Swiss Archives of Neurology, Psychiatry and Psychotherapy

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Die 10 Aufgaben (Ten Missions) der European Federation of Neurological Societies (EFNS)

by EMH Swiss Medical Publishers Ltd.

Swiss Arch. Neurol. Psychiatry Psychother. 2000, 151(4), 175-180; https://doi.org/10.4414/sanp.2000.01172 - 1 Jan 2000

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Abstract

Es ist notwendig, dass alle Erkrankungen des Gehirns, des Rückenmarks, des peripheren Nervensystems und der Muskeln mit Ausnahme der psychiatrischen Erkrankungen von einem Neurologen diagnostiziert, behandelt und versorgt werden, ganz gleich, ob sie nun akut, chronisch, kompliziert oder selten sind [...] Full article

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Kurz-Info zur SNG-Standespolitik

by Hans Rudolf Stöckli

Swiss Arch. Neurol. Psychiatry Psychother. 2000, 151(4), 173-174; https://doi.org/10.4414/sanp.2000.01171 - 1 Jan 2000

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Abstract

Am 29. März 2000 fand für uns Neurologen die «Experten-Runde 2000» statt, die lediglich dazu diente, gravierende Fehler innerhalb des bereits erstellten Leistungskatalogs auszumerzen [...] Full article

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Zur Geschichte der Schweizerischen Neurologischen Gesellschaft

by Marco Mumenthaler

Swiss Arch. Neurol. Psychiatry Psychother. 2000, 151(4), 168-172; https://doi.org/10.4414/sanp.2000.01170 - 1 Jan 2000

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Abstract

Die nachfolgenden Ausführungen stützen sich unter anderem auf die sehr sorgfältige monographische Darlegung der Geschichte der Schweizerischen Neurologie durch M. Minkowski im Jahr 1958 [1] [...] Full article

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Diagnostic et traitement de la sclérose en plaques

by Myriam Schluep and A. Rossetti

Swiss Arch. Neurol. Psychiatry Psychother. 2000, 151(4), 166-167; https://doi.org/10.4414/sanp.2000.01167 - 1 Jan 2000

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Abstract

Le 2^c «State of the Art Symposium» s’est tenu le 22 janvier 2000 à Berne sous la présidence du Professeur Jürg Kesselring de la Clinique de Réhabilitation de Valens [...] Full article

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Therapeutische Probleme beim fortgeschrittenen idiopathischen Parkinson-Syndrom

by Peter Fuhr

Swiss Arch. Neurol. Psychiatry Psychother. 2000, 151(4), 159-165; https://doi.org/10.4414/sanp.2000.01168 - 1 Jan 2000

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Abstract

The treatment of Parkinson’s disease is seemingly simple in its early phase. Levodopa t.i.d. eliminates symptoms and signs completely or almost. Although there is growing evidence that a thorough evaluation of the therapeutic options early in the course of the disease diminishes problems [...] Read more.

The treatment of Parkinson’s disease is seemingly simple in its early phase. Levodopa t.i.d. eliminates symptoms and signs completely or almost. Although there is growing evidence that a thorough evaluation of the therapeutic options early in the course of the disease diminishes problems later on, consultations with the neurologist are often postponed until the situation has become complex. The problems arising at that time can preliminarily be classified in motor and non-motor ones on the one hand, and in disease-related and pharmacologically induced ones on the other hand. The review focuses on non-invasive solutions that are feasible in an out-patient setting. Full article

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Aktuelle Aspekte zur Diagnostik und Therapie der Multisystematrophie

by Gregor K. Wenning, Z. Puschban, K. Seppi and C. Scherfler

Swiss Arch. Neurol. Psychiatry Psychother. 2000, 151(4), 150-158; https://doi.org/10.4414/sanp.2000.01166 - 1 Jan 2000

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Abstract

First described in 1969 by Graham and Oppenheimer, multiple system atrophy (MSA) is increasingly recognised as distinctive neurodegenerative disease. Clinically, it is characterised by autonomic failure, parkinsonism, cerebellar ataxia and pyramidal signs in any combination. The motor disorder is dominated by parkinsonism in [...] Read more.

First described in 1969 by Graham and Oppenheimer, multiple system atrophy (MSA) is increasingly recognised as distinctive neurodegenerative disease. Clinically, it is characterised by autonomic failure, parkinsonism, cerebellar ataxia and pyramidal signs in any combination. The motor disorder is dominated by parkinsonism in 80% of patients (MSA-P) or by cerebellar ataxia in the remaining 20% (MSA-C). Although the clinical syndrome is often highly characteristic in advanced stages clinicopathological and epidemiological data indicate that multiple system atrophy is underdiagnosed in movement disorders clinics as well as in the general population. It remains to be determined whether the recent consensus diagnostic criteria for multiple system atrophy (Gilman et al. 1998) will improve patient recognition. Physical manoeuvres and/or drug therapy may considerably improve orthostatic dysfunction and urogenital complaints, unfortunately these measures are not always implemented. The motor disorder of multiple system atrophy cannot be treated effectively in most patients although transient relief may be obtained by L-Dopa. The latter should therefore be administered to all MSA patients with parkinsonian features. Alternative therapeutic strategies such as neuroprotection and neurotransplantation are currently being explored in experimental multiple system atrophy models. Full article

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Genetik des Parkinson-Syndroms

by Thomas Gasser

Swiss Arch. Neurol. Psychiatry Psychother. 2000, 151(4), 146-149; https://doi.org/10.4414/sanp.2000.01165 - 1 Jan 2000

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Abstract

Over the last few years several genes for monogenically inherited forms of Parkinson’s disease have been mapped and/or cloned. In a large family with autosomal-dominant inheritance and typical Lewy-body pathology, a first gene locus has been mapped to the long arm of chromosome [...] Read more.

Over the last few years several genes for monogenically inherited forms of Parkinson’s disease have been mapped and/or cloned. In a large family with autosomal-dominant inheritance and typical Lewy-body pathology, a first gene locus has been mapped to the long arm of chromosome 4 and mutations in this and a few other families linked to this locus have been identified in the gene for α-synuclein. Aggregation of this protein in Lewybodies may be a crucial step in the molecular pathogenesis of familial and sporadic Parkinson’s disease. A gene causing autosomal-recessive parkinsonism of juvenile onset has been mapped to chromosome 6, and the causative gene has been identified and named parkin. A third locus, again in families with dominant inheritance, typical Lewy-body pathology and late onset, has been mapped to chromosome 2p13, and two additional genes on chromosome 4p have been linked to other dominantly inherited forms of the disease. At present, there is no direct evidence that any of the genes for familial parkinsonian syndromes have a direct role in the aetiology of the common sporadic form of Parkinson’s disease. However, the elucidation of the molecular sequence of events leading to nigral degeneration in these inherited cases is likely to shed light also on the molecular pathogenesis of the common sporadic disorder. Full article

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α-Synuklein und Tau: abnorme Proteinablagerungen beim Parkinson-(plus)-Syndrom

by Markus Tolnay

Swiss Arch. Neurol. Psychiatry Psychother. 2000, 151(4), 136-145; https://doi.org/10.4414/sanp.2000.01164 - 1 Jan 2000

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Abstract

A number of neurodegenerative disorders define the Parkinson-(plus)-syndrome, among them idiopathic Parkinson’s disease, progressive supranuclear palsy, corticobasal degeneration, multiple system atrophy, dementia with Lewy bodies, and familial frontotemporal dementia and parkinsonism (FTDP). Recent studies have revealed that all these disorders are characterised by [...] Read more.

A number of neurodegenerative disorders define the Parkinson-(plus)-syndrome, among them idiopathic Parkinson’s disease, progressive supranuclear palsy, corticobasal degeneration, multiple system atrophy, dementia with Lewy bodies, and familial frontotemporal dementia and parkinsonism (FTDP). Recent studies have revealed that all these disorders are characterised by the presence of abnormal filamentous protein deposits in nerve cells. Depending on the disease, key players are either the presynaptic protein α-synuclein (α-synucleinopathies) or the microtubuleassociated protein tau (tauopathies).The discovery of pathogenic α-synuclein gene mutations in rare familial Parkinson’s disease kindreds and tau gene mutations in FTDP-17 has given new insights into the pathogenic mechanisms leading to these filamentous protein deposits. α-synucleinopathies and tauopathies are within a broad spectrum of neurodegenerative disorders, all of which are characterised by the presence of abnormal filamentous protein deposits. Full article

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Open AccessEditorial

Editorial

by A. J. Steck

Swiss Arch. Neurol. Psychiatry Psychother. 2000, 151(4), 135; https://doi.org/10.4414/sanp.2000.01169 - 1 Jan 2000

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Abstract

Die vorliegende Nummer soll dem Kreis der Leser und Leserinnen des Schweizer Archivs die Ergebnisse eines Parkinson- Symposiums bekannt geben, das in Basel im Herbst 1999 stattgefunden hat [...] Full article

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Swiss Arch. Neurol. Psychiatry Psychother., Volume 151, Issue 4 (01 2000) – 9 articles , Pages 135-180

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