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Olfactory Loss (olfactory + loss)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

The Diagnosis of a Conductive Olfactory Loss,

THE LARYNGOSCOPE, Issue 1 2001
Allen M. Seiden MD, FACS
Abstract Objectives/Hypothesis Two of the most common causes of olfactory loss include upper respiratory infection (URI) and nasal or sinus disease. The etiology of most URI-related losses is thought to be viral and, as yet, there is no available treatment. In contrast, nasal or sinus disease produces an obstructive or conductive loss that often responds dramatically to appropriate therapy. Therefore, the distinction is important but in many cases may be difficult because such patients often present with no other nasal symptoms, and routine physical findings may be nonspecific. The purpose of this report is to characterize those aspects of the history and physical examination that will help to substantiate the diagnosis of a conductive olfactory loss. Study Design A retrospective, nonrandomized study of consecutive patients presenting with a primary complaint of olfactory loss. Methods This study reviewed 428 patients seen at a university-based taste and smell clinic from July 1987 through December 1998. Of this total, 60 patients were determined to have a conductive olfactory loss. All patients were referred specifically because of a primary chemosensory complaint. The University of Pennsylvania Smell Identification Test (UPSIT; Sensonics, Inc., Haddon Heights, NJ) was administered in all cases. Results The most commonly diagnosed etiologies of olfactory loss were head injury (18%), upper respiratory infection (18%), and nasal or sinus disease (14%). Of the 60 patients with a conductive loss, only 30% complained of nasal obstruction, whereas 58% described a history of chronic sinusitis. Only 45% reported that their olfactory loss at times seemed to fluctuate in severity. Anterior rhinoscopy failed to diagnose pathology in 51% of cases, whereas nasal endoscopy missed the diagnosis in 9%. Systemic steroids elicited a temporary reversal of conductive olfactory loss in 83% of patients who received them, offering a useful diagnostic maneuver, whereas topical steroids did so in only 25%. Conclusions The etiology for olfactory loss can in many cases be difficult to determine, but it is important to establish prognosis and to predict response to therapy. Diagnosis requires a thorough history, appropriate chemosensory testing, and a physical examination that should include nasal endoscopy. A trial of systemic steroids may serve to verify that the loss is indeed conductive. [source]

Olfactory loss may be a first sign of idiopathic Parkinson's disease

MOVEMENT DISORDERS, Issue 6 2007
Antje Haehner MD
Abstract Recent studies support the idea of olfactory dysfunction as a very early sign of idiopathic Parkinson's disease (IPD). Aim of the present study was to clinically follow-up patients with idiopathic hyposmia to find out the percentage of patients developing IPD after 4 years time. At baseline, olfactory tests had been combined with transcranial sonography of the substantia nigra and 123I-FP-CIT SPECT imaging. At the present neurological examination, 7% of the individuals with idiopathic hyposmia had developed clinical IPD. Altogether, 13% presented with abnormalities of the motor system. Our data suggest that a combination of olfactory testing and other tests may constitute a screening tool for the risk to develop IPD. © 2007 Movement Disorder Society [source]

Retronasal and Orthonasal Olfactory Function in Relation to Olfactory Bulb Volume in Patients With Posttraumatic Loss of Smell

THE LARYNGOSCOPE, Issue 6 2006
Philippe Rombaux MD
Abstract Objective: The aims of this study were to evaluate olfactory function with orthonasal and retronasal testing in patients with posttraumatic olfactory loss and to investigate the relation between residual olfactory function and olfactory bulb (OB) volume. Method: A retrospective study of 25 patients with posttraumatic olfactory loss was performed. Orthonasal olfactory function was assessed with the Sniffin' Sticks test kit; retronasal olfactory function was assessed with intraorally applied odors. Magnetic resonance imaging was used to determine OB volume and cortical damage in the frontal and temporal areas. Results: The main outcomes of the present study were the demonstration of a correlation between olfactory function and OB volume, which was more pronounced for retronasal than for orthonasal olfactory function; retronasal olfactory function was most affected in the patients with the most extensive cerebral damage and was least compromised in patients without such damage; OB volumes were smaller in patients with parosmia compared with those without; and the presence of parosmia was clearly associated with the presence of cerebral damage. Conclusion: The data confirm that OB volume is an indicator of olfactory function but, interestingly, in this study, it is largely determined by retronasal olfactory sensitivity. In addition, these results emphasize the role of higher cortical centers in olfactory function, and especially in parosmia, which may, at least in some cases, be related to lesions in the fronto-orbital and anterior temporal cortices. It would be of interest to investigate OB volume further in relation to the prognosis of the disorder. [source]

Treatment of Olfactory Dysfunction, II: Studies With Minocycline,

THE LARYNGOSCOPE, Issue 12 2004
R C. Kern MD
Abstract Objectives/Hypothesis: The treatment of anosmia has changed minimally since the early 1970s, despite dramatic advances in the understanding of the molecular biology of olfaction. Recent studies from the authors' laboratory have suggested that most common causes of clinical olfactory dysfunction, including rhinosinusitis, appear to be associated with increased apoptotic death of olfactory sensory neurons. This appears to result in a decline in the number of functioning mature olfactory sensory neurons, despite the capacity of the olfactory epithelium for regeneration. The current study evaluated the ability of the antibiotic minocycline to inhibit olfactory sensory neuron apoptosis. This drug is known to inhibit apoptosis separate from its anti-infective properties. Olfactory sensory neuron apoptosis was triggered by surgical deafferentation ("bulbectomy"), the standard experimental model. Earlier studies have indicated that bulbectomy and sinusitis invoke similar proteolytic enzyme cascades in olfactory sensory neurons. Study Design: Histological analysis of animal olfactory tissue. Methods: Mice underwent unilateral olfactory bulbectomy to induce apoptotic olfactory sensory neuron death, with and without 45 mg/kg intraperitoneal minocycline given 12 hours before surgery and every 12 hours until death. Mice were killed at 2 and 4 days after bulbectomy and assessed for activation of capsase-3 and olfactory sensory neuron survival by immunohistochemical analysis. Results: Minocycline resulted in partial suppression of cell death at 2 days after surgery when compared with untreated animals. Conclusion: Minocycline inhibits olfactory sensory neuron death in the face of a potent pro-apoptotic stimulus. This drug is well tolerated and is currently undergoing human trials for the management of a variety of neurological disorders associated with apoptosis. The current results suggest that minocycline may be efficacious in the management of peripheral olfactory loss as well. [source]

The Diagnosis of a Conductive Olfactory Loss,

THE LARYNGOSCOPE, Issue 1 2001
Allen M. Seiden MD, FACS
Abstract Objectives/Hypothesis Two of the most common causes of olfactory loss include upper respiratory infection (URI) and nasal or sinus disease. The etiology of most URI-related losses is thought to be viral and, as yet, there is no available treatment. In contrast, nasal or sinus disease produces an obstructive or conductive loss that often responds dramatically to appropriate therapy. Therefore, the distinction is important but in many cases may be difficult because such patients often present with no other nasal symptoms, and routine physical findings may be nonspecific. The purpose of this report is to characterize those aspects of the history and physical examination that will help to substantiate the diagnosis of a conductive olfactory loss. Study Design A retrospective, nonrandomized study of consecutive patients presenting with a primary complaint of olfactory loss. Methods This study reviewed 428 patients seen at a university-based taste and smell clinic from July 1987 through December 1998. Of this total, 60 patients were determined to have a conductive olfactory loss. All patients were referred specifically because of a primary chemosensory complaint. The University of Pennsylvania Smell Identification Test (UPSIT; Sensonics, Inc., Haddon Heights, NJ) was administered in all cases. Results The most commonly diagnosed etiologies of olfactory loss were head injury (18%), upper respiratory infection (18%), and nasal or sinus disease (14%). Of the 60 patients with a conductive loss, only 30% complained of nasal obstruction, whereas 58% described a history of chronic sinusitis. Only 45% reported that their olfactory loss at times seemed to fluctuate in severity. Anterior rhinoscopy failed to diagnose pathology in 51% of cases, whereas nasal endoscopy missed the diagnosis in 9%. Systemic steroids elicited a temporary reversal of conductive olfactory loss in 83% of patients who received them, offering a useful diagnostic maneuver, whereas topical steroids did so in only 25%. Conclusions The etiology for olfactory loss can in many cases be difficult to determine, but it is important to establish prognosis and to predict response to therapy. Diagnosis requires a thorough history, appropriate chemosensory testing, and a physical examination that should include nasal endoscopy. A trial of systemic steroids may serve to verify that the loss is indeed conductive. [source]

Predictors of prognosis in patients with olfactory disturbance

ANNALS OF NEUROLOGY, Issue 2 2008
Brian London BA
Objective Although olfaction is often compromised by such factors as head trauma, viruses, and toxic agents, the olfactory epithelium and sectors of the olfactory bulb have the potential for regeneration. This study assessed the degree to which olfactory function changes over time in patients presenting to a university-based smell and taste center with complaints of olfactory dysfunction and the influences of etiology (eg, head trauma, upper respiratory infection), sex, age, smoking behavior, degree of initial dysfunction, and other factors on such change. Methods Well-validated odor identification tests were administered to 542 patients on 2 occasions separated from one another by 3 months to 24 years. Multivariable regression and ,2 analyses assessed the influences of the variables on the longitudinal changes in olfactory test scores. Results On average, smell test scores improved modestly over time. Patient age, severity of initial olfactory loss, and the duration of dysfunction at first testing were significant predictors of the amount of the change. Etiology, sex, time between the two test administrations, and initial smoking behavior were not significant predictors. The percentage of anosmic and microsmic patients exhibiting statistically significant change in function was 56.72 and 42.86%, respectively. However, only 11.31% of anosmic and 23.31% of microsmic patients regained normal age-related function over time. Interpretation Some recovery can be expected in a significant number of patients who experience smell loss. The amount of recovery depends on the degree of initial loss, age, and the duration of loss. Etiology, per se, is not a significant determinant of prognosis, in contrast with what is commonly believed. Ann Neurol 2007 [source]