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3. Entwicklung der Deutschen Neurologie nach 1960

Author

J. Dichgans

Subjects
Psychiatry and Mental health, Neurology, media_common.quotation_subject, Neurology (clinical), General Medicine, Art, Humanities, media_common
Abstract

Die noch immer beschleunigte Entwicklung der Neurologie in Deutschland wird nachfolgend durch einen Zeitzeugen beschrieben, der von 1965 bis 2005 im Fach gearbeitet hat. Naturgemas betreffen die personlichen Erfahrungen des Autors damit nur diese 40 Jahre. So kommt die ruhmreiche Vorgeschichte, die Zeit bis 1933 zu kurz, die Zeit in der die Vater unserer Neurologie weltweit fuhrend waren. Diese Fuhrung wurde durch den Antisemitismus in der Ara des Nationalsozialismus und die Folgen des Zweiten Weltkrieges verloren. Nachdem die deutschen Neurologen nach diesem Krieg zunachst weitgehend isoliert waren und ihnen die Teilnahme an internationalen Kongressen verwehrt war, wurde der Anschluss erst allmahlich in den Jahren nach 1960 zuruckgewonnen. In diesem kurzen Text wird keineswegs Vollstandigkeit angestrebt, sondern eigener Subjektivitat und dem Bestreben nach Kurze Raum gegeben. Es wird versucht mitzuteilen, was ruckblickend wesentlich erscheint. Die Datierung der Fortschritte auf dem Weg war teilweise muhsam. Den Lesern wird Gelegenheit gegeben, die Uberraschung des Autors zu teilen, daruber wie karg das neurologische Wissen und die diagnostischen Methoden vor 50 Jahren noch waren, wie rasch die nachfolgende Entwicklung verlief, wie schnell selbstverstandlich wurde, was vor 20 Jahren noch keiner ahnte, wie sehr wir uns trotz des Fortschritts zu Teilen jeweils nur auf dem neuesten Stand des Irrtums befanden und wahrscheinlich auch heute befinden. Und vor allem, wie ohnmachtig und durchgehend ungepruft die therapeutischen Bemuhungen damals noch waren. Nur aus dem Vergleich von damals, vor 50 Jahren, und heute lasst sich der Fortschritt ermessen. Eine Projektion aufgrund dieser Erfahrung in die Zukunft wird nicht gewagt. Aber es scheint sicher, dass noch viele Zusammenhange, diagnostische Fortschritte und Therapiemoglichkeiten unentdeckt sind und dass auch weiter spannende Zeiten bevor stehen.

Published
2013

4. Analgetika-induzierter Dauerkopfschmerz

Author

Wolf-Dieter Gerber, Hans-Christoph Diener, J. Dichgans, M. Kluck, H. Kukiolka, and E. J. Verspohl

Subjects
Vasomotor, Nausea, business.industry, Codeine, Physical dependence, General Medicine, medicine.disease, Ergotamine Tartrate, Migraine, Anesthesia, medicine, Vomiting, medicine.symptom, Headaches, business, medicine.drug
Abstract

Fifty-two patients, most of whom had had daily headaches for years, were examined and treated. Among them there were 40 who originally had migraine, the others had vasomotor or post-contusional headaches. Average duration of the migraine was 21 years, of chronic headache 7.6 years. All patients had been taking analgesics of a mixed type regularly and for a long time, on average 35.6 tablets or suppositories weekly. All patients had taken more than three different drugs. After an observation period of 3-6 months for grading the headaches and registering the amount of drug intake, all patients were admitted to hospital when all analgesics were at once discontinued. Changing degrees of withdrawal symptoms were the rule: increased headaches, nausea, vomiting, tachycardia, sweating, sleep disorders, and in some also hallucinations and cerebral episodes. At the end of the hospital stay chronic headache had completely disappeared or markedly improved in 77% of patients. Even after an average of 16 months of subsequent observation, chronic headache continued to be significantly improved in 70% of patients. There was a significant reduction in frequency and intensity of attacks in the patients with originally typical migraine. Regular intake of analgesics of the mixed type induces chronic headaches. These are most commonly caused by ergotamine tartrate and aminophenol derivatives, while psychological and physical dependence on anti-migraine drugs is initiated and maintained by additional barbiturates, caffeine and codeine.

Published
2008

9. Evozierte Potentiale : SEP-VEP-AEP-EKP-MEP

Author

Manfred Stöhr, J. Dichgans, Ulrich W. Buettner, C.W. Hess, E. Altenmüller, Manfred Stöhr, J. Dichgans, Ulrich W. Buettner, C.W. Hess, and E. Altenmüller

Subjects
Neurology, Neurosciences, Nervous system—Surgery, Ophthalmology, Psychiatry, Otorhinolaryngology
Abstract

Das aktuelle Wissen auf einem sich rasant entwickelnden Gebiet spiegelt dieses Standardwerk der evozierten Potentiale, das sich seit seinem ersten Erscheinen 1982 als unentbehrliches Lehr- und Nachschlagewerk etabliert hat.'Evozierte Potentiale'o berücksichtigt umfassend sowohl die wissenschaftlichen Grundlagen als auch die praktischen Anwendungsmöglichkeiten der multimodal evozierten Potentiale,o enthält detaillierte Angaben zur Durchführung der einzelnen Verfahren sowie zur Auswertung und Befundung der Untersuchungsergebnisse,o bietet eine besonders hohe Anschaulichkeit durch die Fülle instruktiver Abbildungsbeispiele und Normwerttabellen.Auch die dritte Auflage wird in gewohnter Qualität wieder allen Ansprüchen gerecht.NEU:o Alle klinisch relevanten Modalitäten auf dem aktuellen Stand (SEP, VEP, AEP, Magnetsimulation, ereigniskorrelierte Potentiale, schmerz-evozierte Potentiale).o Berücksichtigung aller Publikationen der letzten Jahre über multimodal evozierte Potentiale.o Verbessertes Abbildungsmaterial mit noch stärkerer Aussagekraft.o Neue Indikationen, veranschaulicht durch einschlägige Beispiele.o Neues Kapitel über schmerz-evozierte Potentiale zur Funktionsprüfung der nozizeptiven Bahnen.Wer über die Ableitung evozierter Potentiale alles wissen muß, ist mit diesem Werk solide, sachkundig und erschöpfend informiert. Wer schon alles weiß, schlägt hier nach und lernt immer noch dazu.

Published
2013

10. Evozierte Potentiale : SEP - VEP - AEP

Author

M. Stöhr, J. Dichgans, H. C. Diener, U. W. Buettner, M. Stöhr, J. Dichgans, H. C. Diener, and U. W. Buettner

Subjects
Neurology, Neurosciences, Pediatrics
Published
2013

11. [Development of neurology in Germany after 1960]

Author

J, Dichgans

Subjects
Neurology, World War II, Germany, National Socialism, Humans, History, 19th Century, History, 20th Century, History, 18th Century, History, 21st Century, Forecasting
Abstract

The still continuing accelerated development of neurology in Germany is described in this article by a contemporary witness who was active in this field from 1965 to 2005. The personal experiences of the author are obviously only reflected over these 40 years so that the glorious antecedents in the period up to 1933, the era in which our predecessors were the world leaders in neurology, is not sufficiently covered. This dominance was lost by the anti-Semitism during the era of National Socialism and the sequelae of World War II. As a result of the war, German neurologists became effectively isolated and their participation in international congresses was forbidden so that a gradual reestablishment of alignment only became possible after 1960. In this brief description no attempt at completeness has been made and only subjectivity and brevity have been considered. An attempt is made to retrospectively convey what essentially happened. An exact dating of advances over the period was sometimes difficult. The readership will have the opportunity to share the surprise of the author on how meagre the neurological knowledge and diagnostic methods were 50 years ago, how rapidly the subsequent development happened, how rapidly things became obvious which 20 years ago nobody was aware of and despite the progress how pleased we were to find ourselves at the most recent state of error and probably still find ourselves nowadays. In particular, how powerless and untested the therapeutic efforts were at that time. The progress can only be measured by a comparison between then, 50 years ago and the present. A projection of the future based on these experiences is not attempted but it seems to be certain that many conceptions, diagnostic advances and therapy options are still undiscovered and that further exciting times can be expected.

Published
2013

12. Altern in Teilen?

Author

J.B. Schulz and J. Dichgans

Subjects
Psychiatry and Mental health, Neurology, Neurology (clinical), General Medicine
Published
1999

13. SELEDO: a 5-y-ear long-term trial on the effect of selegiline in early parkinsonian patients treated with levodopa

Author

Klaus Schimrigk, P. Krauseneck, P.H. Kraus, B. Conrad, J. Schnitker, H.P. Vogel, U. Rinne, Horst Przuntek, G. Pergande, and J. Dichgans

Subjects
Adult, Male, Levodopa, Monoamine Oxidase Inhibitors, Time Factors, Placebo, Placebo group, law.invention, Antiparkinson Agents, Pharmacotherapy, Randomized controlled trial, law, Selegiline, medicine, Clinical endpoint, Humans, Longitudinal Studies, Aged, Dose-Response Relationship, Drug, business.industry, Parkinson Disease, Drug Tolerance, Middle Aged, Clinical trial, Neurology, Anesthesia, Drug Therapy, Combination, Female, Neurology (clinical), business, medicine.drug
Abstract

The SELEDO (from selegiline plus levodopa) study was carried out as a randomized, prospective, placebo-controlled, double- blind, multicenter long-term, 5-year trial to evaluate the possible advantages of combining selegiline and levodopa in the early treatment of Parkinson's disease. One-hundred-and-sixteen patients were randomized either to selegiline or placebo. Before starting the study medication, the levodopa dose was titrated to the individual requirements of each patient. The primary study end point (time when levodopa had to be increased by >50% of the titrated dose) was reached in 23 of 59 patients in the selegiline group and 26 of 48 patients in the placebo group. At the end of the 5 years' treatment period the rates derived from a life-table analysis were 50.4% in the selegiline group and 74.1% in the placebo group (P = 0.027, log-rank test). The median time to reach the primary end point was 4.9 years in the selegiline group and 2.6 years in the placebo group. In patients treated with selegiline, the mean levodopa dose changed only slightly over the 5 years of treatment compared to the initially titrated dose, but rose markedly in the placebo group, where the dose of levodopa had to be adjusted earlier than in the selegiline group. At the same time, the lower levodopa dosage in the selegiline group was accompanied by at least equal therapeutic efficacy (which is necessary for an unambiguous interpretation). Subgroup analyses showed greater benefit for selegiline treated) patients in the earlier stages. Long-term side effects appeared later in the selegiline group, although the difference was not significant. The early combination of selegiline and levodopa proved to be clearly superior to levodopa monotherapy.

Published
1999

14. Manifestation of Hashimoto’s Encephalopathy Years before Onset of Thyroid Disease

Author

R. Peschen-Rosin, M. Schabet, and J. Dichgans

Subjects
Adult, endocrine system, medicine.medical_specialty, Time Factors, endocrine system diseases, Prednisolone, Encephalopathy, Anti-Inflammatory Agents, Hashimoto's encephalopathy, Epilepsies, Myoclonic, Neurological disorder, Gastroenterology, Thyroiditis, Central nervous system disease, Autoimmune thyroiditis, immune system diseases, Internal medicine, medicine, Humans, business.industry, Thyroid disease, Thyroiditis, Autoimmune, Cerebrospinal Fluid Proteins, Electroencephalography, medicine.disease, Magnetic Resonance Imaging, Thyroid Diseases, Carbamazepine, Neurology, Immunoglobulin G, Immunology, Anticonvulsants, Female, Neurology (clinical), medicine.symptom, business, Myoclonus
Abstract

Patients with Hashimoto’s encephalopathy (HE), a steroid-responsive disorder, associated with Hashimoto’s disease and high levels of thyroid-related autoantibodies usually present with a subacute onset of confusion, focal or generalized seizures. Frequent EEG abnormalities include generalized, rhythmic bifrontal or temporal slowing. Elevated protein levels or an intrathecal IgG synthesis may be present in cerebrospinal fluid (CSF). A 39-year-old woman underwent a relapsing course of myocloni and generalized seizures. Initially, thyroid function, thyroid-related autoantibody screening and cerebral MRI were unrevealing. CSF showed oligoclonal bands. Short-term treatment with high doses of prednisolone resolved the myocloni. During the 5th episode of myocloni, signs of hyperthyroidism and elevation of thyroid microsomal antibody titer developed. Hashimoto’s thyroiditis and HE were diagnosed. After subtotal thyroidectomy the patient remained asymptomatic.

Published
1999

15. Cerebellar Functions

Author

J. Bloedel, J. Dichgans, W. Precht, J. Bloedel, J. Dichgans, and W. Precht

Subjects
Neurosciences, Cytology, Nervous system—Surgery
Abstract

Over the past few semesters a group of neurologists, neurophysiologists, and brain theorists in various departments of Tlibingen University have gathered periodically in an effort to review ideas and evidence on cerebel­ lar functions. At times, general solutions seemed close, when credit was given to various theoretical proposals advanced since the early days of cer­ ebellar physiology, however, it became clear in every case that a large part of the available facts refused to submit to the general ideas. As believers in the power of scientific discussion, we felt that the time was ripe for posing the problem of the cerebellum once more to a well­ articulated group of specialists that would include proponents of every disparate point of view. The sponsorship of the Max Planck Society and of the Deutsche Forschungsgemeinschaft, to whom we express our profound gratitude, made it possible to organize an international meeting in Septem­ ber, 1983. The aim of making new, even extravagant ideas palatable to each other was well accomplished by the participants. We trust that some of the ensuing excitement has been carried over into the printed version.

Published
2012

16. Color vision tests for early detection of antiepileptic drug toxicity

Author

Hans-Jürgen Thiel, A. Bayer, D. Schmidt, S. Ried, Walter Paulus, Eberhart Zrenner, M. Kuehn, and J. Dichgans

Subjects
Adult, Phenytoin, Adolescent, genetic structures, Color vision, medicine.medical_treatment, Vision Disorders, Pharmacology, Epilepsy, medicine, Humans, Vision test, Valproic Acid, business.industry, Vision Tests, Osmolar Concentration, Neurotoxicity, Carbamazepine, medicine.disease, eye diseases, Anticonvulsant, Anticonvulsants, Neurology (clinical), business, Color Perception, medicine.drug
Abstract

A previous suggestion that antiepileptic drugs may induce color vision deficiencies prompted us to examine whether color vision deficiencies may occur at lower drug serum concentrations than those associated with symptoms of neurotoxicity. Eighty patients presenting with epilepsy received monotherapies of valproic acid, phenytoin, or carbamazepine; 18 patients did not receive antiepileptic drug therapy. Color vision was tested by the Farnsworth-Munsell 100-hue test, spectral sensitivity, and the newly developed tritan screening plates. Patients treated with phenytoin or carbamazepine developed blue-yellow color vision deficiencies. In contrast, patients exposed to valproic acid or receiving no drug treatment showed normal color vision. There was a significant correlation (p < 0.0001) between signs of neurotoxicity induced by phenytoin or carbamazepine and blue-yellow color vision deficiencies. In contrast, we found no correlation between these signs of neurotoxicity and the drug serum concentrations (p = 0.0637). Color vision testing in epileptic patients treated with phenytoin or carbamazepine appears to be a sensitive method for early detection and monitoring of clinical neurotoxicity.

Published
1997

18. Abstracts Second Congress of the European Society for Clinical Neuropharmacology

Author

G. Collingridge, D. Bruns, A. Teufel, P. Barbier, H. G. Bloß, K. P. Offord, C. Stahl-Hennig, E. N. H. Jansen, T. Sobanski, Carlo Ori, M. Goetz, A. Muratorio, Ulderico Freo, E. Sale, Eldad Melamed, J. M. Maloteaux, Z. Bashir, B. Guschelbauer, D. Fitzgeral, R. Korinthenberg, H. Baas, Armin Heils, I. M. Macrae, T. Kutschka, M. C. Anderson, M. Beeg, G. A. Wiesbeck, P. Del Dotto, P. C. O'Brien, J. Knauber, M. E. Götz, Keith F. Tipton, M. Simanyi, G. Rossi, Max Holzer, I. Svobodová, L. Mancino, L. Calza, Th. Müller, J. P. W. F. Lakke, Mauro Dam, A. Raja, Eri Hashimoto, F. Crépel, U. Pulkowski, R. Ceravolo, D. R. Schroeder, M. Streifler, L. L. Iversen, E. Lossmann, K. Lieb, F. Heinen, T. A. Ibrahim, M. Rösier, F. Siebecker, R. Schinzel, P. Emson, A. H. Rajput, C. H. Lücking, F. Ferraguti, D. Feineis, L. Froelich, Wolf-Dieter Heiss, Ewout R. Brunt, Oliver Griesbeck, N. Pavese, A. Gerstner, J. Putzke, U. Nöth, Paolo Maria Rossini, R. God, G.B. Cassano, R. Nafc, D. Müller, A. Cunningham, Daniela Necchi, Patrick Carroll, C. Lucetti, F. Abel, O. M. Adegemo, E. Braak, B. Molzer, N. Fichter, A. Lugowska, M. L. Rao, S. Roßner, F. Coraddu, A. Gemma, O. Tucha, L. J. Bryan-Lluka, I. Avdiunina, H. Beckmann, P. Fruth, H. W. Clement, F. Müller, E. de la Morena, W. Zieglgänsberger, A. P. Jeanjean, C. H. Lammers, A. Seghers, A. Nuti, A. Steup, M. Schwarz, Michael Sendtner, T. W. van Weerden, M. Li, B. Janetzky, R. Erdmann, R. Winkel, B. Niedermeyer, V. ter Meulen, M. Butà, D. Peckys, Th. Arendt, P. A. Löschmann, S. Strauss, D. Offen, B. Gangus, D. M. Yilmazer, K. Velbinger, T. J. Feuerstein, Klaus V. Toyka, R. S. J. Frackowiak, F. Conquet, K. Gasiorowski, F. Fascetti, C. Grote, A. Barzilai, Thomas A. Sontag, C. G. Parsons, G. Dell’Agnello, Hans-Peter Hartung, Toshikazu Saito, R. Stein, W. D. Rausch, E. Donati, P. Vanhoorde, S. Hartmann, E. Orlov, D. Inglot, Francesca Vaglini, W. Paulus, A. Merico, W. H. Jost, H. H. Borchert, M. Bagli, N. S. Alekseeva, T. Heinemann, B. K. Siesjö, T. Hirning, I. Ziv, C. Wurthman, M. J. Lohse, E. Hermsteiner, J. Coos Verhoef, B. Landwehrmeyer, Félix F. Cruz-Sánchez, Hans Lassmann, R. Jackisch, E. W. Fünfgeld, M. Naumann, Gilberto Pizzolato, M. Bigl, Helmut Heinsen, J. E. Ahlskog, M. Sieklucka, Hiroki Ozawa, S. Hesse, J. Pruim, H. E. Junginger, Andreas Moser, J. Boning, F. Fumagalli, M. Berger, M. Lauk, E. Borroni, M. Gerlach, M. Heider, C. Schwarzer, K. Jellinger, W. H. Oertel, S. Danielcyk, V. Tuulik, J. Bauer, F. Block, Udo Rüb, F. Böcker, Hans Thoenen, L. Komelkova, G. Zürcher, A. Hochman, A. Mesec, G. Jungkunz, G. Charles, P. Vieregge, P. Kalus, Jürgen Fritze, I. Faé, K. Eschrich, H. Standhardt, M. Schüler, W. Kolasiewicz, A. Meister, E. N. H. Janzen, M Melzacka, A. A. Sharkawy, Borwin Bandelow, M. Renna, S. Hauck, Marco A. Riva, U. Lockemann, R. M. Nitsch, Heiko Braak, R. Medori, S. Federspiel, J. Berger, D. Senitz, J. Wissel, Georg W. Kreutzberg, U. McMonagle, H. Przuntek, T. Reum, C. Heim, K. V. Morgunov, R. Maggio, J. Leszek, Gavin P. Reynolds, Gerald Münch, M. Klessaschek, B. Zielke, R. Morgenstern, P. A. Fischer, Y. Agid, B. Volk, H. Schuttes, Konstanze Plaschke, J. Krieglstein, Th. Büttner, D. Blum-Degen, Eleni Koutsilieri, N. Wodarz, Reinhard Schliebs, P. König, Klaus W. Lange, T. Motzek-Noé, Robert Jech, J. Niemann, M. Abdel-moneim, V. V. Peresedov, Juergen Deckert, G. Storm, S. Kamolz, W. Breithaupt, B. Weber, Giovanni Corsini, J. C. Schwartz, M. Hüll, C. Bancher, M. Struck, M. Abdel-mohsen, A. Napolitano, D. Labunsky, M. Sohlbach, T. Winter, J. Sautter, H. J. Degen, Y. Glinka, R. Dörries, C. D. Earl, R. Riederer, G. Bringmann, W. Kuhn, J. A. Protzen, M. Winter, T. Klockgether, B. Fiebich, O. S. Brusov, H. Daniel, B. Bethke, T. R. Tolle, A. Weindl, Michael Bauer, N. Takahata, A. Baumer, Isabella Heuser, V. Gieselmann, Gian Franco Placidi, Giulio Perugi, H. Bönisch, A. Eckert, J. Michaelis, F. von Raison, V. Bigl, S. Harder, Graziella Bernocchi, J. Kuijpers, R. Brückner, U. Bonuccelli, M. José Barro, G. Laux, S. Grüter, W. Retz, M. L. Mimmack, A. Kupsch, Austin Smith, I. Zhirnova, A. M. Sardar, A. I. Svadovsky, Siegfried Hoyer, Peter Riederer, B. Haug, Thomas Arzberger, H. Bernheimer, M. Seemann, Karl-Heinz Sontag, D. Bengel, L. Demisch, W. Danielczyk, Bettina Holtmann, Ullrich Wüllner, E. Hermans, E. V. Khrapova, G. B. Landwehrmeyer, A. Tylki-Szymanska, R. Brinkmann, F. Remeš, B. Kanner, S. L. Timerbaeva, P. Piccini, Susanne Petri, W. Wesemann, G. Ulmar, F. Rausch, Leontino Battistin, U. Ziemann, H. B. Pollard, Gerhard Ransmayr, P. Mečíř, C. Mattern, U. Gärtner, S. Sopper, Moussa B.H. Youdim, Michael Deuschle, M. Pozza, H. Schubert, G. Goping, Rainer Spanagel, Lutz Frölich, L. HaveIec, Martina K. Brückner, W. Gsell, Werner Poewe, M. Da Prada, J. Hartmann, H. J. Stürenburg, B. Löschl, M. Norta, J. Dichgans, G. Stern, J. Mayr, Elda Scherini, D. Bleyl, A. Colzi, P. Rosario, C. D'Avino, J. X Xie, Klaus-Peter Lesch, M. Demuth, M. Ymamoto, A. Toso, K. Lehmann, F. Eblen, J. Thome, R. Burger, S. Šega, G. Farci, Evžen Růžička, F. W. H. M. Merkus, I. Strein, M. Rösler, T. Jaros, D. Barletta, W. W. Chan, U. Havemann-Reinecke, T. Kiauta, R. A. I. de Vos, S. Fähr, A. Körner, A. J. Willemsen, P. J. Neveu, A. V. Moshkin, A. Kleinschroth, L. A. Avdyuna, Johannes Kornhuber, Ryan J. Uitti, R. Häcker, Jan Roth, E. C. Laterre, H. Sternadl, Amos D. Korczyn, G. Künig, Werner E.G. Müller, W. Berger, G. Racagni, S. Salvetti, G. M. Emilien, Parsadanian As, K. Kunze, G. Sperk, D. Högemann, H. Maier, S. Behrens, D. K. Teherani, C Pardini, Karlheinz Reiners, T. S. Chen, C. J. Eggett, L. Popova, H. Reichmann, J. M. Rabey, H. Hartmann, Arvid Carlsson, B. Lawlor, F. Bürklin, O. Gleichauf, and S. Hemm

Subjects
0303 health sciences, medicine.medical_specialty, Public health, 03 medical and health sciences, Psychiatry and Mental health, 0302 clinical medicine, Neurology, medicine, Neurology (clinical), Psychiatry, Psychology, Neuroscience, 030217 neurology & neurosurgery, Biological Psychiatry, Neuropharmacology, 030304 developmental biology
Published
1995

20. Fourth meeting of the European Neurological Society 25–29 June 1994 Barcelona, Spain

Author

H. Hattig, C. Delli Pizzi, M. C. Addonizio, Michelle Davis, A. R. Giovagnoli, L. Florensa, M. Roth, J. de Kruijk, Francisco Lacruz, Ph. Dewailly, A. Toygar, C. Avendano, P.P. De Deyn, J. F. Hurtevent, F. Lomeila, T. W. Wong, Gordon T. Plant, M. Bud, H. J. Willison, DH Miller, D. W. Langdon, R. Cioni, J. Servan, A. Kaygisiz, E. Racadot, D. B. Schens, E. Picciola, L. Falip, C. Bouchard, J. Jotova, A. Jorge-Santamaria, P. Misra, A. Dufour, C. P. Panagopoulos, A. Venneri, B. Sredni, B. Angelard, M. Janelidze, M. Carreno, J. Obenberger, J. Pouget, H. W. Moser, R. Kaufmann, J. A. Molina, D. Linden, A. Martin Urda, E. Uvestad, A. Krone, J. P. Cochin, J. Mallecourt, A. Cambon-Thomsen, K. Violleau, P. Osschmann, A. M. Durocher, E. Bussaglia, D. M. Danielle, H. Efendi, C. Van Broeckhoven, K. G. Jordan, W. Rautenberg, C. Iniguez, J. M. Delgado, Graham Watson, M. Lawden, Gareth J. Barker, K. Stiasny, James T. Becker, G. Campanella, E. Peghi, A. Poli, A. Haddad, T. Yamawaki, Giacomo P. Comi, S. Sotgiu, B. Ersmark, A. Pomes, M. Ziegler, P. Ferrante, P. Ruppi, H. KuÇukoglu, R. Bouton, U. K. Rinne, P. Vieregge, M. Dary, P. Giunti, Peter J. Goadsby, S. Jung, E. Secor, A. Steinberg, N. Vila, M. A. Hernandez, M. Cursi, A. Enqelhardt, A. Engelhardt, J. Veitch, F. Di Silverio, F. Arnaud, B. Neundörfer, R. Brucher, Dominique Caparros-Lefebvre, B. Meyer, Marianne Dieterich, M. H. Snidaro, R. Gomez, R. Cerbo, M. Ragno, J. M. Vance, S. Nemni, A. Caliskan, F. Barros, I. Velcheva, D. Ceballos-Baumann, V. Barak, A. Avila, N. Antonova, F. Resche, S. Pappata, L. Varela, S. R. Silveira Santos, A. Cammarota, L. Naccache, Y. Nara, E. Tournier-Lasserves, R. Mobner, T. Chase, A. Ensenyat, J. Ulrich, G. Giegerich, M. Rother, M. Revilla, N. Nitschke, K. Honczarenko, E. Basart Tarrats, J. Blin, B. Jacob, J. Santamaria, S. Knezevic, J. L. Castillo, M. Antem, J. Colomer, O. Busse, Didier Hannequin, S. Carrier, J. B. Ruidavets, C. Rozman, J. Bogoussslavsky, J. Pascual Calvet, E. Monros, J. M. Polo, M. 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Navasa, J. Ballabriga, G. Broggi, T. Gudeva, C. Rose, J. Vion-Dury, J. A. Gastaut, J. Pniewski, Nicola J. Robertson, G. Kohncke, M. Billot, S. Gok, E. Castellli, F. Denktas, P. Bazzi, F. Spinelli, I. F. Moseley, C. D. Mardsen, B. Barbiroli, O. M. Koriech, A. Miller, Hiroaki Yoshikawa, F. X. Borruat, J. Zielasek, P. Le Coz, J. Pascual, A. Drouet, L. T. Giron, F. Schondube, R. Midgard, M. Alizadeh, M. Liguori, Lionel Ginsberg, L. Harms, C. Tilgner, G. Tognoni, F. Molteni, Mar Tintoré, M. Psylla, C. Goulon-Goeau, M. V. Aguilar, Massimo Filippi, K. H. Mauritz, Thomas V. Fernandez, C. Basset, S. Rossi, P. Meneses, B. Jandolo, T. Locatelli, D. Shechtcr, C. Magnani, R. Ferri, Bruno Dubois, J. M. Warier, S. Berges, F. Idiman, M. Schabet, R. R. Diehl, P. D'aurelio, M. Musior, Reinhard Hohlfeld, P. Smeyers, M. Olivé, A. Riva, C. A. Broere, N. Egund, S. Franceschetti, V. Bonavita, Nicola Canal, E. Timmermans, M. Ruiz, S. Barrandon, G. Vasilaski, B. Deweer, L. Galiano, S. F. T. M. de Bruijn, L. Masana, A. Goossens, B. Heye, K. Lauer, Heinz Gregor Wieser, Stephen R. Williams, B. Garavaglia, A. P. Sempere, F. Grigoletto, P. Poindron, R. Lopez-Pajares, I. Leite, T. A. McNell, C. Caucheteur, J. M. Giron, A. D. Collins, P. Freger, J. Sanhez Del Rio, D. A. Harn, K. Lindner, S. S. Scherer, G. Serve, M. Juncadella, X. Estivill, R. Binkhorst, M. Anderson, B. Tekinsoy, C. Sagan, T. Anastopoulos, G. Japaridze, S. Guillou, F. Erminio, Jon Sussman, P. G. Oomes, D. S. Rust, S. Mascheroni, O. Berger, M. Peresson, K. V. Toyka, T. W. Polder, M. Huberman, B. Arpaci, H. Ramtami, I. Martinez, Ph. Violon, P. P. Gazzaniga Pozzill, R. Ruda, P. Auzou, J. Parker, S. P. Morrissey, Jiahong Zhu, F. Rotondi, P. Baron, W. Schmid, P. Doneda, M. Spadaro, M. C. Nargeot, I. Banchs, J.S.P. van den Berg, R. Ferrai, M. Robotti, M. Fredj, Pedro M. Rodríguez Cruz, B. Erne, D. G. Piepgras, M. C. Arne-Bes, J. Escudero, C. Goetz, A. R. Naylor, M. Hallett, O. Abramsky, E. Bonifacio, L. E. Larsson, R. Pellikka, P. Valalentino, D. Guidetti, B. Buchwald, C. H. Lücking, D. Gauvreau, F. Pfaff, A. Ben Younes-Chennoufi, R. Kiefer, R. Massot, K. A. Hossmann, L. Werdelin, P. J. Baxter, U. Ziflo, S. Allaria, C. D. Marsden, M. Cabaret, S. P. Mueller, E. Calabrese, R. Colao, S. I. Bekkelund, M. Yilmaz, O. Oktem-Tanor, R. Gine, M. E. Scheulen, J. Beuuer, A. Melo, Z. Gulay, M. D. Have, C. Frith, D. Liberati, J. Gozlan, P. Rondot, Ch. Brunholzl, M. Pocchiari, J. Pena, L. Moiola, C. Salvadori, A. Cabello, T. Catarci, S. Webb, C. Dettmers, N. A. Gregson, Alexandra Durr, F. Iglesias, U. Knorr, L. Ferrini-Strambi, F. Kruggel, P. Allard, A. Coquerel, P. Genet, F. Vinuels, C. Oberwittler, A. Torbicki, P. Leffers, B. Renault, B. Fauser, C. Ciano, G. Uziel, J. M. Gibson, F. Anaya, C. Derouesné, C. N. Anagnostou, M. Kaido, W. Eickhoff, G. Talerico, M. L. Berthier, A. Capdevila, M. Alons, D. Rezek, E. Wondrusch, U. Kauerz, D. Mateo, M. A. Chornet, Holon, N. Pinsard, I. Doganer, E. Paoino, H. Strenge, C. Diaz, J. R. Brasic, W. Heide, I. Santilli, W. M. Korn, D. Selcuki, M. J. Barrett, D. Krieger, T. Leon, T. Houallah, M. Tournilhac, C. Nos, D. Chavot, F. Barbieri, F. J. Jimenez-Jimenez, J. Muruzabal, K. Poeck, A. Sennlaub, L. M. Iriarte, L. G. Lazzarino, C. Sanz, P. A. Fischer, S. D. Shorvon, R. Hoermann, F. Delecluse, M. Krams, O. Corabianu, F. H. Hochberg, Christopher J. Mathias, B. Debachy, C. M. Poser, L. Delodovici, A. Jimenez-Escrig, F. Baruzzi, F. Godenberg, D. Cucinotta, P. J. Garcia Ruiz, K. Maier-Hauff, P. R. Bar, R. Mezt, R. Jochens, S. Karakaneva, C. Roberti, E. Caballero, Joseph E. Parisi, M. Zamboni, T. Lacasa, B. Baklan, J. C. Gautier, J. A. Martinez-Matos, W. Pollmann, G. Thomas, L. Verze, E. Chleide, R. Alvarez Sala, I. Noel, E. Albuisson, O. Kastrup, S. I. Rapoport, H. J. Braune, H. Lörler, M. Le Merrer, A. Biraben, S. Soler, S. J. Taagholt, U. Meyding-Lamadé, K. Bleasdale-Barr, Isabella Moroni, Y. Campos, J. Matias-Guiu, G. Edan, M. G. Bousser, John B. Clark, J. Garcia de Yebenes, N. K. Olsen, P. Hitzenberger, S. Einius, Aj Thompson, Ch. J. Vecht, T. Crepin-Leblond, Klaus L. Leenders, A. Di Muzio, L. Georgieva, René Spiegel, K. Sabey, D. Ménégalli, J. Meulstee, U. Liszka, P. Giral, C. Sunol, J. M. Espadaler, A. D. Crockar, K. Varli, G. Giraud, P. J. Hülser, A. Benazzouz, A. Reggio, M. Salvatore, K. Genc, M. Kushnir, S. Barbieri, J. Ph. Azulay, M. Gianelli, N. Bathien, A. AlMemar, F. Hentati, I. Ragueneau, F. Chiarotti, R. C. F. Smits, A. K. Asbury, F. Lacruz, B. Muller, Alan J. Thompson, Gordon Smith, K. Schmidt, C. Daems Monpeun, Juergen Weber, A. Arboix, G. R. Fink, A. M. Cobo, M. Ait Kaci Ahmed, E. Gencheva, Israel-Biet, G. Schlaug, P. De Jonghe, Philip Scheltens, K. Toyka, P. Gonzalez-Porque, A. Cila, J. M. Fernandez, P. Augustin, J. Siclia, S. Medaglini, D. E. Ziogas, A. Feve, L. Kater, G. J. E. Rinkel, D. Leppert, Rüdiger J. Seitz, S. Ried, C. Turc-Carel, G. Smeyers, F. Godinho, M. Czygan, M. Rijntjes, E. Aversa, M. Frigo, Leif Østergaard, J. L. Munoz Blanco, A. Cruz-Matinez, J. De Reuck, C. Theillet, T. Barroso, V. Oikonen, Florence Lebert, M. Kilinc, C. Cordon-Cardon, G. Stoll, E. Thiery, F. Pulcinelli, J. Solski, M. Schmiegelow, L. J. Polman, P. Fernandez-Calle, C. Wikkelso, M. Ben Hamida, M. Laska, E. Kott, W. Sulkowski, C. Lucas, N. M. Bornstein, D. Schmitz, M. W. Lammers, A. de Louw, R. J. S. Wise, P. A. van Darn, C. Antozzi, P. Villanueva, P. H. E. Hilkens, C. Constantin, W. Ricart, A. Wolf, M. Gamba, P. Maguire, Alessandro Padovani, B. M. Patten, Marie Sarazin, H. Ackermann, L. Durelli, S. Timsit, Sebastian Jander, B. W. Scheithauer, G. Demir, J. P. Neau, P. Barbanti, A. Brand, N. AraÇ, V. Fischer-Gagnepain, R. Marchioli, G. Serratrice, C. Maugard-Louboutin, G. T. Spencer, D. Lücke, G. Mainardi, K. Harmant Van Rijckevorsel, G. B. Creel, R. Manzanares, Francesco Fortunato, A. May, J. Workman, K. Johkura, E. Fernandez, Carlo Colosimo, L. Calliauw, L. Bet, Félix F. Cruz-Sánchez, M. Dhib, H. Meinardi, F. Carrara, J. Kuehnen, C. Peiro, H. Lassmann, K. Skovgaard Olsen, A. McDonald, L. Sciulli, A. Cobo, A. Monticelli, B. Conrad, J. Bagunya, J. Benitez, V. Desnizza, B. Dupont, O. Delrieu, D. Moraes, J. J. Heimans, F. Garcia Rio, M. Matsumto, A. Fernandez, R. Nermni, R. Chalmers, M. J. Marchau, F. Aguado, P. Velupillai, P. J. Martin, P. Tassan, V. Demarin, A. Engelien, T. Gerriets, Comar, J. L. Carrasco, J. P. Pruvo, A. Lopez de Munain, D. Pavitt, J. Alarcon, Chris H. Polman, B. Guldin, N. Yeni, Hartmut Brückmann, N. Wilczak, H. Szwed, R. Causaran, G. Kyriazis, M. E. Westarp, M. Gasparini, N. Pecora, J. M. Roda, E. Lang, V. Scaioli, David R. Fish, D. Caputo, O. Gratzl, R. Mercelis, A. Perretti, G. Steimetz, I. Link, C. Rigoletto, A. Catafau, G. Lucotte, M. Buti, G. Fagiolari, A. Piqueras, C. Godinot, J. C. Meurice, Erodriguez J. Dominigo, F. Lionnet, H. Grzelec, David J. Brooks, P. M. G. Munro, F. X. Weilbach, M. Maiwald, W. Split, B. Widjaja-Cramer, V. Ozturk, J. Colas, E. Brizioli, J. Calleja, L. Publio, M. Desi, R. Soffietti, P. Cortinovis-Tourniaire, E. F. Gonano, G. Cavaletti, S. Uselli, K. Westerlind, H. Betuel, C. O. Dhiver, H. Guggenheim, M. Hamon, R. Fazio, P. Lehikoinen, A. Esser, B. Sadzot, G. Fink, Angelo Antonini, D. Bendahan, V. Di Carlo, G. Galardi, A. F. Boller, M. Aksenova, Del Fiore, V. de la Sayette, H. Chabriat, A. Nicoletti, A. Dilouya, M. L. Harpin, E. Rouillet, J. Stam, A. Wolters, M. R. Delgado, Eduardo Tolosa, G. Said, A. J. Lees, L. Rinaldi, A. Schulze-Bonhage, MA Ron, C. Lefebvre, E. W. Radü, R. Alvarez, M. L. Bots, P. Reganati, S. Palazzi, A. Poggi, N. J. Scolding, V. Sazdovitch, T. Moreau, E. Maes, M. A. Estelies, P. Petkova, Jose-Felix Marti-Masso, G De La Meilleure, N. Mullatti, M. Rodegher, N. C. Notermans, T. A. T. Warner, S. Aktan, J. P. Louboutin, L. Volpe, C. Scheidt, W. Aust, C. M. Wiles, U. Schneider, S. K. Braekken, W. R. Willems, K. Usuku, Peter M. Rothwell, C. Talamon, M. L. Sacchetti, A. Codina, M. H. Marion, A. Santoro, J. Roda, A. Bordoni, D. J. Taylor, S. Ertas, H. H. Emmen, J. Vichez, V. BesanÇon, R. E. Passingham, M. L. Malosio, A. Vérier, M. Bamberg, A. W. Hansen, E. Mostacero, G. Gaudriault, Marie Vidailhet, B. Birebent, K. Strijckmans, F. Giannini, T. Kammer, I. Araujo, J. Nowicki, E. Nikolov, A. Hutzelmann, R. Gherardi, J. Verroust, L. Austoni, A. Scheller, A. Vazquez, S. Matheron, H. Holthausen, J. M. Gerard, M. Bataillard, S. Dethy, V. H. Patterson, V. Ivanez, N. P. Hirsch, F. Ozer, M. Sutter, C. Jacomet, M. Mora, Bruno Colombo, A. Sarropoulos, T. H. Papapetropoulos, M. Schwarz, D. S. Dinner, N. Acarin, B. Iandolo, J. O. Riis, P. R. J. Barnes, F. Taroni, J. Kazenwadel, L. Torre, A. Lugaresi, I. L. Henriques, S. Pauli, S. Alfonso, Pedro Quesada, A. S. T. Planting, J. M. Castilla, Thomas Gasser, M. Van der Linden, A. Alfaro, E. Nobile-Orazio, G. Popova, W. Vaalburg, F. G. A. van der Mech, L. Williams, F. Medina, J. P. Vernant, J. Yaouanq, B. Storch-Hagenlocher, A. Potemkowski, R. Riva, M. H. Mahagne, M. Ozturk, Ve. Drory, N. Konic, C. Jungreis, A. Pou Serradell, J. L. Gauvrit, G. J. Chelune, S. Hermandez, T. Dingus, L. Hewer, Ch. Koch, M. N. Metz-Lutz, G. Parlato, M. Sinaki, Charles Pierrot-Deseilligny, H. C. Diener, J. Broeckx, J. Weill-Fulazza, M. L. Villar, M. Rizzo, O. Ganslandt, C. Duran, N. A. Fletcher, G. Di Giovacchino, Susan T. Iannaccone, C. Kolig, N. Fabre, H. A. Crockard, Rita Bella, M. Tazir, E. Papagiannuli, K. Overgaard, Emma Ciafaloni, I. Lorenzetti, F. Viader, P. A. H. Millac, I. Montiel, L. H. Visser, M. Palomar, P. L. Murgia, H. Pedersen, Rafael Blesa, S. Seddigh, W. O. Renier, I. Lemahieu, H. M. L. Jansen, L. Rosin, J. Galofre, K. Mattos, M. Pondal, G. M. Hadjigeorgiou, D. Francis, L. Cantin, D. Stegeman, M. Rango, A. B. M. F. Karim, S. Schraff, B. Castellotti, I. Iriarte, E. Laborde, T. J. Tjan, R. Mutani, D. Toni, B. Bergaasco, J. G. Young, C. Klotzsch, A. Zincone, X. Ducrocq, M. Uchuya, O. J. Kolar, A. Quattrone, T. Bauermann, Nereo Bresolin, J. Vallée, B. C. Jacobs, A. Campos, Werner Poewe, J. A. Villanueva, A. W. Kornhuber, A. Malafosse, E. Diez-Tejedor, G. Jungreia, M. J. A. Puchner, A. Komiyama, O. Saribas, V. Volpini, L. Geremia, S. Bressi, A. Nibbio, Timothy E. Bates, T. z. Tzonev, E. Ideman, G. A. Damlacik, G. Martino, G. Crepaldi, T. Martino, Kjell Någren, E. Idiman, D. Samuel, J. M. Perez Trullen, Y. van der Graaf, J. O. Thorell, M. J. M. Dupuis, E. Sieber, R. D'Alessandro, C. Cazzaniga, J. Faiss, A. Tanguy, A. Schick, I. Hoksergen, A. Cardozo, R. Shakarishvili, G. K. Wennlng, J. L. Marti-Vilalta, J. Weissenbach, I. L. Simone, Amalia C. Bruni, Darius J. Adams, C. Weiller, A. Pietrangeli, F. Croria, C. Vigo-Pelfrey, Patricia Limousin, A. Ducros, G. Conti, O. Lindvall, E. Richter, M. Zuffi, A. Nappo, T. Riise, J. Wijdenes, M. J. Fernandez, J. Rosell, P. Vermersh, S. Servidei, M. S. C. Verdugo, F. Gouttiere, W. Solbach, M. Malbezin, I. S. Watanabe, A. Tumac, W. I. McDonald, D. A. Butterfield, P. P. Costa, F. deRino, F. Bamonti, J. M. Cesar, C. H. Lahoz, I. Mosely, M. Starck, M. H. Lemaitre, K. M. Stephan, S. Tex, R. Bokonjic, I. Mollee, L. Pastena, M. Gutierrez, F. Boiler, M. C. Martinez-Para, M. Velicogna, O. Obuz, A. Grinspan, M. Guarino, L. M. Cartier, E. Ruiz, D. Gambi, S. Messina, M. Villa, Michael G. Hanna, J. Valk, Leone Pascual, M. Clanet, Z. Argov, B. Ryniewicz, E. Magni, B. Berlanga, K. S. Wong, C. Gellera, C. Prevost, F. Gonzalez-Huix, R. Petraroli, J. E. G. Benedikz, I. Kojder, C. Bommelaer, L. Perusse, M. R. Bangioanni, Guy M. McKhann, A. Molina, C. Fresquet, E. Sindern, Florence Pasquier, M. J. Rosas, M. Altieri, O. Simoncini, M. Koutroumanidis, C. A. F. Tulleken, M. Dary-Auriol, S. Oueslati, H. Kruyer, I. Nishisho, C. R. Horning, A. Vital, G. V. Czettritz, J. Ph. Neau, B. Mihout, A. Ameri, M. Francis, S. Quasthoff, D. Taussig, S. Blunt, P. Valentin, C. Y. Gao, O. Heinzlef, H. d'Allens, C. Coudero, M. Erfas, G. Borghero, P. J. Modrego Pardo, M. C. Patrosso, N. L. Gershfeld, P. A. J. M. Boon, O. Sabouraud, M. Lara, J. Svennevig, G. L. Lenzi, A. Barrio, H. Villaroya, JosÇ M. Manubens, O. Boespflug-Tanguy, M. Carreras, D. A. Costiga, J. P. Breux, S. Lynn, C. Oliveras Ley, A. G. Herbaut, J. Nos, C. Tornali, Y. A. Hekster, J. L. Chopard, J. M. Manubens, P. Chemouilli, A. Jovicic, F. Dworzak, S. Smirne, S. E. Soudain, B. Gallano, D. Lubach, G. Masullo, G. Izquierdo, A. Pascual Leone Pascual, A. Sessa, V. Freitas, O. Crambes, L. Ouss, G. W. Van Dijk, P. Marchettini, P. Confalonieri, M. Donaghy, A. Munnich, M. Corbo, and M. E. L. van der Burg

Subjects
Neurology, business.industry, Media studies, Library science, Medicine, Neurology (clinical), business
Published
1994

23. Pathophysiology of cerebellar ataxia

Author

Hans-Christoph Diener and J. Dichgans

Subjects
Cerebellum, Ataxia, Cerebellar Ataxia, Posture, Electromyography, Dysdiadochokinesia, Dysmetria, Tremor, medicine, Humans, Gait, Neurologic Examination, Myoclonic Cerebellar Dyssynergia, Cerebellar ataxia, medicine.diagnostic_test, medicine.disease, Hypotonia, medicine.anatomical_structure, Neurology, Neurology (clinical), medicine.symptom, Psychology, Neuroscience, Motor cortex
Abstract

Human and animal experiments performed recently have resulted in a more detailed understanding of limb movement and body posture disorders associated with cerebellar dysfunction. The delay in movement initiation can be explained by a delay in onset of phasic motor cortex neural discharge owing to decreased input from the cerebellar hemispheres. Disorders of movement termination (dysmetria), which can occur for movements at proximal and distal joints, result from disturbances of the timing and intensity of antagonist electromyographic (EMG) activity necessary to break the movement. Disorders in velocity and acceleration of limb movements result from muscular activity that is smaller in amplitude and more prolonged. The cerebellum is important for control of constant force but not for generation of maximal force. Dysdiadochokinesia is explained by a combination of the above mentioned mechanisms. During complex movements in three-dimensional space, the cerebellum contributes to timing between single components of a movement, scales the size of muscular action, and coordinates the sequence of agonists and antagonists. The basic structure of motor programs is not generated in the cerebellum. Hypotonia can be observed only in acute cerebellar lesions. Cerebellar tremor appears to result from a central mechanism, but is modulated or provoked through increased long-loop EMG responses. The common assumption that cerebellar ataxia of stance does not improve with visual feedback is true only of vestibulocerebellar lesions, not for ataxia resulting from atrophy of the anterior lobe of the cerebellum.

Published
1992

26. Adaptive Mechanisms of VOR Compensation After Unilateral Peripheral Vestibular Lesions in Humans

Author

M. Fetter and J. Dichgans

Subjects
Vestibular system, General Neuroscience, Stimulation, Anatomy, Nystagmus, Inhibitory postsynaptic potential, Sensory Systems, Peripheral, Tonic (physiology), Lesion, Otorhinolaryngology, otorhinolaryngologic diseases, medicine, sense organs, Neurology (clinical), Spontaneous nystagmus, medicine.symptom, Psychology
Abstract

o Abstract - To further elucidate possible central plastic adaptive processes during the recovery from a unilateral peripheral vestibular lesion, we inves­ tigated vestibular functions in humans over a period of 2 months after an acute unilateral labyrinthine lesion. A unilateral peripheral vestibular lesion cre­ ates both a tonic imbalance that causes spontane­ ous nystagmus and a decrease and directional asymmetry of dynamic vestibular responses. We es­ tablish that the tonic imbalance expressed by the spontaneous nystagmus rapidly decreased (similar to other species), whether the lesion remained com­ plete or not. This rebalancing, in the case of com­ plete lesions, is at least partly due to restoration of central vestibular tone on the lesioned side. This restoration of tone also explains, in the case of a complete lesion, the recovery of dynamic vestibu­ lar responses for high-velocity inhibitory stimula­ tion of the remaining labyrinth. A clear recovery of the dynamic response for excitatory stimulation of the remaining labyrinth cannot be proven, as has been shown in monkeys during the first 4 days af­ ter a unilateral vestibular lesion. This is probably due to the fact that in our patients the first record­ ing could not be performed before day 3 after the onset of symptoms. Therefore, any fast dynamic recovery may have been missed. o Keywords - VOR compensation; unilateral labyrinthine lesion; vestibular system, human.

Published
1990

27. Upbeat nystagmus changing to downbeat nystagmus with convergence in a patient with a lower medullary lesion

Author

M. Fetter and J. Dichgans

Subjects
Vestibular system, medicine.medical_specialty, Pathology, Stereotactic biopsy, genetic structures, medicine.diagnostic_test, business.industry, Downbeat nystagmus, Lesion, Ophthalmology, Hemiparesis, Swallowing, medicine, Neurology (clinical), Upbeat nystagmus, Radiology, medicine.symptom, business, Medulla
Abstract

The authors report an 18-year-old male patient with acute onset hemiparesis on the right side, difficulties in speaking and swallowing, and upbeat nystagmus changing to downbeat nystagmus on convergence, with a circumscribed structural lesion in the lower medulla on MRI scan. Stereotactic biopsy did not disclose the diagnosis, only nonspecific edema with gliosis and siderophages was found. Accordingly, a nonspecific inflammation was suspected. Over several months most of the symptoms, except the hemiparesis, subsided despite the fact that the lesion did not change in size or enhancement on MRI scan. To our knowledge, this is the first case with a localized structural lesion that shows this unusual oculomotor syndrome. The syndrome is discussed in the light of recent results on the origin of vertical spontaneous nystagmus.

Published
1990

28. [Does youth mean vigorous and age, feeble biological repair mechanisms?]

Author

J, Dichgans and J B, Schulz

Subjects
Aging, Models, Neurological, Age Factors, Brain, Neurodegenerative Diseases, Nerve Regeneration
Abstract

All living creatures are subject to aging, but our understanding of what governs aging is limited. In the course of a lifetime, with the constant renewal of the organic substance of living creatures errors arise, e.g. in the formation, disposal, and reproduction of DNA, proteins and lipids or in the constant substitution of aging cells in the organs. These errors are recognized and generally counterbalanced by appropriate repair mechanisms. This process is obviously determined partly by environmental influences (e.g. UV radiation, oxidizing influences, thermal shock) and genetic factors (such as the significance of so-called survival genes and gene mutations). In this paper the authors both explain and test the hypothesis that the aging of organs and organisms is the consequence of and not the reason for a progressive weakening of the repair mechanisms throughout life.

Published
2007

31. [Familial cavernous malformations of the central nervous system. A clinical and genetic study of 15 German families]

Author

A M, Siegel, H, Bertalanffy, J J, Dichgans, C E, Elger, H, Hopf, N, Hopf, M, Keidel, A, Kleider, G, Nowak, R A, Pfeiffer, J, Schramm, S, Spuck, H, Stefan, U, Sure, C R, Baumann, G A, Rouleau, D J, Verlaan, E, Andermann, and F, Andermann

Subjects
Adult, Intracranial Arteriovenous Malformations, Male, Polymorphism, Genetic, DNA Mutational Analysis, Brain, Risk Assessment, Pedigree, Risk Factors, Germany, Proto-Oncogene Proteins, Prevalence, Humans, Female, Genetic Predisposition to Disease, Genetic Testing, Carrier Proteins, KRIT1 Protein, Microtubule-Associated Proteins
Abstract

In 1928, Hugo Friedrich Kufs reported on a family with cerebral, retinal, and cutaneous cavernous malformations. Since then, more than 300 families with inherited cavernous malformations have been reported. Genetic studies showed three loci, on chromosomes 7q21-q22 (with the gene CCM1), 7p15-p13 (CCM2), and 3q25.2-q27 (CCM3). The gene product of CCM1 is Krit 1 (Krev interaction trapped 1), a protein interacting with angiogenesis by various mechanisms. Recently, CCM2 has also been identified; its product is a protein which might have a function similar to that of Krit 1. However, the CCM3 gene has still not been found. In this study, we present clinical and genetic findings on 15 German families.

Published
2005

32. A patient with Marfan's syndrome and neurofibromatosis type 1 with polyneuropathy

Author

S. Isenmann, J. Dichgans, U. Bühring, and I. Hartlapp

Subjects
Adult, medicine.medical_specialty, Neurofibromatosis 1, Neural Conduction, Schwannoma, Marfan Syndrome, Polyneuropathies, Rare case, Medicine, Neurofibroma, Humans, Family history, Neurofibromatosis, De novo mutations, S syndrome, business.industry, Brain, medicine.disease, Dermatology, Surgery, Electrophysiology, Neurology, Spinal Cord, Female, Neurology (clinical), business, Polyneuropathy
Abstract

Both Marfan's syndrome and neurofibromatosis type 1 are hereditary, autosomal dominant conditions. Here, we report the rare case of a patient fulfilling the clinical criteria for both diseases. In the absence of a family history of either of the two conditions, two independent de novo mutations are the most likely cause.

Published
2004

34. The cerebellum and cognition. Intellectual function in spinocerebellar ataxia type 6 (SCA6)

Author

C, Globas, S, Bösch, Ch, Zühlke, I, Daum, J, Dichgans, and K, Bürk

Subjects
Adult, Male, Cognition, Cerebellum, Humans, Spinocerebellar Ataxias, Female, Middle Aged, Neuropsychological Tests, Cognition Disorders, Aged
Abstract

The aim of this study was to assess cognitive function in patients with spinocerebellar ataxia type 6 (SCA6), an autosomal-dominantly inherited disease leading to a progressive cerebellar syndrome. In contrast to other SCA types, the pathological changes are mostly restricted to the cerebellum. Cognitive function was studied in 12 patients with genetically confirmed SCA6 (mean duration of disease: 9.2 +/- 11.6 years) and 12 age- and IQ-matched controls using a test battery comprising tests for IQ, attention, verbal and visuospatial memory, as well as executive function. While none of the SCA6 subjects had features of general intellectual impairment, only mild deficits in single subtests especially in fronto-executive tasks were observed, but without reaching statistical significance. Thus the current findings do not demonstrate severe cognitive dysfunction in SCA6.

Published
2003

35. Motor reorganization after spinal cord injury: evidence of adaptive changes in remote muscles

Author

U., Laubis-Herrmann, J., Dichgans, H., Bilow, and H., Topka

Abstract

Purpose: Given that SCI leads to substantial changes in biomechanical properties of the body and to widespread postlesional reorganization of the motor system as determined by functional imaging studies, we sought to identify neurophysiological correlations and time course of reorganization affecting muscles more distant to a SCI. Methods: Two arm muscles distant to a SCI (T2-L3), M.biceps brachii (BIC), M.abductor pollicis brevis (APB), were studied in 13 SCI-patients and 15 controls. Motor thresholds at rest (MT), facilitatory effects on MEP-amplitudes (FE) with voluntary activation, MEP-amplitudes with maximal stimulation (MA) and recruitment curves (RC) were measured and correlated with level, age and severity of the lesion. Follow-up studies (t2) were performed in five patients with clinical recovery. Results: Patients exhibited smaller MA from activated BIC, a tendency towards smaller FE and smaller RC-slopes at t1. With clinical recovery, activated BIC-FE, MA and RC-slopes tended to normalize. Conclusions: Our data support the hypothesis that postlesional reorganization of the motor system also involves remote muscles. Considering pattern and time course of reorganization, we speculate that they appear as sequelae of the trauma, possibly representing an adaptation of the motor system to an altered biomechanical status after SCI.

Published
2001

36. Sublethal irradiation promotes migration and invasiveness of glioma cells: implications for radiotherapy of human glioblastoma

Author

C, Wild-Bode, M, Weller, A, Rimner, J, Dichgans, and W, Wick

Subjects
Male, Brain Neoplasms, 3T3 Cells, Glioma, Radiation Tolerance, Rats, Inbred F344, Rats, Mice, Matrix Metalloproteinase 9, Proto-Oncogene Proteins c-bcl-2, Cell Movement, Spheroids, Cellular, Tumor Cells, Cultured, Animals, Humans, Matrix Metalloproteinase 2, Neoplasm Invasiveness, Receptors, Vitronectin, Glioblastoma
Abstract

Human malignant gliomas are highly lethal neoplasms. Involved-field radiotherapy is the most important therapeutic measure. Most relapses originate from the close vicinity of the irradiated target field. Here, we report that sublethal doses of irradiation enhance the migration and invasiveness of human malignant glioma cells. This hitherto unknown biological effect of irradiation is p53 independent, involves enhanced alphavbeta3 integrin expression, an altered profile of matrix metalloproteinase-2 and matrix metalloproteinase-9 (MMP-2 and MMP-9) expression and activity, altered membrane type 1 MMP and tissue inhibitor of metalloproteinases-2 expression, and an altered BCL-2/BAX rheostat favoring resistance to apoptosis. BCL-2 gene transfer and irradiation cooperate to enhance migration and invasiveness in a synergistic manner. Sublethal irradiation of rat 9L glioma cells results in the formation of a greater number of tumor satellites in the rat brain in vivo concomitant with enhanced MMP-2 and reduced tissue inhibitor of metalloproteinases-2 expression. Collectively, these data suggest that the current concepts of involved-field radiotherapy for malignant glioma need to be reconsidered and that the pharmacological inhibition of migration and invasion during radiotherapy may represent a new therapeutic approach to improve the therapeutic efficacy of radiotherapy for malignant glioma.

Published
2001

37. Treosulfan chemotherapy for recurrent malignant glioma

Author

F, Schmidt, W, Wick, U, Herrlinger, J, Dichgans, and M, Weller

Subjects
Adult, Male, Salvage Therapy, Brain Neoplasms, Astrocytoma, Middle Aged, Survival Analysis, Cohort Studies, Treatment Outcome, Bone Marrow, Retreatment, Humans, Female, Neoplasm Recurrence, Local, Glioblastoma, Antineoplastic Agents, Alkylating, Busulfan, Aged
Abstract

Treosulfan is a bifunctional alkylating prodrug with activity against various solid tumors. To improve the outcome for patients with recurrent malignant glioma, we assessed the efficacy of intravenous treosulfan (6-10 g/m2 4-weekly) as salvage therapy for patients with recurrent or progressive glioblastoma (GB, n = 14) or anaplastic astrocytoma (AA, n = 2). All patients had prior involved-field radiotherapy and adjuvant nitrosourea-based chemotherapy. A total of 56 cycles were administered. Tumor responses were assessed radiologically and clinically prior to each cycle. All patients were assessable for toxicity, response and survival. There were no complete or partial responses (CR, PR). Two patients progressed after the first cycle, 14 patients had initially stable disease (SD). Median progression-free survival was 3.25 months for the GB patients. Five patients were progression-free at 6 months (30%), including the 2 AA patients. The 2 AA patients are stable at 22 months. Myelosuppression was the dose-limiting toxicity in this cohort of nitrosourea-pretreated patients. Treosulfan has modest activity in patients with recurrent malignant glioma. Further evaluation of treosulfan in chemonaive malignant glioma patients is warranted.

Published
2001

38. Heat shock protein expression in human gliomas

Author

H M, Strik, M, Weller, B, Frank, M, Hermisson, M H, Deininger, J, Dichgans, and R, Meyermann

Subjects
Oligodendroglioma, HSC70 Heat-Shock Proteins, Humans, HSP70 Heat-Shock Proteins, HSP90 Heat-Shock Proteins, Astrocytoma, Carrier Proteins, Prognosis, Crystallins, Heat-Shock Proteins, Neoplasm Proteins
Abstract

Heat shock proteins (HSP) are cytoprotective, antiapoptotic proteins which may predict clinical prognosis in various types of cancer. Here, we asked whether the differential response to radiochemotherapy and different overall prognosis for astrocytic and oligodendroglial tumours can be accounted for by differences in HSP expression.We examined aB-crystallin, HSP27, HSP70, HSC70 (HSP73) and HSP90 expression in 44 human gliomas (5 anaplastic and 5 low-grade astrocytomas, 5 anaplastic and 5 low-grade oligodendrogliomas and 24 glioblastomas) by immunohistochemistry.HSP were expressed in the tumour parenchyma of all high-grade and most low-grade gliomas, including oligodendrogliomas. Endothelial cells were more often positive for HSC70 and HSP90, but more often negative for HSP27, in glioblastomas than in the other tumours. HSP were also observed in macrophages/microglial cells, but not in a tumour-specific pattern.Different patterns of HSP expression seem not to account for the differential response of these tumours to adjuvant cytotoxic therapy.

Published
2001

39. Glutathione, oxidative stress and neurodegeneration

Author

J B, Schulz, J, Lindenau, J, Seyfried, and J, Dichgans

Subjects
Oxidative Stress, Alzheimer Disease, Friedreich Ataxia, Nerve Degeneration, Animals, Humans, Parkinson Disease, Motor Neuron Disease, Glutathione, Mitochondria
Abstract

There is significant evidence that the pathogenesis of several neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, Friedreich's ataxia and amyotrophic lateral sclerosis, may involve the generation of reactive oxygen species and mitochondrial dysfunction. Here, we review the evidence for a disturbance of glutathione homeostasis that may either lead to or result from oxidative stress in neurodegenerative disorders. Glutathione is an important intracellular antioxidant that protects against a variety of different antioxidant species. An important role for glutathione was proposed for the pathogenesis of Parkinson's disease, because a decrease in total glutathione concentrations in the substantia nigra has been observed in preclinical stages, at a time at which other biochemical changes are not yet detectable. Because glutathione does not cross the blood-brain barrier other treatment options to increase brain concentrations of glutathione including glutathione analogs, mimetics or precursors are discussed.

Published
2000

40. Human malignant glioma cell lines are refractory to retinoic acid-mediated differentiation and sensitization to apoptosis

Author

F, Schmidt, P, Groscurth, J, Dichgans, and M, Weller

Subjects
Interferon-alpha, Apoptosis, Cell Differentiation, Stereoisomerism, Tretinoin, Glioma, Rats, Interferon-gamma, Proto-Oncogene Proteins c-bcl-2, Astrocytes, Animals, Humans, Drug Interactions, Tumor Suppressor Protein p53
Abstract

Retinoids are candidate differentiation-inducing agents for glial tumors. Differentiation therapy is an attractive approach to cancers that resist surgery, irradiation and chemotherapy.We examined the effects of retinoids on proliferation, morphology and sensitivity to apoptosis in human malignant glioma and neuroblastoma cell lines.In contrast to neuroblastoma cells, retinoids are devoid of acute cytotoxic effects and have only moderate antiproliferative effects on human glioma cell lines upon long-term exposure at high concentrations. Electron microscopy fails to reveal features of differentiation or apoptosis in retinoid-treated glioma cells and untransformed rat astrocytes. Retinoids do not modulate CD95 or CD95L expression or susceptibility to CD95-mediated apoptosis and fail to act in synergy with interferon (IFN)-alpha or IFN-gamma or cancer chemotherapy drugs to promote growth inhibition or apoptosis.Glioma cell lines are refractory to the induction of differentiation or apoptosis by retinoids.

Published
2000

42. Evoked potentials in multiple system atrophy (MSA)

Author

M, Abele, J B, Schulz, K, Bürk, H, Topka, J, Dichgans, and T, Klockgether

Subjects
Adult, Male, Afferent Pathways, Analysis of Variance, Chi-Square Distribution, Cerebellar Ataxia, Neural Conduction, Pyramidal Tracts, Magnetoencephalography, Middle Aged, Multiple System Atrophy, Evoked Potentials, Motor, Statistics, Nonparametric, Parkinsonian Disorders, Evoked Potentials, Somatosensory, Evoked Potentials, Auditory, Brain Stem, Reaction Time, Evoked Potentials, Visual, Humans, Female, Visual Pathways, Evoked Potentials, Aged
Abstract

To study the involvement of pyramidal tracts and sensory pathways in multiple system atrophy (MSA).Evoked potential studies were performed in 45 MSA patients suffering from either MSA of cerebellar type (MSA-C) or MSA of parkinsonian type (MSA-P).Motor evoked potentials were normal in all MSA patients, whereas visual and somatosensory evoked potential abnormalities were found in about 40% of the MSA patients with no significant difference between the cerebellar (MSA-C) and parkinsonian (MSA-P) subgroup. Abnormal latencies of wave III in brainstem auditory evoked potentials were significantly more frequent in MSA-C.Abnormalities of somatosensory, visual and auditory evoked potentials are frequent findings in MSA, whereas abnormal motor evoked potentials are not a characteristic feature of the disease.

Published
2000

43. Transforming growth factors beta(1) (TGF-beta(1)) and TGF-beta(2) promote glioma cell migration via Up-regulation of alpha(V)beta(3) integrin expression

Author

M, Platten, W, Wick, C, Wild-Bode, S, Aulwurm, J, Dichgans, and M, Weller

Subjects
Transcriptional Activation, Integrins, Gene Expression Regulation, Cell Movement, Transforming Growth Factor beta, Tumor Cells, Cultured, Humans, Intercellular Signaling Peptides and Proteins, Glioma, RNA, Messenger, Peptides, Up-Regulation
Abstract

The migratory behaviour of malignant gliomas relies on the interaction of integrins with extracellular matrix (ECM) components. Transforming growth factor-beta(1) (TGF-beta(1)) potently stimulates glioma cell motility whereas TGF-beta(2) is known for its immunosuppressive properties. Here, we show that both TGF-beta(1) and TGF-beta(2) promote migration of glioma cells. In parallel, TGF-beta(1) and TGF-beta(2) induce alpha(V) and beta(3) intergrin mRNA expression and enhance cell surface expression of alpha(V)beta(3) integrin. TGF-beta-mediated promotion of migration is abrogated by echistatin, a Arg-Gly-Asp (RGD) peptide antagonist of alpha(V)beta(3) integrin, and by a neutralizing anti-alpha(V)beta(3) integrin antibody. Taken together, we report a novel mechanism by which TGF-beta modulates cell ECM interactions and promotes glioma cell motility.

Published
2000

44. [Aging in parts? Systemic aging of the nervous system]

Author

J, Dichgans and J B, Schulz

Subjects
Central Nervous System, Male, Neurons, Animals, Humans, Female, Nerve Tissue Proteins, Neurodegenerative Diseases, Magnetic Resonance Imaging, Cellular Senescence
Abstract

Neurons of the central nervous system in general do not multiply after birth. Therefore, no replacement or biological renewal of individual cells affected by aging or death is possible. Morphological changes occurring in the aging brain are found substantially more pronounced in neurodegenerative diseases. Systemic degenerations of selective brain areas in these disorders, e.g. in Alzheimer's, Parkinson's, Huntington's disease or in amyotrophic lateral sclerosis, may be considered as models of accelerated aging and may allow to study the genetic and environmental influences of selective aging and cell death in modules of the central nervous system. Although neurodegenerative diseases are disparate disorders on the basis of their symptomatology and the anatomic distribution of pathologic lesions, they actually share key attributes with respect to biochemical and cellular determinants of selective vulnerability. Most strikingly, many show a conversion of disease specific and only recently identified proteins into unsoluble aggregates which form intra- or extracellular deposits. These protein aggregates may, over time, affect neuronal function, eventually leading to neurodegeneration and neurodegenerative pathology. The pathological process is counterbalanced by protective mechanisms that may loose their efficacy during normal aging. This could explain the late onset of even the inherited neurodegenerative disorders. Since the expression of disease-specific proteins is often not restricted to the affected brain areas (as exemplified by the expression of polyglutamine containing proteins in trinucleotide repeat disorders in non-affected brain areas and even outside the brain), the anatomical specificity of the degenerative process may be determined by associated binding proteins. Therapeutic strategies include the reinforcement of physiological defense mechanisms and intervention at early phases of the pathological biochemistry of disease specific proteins.

Published
2000

45. [New insights in the molecular genetics and pathophysiology of hereditary ataxias]

Author

K, Bürk, T, Klockgether, and J, Dichgans

Subjects
Adult, Chromosome Aberrations, Male, Adolescent, Nuclear Proteins, Proteins, Chromosome Disorders, Nerve Tissue Proteins, Repressor Proteins, Phosphotransferases (Alcohol Group Acceptor), Ataxins, Trinucleotide Repeats, Friedreich Ataxia, Iron-Binding Proteins, Mutation, Humans, Protein Isoforms, Ataxia, Female, Ataxin-3, Ataxin-1, Spinocerebellar Degenerations
Abstract

The hereditary ataxias are a heterogeneous group of inherited neurodegenerative disorders characterised by progressive ataxia that results from degeneration of the cerebellum and its afferent and efferent connections. With respect to the pathogenic mechanisms, the hereditary ataxias may be tentatively divided into three groups: (1) The recessive ataxias are induced by the functional impairment of a protein that is essential for the survival of specific neurons while the autosomal dominant ataxias are either caused by (2) mutations of genes coding for ion channels thus resulting in a channelopathy or by (3) a novel deleterious function of a extended polyglutamine sequence within the proteins encoded by the respective genes.

Published
1999

46. Tremorlytic activity of budipine in Parkinson's disease

Author

S, Spieker, S, Breit, T, Klockgether, and J, Dichgans

Subjects
Antiparkinson Agents, Levodopa, Male, Double-Blind Method, Piperidines, Electromyography, Tremor, Humans, Female, Parkinson Disease, Aged
Abstract

In order to objectively quantify the tremorlytic activity of budipine in Parkinson's disease (PD) we performed longterm tremor recordings in a subset of patients enrolled in two clinical trials. Eleven PD patients with marked tremor participating in an open-label study underwent longterm recording before and during medication. Nine patients completed the study. Tremor occurrence was reduced from 52 +/- 18.6% to 34.7 +/- 19.3% (p0.05); tremor intensity decreased from 15.3 +/- 4.8 (SNR) to 11.3 +/- 4.8 (p0.01). UPDRS tremor subscores were also significantly improved. Fourteen patients who enrolled in a multicenter, double-blind, placebo-controlled study underwent longterm tremor analysis in addition to the Columbia University Rating Scale (CURS). Tremor occurrence was improved in the budipine group (n = 7) from 24.7 +/- 15.5% to 14.8 +/- 14.5% (p0.05). Tremor intensity decreased from 9.1 +/- 2.5 (SNR) to 7.2 +/- 1.6. However, the latter result was statistically not significant, probably due to the small patient number. In the placebo-group (n = 7) there was no reduction of tremor occurrence or of tremor intensity. The CURS sum score was improved from 5.7 to 3.0 in the budipine group, whereas there was only a smaller improvement in the placebo group (from 7.1 to 5.5). These data suggest that budipine is an effective tremorlytic agent in PD, which may be used as an alternative to anticholinergics.

Published
1999

47. Betulinic acid-induced apoptosis in glioma cells: A sequential requirement for new protein synthesis, formation of reactive oxygen species, and caspase processing

Author

W, Wick, C, Grimmel, B, Wagenknecht, J, Dichgans, and M, Weller

Subjects
Cyclin-Dependent Kinase Inhibitor p21, Fas Ligand Protein, Cell Survival, bcl-X Protein, Apoptosis, DNA Fragmentation, Cysteine Proteinase Inhibitors, Cyclins, Proto-Oncogene Proteins, Tumor Cells, Cultured, Humans, fas Receptor, Cycloheximide, Betulinic Acid, bcl-2-Associated X Protein, Membrane Glycoproteins, Cell Cycle, Glioma, Antineoplastic Agents, Phytogenic, Triterpenes, Enzyme Activation, Kinetics, Proto-Oncogene Proteins c-bcl-2, Caspases, Pentacyclic Triterpenes, Reactive Oxygen Species, Oligopeptides, Cell Division
Abstract

Betulinic acid (BA), a pentacyclic triterpene, is an experimental cytotoxic agent for malignant melanoma. Here, we show that BA triggers apoptosis in five human glioma cell lines. BA-induced apoptosis requires new protein, but not RNA, synthesis, is independent of p53, and results in p21 protein accumulation in the absence of a cell cycle arrest. BA-induced apoptosis involves the activation of caspases that cleave poly(ADP ribose)polymerase. Interactions of death ligand/receptor pairs of the CD95/CD95 ligand family do not mediate BA-induced caspase activation. BA enhances the levels of BAX and BCL-2 proteins but does not alter the levels of BCL-xS or BCL-xL. Ectopic expression of BCL-2 prevents BA-induced caspase activation, DNA fragmentation, and cell death. Furthermore, BA induces the formation of reactive oxygen species that are essential for BA-triggered cell death. The generation of reactive oxygen species is blocked by BCL-2 and requires new protein synthesis but is unaffected by caspase inhibitors, suggesting that BA toxicity sequentially involves new protein synthesis, formation of reactive oxygen species, and activation of crm-A-insensitive caspases.

Published
1999

48. Predicting chemoresistance in human malignant glioma cells: the role of molecular genetic analyses

Author

M, Weller, J, Rieger, C, Grimmel, E G, Van Meir, N, De Tribolet, S, Krajewski, J C, Reed, A, von Deimling, and J, Dichgans

Subjects
Proto-Oncogene Proteins c-bcl-2, Brain Neoplasms, Drug Resistance, Neoplasm, Mutation, Tumor Cells, Cultured, Humans, Antineoplastic Agents, Apoptosis, Glioma, Drug Screening Assays, Antitumor, Genes, Retinoblastoma, Genes, p53
Abstract

Less than 30% of malignant gliomas respond to adjuvant chemotherapy. Here, we asked whether alterations in the p53 and RB pathways and the expression of six BCL-2 family proteins predicted acute cytotoxicity and clonogenic cell death induced by BCNU, vincristine, cytarabine, teniposide, doxorubicin, camptothecin or beta-lapachone in 12 human malignant glioma cell lines. Neither wild-type p53 status, nor p53 protein accumulation, nor p21 or MDM-2 levels, nor differential expression of BCL-2 family proteins predicted drug sensitivity, except for an association of BAX with higher beta-lapachone sensitivity in acute cytotoxicity assays. p16 protein expression was associated with high doubling time and chemoresistance. We conclude that some important molecular changes, which are involved in the development of gliomas and attributed a role in regulating vulnerability to apoptosis, may not determine the response to chemotherapy in these tumors.

Published
1998

49. Chemosensitivity of human malignant glioma: modulation by p53 gene transfer

Author

M, Trepel, P, Groscurth, U, Malipiero, E, Gulbins, J, Dichgans, and M, Weller

Subjects
Recombinant Fusion Proteins, Antineoplastic Agents, Apoptosis, Transfection, Mice, Proto-Oncogene Proteins, Tumor Cells, Cultured, Animals, Humans, Point Mutation, Teniposide, bcl-2-Associated X Protein, Brain Neoplasms, Cytarabine, Temperature, Glioma, Genes, p53, Carmustine, Genes, bcl-2, Gene Expression Regulation, Neoplastic, Amino Acid Substitution, Proto-Oncogene Proteins c-bcl-2, Doxorubicin, Drug Resistance, Neoplasm, Vincristine, Tumor Suppressor Protein p53, Cell Division, Gene Deletion
Abstract

Loss of wild-type p53 activity is one of the most common molecular abnormalities in human cancers including malignant gliomas. The p53 status is also thought to modulate sensitivity to irradiation and chemotherapy. Here, we studied the effect of a p53 gene transfer on the chemosensitivity of three human glioma cell lines with different endogenous p53 status (LN-229, wild-type; LN-18, mutant; LN-308, deleted), using the murine temperature-sensitive p53 val135 mutant. Expression of mutant p53 enhanced proliferation of LN-308 cells but reduced proliferation in the other cell lines. Expression of wild-type p53 caused reversible growth arrest of all cell lines but failed to induce apoptosis. Growth arrest induced by wild-type p53 was associated with strong induction of p21 expression. Strong induction of BAX expression and loss of BCL-2 expression, which are associated with p53-dependent apoptosis rather than growth arrest, were not observed. Wild-type p53 failed to sensitize glioma cells to cytotoxic drugs including BCNU, cytarabine, doxorubicin, teniposide and vincristine. The combined effects of wild-type p53 gene transfer and drug treatment were less than additive rather than synergistic, suggesting that the intracellular cascades activated by p53 and chemotherapy are redundant. Unexpectedly, forced expression of mutant p53 modulated drug sensitivity in that it enhanced the toxicity of some drugs but attenuated the effects of others. These effects may represent a dominant negative effect of mutant p53 in LN-229 cells which have wild-type p53 activity but must be considered a gain of function-type effect in the other two cell lines which have no wild-type p53 activity. Importantly, no clear-cut pattern emerged among the three cell lines studied. We conclude that somatic gene therapy based on the reintroduction of p53 will limit the proliferation of human malignant glioma cells but is unlikely to induce clinically relevant sensitization to chemotherapy in these tumors.

Published
1998

50. Multijoint arm movements in cerebellar ataxia: abnormal control of movement dynamics

Author

H, Topka, J, Konczak, K, Schneider, A, Boose, and J, Dichgans

Subjects
Adult, Male, Cerebellar Ataxia, Movement, Arm, Humans, Female, Joints, Middle Aged, Hand, Muscle, Skeletal, Psychomotor Performance, Gravitation
Abstract

In cerebellar ataxia, kinematic aberrations of multijoint movements are thought to originate from deficiencies in generating muscular torques that are adequate to control the mechanical consequences of dynamic interaction forces. At this point the exact mechanisms that lead to an abnormal control of interaction torques are not known. In principle, the generation of inadequate muscular torques may result from an impairment in generating sufficient levels of torques or from an inaccurate assessment and prediction of the mechanical consequences of movements of one limb segment on adjacent joints. We sought to differentiate the relative contribution of these two mechanisms and, therefore, analyzed intersegmental dynamics of multijoint pointing movements in healthy subjects and in patients with cerebellar degeneration. Unrestrained vertical arm movements were performed at three different target movement velocities and recorded using an optoelectronic tracking system. An inverse dynamics approach was employed to compute net joint torques, muscular torques, dynamic interaction torques and gravitational torques acting at the elbow and shoulder joint. In both groups, peak dynamic interaction forces and peak muscular forces were largest during fast movements. In contrast to normal subjects, patients produced hypermetric movements when executing fast movements. Hypermetric movements were associated with smaller peak muscular torques and smaller rates of torque change at elbow and shoulder joints. The patients' deficit in generating appropriate levels of muscular force were prominent during two different phases of the pointing movement. Peak muscular forces at the elbow were reduced during the initial phase of the movement when simultaneous shoulder joint flexion generated an extensor influence upon the elbow joint. When attempting to terminate the movement, gravitational and dynamic interaction forces caused overshooting extension at the elbow joint. In normal subjects, muscular torque patterns at shoulder and elbow joint were synchronized in that peak flexor and extensor muscular torques occurred simultaneously at both joints. This temporal pattern of muscular torque generation at shoulder and elbow joint was preserved in patients. Our data suggest that an impairment in generating sufficient levels of phasic muscular torques significantly contributes to the patients' difficulties in controlling the mechanical consequences of dynamic interaction forces during multijoint movements.

Published
1998

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