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PubMed2001

Taste and smell dysfunction in patients receiving chemotherapy: a review of current knowledge.

Disorders of taste are prevalent in patients undergoing chemotherapy and often have a negative impact on quality of life and nutrition. We now present a review of the physiology of taste and smell and a discussion of the multiple causes of disturbances in these senses in patients undergoing standard- and high-dose chemotherapy. A better understanding of the complex and often multifactorial etiology of taste dysfunction should enable the clinician to institute measures to minimize the impact of these disturbing changes.

Antineoplastic Agents↗
PubMed1996

Differential effects of cocaine, alcohol, and nicotine dependence on olfactory evoked potentials.

Olfactory evoked potentials (OEP) were elicited by odorous and nonodorous stimuli in 50 adult subjects: 26 subjects with histories of either cocaine (n = 19) or alcohol (n = 7) dependence, 10 with histories of nicotine but no other drug dependence, 2 with clinical anosmia of peripheral origin, and 12 subjects without drug or olfactory disorders. The presentation of nonodorous stimuli (i.e. a nasal air puff) did not elicit OEP component amplitude and latency differences among the groups. However, the presentation of odorous stimuli elicited a significantly smaller P1 component in the cocaine-dependent and alcohol-dependent groups than in the normal control and nicotine-dependent groups. The P1 amplitude deficit in the cocaine-dependent group is consistent with case report data associating cocaine use with lesions of the peripheral and/or central olfactory apparatus.

Adult↗
PubMed1999

Increased olfactory sensitivity in first episode psychosis and the effect of neuroleptic treatment on olfactory sensitivity in schizophrenia.

Olfactory sensitivity to two odorants, isoamyl acetate and androstenone, was assessed in 19 male schizophrenic patients and 10 control subjects. Tests were performed during a drug-free period and 2-3 weeks after initiation of neuroleptic drug therapy. Olfactory sensitivity in schizophrenic patients was significantly impaired during the drug-free period and neuroleptic treatment further reduced olfactory sensitivity in these patients. The same olfactory tests were administered to 22 first-episode-psychosis patients, 12 first-episode-schizophrenia and 10 brief-psychotic-disorder patients, as well as to 20 age-matched control subjects. The first-episode-psychosis patients had significantly higher sensitivity to isoamyl acetate and to androstenone, but the incidence of anosmia to androstenone was not higher in the first episode patient group as compared to the control group. We conclude that olfactory dysfunction in schizophrenic patients, and possibly other forms of psychosis, is mainly due to long-term effects of commonly used neuroleptic drugs.

Acute Disease↗
PubMed1987

[Classification and definition of smell and taste disorders].

The smell and taste disorders are defined in terms due to two principles - the type and site of lesion. The quantitative dysosmias (anosmia, hyposmia, hyperosmia) correspond to the quantitative dysgeusias (ageusia, hypogeusia, hypergeusia) and the qualitative dysosmias (parosmia, pseudo-osmia, phantosmia, agnosmia) correspond to the qualitative dysgeusias (parageusia, pseudogeusia, phantogeusia, agnogeusia). Due to the site of lesion we can differentiate between respiratory, epithelial, combined, neural, and central dysosmias as well as epithelial, neural, and central dysgeusias. Typical examples are demonstrated, denying other classifications and terms as not precisely enough or negligible ones.

Ageusia↗
PubMed1999

Relationship between uninasal anatomy and uninasal olfactory ability.

OBJECTIVE: To examine the relationship between uninasal anatomy and olfactory ability. DESIGN: A stepwise analysis of variance was used to regress the logarithm of the percentage of correct responses on the Odorant Confusion Matrix (a measure of olfactory ability) against the logarithm of nasal volume measurements determined from computed tomographic scans. PARTICIPANTS: Nineteen patients with hyposmia whose olfactory losses were thought to be related to conductive disorders. RESULTS: After correcting for sex differences, a mathematical model was developed in which the volume of 6 regions of the nasal cavity, 6 first-order interactions, and 3 second-order interactions accounted for 97% of the variation in the measure of olfactory ability. CONCLUSIONS: Increases in the size of compartments of the nasal cavity around the olfactory cleft generally increase olfactory ability. Also, anatomical differences in the nasal cavities of men and women may account, in part, for sex differences in olfactory ability.

Adult↗
PubMed2002

Anti-inflammatory and surgical therapy of olfactory disorders related to sino-nasal disease.

Olfactory loss may be caused by mechanical obstruction or inflammation of the olfactory epithelium due to allergic/non-allergic rhinitis and chronic sinusitis with or without polyps. Treatment of olfactory loss related to sino-nasal disease is possible. Apart from surgical approaches and/or treatment with antibiotics, both systemic and topical steroids are effectively used in the therapy of olfactory loss related to sino-nasal disease. In most cases improvement of olfactory function appears to relate to the anti-inflammatory actions of the steroids used. While some details of therapeutic effect and dose regimen are not clear, systemic steroids are often helpful even in patients without nasal obstruction due to polyps or obvious inflammatory changes.

Anti-Bacterial Agents↗
PubMed2006

Nasal health in Down syndrome: a cross-sectional study.

OBJECTIVE: To investigate peripheral nasal pathology as a contributor to olfactory impairment in DS. STUDY DESIGN: Twenty DS and 16 non-DS subjects were recruited. Nasal history and symptoms were assessed by self-report or informant. Olfactory threshold, odor identification, and nasal endoscopy were assessed on each subject. RESULTS: DS subjects were impaired on olfactory threshold (P<0.0001) and odor identification (P<0.001). Although DS subjects tended toward upper-respiratory infections, sleep-disordered breathing, and nasal itching, differences were not significant (P=0.07, 0.06, and 0.058, respectively). There were no significant differences on self-reported nasal history or symptoms. Endoscopy showed equivalent health in DS and control subjects. CONCLUSION: This DS population shows olfactory impairment. However, nasal health is comparable in DS subjects and controls. Nasal dysfunction is unlikely to contribute to olfactory impairment in DS. SIGNIFICANCE: Olfactory deficits in DS appear to be secondary to central, rather than rhinologic, pathology. EBM RATING: B-2b.

Adolescent↗
PubMed1999

Decreased parotid saliva gustin/carbonic anhydrase VI secretion: an enzyme disorder manifested by gustatory and olfactory dysfunction.

BACKGROUND: Taste and smell dysfunction has been reported to occur in patients with a variety of clinical problems. We wanted to investigate a specific group of patients in whom taste and smell dysfunction occurred putatively related to a specific biochemical abnormality in a salivary growth factor [gustin/carbonic anhydrase (CA) VI] considered responsible for maintenance of taste bud function. METHODS: Eighteen patients developed loss and/or distortion of taste and smell after an acute influenza-type illness. They were evaluated clinically, by psychophysical tests of taste and smell function, by measurement of parotid salivary gustin/CAVI by a radioimmunoassay and by measurement of serum, urine, and salivary zinc. Biopsies of circumvallate papillae were obtained in 6 patients and examined by transmission electron microscopy. Similar studies were performed in 55 asymptomatic volunteers with biopsies of circumvallate papillae performed in 4. RESULTS: Taste and smell acuity were impaired in patients compared with healthy volunteers and parotid gustin/CAVI, salivary, and serum zinc concentrations were lower in patients than in healthy volunteers. Taste buds in circumvallate papillae of patients exhibited severe vacuolization, cellular degeneration, and absence of dense extracellular material. CONCLUSIONS: These results describe a clinical disorder formulated as a syndrome of hyposmia (decreased smell acuity), hypogeusia (decreased taste acuity), dysosmia (distorted smell function), dysgeusia (distorted taste function), and decreased secretion of parotid saliva gustin/CAVI with associated pathological changes in taste bud anatomy. Because gustin/CAVI is found in humans only in parotid saliva and has been associated with taste bud growth and development these results suggest that inhibition of synthesis of gustin/CAVI is associated with development of taste bud abnormalities and thereby loss of taste function.

Adult↗
PubMed1998

Olfactory function in restless legs syndrome.

Restless leg syndrome (RLS) is usually idiopathic but may occur in patients with Parkinson's disease (PD). Both respond to dopaminergic medications. Whether these disorders share a common pathophysiology is unclear. Because PD is associated with a loss of olfactory function, we compared the olfactory function of patients with RLS with control and PD patients. Using the University of Pennsylvania Smell Identification Test (UPSIT), olfactory function was found to be normal in patients with idiopathic RLS and significantly reduced in patients with PD. This suggests that the pathophysiology of RLS differs from PD, and that RLS likely is not a "forme fruste" or a preclinical sign of PD.

Aged↗
PubMed2006

Olfactory disorders following upper respiratory tract infections.

Postviral olfactory disorders usually occur after an upper respiratory tract infection (URTI) associated with a common cold or influenza. With a prevalence between 11 and 40% they are among the common causes of olfactory disorders. Women are more often affected than men and post-URTI disorders usually occur between the fourth and eighth decade of life. The exact location of the damage in post-URTI is not yet known even though from biopsies a direct damage of the olfactory receptor cells is very likely. Nevertheless, central mechanisms cannot completely be ruled out. The diagnosis is made according to the history, clinical examination and olfactory testing. Affected patients usually recall the acute URTI and a close temporal connection should be present to establish the diagnosis. Spontaneous recovery might occur within 2 years. So far, no effective therapy exists even though specific olfactory training might be promising.

Humans↗
PubMed2006

Effects of ageing on smell and taste.

Disorders of taste and smell commonly present diagnostic dilemmas to the medical profession. This may be secondary to the lack of knowledge and understanding of these conditions. There seems to be a low level of interest in the disorders, when compared with disruption of the other senses such as sight and hearing. Nevertheless, impairment of these senses are common and may be life threatening, especially when they involve the elderly patient. The aetiology of the conditions is widespread, and extend beyond the content of this article. This article will relate only to how the ageing process may contribute to sensory dysfunction. It will focus on how the ageing process changes the normal anatomy and physiology of the senses, how this effects the person's quality of life, and the current management of these conditions.

Aged↗
PubMed1999

Is Parkinson's disease a primary olfactory disorder?

It has been known for over 30 years that olfactory function is disordered in idiopathic Parkinson's disease (IPD). The severity and partial specificity of anosmia was not realized until recently, with the advent of more detailed analysis and sophisticated measurement. The olfactory vector hypothesis suggests that the causative agent for IPD enters the brain via the nasal route, but the reason for olfactory dysfunction may be more subtle. Evidence for olfactory disturbance is reviewed from pathological, psychological, neurophysiological and genetic stand-points. It is proposed that the initial causative event in IPD may start in the rhinencephalon (olfactory brain) prior to damage in the basal ganglia.

Aging↗
PubMed2005

[The genetics of hypogonadotropic hypogonadism in the male].

Underlying causes of hypogonadotropic hypogonadism are acquired or congenital disorders of the hypothalamus or pituitary (e.g. pituitary adenoma, craniopharyngioma, prior radiotherapy, trauma, severe general diseases, extreme stress, genetic mutations). In addition to a comprehensive history and physical examination, the diagnostic work-up includes measurement of testosterone, LH and FSH, with the aim of differentiating between primary and secondary hypogonadism. Where indicated, investigation of pituitary function, the use of imaging procedures, possibly an olfactory test, a GnRH stimulation test or genetic analyses may be added. Depending upon the indication, treatment is effected with testosterone, GnRH or gonadotropines.

Adolescent↗
PubMedDate not supplied

CT of the brain in taste and smell dysfunction.

Three hundred fifty-four patients with taste and/or smell disorders were evaluated with computed tomography (CT). The largest group was characterized by head trauma (27%), followed by idiopathic causes (26%), postinfluenza-like hyposmia and hypogeusia (15%), and congenital etiologies (14%). Hyposmia and hypogeusia occurred concomitantly in 21%-45%, the percentage varying according to etiologic subgroup. CT abnormalities were found in 108 (31%) of the 354 patients. The most frequent pathologies were frontal encephalomalacia, subfrontal atrophy in the region of the olfactory bulbs, and anterior temporal lobe atrophy. These changes were found alone or in tandem. Some CT findings suggest common cerebral taste and smell centers and common neural pathways and association centers.

Ageusia↗
PubMed1991

Juvenile onset diabetes mellitus, central diabetes insipidus and optic atrophy (Wolfram syndrome)--neurological findings and prognostic implications.

The authors report on one case of Wolfram syndrome, a rare condition, which is characterized by juvenile onset diabetes mellitus, diabetes insipidus, optic atrophy and sensorineural deafness. The findings of this 13-year follow-up show that this patient developed typical neurological complications of long-standing diabetes mellitus as in the common type 1 variant. Moreover, some peculiar signs occurred such as anosmia, ophthalmoplegia interna, and central nystagmus. Since Wolfram syndrome is probably part of a more generalized neurodegenerative disorder, long-term prognosis will depend both upon the severity of chronic diabetic complications and upon the rapidity, by which degeneration of cerebellar, pontine and brain stem structures appear. Prognosis of the cardinal clinical signs is such that optic atrophy, though usually quite rapid in the beginning, generally does not lead to complete blindness. Sensorineural hearing loss progresses very slowly so that deafness might be expected exceptionally only. The hearing deficit in classical diabetics, however, is of retrocochlear origin. Therefore, in Wolfram syndrome, a combined inner-ear and retrocochlear hearing loss may occur.

Adolescent↗
PubMed2002

Rare cause for short stature--Kallmann's syndrome--a case report.

Kallmann's syndrome is a neuroendocrine disorder, characterized by hypogonadotropic hypogonadism with hyposmia. We report a 27 year old male who presented with short stature and pain in the lumbar region. On detailed evaluation he had growth retardation, features of hypothalamic hypogonadism as evidenced by endocrimological tests and anosmia since birth. He had co-existent caries spine T10,T11 causing pain in the lumbar region-MRI brain showed normal olfactory pathway while the response to nasal stimulants was markedly attenuated. We present this case for its very care occurrence in the eastern part of the world and the typical feature being normal MRI brain with functional defect of the olfactory pathway.

Adolescent↗
PubMed2000

[The problem of anosmia].

Olfactory problems have deleterious consequences to systemic health, nutritional status and quality of life. Olfactory disorders are not as rare as generally assumed. Chemosensory dysfunction is most often secondary to one of only a few causes: nasal/sinus disease, viral infection, toxic chemical exposure, head trauma, as well as medication-related and idiopathic conditions. Many olfactory disorders are secondary to a wide variety of diseases, e.g. Alzheimer's disease. The patient's history may provide clues to these and other problems (e.g. toxin exposure, congenital dysosmia). Therapy should not begin until a standardized test has been established the impairment of the sense of smell. Treatment of the underlying diseases may restore chemosensory function. The only truly reversible cause is inflammation, which is confirmed when smell returns after administration of corticosteroids. Reference is made to the need for adequate psychologic guidance of patients with chemosensorial problems. If restoration of their sense of smell is unlikely, patients should be educated to ensure safety in regard to such dangers as gas leaks, smoke, and spoiled foods.

Diagnosis, Differential↗
PubMed2000

Assessment of smell and taste in patients with allergic rhinitis.

We examined the senses of smell and taste in 240 patients with verified hypersensitivity reactions of the respiratory tract. Olfactometry was performed according to Elsberg and Levy's method and followed by electrogustometry. The examinations revealed that the incidence of smell and taste disorders in patients with allergic rhinitis is 21.4% and 31.2%, respectively. No significant relationships between smell and taste dysfunction were found. We evaluated statistically positive correlations between the olfactory and gustatory thresholds compared with 78 qualitative and quantitative factors assessed in the study. There was a statistically significant relationship between the olfactory thresholds and levels of eosinophils in blood and in nasal discharge. acid reaction of the nasal mucosa, coexisting nasal polyps and X-ray changes in the ethmoid sinuses. There was a positive influence of pharmacotherapy as well as specific desensitization and surgery on the impairment of the sense of smell in allergic rhinitis.

Adolescent↗