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1.
为分析静压变化对中耳听骨链运动和耳蜗输入的影响,运用有限元模型研究外耳道静压导致的中耳声音传递功能和耳蜗激励输入改变。首先,根据相关实验测量数据并结合有限元分析,拟合了耳道静压力与中耳各构件有效弹性模量关系的经验公式;然后,通过材料参数的改变模拟压力造成的中耳结构刚度增加,分析耳道静压对中耳机动性的影响和不同耳道压力下镫骨底板位移、速度和耳蜗两窗压力差的变化。计算结果与相关的文献实验数据有较好的符合,说明所建立的计算模型在模拟静压条件下中耳传递功能方面的合理性。结果表明在低频范围(0~0.6 kHz)外耳道静压对两窗压力差的影响稍大于对镫骨位移的影响。  相似文献   

2.
内耳圆窗膜解剖   总被引:1,自引:0,他引:1  
圆窗膜是间隔于中耳和内耳之间的重要屏障,其结构及正常的功能对保证内耳正常生理功能具有重要意义。准确测量圆窗膜的面积和形态有助于对其进行深入的病理生理学研究,进而计算圆窗膜在病理状态下对各种物质的转运速率,测试内耳各腔隙离子浓度变化等,为阐明中耳和内耳疾病的相互影响,中耳腔内毒素和药物等影响内耳功能的机理,及更好的开展内耳显微手术,电子耳蜗手术等治疗奠定基础。  相似文献   

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目的探讨中耳传音功能异常对畸变产物耳声发射(DPOAE)测试结果的影响程度并在临床应用中加以识别和剔除.方法将年龄2月~11岁56例(107耳)小儿依听力损失类型分为感音性聋组和传导性聋组,并设置正常听力对照组,应用GSI 60耳声发射仪分别观察其DPOAE的DP检出率、DP幅值、DP与NF幅值差及相同参数条件下DPOAE测试时间.结果耳蜗功能严重受损和渗出性中耳炎所记录到的DPOAE各测量参数之间的差异无统计学意义(p>0.05).结论中耳积液导致的中耳传音功能障碍对DPOAE测试结果的影响,与耳蜗功能严重损害时所记录到的DPOAE参数变化,在临床检测中难以区分.因此,临床上在应用DPOAE进行听力评估之前,首先要检测受检者的中耳功能,剔除其对DPOAE检测结果的影响,确保结果的可靠性.  相似文献   

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目的研究采用传统基底膜位移评价标准评估圆窗激振式人工中耳听力补偿性能的准确性,为圆窗激振式人工中耳的性能评估提供理论基础。方法基于耳蜗几何结构的实验数据,建立耳蜗感声微观有限元模型,通过对比内听毛细胞、外听毛细胞、盖膜等部位位移响应的实验测量值,验证模型的可靠性。基于该模型,对比分析正向激振、圆窗激振下的基底膜位移与内听毛细胞静纤毛剪切位移;以内听毛细胞静纤毛剪切位移作为感声标准,研究圆窗激振时采用传统人工中耳基底膜评价标准的等效声压级偏差。结果在所研究耳蜗微段对应的5 k Hz特征频率处,相同幅值的声压作用下,圆窗激振的基底膜位移和内听毛细胞静纤毛剪切位移均小于正向激振的对应值。结论正向激振下的内听毛细胞更兴奋,感声效果更强。同时,采用正向激振的基底膜位移评价方法评估圆窗激振的听力补偿效果,会高估圆窗激振的听力补偿性能;但偏差较小,是一种相对可靠的评价方法。  相似文献   

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目的研究耳蜗圆窗病变对中耳结构力学行为的影响。方法依据临床健康志愿者右耳CT扫描结果,将CT扫描数据数值化导入PATRAN软件进行人耳三维有限元模型重建,并应用NASTRAN软件进行流固耦合频率响应分析,通过数值模拟方法探讨中耳结构动力响应对内耳耳蜗圆窗病变的反馈。结果硬化症导致的圆窗封闭比先天性圆窗封闭使镫骨振幅下降更多,最大达到30. 2 d B,且后者不会对镫骨振动速度产生明显影响。相位角方面,硬化症情况下镫骨和圆窗均最多产生90°变化,且两者保持180°差值;而先天性圆窗封闭情况下镫骨最大有270°变化,同时圆窗相位角变化消失。结论基于振幅、速度和相位角,镫骨动力行为会对先天性和硬化症导致的圆窗封闭形成不同的反馈表现,研究结果可为未来临床上诊断及修复圆窗病变提供理论支撑。  相似文献   

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目的探讨常压和高压环境下噪声对耳蜗的影响,用数值模拟方法弥补试验手段不足导致的噪声对耳蜗听力行为特征研究的缺失。方法基于健康人耳蜗CT扫描图像,结合自编程序,利用PATRAN软件建立三维螺旋耳蜗有限元模型。应用NASTRAN软件进行流固耦合频率响应分析和瞬态响应分析,通过数值模拟方法模拟常压和高压环境中噪声对耳蜗的影响。结果模型计算结果与文献中已报道的试验结果相吻合,验证了模型的正确性。当频率小于5 kHz时,常压和高压环境中噪声激励下基底膜位移基本一致;当频率大于5 kHz时,常压环境中噪声激励下基底膜位移逐渐减小,而高压环境中噪声激励下基底膜位移却持续增加。结论高压环境中噪声对基底膜高频影响更加明显。数值模拟结果弥补了试验手段不足导致的噪声对人耳蜗听力行为特征研究的缺失,为今后对耳蜗进行针对性试验研究提供了新的思路和理论支撑。  相似文献   

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目的研究中耳畸形对圆窗激振性能的影响,为圆窗激振式人工中耳的优化提供理论支持。方法构建包含两腔不对称的非螺旋耳蜗的人耳有限元模型,并与实验数据进行对比,验证模型的可靠性。基于该模型,通过改变相应组织的材料属性,分别模拟听骨链固定、听骨链融合、听小骨缺损3种中耳畸形对圆窗激振性能的影响。结果中耳畸形主要影响圆窗激振式人工中耳的低频性能,听骨链固定和听骨链融合对圆窗激振起恶化效果。镫骨固定对圆窗激振补偿性能的影响最大,恶化量高达47.93 dB;听小骨缺损可提高圆窗激振的性能,最大改善量为6.24 dB。结论中耳畸形对圆窗激振的低频性能有影响,临床植入圆窗激振式人工中耳时需要针对性地提高其作动器的输出量。  相似文献   

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目的研究高压对中耳结构造成的损伤。方法基于CT扫描建立中耳结构有限元数值模型,对模型施加随时间变化的压力,分析鼓膜以及镫骨足板的应力、应变和位移变化。结果获得的计算结果与相关文献中的试验数据吻合,验证了所建中耳模型的准确性。高压会对中耳造成损伤,随着压力的增加,损伤加重;快速加压使得中耳损伤严重,对内耳的影响较小;慢速加压也能导致中耳损伤,但在中耳损伤前,内耳会损伤。结论高压容易导致人耳出现损伤,为避免听力受到影响,在加压过程中要控制好加压速率。  相似文献   

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目的研究典型中耳病变对圆窗激振听力补偿效果的影响,为圆窗激振式人工中耳的优化设计提供参考。方法利用CT扫描和逆向成型技术建立包括中耳和耳蜗的有限元模型,并验证模型的可靠性。再基于该模型,通过改变相应组织的材料属性,分别模拟镫骨环韧带硬化、镫骨不正常发育和锤骨前韧带硬化3种典型中耳病变。通过对比相应的基底膜响应,分析这3种病变对圆窗激振听力补偿效果的影响。结果镫骨不正常发育主要在高频处降低圆窗激振的效果,镫骨环韧带硬化和锤骨前韧带硬化主要恶化圆窗激振低频段的响应。3种病变中,镫骨环韧带硬化对圆窗激振听力补偿效果影响较大,等效声压的减小量可高达17 d B。结论中耳病变恶化圆窗激振的听力补偿效果,且恶化量较大,故在设计圆窗激振式人工中耳时需要针对性地提高其作动器的输出量。  相似文献   

10.
王威  吴辉 《医学信息》2008,21(6):882-884
目的 检测基质金属蛋白酶-2(matrix metalloproteinase-2 mmp-2)在中耳胆脂瘤中的表达,探讨其与中耳胆脂瘤骨质破坏的关系.方法 用逆转录聚合酶链反应(ILT-PCR)技术检测胆脂瘤和外耳道皮肤中MMP-2的mRNA表达情况.结果 MMP-2 mRNA在胆脂瘤中阳性表达水平明显高于在外耳道中的表达水平(P<0.01).结论 MMP-2与胆脂瘤的骨质破坏密切相关;胆脂瘤基质细胞在胆脂瘤的破坏作用中可能起了重要的作用.  相似文献   

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A further analysis of already published data supports the position that retardates of low ability level less frequently have retarded siblings, retarded parents, and parents low in occupational level than do retardates higher in ability level. The analysis supports the position that there are two types of retarded individuals, persons retarded as a result of gene or chromosomal anomalies, brain injury, etc., who more frequently occur in the lower-level retardate group, and persons whose retardation represents polygenic segregation, who more frequently occur in the higher-level group.  相似文献   

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Modes of Inheritance of Errors of Refraction   总被引:5,自引:0,他引:5       下载免费PDF全文
Eighteen families in which both parents had refractions within the range of +4·0 D to −4·0 D and axial lengths seen in emmetropia (22·3-26·0 mm) showed coefficients of correlation of the order 0·5 indicative of polygenic inheritance. Such coefficients were seen for axial length (0·407) and for the cornea (0·487), but not for the lens (which is known to be yoked to the axial length). No such coefficients were seen in 19 families in which one of the parents had axial length outside the emmetropic range (nine families with long axes and 10 with short axes).

The pattern of polygenic inheritance for emmetropia (completely correlated optical components) and errors of refraction up to 4·0 D (inadequately correlated components: correlation ametropia) follows that seen in stature and other measurable characters. In contrast the high refractive errors with their abnormal axial lengths (component ametropia) are—like the extremes in stature—pathological anomalies with monofactorial inheritance.

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1. Recovery of responsiveness of single cells in lateral geniculate nucleus of rat has been determined in both P and I cells. There are three types of recovery curve among P cells; (a) early recovery, (b) early partial recovery followed by depression and then complete recovery, (c) prolonged depression followed by cyclic recovery. Type (c) is by far the commonest recovery curve. In contrast to the spike in a P cell, the synaptic potential recovers to its full amplitude in about 20 msec. All I cells exhibit similar rapid recovery curves after a prolonged depression.2. Conditioning stimuli applied to visual cortex also produce a prolonged depression in most P cells but I cells can be re-excited at short intervals from cortex. Decortication does not prevent the prolonged depression of the multineuronal response produced by optic nerve stimulation.3. A neuronal model is proposed to explain these observations. It is supposed that I cells (interneurones) are innervated by axon collaterals of the P cells (principal cells, projecting to visual cortex) and that the I cells exert an inhibitory influence on the P cells.  相似文献   

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It was established, in experiments on isolated spinal ganglia of adult rats in concluons of intracellular recording, that dopamine (1 M/liter) elicits depolarized responses in 61% of neurons, hyperpolarized in 20% of neurons, and depolarized-hyperpolarized in 19% of neurons. The depolarized responses are associated with the activation of D1 dopamine receptors, and are governed by the shift of cAMP-dependent cation (sodium) channels to the conducting state. The hyperpolarized responses are triggered by the activation of D2 dopamine receptors, which by means of HTP-binding protein convert the potassium channels to the conducting state. The change in the polarization of neurons with the action of dopamine influences their electrical excitability variously.Translated from Fiziologicheskii Zhurnal SSSR imeni I. M. Sechenova, Vol. 76, No. 6, pp. 739–745, June, 1990.  相似文献   

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