1 1 Symposium Chemosensory Receptors Satellite DEVELOPMENT ...

105 Poster Chemosensory Coding and ClinicalCHEMOSENSORY MEASUREMENT IN ESSENTIAL TREMORNoyce A. 1 , Shah M. 1 , Deeb J. 1 , Findley L.J. 1 , Hawkes C.H. 1 1 Smell &Taste Research Unit, Essex Neuroscience Centre, London, UnitedKingdomObjective: Tremulous Parkinson´s disease (PD) may be confusedwith Essential Tremor (ET). Smell and taste are abnormal in early stagePD but probably not at any stage in ET. We wished to determinewhether chemosensory testing is normal in ET and if so this might helpdistinguish it from PD. Methods: Three procedures were used: (1)University of Pennsylvania Smell Identification test (UPSIT); (2) SmellThreshold Test (Sensonics Inc.) using phenylethylalcohol in (i) 45healthy controls, mean age 49y (17-93 y), and (ii) 50 ET patients meanage 62y (17-82y); (3) taste threshold measurement with Rion TR-06electrogustometer applied to (a) tip of tongue (chorda tympani; CT) or(b) base of tongue over the most lateral vallate papilla (VP; IX). Allparticipants scored at least 27/30 on the Mini-Mental Status Test.Results: There were no significant differences in any control vs. ETcomparisons as follows (t-test, p > 0.05): (1) Mean UPSIT scoresbetween controls and ET (32.8/40 vs. 32.3/40. (2) mean control smellthresholds: -6.7 vol/vol compared to -6.3 vol/vol for ET. (3) Mean tastethreshold: controls CT: 11.2 dB; VP: 13.5 dB. ET CT: 13.5 dB and VP14.6 dB. Conclusions: Smell sense and taste threshold are normal in ETcompared to healthy controls. This information may be of value indistinguishing ET from tremulous PD patients.106 Poster Chemosensory Coding and ClinicalNASAL MUCOSA IN PATIENTS WITH PARKINSON´SDISEASEWitt M. 1 , Gudziol V. 1 , Haehner A. 1 , Reichmann H. 2 , Hummel T. 11 Otorhinolaryngology, University of Technology, Dresden, Med. Sch.,Dresden, Germany; 2 Neurology, University of Technology, Dresden,Med. Sch., Dresden, GermanyIdiopathic Parkinson´s disease (PD) is a neurodegenerative disorderinvolving several neuronal systems. The pathognomonic formation ofneuronal inclusion bodies (Lewis bodies) usually starts in the medullaoblongata and the anterior olfactory nucleus, before motor symptomsbecome evident. Thus, an impaired olfactory function, when tested, mayconstitute one of the earliest symptoms of PD. However, it is stillunknown to what degree eventual changes of the olfactory epitheliummay contribute to dysmosmia in these patients. The aim of this pilotstudy was to investigate the morphology of the olfactory epithelium insubjects diagnosed with PD since several years. Methods: Biopsies ofseven individuals diagnosed with PD (mean age: 76 years) as well asfour anosmic controls (mean age: 53 years) were taken from differentsites of the nasal mucosa. For immunohistochemistry, antibodies againstolfactory marker protein (OMP), neurotubulin, protein gene product 9.5(PGP 9.5) were applied to paraffin embedded tissue sections. Further,mRNA for OMP was isolated from olfactory and respiratory mucosausing RT-PCR. Results and conclusions: Preliminaryimmunohistochemical findings showed irregular areas of olfactoryepithelium positive for PGP 9.5 and neurotubulin, but mostly negativefor OMP. However, mRNA for OMP was found in mucosa of theolfactory cleft as well as in the respiratory mucosa. There were noapparent differences to the olfactory epithelium of patients withidiopathic anosmia. With due caution in this small number ofindividuals tested, we conclude from these data that PD-relatedolfactory impairment is not immediately associated with specificchanges in the olfactory epithelium.107 Poster Chemosensory Coding and ClinicalIDIOPATHIC PARKINSON'S DISEASE IS A PRIMARYOLFACTORY DISORDERHawkes C.H. 1 1 Essex Neuroscience Centre, Romford, United KingdomIn 1999 I proposed that idiopathic parkinson´s disease (IPD) was aprimary olfactory disorder and that the pathogen gained access to thebrain through the nose. Since then there have been further supportivedevelopments: (1) confirmation of alpha-synuclein deposits in theolfactory bulb in nearly all cases (2) observations by Braak et al (2003)that the earliest changes are in the olfactory bulb and dorsal medullarynuclei of IX and X. (3) virtual absence of mitral cells - the first relay inthe olfactory path (4) demonstration of hyposmia in at least 80%patients measured by identification score or olfactory event relatedpotentials (5) correlation in some studies of smell tests and disability (6)association of impaired dopamine transporter uptake or abnormal s.nigra transcranial Doppler in about one third cases with idiopathicanosmia (7) prospective community-based studies from the Honolulu-Asian Aging study show predictive value of olfactory testing for IPD onthe basis of clinical and pathological examination. It is proposed that inIPD, olfactory impairment is the earliest change along with damage incranial nuclei IX and X; that these alterations predate the motorcomponent by several years and that the likely agent is a neurotropicvirus which accesses the olfactory nerves and medulla through thenasopharynx.108 Poster Chemosensory Coding and ClinicalCLARIFYING THE NATURE OF THE OLFACTORYIMPAIRMENT FOUND IN PARKINSON´S DISEASEBailie J.M. 1 , Rybalsky K.A. 1 , Hastings L. 2 , Revilla F.J. 3 , GestelandR.C. 4 , Frank R.A. 5 1 Psychology, University of Cincinnati, Cincinnati,OH; 2 Osmic Enterprises, Inc., Cincinnati, OH; 3 Neurology, Universityof Cincinnati, Cincinnati, OH; 4 Cell Biology, Neurobiology & Anatomy,University of Cincinnati, Cincinnati, OH; 5 Psychology/Office of VicePresident for Research and Advance, University of Cincinnati,Cincinnati, OHOver the last 30 years investigators have shown that patients withParkinson´s disease (PD) perform poorly on odor identification tests.However, the relative contributions of sensory and cognitiveimpairment to this decline in performance are not well understood. Thisstudy investigated the possible role of a decrease in olfactory signalstrength on odor identification in PD patients. Patients were assessedusing a nine-odor olfactory identification test (OIT) and the SniffMagnitude Test (SMT). The SMT is a reliable measure of olfactoryfunction that examines sniffing behavior to quantify olfactory abilities.The tests were modified to incorporate odorants that could beadministered in increasing concentrations under the hypothesis thatpatient performance on both measures would improve as odors areintensified. Repeated measures ANOVA revealed that patients with PDcorrectly identified more high concentration (M = 5.36, SD = 2.28) thanlow concentration odorants (M = 4.09, SD=2.20) on the OIT, F(1,21) =13.77, p < 0.001. Similarly, higher odor intensities produced more sniffsuppression when taking the SMT, F(1,21) = 13.69, p < 0.001. Theresults suggest that a portion of the olfactory identification deficit inpatients with PD is the result of decreased olfactory signal strength. Thefindings are discussed in terms of the theoretical understanding ofolfactory functioning in PD and stimulus selection in olfactory tests.This Project was supported by NIH grant DC004139, R. Gesteland, PI27