先天性TORCH感染暴露婴儿的听性脑干异常：对纵向听力学监测的意义
Auditory Brainstem abnormalities in infants exposed to congenital TORCH infections: implications for longitudinal audiological monitoring.
文献信息
| PMID | 42911281 |
|---|---|
| 原文 | 在 PubMed 查看原文 ↗ |
| 发表日期 | 2026 |
| 作者 | Glauciene Amaral Martins |
| 作者单位 | Department of Physical Therapy, Speech-Language Pathology and Occupational Therapy, School of Medicine, University of São Paulo, São Paulo, Brazil. glaucienemartins24@usp.br. |
| 期刊 | European journal of pediatrics |
| SCI 分区 | Q1 |
| IF | 3 |
| 研究类型 | 临床研究 · 临床 |
| 所属专科 | 耳科 |
中文摘要
未标注： 通过将先天性感染暴露婴儿与无听力损失风险指征的婴儿进行比较，评估其听觉通路的完整性与成熟度。本前瞻性纵向研究纳入55名先天性TORCH感染暴露婴儿（研究组-SG）和38名无听力损失风险指征的婴儿（对照组-CG），均来自巴西圣保罗一家公立医院的新生儿听力筛查项目。对先天性TORCH感染暴露婴儿及无听力损失风险指征的对照组婴儿进行了评估。参与者接受三次评估：3月龄前（T1）、首次评估后3个月（T2）以及首次评估后6个月（T3）。记录听性脑干反应（ABR）和长潜伏期听觉诱发电位（LLAEP）。分析ABR的绝对潜伏期和峰间期，以及LLAEP的P1成分潜伏期。先天性感染暴露婴儿显示出更高频率的ABR异常，涉及III波和V波、I-III和I-V峰间期以及总体ABR结果，尤其在初始评估时。两组随时间均观察到ABR波和峰间潜伏期以及LLAEP P1潜伏期的进行性缩短。两组间P1潜伏期未见显著差异。
结论： 先天性感染暴露婴儿表现出脑干听觉通路成熟的改变，提示其成熟轨迹较无听力损失风险指征的婴儿更慢或不同。纵向听力学随访对于该人群听觉通路异常的早期识别至关重要。
已知： • 先天性感染可能通过影响外周和中枢听觉通路而损害听觉发育。
新发现： • 先天性TORCH感染暴露婴儿显示出更高频率的听性脑干反应异常，提示脑干听觉成熟轨迹更慢或不同。
英文摘要
UNLABELLED: To evaluate the integrity and maturation of the auditory pathway in infants exposed to congenital infections by comparing them with infants without risk indicators for hearing loss. This prospective longitudinal study included 55 infants exposed to congenital TORCH infections (study group-SG) and 38 infants without risk indicators for hearing loss (control group-CG) enrolled in a Neonatal Hearing Screening program at a public hospital in São Paulo, Brazil. Infants exposed to congenital TORCH infections and a control group without risk indicators for hearing loss were evaluated. Participants underwent three assessments: before 3 months of age (T1), 3 months after the first assessment (T2), and 6 months after the first assessment (T3). Auditory Brainstem Response (ABR) and Long-Latency Auditory Evoked Potentials (LLAEP) were recorded. Absolute latencies and interpeak intervals of the ABR, as well as the P1 component latency of the LLAEP, were analyzed. Infants exposed to congenital infections showed a higher frequency of ABR abnormalities involving waves III and V, interpeak intervals I-III and I-V, and the overall ABR outcome, particularly at the initial assessments. Progressive reductions in ABR wave and interpeak latencies, as well as in LLAEP P1 latency, were observed over time in both groups. No significant between-group differences were found in P1 latency.
CONCLUSION: Infants exposed to congenital infections exhibit alterations in brainstem auditory pathway maturation, suggesting a slower or distinct maturational trajectory than infants without risk indicators for hearing loss. Longitudinal audiological follow-up is essential for the early identification of auditory pathway abnormalities in this population.
WHAT IS KNOWN: • Congenital infections may impair auditory development by affecting the peripheral and central auditory pathways.
WHAT IS NEW: • Infants exposed to congenital TORCH infections showed a higher frequency of Auditory Brainstem Responses abnormalities, suggesting a slower or distinct brainstem auditory maturation trajectory.