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PubMed2001

Olfactory identification is impaired in clinic-based patients with vascular dementia and senile dementia of Alzheimer type.

AIMS: It is now well established that there are abnormalities in the sense of smell in patients suffering from Alzheimer's disease (AD). They have both raised olfactory thresholds and impaired odour identification. The situation in vascular dementia is unclear. We used the University of Pennsylvania Smell Identification Test (UPSIT), a 40-item, forced choice, cued, 'scratch-and- sniff' test, to examine olfactory identification in vascular dementia and to determine whether it would differentiate the disorder from AD and normal elderly. METHODS: We investigated three matched subject groups: 13 people having a Cambridge Examination for Mental Disorders in the Elderly (CAMDEX) diagnosis of definite senile dementia of Alzheimer type, 13 having a CAMDEX diagnosis of definite vascular dementia and 13 non-cognitively impaired controls. The subjects were then tested with the UPSIT in their own home by an independent blind researcher to see if the test could distinguish the different diagnostic groups in this setting. RESULTS: The median UPSIT score was 30 (out of a maximum of 40) for controls, 12 for the vascular group and 15 for the AD group. The difference was significant (p = 0.05) between both demented groups and the normal controls. Similarly there was a significant difference in the UPSIT score between the AD group and controls (p = 0.001) and between the vascular dementia group and controls (p = 0.001), but there was no significant difference between the AD group and the vascular dementia group. The UPSIT score correlated strongly with the degree of cognitive impairment as measured by the CAMCOG (r(s) = 0.683, p = 0.01) CONCLUSIONS: Patients with vascular dementia had a similar degree of olfactory impairment to those with AD. The UPSIT successfully differentiated between dementia patients and normal elderly British subjects tested in their own homes. The UPSIT did not differentiate between those with AD and vascular dementia.

Aged↗
PubMed2004

[Diffuse nasal polyposis and comorbidity: study of 65 cases treated by endonasal endoscopic surgery].

INTRODUCTION: Nasal polyposis is an inflammatory disorder which pathophysiology remains unclear. Several clinical associations are described according to co-morbidities (asthma, allergy...). OBJECTIVE: To analyze the efficacy of a standardized surgical procedure in 65 patients with nasal polyposis, enrolled in three categories according to the presence of co-morbidities (asthma, allergy...). STUDY DESIGN: Open prospective study of non-randomized cases from a single institution. METHODS: An inception cohort of 65 consecutive patients with nasal polyposis observed from January 1994 to December 1997. The same surgical procedure was performed in all patients. At the end of the study, an evaluation was performed to collect all the information concerning nasal and bronchial symptoms, asthma conditions, and medical treatment. RESULTS: 60 patients have finally completed the study. Polyposis was isolated in 29 patients, asthma was present in 21 patients, associated with aspirin intolerance in 10 patients (ASA Triad). Nasal obstruction and olfactory dysfunction was improved in 37 and 42 patients, respectively (p<0.0001), without a statistical significance between all groups. After surgery, topical treatment with steroids and local recurrences were more frequently observed in the ASA Triad group without statistical significance. CONCLUSION: Nasal polyposis appears to be less controlled in the ASA Triad group compared to isolated nasal polyposis, although such conclusion is not statistically significant.

Adolescent↗
PubMed1994

Drug-induced taste and smell disorders. Incidence, mechanisms and management related primarily to treatment of sensory receptor dysfunction.

Drugs in every major pharmacological category can impair both taste and smell function and do so more commonly than presently appreciated. Impairment usually affects sensory function at a molecular level, causing 2 major behavioural changes--loss of acuity (i.e. hypogeusia and hyposmia) and/or distortion of function (i.e. dysgeusia and dysosmia). These changes can impair appetite, food intake, cause significant lifestyle changes and may require discontinuation of drug administration. Loss of acuity occurs primarily by drug inactivation of receptor function through inhibition of tastant/odorant receptor: (i) binding; (ii) Gs protein function; (iii) inositol trisphosphate function; (iv) channel (Ca++,Na++) activity; (v) other receptor inhibiting effects; or (vi) some combination of these effects. Distortions occur primarily by a drug inducing abnormal persistence of receptor activity (i.e. normal receptor inactivation does not occur) or through failure to activate: (i) various receptor kinases; (ii) Gi protein function; (iii) cytochrome P450 enzymes; or other effects which usually (iv) turn off receptor function; (v) inactivate tastant/odorant receptor binding; or (vi) some combination of these effects. Termination of drug therapy is commonly associated with termination of taste/smell dysfunction, but occasionally effects persist and require specific therapy to alleviate symptoms. Treatment primarily requires restoration of normal sensory receptor growth, development and/or function. Treatment which restores sensory acuity requires correction of steps initiating receptor and other pathology and includes zinc, theophylline, magnesium and fluoride. Treatment which inhibits sensory distortions requires reactivation of biochemical inhibition at the receptor or inactivation of inappropriate stimulus receptor binding and/or correction of other steps initiating pathology including dopaminergic antagonists, gamma-aminobutyric acid (GABA)-ergic agonists, calcium channel blockers and some orally active local anaesthetic, antiarrhythmic drugs.

Anti-Infective Agents↗
PubMed2002

Clinical assessment of retronasal olfactory function.

OBJECTIVES: To develop a test kit for the simple assessment of retronasal olfactory function and to compare orthonasal and retronasal olfactory function in healthy subjects and patients with olfactory disorders. DESIGN AND PATIENTS: We tested 230 individuals with normosmia, hyposmia, and anosmia using grocery-available powders. Initially, 30 different substances were investigated. Subjects identified each substance using a list with 4 verbal items (forced choice). After preliminary experiments, 20 items were selected according to the degree to which they were identified by normosmic and anosmic subjects. Orthonasal olfactory function was assessed psychophysically using "sniffin' sticks," which includes tests for odor identification, discrimination, and butanol odor thresholds. In addition, anosmia was confirmed electrophysiologically by means of olfactory-evoked potentials. RESULTS: In healthy subjects, there was a test-retest reliability correlation of r(27) = 0.76 for retronasal olfactory function, which is similar to other odor identification tests. Retronasal testing in normosmic subjects allowed for the discrimination of sex-related differences, with women scoring higher than men (P =.007), and the identification of a slight decrease with age (r(120) = -0.20; P =.03). Orthonasal and retronasal identification of odors was found to correlate (r(86) = 0.78; P<.001). Retronasal testing allowed for the discrimination between normosmia, hyposmia, and anosmia (P<.001). In addition, retronasal performance of anosmic patients appeared to improve with duration of anosmia (P =.03). No difference was found between patients with anosmia of different origin. CONCLUSION: Results of the present investigation indicate that the assessment of retronasal olfactory function is possible using oral stimulus presentation.

Adolescent↗
PubMed2005

Permanent deficits in serotonergic functioning of olfactory bulbectomized rats: an in vivo microdialysis study.

BACKGROUND: Bilateral removal of the olfactory bulbs (OBX) in rats results in a complex constellation of behavioral, neurochemical, neuroendocrine, and neuroimmune alterations, many of which are also reported in patients with major depressive disorder (MDD). Drawing on clinical findings, there has been considerable interest in the role of serotonin in the mechanism of action of OBX. However, to date, there has been no report of direct measurement of serotonergic functioning of bulbectomized animals using microdialysis. The present study describes the effects of olfactory bulbectomy on functioning of the serotonergic system. METHODS: In vivo microdialysis was performed in conscious rats that underwent OBX or sham surgery. Alterations in the functioning of the serotonergic system were assessed by administration of fluvoxamine, fenfluramine, and 3-hydroxybenzylhydrazine (NSD-1015). Animals were also repeatedly tested in an open field. RESULTS: Bilateral removal of the olfactory bulbs decreased basal extracellular levels by decreasing the releasable pool of serotonin (5-HT) in the basolateral amygdala 2 weeks after surgery and in the dorsal hippocampus 2 weeks and 5 months after surgery. Olfactory bulbectomized animals showed a lower rate of 5-HT synthesis under basal conditions. However, the capacity of the system to synthesize 5-HT was not affected. Olfactory bulbectomized rats were hyperactive in the open field. This hyperactivity remained after successive testing, indicating permanent behavioral changes. CONCLUSIONS: This microdialysis study shows that OBX has profound and long-lasting effects on serotonergic functioning and on activity levels and is therefore considered an intriguing and promising animal model for affective processes in the brain.

Animals↗
PubMed2002

[Hearing disorders, dysosmia and dysgensia in patients undergoing irradiation for head and neck cancer].

UNLABELLED: The study included 30 patients who underwent irradiation for head and neck cancer in the Regional Oncology Center. Cobalt 60 was used to irradiate facial--cervical area bilaterally and parotid glands partially. Before and after the irradiation, audiometric test, examination for osmaesthesia and sense of taste were performed. MATERIAL AND METHOD: All patients underwent laryngologic examination. The sense of smell was estimated by using quantitative method (smell threshold test) and qualitative method (identificational test). Butyl alcohol with serial watery dilution from 0, 002 to 4 were used in the threshold tests. The identificational test relies on recognition of seven commonly known smells. The examination of taste was performed using the quantitative and qualitative methods. The assessment of taste threshold was made with electrogustometer. The organ of hearing was examined with tone audiometry. RESULTS: Audiometric examination of the patients before irradiation revealed sensorineural hearing loss in 14 patients while 6 patients proved mixed hearing loss. After the irradiation, 50% of the patients showed further hearing loss in the range of 5-30 dB. After the irradiation, the percentage of patients with anosmia was elevated to 20%. Normosmic patients were not observed. The quantitative method of the sense of taste before and after irradiation did not show a significant difference. Only 10% of patients who underwent irradiation recognized 4 basic tastes, 30% of them did not show the sense of taste in the qualitative method. CONCLUSION: 1. After the irradiation, 50% of the patients developed further hearing loss. 2. Olfactometric examination of the patients after laryngectomy showed different degree of hyposmia. 3. The quantitative method of smell performed in patients before and after irradiation showed no significant differences. 4. Distinct deterioration of taste recognition was observed in the qualitative method compared to the examination before irradiation.

Adult↗
PubMed2006

Olfactory deficit in idiopathic rapid eye movements sleep behavior disorder.

INTRODUCTION: REM sleep behavior disorder (RBD) is a parasomnia characterized by a loss of atonia and an increased phasic muscle activity during REM sleep. Idiopathic RBD frequently herald an alpha-synucleinopathy, including such as Parkinson's disease (PD) and dementia with Lewy Body (DLB). Pathological changes in the anterior olfactory nucleus and olfactory loss occur very early in the course of PD and DLB. The aim of the study was to assess olfactory function in a large group of idiopathic RBD patients. METHODS: Fifty-four consecutive polysomnographically-confirmed iRBD patients (44 men, 10 women; mean age: 69.2+/-8.3 years; mean Unified Parkinson's Disease Rating Scale Part III (UPDRS-III) score: 4.9+/-4.3) and 54 age and gender-matched control subjects underwent the Brief University of Pennsylvania Smell Identification Test (B-SIT). RESULTS: A marked olfactory impairment was observed in the RBD group (mean B-SIT score: 7.1+/-2.5 versus 9.4+/-1.8; p < 0.0001), with 33 (61.1%) RBD patients versus 9 (16.6%) controls showing abnormal olfactory function (p < 0.0001). No correlation was found between the degree of olfactory loss and either duration of RBD symptoms or UPDRS-III score. Deficit in recognize paint thinner odorant showed the highest positive predictive value (0.95) for identifying idiopathic RBD. CONCLUSIONS: The olfactory deficit found in most idiopathic RBD patients shares similarities with that described in PD and may be a sign of a widespread neurodegenerative process. Its detection may help in identifying subjects at higher risk of developing an alpha-synucleinopathy-mediated neurodegeneration.

Aged↗
PubMed2006

Extrapyramidal symptoms in Wilson's disease are associated with olfactory dysfunction.

Wilson's disease is a rare autosomal recessive disorder characterized by the accumulation of copper, mainly in the liver and the brain. As copper accumulation in the brain leads to disturbances in basal ganglia function, neurological-type patients typically present with hypo- and hyperkinetic extrapyramidal symptoms, with Parkinsonism being very common. Although there are numerous reports on olfactory deficits in primary neurodegenerative disorders, olfactory function has not been investigated in metabolic disorders presenting with extrapyramidal features. Twenty-four patients with Wilson's disease participated in the investigation. All patients were treated pharmacologically. They comprised patients with liver disease alone (including mild enzyme elevation in asymptomatic individuals; n = 11) and/or neurological symptoms (n = 13) at the time of testing. Twenty-one patients underwent both [18F]fluoro-2-deoxy-D-glucose positron emission tomography ([18F]FDG-PET) and magnetic resonance imaging (MRI). The severity of extrapyramidal symptoms was judged using a clinical score system ranging from 0 (no symptoms) to 3 (severe symptoms). In all patients, psychophysical testing was performed using the Sniffin' Sticks, which involved tests for odor threshold, discrimination, and identification. Results from the present study revealed that Wilson's disease patients with neurological symptoms show a significant olfactory dysfunction compared to hepatic-type patients. Individuals who are more severely neurologically affected also present with a more pronounced olfactory deficit. Of interest, there was no significant effect of long-term treatment with penicillamine on olfactory function. Olfactory function did not correlate significantly with the presence of MRI visible lesions in the basal ganglia or with any regional glucose metabolism as measured by [18]F-FDG-PET. In conclusion, these findings indicate that the underlying pathological alterations with degeneration in the basal ganglia and neuronal loss in association with a marked increase of the copper content in this brain region play a role in the olfactory deficit.

Adult↗
PubMed2006

Novel fibroblast growth factor receptor 1 mutations in patients with congenital hypogonadotropic hypogonadism with and without anosmia.

CONTEXT: Kallmann syndrome is a clinically and genetically heterogeneous disorder. To date, loss-of-function mutations in the genes encoding anosmin-1 (KAL1) and fibroblast growth factor receptor 1 (FGFR1) have been described in the X-linked and autosomal dominant forms of this syndrome, respectively. OBJECTIVE: The objective was to investigate genetic defects in the KAL1 and FGFR1 genes in patients with congenital isolated hypogonadotropic hypogonadism (IHH). PATIENTS: Eighty patients (71 males and nine females) with IHH were studied, of which 30 were familial. Forty-six of them had olfactory abnormalities. METHODS: The coding regions of both KAL1 and FGFR1 genes were amplified and automatically sequenced. The KAL1 mutations were investigated only in patients with olfactory abnormalities, whereas FGFR1 was studied in the entire group. RESULTS: Two novel KAL1 mutations, an intragenic deletion of exons 3-6 and a splicing mutation IVS7 + 1G>A, were identified in two of 46 patients with Kallmann syndrome. Eight novel heterozygous FGFR1 mutations (G48S, L245P, R250W, A343V, P366L, K618fsX654, P722S, and V795I) were identified in nine of 80 patients with IHH. Eight of them had olfactory abnormalities. Interestingly, the G48S mutation was identified in a normosmic IHH patient. Two unrelated females, who carried FGFR1 mutations, had anosmia and normal reproductive function. CONCLUSION: We identified novel mutations in KAL1 and FGFR1 genes in IHH patients. FGFR1 mutations were identified in 17% of the patients with olfactory abnormalities and in one of 34 normosmic IHH patients. In addition, isolated anosmia was identified in two unrelated females as a partial phenotypic manifestation of FGFR1 defects.

Adolescent↗
PubMed2006

Clinical significance of results from olfactory testing.

BACKGROUND: Although widely used in healthy subjects and patients with olfactory loss, the significance of changes of scores from validated olfactory tests is unknown. AIM AND METHODS: The aim of the present study was to relate the self-assigned changes of olfactory function in terms of "better," "unchanged," and "worse" in patients with smell disorders with the results from olfactory testing by means of a validated test set. Olfactory function of 83 anosmic or hyposmic patients (40 women, 43 men; age 12-84 yr) was tested on two occasions (mean interval 136 days, minimum 7 days, maximum 6.7 yr). Olfactory function was assessed using a validated technique ("Sniffin' Sticks"). This test consists of three subtests, one for odor threshold (T), odor discrimination (D), and odor identification (I), with possible results ranging up to 16 points each. From the sum of the results from the three subtests a composite "TDI" score was obtained. RESULTS: Forty-four patients indicated an improvement of olfactory function, whereas 39 patients reported no change. No subject reported deterioration of olfactory sensitivity. Subjects assigned to group BETTER had higher TDI scores in the second olfactory tests than subjects assigned to the group UNCHANGED, both in absolute terms and as compared with the first olfactory test (effect "test occasion" by "self-assessed improvement," P < .001). There was no significant difference between groups with respect to age and sex (P = .99 and .84, respectively). Logistic regression showed that more than 60% of the subjects reported an improvement of olfactory sensitivity when the TDI score increased by 5.5 points. CONCLUSION: We show that there is a statistically significant relation between measured and perceived improvement of olfactory function in patients who first presented with the diagnosis of anosmia or hyposmia. The results indicate that improved olfactory function in patients with olfactory deficiency is perceived as such in everyday life and is quantitatively related to an improvement in the composite TDI score of the "Sniffin' Sticks" olfactory test battery. This is the basis for the application of a specific therapy for olfactory loss because of a possible gain in quality of life for the patients.

Adolescent↗
PubMed1996

[Magnetic resonance imaging of the olfactory pathways in Kallmann de Morsier syndrome].

INTRODUCTION: Kallmann syndrome is a disease clinically characterized by the association of hypogonadotrophic hypogonadism and anosmia or hyposmia. Most cases have been recorded among men. It is a genetic disorder with a specific gene location on the X chromosome. The cells that normally express luteinizing hormone-releasing hormone or LHRH fail to migrate the olfactory placode to the forebrain. The lateral projections of the olfactory placode also fail to induce development of the olfactory bulbs and tracts. MATERIAL AND METHODS: The aim of this study was to compare the MRI appearance of the olfactory sulci, the olfactory bulbs and frontal lobe between groups. The first reference group was composed of 20 subjects and the second group of 18 patients suffering from Kallmann syndrome. For all studies we used a 1.5 T magnet system (Signa GE). We performed two sagittal and coronal T1-weighted sequences in spin echo (TR = 600 ms, TE = 12 ms) with interleaved 3 mm slices and a 14 cm field of view. RESULTS: In the first group, the two olfactory bulbs were always seen on coronal slices just behind the crista galli measuring 2 to 3.2 mm transversally. On sagittal slices, in 60% of the cases two bulbs were seen (3 mm laterally of the pituitary stalk) and in the other 40% only one bulb was seen. The length of the bulb has been measured between 6 and 11 mm. We noticed a plat frontal lobe in 85% of the cases. In the second group the olfactory bulbs were never visible among the 18 patients suffering from Kallmann syndrome. The hypoplasic sulci were hardly visible and their size was less or equal to 1 cm and the frontal lobe was triangular in 80% of the cases. One patient had hypoplasia of corpus callosum. CONCLUSION: MRI is helpful tool to demonstrate abnormalities of the olfactory system which are always present among patients suffering from Kallmann syndrome. MRI can also show, at the same time, a possible associated brain abnormality.

Adult↗
PubMed2006

Mutations in fibroblast growth factor receptor 1 cause Kallmann syndrome with a wide spectrum of reproductive phenotypes.

BACKGROUND: Kallmann's syndrome (KS) is a clinically and genetically heterogeneous disorder consisting of idiopathic hypogonadotropic hypogonadism (IHH) and anosmia. Mutations in KAL1 causing the X-linked form of KS have been identified in 10% of all KS patients and consistently result in a severe reproductive phenotype. KAL1 gene encodes for anosmin-1, a key protein involved in olfactory and GnRH neuronal migration through a putative interaction with FGFR1. Heterozygous mutations in the FGFR1 gene accompanied by a high frequency of cleft palate and other facial dysmorphisms were recently identified in 8% of a large KS cohort, yet the reproductive phenotype of KS patients harboring FGFR1 mutations has not been described. RESULTS: One hundred and fifty probands with KS (130 males and 20 females) were studied to determine the frequency and distribution of FGFR1 mutations and their detailed reproductive phenotypes. Fifteen heterozygous mutations in unrelated probands were identified. Twelve missense mutations (p.R78C, p.V102I, p.D224H, p.G237D, p.R254Q, p.V273M, p.E274G, p.Y339C, p.S346C, p.I538V, p.G703S and p.G703R) were distributed among the first, second and third immunoglobulin-like domains (D1-D3), as well as the tyrosine kinase domain (TKD). The mutations Y339C and S346C are located in exon 8B and code for the isoform FGFR1c. Additionally, two nonsense mutations (p.T585X and p.R622X) were documented in the TKD of the protein. A wide spectrum of reproductive function was observed among KS probands including: (1) a severe phenotype demonstrated by microphallus, cryptorchidism, no pubertal development, undetectable serum gonadotropins and low serum testosterone (T) and inhibin B; (2) partial pubertal development; (3) the fertile eunuch variant of IHH with normal testicular size and active spermatogenesis with a reversal of HH after T therapy. In addition, we found an even wider spectrum of reproductive function within pedigrees carrying an FGFR1 mutation ranging from IHH to delayed puberty to normal reproductive function (anosmia only or asymptomatic carriers). These observations strongly suggest a role for other genes that modify the phenotype of FGFR1 mutations. CONCLUSION: KS patients and family members carrying an FGFR1 mutation present a broad spectrum of pubertal development in contrast to the almost uniform severe clinical phenotype described in KS subjects with a KAL1 mutation. Additionally, this report implicates the isoform FGFR1c in the pathogenesis of KS.

Adolescent↗
PubMed2004

Combination of 'idiopathic' REM sleep behaviour disorder and olfactory dysfunction as possible indicator for alpha-synucleinopathy demonstrated by dopamine transporter FP-CIT-SPECT.

REM sleep behaviour disorder (RBD) and olfactory dysfunction are common and very early features of alpha-synucleinopathies, in particular Parkinson's disease. To investigate the hypothesis that these two clinical features in combination are an indicator of evolving alpha-synucleinopathy, olfactory function was assessed in RBD. We studied 30 patients (18 male, 12 female; mean age 48 +/- 14 years, range 19-78 years) with clinical (idiopathic, n = 6; symptomatic, n = 13, mostly associated with narcolepsy) or subclinical (n = 11, associated with narcolepsy) RBD according to standard criteria and 30 age- and gender-matched healthy control subjects using standardized 'Sniffin' Sticks'. RBD patients had a significantly higher olfactory threshold (P = 0.0001), lower discrimination score (P = 0.003), and lower identification score (P = 0.001). Compared with normative data, 97% of the RBD patients had a pathologically increased olfactory threshold, 63% an impaired odour discrimination score, and 63% a decreased identification score. On neurological examination, signs of parkinsonism were newly found in five patients with clinical RBD (not associated with narcolepsy), who usually had a long history of 'idiopathic' RBD. Four of the five patients fulfilled the UK Brain Bank criteria for the clinical diagnosis of Parkinson's disease. The underlying nigrostriatal degeneration of clinical Parkinson's disease was confirmed by I-123-FP-CIT SPECT in one patient and early nigrostriatal degeneration was identified by SPECT in a further two patients with 'idiopathic' clinical RBD out of 11 RBD patients who agreed to undergo SPECT studies. Our study shows that RBD patients have a profound impairment of olfactory function. Five patients with clinical RBD not associated with narcolepsy had clinical or imaging signs of nigrostriatal degeneration. This new clinical finding correlates with the neuropathological staging of Parkinson's disease (stages 1-3) as proposed by Braak. In stage 1, the anterior olfactory nucleus or the olfactory bulb is affected (along with the dorsal motor nucleus of the glossopharyngeal and vagal nerves). In stage 2, additional lesions consistently remain confined to the medulla oblongata and pontine tegmentum, which are critical areas for RBD. Midbrain lesions are found only in stage 3, in particular degeneration of dopaminergic neurons in the substantia nigra pars compacta. Thus, 'idiopathic' RBD patients with olfactory impairment might present with stage 2 preclinical alpha-synucleinopathy. Since narcoleptic patients are not known to have an increased risk of developing parkinsonism, the pathophysiology and clinical relevance of hyposmia in RBD/narcolepsy patients requires further research.

Adult↗
PubMed1975

Moebius syndrome in Kallmann syndrome.

A girl born with congenital paresis of cranial nerves III, IV, and VII (Moeblus syndrome) subsequently developed a progressive peripheral neuropathy. There was suggestive evidence of a familial neuropathy with autosomal dominant inheritance in three family members. The patient also had hypogonadotrophic hypogonadism and anosmia (Kallmann syndrome).

Abducens Nerve↗
PubMed1989

Post-traumatic anosmia. Ultrastructural correlates.

Five patients suffering post-traumatic anosmia were studied at the University of Colorado Health Sciences Center, Denver. Each patient underwent psychophysical testing, clinical evaluation, and olfactory biopsy. The biopsy specimens were examined ultrastructurally and were found to vary from normal tissues. The overall appearance of the olfactory epithelium in the post-traumatic patient is disrupted and the receptor cells are distorted. Large numbers of axons are located near the basement membrane and can often be found in bundles throughout the epithelium, extending even to the mucosal surface. Olfactory cilia are rarely seen in epithelia obtained from post-traumatic patients. Bald olfactory vesicles, often containing basal bodies, are frequently observed. We postulate that in these cases, the olfactory epithelium regenerates following head trauma and the receptor cells attempt to send axons centrally. However, the cribriform plate has undergone fibrotic healing and the axons are unable to penetrate it and make contact with olfactory bulb neurons.

Adult↗
PubMed1989

Persistent high-altitude headache and aguesia without anosmia.

High-altitude headache and taste dysfunction are usually cured within a few months by descent to sea level. We studied a patient who had persistent bitemporal throbbing headache with the associated findings of high-altitude headache syndrome 15 years after a compression chamber accident. He also had loss of taste without loss of smell since the incident.

Adult↗
PubMed1997

Olfactory dysfunction in patients with head trauma.

BACKGROUND: The ability to smell is commonly altered by head trauma (HT). However, the nature, prevalence, prognosis, and etiology of such alterations are poorly understood. OBJECTIVES: To quantitatively determine the degree of olfactory function in patients with HT-related chemosensory complaints and to examine the influences of age, sex, HT severity, time since HT, and other variables on such function. Also, to use quantitative magnetic resonance imaging (MRI) to establish whether and to what degree damage to the olfactory bulbs and tracts, frontal lobes, and temporal lobes occurs. PATIENTS AND METHODS: Two hundred sixty-eight patients with HT from the University of Pennsylvania Smell and Taste Center, Philadelphia, were administered a quantitative odor identification test, a depression inventory, and a medical history questionnaire; 66 were retested after individual test-retest periods ranging from 1 month to 13 years. The volume of olfactory-related brain structures was determined in 15 patients and 15 controls using MRI. RESULTS: One hundred seventy-nine patients (66.8%) had anosmia, 55 (20.5%) had microsmia, and 34 (12.7%) had normosmia. Frontal impacts produced less dysfunction than back or side impacts. Of the 66 retested patients, 24 (36%) improved slightly, 30 (45%) had no change, and 12 (18%) worsened; only 3 patients, none of whom initially had anosmia, regained normal olfactory function. Trauma severity was related to olfactory test scores in patients with microsmia. Parosmia prevalence decreased from 41.1% to 15.4% over an 8-year posttrauma period. Olfactory bulb and tract volumes of male, but not female, patients with HT were greatly reduced relative to volumes of controls. CONCLUSIONS: Patients complaining of HT-related olfactory dysfunction typically have anosmia and rarely regain normal olfactory ability, parosmia prevalence decreases over time in such patients, and damage to olfaction-related brain structures can be observed in most such patients using an appropriate MRI protocol.

Adult↗