PLP139-151多肽诱导实验性自身免疫性脑脊髓炎大鼠的听觉和形态学改变

目的制作实验性自身免疫性脑脊髓炎(experimntalautoimmuneencephalomyelitis,EAE)动物模型,研究髓鞘蛋白脂质蛋白(proteolipidprotein,PLP)139-151多肽诱导的EAE大鼠听觉和听觉传导径路组织学改变,探讨其对大鼠听力的影响。方法动物分实验组和对照组,实验组大鼠用PLP139-151和含结核杆菌的完全福氏佐剂混合制成的抗原配剂行双侧后肢足垫下注射,制作EAE大鼠模型,对照组用生理盐水混合完全福氏佐剂注射。观察大鼠免疫前后体重变化和临床症状评分,检测EAE大鼠免疫前后听性脑干反应(auditorybrainstemresponse,ABR)、听神经复合动作电位(compoundactionpotential,CAP)、中潜伏期反应(middlelatencyresponse,MLR)及畸变产物耳声发射(distor-tionproductsotoacousticemissions,DPOAE)的变化,并利用电镜、免疫组织化学染色和Westernblot等方法观察EAE大鼠听神经及脑干组织学改变。结果免疫后EAE大鼠体重降低,症状评分在免疫后第14~21天达最高峰;ABR反应阈升高,ABR的波Ⅱ、Ⅴ潜伏期,Ⅰ-Ⅴ、Ⅱ-Ⅴ波间期和CAP的N2波潜伏期延长、波幅降低;MLR的Na、Pa潜伏期明显延长;DPOAE可正常引出,于免疫早期可见低频幅值升高;对照组听力学检测无明显改变。电镜下可见EAE大鼠听神经中枢端髓鞘松散、局部变薄或融合,免疫组织化学染色可见脑干白质局灶性脱髓鞘改变,可累及耳蜗核;Westernblot显示听神经PLP蛋白表达减少,髓鞘碱性蛋白(MBP)未见明显改变。结论EAE大鼠的病理改变主要浸润白质,可引起听觉中枢和听神经中枢端少突胶质细胞脱髓鞘,导致听觉中枢传导径路的听力学改变。     

P0蛋白免疫豚鼠的听力学研究

目的:探讨内耳纯化PO蛋白免疫豚鼠的听力学变化.方法:制备纯化内耳PO蛋白.分析20只经内耳纯化PO蛋白免疫后豚鼠的ABR、听神经动作电位(CAP)、畸变产物耳声发射(DPOAE)的检查结果.结果:20只动物经PO蛋白免疫后死亡4只,余16只(32耳)动物中,7耳(22%,7/32)出现ABR反应阈升高,波Ⅰ、Ⅲ潜伏期及Ⅰ-Ⅲ、Ⅰ-Ⅳ波间期明显延长(P<0.01),但Ⅲ-Ⅳ间期无明显变化;CAP(N1)幅值均有不同程度的下降,潜伏期延长(P<0.01));POAE各频率的幅值无明显改变,对侧白噪声抑制效应存在,有减弱的趋势,但与对照组无明显差异(P>0.05).结论:纯化的内耳P0蛋白是内耳重要的自身抗原之一,可导致部分豚鼠的听神经和内耳出现自身免疫性疾病.     

PLP139-151多肽诱导实验性自身免疫性脑脊髓炎女鼠的听带和形态学改变

目的 制作实验性自身免疫性脑脊髓炎（experimntal autoimmune encephalomyelitis，EAE）动物模型，研究髓鞘蛋白脂质蛋白（proteolipid protein，PLP）139-151多肽诱导的EAE大鼠听觉和听觉传导径路组织学改变，探讨其对大鼠听力的影响。方法 动物分实验组和对照组，实验组大鼠用PLP139-151和含结核杆菌的完全福氏佐剂混合制成的抗原配剂行双侧后肢足垫下注射，制作EAE大鼠模型，对照组用生理盐水混合完全福氏佐剂注射。观察大鼠免疫前后体重变化和临床症状评分，检测EAE大鼠免疫前后听性脑干反应（auditory brajnstem response，ABR）、听神经复合动作电位（compound action potential，CAP）、中潜伏期反应（middle latency response，MLR）及畸变产物耳声发射（distortion products otoacoustic emissiom，DPOAE）的变化，并利用电镜、免疫组织化学染色和Western blot等方法观察EAE大鼠听神经及脑干组织学改变。结果 免疫后EAE大鼠体重降低，症状评分在免疫后第14～21天达最高峰；ABR反应阈升高，ABR的波Ⅱ、Ⅴ潜伏期，Ⅰ-Ⅴ、Ⅱ-Ⅴ波间期和CAP的N2波潜伏期延长、波幅降低；MLR的Na、Pa潜伏期明显延长；DPOAE可正常引出，于免疫早期可见低频幅值升高；对照组听力学检测无明显改变。电镜下可见EAE大鼠听神经中枢端髓鞘松散、局部变薄或融合，免疫组织化学染色可见脑干白质局灶性脱髓鞘改变，可累及耳蜗核；Western blot显示听神经PLP蛋白表达减少，髓鞘碱性蛋白（MBP）未见明显改变。结论 EAE大鼠的病理改变主要浸润白质，可引起听觉中枢和听神经中枢端少突胶质细胞脱髓鞘，导致听觉中枢传导径路的听力学改变。     

免疫性脑脊髓膜炎模型中听神经脱髓鞘病变与听觉诱发电位的变化

目的探索实验性免疫性脑脊髓膜炎模型中听神经脱髓鞘病变和ABR随时间的变化,以及这两种变化之间的关系。方法选取Wistar大鼠60只,随机分为实验组、对照组和正常组,分别皮下注射牛坐骨神经髓鞘碱蛋白和完全弗氏佐剂、完全弗氏佐剂、生理盐水。对所有实验动物在免疫前、免疫结束后1、2、3、4、5、6周进行ABR检查。每周随机抽取各组2只动物,2.5%戊二醛活体灌注后处死,电镜下观察听神经的变化。结果实验组动物听神经在给药后1周均出现脱髓鞘病变,给药后第3周达到高峰,随后自行缓解,在第6周基本恢复;ABR的阈值各组间无明显差异,实验组Ⅲ波潜伏期延长。结论免疫性脑脊髓膜炎模型中听神经的脱髓鞘病变发病后随时间自行缓解,与ABR的变化并不同步。     

急性高胆红素血症豚鼠听功能研究

目的 探讨急性高胆红素血症对听功能的影响及病损部位。方法建立急性高胆红素血症豚鼠模型，检测其听性脑干反应（ABR）、听神经复合动作电位（CAP）阈值及潜伏期、耳蜗微音器电位（CM）、畸变产物耳声发射（DPOAE）。结果实验组动物出现ABR反应阈升高，伴波Ⅰ、Ⅲ、Ⅳ潜伏期及Ⅰ-Ⅲ、Ⅲ-Ⅳ波间期明显延长，与对照组比较有显著差异（P〈0．01）；CAPN1、N2波潜伏期延长，与对照组比较有显著差异（P〈0．01）；实验组有2只动物（3耳）ABR、CAP未引出；CM在8、4、1kHz处幅值下降，DPOAE各频率幅值下降；电镜示螺旋神经节细胞胞浆空泡状改变、包绕髓鞘板层松解。结论高胆红素血症不但引起中枢听觉传导通路的损害，亦可累及耳蜗，其耳蜗毒性机制尚需进一步探讨。     

自身免疫性听神经病动物模型的建立及听性脑干反应和畸变产物耳声发射的变化

目的建立自身免疫性听神经病动物模型，探讨其听性脑干反应（auditory brainstem response ABR）和畸变产物耳声发射（distortion product otoacoustic emission DPOAE）的变化特征。方法选取耳廓反射正常的白色豚鼠250只，分离、电泳与纯化豚鼠螺旋神经节及蜗轴内的耳蜗神经纤维抗原，然后与等量完全弗氏佐剂免疫同种豚鼠，其中正常组10只，对照组10只，试验组50只。观察ABR、DPOAE、血清IgG水平、螺旋神经节和耳蜗核团形态学的改变、听神经抗原蛋白在螺旋神经节和耳蜗神经的表达、听神经纤维超微结构的变化。结果免疫后16只动物（32／100耳）出现听性脑干反应阈提高10～25dB，Ⅰ、Ⅲ波潜伏期延长，到免疫后第3周最为明显，随后有逐渐恢复的趋势，其中Ⅲ波潜伏期到第6周恢复正常；该组豚鼠DPOAE没有变化，动物血清IgG显著性升高，与对照组相比差异有统计学意义（F=10．03，P〈0．05）；均有不同程度的螺旋神经节细胞变性、数目减少，螺旋神经节和小血管周围有淋巴细胞浸润；听神经纤维出现脱髓鞘、髓鞘断裂等现象。豚鼠耳蜗核各亚核团平均细胞密度和细胞平均面积各组差异比较没有统计学意义；听神经蛋白完全分布于耳蜗螺旋神经节和听神经纤维组织。免疫后34只动物（68／100耳）没有出现ABR反应阈升高，血清IgG没有升高，与对照组相比差异没有统计学意义，螺旋神经节、耳蜗核团、听神经纤维超微结构没有变化。结论建立了豚鼠自身免疫性听神经病动物模型，该动物模型的ABR反应阈轻中度提高，Ⅰ、Ⅲ波有自然恢复的趋势。DPOAE没有变化。     

早期听神经瘤的听性脑干反应

听力损失较少的听神经瘤(平均损失36.9dB)6例与同等听力损失的内耳感觉神经性聋(平均损失36.3dB)6例,就其ABR的以下各参数进行比较;①波Ⅰ、波Ⅲ、波Ⅴ的潜伏期;②波Ⅰ～Ⅲ间潜伏期,波Ⅰ～Ⅴ间潜伏期;③两耳波Ⅴ潜伏期差,两耳波Ⅰ～Ⅴ间潜伏期差;④波的再现性。结果:①波Ⅰ、波Ⅴ潜伏期的绝对值:听神经瘤波Ⅰ潜伏期的平均值为1.98ms,比正常者1.9ms仅稍延长;耳蜗性聋波Ⅰ潜伏期延长,其平均值为2.1ms。听神经瘤波Ⅴ潜伏期为6.9ms(6.0～7.7ms),比正常者延长,耳蜗性聋为6.2ms(5.6～6.9ms),也有延长的病例,因     

谷氨酸对豚鼠畸变产物耳声发射和听性脑干反应的影响

目的 研究外源性谷氨酸对畸变产物耳声发射(distortion product otoacoustlcemission，DPOAE)、听性脑干反应(auditory brainstem response，ABR)及耳蜗形态学的影响。方法应用豚鼠全耳蜗灌流技术，耳蜗灌流10mmol/L谷氨酸2h，分别记录灌流前、后DPOAE和ABR；耳蜗微音电位(cochlear microphonics，CM)和听神经复合动作电位(compound action potential，CAP)；应用透射电镜进行耳蜗形态学观察。结果灌流人工外淋巴液前、后CM及CAP无改变；灌流10mmol／L谷氨酸后DPOAE无改变，ABR潜伏期延长；同样灌流10mmol／L谷氨酸后CM幅度虽有下降、但是其非线性特点无改变；CAP阈值平均升高了35dB；灌流谷氨酸后内毛细胞及其下方神经纤维出现空泡。结论谷氨酸作为耳蜗主要的兴奋性传入神经递质，过度释放可以产生兴奋性毒性，损伤耳蜗内毛细胞及传入神经。同时本实验为建立听神经病的动物模型提供了一个参考方法。     

双侧耳蜗切除术致听力剥夺大鼠的听性脑干反应改变

目的：通过比较大鼠在双侧耳蜗切除术后不同时间点听性脑干反应（ABR）的变化,探讨ABR在测试听力剥夺大鼠模型中的应用价值。方法：选取2周龄SD大鼠40只,随机分为实验组4组（2周组、4周组、6周组、8周组）和对照组4组,每组5只（10耳）。实验组动物在双侧耳蜗损毁术后不同时间点与其对照组行ABR检测,记录ABR阈值及各波潜伏期和波间期。结果：实验组ABR反应阈明显升高,与对照组相比,差异有统计学意义（P〈0．01）,各波潜伏期和波间期明显延长（P〈0．01）;实验2周组、4周组与6周组和8周组相比,ABR反应阈的差异也有统计学意义（P〈0．01）。结论：双侧耳蜗切除术可导致大鼠ABR反应阈明显增高,各波潜伏期和波间期明显延长;听力剥夺效果从术后4周开始越发明显。     

分泌性中耳炎患儿听性脑干反应的应用及特征

目的 通过比较分泌性中耳炎(otitis media with effusion, OME)患儿鼓膜置管术前、后听性脑干反应(auditory brainstem response, ABR)的变化,探讨ABR测试在儿童分泌性中耳炎诊治中的临床应用价值.方法 对50例(100耳)分泌性中耳炎患儿行鼓膜置管术前进行ABR测试,其中有30例(60耳) 术后再次行ABR测试,并与50例(100耳)正常对照组儿童进行比较;另外将该30例(60耳)患儿根据鼓室分泌物黏稠度分两组,分泌物黏稠组16例(32耳),分泌物稀薄组14例(28耳),将两组ABR波Ⅴ阈值结果进行比较.结果 50例(100耳)分泌性中耳炎患儿术前ABR波Ⅴ阈值及波Ⅰ潜伏期均正常者占13%,漏诊率为13%;波Ⅴ阈值正常占41%,轻度异常52%,中度异常7%;波Ⅰ潜伏期正常19%,72%波Ⅰ潜伏期延长,9%出现波Ⅰ缺失.术前OME组患儿的ABR波Ⅰ、Ⅲ、Ⅴ各波潜伏期比正常儿童延长,阈值升高,差异有显著统计学意义(P＜0.01).Ⅰ-Ⅲ、Ⅰ-Ⅴ波间期缩短,与正常组比较差异有显著统计学意义(P＜0.01).术后ABR波Ⅴ阈值及波Ⅰ潜伏期均正常者占46.7%;波Ⅴ阈值正常占70.5%,轻度异常29.5%;波Ⅰ引出率100%,潜伏期正常占50.2%;OME组中术前、术后ABR各波潜伏期、波Ⅴ阈值比较差异有显著统计学意义(P＜0.01),各波波间期比较无差异,术后听力有明显改善,但与正常组比较部分患儿波Ⅴ阈值仍高,波Ⅰ、Ⅲ潜伏期仍延长,Ⅰ-Ⅲ、Ⅰ-Ⅴ波间期缩短(P＜0.05);分泌物黏稠组波Ⅴ阈值较稀薄组高.结论 单用ABR作为诊断OME的依据是有欠缺的,但大部分患儿可以通过该检查进行听力损失的评估,以了解鼓膜置管术后的听力状况及恢复程度.     

Effects of acute infrasound exposure on vestibular and auditory functions and the ultrastructural changes of inner ear in the guinea pig]

OBJECTIVE: To define the effects of acute infrasound exposure on vestibular and auditory functions and the ultrastructural changes of inner ear in guinea pigs. METHODS: The animals involved in the study were exposed to 8 Hz infrasound at 135dB SPL for 90 minutes in a reverberant chamber. The sinusoidal pendular test (SPT), auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAE) were respectively detected pre-exposure and at 0(within 2 hrs), 2 and 5 day after exposure. The ultrastructures of the inner ear were observed by scanning electron microscopy. RESULTS: The slow-phase velocity and the frequency of the vestibular nystagmus elicited by sinusoidal pendular test (SPT) declined slightly following infrasound exposure, but the changes were not significant (P > 0.05). No differences in the ABR thresholds, the latencies and the interval peak latencies of I, III, V waves were found between the normal and the experimental groups, and among experimental groups. The amplitudes of DPOAE at any frequency declined remarkably in all experimental groups. The ultrastructures of the inner ear were damaged to different extent. CONCLUSION: Infrasound could transiently depress the excitability of the vestibular end-organs, decrease the function of OHC in the organ of Corti and cause damage to the inner ear of guinea pigs.     

急性次声波暴露后豚鼠位听功能及内耳超微结构的变化

目的观察次声波对豚鼠位听功能和内耳超微结构的影响。方法将豚鼠置于频率8Hz、声压级135dBSPL的次声声场中连续暴露90min。应用正弦摆动试验(sinusoidalpendulartest,SPT)、听性脑干反应（auditorybrainstemresponse,ABR）和畸变产物耳声发射(distortionproductionotoacousticemission,DPOAE)评价次声波暴露前后豚鼠前庭功能和听功能的变化,扫描电镜观察豚鼠内耳各结构表面超微形态的变化。结果次声波暴露后不同时间正弦摆动诱发的豚鼠前庭性眼震的最大慢相速度(slow-phasevelocity,SPV)和频率较次声暴露前轻微降低,但无显著性意义(P>0.05)。次声波暴露后各组动物ABR阈值较正常时略有升高,亦无统计学差异(P>0.05),各组动物ABR各波潜伏期和波间期与次声暴露前比较差异均无显著性(P>0.05);DPOAE的幅度值在各个频率段均有明显的降低(P<0.01)。扫描电镜下见各实验组动物内耳半规管壶腹嵴两囊斑及Corti器感觉毛细胞纤毛缺失、散乱、倒伏及融合,表皮板等结构均有不同程度的损伤。结论次声波对豚鼠前庭末梢感受器兴奋性可能有一过性的轻微抑制作用,但SPT无有意义改变。次声波可引起豚鼠内耳毛细胞超微结构的损伤,可导致豚鼠耳蜗外毛细胞功能明显减退,这种功能减退尚不足以引起听力的明显改变。     

Anesthesia and surgical traum: their influence on the guinea pig compound action potential

A chronic implant consisting of a fine thermocouple placed on the round window permitted measurement of temperature and of the compound action potential (CAP) of the cochlear nerve in guinea pigs. Thresholds and latencies of the CAP, in response to tone bursts (2–40 kHz), were measured when the animal was awake and unrestrained, and again after several hours of anesthesia. The CAP remained unchanged with a variety of common anesthetics when precise control of round window temperature was maintained. However, when anesthesia was accompanied by several hours of slight cochlear cooling, thresholds were elevated for CAPs evoked by frequencies above 24 kHz and latencies were increased for CAPs evoked by all frequencies tested.

The effects of surgery on CAP threshold and latency were also examined. Guinea pigs were tested while still anesthetized at the conclusion of the implantation procedure, and then again several days later while awake. Thresholds and latencies were unchanged. In two anesthetized guinea pigs already implanted with thermocouples, ventral and post-auricular surgery to expose the middle ear had no effect on the CAP, when low-speed drilling was used to open the auditory bulla. However, when small portions of the bulla were broken away with forceps, the CAP in response to high-frequency tone bursts immediately showed elevated thresholds. This alteration of the CAP was clearly different from that produced by lowered temperature, since the latencies at threshold were significantly decreased.     

No evidence of auditory dysfunction in guinea pigs immunized with myelin P0 protein

Recent data have focused on the peripheral nerve myelin glycoprotein P0 as a putative autoantigen involved in the autoimmune etiology of some cases of Meniere's disease, idiopathic sensorineural hearing loss and sudden deafness. To determine whether antibodies to myelin P0 can alter cochlear function, 13 healthy guinea pigs were immunized with purified porcine myelin P0 while 10 controls were injected with saline water. The animals were then evaluated for evidence of evolving inner ear disease using immunological, electrophysiological and morphological methods. Twenty-six experimental ears were tested weekly with a brainstem auditory evoked potential technique for a period of 4 months and were compared to 20 control ears. Uniformly, all P0-sensitized guinea pigs showed antibodies to myelin protein P0 as evidenced by ELISA. Clinical signs of inflammatory demyelination were not discernible in P0-sensitized guinea pigs and all the animals were qualitatively normal. No significant increase of evoked potential thresholds was found in the P0-sensitized animals when compared to controls (P>0.05). Peak latencies of waves I, II, III, IV and V and inter-peak latencies in P0-sensitized guinea pigs did not significantly differ from those of controls (P>0.05). Histological sections of inner ear and peripheral nerves were free of disease in both groups. These findings indicate that the sole presence of antibodies to myelin P0 in the sera of guinea pigs or patients suspected of having autoimmune inner ear diseases is unlikely to elicit auditory abnormalities and that additional factors are necessary for the pathogenic development of these disorders.     

Effects of experimental cochlear thrombosis on oxygenation and auditory function of the inner ear

To elucidate the etiology and pathogenesis of sudden hearing loss, the effect of experimental cochlear thrombosis on oxygenation and the auditory function of the inner ear was investigated in anesthetized guinea pigs. Impairment of cochlear blood flow (CBF) was induced by ferromagnetic obstruction of cochlear blood vessels at lowered body temperature. Perilymphatic oxygen partial pressure (PO₂) in the basal scala tympani (about 200 m below the round window membrane) was measured polarographically using micro-coaxial needle electrodes. Auditory function was examined by recording cochlear microphonic (CM) frequency responses, compound action potentials (CAP) and auditory evoked brainstem responses (ABR). Findings demonstrated a considerable decrease in the mean perilymphaticPO₂ of 40%, 2 h after the start of the experiment. Mean CM and N₁ CAP amplitudes were reduced by about 25% each and ABR by 18%. No significant changes were observed in the latencies of either CAP or ABR. Mean basal CBF was found to decrease by 35%, as measured by laser Doppler flowmetry in a parallel study. The present findings demonstrate that vascular impairment in the inner ear results in a considerable drop in intracochlear oxygenation, causing a significant loss in the auditory response.     

Age-related Alterations in the Auditory Brainstem Responses and the Compound Action Potentials in Guinea Pigs

The auditory brainstem response (ABR) and the eighth nerve compound action potential (CAP) were measured using click stimuli to investigate the agerelated alteration in the auditory function in 66 guinea pigs consisting of four age groups. With advancing age, a gradual elevation of the thresholds in both the ABR and CAP was clearly seen, together with the prolonged latencies for waves I, II, III, and IV to clicks at 95 dBpeSPL in the ABR. There were some individual differences in either threshold elevation or latency prolongation of both the ABR and CAP in aged guinea pigs. These findings suggest that the effect of individual differences on degenerative aging processes of the auditory system should be considered in selected aged animals, although a significant elevation of the neural auditory threshold is clearly found with advancing age as a whole.     

纯化内耳P0蛋白诱发听神经脱髓鞘的实验研究

目的用从豚鼠内耳组织中纯化的P0蛋白免疫大鼠,观察实验动物听神经髓鞘变化,推测P0蛋白在听神经病的发生发展中的作用。方法采用SDS PAGE从内耳组织中分离、纯化P0蛋白,用Western Blot法鉴定纯化的P0蛋白。用纯化的P0蛋白作为抗原免疫大鼠,观察其听性脑干反应阈、耳声发射的变化、动物血清IgG水平以及听神经的髓鞘在光镜电镜下的形态学变化,免疫组织化学技术观察P0蛋白在听神经上的分布。结果免疫后实验组大鼠听力学显示听神经病的特征：耳声发射正常,而听性脑干反应严重异常;实验组血清IgG水平显著升高。电镜下可见听神经的脱髓鞘病变,免疫组织化学技术显示P0分布在蜗神经纤维的髓鞘上。结论P0蛋白作为抗原能诱发蜗神经的脱髓鞘病变,可能是听神经病的重要发病机制之一。     

不同病因引起的新生儿高胆红素血症听性脑干反应的特点

目的 探讨不同病因引起的新生儿高胆红素血症的听性脑干反应(ABR)特点及其与临床的关系.方法 将88例(176耳)高胆红素血症患儿按病因分为6组,同时选取15名(30耳)健康新生儿作为正常对照,均进行ABR测试,并比较各组间的差异,42 d后患儿复查ABR.结果 不同病因中,葡萄糖6-磷酸脱氢酶(glucose-6-phosphate dehydrogenase,G-6-PD)缺乏症所致的高胆红素血症ABR反应阈增高最明显,异常率最高.不同病因组之间及与对照组间ABR的Ⅲ波、Ⅴ波潜伏期及Ⅲ-Ⅴ、Ⅰ-Ⅴ波间期差异均具有统计学意义(P值均＜0.05).高胆红素血症患儿ABR各波潜伏期及波间期均较对照组延长,其中新生儿感染最容易引起ABR各波潜伏期及波间期延长,其次是ABO溶血与其他不明原因组,母乳性黄疸组潜伏期与波间期相对要短.多病因组ABR反应阈的异常率明显高于单病因组(P＜0.05);单种病因与多种病因引起的高胆红素血症组间比较,ABR各波潜伏期及波间期差异无统计学意义(P值均＞0.05).30例患儿进行了复查,复查前后除Ⅰ-Ⅲ波间期外,各波潜伏期及波间期差异均具有统计学意义(P值均＜0.05).结论 高胆红素血症对听觉系统的损害与病因的种类及数量有关.由G-6-PD缺乏、新生儿感染、ABO溶血、多病因以及不明原因引起的高胆红素血症与母乳性黄疸相比,更易导致听觉功能损害.高胆红素血症对听觉的损害存在一定的可逆性.

Abstract：

Objective To explore the characteristics of auditory brainstem response (ABR) in neonatal hyperbilirubinemia induced by different causes. Methods A total of 88 neonates ( 176 ears) with hyperbilirubinemia were divided into several groups according to the causes and followed up after 42 d, and 15 nomal neontes (30 ears) were measured ABR and analyzed the results. Results The thresholds of ABR in glucose-6-phosphate dehydrogenase were the highest in all the groups and had the lowdest incidence rate.The wave Ⅲ, Ⅴ latencies and Ⅲ-Ⅴ, Ⅰ -Ⅴ interwave intervals of the ABR were significantly difference and prolonged during test in comparison to the latencies in the control group ( P ＜ 0. 05 ). The neonatal infections group had the longest wave and interwave intervals, followed by ABO incompatibility hemolytic diseases and the unknown cause groups, while the breastfeeding jaundice were the shortest in the groups of neonatal hyperbilirubinemia. The thresholds of ABR in the hyperbilirubinemia caused by several etiologies were significant abnomality when compared with the single etiology. However, they were similar in the wave latencies and interwave intervals of ABR. During the follow up, the ABR wave latencies and interwave intervals except for interwave latency Ⅰ-Ⅲ were significantly shorter. Conclusions The toxicity of hyperbilirubinemia to the auditory nervous system are related to the species and number of etiologies. The neonate hyperbilirubinemia cuased by glucose-6-phosphate dehydrogenase, infections, ABO incompatibility hemolytic diseases and many etiologies are much more dangerous to the auditory system than the breastfeeding jaundice. The damages of hyperbilirubinemia to the auditory nervous system are reversible probably.