可逆转的深度感音神经性听力损失并发隐球菌脑膜炎在免疫正常的成年人:诊断和治疗的见解。

IF 0.7
Ahmad Alkheder, Lin Ahmad Ibrahim, Khaled Ziadah, Aliaa Issa, Mona Abbas, Ghassan Hamzeh
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引用次数: 0

摘要

本报告描述了一例51岁男性hiv阴性伴糖尿病、高血压和牛皮癣的非典型隐球菌性脑膜炎(CM)。患者有10天的亚急性头痛、呕吐和发热病史,随后突然出现重度双侧感音神经性听力损失(SNHL)、共济失调、复视、嗅觉丧失、老年、嗜睡、脑膜、呕吐反射缺失和双侧外展肌麻痹。脑MRI显示炎症改变累及鞍膈、丘脑和垂体柄。脑脊液分析证实CM(多细胞增多,蛋白升高,低血糖,开压bbb60 cmH2O,隐球菌抗原阳性),HIV和恶性肿瘤筛查阴性。听力测定证实双侧重度SNHL。治疗方法包括静脉注射两性霉素B脂质体,随后口服大剂量氟康唑,并辅以连续腰椎穿刺治疗以控制颅内压。随访1个月听力部分恢复。该病例强调,即使在没有明显免疫抑制的宿主中,突发性双侧snhl(很少是主要的初始表现)也可能预示CM,这给诊断带来了重大挑战。深度SNHL、多发性颅神经病变(包括VIII)、小脑体征和明显升高的ICP强烈暗示耳蜗后病变,可能由脑膜炎症、直接前庭耳蜗神经侵犯和/或神经压迫引起。关键的是,及时的抗真菌治疗结合积极的ICP降低促进神经系统恢复,显示潜在的可逆性和避免过早的人工耳蜗植入。临床医生应考虑急性双侧听前庭功能障碍伴颅神经病变或颅内压升高的CM患者,特别是亚急性前驱症状。该病例强调了icp指导下的并发治疗与抗真菌药物在优化神经预后(包括听力恢复)方面的重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Reversible Profound Sensorineural Hearing Loss Complicating Cryptococcal Meningitis in an Immunocompetent Adult: Diagnostic and Therapeutic Insights.

This report describes an atypical presentation of cryptococcal meningitis (CM) in a 51 year-old HIV-negative male with diabetes, hypertension, and psoriasis. The patient presented with a 10 day history of subacute headache, vomiting, and fever, followed by the abrupt onset of profound bilateral sensorineural hearing loss (SNHL), ataxia, diplopia, anosmia, ageusia, drowsiness, meningismus, absent gag reflex, and bilateral abducens palsy. Brain MRI revealed inflammatory changes involving the sellar diaphragm, thalamus, and pituitary stalk. Cerebrospinal fluid analysis confirmed CM (pleocytosis, elevated protein, hypoglycorrhachia, opening pressure >60 cmH2O, positive cryptococcal antigen), with negative HIV and malignancy screens. Audiometry confirmed profound bilateral SNHL. Treatment included intravenous liposomal amphotericin B followed by high-dose oral fluconazole, augmented by serial therapeutic lumbar punctures for intracranial pressure (ICP) control. Partial hearing recovery was observed at 1 month follow-up. This case highlights that sudden bilateral SNHL-rarely the dominant initial manifestation-can herald CM even in hosts without overt immunosuppression, posing significant diagnostic challenges. The constellation of profound SNHL, multiple cranial neuropathies (including VIII), cerebellar signs, and markedly-elevated ICP strongly implicates retrocochlear pathology, likely resulting from meningeal inflammation, direct vestibulocochlear nerve invasion, and/or neural compression. Critically, timely-antifungal therapy combined with aggressive ICP reduction facilitated neurological recovery, demonstrating potential reversibility and avoiding premature cochlear implantation. Clinicians should consider CM in patients presenting with acute bilateral audiovestibular dysfunction accompanied by cranial neuropathies or elevated ICP, particularly with subacute prodromal symptoms. This case underscores the essential role of concurrent ICP-directed management alongside antifungals to optimize neurological outcomes, including hearing recovery.

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