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Results for “Olfaction Disorders”

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PubMed1997

Olfactory identification deficits in schizophrenia: correlation with duration of illness.

OBJECTIVE: The authors examined the relationship between deficits in olfactory identification and duration of illness in young and elderly patients with schizophrenia. METHOD: Olfactory identification performance of 38 patients with schizophrenia and 40 normal subjects was compared by using the University of Pennsylvania Smell Identification Test. RESULTS: The schizophrenic patients demonstrated olfactory deficits relative to the comparison group, and the elderly schizophrenic patients displayed a greater magnitude of olfactory deficit than the younger patients. Independent of normal aging effects and cognitive deficit, patients with schizophrenia showed a strong relationship between olfactory identification scores and duration of illness, which suggests that olfactory abilities decline progressively over the course of the disorder. CONCLUSIONS: In contrast to other neuropsychological measures that have been reported to be stable over the course of illness, olfactory identification abilities deteriorate steadily in patients with schizophrenia, even for those with relatively recent onset.

Adolescent↗
PubMed2005

Challenging conventional wisdom: the etiologic role of dopamine oxidative stress in Parkinson's disease.

Oxidative stress is well documented in Parkinson's disease (PD) and has been attributed to dopamine oxidative metabolism. However, evidence of oxidative stress is found in a variety of neurodegenerative disorders, suggesting that more general factors are responsible or that cytodestructive processes secondarily generate oxyradical products. Increasing evidence points away from dopamine metabolism as an important contributor to PD neurodegeneration. Predictions from the dopamine oxidative stress hypothesis of PD reveal multiple inconsistencies. Although the clinical and therapeutic importance of the nigrostriatal dopaminergic system is undeniable, PD neuropathology is much more widespread.

Brain Stem↗
PubMed1999

Investigation of a unique male and female sibship with Kallmann's syndrome and 46,XX gonadal dysgenesis with short stature.

A sibship is described where the brother and a sister both have Kallmann's syndrome (anosmia and deficiency of gonadotrophin releasing hormone) and the woman also has streak ovaries. Although there are several conditions that may occur with Kallmann's syndrome, there are no known reports of ovarian dysgenesis being associated with this disorder. Cytogenetic analysis showed no rearrangement or major deletions of the chromosomes. Linkage analysis using informative microsatellite markers predicts that a gene other than KAL1 (at Xp22.3) is implicated in the Kallmann's syndrome manifesting concurrently with ovarian dysgenesis found in this family.

Adult↗
PubMed1992

Audiological, vestibular and radiological abnormalities in Kallman's syndrome.

Kallman's syndrome is a multifaceted congenital disorder with predominantly endocrine abnormalities. We have characterized the associated mixed hearing loss and identified consistent radiological evidence of abnormal temporal bone anatomy. Abnormal labyrinthine morphology is accompanied by a complete absence of response to vestibular stimulation with caloric or rotational chair testing. The endocrine abnormalities are correctable and Kallman's syndrome is a diagnosis worthy of consideration when assessing children with congenital hearing loss.

Adult↗
PubMed2001

Stability of olfactory identification deficits in neuroleptic-naive patients with first-episode psychosis.

OBJECTIVE: Olfactory identification deficits and their relationship to negative symptoms in patients with schizophrenia were examined in patients with recent-onset psychosis, the majority of whom were neuroleptic naive. METHOD: Seventy-four inpatients with a first episode of psychosis (27 with schizophrenia or schizophreniform disorder, nine with schizoaffective disorder, 17 with affective psychoses, and 21 with other psychoses), 49 of whom had not received antipsychotic medication, were compared to 38 age- and gender-matched normal subjects. Olfactory identification ability was assessed with the University of Pennsylvania Smell Identification Test. Forty patients and 13 comparison subjects were reassessed at 6 months to examine whether olfactory deficits were specific to schizophrenia or schizophreniform disorder and were stable over time. RESULTS: At baseline, the patients had significant impairment in olfactory identification ability compared to the normal subjects. This difference persisted after controlling for gender, premorbid or current IQ, smoking history, cannabis use, or the effects of medication. Diagnostic subgroups did not differ in olfactory identification ability. The deficits remained stable at 6-month follow-up and were associated with negative symptoms at both time points. No relationship was found between olfactory identification ability and length of either untreated psychosis or illness prodrome. CONCLUSIONS: Impairment in olfactory identification ability was apparent from the outset of psychotic illness and was not specific to schizophrenia or schizophreniform disorder. No change in the degree of this deficit was found after patients were stabilized and had responded to medication. The deficit could not be explained by peripheral factors that might contribute to olfactory identification ability, suggesting that it reflects central mechanisms.

Adolescent↗
PubMed1988

The nature of unilateral neglect in the olfactory sensory system.

This study investigated two major theories of unilateral neglect utilizing the ipsilaterally innervated olfactory sense. The sensory theory states that unilateral neglect is due to a diminished or attenuated sensory input. The representational theory states that unilateral neglect is due to a disordered internal representation, which is not dependent on sensory input. Results of the study revealed that right hemisphere lesion patients with left unilateral neglect failed to respond to their left contralateral nostril on olfactory double simultaneous stimulation, consistent with the representational theory because the left nostril has no direct sensory input to the right hemisphere.

Attention↗
PubMed1992

Office management of taste and smell disorders.

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.

Ambulatory Care↗
PubMedDate not supplied

Calcification of the olfactory bulbs in three patients with hyposmia.

An estimated two million Americans suffer from chemosensory disorders. We present the clinical and imaging findings in three hyposmic patients with bilateral olfactory bulb calcification detected by CT. To our knowledge, these are the first cases of olfactory bulb calcification reported in the literature. A review of the literature concerning calcification of cranial nerves, olfactory neuritis, and the potential etiology and clinical significance of olfactory bulb calcification in our patients is presented.

Adult↗
PubMed1976

FSH and LH response to LHRF in Kallman's syndrome.

The olfacto-genital syndrome (Kallman's syndrome) is believed to be primarily an hypothalamic disorder resulting in hypogonadotropic hypogonadism or hypo-ovarianism and anosmia. The pituitary response in 2 patients was measured on dialy subcutaneous injections of 100 mug of LHRF. One of the patients was also studied in a similar fashion by administration of LHRF intravenously for 4 consecutive days. A greater response occurred with the subcutaneous route.

Adult↗
PubMed1987

Dysosmia caused by encephalitis in a dog.

A 1- to 2-year-old Beagle was referred for evaluation of a disorder of the sense of smell. The dog had suddenly lost the ability to find rabbits, even though it previously had won field trials. Clinical findings indicated mild encephalitis with some capability to respond to odoriferous stimuli. An unusual test of the sense of smell is described; results indicated some sense of smell, although behavioral response to the odor was inappropriate. It was suspected that canine distemper encephalitis may have been associated with the dysosmia.

Animals↗
PubMed2006

Euosmia: a rare form of parosmia.

The nature of qualitative olfactory disorders such as phantosmia and parosmia is a matter of debate. Parosmia and phantosmia mainly occur in combination with post-traumatic or post-infectious olfactory loss. Rare causes of these disorders such as brain tumors, side-effects of drugs, paraneoplastic syndromes, psychiatric disorders or intracerebral haemorrhage have been reported. Parosmias are distorted sensations of smell elicited by an odor, whereas phantosmias persist permanently or occur without the presence of an odor source. Phantosmias differ widely in terms of their nature. In contrast, parosmias always seem to be unpleasant. We report the case of a female with post-infectious hyposmia who reported a pleasant parosmia to selected odorants. We have called this rare clinical presentation euosmia.

Antioxidants↗
PubMed2004

[Testing the sense of smell using validated procedures].

There is a growing interest into the investigation of smell disorders in both research and clinical practice. For psychophysical ("subjective") investigations related to the sense of smell a variety of test kits are available, namely the various "Sniffin' Sticks" kits, the UPSIT (University of Pennsylvania Smell Identification Test) or the CCSIT (Cross-Cultural Smell Identification Test). Recording of olfactory evoked potentials (OEPs) and respiration olfactometry can be used for diagnosing smell dysfunctions in a more objective way.

Humans↗
PubMed1999

Efficacy of exogenous oral zinc in treatment of patients with carbonic anhydrase VI deficiency.

BACKGROUND: We previously described a disorder in 18 patients with decreased parotid saliva gustin/carbonic anhydrase (CA) VI secretion associated with loss of taste (hypogeusia) and smell (hyposmia) and distorted taste (dysgeusia) and smell (dysosmia). Because gustin/CAVI is a zinc-dependent enzyme we instituted a study of treatment with exogenous zinc to attempt to stimulate synthesis/secretion of gustin/CAVI and thereby attempt to correct the symptoms of this disorder. METHODS: Fourteen of the 18 patients with this disorder completed the study. They were treated with 100 mg of exogenous zinc daily for 4 to 6 months, in an open clinical trial. Both before and after treatment, measurements were obtained of parotid saliva gustin/CAVI, parotid saliva, serum and urine zinc, taste and smell function, and, in some patients, examination of circumvallate taste buds by electron microscopy. RESULTS: Treatment success was predicated upon significant increases in parotid saliva gustin/CAVI. This occurred in 10 of the 14 patients who were labeled responders; they also exhibited improvement in taste and smell acuity, a diminution in dysgeusia and dysosmia and increased zinc concentrations in parotid saliva, serum, and urine. Taste bud morphology returned to normal in each responder in whom it was measured. No increase in gustin/CAVI occurred in 4 patients who were labeled nonresponders; they exhibited no improvement in taste or smell acuity and no increases in parotid saliva zinc. However, serum and urine zinc increased to levels similar to those measured in the 10 responders. Two of 4 nonresponders reported diminution in dysgeusia and dysosmia. Taste bud morphology did not change from the abnormal state in the 1 nonresponder in whom it was measured. CONCLUSIONS: Zinc treatment is effective in patients in whom this trace metal increases synthesis/secretion of gustin/CAVI and ineffective in those in whom it does not. Increased gustin/CAVI in this disorder is probably associated with zinc stimulation of the gene responsible for the synthesis/secretion of gustin/CAVI. Among nonresponders, zinc was ineffective for several possible reasons, including resistance to zinc and possible sialylation of gustin/CAVI, which may render it functionally ineffective. Results suggest the hypothesis that gustin/CAVI is a trophic factor that promotes growth and development of taste buds through its action on taste bud stem cells.

Administration, Oral↗
PubMed2004

Taste and smell disturbance with the alpha-adrenoceptor agonist midodrine.

OBJECTIVE: To report a case of a disturbance of taste and smell associated with the alpha-adrenoceptor agonist midodrine. CASE SUMMARY: A 64-year-old white man with autonomic failure was started on midodrine 5 mg/day as treatment for orthostatic hypotension. After 3 months, the dose was increased to 12.5 mg/day, whereupon he noted a new onset of taste and smell disturbance. These symptoms made eating so unpleasant that the man greatly reduced his food intake, leading to significant weight loss. In addition, he experienced well-recognized adverse effects of midodrine, such as scalp pruritus, after the dose increase. All symptoms resolved with a dose reduction of midodrine (to 5 mg/day), and the patient increased his food intake, resulting in a return to his initial body weight. DISCUSSION: Midodrine is commonly associated with dose-dependent adverse effects, such as scalp pruritus and cutis anserina. Disorders of taste and smell have not been previously reported with midodrine, although it has been suggested that other sympathomimetic drugs may have effects on the olfactory threshold. Severe disorders of taste and smell may impact not only on a patient's quality of life, but also on their physical well-being, with significant weight loss being reported in this case. According to the Naranjo probability scale, this patient's taste and smell disturbance was probably associated with midodrine. CONCLUSIONS: The use of midodrine may be associated with taste and smell disturbance. This case suggests that such an association is likely to be dose dependent.

Adrenergic alpha-Antagonists↗
PubMed2000

Preclinical (premotor) Parkinson's disease.

Parkinson's disease (PD) is an idiopathic disease caused by necrosis and apoptosis of dopaminergic cells in the brainstem, which are probably induced by oxidative stress. Current therapeutic strategies comprise symptomatic and restorative treatment. Neuroprotective treatment, however, is close to becoming reality. As neuroprotective therapy may be of particular benefit to the preclinical and/or very early PD patients, identifying patients in the early stages of the disease is a priority. Both [18F]dopa positron emission tomography (PET) and [123I]beta-CIT single photon emission computed tomography (SPECT) imaging may be useful tools in diagnosing early (preclinical) PD. As screening the whole population for preclinical PD is not realistic, one has to select subjects with a high risk for this disease. Olfactory disturbances, subtle neurocognitive dysfunction, visuomotor control abnormalities and, to a lesser degree, mood and personality disorders, have lately been suggested to precede or accompany early clinical motor hallmarks of PD. In an epidemiological study, 500 first-degree relatives of PD patients were assessed for these signs and symptoms, and [123I]beta-CIT SPECT was performed on patients in the top 10% and the bottom 10% with regard to sense of smell. In this report, the study design and initial data from this ongoing study will be presented.

Humans↗
PubMed2001

[Disorders of taste and smell].

Disorders of taste and smell not only are uncomfortable to the person involved, e.g. because of an impaired hedonic and sensory experience of food or the continuous presence of a nasty taste, but can also result in loss of body weight and may have a negative influence on the quality of life. In this article both the physiology of chemosensory function and dysfunction of taste and smell are discussed as well as some clinical consequences and their treatment.

Ageusia↗
PubMed1982

Posttraumatic anosmia.

Two hundred twelve patients with traumatic anosmia had been seen at a clinic during the past 16 years. Sequelae of olfactory disorders were observed in 212 (4.2%) of the 5,000 cases seen that involved head and face injuries. The two most severe olfactory disorders were anosmia in 154 (72.6%) cases and hyposmia in 58 (27.4%) cases. The most frequent trauma site was the occipital region followed by the facial and frontal regions. Follow-up investigative results revealed olfactory improvement in eight (14%) of 56 cases. Six (10%) of the 56 cases prompted an aggravation of the olfactory problem. The fragmentation of olfactory nerve fibers appeared to be the most frequent cause of the anosmia after head injury.

Adolescent↗
PubMed2003

Reversible anosmia after amikacin therapy.

Olfactory disorders are among the rare adverse effects of antibiotic therapy. To date, olfactory losses or distortions have been reported after the use of doxycycline, amoxicillin, clarithromycin, roxithromycin, kanamycin sulfate, and streptomycin sulfate. We describe what we believe to be the first case of transient anosmia associated with the use of intravenous amikacin sulfate. The appearance of the disorder and its subsequent resolution were demonstrated by psychometric testing as well as by chemosensory evoked potentials. Based on the well-documented temporal course of the anosmia, there is a probable causal correlation between the administration of amikacin and the appearance of the olfactory disturbance. However, the exact pathogenesis of the anosmia is still a matter of conjecture.

Amikacin↗