| Objective:Research on upper airway sensory nerve,motor nerve pathological role in the pathogenesis of OSAHS.Methods:The first part: the experimental group were 58 patients with OSAHS confirmed by PSG in changhai hospital from August 2016 to May 2017.Thirteen normal volunteers who were excluded from OSAHS by PSG were treated as the control group.,tactile sense is measured by Semmes-Weinstein Monofilaments on both sides of the hard palate and the middle of uvula in experimental group and control group.Then the uvula tactile threshold minus the hard palatal tactile threshold was used as standardized palatal sensory threshold(SPST),By comparing the differences among the hard palate,soft palate and SPST of two groups,and checking its correlation with the severity of OSAHS,making a judgment on whether OSAHS patients have a feeling dysfunction.In the second part,the experimental group were 31 patients diagnosed with OSAHS from June 2015 to June 2017,and the control group were 9 patients with tonsillar benign lesions excluded OSAHS by PSG..In the experimental group,the palatopharyngoplasty was performed,and the control group had bilateral tonsillectomy,and the soft palate was collected during the operation.The specimens were made into wax blocks,and the histopathological changes of the soft palate were analyzed by HE and Masson staining.Immunohistochemical staining was used to analyze the changes of myelin basic protein(MBP),neural cell adhesion molecule(NCAM)and Agrin in the soft palatal tissue,and to study the sensory and motor changes of the upper airway.Results:the first part: 1.there was no significant difference in lips tactile threshold between the two groups;2.OSAHS group was larger than the control group in the hard and soft palatal tactile threshold,with the aggravation of the disease,both of them gradually increase.3.In OSAHS group,the tactile threshold of soft palate was larger than that of hard patate;4.The SPST of OSAHS group was larger than that of the control group,with the aggravation of the disease,it gradually increases,and SPST was positively correlated with AHI and was negatively correlated with the lowest blood oxygen in sleep.The second part: 1.HE and Masson staining showed that OSAHS Patients had a disorganization of soft palate tissue,the soft palate mucosa epithelial keratinization,swelling,and thickening of the lamina propria,interstitial vasodilation and congestion,inflammatory cells infiltration in organization,variation in gland bubble sizes and fat vacuoles increase,fibrous tissue hyperplasia,muscle atrophy,hypertrophy,fracture,as the OSAHS condition worsens,The degree of pathological tissue injury is also increasing;2.Immunohistochemical staining shows that the average cumulative light density ofmyelin basic protein MBP located in mucous membrane is less than that in the control group,With the aggravation of OSAHS disease,MBP average cumulative light density of OSAHS patients becomes increasingly smaller;In the experimental group,the average cumulative light density of NCAM is greater than that of the control group,and the average cumulative light density of NCAM increases with the increase of OSAHS in the OSAHS group.The average cumulative light density of Agrin is greater in the OSAHS group than that of the control group.In the OSAHS group,with the aggravation of OSAHS,the average cumulative light density of Agrin increases.Conclusion:Patients with OSAHS have sensory and motor neuropathy in the upper airway,which is the key pathogenesis of OSAHS. |
