Swiss Archives of Neurology, Psychiatry and Psychotherapy

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Jacqueline M. Washington, editor: Neurologic Disorders in Pregnancy

by EMH Swiss Medical Publishers Ltd.

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 342; https://doi.org/10.4414/sanp.2006.01785 - 1 Jan 2006

Abstract

Diagnostik und Therapie neurologischer Erkrankungen im Rahmen von Schwangerschaft sind ein wichtiger Bestandteil bei der Betreuung von Frauen im gebährfähigen Alter, und zwar sowohl für den Neurologen als auch für den Gynäkologen und den Allgemeinmediziner[...] Full article

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Barry S. Oken, editor: Complementary Therapies in Neurology

by EMH Swiss Medical Publishers Ltd.

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 342; https://doi.org/10.4414/sanp.2006.01784 - 1 Jan 2006

Abstract

Wer sich rasch und sachlich über den möglichen Einsatz von alternativmedizinischen Behandlungen bei neurologischen[...] Full article

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Karl F. Masuhr, Marianne Neumann: Neurologi

by EMH Swiss Medical Publishers Ltd.

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 341-342; https://doi.org/10.4414/sanp.2006.01783 - 1 Jan 2006

Abstract

Die neue, 5., vollständig überarbeitete Auflage des altbewährten[...] Full article

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Holger Grehl, Frank Reinhardt: Checkliste Neurologie. (Checklisten der aktuellen Medizin)

by EMH Swiss Medical Publishers Ltd.

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 341; https://doi.org/10.4414/sanp.2006.01782 - 1 Jan 2006

Abstract

Vor 6 Jahren erschien erstmals die Checkliste Neurologie und 2005 bereits die vorliegende 3[...] Full article

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Eva L. Feldmann, Wolfgang Grisold, James W. Russell, Udo A. Zifko: Atlas of Neuromuscular Diseases. A Practical Guideline

by EMH Swiss Medical Publishers Ltd.

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 341; https://doi.org/10.4414/sanp.2006.01781 - 1 Jan 2006

Abstract

Dieses Buch ist ein hervorragender Begleiter, besonders für die sehr seltenen neuromuskulären Erkrankungen[...] Full article

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J. Bogousslavsky, F. Boller: Neurological Disorders in Famous Artists

by EMH Swiss Medical Publishers Ltd.

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 341; https://doi.org/10.4414/sanp.2006.01780 - 1 Jan 2006

Abstract

Die Auswirkungen von Hirnaffektionen auf die künstlerische Ausdrucksfähigkeit haben Neurologen immer wieder fasziniert[...] Full article

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Frank Block, Herausgeber: Infektiöse und entzündliche Erkrankungen des ZNS. Diagnostik, Therapie und Prophylaxe

by EMH Swiss Medical Publishers Ltd.

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 340-341; https://doi.org/10.4414/sanp.2006.01779 - 1 Jan 2006

Abstract

Eine Arbeitsgruppe aus der Neurologischen Universitätsklinik Aachen um Frank Block hat sich die dankenswerte Aufgabe zu eigen gemacht[...] Full article

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Ralf W. Baumgartner, editor: Handbook on Neurovascular Ultrasound

by EMH Swiss Medical Publishers Ltd.

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 340; https://doi.org/10.4414/sanp.2006.01778 - 1 Jan 2006

Abstract

Im vorliegenden Buch trugen renommierte internationale Experten das Wissen über neurovaskulären Ultraschall und dessen Entwicklung der vergangenen Jahre zu einer Monographie zusammen[...] Full article

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R. W. Baumgartner, J. Bogousslavsky, V. Caso, M. Paciaroni, Volume Editors: Handbook on Cerebral Artery Dissection

by H. Mattle

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 340; https://doi.org/10.4414/sanp.2006.01777 - 1 Jan 2006

Abstract

Dissektionen der extrakranialen Hirnarterien stellen im jungen und mittleren Erwachsenenalter nach arteriosklerotischen Läsionen die häufigste Ursache von Hirninfarkten dar. Es erstaunt daher[...] Full article

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Fuat Aksu: Neuropädiatrie. Diagnostik und Therapieneurologischer Erkrankungen im Kindesund Jugendalter

by EMH Swiss Medical Publishers Ltd.

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 340; https://doi.org/10.4414/sanp.2006.01776 - 1 Jan 2006

Abstract

Das Buch «Neuropädiatrie Diagnostik und Therapie neurologischer Erkrankungen im Kindes- und Jugendalter» ist ein didaktisch hervorragend gegliedertes Werk[...] Full article

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177. Tagung der Schweizerischen Neurologischen Gesellschaft 177e Réunion de la Société Suisse de Neurologie

by H. Grötzsch,, A. Truffert, A. Kohler and M. R. Magistris

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 333-339; https://doi.org/10.4414/sanp.2006.01771 - 1 Jan 2006

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Abstract

Interlaken, 19.–21. Oktober 2006 Full article

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Swiss neurology: a leading force in Europe

by Clay E. Reilly

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 330-332; https://doi.org/10.4414/sanp.2006.01772 - 1 Jan 2006

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Abstract

Introduction Why does one country excel in the sciences, but another does not [...] Full article

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Neurologist-in-training

by Patrik Michel

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 327-329; https://doi.org/10.4414/sanp.2006.01775 - 1 Jan 2006

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Abstract

The aim of this section is to prepare the neurologist-in-training for the FMH examination, to confront her or him with specific problems of everyday neurological practice and to give him or her updates on recent controversies in clinical neurology. Full article

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Morbus Wilson: eine klinische und molekularbiologische Kasuistik

by Christoph Noppen, J. Wyrsch, E. H. Viollier, K. Hess and C. Schaefer

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 323-326; https://doi.org/10.4414/sanp.2006.01770 - 1 Jan 2006

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Abstract

Wilson’s disease is a rare autosomal recessively inherited disorder of copper metabolism resulting in accumulation of copper in many organs. The Kayser-Fleischer corneal ring represents a typical symptom in Wilson patients. ATP7B, the gene product of the Wilson’s disease gene, is expressed in [...] Read more.

Wilson’s disease is a rare autosomal recessively inherited disorder of copper metabolism resulting in accumulation of copper in many organs. The Kayser-Fleischer corneal ring represents a typical symptom in Wilson patients. ATP7B, the gene product of the Wilson’s disease gene, is expressed in hepatocytes and plays a critical role in copper transport and secretion. Mutations encompassing this gene leading to amino acid substitutions reduce the affinity of the ATPase enzyme to copper and prevent the transport of copper through the hepatocytes into the bile duct. More than 200 mutations in the 21 coding exons of the Wilson’s disease gene ATP7B have been described, the most common European one being His1069Gln (30–60% in European patients).Wilson’s disease may present with various clinical symptoms, commonly as liver and neuropsychiatric disease. The diagnosis of Wilson’s disease (prevalence 1:30 000) is based on a combination of clinical and neurological symptoms (Kayser-Fleischer corneal ring, MRI), a multi-parametric clinical chemistry panel (ceruloplasmin, 24 h-copper excretion in urine, serum copper) and molecular genetic analysis of ATP7B gene mutations. Symptomatic patients are treated with the chelating agents D-penicillamine or trientine, and in a second phase often with zinc. Lifelong therapy is required and provides life expectancy near to normal. Here, we report on the long-term follow-up of a 30-year-old Wilson patient displaying a compound heterozygosity of His1069Gln – Asn1270Ser mutations in the ATP7B gene as diagnosed by LightCycler real time polymerase chain reaction and DNA sequencing of exon 18. Molecular family-pedigree analysis over four generations revealed seven additional heterozygous mutation carriers. Treatment of the index patient with high doses of chelating agent D-penicillamine (1500 mg/d) in combination with zinc (150 mg/d) could reverse copper encephalopathy to normal and markedly reduced neurological symptoms. Kayser-Fleischer corneal ring was persistent. Wilson’s disease should be taken into consideration in case of any liver disease of unknown origin or neuropsychiatric symptoms. Current diagnostic panels (international scoring system) encompassing clinical chemistry and molecular genetics for screening and confirmation of Wilson’s disease are discussed. Full article

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Amyotrophic lateral sclerosis: can we predict the course of disease?

by Adam Czaplinski, and S. H. Appel

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 317-322; https://doi.org/10.4414/sanp.2006.01773 - 1 Jan 2006

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Abstract

A variety of prognostic factors have been associated with survival and disease progression in amyotrophic lateral sclerosis (ALS).With knowledge of factors that affect prognosis, clinicians can best advise their patients about their future clinical course. Moreover, the evaluation of early prognostic variables and [...] Read more.

A variety of prognostic factors have been associated with survival and disease progression in amyotrophic lateral sclerosis (ALS).With knowledge of factors that affect prognosis, clinicians can best advise their patients about their future clinical course. Moreover, the evaluation of early prognostic variables and the understanding of “at first exam” factors related to outcome may impact on the selection of patient cohorts for clinical trails. This goal is highly desirable, since the appropriate stratification of eligible patients based on the described predictors could result in reduction of sample size and study duration. It is well known that factors like age, sex, site of symptom onset and diagnostic delay, if imbalanced among treatment groups, may have a larger effect on outcome in the clinical ALS trials than the treatment itself. Thus, matching patients for established demographic and clinical parameters is particularly important in planning clinical trials. However, the randomisation for too many variables in the entry criteria may cause a large increase in the number of patients needed to balance the trial. Based on our own data we describe here the value of prognostic factors related to outcome in patients with ALS and review the literature. The identification of younger age, limb site of onset and longer FS-FE delay as predictors of prolonged survival in an ALS clinic population is in agreement with the findings of several earlier studies that were based on smaller groups of patients. Moreover, given the well-known correlation between disease value of several “at first examination” clinical parameters – baseline value of functional rating scales such as ALSFRS and Appel score, initial progression rate and baseline value of the forced vital capacity (FVC) – all of which may have significant utility in patient management. Full article

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Dysimmune polyneuropathies – new diagnostic and therapeutic insights

by Susanne Renaud,

Swiss Arch. Neurol. Psychiatry Psychother. 2006, 157(7), 307-316; https://doi.org/10.4414/sanp.2006.01774 - 1 Jan 2006

Cited by 1 | Viewed by 110

Abstract

Polyneuropathies are systemic diseases of the nervous system that affect peripheral motor, sensory and vegetative autonomous nerve fibres. The prevalence is 2.4% in the general population and 8% in those older than 55 years. Although inflammatory polyneuropathies represent only about 10% of all [...] Read more.

Polyneuropathies are systemic diseases of the nervous system that affect peripheral motor, sensory and vegetative autonomous nerve fibres. The prevalence is 2.4% in the general population and 8% in those older than 55 years. Although inflammatory polyneuropathies represent only about 10% of all polyneuropathies, they are important since they are potentially treatable. They encompass the Guillain-Barré syndrome (GBS) and its chronic sibling chronic inflammatory demyelinating polyneuropathy (CIDP), the vasculitides of the peripheral nervous system (VAS) and polyneuropathies that are associated with autoantibodies, e.g. in the context of a paraproteinaemia. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an acquired immunemediated neuropathy that causes significant neurological morbidity. Despite the resemblance to the Guillain-Barré syndrome and the observation that immunosuppressive therapies can lead to a clinical improvement the pathogenesis of CIDP is poorly understood. Since CIDP responds to plasmapheresis and intravenous immunoglobulins (IVIG), humoral mechanisms seem to be involved. But so far autoantibodies against various proteins like P0, glycoproteins and glycolipid components such as GM1, LM1, chondroitin sulfate C have only been found in a minority of patients. Most of the mononuclear inflammatory cells in nerve biopsies are macrophages and activated T-lymphocytes. But 7 had improved nerve conduction studies by at least 10%.These findings were accompanied by laboratory evidence of reduction of B cells, anti-MAG antibodies and total IgM. IgM levels fell to a median of 58% and anti-MAG antibody titres fell to a median of 38% of the initial values one year after treatment.A follow-up study with the double dose of rituximab in the same patients led to improvement in 4 patients for 2 of them for the first time. In comparison to the baseline before the first treatment with rituximab 375 mg/m2 4 out of the 7 patients who were retreated improved and all 6 of the patients in whom neurography could be done had significant improvement of nerve conduction velocities.The IgM fell to a median of 38% and the anti-MAG antibody titres fell to a median of 16% of the initial values. Rituximab was well tolerated which is important since conventional treatments like chlorambucil or interferon-alpha have produced inconsistent or no beneficial effects in placebocontrolled trials and longer follow-up studies, and may even be associated with long-term complications. Recently, a double-blind multicentre study on rituximab in anti-MAG associated polyneuropathy has been started in collaboration with French neuropathy centres. Full article

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Swiss Arch. Neurol. Psychiatry Psychother., Volume 157, Issue 7 (01 2006) – 16 articles

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