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目的:分析外伤性嗅觉障碍患者的临床特点及预后。方法:回顾性分析2015-01-2016-12首次诊断为外伤性嗅觉障碍并完成14~473d随访的202例患者(来自11个省、自治区及直辖市)的临床资料。按嗅觉障碍病因进行分组(外伤性嗅觉障碍患者65例,非外伤性嗅觉障碍患者137例),用统计学方法比较各组年龄(岁)、性别、嗅觉功能(SniffinSticks)、味觉功能(三滴法)、嗅觉诱发电位及嗅通路MRI特点。结果:外伤性嗅觉障碍组年龄(40±11岁)与非外伤性嗅觉障碍组年龄(47±15岁)相比,差异有统计学意义(P<0.05);在性别分布上差异无统计学意义(P>0.05)。在嗅觉功能上,外伤性嗅觉障碍组分值(TDI)为(12±5),非外伤性嗅觉障碍组为(19±8),差异有统计学意义(P<0.05)。在嗅觉诱发电位中经嗅觉特异刺激剂刺激引出P2波潜伏期在外伤性嗅觉障碍组(483±82ms)与非外伤性嗅觉障碍组(418±64ms)间差异有统计学意义(P<0.05)。但在味觉功能(三滴法)上,经嗅觉特异刺激剂刺激波的振幅、经三叉神经刺激波的振幅和潜伏期及嗅通路MRI均差异无统计学意义(P>0.05)。通过14~473d随访,65例外伤性嗅觉障碍患者中有9例失访,8.9%(5/56)的患者嗅觉功能有提升,5.4%(3/56)的患者味觉功能有提升,5.4%(3/56)的患者嗅味觉功能同时有提升。结论:头部外伤是导致嗅觉丧失的主要病因。在本临床观察中,外伤性嗅觉障碍患者表现更为年轻,可能与年轻患者在社会活动中更为活跃有关。且在嗅觉功能上多表现为嗅觉丧失。外伤性嗅觉障碍患者味觉功能相对于嗅觉功能更难恢复,推测味觉中枢在外伤中相对于嗅觉中枢更易受损。
Objective: To analyze the clinical characteristics and prognosis of traumatic olfactory dysfunction. Methods: The clinical data of 202 patients (from 11 provinces, autonomous regions and municipalities directly under the Central Government) who were initially diagnosed with traumatic olfactory disorder and were followed up from 14 to 473 days were retrospectively analyzed. According to the causes of olfactory dysfunction, 65 patients with traumatic olfactory dysfunction and 137 patients with non-traumatic olfactory dysfunction were divided into groups according to the age, sex, olfactory function (Sniffin ’Stuks), taste function Three drops), olfactory evoked potential and olfactory pathway MRI features. Results: There was significant difference between the age of traumatic olfactory dysfunction group (40 ± 11 years) and the age of non-traumatic olfactory disorder group (47 ± 15 years old) (P <0.05). There was no significant difference in gender distribution Significance (P> 0.05). Olfactory function, traumatic olfactory dysfunction component (TDI) was (12 ± 5), non-traumatic olfactory dysfunction group was (19 ± 8), the difference was statistically significant (P <0.05). The latent period of P2 wave induced by olfactory specific stimulant in olfactory evoked potentials was significantly different between the traumatic olfactory dysfunction group (483 ± 82ms) and the non-traumatic olfactory dysfunction group (418 ± 64ms) (P <0.05). However, there was no significant difference in the amplitudes of the wave stimulated by the olfactory specific stimulants, the amplitude and latency of the trigeminal nerve stimulation and the olfactory pathways in the taste function (three drops method) (P> 0.05). After 14 to 473 days of follow-up, 9 of 65 patients with traumatic olfactory dysfunction were lost to follow-up, while olfactory function was improved in 8.9% (5/56) of patients and 5.4% (3/56) (3/56) of patients with smell and taste function also improved. Conclusion: Head trauma is the main cause of loss of smell. In this clinical observation, patients with traumatic olfactory dysfunction are younger and may be more active in young people’s social activities. And in the sense of smell more performance for the loss of smell. Patients with traumatic olfactory dysfunction have a more impaired taste function than olfactory function, presumably the taste center is more susceptible to injury than the olfactory center in trauma.