Mishra Amit Kumar, Bishowkarma Sagar, Gyawali Bigyan Raj
Maharajgunj Medical Campus, Institute of Medicine, Tribhuvan University Teaching Hospital, Kathmandu, 44600 Nepal.
Department of ENT-HNS, Maharajgunj Medical Campus, Institute of Medicine, Tribhuvan University Teaching Hospital, Kathmandu, Nepal.
Indian J Otolaryngol Head Neck Surg. 2024 Dec;76(6):5057-5065. doi: 10.1007/s12070-024-05093-w. Epub 2024 Sep 24.
This study aimed to consolidate evidence linking vocal cord palsy (VCP) to hypoxic injury, and its pathophysiology, and explore related topographical representations along laryngeal innervation. PubMed, Embase, and Scopus were the databases used. This review adheres to PRISMA guidelines. We included case series or case reports published before December 6, 2023. These studies must document VCP, diagnosed via direct or indirect laryngoscopic evaluation, resulting from hypoxic injury with imaging documentation specifying the level of injury. Screening, review, quality assessment, and extraction were done using Covidence. Our search strategy yielded 380 articles, of which 11 papers met the inclusion criteria for final review. A total of 12 patients were included across the selected studies, evenly split between genders. The causes of hypoxic injury were stroke in 11 cases and perinatal asphyxia in one. The hypoxic injury affected the medulla, pons, basal ganglia, thalamus, internal capsule, cortex, and cerebellum. The distribution of hypoxic injuries was: left side (6), bilateral (2), right side (2), and not mentioned (2). Vocal cord involvement was unilateral in eight cases and bilateral in four cases. In five cases, the involvement was ipsilateral to the hypoxic injury, bilateral when the injury was bilateral, and contralateral in two cases. Our study provides insights into how hypoxic brain injury can cause VCP and correlates the level of lesions along the innervation pathway with the clinical presentation. VCP can be induced by hypoxic injuries to the neurons extending from the laryngeal motor cortex to the laryngeal motor neurons in the medulla.
本研究旨在巩固将声带麻痹(VCP)与缺氧性损伤及其病理生理学联系起来的证据,并探索沿喉神经支配的相关拓扑学表现。使用的数据库为PubMed、Embase和Scopus。本综述遵循PRISMA指南。我们纳入了2023年12月6日前发表的病例系列或病例报告。这些研究必须记录经直接或间接喉镜评估诊断出的因缺氧性损伤导致的VCP,并有影像学记录明确损伤水平。使用Covidence进行筛选、综述、质量评估和提取。我们的检索策略共获得380篇文章,其中11篇论文符合最终综述的纳入标准。所选研究共纳入12例患者,男女各半。缺氧性损伤的原因中,11例为中风,1例为围产期窒息。缺氧性损伤累及延髓、脑桥、基底神经节、丘脑、内囊、皮质和小脑。缺氧性损伤的分布情况为:左侧(6例)、双侧(2例)、右侧(2例)、未提及(2例)。声带受累情况为单侧8例,双侧4例。5例中,受累与缺氧性损伤同侧,损伤为双侧时则为双侧受累,2例为对侧受累。我们的研究深入探讨了缺氧性脑损伤如何导致VCP,并将神经支配途径上的病变水平与临床表现相关联。从喉运动皮质延伸至延髓的喉运动神经元的缺氧性损伤可诱发VCP。