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Background: Olfactory disorders affect approximately 3 to 22% of the general population and impact on human quality of life. These symptoms have gained more attention after the COVID-19 pandemic, as anosmia emerged as a common presentation. A large number of patients with smell dysfunction have exhibited limited response to clinical therapy. Therefore, we propose a transnasal endoscopic nerve transfer technique for stimulate the olfactory neuroepithelium as a potential treatment option for olfactory dysfunction. We aimed to demonstrate preliminary results of nerve transfer surgery for the treatment of olfactory disorders, as well as to present the surgical technique. Methods: Eight patients with olfactory disorders, unresponsive to usually recommended treatments, underwent nerve transfer surgery between March 2022 and March 2023. The Connecticut olfactory test was administered to all patients before and after the surgery and quality of life was evaluated using the Visual Analogue Scale. Results: The average age of the patients was 46.3 years, and the olfactory disturbance has duration of approximately 27.5 months. Objective improvement in quality of life and olfactory scores was observed in 62,5% of the patients who underwent the surgery. Conclusions: Transnasal endoscopic nerve transfer technique may be a promissing therapeutic method in cases of olfactory dysfunction. The follow-up of these patients over a longer period, as well as more patients undergoing nerve transfer will provide more conclusive statistical data. Level of evidence: Level V, Therapeutic study. [ABSTRACT FROM AUTHOR]

Introduction: Zinc deficiency may worsen the severity of olfactory dysfunction; however, the relationship between serum zinc levels and therapeutic effects on olfactory dysfunction remains uncertain. This study investigated the relationship between normalising serum zinc levels and the therapeutic effects on olfactory dysfunction. Methods: Forty-two patients diagnosed with post-infectious, post-traumatic, and idiopathic olfactory dysfunction, with serum zinc levels <70 μg/dL, were included in the study. All patients were treated with mecobalamin, tokishakuyakusan, and polaprezinc. The patients were divided into 2 groups: the zinc-normalised (≥70 μg/dL) and zinc-deficient (<70 μg/dL) groups, based on their post-treatment serum zinc levels. Olfactory test results were compared in each of the 2 groups. Results: The patients were treated for a median of 133 days. The zinc-normalised group had significantly better results in all olfactory tests (detection/recognition thresholds of the T&T olfactometer, odour identification test (Open Essence), Visual Analogue Scale for olfactory dysfunction, and self-administered odour questionnaire). In contrast, only the self-administered odour questionnaire showed a significant improvement in the zinc-deficient group, with no significant differences observed in the other olfactory tests. When comparing the changes in the olfactory test scores between the 2 groups, significant differences were observed in the detection/recognition thresholds of the T&T olfactometer test and Open Essence results. Conclusion: These findings suggest that patients with olfactory dysfunction may have difficulty improving their olfactory function if they also have zinc deficiency. Furthermore, normalisation of zinc deficiency may contribute to the improvement of olfactory dysfunction with general treatment. Plain Language Summary: This study examined how zinc levels relate to problems with smelling, which is called olfactory dysfunction. We studied 42 participants who had trouble smelling due to infections, injuries, or unknown reasons and who also had low zinc levels in their blood. After the participants consumed a zinc supplement to treat their low zinc levels, we placed the participants either in the group for those who had their zinc levels go back to normal or in the group for those who remained zinc deficient. We tested the participants' sense of smell in different ways, including using an olfactometer, a card with different scents, and questionnaires. The group with normal zinc levels did much better in all the smell tests; the zinc-deficient group only improved in 1 test, which was the questionnaire. These results suggest that if someone has trouble smelling and they also lack the appropriate level of zinc, it might be difficult for them to get better. However, if they can improve their zinc level and bring it to a normal level, their sense of smell could improve. In summary, this study demonstrated a connection between zinc levels and smelling ability, indicating that repairing zinc deficiency may aid in treating olfactory dysfunction. [ABSTRACT FROM AUTHOR]

Background: A subset of patients diagnosed with COVID-19 is encountering persistent post-COVID symptoms. These symptoms can significantly impede their quality of life and exert profound effects on their day-to-day functioning. Purpose: This study aimed to identify the dimensions of quality of life most affected in patients with long COVID symptoms. Methods: A cross-sectional survey was applied using the SF-36 questionnaire which was distributed on Twitter and Instagram. Furthermore, a total of 122 respondents were obtained through accidental sampling. The association between variables was analyzed using Chi-square and Mann-Whitney tests. Results: Respondents who completed the questionnaire (n=122) came from different regions, with West Java as the largest area of origin (37.70%). In addition, the majority were female (n=103, 84.4%) under 25 years old (n=92, 75.41%), and the three symptoms experienced were fatigue (n=108; 35.29%), brain fog (n=61;19.93%), and olfactory disturbances (n=54; 17.65%). There was an association between long COVID duration and gender (p= 0.03). However, there was no association between other demographic characteristics with long COVID duration (p > 0.05). General health (41.67 (IQR=29), p= 0.00) and vitality (40.00 (IQR=20), p= 0.02) were the two aspects of quality of life significantly altered in patients with long COVID symptoms more than 3 months. Conclusion: The aspects of quality of life, particularly general health and vitality, experienced a significant decline in post-COVID-19 patients with long COVID symptoms for more than 3 months. [ABSTRACT FROM AUTHOR]

Purpose: Although the association between zinc deficiency and olfactory dysfunction is inconclusive, zinc deficiency causes apoptosis of the olfactory ensheathing cells which is involved in olfactory nerve turnover and axon regeneration, thereby suggesting a possible relationship. We investigated the relationship between serum zinc levels and olfactory function in patients with olfactory dysfunction. Methods: Ninety patients who had been diagnosed with post-infectious, posttraumatic, drug-induced, neurological and idiopathic olfactory dysfunction were included. Patients were divided into zinc normal group and zinc deficiency groups according to three reference values for serum zinc levels (60, 65, 70 µg/dL). The results of olfactory tests and patient backgrounds were used to compare the differences between the two groups. Results: There were significantly worse detection and recognition thresholds in the T&T olfactometer and Open Essence (odor identification test) results in the zinc deficiency group (< 60 µg/dL). In addition, significant correlations between olfactory tests (detection/recognition thresholds in the T&T olfactometer and Open Essence results) and serum zinc levels < 65 µg/dL were observed. The zinc deficiency group < 70 µg/dL with idiopathic olfactory dysfunction had significantly worse olfactory tests (detection/recognition thresholds in the T&T olfactometer and Open Essence). In addition, there was a significant correlation between the detection/recognition thresholds in the T&T olfactometer and serum zinc levels in idiopathic olfactory dysfunction. Conclusions: Our findings suggest that zinc deficiency may exacerbate the severity of olfactory dysfunction. Furthermore, idiopathic olfactory dysfunction may be partly caused by zinc deficiency. [ABSTRACT FROM AUTHOR]

Introduction: Olfactory changes are quite common in the population, causing a significant impact on the quality of life. Documentation of the olfactory function is essential for the diagnosis, treatment and follow-up of patients with inflammatory diseases of the upper airways, neurodegenerative diseases or viral infections. Among the different existing smell tests, the CCCRC is an inexpensive test, easy to apply, but it has not yet been evaluated on a large scale in the Brazilian population. Objective: To validate the CCCRC smell test, after adaptation for the Brazilian population, evaluating the performance of healthy volunteers and the stability of the test in retests. Methods: In this study, we carried out a cultural adaptation of the CCCRC test to Brazil. To validate and determine the normality scores, we applied the test to 334 healthy volunteers, aged >18 years of age. The retest was also carried out in up to four weeks on 34 additional volunteers to assess validity of the results. Results: When evaluating the participants’ performance, normosmia and mild hyposmia values were obtained in more than 95% of them. Women (58.4%) showed better accuracy than men (41.6%): p

Objectives: We sought to determine whether SARS-CoV-2 infections are associated with anosmia and if this virus infects other neuronal cells. We utilized male and female olfactory neuronal cell lines and other olfactory cell lines to determine the viral targets. Methods: We used four undifferentiated and two partially differentiated human developing neuronal cell lines. Infectivity was confirmed by reverse transcription quantitative realtime polymerase chain reaction (RT-qPCR), immunofluorescence assay (IFA) probing with anti-SARS-CoV-2 antibody, evaluation of cytopathic effects, and neurite formation. We induced partial differentiation of all cell lines (since both olfactory cell lines were terminally differentiated) with retinoic acid (RA) to determine whether differentiation was a factor in viral permissiveness. The expression of serine protease, transmembrane serine protease 2 (TMPRSS2), and angiotensin-converting enzyme II (ACE2) receptors were examined by RT-qPCR and IFA to determine the mechanism of viral entry. Results: Four to five days after exposure, both olfactory cell lines exhibited morphological evidence of infection; IFA analyses indicated that ~30% of the neurons were SARS-CoV-2 positive. At two weeks, 70-80% were positive for SARS-CoV-2 antigens. The partially differentiated (CRL-2266 and CRL-2267) and undifferentiated cell lines (CRL-2142, CRL-2149, CRL-127, and CDL-2271) were essentially non-permissive. After RA treatment, only CRL-127 exhibited slight permissiveness (RT-qPCR). The TMPRSS2 receptor showed high expression in olfactory neurons, but low expression in RA treated CRL-127. ACE2 exhibited high expression in olfactory neurons, whereas other cell lines showed low expression, including RA-treated cell lines. ACE2 expression slightly increased in CRL-127 post RA-treatment. Conclusions: Our studies confirm neurotropism of SARS-CoV-2 to olfactory neurons with viral entry likely mediated by TMPRSS2/ACE2. Other neuronal cell lines were non-permissive. Our results established that the nerve cells were infected regardless of male or female origin and strengthened the reported association of COVID-19 with loss of smell in infected individuals. [ABSTRACT FROM AUTHOR]

The article discusses about post-infectious olfactory dysfunction. Topics of discussion includes it is caused by damage to the olfactory epithelium and/or central olfactory processing pathways and was being observed in individuals infected with SARS-CoV-2. It further discusses about how olfactory training can help in PIOD and Aromatherapy can contribute to the development of therapeutic strategies.

Background Evidence suggests that olfactory impairment (OI) may be a degenerative neurologic complication of diabetes; however, the association is not yet well established. The objective of this work was to systematically review existing literature on the association between diabetes and OI in adults, with meta‐analysis of evaluable studies. Methods A literature search encompassing 358 abstracts from the last 75 years in PubMed, EMBASE, and Cochrane was performed. English‐language articles investigating adults with diabetes and OI in comparison to control groups with original data and ≥7 subjects were included. The Newcastle‐Ottawa scale was applied for quality assessment. Two investigators independently reviewed all articles. For meta‐analysis, the odds ratio of OI in diabetes compared with control groups was calculated using the fixed effects model. Results The initial search yielded 358 abstracts, from which 21 articles were reviewed and 11 articles (n = 6,747) were included. Studies included were case‐control (64%) or cross‐sectional (36%) with evidence level 3b. On the Newcastle‐Ottawa scale, the mean quality assessment score for case‐control and cross‐sectional studies was 7.4 (maximum of 9) and 7.0 (maximum of 10), respectively. A statistically significant association between diabetes and olfaction compared with controls was found in 6 (55%) of the 11 articles. Four studies were eligible for meta‐analysis, which yielded an overall odds of having OI with diabetes as 1.58 times more likely than in control groups (95% CI [1.16, 2.16]; I2 = 10.3%). Conclusions The reviewed studies support a significant association between diabetes and OI. Further studies are warranted to characterize this association. Level of Evidence 3a

The article offers information on olfactory dysfunction (OD), including hyposmia and anosmia, as frequent in patients infected with severe acute respiratory syndrome coronavirus 2. It mentions that plasmatic concentrations of systemic inflammatory biomarkers such as CRP (C-reactive protein), fibrinogen, or LDH (lactate dehydrogenase) gradually increased over the first ten days after the onset of symptoms.

Objective: Recent scientific literature has widely described a possible major role of smell dysfunction as a specific symptom of coronavirus disease 2019. This systematic review may provide a more holistic approach to current knowledge of the disease. Methods: A systematic review was completed using Embase, PubMed and Web of Science databases that considered original articles focused on olfactory evaluation in coronavirus disease 2019 patients, published between March and May 2020, in English language. Results: From the 483 research papers initially identified, 32 original studies were selected, comprising a total of 17 306 subjects with a laboratory confirmed diagnosis of coronavirus disease 2019. Individual study sample sizes ranged from 6 to 6452 patients. This comprehensive analysis confirmed that olfactory disorders represent an important clinical feature in coronavirus disease 2019, with a prevalence of 11–100 per cent in included patients, although there was heterogeneity in terms of assessment tools and population selection criteria. Conclusion: The results indicate that an accurate clinical evaluation should be carried out using structured questionnaires and tests with olfactory substances. [ABSTRACT FROM AUTHOR]

Background: Evidence suggests that olfactory impairment (OI) may be a degenerative neurologic complication of diabetes; however, the association is not yet well established. The objective of this work was to systematically review existing literature on the association between diabetes and OI in adults, with meta‐analysis of evaluable studies. Methods: A literature search encompassing 358 abstracts from the last 75 years in PubMed, EMBASE, and Cochrane was performed. English‐language articles investigating adults with diabetes and OI in comparison to control groups with original data and ≥7 subjects were included. The Newcastle‐Ottawa scale was applied for quality assessment. Two investigators independently reviewed all articles. For meta‐analysis, the odds ratio of OI in diabetes compared with control groups was calculated using the fixed effects model. Results: The initial search yielded 358 abstracts, from which 21 articles were reviewed and 11 articles (n = 6,747) were included. Studies included were case‐control (64%) or cross‐sectional (36%) with evidence level 3b. On the Newcastle‐Ottawa scale, the mean quality assessment score for case‐control and cross‐sectional studies was 7.4 (maximum of 9) and 7.0 (maximum of 10), respectively. A statistically significant association between diabetes and olfaction compared with controls was found in 6 (55%) of the 11 articles. Four studies were eligible for meta‐analysis, which yielded an overall odds of having OI with diabetes as 1.58 times more likely than in control groups (95% CI [1.16, 2.16]; I2 = 10.3%). Conclusions: The reviewed studies support a significant association between diabetes and OI. Further studies are warranted to characterize this association. Level of Evidence: 3a [ABSTRACT FROM AUTHOR]

Olfactory dysfunction and tinnitus are age-related otorhinolaryngological disorders with a high prevalence in the elderly population and share several common clinical features. However, there is no study investigating the relationship between these two diseases. We studied the prevalence of olfactory dysfunction and tinnitus among Koreans and studied the relationship between these two diseases based on the Korean National Health and Nutrition Examination Survey. The subjects of this study were enrolled from the Fifth Korean National Health and Nutrition Examination Survey (2010–2012, n = 25,534). Data of subjects aged 40 years and older who underwent physical examination and completed a self-reported questionnaire and other anthropometric variables were statistically analyzed. Odds ratios were calculated to identify the relationship between olfactory dysfunction and tinnitus, using multiple logistic regression models. Older males, non-smokers, non/lower alcohol drinker groups exhibited the relationship between olfactory dysfunction and tinnitus. Metabolic syndrome and mental health problems were associated with both olfactory dysfunction and tinnitus. After adjusting for confounding factors, olfactory dysfunction was significantly associated with tinnitus (OR 1.318). There was a dose-response relationship between tinnitus severity and the odds of olfactory dysfunction (ORs for mild, moderate and severe tinnitus were, respectively, 1.134, 1.569 and 2.044). Additional molecular genetics and animal studies are needed to determine the shared pathophysiology of the two diseases. [ABSTRACT FROM AUTHOR]

Abstract MnFe 2 O 4 nanoparticles (NPs) are commonly produced in some occupational settings and may reach high concentration in activities such as arc-welding or ferroalloy metallurgy. Manganese is an essential cofactor in enzyme activities but it has been demonstrated that long-term exposure to excessive levels can lead to “manganism”, a neurodegenerative disease resembling Parkinson features. Inhaled NPs deposit partially in pharynx and nasopharynx and may reach the central nervous system through the olfactory nerve, which is completely enveloped by the meningeal membranes throughout its course from the nasal cavity to the olfactory bulb or through the trigeminal nerves. This study investigated in vitro the transmeningeal absorption of 50 nm MnFe 2 O 4 NPs, using excised porcine meninges mounted on Franz diffusion cells. We tested two donor solutions: the first containing MnFe 2 O 4 NPs (2.0 g/L) and the second obtained by the ultrafiltration of the first one, in order to test only the NPs water soluble fraction. Each experiment was carried separately for 4 h. Results showed that no Mn flux permeation through the meninges occurred, since only trace of the metal was found in receivers solutions of cells exposed to MnFeNPs (5.5 ± 2.2 ng/cm2), ultrafiltered solution (3.5 ± 1.5 ng/cm2) and blank cells. (2.1 ± 0.6 ng/cm2) (mean and SE). Differences did not reach the statistical significance. Our study shows – for the first time - that MnFe 2 O 4 NPs penetrate the meningeal membrane in a negligible amount, thus making unlikely the hypothesis of a transcellular and paracellular absorption through the olfactory nerve but not excluding the hypothesis of an active intraneuronal absorption. Highlights • MnNPs are inhaled during arch welding processes, their potential intranasal absorption is poorly known. • Mn in the basal ganglia of CNS could lead to neurological Parkinson-like syndrome. • Our study investigated MnFe2O4NPs permeation through the meninges, which are involved in this absorption route. • Results showed that a negligible amount of the metal pass through this membrane. [ABSTRACT FROM AUTHOR]

Olfactory impairment is the most common clinical manifestation among the elderly, and its prevalence increases sharply with age. Notably, growing evidence has shown that olfactory dysfunction is the first sign of neurodegeneration, indicating the importance of olfactory assessment as an early marker in the diagnosis of neurological disorders. In this review, we describe the nature of olfactory dysfunction and the advantage of using animal models in olfaction study, and we include a brief introduction to olfactory behavior tests widely used in this field. The contribution of microglia in the neurodegenerative processes including olfactory impairment is then discussed to provide a comprehensive description of the physiopathological role of interactions between neurons and microglia within the olfactory system. [ABSTRACT FROM AUTHOR]

Introduction Little is known about the etiology of olfactory dysfunction in the pediatric population. The aim of this study is to characterize the etiology and clinical features of anosmia and to explore evaluation options in a pediatric population. Methods Olfactory dysfunction was identified at a tertiary pediatric hospital between January 2003 and October 2014 using a text-based and ICD-9 search of the electronic health record system. Clinical information gathered included history, physical examination and imaging study. A phone questionnaire was completed to determine persistence and development of other rhinologic, endocrine, or neurologic symptoms. Results 37 children (male/female = 17/20) with mean/median ages of 13.28/14. 19 years were identified. The distribution of etiology was: rhinologic disease (N = 16), congenital (N = 4), trauma (N = 1), neoplasm (N = 1) and unknown (N = 15). Rhinologic disease included chronic rhinosinusitis (N = 3) and other nasal anatomic lesions. None of the four subjects with congenital anosmia had classic Kallmann syndrome. The utility of imaging in confirming an etiology of anosmia was noted in 1 of 8 CT and 5 of 22 MRI. The most significant finding of the questionnaire was confirmation of normal puberty in the congenital group. Conclusion Similar to the adult population, rhinologic disease is the most common cause. Absence or hypoplasia of the olfactory bulbs without associated delayed puberty is the presentation of congenital anosmia in our cohort. MRI had a higher utility than CT in evaluating anosmia in general and congenital anosmia in specific. MRI to evaluate children with a history of congenital olfactory dysfunction is recommended. [ABSTRACT FROM AUTHOR]

Background: In this work we assess the association between olfactory dysfunction and cognition in a nationally representative sample of older adults in the United States. Methods: Participants aged ≥60 years (n = 1236) from the 2013–2014 National Health and Nutritional Examination Survey underwent both olfactory and cognitive testing. Olfaction was assessed by both objective test (8‐odor Pocket Smell Test: smell impairment defined as score ≤2) and self‐report. Cognitive assessment consisted of the Digit Symbol Substitution Test (DSST), the Animal Fluency Test, and the Consortium to Establish a Registry for Alzheimer's Disease (CERAD). Regression models were used to examine the association between olfaction and cognition while adjusting for demographics, cardiovascular factors, and associated medical history. Results: The prevalence of smell impairment in US older adults was 18.0% (95% confidence interval [CI], 14.0‐22.0%) and 22.0% (95% CI, 18.5‐25.6%) based on objective smell test and self‐report, respectively. In a multivariate model adjusted for relevant factors, low smell test scores were consistently associated with low scores on cognitive assessments, with a DSST score difference of −1.5 (95% CI, −2.2 to −0.8), Animal Fluency Test score difference of −0.4 (95% CI, −0.7 to −0.1), and CERAD Word List score difference of −0.4 (95% CI, −0.6 to −0.2) per 1‐point decrease in smell test score. There was no association between self‐reported smell impairment and cognition. Conclusion: Objectively measured olfactory dysfunction is independently associated with cognitive impairment. These findings are consistent with previous studies and suggest the utility of objective olfactory tests as an indicator for cognitive impairment as compared with self‐reported olfactory dysfunction, which is an uncertain indicator. [ABSTRACT FROM AUTHOR]

Background: The clinical features of postoperative delirium are similar to the core features of alpha synuclein-related cognitive disorders, such as Parkinson’s disease dementia (PDD) or dementia with Lewy bodies (DLB). Therefore, we hypothesized that the non-motor symptoms (NMSs) in Parkinson’s disease (PD), which precede the cardinal motor features of PD, are likely to be risk factors for developing postoperative delirium. We investigated the association between PD-related NMSs and postoperative delirium in old people undergoing elective spinal surgery. Methods: This study was a prospective study. Participants were aged 65 years and older and scheduled to undergo elective spinal surgery. During the enrollment period, 338 individuals were screened, 104 participants were included in the analysis. We assessed eight easily-assessed and representative PD-related NMSs 1 day before the scheduled surgery using tests or questionnaires for each symptom. The presence of delirium was determined by using the short version of the Confusion Assessment Method (CAM). Results: Fifteen (14.4%) of the 104 participants (age, 71.7 ± 4.7 years; men, 34.6%) met the CAM criteria for post-operative delirium. Multivariate logistic analysis showed that decreased olfactory function (odds ratio [OR] 0.63, 95% CI 0.44–0.91) and exhibiting rapid eye movement sleep behavior disorder (RBD, OR 1.45, 95% CI 1.09–1.93) were significantly independent predictors of postoperative delirium. Conclusions: Our study shows that hyposmia and RBD are significantly independent risk factors for postoperative delirium in general elderly population. Considering that NMSs may represent burden of alpha synuclein deposit, we postulate that an underlying alpha synucleinopathy may correlates with postoperative delirium. Significance: This study gives a novel insight for the risk factor of postoperative delirium. [ABSTRACT FROM AUTHOR]

Recent data suggest that olfactory deficits could represent an early marker and a pathogenic mechanism at the basis of cognitive decline in type 2 diabetes (T2D). However, research is needed to further characterize olfactory deficits in diabetes, their relation to cognitive decline and underlying mechanisms. The aim of this study was to determine whether T2D impairs odour detection, olfactory memory as well as neuroplasticity in two major brain areas responsible for olfaction and odour coding: the main olfactory bulb (MOB) and the piriform cortex (PC), respectively. Dipeptidyl peptidase-4 inhibitors (DPP-4i) are clinically used T2D drugs exerting also beneficial effects in the brain. Therefore, we aimed to determine whether DPP-4i could reverse the potentially detrimental effects of T2D on the olfactory system. Non-diabetic Wistar and T2D Goto-Kakizaki rats, untreated or treated for 16 weeks with the DPP-4i linagliptin, were employed. Odour detection and olfactory memory were assessed by using the block, the habituation-dishabituation and the buried pellet tests. We assessed neuroplasticity in the MOB by quantifying adult neurogenesis and GABAergic inhibitory interneurons positive for calbindin, parvalbumin and carletinin. In the PC, neuroplasticity was assessed by quantifying the same populations of interneurons and a newly identified form of olfactory neuroplasticity mediated by post-mitotic doublecortin (DCX) + immature neurons. We show that T2D dramatically reduced odour detection and olfactory memory. Moreover, T2D decreased neurogenesis in the MOB, impaired the differentiation of DCX+ immature neurons in the PC and altered GABAergic interneurons protein expression in both olfactory areas. DPP-4i did not improve odour detection and olfactory memory. However, it normalized T2D-induced effects on neuroplasticity. The results provide new knowledge on the detrimental effects of T2D on the olfactory system. This knowledge could constitute essentials for understanding the interplay between T2D and cognitive decline and for designing effective preventive therapies. [ABSTRACT FROM AUTHOR]

Introduction: The primary aim of the current study was to examine the usefulness of our proposed olfactory scoring system in chronic rhinosinusitis (CRS) patients with olfactory disorders (n = 213) receiving endoscopic sinus surgery (ESS).Materials and methods: Analyzed patients were divided into two groups: an eosinophilic CRS (ECRS) group (n = 153); and a non-ECRS group (n = 60). The T&T recognition threshold test was used to evaluate olfaction at baseline and at 3 and 12 months after ESS. Patients with mean recognition threshold < 2.0 at 3 or 12 months or with a decrease of ≥ 1.0 as compared with baseline were defined as showing clinical improvement. We scored mucosal conditions as normal (0 points), edema (1 point), and polyp (2 points) at the canopy of olfactory cleft (OC), middle and superior turbinates, superior nasal meatus, and sphenoethmoidal recess during ESS. The total score of OCs (SOCs) was calculated (range 0–20 points). We compared SOCs between ECRS and non-ECRS groups. Factors related to olfactory improvement were also investigated using uni- and multivariate analyses.Results: SOCs in the ECRS and non-ECRS groups showed significant correlations with mean recognition thresholds at baseline and at 3 and 12 months. In the multivariate analysis for predicting improvement of mean recognition threshold, lower SOCs were significantly associated with olfactory improvement factors at 3 and 12 months postoperatively in the ECRS group.Conclusion: SOCs appears promising for estimating olfactory prognosis after ESS in CRS patients. [ABSTRACT FROM AUTHOR]

Background/objectives: Loss of olfactory function is largely found with aging. Such a reduction in olfactory function affects quality of life and enhances likelihood of depressive symptoms. Furthermore, it has been shown that reduction in olfactory function is associated with cognitive impairment and several diseases such as major depression. Because several studies suggest that discontinuous exposure to odors may improve general olfactory function, the primary aim of this study was to investigate whether such "olfactory training" has positive effects on subjective well-being and cognitive function.Design: We performed a controlled, unblinded, longitudinal study SETTING: The study took place at an outpatients' clinic of a Department of Otorhinolaryngology at a Medical University.Participants: A total of 91 participants (age 50 to 84 years) completed testing. They were randomly assigned to an olfactory training (OT) group (N = 60) and a control group (N = 31). The study included two appointments at the Smell and Taste Clinic.Measurements: Olfactory and cognitive function as well as subjective well-being was tested using standardized tests.Intervention: During the 5-month interval between sessions, the OT group completed daily olfactory exposure. During the same time, the control group completed daily Sudoku problems.Results: Analyses show a significant improvement of olfactory function for participants in the OT group and improved verbal function and subjective well-being. In addition, results indicated a decrease of depressive symptoms.Conclusion: Based on the present results, OT may constitute an inexpensive, simple way to improve quality of life in older people. Copyright © 2017 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Head trauma is considered to be the third cause of olfactory function disorders. Olfactometric assessment in patients accusing anosmia following head injury produced by car accident or aggression is important, because most of them are involved in law trials in order to obtain financial compensations from the author. It is compulsory to use both subjective and objective olfactory evaluation methods combined with a detailed anamnesis, a complete ENT examination and a good cranio-facial imaging (computed tomography or MRI) in order to exclude malingerers and to obtain an accurate diagnosis. "Sfanta Maria" ENT Department from Bucharest is the only center in Romania where the olfactory function in completely investigated. We use chemosensory (Snap and Sniff Test and n-Butanol Dynamic Olfactometry) and electrophysiological tests (electric olfactory evoked potentials of the olfactory bulb). Unfortunately, we confront with a series of difficulties in what concerns the smell function evaluation: 1) there is scarce information in the literature regarding the olfactory electric evoked potentials; 2) the electric olfactory evoked potentials register only the electrical activity in the olfactory bulb; 3) in case of olfactory impairment medically confirmed, we cannot establish a cause-effect relationship between the disturbance and the event; 4) the most accurate electrophysiological assessment method currently available in Europe is the time-frequency analysis of chemosensory event-related potentials, but we do not dispose of the necessary equipment yet; 5) sometimes patients do not give us the informed consent for a complete olfactory evaluation. [ABSTRACT FROM AUTHOR]

Determining how synaptic coupling within and between regions is modulated during sensory processing is an important topic in neuroscience. Electrophysiological recordings provide detailed information about neural spiking but have traditionally been confined to a particular region or layer of cortex. Here we develop new theoretical methods to study interactions between and within two brain regions, based on experimental measurements of spiking activity simultaneously recorded from the two regions. By systematically comparing experimentally- obtained spiking statistics to (efficiently computed) model spike rate statistics, we identify regions in model parameter space that are consistent with the experimental data. We apply our new technique to dual micro-electrode array in vivo recordings from two distinct regions: olfactory bulb (OB) and anterior piriform cortex (PC). Our analysis predicts that: i) inhibition within the afferent region (OB) has to be weaker than the inhibition within PC, ii) excitation from PC to OB is generally stronger than excitation from OB to PC, iii) excitation from PC to OB and inhibition within PC have to both be relatively strong compared to presynaptic inputs from OB. These predictions are validated in a spiking neural network model of the OB±PC pathway that satisfies the many constraints from our experimental data. We find when the derived relationships are violated, the spiking statistics no longer satisfy the constraints from the data. In principle this modeling framework can be adapted to other systems and be used to investigate relationships between other neural attributes besides network connection strengths. Thus, this work can serve as a guide to further investigations into the relationships of various neural attributes within and across different regions during sensory processing. recorded spiking activity from multiple regions simultaneously is feasible. However, other important quantities- such as inter-region connection strengths-cannot yet be measured. Here, we develop new theoretical tools to leverage data obtained by recording from two different brain regions simultaneously. We address the following questions: what are the crucial neural network attributes that enable sensory processing across different regions, and how are these attributes related to one another? With a novel theoretical framework to efficiently calculate spiking statistics, we can characterize a high dimensional parameter space that satisfies data constraints. We apply our results to the olfactory system to make specific predictions about effective network connectivity. Our framework relies on incorporating relatively easy-to-measure quantities to predict hard-to-measure interactions across multiple brain regions. Because this work is adaptable to other systems, we anticipate it will be a valuable tool for analysis of other larger scale brain recordings. [ABSTRACT FROM AUTHOR]

Olfactory impairment in older adults is associated with cognitive decline. This study describes the development of a Brief Odor Detection Test (B-ODT), and its pilot administration in community-dwelling older adults. The study aimed at examining whether the test could differentiate older adults with very mild cognitive impairment from their cognitively healthy counterparts. The sample consisted of 34 older adults (22 women), aged from 65 to 87 years. Participants were divided into two groups according to their general cognitive functioning. Odor detection was measured via vanillin solutions at the following concentrations: 150 mg/L, 30 mg/L, 15 mg/L, 3 mg/L, and .03 mg/L. The first condition of the test involved a scale administration of vanillin solutions. The second condition examined the change in air odour and it required vanillin solution of 30 mg/L and a metric ruler of 30 cm. The examiner had to place the solution at a specific distance point from each nostril. Odour identification sensitivity was secondarily measured. The results showed statistically significant differences in odour detection threshold between the two groups. In the unirhinal testing, left nostril differences of the two groups were definite. Hence, the B-ODT seems a promising instrument for very early cognitive impairment screening in older adult population. [ABSTRACT FROM AUTHOR]

Background:Olfactory neuroblastoma is a rare sinonasal malignancy, with poorly defined treatment protocols. Management at a tertiary centre was retrospectively evaluated to inform future treatment and follow up.Methods:Cases treated with curative intent (2000–2014) were included. Data were collected, and overall and disease-free survival rates were calculated.Results:Eleven cases were identified, with a median follow up of 87 months. One patient was Kadish stage A, one was stage B, eight were stage C and one was stage D. The latter patient underwent chemoradiotherapy alone. The remaining patients proceeded to: endoscopic-assisted wide local excision (n = 2), anterior craniofacial resection (n = 4) or endoscopic craniofacial resection (n = 4). No patients had primary nodal disease or elective neck treatment. One patient had neoadjuvant chemoradiation. Six patients had post-operative radiotherapy; three received adjuvant chemotherapy. Two patients had late cervical node failure, and proceeded to neck dissection and post-operative radiotherapy. Two patients had late local recurrence. Ten-year overall and disease-free survival rates were 68.2 and 46.7 per cent, respectively.Conclusion:Longer-term follow up is supported given the incidence of late regional and local recurrence. Prophylactic treatment of cervical nodes in locally advanced disease is an area for further investigation. [ABSTRACT FROM AUTHOR]

Drug-induced parkinsonism ( DIP) is common, and the motor symptoms can be indistinguishable from Parkinson's disease ( PD). When symptoms persist after drug withdrawal, this may represent 'unmasking' of underlying PD. We previously reported that hyposmia, a common nonmotor feature of PD, was associated with persistent DIP. Here, we report on a series of 33 consecutive patients who underwent dopamine transporter imaging to evaluate DIP. We examined the clinical correlates of underlying dopaminergic denervation by comparing subjects with normal and abnormal scans. Imaging was abnormal in 7 of 33 (21%) cases. Motor features were similar in patients with normal and abnormal scans. Olfactory testing was available for 30 subjects and was concordant with imaging in 27 of 30 (odds ratio = 63; 95% confidence interval: 4.8-820; P = 0.002). Olfactory testing may be a simple screen to help identify DIP patients with underlying dopaminergic denervation, consistent with unmasking of incipient PD. [ABSTRACT FROM AUTHOR]

In patients with neurodegenerative diseases, there is a spectrum of smell dysfunction ranging from severe loss, as seen in Alzheimer's disease and Parkinson's disease, to relatively little loss, as seen in progressive supranuclear palsy. Given the ubiquitous but varying degrees of olfactory dysfunction among such diseases, it is conceivable that differential disruption of a common primordial neuropathological substrate causes these differences in olfactory function. For example, the amount of damage to forebrain neurotransmitter and neuromodulator circuits, most notably those involving cholinergic transmission, appears to be correlated with quantitative smell test scores across a wide range of neurodegenerative diseases. Thus, a key question is whether damage to such a substrate is the basis for the perceptual differences in olfaction or whether disease-specific or other entities, such as respiratory infections or pollution, are responsible. In light of the early preclinical onset of smell deficits in many neurodegenerative diseases, the answer to this question might provide crucial insight into the cause of disease pathology at its earliest stages of development. [ABSTRACT FROM AUTHOR]

Background Chronic rhinosinusitis (CRS) is a common inflammatory condition and a major cause of olfactory loss. Olfactory dysfunction has been associated with reduced olfactory bulb (OB) volume and gray matter (GM) density in the olfactory-related brain areas. The aim of this study was to investigate brain GM structural and OB volume alterations in patients with CRS. Methods Structural brain images were collected from 21 CRS patients and 31 healthy controls on a 3-T scanner. Voxel-based morphometry (VBM) was performed to investigate GM. Olfactory bulb volumes were measured using AMIRA software. Psychophysical olfactory testing for odor threshold (T) and identification (I) was performed using the Sniffin' Sticks battery. Results CRS patients had significantly lower scores for Sniffin' Sticks olfactory tests than controls ( p < 0.001 for T, I, and combined T and I [TI] scores). Region-of-interest analyses revealed no difference in GM volume between CRS patients and healthy controls; however, in CRS patients with severe olfactory dysfunction, GM reduction was observed in the gyrus rectus, orbitofrontal cortex, thalamus, and the insula. In addition, no difference was observed for OB volume in CRS patients compared with healthy controls. Conclusion In this study we identified a reduction in gray matter in olfactory brain regions in CRS patients with severe olfactory dysfunction. [ABSTRACT FROM AUTHOR]

Background Olfactory function deteriorates in patients with severe obstructive sleep apnea syndrome (OSAS). The effect of positive airway pressure (PAP) therapy on olfactory function has not been investigated before. In this study, we aimed to investigate the role of PAP therapy on olfactory impairment in patients with OSAS. Methods Thirty patients who had OSAS and planned for PAP therapy were included in the study. All participants underwent a detailed otorhinolaryngological examination and polysomnography. The 'Sniffin' Sticks' test was used for the analysis of olfactory function. The participants underwent the smell test before the PAP therapy, and about 3 months after the therapy. Pretreatment and posttreatment results were compared. Results The pretreatment and the posttreatment apnea-hypopnea index (AHI) were 57.6 ± 29.8/hour and 9.5 ± 7.9/hour, respectively. Odor threshold (OT), odor discrimination (OD), odor identification (OI), and threshold-discrimination-identification (TDI) scores significantly increased after PAP therapy ( p = 0.001, p = 0.002, p = 0.001, and p = 0.001, respectively). The pretreatment and posttreatment total TDI scores were 28.48 ± 4.71 and 32.50 ± 3.88, respectively ( p = 0.001). Conclusion This study demonstrates olfactory dysfunction in patients with OSAS. We achieved a significant improvement in olfactory function of patients with OSAS after PAP therapy. Further studies are needed to illuminate the pathogenesis of olfactory dysfunction in OSAS, and the role of PAP therapy on olfactory improvement. [ABSTRACT FROM AUTHOR]

Background: Olfactory deficits are present in early Alzheimer's disease (AD) and mild cognitively impaired (MCI) patients. However, whether these deficits are due to dysfunction of the central or peripheral olfactory nervous system remains uncertain. This question is fundamentally important for developing imaging biomarkers for AD using olfactory testing.Objective: This study sought to use olfactory functional magnetic resonance imaging (fMRI) to further demonstrate the involvement of the central olfactory system in olfactory deficits in MCI and AD.Methods: We investigated the central olfactory system in 27 cognitively normal controls (CN), 21 MCI, and 15 AD subjects using olfactory fMRI with an odor-visual association paradigm during which a visual cue was paired with lavender odorant (odor condition) or odorless air (no-odor condition).Results: The CN subjects had significantly greater activated volume in the primary olfactory cortex during both the odor and no-odor conditions compared to either the MCI or AD groups (p < 0.05). No significant differences were observed between the odor and no-odor conditions within each group. No-odor condition activation in AD and MCI correlated with the cognitive and olfactory assessments.Conclusion: The no-odor condition, allowing investigation of activation patterns when the peripheral olfactory system was not directly involved, elicited the same functional response as the odor condition for each of the three groups. Thus, the olfactory activation deficits present in AD and MCI patients are most likely caused by degeneration of the central olfactory nervous system. [ABSTRACT FROM AUTHOR]

Although early olfactory dysfunction has been found in patients with Alzheimer's disease, the underlying mechanisms remain unclear. In this study, we investigated whether and how oligomeric amyloid-β peptide (Aβ) affects the responses of mitral cells (MCs). We found that oligomeric Aβ1–42 increased spontaneous and evoked firing rates but decreased the ratio of evoked to spontaneous firings in MCs. Aβ1–42 oligomers showed no impact on the hyperactivity exerted by pharmacological blockage of GABA A receptors, suggesting an involvement of GABAergic inhibitory transmission in Aβ1 to 42–induced over-excitability. It was further determined that Aβ1–42 oligomers inhibited the frequency of spontaneous inhibitory postsynaptic currents and miniature inhibitory postsynaptic currents, as well as the amplitude of miniature inhibitory postsynaptic currents in MCs. Both recurrent and lateral inhibition of MCs, which are critical for odor discrimination, were also disrupted by Aβ1–42 oligomers. The above data indicate that Aβ impairs local inhibitory circuits and thereby leads to perturbations of olfactory information output in the olfactory bulb. This study reveals a cellular and synaptic basis of olfactory deficits associated with Alzheimer's disease. [ABSTRACT FROM AUTHOR]

Introduction: Olfactory groove schwannomas (OGSs) are extremely rare tumours, particularly in the paediatric population. Case report: A 13-year-old girl presented with two epileptic seizures, papilloedema and incomplete binasal quadrantanopia. Computed tomography (CT) and magnetic resonance imaging (MRI) demonstrated a large heterogeneously enhancing tumour of the anterior skull base with a prominent dorsal pseudocyst. Interestingly, the pseudocyst embraced the right ICA bifurcation and displaced the optic tracts, optic chiasm and optic nerves and the ipsilateral basal ganglia. The patient underwent surgery via the frontolateral approach, and the tumour was completely removed. The pseudocyst was opened, and its wall was partially resected. It subsequently resolved completely. Histopathological examination yielded the rare diagnosis of schwannoma of the anterior skull base. Conclusion: Although extremely rare, olfactory groove schwannomas can be seen in paediatric patients. Our patient is the youngest ever reported with this histopathological diagnosis along with the formation of a large pseudocyst. [ABSTRACT FROM AUTHOR]

BACKGROUND: Olfactory dysfunction affects millions of people worldwide. This sensory impairment is associated with neurodegenerative disease and significantly decreased quality of life. Exposure to airborne pollutants has been implicated in olfactory decline, likely due to the anatomic susceptibility of the olfactory nerve to the environment. Historically, studies have focused on occupational exposures, but more recent studies have considered effects from exposure to ambient air pollutants. OBJECTIVES: To examine all relevant human data evaluating a link between ambient pollution exposure and olfaction and to review supporting animal data in order to examine potential mechanisms for pollution-associated olfactory loss. METHODS: We identified and reviewed relevant articles from 1950 to 2015 using PubMed and Web of Science and focusing on human epidemiologic and pathophysiologic studies. Animal studies were included only to support pertinent data on humans. We reviewed findings from these studies evaluating a relationship between environmental pollutant exposure and olfactory function. RESULTS: We identified and reviewed 17 articles, with 1 additional article added from a bibliography search, for a total of 18 human studies. There is evidence in human epidemiologic and pathologic studies that increased exposure to ambient air pollutants is associated with olfactory dysfunction. However, most studies have used proxies for pollution exposure in small samples of convenience. Human pathologic studies, with supporting animal work, have also shown that air pollution can contact the olfactory epithelium, translocate to the olfactory bulb, and migrate to the olfactory cortex. Pollutants can deposit at each location, causing direct damage and disruption of tissue morphology or inducing local inflammation and cellular stress responses. CONCLUSIONS: Ambient air pollution may impact human olfactory function. Additional studies are needed to examine air pollution--related olfactory impacts on the general population using measured pollution exposures and to link pollution exposure with olfactory dysfunction and related pathology. CITATION: Ajmani GS, Suh HH, Pinto JM. 2016. Effects of ambient air pollution exposure on olfaction: a review. Environ Health Perspect 124:1683-1693; http://dx.doi.org/10.1289/EHP136 [ABSTRACT FROM AUTHOR]

Background: Scans without evidence of dopaminergic deficit (SWEDD), a heterogeneous disorder, refers to patients with normal dopamine transporter scan presumed to have Parkinson's disease (PD). Although clinically hard to discriminate, it is important to differentiate SWEDD from PD in the early stage of disease in practice. Olfactory dysfunction is a sensitive biomarker of neurodegeneration. A considerable number of SWEDD patients show abnormal olfaction. We investigated the olfaction and non-motor symptoms in SWEDD, PD, and healthy controls. A subgroup analysis of SWEDD by olfactory function was also conducted. Methods: This study enrolled 40 SWEDD, 28 PD, and 26 healthy controls. The Korean version of Sniffin's stick test II (KVSS II) and the Korean version of non-motor symptoms scale for PD (K-NMSS) were used to evaluate olfaction and non-motor symptoms. Patients with SWEDD were categorized into normal olfaction (SWEDD-N) and olfactory dysfunction (SWEDD-D) subgroups. Results: Overall KVSS II scores of SWEDD group was distinctive when compared to those of PD or controls. K-NMSS scores were increased in PD compared to those in SWEDD or controls. In subgroup analysis, KVSS II scores in SWEDD-D were similar to those in PD. K-NMSS scores in SWEDD-D were also significantly higher than those in SWEDD-N but lower than those in PD. Conclusions: Olfactory dysfunction could be a biomarker to differentiate SWEDD from PD. Non-motor symptoms differed between the two SWEDD subgroups classified by olfaction. These findings suggest that the underlying pathophysiology of SWEDD with normal olfaction and olfactory dysfunction might be different. [ABSTRACT FROM AUTHOR]

Background: Loss of olfaction has been considered inevitable in endoscopic endonasal resection of olfactory groove meningiomas. Olfaction preservation may be feasible through an endonasal unilateral transcribriform approach, with the option for expansion using septal transposition and contralateral preservation of the olfactory apparatus. Methods: An expanded unilateral endonasal transcribriform approach with septal transposition was performed in five cadaver heads. The approach was applied in a surgical case of a 24 × 26-mm olfactory groove meningioma originating from the right cribriform plate with partially intact olfaction. Results: The surgical approach offered adequate exposure to the anterior skull base bilaterally. The nasal/septal mucosa was preserved on the contralateral side. Gross total resection of the meningioma was achieved with the successful preservation of the contralateral olfactory apparatus and preoperative olfaction. Six months later, the left nasal cavity showed no disruption of the mucosal lining and the right side was at the appropriate stage of healing for a harvested nasoseptal flap. One year later, the preoperative olfactory function was intact and favorably viewed by the patient. Objective testing of olfaction showed microsomia. Conclusions: Olfaction preservation may be feasible in the endoscopic endonasal resection of a unilateral olfactory groove meningioma through a unilateral transcribriform approach with septal transposition and preservation of the contralateral olfactory apparatus. [ABSTRACT FROM AUTHOR]

Background Vitamin B12 plays a major role in the maintenance of central and peripheral nervous systems. Vitamin B12 deficiency may affect the spinal cord, brain, optic nerve, and peripheral nerve functions; however, the effect of vitamin B12 deficiency on olfactory function has not been studied, so our study aimed to investigate that. Methods Thirty-nine patients with low vitamin B12 levels and 34 controls were included in the study. All participants had detailed otorhinolaryngological examinations and laboratory tests. The Sniffin' Stick test was used for analysis of olfactory function. The 2 groups were compared for smell test results. Correlations of smell test results with demographic and laboratory data were investigated in the vitamin B12-deficient group. Results The threshold discrimination identification scores were (mean ± standard deviation) 28.04 ± 5.58 and 35.10 ± 2.84 in the vitamin B12-deficient and control groups, respectively ( p < 0.001). In the vitamin B12-deficient group, hyposmia and anosmia were evident in 56.4% and 5.1% of the patients, respectively, but no subjects in the control group had olfactory dysfunction ( p < 0.001). Correlation analysis showed that age and odor identification score showed a negative correlation ( p < 0.001); however, there was a positive correlation between threshold, discrimination and identification (TDI) score and vitamin B12 levels. Conclusion In this study, we showed for the first time that olfactory dysfunction may be present in patients with vitamin B12 deficiency. Apart from a negative correlation of age with odor identification score, none of the other parameters studied showed correlations with olfactory dysfunction. [ABSTRACT FROM AUTHOR]

Background: Kallmann syndrome (KS) is defined by the association of hypogonadotropic hypogonadism and anosmia. It is characterized by a significant clinical and genetic heterogeneity; actually, it may present several non-reproductive non-olfactory anomalies, and all the ways of genetic transmission can be involved in the inheritance of the disease. Although six pathogenesis-related genes have been identified so far, KS remains sporadic in 70 % of the cases, and the genetic diagnosis is not available for all of them. The purpose of this paper is to present a further disease that can enrich the wide spectrum of KS variability, that is cerebral arachnoid cyst. Case description: This 11-year-old boy presented with the typical characteristics of KS together with those related to a sylvian arachnoid cyst. He was admitted because of worsening headache. At the admission, the physical examination revealed eunuchoid aspect, micropenis, previous cryptorchidism, and anosmia. MRI pointed out a large, left sylvian arachnoid cyst, agenesia of the olfactory bulbs/tracts complex, and hypoplasia of the left olfactory sulcus. The child was operated on by endoscopic fenestration of the cyst, followed by transient external drainage for subdural hygroma and microscopic fenestration for recurrence of the cyst. His statural growth is normal but the sexual development still delayed in spite of hormone replacement therapy. Conclusion: According to the present and the other four cases in the literature, arachnoid cyst should be included among the anomalies possibly accompanying KS date although this association seems to be occasional as far as embryogenesis and physiopathology are concerned. [ABSTRACT FROM AUTHOR]

Background: Behavioral and cognitive impairment are common in amyotrophic lateral sclerosis (ALS) and represent a continuum with frontotemporal dementia (FTD). Olfactory dysfunction has been described in a subset of ALS patients and might be associated with frontotemporal and insular cortex dysfunction. Objective: To evaluate olfaction dysfunction in ALS patients and its relationship with either cognition or behavioral impairment. Methods: 28 consecutive ALS patients underwent an extensive cognitive and behavioral battery and were classified as patients with normal cognition (ALS-N, n = 11) or with part of the ALS-FTD spectrum (n = 17), including either cognitive or behavioral im-pairment or dementia. Odor verbal and visual identification and discrimination were investigated in patients and agematched controls using a test adapted from the Sniffin' Sticks. Results: Olfactory function was significantly different between ALS-FTD spectrum patients and controls (p < 0.001) and inversely correlated with behavioral and cognitive performance. The 10-point cutoff distinguished ALS-N from ALS-FTD spectrum patients with a sensitivity and specificity of 71 and 100%, respectively. Conclusions: Hyposmia is common in a subset of ALS patients and strongly associated with behavioral and cognitive impairment. Olfactory testing may represent an early screening tool in order to identify ALS subjects with cognitive/behavioral dysfunction. Further studies in larger series are mandatory in order to better investigate clinical and pathological aspects in this group of patients. [ABSTRACT FROM AUTHOR]

Background: Olfactory dysfunction is common in Parkinson's disease (PD) and idiopathic rapid eye movement sleep behavior disorder (iRBD), which is a risk factor in the development of PD. However, a few studies have conflicting results when comparing dysosmia in the patients with iRBD and PD. There is no study investigating the olfactory function in Chinese patients with iRBD. Additionally, the Sniffin’ Sticks screening 12 test (SS-12) contains several odors that are not familiar to people in different cultures. Methods: Odor identification was evaluated in iRBD patients (n = 54), PD patients (n = 54) and healthy controls (n = 54). With the identification data, a brief odor identification test was established and then validated in other subjects. Results: Odor identification scores in iRBD patients were significantly higher than those in PD patients (P<0.001) but lower than those in controls (P<0.001). At the cut-off value of 7.5, the Sniffin’ Sticks clearly differentiated iRBD and PD patients from the controls, and the brief test could increase the specificity in diagnosing PD. Neither the Sniffin’ Sticks nor the brief test could clearly differentiate PD and iRBD patients from each other. Conclusions: Olfaction is more impaired in PD patients than in iRBD patients, possibly due to the heterogeneity of iRBD patients. The Sniffin’ Sticks could be a useful tool for differentiating iRBD patients from the healthy population, and it could be useful for screening people at high-risk of PD in China, especially when combined with polysomnography. To reduce the expense and time required for the Sniffin’ Sticks test, this study shows that a brief test is feasible. [ABSTRACT FROM AUTHOR]

To report on the presence of olfactory arachnoid dilatations (OAD), a previously undescribed radiologic feature of spontaneous cerebrospinal fluid (CSF) rhinorrhea originating from the cribriform plate of the ethmoid bone. The medical records of all patients treated between 2001 and 2011 at a tertiary care center for a spontaneous CSF rhinorrhea originating from the cribriform plate were retrospectively reviewed. The radiological work-up included high-resolution computed tomography and magnetic resonance imaging with at least the following sequences: T1, T2, and T2 with fast imaging employing steady state acquisition (FIESTA). Thirty cases were identified. The mean age at diagnosis was 49. Fourteen patients (47 %) had a body mass index (BMI) of 30 or more and 3 patients (10 %) had a BMI between 25 and 29.9. Five patients had a history of meningitis. The imaging work-up revealed a bone defect of the cribriform plate in 6 cases (20 %), associated to a typical meningocele in 14 cases (47 %). In ten patients (33 %), there was no defect of the cribriform plate, but ultrathin coronal T2-FIESTA sequences revealed an OAD, i.e. a dilatation of the arachnoid sheath of the olfactory fibers, in nine cases (30 %), or a 'pseudo-polyp' outlined by a thin layer of arachnoid (1 patient, 3 %). Preoperative imaging should be carefully analyzed for the presence of OAD or 'pseudo-polyp' in patients presenting with a CSF rhinorrhea without bony defect of the cribriform plate. [ABSTRACT FROM AUTHOR]

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Association of changes in olfactory-related structures with olfactory function in patients with multiple sclerosis (MS) is not well understood. We used a T&T olfactometer test kit to evaluate olfactory function in 26 patients with MS and 26 age- and sex-matched healthy controls (HC). Then, Brain MRI were performed and olfactory-related structures were analyzed in these subjects. Olfactory detection and recognition threshold were significantly higher in the MS group, interestingly olfactory recognition threshold positively correlated with expanded disability status scale scores in these patients. Olfactory bulb (OB) volume reduced in patients with olfactory dysfunction (ODF). At the same time, reductions in gray matter (GM) volume were observed in the parahippocampal gyrus (PCG), amygdala, piriform cortex, and inferior frontal gyrus in patients with MS compared to HC. Atrophy of the PCG was more obvious in patients with ODF than patients without ODF and the PCG volume correlated with the olfactory recognition threshold, while no difference was found in fractional anisotropy values of tract-based spatial statistics analysis in the two groups. Olfactory function in patients with MS tends to become gradually more impaired with disability aggravation. Decreases in the volume of the OB and olfactory-related GM might provide valuable information about disease status in patients with MS with olfactory impairment. [ABSTRACT FROM AUTHOR]

In the adult olfactory epithelium, the transcription factors Pax6 and Sox2 are co-expressed in sustentacular cells, horizontal basal cells (HBCs), and less-differentiated globose basal cells (GBCs)–both multipotent and transit amplifying categories—but are absent from immediate neuronal precursor GBCs and olfactory sensory neurons (OSNs). We used retroviral-vector transduction to over-express Pax6 and Sox2 individually and together during post-lesion recovery to determine how they regulate neuronal differentiation. Both Pax6 and Sox2, separately and together, can suppress the production of OSNs, as fewer clones contain neurons than with empty vector (EV), although this effect is not absolute. In this regard, Pax6 has the strongest effect when acting alone. In clones where neurons form, Pax6 reduces neuron numbers by comparison with EV, while Sox2 expands their numbers. Co-transduction with Pax6 and Sox2 produces an intermediate result. The increased production of OSNs driven by Sox2 is due to the expansion of neuronal progenitors, since proliferation and the numbers of Ascl1, Neurog1, and NeuroD1-expressing GBCs are increased. Conversely, Pax6 seems to accelerate neuronal differentiation, since Ascl1 labeling is reduced, while Neurog1- and NeuroD1-labeled GBCs are enriched. As a complement to the over-expression experiments, elimination of Sox2 in spared cells of floxed Sox2 mice, by retroviral Cre or by K5-driven CreERT2, reduces the production of OSNs and non-neuronal cells during OE regeneration. These data suggest that Pax6 and Sox2 have counteracting roles in regulating neurogenesis, in which Pax6 accelerates neuronal production, while Sox2 retards it and expands the pool of neuronal progenitors. [ABSTRACT FROM AUTHOR]

Olfactory dysfunction is a common and early symptom of many neurodegenerative diseases, particularly of Alzheimer's disease (AD) and mild cognitive impairment, pointing to the progression to dementia. Recent studies have revealed that valproic acid (VPA) has neuroprotective effects in rodent models of AD. In this study, we investigated the effects of VPA on olfactory dysfunction of APP/PS1 double transgenic mouse models of AD. After continuous treatment with a 100 mg/kg daily dose of VPA for 3 months, APP/PS1 mice showed improved olfactory performances. In agreement with the behavioral findings, VPA treatment reduced amyloid β (Aβ) burden in the olfactory epithelium (OE) of transgenic mice. And, VPA increased epithelial thickness of the olfactory mucosa through decreased cell apoptosis and increased cell proliferation. In the olfactory bulb (OB), VPA administration also reduced senile plaques and levels of soluble and insoluble Aβ42 peptides. Besides, VPA promoted the increase of mitral cells and decrease of neurofilament immunostaining. In hence, VPA treatment completely improved the olfactory performances and prevented degenerative changes of the OE and OB. Our study raises the possibility of AD diagnosis by OE biopsy. Moreover, VPA may provide a novel therapeutic strategy for the treatment of olfactory dysfunction in AD patients. [ABSTRACT FROM AUTHOR]

Most forms of suprathreshold sensory stimulation perturb sleep. In contrast, presentation of pure olfactory or mild trigeminal odorants does not lead to behavioral or physiological arousal. In fact, some odors promote objective and subjective measures of sleep quality in humans and rodents. The brain mechanisms underlying these sleep-protective properties of olfaction remain unclear. Slow oscillations in the electroencephalogram (EEG) are a marker of deep sleep, and K complexes (KCs) are an EEG marker of cortical response to sensory interference. We therefore hypothesized that odorants presented during sleep will increase power in slow EEG oscillations. Moreover, given that odorants do not drive sleep interruption, we hypothesized that unlike other sensory stimuli odorants would not drive KCs. To test these hypotheses we used polysomnography to measure sleep in 34 healthy subjects (19 women, 15 men; mean age 26.5 ± 2.5 yr) who were repeatedly presented with odor stimuli via a computer-controlled air-dilution olfactometer over the course of a single night. Each participant was exposed to one of four odorants, lavender oil (n = 13), vetiver oil (n = 5), vanillin (n = 12), or ammonium sulfide (n = 4), for durations of 5, 10, and 20 s every 9-15 min. Consistent with our hypotheses, we found that odor presentation during sleep enhanced the power of delta (0.5-4 Hz) and slow spindle (9-12 Hz) frequencies during non-rapid eye movement sleep. The increase was proportionate to odor duration. In addition, odor presentation did not modulate the occurrence of KCs. These findings imply a sleep-promoting olfactory mechanism that may deepen sleep through driving increased slow-frequency oscillations. [ABSTRACT FROM AUTHOR]

It is well known that patients with Parkinson's Disease (PD) suffer from olfactory impairments, but it is not clear whether patients are aware of their level of deficit in olfactory functioning. Since PD is a neurodegenerative disorder and its progression may be correlated with olfactory loss (Ansari & Johnson, 1975; but see also Doty, Deems, & Stellar, 1988), it is possible that these patients would be subject to metacognitive errors of over-estimation of olfactory ability (White & Kurtz, 2003). Nineteen non-demented PD patients and 19 age-matched controls were each given an objective measure of olfactory identification (the UPSIT, Doty, Shaman, Kimmelman, & Dann, 1984) and a subjective measure involving a questionnaire that asked them to self-rate both their olfactory function generally and their ability to smell each of 20 odors, 12 of which were assessed on the UPSIT. All of the PD patients showed impaired olfactory ability, as did 7 of the controls, according to the UPSIT norms. Self-rated and performance-based olfactory ability scores were significantly correlated in controls (r=.49, p=.03) but not in patients with PD (r=.20, p=.39). When the 12 odors common to both the self-rated questionnaire and UPSIT were compared, PD patients were less accurate than controls (t(36)=-4.96, p<.01) at estimating their own ability and the number of over-estimation errors was significantly higher (tone-tailed(29)=1.80, p=.04) in PD patients than in the control group, showing less metacognitive awareness of their ability than controls. These results support the idea that olfactory metacognition is often impaired in PD, as well as in controls recruited for normosmic ability (Wehling, Nordin, Espeseth, Reinvang, & Lundervold, 2011), and indicate that people with PD generally exhibit over-estimation of their olfactory ability at a rate that is higher than controls. These findings imply that PD patients, unaware of their olfactory deficit, are at greater risk of harm normally detected through olfaction, such as smoke or spoiled foods. [ABSTRACT FROM AUTHOR]

The effect of an olfactory stimulation on the perception of time was investigated through two different experiments based on temporal bisection tasks. In experiment 1, the durations to be classified as either short or long were centered on 400 ms while in Experiment 2 there were centered on 2000 ms. The participants were different in the two experiments (36 subjects in each one). In each experiment, half of the subjects learnt the anchor durations when smelling an unpleasant odor (decanoic acid) and the other half when smelling no odor. After the learning phase, both groups were tested with and without odor. The results showed opposite effects depending on the duration range. The subjects underestimated the time in the presence of the unpleasant odor in the short duration range while they overestimated it in the long duration range. The results have been discussed in the framework of the pacemaker-counter clock model and a potential emotional effect induced by the odor on the subjective time perception has also been considered. [ABSTRACT FROM AUTHOR]

Chronic renal disease is known to alter olfactory function, but the specific changes induced in olfactory organs during this process remain unclear. Of the uraemic toxins generated during renal disease, high levels of urea are known to induce hyposmic conditions. In this study, the effects of environmental exposure to elevated concentrations of urea (7, 13.5 and 20 g L-1) on the sensory mucosa of zebrafish in acute toxicity and chronic toxicity tests were described. It was observed that lamellae maintained structural integrity and epithelial thickness was slightly reduced, but only following exposure to the highest concentrations of urea. Panneuronal labelling with anti-Hu revealed a negative correlation with levels of urea, leading to investigation of whether distinct neuronal subtypes were equally sensitive. Using densitometric analysis of immunolabelled tissues, numbers of Gα olf-, TRPC2- and TrkA-expressing cells were compared, representing ciliated, microvillous and crypt neurons, respectively. The three neuronal subpopulations responded differently to increasing levels of urea. In particular, crypt cells were more severely affected than the other cell types, and Gα olf-immunoreactivity was found to increase when fish were exposed to low doses of urea. It can be concluded that exposure to moderate levels of urea leads to sensory toxicity directly affecting olfactory organs, in accordance with the functional olfactometric measurements previously reported in the literature. [ABSTRACT FROM AUTHOR]

Olfactory neuroblastoma (ON) is a rare type of malignant neoplasm originating from the olfactory neuroepithelial cells of the nasal cavity. ON is also known as esthesioneuroblastoma or neuroendocrine carcinoma. The malignancy accounts for <3% of tumors originating in the nasal cavity. Through the nasal cavity, ON may infiltrate the sinuses, the orbit and the cranium. The tumor is characterized by a pattern of slow growth and local recurrences. Treatment options are surgical excision or surgery combined with a radiotherapy (RT) and/or chemotherapy combination treatment. The present study reports the case of a 69-year-old patient with a mass in the nasal cavity who was treated by combined surgical excision and RT. The literature for ON and the treatment of the tumor are also discussed. [ABSTRACT FROM AUTHOR]