"published-print":{"date-parts":[[2025,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Neuroleptic malignant syndrome (NMS) is a rare but life\u2010threatening reaction associated with the use of dopamine\u2010modulating agents, which presents with symptoms like high fever, muscle rigidity, and autonomic instability. It is known that both the use of dopamine receptor antagonists and the sudden withdrawal of dopamine receptor agonists can trigger NMS. Benzodiazepine withdrawal can create a GABA\u2010deficient state, linked to catatonia and possibly predisposing individuals to NMS. The case was a 53\u2010year\u2010old male patient with a history of high\u2010dose benzodiazepine dependency, who developed NMS after the abrupt withdrawal of alprazolam and the single\u2010dose intramuscular (IM) haloperidol. He presented with the symptoms of stupor, generalized rigidity, and fever, requiring admission to the Respiratory Care Unit. His medical history included long\u2010term use of clonazepam, alprazolam, and methadone maintenance therapy (MMT). The laboratory findings also demonstrated elevated creatine phosphokinase (CPK) levels, peaking at 7896\u2009IU\/L. The treatments with bromocriptine and lorazepam further led to gradual improvement, and the patient was discharged after 11\u2009days following the resolution of NMS symptoms. This case highlights the potential role of benzodiazepine withdrawal as a risk factor for NMS, especially when combined with antipsychotic medication like haloperidol. The shared mechanisms between the pathophysiology of NMS and benzodiazepine withdrawal suggest that the abrupt cessation of GABAergic agents may lower dopaminergic activity, contributing to the onset of NMS. Clinicians must be accordingly cautious in distinguishing benzodiazepine withdrawal from other causes of delirium and then option for appropriate treatment approaches to mitigate risks.<\/jats:p>","DOI":"10.1002\/ccr3.70632","type":"journal-article","created":{"date-parts":[[2025,7,10]],"date-time":"2025-07-10T06:50:19Z","timestamp":1752130219000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Is Abrupt Withdrawal of Benzodiazepines a Risk Factor for Neuroleptic Malignant Syndrome? A Case Report With Single\u2010Dose Haloperidol"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-3208-0734","authenticated-orcid":false,"given":"Behnam","family":"Abbasi","sequence":"first","affiliation":[{"name":"Department of Psychiatry, Faculty of Medicine Mazandaran University of Medical Sciences  Sari Iran"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6872-481X","authenticated-orcid":false,"given":"Forouzan","family":"Elyasi","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, Faculty of Medicine Mazandaran University of Medical Sciences  Sari Iran"},{"name":"Sexual and Reproductive Health Research Center, Psychiatry and Behavioral Sciences Research Center, Addiction Institute Mazandaran University of Medical Sciences  Sari Iran"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masoud","family":"Aliyali","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Faculty of Medicine Mazandaran University of Medical Sciences  Sari Iran"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2025,7,9]]},"reference":[{"key":"e_1_2_12_2_1","doi-asserted-by":"publisher","DOI":"10.1177\/070674371205700810"},{"key":"e_1_2_12_3_1","doi-asserted-by":"publisher","DOI":"10.1002\/npr2.12315"},{"key":"e_1_2_12_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-030-73503-6_38"},{"key":"e_1_2_12_5_1","doi-asserted-by":"publisher","DOI":"10.4103\/ipj.ipj_265_21"},{"key":"e_1_2_12_6_1","doi-asserted-by":"publisher","DOI":"10.1177\/2324709620969498"},{"key":"e_1_2_12_7_1","doi-asserted-by":"publisher","DOI":"10.2174\/1573400511309020005"},{"key":"e_1_2_12_8_1","doi-asserted-by":"publisher","DOI":"10.1038\/clpt.1981.154"},{"key":"e_1_2_12_9_1","doi-asserted-by":"publisher","DOI":"10.1186\/s42077\u2010022\u201000283\u20106"},{"key":"e_1_2_12_10_1","doi-asserted-by":"publisher","DOI":"10.1176\/ajp.2007.164.6.870"},{"key":"e_1_2_12_11_1","doi-asserted-by":"publisher","DOI":"10.1055\/s\u20102001\u201015188"},{"key":"e_1_2_12_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.biopha.2024.116329"},{"key":"e_1_2_12_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.genhosppsych.2006.07.007"},{"key":"e_1_2_12_14_1","doi-asserted-by":"publisher","DOI":"10.1097\/jcp.0000000000001019"},{"key":"e_1_2_12_15_1","doi-asserted-by":"publisher","DOI":"10.2174\/1570159x13999150424113345"},{"key":"e_1_2_12_16_1","doi-asserted-by":"publisher","DOI":"10.1159\/000118713"},{"key":"e_1_2_12_17_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature08758"},{"key":"e_1_2_12_18_1","first-page":"207","volume-title":"Progress in Brain Research","author":"Kellogg C. 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