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At least 19 recordsLinked to original sources
PubMed2006

Intranasal zinc and anosmia: the zinc-induced anosmia syndrome.

OBJECTIVE: Commercial preparations of intranasal zinc gluconate gel are marketed as a remedy for the common cold. However, intranasal zinc has been reported as a cause of anosmia in humans and animals. Seventeen patients presenting with anosmia after the use of intranasal zinc gluconate are described. METHODS: The authors conducted a retrospective case series of patients presenting to a nasal dysfunction clinic and conducted complete history and physical examination on all patients, including nasal endoscopy. All patients underwent detailed odor threshold and identification testing. RESULTS: Threshold and identification testing revealed impaired olfaction in all patients. Inflammatory and traumatic causes of anosmia were excluded based on history, physical examination, and imaging. All patients diagnosed with zinc-induced anosmia or hyposmia reported sniffing deeply when applying the gel. This was followed by an immediate sensation of burning lasting minutes to hours. Loss of sense of smell was then perceived within 48 hours. Seven of 17 patients never developed symptoms of an upper respiratory infection. CONCLUSIONS: The zinc-induced anosmia syndrome, characterized by squirt, sniff, burn, and anosmia, occurs after the exposure of olfactory epithelium to zinc cation. It can be distinguished from postviral anosmia based on history.

Administration, Intranasal↗
PubMed1986

[Anosmia or hyposmia after long-term oral administration of tegafur--improved anosmia].

Seventeen patients who manifested anosmia or hyposmia after long-oral administration of Tegafur (FT-207) in postoperative chemotherapy for cancer were followed up. Anosmia improved in 9 of 17 patients (52.9%), and the recovery period was between 3 and 42 months after the manifestation, and between 1 and 35 months after discontinuation of FT-207. Rhinoscopy and radiography revealed no abnormal findings in the nasal septum, rima oflactoria, concha nasalis media, sinus ethmoidales, etc. As it took a long time to recover from these signs and symptoms, they were presumed to be due to reversible neurological anosmia or hyposmia.

Aged↗
PubMed2005

Anosmia is very common in the Lewy body variant of Alzheimer's disease.

BACKGROUND: Olfactory abnormalities are reported in Alzheimer's disease and Parkinson's disease. Anosmia appears to be common in dementia with Lewy bodies but not in pure Alzheimer's disease. OBJECTIVE: To determine whether anosmia improves discrimination between the Lewy body variant (LBV) of Alzheimer's disease and "pure" Alzheimer's disease. METHODS: 106 cases of necropsy confirmed pure Alzheimer's disease (n = 89) or LBV (n = 17) were reviewed. All had received butanol odour threshold testing. Anosmia was defined as a score < or = 1.0 on a 0-9 point scale. Logistic regression analysis was used to model potential predictors (for example, parkinsonism, smoking, hallucinations) of neuropathological diagnosis and anosmia. RESULTS: LBV cases had an increased prevalence of anosmia (65%) compared with Alzheimer's disease (23%; odds ratio (OR) = 6.3, p = 0.00045), or normal elderly people (6.7%). Within the dementia cases, the negative predictive value (92%) and specificity (78%) of anosmia were both good; sensitivity for detecting LBV was 65%, but the positive predictive value (PPV) was only 35%. Logistic regression models showed anosmia (OR = 5.4, p = 0.005) and visual hallucinations (OR = 7.3, p = 0.007) were strong independent predictors of Lewy body pathology. When anosmia was added as a core feature to consensus diagnostic criteria for probable Lewy body dementia, five additional cases of LBV were detected (29% increased sensitivity), but with four additional false positives (1% increased discrimination, 4% decreased specificity, 33% decreased PPV). CONCLUSIONS: Anosmia is very common in LBV. Adding anosmia as a core feature improved sensitivity for detecting LBV, but did not improve discrimination between Alzheimer's disease and LBV owing to a concomitant increase in false positives.

1-Butanol↗
PubMed2000

[Psychoosmology at the turn of the millennium: From "nasal reflex neurosis" to the modern psychosomatics of sudden anosmia].

This article offers a psychosomatic description of the medical disorder known as sudden anosmia, an illness which previously has been unjustly neglected. The authors present an operational definition of sudden anosmia and describe the illness's multi-facetted symptomatology. Sudden anosmia is influenced by a number of etiological factors. In this regard, it can be seen that not only classical medical factors such as neurophysiology and anatomy prove to be relevant, but also various characteristics of the fields of personality psychology, family psychology, and behavioral psychology as well. The modern diagnostics of sudden anosmia are conceived interdisciplinarily and span from olfactory measurements to rhino-psychological testing. The treatment of patients suffering from sudden anosmia is based on a multi-staged treatment concept. This concept equally considers both medical and psychological approaches, whereby behavior psychological treatment will be given particular importance in discussion of the latter. Processes for evaluation and quality assurance to monitor the methods of diagnostics and therapy provided for persons afflicted by sudden anosmia are still in their beginning stages.

Humans↗
PubMed1975

Effects of pinealectomy, anosmia and blinding alone or in combination on gonadotropin secretion and pituitary and target gland weight in intact and castrated male rats.

Pinealectomy had inconstant effects on serum gonadotropins when blood samples were taken during the day, however late nocturanal titers of both FSH and LH tended to decline and this decline tended to be reversed by pinealectomy. Either anosmia or blinding elevated nocturnal FSH and had a tendency to elevate nocturnal LH titers- effects which were only inconstantly modified by pinealectomy. Blinding plus anosmia lowered both daytime and nocturnal FSH titers; the lowering of nocturnal levels was reversed by pinealectomy. There was a less pronounced lowering of nocturnal LH titers in these doubly-operated animals and again this was partially reversed by pinealectomy. These changes in gonadotropin titers probably accounted at least in part for the testicular atrophy seen in the doubly-operated animals and its reversal by pinealectomy. Following castration, plasma gonadotropin titers rose in all groups and the final level of FSH attained was highest in the pinealectomized animals. Similarly, final levels of FSH and LH were further increased in castrates by blinding, anosmia or blinding plus anosmia, but these changes were not consistently modified by pinealectomy. At sacrifice of the castrates, pituitary FSH and LH concentrations were not modified by pinealectomy, however they were elevated by anosmia or by the double sensory-deprivation. The atrophy of the seminal vesicles induced by castration was partially prevented by pinealectomy, which suggests that the pineal also exerts a direct inhibitory effect on this accessory organ. Alterations in anterior and posterior pituitary weight were also observed.

Animals↗
PubMed1997

Posttraumatic anosmia in craniofacial trauma.

Although the clinical implications of anosmia can be significant, posttraumatic anosmia is generally given relatively little attention in the clinical setting. Patients who sustain craniofacial trauma are most at risk. The incidence of posttraumatic anosmia varies according to the severity of injury and has an overall estimated incidence of 7%. Factors that increase the risk of developing anosmia include anterior skull base fractures, bilateral subfrontal lobe injury, dural lacerations, and cerebrospinal fluid leakage. Recovery of function has been estimated to be approximately 10%. Time of recovery, if it occurs, varies between 8 weeks and 2 years. Presented herein are the clinical, radiographic, pathophysiologic, and anatomic substrata of posttraumatic anosmia.

Adolescent↗
PubMed1987

Steroid-dependent anosmia.

In steroid-dependent anosmia (nasal polyps, inhalant allergy, anosmia), high doses of steroids will temporarily restore the sense of smell, a diagnostic test. Appropriate surgery can then be carried out, followed by low-dose, long-term steroid therapy to maintain the sense of smell. Olfactory biopsy specimens taken during the course of evaluation and treatment show electron-optically normal olfactory receptors, meaning that the probable pathogenesis of the sensory deficit is an obstruction, mechanical and possibly biochemical. Two cases of steroid-dependent anosmia are presented to detail a fully reversible anosmia using state-of-the-art techniques.

Adrenal Cortex Hormones↗
PubMed1982

Anosmia and play fighting behavior in prepubescent male and female rats.

Prepubescent male and female rats were paired after intranasal treatment with isotonic zinc sulfate or saline solutions to determine the influence of peripheral anosmia upon play fighting behavior. In Experiment 1, male isolate residents pinned intruders significantly more often than intruders pinned residents but anosmia treatment had no influence on pinning behavior. In Experiment 2, males and females differed significantly in all major categories of play fighting but anosmia treatment had no influence on play fighting of either males or females. In Experiment 3, male groups matched for play fighting behavior prior to intranasal zinc or saline treatment were paired with like-treated males. All males in all pairings engaged in play behavior but anosmic males played less than controls. Evidently, intranasal zinc treatment depresses play behavior only when both members of a pair are anosmic. Play behavior is more markedly affected by resident-intruder status and by gender than by peripheral anosmia.

Aggression↗
PubMed1996

Anosmia and chronic sinus disease.

Chronic sinus disease associated with progressive mucosal disease is often a cause for anosmia. Despite aggressive allergic, medical, and surgical intervention, long-term relief of anosmia has been difficult to document. Fifty patients sought treatment for subjective anosmia and symptoms of progressive sinusitis and underwent endoscopic sinus surgery. After surgery 52% maintained significant improvement in smell by subjective measures that correlated with objective olfactory University of Pennsylvania Small Identification test ("UPSIT") results. Of the remaining patients, some had intermittent improvement, but most remained hyposmic or anosmic despite clinically well-healed ethmoid surgical beds. Of the preoperative and postoperative historical, clinical, and radiological data analyzed, severity of the presenting sinus disease (defined as stage II In the Kennedy staging criteria or disease extending beyond the ethmoids on preoperative computed tomography scan) and persistent mucosal disease in the surgical bed are associated with persistent anosmia (p = 0.005).

Adult↗
PubMed1996

[Pathophysiology of post-traumatic anosmia].

BACKGROUND: Head injury is one of the most common causes of olfactory disturbances. The incidence of posttraumatic anosmia depending from the severity of the injury lies between 5% and over 80%. METHODS: Clinical assessments were performed in 26 cases with posttraumatic anosmia using subjective olfactometric tests. Additionally, morphological studies were performed in 26 other patients, who died between 36 hours and six weeks after head injuries. RESULTS: Frontal basal injuries as well as minor occipital blows are capable of causing complete olfactory loss. About one-third of all patients were not aware of their chemosensory deficits, especially when associated neurological deficits occurred. Moreover, the studies show that: 1: The vulnerability of the fila olfactoria varies extremely and depends on unknown, highly individual parameters. 2: Trauma can induce local hemorrhage within the olfactory tracts and bulbs without any other intracranial lesions. 3: An intracerebral contusion is often misunderstood as the direct substrate of a posttraumatic anosmia. However, in a number of cases it is merely the sign of a strong injuring force, potentially capable of injuring the fila or the olfactory bulbus. CONCLUSIONS: The findings indicate that the pathophysiology and biomechanics of posttraumatic anosmia should be the subject of critical discussion.

Accidents, Traffic↗
PubMed2002

Sensory detection of glutaraldehyde in drinking water-emergence of sensitivity and specific anosmia.

A study of 30 young adults (15 males, 15 females), screened to have normal olfaction, measured detection of the flavor of glutaraldehyde, a biocide that could occur in disinfected potable water. Over the range of interest, up to 100 p.p.m., flavor derived from olfactory stimulation. Higher concentrations would cause oral irritation. Fourteen subjects failed to detect the glutaraldehyde in the first of four sessions of testing. Eight of the 14 (seven males, one female) continued to exhibit the anosmia throughout testing. The other six (one male, five females) began to detect the material in session two and exhibited increasing sensitivity over sessions two to four. Their average sensitivity never reached that of the 16 subjects who evinced no anosmia and who also improved their performance over sessions. The combined group of 22 could detect 17 p.p.m. Less thorough testing would have yielded much higher values. Specific anosmia for this dialdehyde has precedence in anosmia for various monoaldehydes, most notably isobutyraldehyde. The positive influence of experience with a material on detection has been found previously, most intriguingly by Wysocki and colleagues, who showed that experience could differentially induce sensitivity to the odorant androstenone and suggested that the phenomenon might occur for other compounds. Glutaraldehyde appears to be one, perhaps of many.

Adolescent↗
PubMed2005

Anosmia in association with occupational use of a waterproof coating chemical.

A case of acute permanent anosmia is described in a renovation worker during exposure to a waterproof coating chemical. The chemical consisted of several substances of which four (acetone, acrylates, butyl acetate and carbon disulfide) has been previously reported to induce hyposmia or anosmia in workers. Other aetiologies were clinically excluded but a large arachnoidea cyst in the frontal part of the left temporobasal fossa with possible compression of the left entorhinal cortex. The toxic aetiology of anosmia is supported by the acute onset and the temporal relationship with occupational exposure. The silent cyst as the cause of anosmia is improbable, but it may have had some contributory role. Our case illustrates both the challenges when clinically examining patients with work-related olfactory impairment and the importance of multi-disciplinary approach to such patients.

Adult↗
PubMed2001

Quantitative PET findings in patients with posttraumatic anosmia.

OBJECTIVE: To investigate quantitative positron emission tomography (PET) findings, particularly from orbitofrontal cortex, in patients with posttraumatic anosmia. SETTING: Neuropsychology outpatient clinic and university brain imaging center. SUBJECTS: Eleven patients with head injury resulting in severe anosmia and 11 controls matched for age. All 11 head-injured patients had their head injuries at least 2 years before involvement in the study. MEASURES: Regional cerebral glucose metabolism was measured with PET. RESULTS: Quantitative evaluation of PET findings for anosmic patients as a group showed orbitofrontal hypometabolism compared with controls. Decreased activity was also noted in mesial temporal lobe. Activity in subcortical white matter was essentially identical between groups. CONCLUSIONS: Findings strongly suggest that posttraumatic anosmia is closely associated with hypometabolism in the orbitofrontal cortex and the medial prefrontal cortex. The results also underscore the importance of posttraumatic anosmia as a clinical sign of orbitofrontal damage, as has been shown previously with neuroSPECT (single photon emission computed tomography).

Adult↗
PubMed1998

Interferon-induced anosmia in a patient with chronic hepatitis C.

We report a patient with chronic active hepatitis C developing acute anosmia during interferon (IFN) therapy. On July 31, he began receiving 6 MU of IFN-alpha daily. On September 26, he failed to smell gas leaking from a gas cooker, so IFN therapy was discontinued. He showed no reaction on a standard olfactory acuity test. As the patient had borderline diabetes, the association of anosmia with impaired glucose tolerance cannot completely be excluded, but his anosmia was probably induced by IFN therapy, since anosmia developed 10 days after the initiation of the IFN therapy, without any deterioration of his glucose intolerance.

Antiviral Agents↗