Læknablaðið : fylgirit - 01.05.2002, Blaðsíða 28

Læknablaðið : fylgirit - 01.05.2002, Blaðsíða 28
ABSTRACTS / 33RD SNC & 2ND SCNN diagnosis unless the patient is female with tremor dominant disease. 3) anosmia in progressive supranuclear palsy and corticobasal degeneration is rare and should likewise provoke diagnostic review. 4) hyposmia is an early feature of IPD and AD and may precede motor and cognitive signs respectively. 5) subjects with anosmia and one ApoE-4 allele have an approximate 5-fold increased risk of later AD. 6) impaired smell sense is seen in some patients at 50% risk of parkinsonism 7) smell testing in HC and MND are not likely to be of clinical value. 8) biopsy of olfactory nasal neurons reveals non-specific changes in IPD and AD and at present will not aid diagnosis. 31 - Epilepsy and driving licence Brodtkorb E, Bráthen G, Helde G Dept. of Neurology, St. Olavs Hospital, Trondheim, Norway Objective: To find out how current regulations are applied in clinical practice in Norway. Material and methods: A questionnaire was sent to all 344 members of the Norwegian Neurological Association. Results: Fifty-six percent responded within 3 months. Most responders (152) worked in the field of clinical neurology and filled in the questionnaire. The majority (73%) did not regard reporting a “situation-related” seizure to the authorities as obligatory, but almost all of these responders (94%) would temporarily disallow driving. Sixty percent did not consider it obligatory to report the exclusive occurrence of simple partial seizures with retained cons- ciousness and motor control. A surprisingly large number (36%) would never recommend dispensation from the 1 year driving ban rule. Thirty-nine % generally used EEG in the assessment of driving fitness, whereas 17% rarely did so. Almost all (93%) would withdraw AEDs after longstanding freedom from seizures in patients allowed to drive, but only 44% recalled having done so within the past year. Most responders (75%) considered a necessity to drive to weigh against drug withdrawal. Only 50% instructed the patients not to drive in relation to AED withdrawal. Forty-five % did not consider seizure recurrence resulting from consented withdrawal to activate the obligation to report. Conclusion: There is poor consensus among neurologists about many aspects of driving and epilepsy, particularly in assessing the risk when stopping drug treatment. The regulations should be more specific and these issues should be focused during postgraduate teaching in clinical neurology. 32 - Could Multiple Sclerosis Be A Sexually Transmitted lllness? Hawkes C Oldchurch Hospital, Essex Neuroscience Centre, Romford, United Kingdom Many aspects of Multiple'Sclerosis (MS) are not explained by genetic mechanisms. Evidence supporting the theory includes: 1) age and gender pattern of MS is similar to many STI. 2) migration studies imply MS is acquired around puberty i.e. time of sexual debut 3) some MS clusters occur after influx of large numbers of males e.g. Faroes, Orkneys, Shetlands, Iceland. Space-time cluster analysis suggests MS is acquired in adolescence. 4) tropical spastic paraplegia, a known STI with low conjugal rate, has similarity to primary progressive MS. HTLV-1 infection is transmitted ineffi- ciently from husband to wife and children are infected only if mother has disease - not father alone. This asymmetry of risk is similar to MS 5) twin studies give conflicting, support to the genetic component of MS 6) reanalysis of data on oral contraceptive use in the US-Nurse Health Survey suggests increased risk of MS after 6 years’ use. 7) MS prevalence is high in permissive societies and low in strict or isolated cultures. Much of the world distribution of MS can be explained on the basis of sexual morality and racial separation. 8) during the sexual revolution of 1960s MS incidence increased particularly for females e.g. Denmark 9) conjugal studies from Sardinia but not Canada suggest elevated risk of transmission to spouse. 10) childhood MS may result from maternal infection or sexual abuse. It is proposed that: MS is an infection which is rarely symptomatic but widely present in Caucasians; it transmits to nai've populations especially female; adolescents are at particular risk from infected but not necessarily symptomatic males. 33 -A genome wide linkage disequilibrium screen in Scandi- navian multiple sclerosis patients shows association to chromosome regions at 1q (D1S1601) and 11q (D11S1986) Harbo HF*', Datta P*2, Spurkland A', Ryder LP2, Sawcer S3, Celius EG*, Modin H5, Ákesson E5, Sandberg-Wollheim M6, Myhr K-M7, Andersen O8, Hillert J5, Soerensen PS2, Svejgaard A2, Compston A3, Vartdal F', Oturai A2 'The National Hospital, Oslo, Norway; 2Copenhagen University Hospital, Rigs- hospitalet, Copenhagen, Denmark; ’Addenbrookes Hospital, Cambridge, United Kingdom; 4Ullevál UniversityHospital, Oslo, Norway; 5Huddinge University Hospital, Huddinge, Sweden; hLund University Hospital, Lund, Sweden; 7Hauke- land Hospital, Bergen, Norway; "Gothenburg University Hospital, Gothenburg, Sweden. *These authors contributed equally. Objective: This study attempts to identify gene regions encom- passing putative susceptibility genes in multiple sclerosis (MS) in the genetically homogenous Scandinavian population. Materials and methods: Linkage disequilibrium mapping of the genome was performed by analysing two pools of DNA from MS patients (n=199 and n=201) and two pools from healthy controls (both n=200). These pools which contain equal amounts of DNA from each individual were analysed in two separate screens using the same 6000 microsatellite markers evenly spaced throughout the genome. Differences in microsatellite allele image patterns bet- ween one MS pool and one control pool were identified in each screen. Furthermore, data from both screens (i.e. from 400 patients and 400 controls) were analysed together. A few selected markers which displayed significant deviations were reanalysed in both sets of pools. Results: A total of 4212 markers were successfully analysed, when data from both screens were analysed together. The HLA markers D6S2447 and D6S2444 are among the markers displaying associa- tion in this analysis. Fourteen markers appeared to be significantly associated with MS in both screens when analysed separately. Among these the D1S1601 marker at lq and the D11S1986 marker at llq were confirmed to be associated with MS in a repeat experiment. Conclusion: Two novel genetic regions (lq and llq) which seem to contribute to the genetic susceptibility to MS were identified. More susceptibility gene regions are expected to be identified when this study is included in a European meta-analysis in the Genetic Analysis of Multiple sclerosis in EuropeanS study (GAMES). 28 Læknabladið/Fylgirit 43 2002/88
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