Generally, there were no significant differences in recurrence rates according to clinical stage or surgical approach. Given the rate of delayed recurrence, follow-up of >3 years is required. Moreover, surgeons should always consider combined approaches to reduce the chances of recurrence.

Even if multiplicity of obstruction pattern was most commonly associated with severe OSA, almost one third of mild OSA patients also showed multiple anatomic structures and levels of obstruction. Therefore, a precise evaluation for multiplicity of obstruction patterns should precede the decision of a treatment plan, regardless of disease severity.

Background Postviral olfactory loss after upper respiratory tract infection (URI) is not uncommon. However, its exact location and nature are not fully understood. Although it is likely to be caused by a direct damage of olfactory epithelium, a damage of the central pathway has also been suspected as its possible mechanism. This study will show basal metabolism in the brain of patients with postviral olfactory loss using fluorodeoxyglucose-positron emission tomography (FDG PET). Methods Nine patients with postviral olfactory dysfunction were enrolled. All of the patients had neither apparent sinusitis nor rhinitis. All of them recalled causative URI and temporal connection with development of their olfactory loss. After olfactory function tests using the butanol threshold test and smell identification test confirmed olfactory impairment, FDG PET studies were performed during a rest state. The cerebral metabolic abnormality was compared between the patients and age/gender-matched healthy controls using a voxel-wised analysis. Results In comparison with healthy controls, the patients showed a significant hypometabolism in the right piriform cortex and bilateral amygdala and parahippocampal areas where the olfactory neurons primarily project. Furthermore, hypometabolism was also shown in the bilateral insular cortices, medial and lateral temporal cortex where the olfactory information is integrated to produce the sensation. Increased metabolism was not found in any brain area. Conclusion This study showed that the postviral olfactory loss is likely to be associated with decreased metabolism in the specific brain regions where the olfactory information is received and integrated.

Our study showed that olfactory impairment was correlated with olfactory neuronal population in mice treated with 3-methylindole. The food-finding test would be a useful tool that could be easily performed without special training in the 3-methylindole-treated C57BL6 anosmic mouse model.

An animal model of OSA could be developed by paralyzing the genioglossus in rabbits. This model may contribute to identifying the pathogenesis of upper airway obstruction in OSA and to developing new diagnostic or treatment devices targeting specific obstruction sites.