xRead - Olfactory Disorders (September 2023)

20426984, 2022, 4, Downloaded from https://onlinelibrary.wiley.com/doi/10.1002/alr.22929, Wiley Online Library on [04/09/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License

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smoking to be associated with postoperative OD. 985,1010 In two studies, smokers with CRS had greater risk of OD, par ticularly those with eosinophilic CRS. 145,1013 When evaluating patients with PD, a case-control anal ysis found greater overall risk of OD in smokers compared with nonsmokers but lower relative risk in smokers with PD. In another study, first-degree nonsmoker relatives of patients with PD showed nonsignificant smoking-OD risk associations. 1011,1012 One observational study of patients seen in an ear, nose, and throat outpatient clinic reported that smokers had a higher risk of OD. 1015 Two studies found worse OF in smokers (versus non smokers): one reported temporal associations between smoking and reduced nasal pungency, whereas one found no difference in retronasal perception in smokers. One study reported that swallow-related muscle compensation was associated with worse OF in smokers,while another reported lower OBV in smokers. In addition, one study reported better OF with brief (16- to 20-hour) abstinence from smoking. 1016–1022 Chronic cigarette smoking increases the risk of OD. Former smokers may recover OF, although the length of smoking may influence recovery. Aggregate grade of evidence : B (Level 1: one study; Level 2: 21 studies; Level 3: one study; Level 4: 24 studies). P Idiopathic Idiopathic OD (IOD), by definition, is without an identi fied cause despite a comprehensive workup. Likewise, lit tle is known regarding the pathophysiology of IOD, despite this clinical entity accounting for up to one sixth of patients withOD. 916,1023,1024 It is possible that IOD may represent an early manifestation of neurodegenerative disease in a select group of patients. For instance, Haehner et al 1025 found that 10% of patients who were diagnosed with IOD ultimately developed PD after an 11-year interval. Thus, in some instances, the designation of IOD may be a misclas sification, and current estimations of IOD prevalence may be artificially inflated. In cases of true IOD, a small body of literature utilizing neurophysiologic and neuroimaging techniques has attempted to elucidate the pathophysiology with limited success. Perturbations in the CNS and olfactory pathways are potentially implicated in the pathogenesis of IOD. Sev eral studies have shown that olfactory performance corre lates with cortical volume of the OFC and insular cortex in healthy adults. 1026,1027 Moreover, these portions of the brain decline in volume in patients with diverse causes of OD. 1028 Yaoetal 1029 showed that in a population of patients with IOD, significant grey matter volume decline was seen in the POC and secondary olfactory areas (OFC, insu

lar cortex, anterior cingulate cortex, and parahippocam pal cortex). OBV changes are common in many causes of OD, including patients with IOD, and are thought to represent a declining population of olfactory neurons sec ondary to decreased olfactory signal transduction from the neuroepithelium. 1030–1032 Despite the concordance of these findings in patients with IOD, there are conflict ing reports that fail to demonstrate identifiable radiologic irregularities. 1024 Moreover, it is unknown whether struc tural changes in the brain are a consequence of the patho physiologic mechanism of IOD, or, rather, a secondary manifestation of diminished OF. Beyond radiologic findings, patients with IOD may have alteration in olfactory signal transduction. Liu et al 1032 compared the amplitude and latency of chemosensory ERPs in patients with IOD and normal healthy controls. In patients with IOD, a significant decrease in amplitude of ERPs likely represented either decreased populations of peripheral olfactory neurons or alterations in central olfac tory pathways. The current body of literature implicates CNS structural changes and electrophysiologic signal transduction damp ening in the pathophysiologic mechanism of disease. Sig nificant work remains to fully elucidate this disease pro cess, which may, in fact, reflect multiple underlying causes. A significant portion of patients with olfactory loss are placed into an idiopathic category, with likely multiple different causes leading to this diagnosis. More research is needed to better elucidate and therefore treat the underlying mechanisms. Aggregate grade of evidence : C (Level 4: six studies). EVALUATION AND DIAGNOSIS A History and physical examination History and physical examinations are essential parts of the evaluation of patients with OD. 14,23,69,135, 137,370,914,1033,1034 A thorough history provides a diagnosis of OD in most cases and a complete head and neck examination helps to confirm the diagnosis. Multiple retrospective case series and a prospective cohort study have used clinical history and physical examination to delineate potential causes among patients presenting with OD (Table VIII-1). 23,69,135,137,370,914,1033 There were no ran domized studies investigating the utility of history-taking or physical examination on the diagnosis of OD. Lack of higher-level evidence is expected given that history and physical examinations are essential to any medical diagnosis. Clinical assessment of patients with OD should include general clinical history and specific questions related to VIII