Solanki Anshu, Mukerjee Dev, Bhadauria Naveen, Barve Rudra
Rheumatology, North Middlesex University Hospital, London, GBR.
Internal Medicine, St. George's University School of Medicine, St. George's, GRD.
Cureus. 2025 Aug 21;17(8):e90706. doi: 10.7759/cureus.90706. eCollection 2025 Aug.
Olanzapine, a second-generation antipsychotic, is generally well tolerated but can rarely be associated with serious complications such as rhabdomyolysis and hyponatremia. We report the case of a woman in her early forties with a 15-year history of paranoid schizophrenia who developed bilateral foot drop and seizures in the context of severe hyponatremia and markedly elevated creatine phosphokinase (CPK) levels. Symptoms arose after olanzapine dose escalation from 10 to 20 mg daily to address difficult psychiatric symptoms. Magnetic resonance imaging (MRI) showed diffuse T2 hyperintensity in calf muscles, and nerve conduction studies revealed bilateral common peroneal neurapraxia. The presentation was attributed to olanzapine-induced syndrome of inappropriate antidiuretic hormone secretion (SIADH) and rhabdomyolysis. Both olanzapine and Lurasidone were stopped on admission; sequential re-challenge identified olanzapine as the probable causative agent. This case highlights the importance of early recognition of muscle symptoms and electrolyte disturbances in patients on antipsychotics, particularly following dose adjustments.
奥氮平是一种第二代抗精神病药物，通常耐受性良好，但很少会引发严重并发症，如横纹肌溶解和低钠血症。我们报告了一例四十出头的女性病例，该患者患有偏执型精神分裂症15年，在严重低钠血症和肌酸磷酸激酶（CPK）水平显著升高的情况下出现了双侧足下垂和癫痫发作。症状出现在奥氮平剂量从每日10毫克增加到20毫克以应对难治性精神症状之后。磁共振成像（MRI）显示小腿肌肉弥漫性T2高信号，神经传导研究显示双侧腓总神经失用。该表现归因于奥氮平引起的抗利尿激素分泌不当综合征（SIADH）和横纹肌溶解。入院时停用了奥氮平和鲁拉西酮；后续的重新激发试验确定奥氮平为可能的致病因素。该病例强调了早期识别抗精神病药物治疗患者的肌肉症状和电解质紊乱的重要性，尤其是在剂量调整之后。
