Search

Smell loss (hyposmia) and hypertension are common but related medical problems. Associated with hyposmia is loss of ability to obtain flavor from food. To compensate for flavor loss hyposmic patien...

The notion that the classic motor features of Parkinson disease (PD) are preceded by a prodrome has received renewed interest in the past decade. A recent study corroborates previous findings that smell loss and constipation are signifiers of nigral degeneration. But can we really predict who is going to get PD?

Objective Smell loss (hyposmia) inhibits flavor perception and influences food intake. To compensate for flavor loss, some patients with hyposmia appear to increase salt usage. The purpose of this study was to compare self-reported salt usage in patients with hyposmia with that in normal volunteers. Methods Salt usage was compared in 56 patients with hyposmia but with normal taste function with that in 27 normal volunteers. Salt usage was formulated with respect to 1) a standard quantitative salt intake scale, 2) salt addition related to food intake, 3) intake of foods and beverages with high salt content, and 4) salt intake related to presence or absence of hypertension. Results Eighteen (32%) of the 56 patients self-reported increased salt usage; they were labeled “increased users.” The other 38 hyposmic patients (68%) did not report increased salt usage; they were labeled “non-changers.” Increased users estimated their salt usage rose an average 2.8 times that experienced before their hyposmia onset. They also reported adding salt to their food before tasting it and ate more highly salted foods than did the non-changers. Salt usage was not increased further among increased users with hypertension but was increased further among non-changers with hypertension. Conclusions Salt usage is increased among some patients with hyposmia presumably to enhance flavor perception to compensate for diminished flavor perception related to loss of smell.

Hyposmia is generally considered a rare occurrence among patients in the U.S. It is also considered a minor loss of sensory function compared to loss of vision or hearing. However, it occurs much m...

Chemosensory disorders have been receiving increasing clinical attention but remain a difficult diagnostic problem. With the development of several well-standardized testing methods, taste or smell loss can now be verified, and this has added to knowledge concerning the common causes of dysfunction. Diagnosis typically rests upon the history and physical examination, but, except in the case of obstructive nasal and sinus pathologic conditions, therapy usually remains elusive.

Previous data on the prevalence of olfactory dysfunction in Parkinson's disease (PD) range from 45% to 90%. The present multicenter study aimed to provide data on the prevalence of smell loss in a large sample of PD patients from three independent populations. Olfactory sensitivity was tested in 400 patients from Australia, Germany, and The Netherlands by means of a psychophysical olfactory test, the "Sniffin' Sticks", which is comprised of 3 subtests of olfactory function. Out of the total number of patients 45.0% presented as functionally anosmic, 51.7% were hyposmic, whereas only 3.3% were normosmic. This indicates that 96.7% of PD patients present with significant olfactory loss when compared to young normosmic subjects. This figure falls to 74.5%, however, when adjusted to age-related norms. Thus, olfactory dysfunction should be considered as a reliable marker of the disease.

Purpose: To evaluate nasal mucus levels of cAMP and cGMP in patients with taste and smell dysfunction with respect to severity of their smell loss. Methods: cAMP and cGMP were measured in nasal mucus using a sensitive spectrophotometric 96 plate ELISA technique. Smell loss was measured in patients with taste and smell dysfunction by standardized psychophysical measurements of olfactory function and classified by severity of loss into four types from most severe to least severe such that anosmia > Type I hyposmia > Type II hyposmia > Type III hyposmia. Measurements of nasal mucus cyclic nucleotides and smell loss were made independently. Results: As smell loss severity increased stepwise cAMP and cGMP levels decreased stepwise [cAMP, cGMP (in pmol/ml); anosmia – 0.004, 0.008: Type I hyposmia – 0.12±0.03, 0.10±0.03: Type II hyposmia – 0.15±0.02, 0.16±0.01: Type III hyposmia – 0.23±0.05, 0.20±0.15]. Conclusions: These results confirm the association of biochemical changes in cyclic nucleotides with systematic losses of smell acuity. These results confirm the usefulness of the psychophysical methods we defined to determine the systematic classification of smell loss severity. These changes can form the basis for the biochemical definition of smell loss among some patients with smell loss as well as for their therapy.

Environmental agents, including viruses, prions, and toxins, have been implicated in the cause of a number of neurodegenerative diseases, most notably Alzheimer's and Parkinson's diseases. The presence of smell loss and the pathological involvement of the olfactory pathways in the formative stages of Alzheimer's and Parkinson's diseases, together with evidence that xenobiotics, some epidemiologically linked to these diseases, can readily enter the brain via the olfactory mucosa, have led to the hypothesis that Alzheimer's and Parkinson's diseases may be caused or catalyzed by agents that enter the brain via this route. Evidence for and against this concept, the "olfactory vector hypothesis," is addressed in this review.

Chronic rhinosinusitis encompasses a group of disorders characterized by inflammation of the mucosa of the nose and paranasal sinuses of at least 12 weeks' duration. In addition to nasal obstruction and discharge, chronic sinusitis is a common cause of olfactory dysfunction. Smell loss can result in problems including safety concerns, hygiene matters, appetite disorders, and changes in emotional and sexual behavior. Although smell loss related to sinonasal disease is probably the most treatable form of olfactory dysfunction and treatment can improve olfactory sensation in the setting of sinusitis, most studies show that the effects are usually transient and incomplete.

We have observed that, in cases of smell loss, patients often complain of taste loss as well even though they actually have normal gustatory acuity according to gustatory tests; we have defined such symptoms as "flavor disturbance". The clinical features of flavor disturbance are reported in this paper.A total of 297 patients (99 males, 198 females; mean age 55.5 years) were treated for olfactory disturbance at the hospital of Hyogo College of Medicine between July 1995 and August 2001. Sixty-six out of 297 patients (22.5%) also experienced taste disturbance, and 49 of these 66 cases were evaluated by means of smell and taste tests. These 49 patients who complained of taste and smell loss were classified into two groups according to the results of their smell and taste tests. Patients who only complained of olfactory disturbance were also reviewed.There was no relationship between the severity of olfactory disturbance and the degree of flavor disturbance. The incidence of flavor disturbance was high in patients with sudden olfactory disturbance after upper respiratory tract infection or head trauma and low in those with slowly progressive olfactory disturbance. The symptoms of flavor disturbance improved regardless of whether smell was improved or not.The patients with flavor disturbance tended to misrecognize that they had taste loss because of sudden smell loss, and there were more of these cases than we expected. When patients with smell and taste loss are treated, flavor disturbance should also be considered.

Smell loss associated with nasal sinus disease can be a frustrating condition for patients and their physicians. A better understanding of the causes and pathophysiology of olfactory dysfunction can provide a framework from which the physician can plan appropriate treatment and counsel patients as to probable outcomes. This article reviews the pathophysiology of smell loss and the diagnostic paradigms and treatment approaches for the more common causes of anosmia.

Disorders of the sense of smell can be frustrating for both the patient and physician. Ongoing research in this field has provided insight into the possible mechanisms for smell loss; however, therapy is still limited. Commercially distributed smell testing kits and newer screening tests using material available in all clinical settings have made diagnosis and measurement of the degree of impairment available to all physicians. A detailed history and physical examination are the most powerful tools in the evaluation of smell disorders, whereas imaging studies are reserved for preoperative planning or detailed assessment of positive physical findings.

Atrophic rhinitis is a chronic inflammatory disease of nasal cavity and lovs of smell is an important feature of this condition. An attempt has been made to measure the olfactory status both qualitatively and quantitatively in these cases. The study has been conducted for seven basic odours and a varying degree of smell loss is reported for different odours in different cases.

The University of Pennsylvania Smell Identification Test (UPSIT) and a smell ability questionnaire were administered to 167 Japanese volunteers ranging in age from 20 to 59 years. Of these subjects, 80 also received the T&T olfactometer threshold test. Of the latter subjects, 36 were patients tested before endoscopic nasal surgery for sinusitis and polyposis. The patients exhibited decreased smell function, as measured by the T&T olfactometer, the UPSIT, and a 30-item version of the UPSIT in which the 10 least familiar items were removed (ps < 0.001). Spearman correlations ranging from 0.53 to 0.70 were found between (i) scores on the 30- and 40-item UPSITs and (ii) the T&T detection and recognition threshold values. Significant correlations were found between scores on the smell ability questionnaire and the olfactory test measures (UPSIT30 r = 0.56; UPSIT40 r = 0.58; T&T detection r = 0.56; T&T recognition r = 0.69, p < 0.001), indicating that subjects are relatively accurate in assessing their olfactory ability. This study suggests that the 30 and 40-item UPSITs correlate well with measures derived from the T&T olfactometer, and that all three tests are sensitive to the smell loss of Japanese sinusitis/polyposis patients.

Awareness of loss in smell sensitivity was assessed in 80 normal elderly subjects, 80 patients with probable Alzheimer's disease (AD), and 80 patients with sinusitis by comparing measured smell sensitivity to questionnaire-based, self-reported sensitivity. Both AD patients and sinusitis patients had significantly poorer diagnosed smell sensitivity than the normal elderly. Both patient groups had thresholds which on average were about nine times more concentrated than those of the normal elderly. However, 74% of the AD patients and 77% of the normal elderly with smell loss reported normal smell sensitivity. In contrast, only 8% of the sinusitis patients with loss reported normal smell sensitivity.

BACKGROUND: Olfactory dysfunction in MS patients is reported in the literature. MRI of the olfactory bulb (OB) is discussed as a promising new testing method for measuring olfactory function (OF). Aim of this study was to explore reasons for and optimize the detection of olfactory dysfunction in MS patients with MRI. MATERIALS AND METHODS: OB and olfactory brain volume was assessed within 34 MS patients by manual segmentation. Olfactory function was tested using the Threshold-Discrimination-Identification-Test (TDI), gustatory function was tested using Taste Strips (TST). RESULTS: 41% of the MS patients displayed olfactory dysfunction (8% of the control group), 16% displayed gustatory dysfunction (5% of the control group). There was a correlation between the OB volume and the number and volume of MS lesions in the olfactory brain. Olfactory brain volume correlated with the volume of lesions in the olfactory brain and the EDSS score. The TST score correlated with the number and volume of lesions in the olfactory brain. CONCLUSION: The correlation between a higher number and volume of MS lesions with a decreased OB and olfactory brain volume could help to explain olfactory dysfunction.

It has been estimated that at least 2 million Americans suffer from a disorder of taste or smell,1 but this is probably an underestimation, particularly if one considers the significant degree of smell impairment in the elderly population. Although there are over 200,000 visits to physicians each year for chemosensory disorders, many more of these problems go unreported; they tend to be dismissed by patients as well as by physicians. It is quite obvious, however, that individuals with a taste or smell loss may suffer a significant impairment to their quality of life, both aesthetically and emotionally. Smell and taste alert us to fires, poisonous fumes, leaking gas, and spoiled foods. For this reason, loss of smell is of particular concern to elderly individuals and to those who live alone. The natural pleasures associated with eating can be severely impaired in a person with a taste or smell loss or distortion. Smell and taste impairment can also lead to depression, especially in persons whose occupations (e.g., fireman, chef) critically depend upon these senses.

• Cocaine has been used for many decades as both a stimulant and as a topical anesthetic/vasoconstrictor. Illicit "snorting" or freebase smoking has increased markedly in recent years. Decreased olfaction has been an often reported subjective complaint of cocaine abusers, but quantification of smell loss using sensitive psychophysical tests has not yet been done, leading to the present study. Eleven cocaine abusers were recruited from a drug treatment clinic. Olfaction was assessed using a butanol threshold test, the UPSIT, and a 7-item discrimination test. One patient tested anosmic, one had a mild discrimination problem, and one had a large septal perforation but was normosmic. From the present study, it appears that most cocaine abusers, even heavy users or those with intranasal damage, do not develop permanent olfactory dysfunction. It is not clear what factors may have resulted in complaints of olfactory loss in previous studies. ( Arch Otolaryngol Head Neck Surg. 1990; 116: 1415-1418)

This article has reviewed studies that document a relationship between loss of smell function and disturbances in nasal airflow function. In some cases (for example, hypertrophied adenoids and nasal sinus disease), medical or surgical intervention appears to be useful in restoring some, if not all, of the smell loss associated with the disorder. In other cases (for example, septoplasty), empirical evidence of such efficacy is wanting. Given the current research interest on these topics, however, a clear understanding of both the positive and negative influences of surgical and medical interventions in most cases of obstructive nasal disease or malformities will be forthcoming.

Several studies have shown a significant relationship between smelling and olfactory imagery abilities. The primary aim of the present study was to validate a French version of the Vividness of Olfactory Imagery Questionnaire (VOIQ). The secondary aim was to investigate its capability to differentiate individuals with smell loss from healthy individuals. After having elaborated a French translation of the VOIQ (fVOIQ), we evaluated olfactory imagery abilities of 387 French participants who anonymously self-completed the fVOIQ: 121 pathologic individuals (hyposmic and anosmic), 244 normosmic individuals (healthy non-expert), and 22 fragrance experts. Significant split-half reliability as expressed by Spearman correlation coefficients for the global sample, as well as for each group separately, indicated the excellent internal consistency of the fVOIQ. Moreover, results revealed a significant effect of the smelling ability group on fVOIQ score, suggesting that daily olfactory stimulation is fundamental to maintaining the ability to create a vivid image and that severe loss of smell may result in progressive impairment of olfactory imagery. Our fVOIQ and the original English version seemingly have similarly high benefit in differentiating experts and normosmic individuals based on their olfactory imagery ability. Moreover, the fVOIQ seems capable of differentiating individuals with loss of smell from healthy individuals. These findings demonstrate the reliability and validity of the fVOIQ, and its capability to differentiate individuals’ smelling ability according to their olfactory imagery ability.

Recently, olfactory training has been introduced as a promising treatment for patients with olfactory dysfunction. However, less is known about the neuronal basis and the influence on functional networks of this training. Thus, we aimed to investigate the neuroplasticity of chemosensory perception through an olfactory training program in patients with smell loss. The experimental setup included functional MRI (fMRI) experiments with three different types of chemosensory stimuli. Ten anosmic patients (7f, 3m) and 14 healthy controls (7f, 7m) underwent the same testing sessions. After a 12-week olfactory training period, seven patients (4f, 3m) were invited for follow-up testing using the same fMRI protocol. Functional networks were identified using independent component analysis and were further examined in detail using functional connectivity analysis. We found that anosmic patients and healthy controls initially use the same three networks to process chemosensory input: the olfactory; the somatosensory; and the integrative network. Those networks did not differ between the two groups in their spatial extent, but in their functional connectivity. After the olfactory training, the sensitivity to detect odors significantly increased in the anosmic group, which was also manifested in modifications of functional connections in all three investigated networks. The results of this study indicate that an olfactory training program can reorganize functional networks, although, initially, no differences in the spatial distribution of neural activation were observed.