人Corti‘s器扫描电镜观察

目的 了解正常人Corti’s器的超微结构特征。方法 用扫描电镜观察成年人和胎儿的Corti’s器。结果成人和胎儿Corti’s器基底圈内、外毛细胞排列规则,中圈和顶圈毛细胞排列不规则,内毛细胞以一排,外毛细胞以三排排列。可观察到列外的内、外毛细胞,四排排列和自然缺失的外毛细胞。外毛细胞粗大的静纤毛以及由于固定不及时引起的外毛细胞静纤毛气球样改变。结论 用扫描电镜观察成人和胎儿Corti’s器的精细结构,发现了毛细胞排列的基本规律和一些异常的形态。及时固定是保存Corti’s器结构完好的必要条件。     

Functional organization of the forebrain auditory centres of the European starling: a study based on natural sounds

The field L complex is thought to be the highest auditory centre and the input in the song vocal nuclei. Different anatomical and functional subdivisions have been described in field L. Auditory neurons of field L are well activated by natural sounds and especially by species-specific sounds. A complex sound coding appears to exist in field L. However, until now, the spatial organization of the different functional subdivisions has been described only using artificial sounds. Here, we investigated the spatial distribution of neuronal responses in field L to species-specific songs. Starlings seemed to be a very appropriate species for this investigation, both because of their complex vocal behaviour that implies different levels of categorization and their neuronal responses towards complex song elements. Multi-unit recordings were performed in wild starlings that were awake. The method of backward correlation was used to visualize the functional organization and we represented the neuronal responses as both activity maps and correlation maps. The use of natural sounds allowed us to define several functional sub-areas with different neuronal processing. These results show that field L is involved in a more complex task than simple frequency processing.     

Histopathology of noise deafness

The psychophysical effects of sound stimulation at increasing intensity include adaptation, temporary threshold shift, and permanent hearing loss. The mechanisms involved in permanent loss are direct mechanical destruction, following high intensity noise exposure, and metabolic decompensation with subsequent degeneration of sensory elements, following moderate intensity noise exposure. Both these cause their own pattern of cochlear histological abnormality, while the only morphological correlate to temporary threshold shift is an increase in the number and size of liposomes, mainly in the outer hair cells after longer periods of repeated temporary threshold shift. There are critical intensity levels which determine the type and extent of damage, and for any given exposure intensity a saturation of damage is reached over time. There is great variability in acoustic cochlear damage, especially that of the delayed metabolic type, the type which results from conditions which predominate in our actual noise environment.     

Histopathology of the stapes in osteogenesis imperfecta

Conventional histological studies of stapes footplates from patients with osteogenesis imperfecta revealed, in nine out of 15 stapes examined, an otospongiotic-like lesion. Although the morphology of the stapedial lesion was comparable to the early otosclerotic focus, a greater structural disorganization and larger resorption spaces in osteogenesis imperfecta distinguished the two conditions. The histopathology of the stapes was related to the morphology of cortical and trabecular bone from the iliac crest. Various degrees of immature, osteogenic bony tissue were found in the iliac crest, showing no resemblance to the otospongiotic-like focus in the footplate. Even though the histologic appearance of the stapes footplates differed from the findings in peripheral bone, the present study indicates that the stapedial lesion in osteogenesis imperfecta is most likely a manifestation of the generalized bone and connective tissue disorder. The study further supports the view that osteogenesis imperfecta and otosclerosis are of different aetiology.     

Exostoses and Cavernous Venous Formation in the External Auditory Canal of the Hooded Seal as a Functional Physiological Organ

Exostoses of the external auditory canal (EAC) develop after protracted mechanical, chemical or thermal irritation in particular. This is a common disorder among aquatic sportsmen and has been considered unique to Man. We dissected and photodocumented the EACs of 5 newborn and 3 adult Hooded Seals (Cystophora cristata). Serial sections of the EACs were prepared for light microscopic evaluation after staining with haematoxylin-eosin or toluidine blue. All EACs exhibited a firm, broad-based, mountain peak-shaped exostosis on the floor of the meatus, lateral to the eardrum. In addition, the meatal skin of the bony EAC harboured large venous sinuses. The exostosis and venous sinuses of the seal EAC participate in the protection of the sensitive hearing apparatus, particularly the pars tensa portion of the drum, during diving.     

Histopathology of the temporal bones of deaf dogs

Histopathological studies were done in 22 deaf dogs consisting of 10 Dalmatians, 5 English setters, 2 Great Danes, 2 foxhounds, 1 shepherd, 1 bulldog and 1 Australian sheep dog. Hypoplasia or aplasia of the sensory cells of the organ of Corti, stria vascularis and macula sacculi (pars inferior) was noted in all deaf dogs examined, indicating the pathology of inner ear malformation in these dogs to be of Scheibe's type. A solidified and calcified tectorial membrane was noted in 19 out of the 22 deaf dogs. A calcified sclerosis of the tectorial membrane is thought to be a characteristic finding of genetically inherited anomaly of the inner ear in deaf dogs. Distortion of the tectorial membrane, absence of the sensory cells in the organ of Corti, agenesis of the stria vascularis and abnormalities of the saccule described Scheibe's dysgenesis of the pars inferior as the pathological correlate for deafness in these dogs as assessed functionally.     

鼠和人胎儿嗅粘膜与犁鼻器官的免疫组织化学观察

应用免疫组织化学方法观察了神经原特异性烯醇化酶（ＮＳＥ）、神经胶质特异性Ｓ－１００蛋白（Ｓ－１００）和细胞角质素（ＣＫ）三种抗体在豚鼠。大鼠和人胎儿嗅粘膜和犁鼻器官的正常分布情况。结果发现以上三种抗体联合应用可以显示除支持细胞和微绒毛细胞外所有的嗅粘膜结构，是研究正常嗅粘膜和嗅粘膜病理改变的良好方法。豚鼠、大鼠犁鼻器官内侧被覆ＮＳＥ阳性的嗅上皮，具有感觉功能。７个月人胎儿鼻中隔两侧的犁鼻器官对ＮＳＥ染色呈阴性反应，因此，新生儿和成年人的犁鼻器官不可能具有象低等动物那样的辅助嗅觉的功能。     

面神经管裂缺处面神经组织学观察

目的探讨先天性面神经管裂处神经外膜缺陷可能引起的病理学改变。方法采用光学显微镜对美国明尼苏达大学颞骨病理实验室１５２６具颞骨连续切片的面神经颞骨全程进行组织病理学观察。结果发现先天性面神经管裂者８８５耳，其中４８耳在管裂处神经外膜缺损，其中４０耳面神经从管裂处疝出，有１３耳在管裂处形成外生性面神经鞘瘤。３耳在管裂处面神经受炎性细胞浸润。而管裂处有神经外膜覆盖的８３７耳均未见此类病变。结论面神经管裂处神经外膜的缺损是此处面神经疝出、外生性神经鞘瘤形成和面神经易于受炎症浸润的组织解剖学原因。     

Histopathology of congenital subglottic stenosis

A precise delineation of each laryngeal abnormality is critical to planning rational therapy. Since congenital cricoid cartilage anomalies are easily overlooked, a systematic approach to their identification is as important as a clear concept of their classification. The purpose of this communication is to present the pathologic findings and classification of congenital cricoid cartilage deformities and to summarize updated information derived by the whole organ macrosection technique. The classification of congenital subglottic stenosis is based on study of the English-language literature and the collection in the Laryngeal Development Laboratory at The Children's Memorial Hospital in Chicago. Twenty-nine specimens with congenital cricoid abnormalities have been identified. Fourteen have an elliptical cricoid cartilage; 12, a laryngeal cleft; 5, a flattened shape: 1, a large anterior lamina; and 3, generalized thickening. Some specimens have more than 1 anomaly. Eight cases of fragmented or distorted cricoid cartilages are thought to be acquired lesions. An anterior submucous cricoid cleft has been identified and is presented for the first time.     

Histopathology of sudden hearing loss

Eleven temporal bones from eight patients who had clinical histories of sudden hearing loss (SHL) were studied to assess the possible etiopathogenesis. The origin of SHL in seven ears from five patients was obscure, but appeared to be due to multiple causes. Common histopathologic changes in the cochlea, although complex, included atrophy of the organ of Corti and loss of cochlear neurons. Loss of cochlear neurons was the main finding in ears of viral infection. Labyrinthine fibrosis and formation of new bone were seen in two ears associated with vascular insult and in two ears of autoimmune disease. Different histopathologic findings causing SHL were observed even in cases with the same etiology. A case of SHL showing endolymphatic hydrops as the main histopathologic finding is described.     

Histopathology of the olfactory pathway due to ischemia

Various agents, such as trauma, viral infections and neoplasms cause olfactory dysfunction. However, little is understood concerning the role of ischemia. An experimental model of brain ischemia was developed in the Mongolian gerbil, and the olfactory pathway was studied. This animal was chosen because of its incomplete circle of Willis, since poor patency of the circle of Willis is not an uncommon finding in the aging human. Ischemia was induced by unilateral ligation of one common carotid artery or temporary occlusion of both common carotid arteries. Under both circumstances, ischemic changes occurred in the lateral olfactory tract, the olfactory ventricle, and the olfactory tubercle. Damage is more severe with bilateral temporary occlusion than unilateral ligation. The olfactory bulbs and neuroepithelium, however, are resistant to ischemia.     

面神经管裂缺处面神经组织学观察

目的 探讨先天性面神经管裂处神经外膜缺陷可能引起的病理学改变。方法 采用光学显微镜对美国明尼苏达大学颞骨病理实验室１５２６具颞骨连续切片的面神经颞骨全程进行组织病理学观察。结果 发现先天性面神经管裂者８８５耳，其中４８耳在管裂处神经外膜缺损，其中４０耳面神经从管裂处疝出，有１３耳在管裂处形成外生性面神经鞘瘤。３耳在管裂处面神经受炎性细胞浸润。而管裂处有神经外膜覆盖的８３７耳均未见此类病变。结论 面     

Histopathology of the temporal bone after open mastoid surgery

Histopathology of the temporal bone after open mastoid surgery The ear that is deaf and continues to discharge after radical or modified radical mastoidectomy remains an unsolved problem for the otologist. The temporal bones of 17 patients in whom open mastoidectomy had been done during their life time were serially sectioned and examined. Histological changes secondary to surgery and chronic infection are described. The study fails to reveal a specific cause for unhealed areas in the mastoid bowl. It is suggested that the unhealed areas are caused by the unhealthy physical environment for the surface epithelium.