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4. Unusual presentations and intrafamilial phenotypic variability in infantile onset Alexander disease

Author

Isabella Moroni, Laura Farina, Davide Tonduti, Giorgio Giaccone, Isabella Ceccherini, and Anna Ardissone

Subjects
Adult, Male, 0301 basic medicine, medicine.medical_specialty, Pathology, Neurology, Adolescent, Dermatology, Biology, White matter, 03 medical and health sciences, 0302 clinical medicine, Glial Fibrillary Acidic Protein, medicine, Humans, Child, Neuroradiology, Family Health, Glial fibrillary acidic protein, Leukodystrophy, Brain, General Medicine, medicine.disease, Magnetic Resonance Imaging, Phenotype, Alexander disease, Psychiatry and Mental health, 030104 developmental biology, medicine.anatomical_structure, biology.protein, Female, Alexander Disease, Neurology (clinical), Neurosurgery, 030217 neurology & neurosurgery
Abstract

Alexander disease is an hereditary leukodystrophy related to mutations of GFAP. Classically AxD was divided in infantile, juvenile, and adult subgroups. Recent data suggested considering only two subtypes: type I (infantile onset with lesions extending to the cerebral hemispheres); type II (adult onset with primary involvement of subtentorial structures). We report two related and one unrelated patients presenting with a peculiar association of clinical and neuroradiological features. GFAP analysis disclosed the presence of one novel and two previously reported mutations. Our patients underline the importance of considering AxD in patients with bulbar symptoms and autonomic dysfunction even if MRI shows only posterior fossa abnormalities, supporting the hypothesis of a third type of AxD sharing features of both type I and type II. The evidence of an intrafamilial phenotypic variability suggests the possible role of still unknown factors influencing the effect of GFAP mutation and determining the phenotype.

Published
2016

5. KARS-related diseases: progressive leukoencephalopathy with brainstem and spinal cord calcifications as new phenotype and a review of literature

Author

Isabella Moroni, Odile Boespflug-Tanguy, Anna Pichiecchio, Rita Barone, Gabriella Nebbia, Imen Dorboz, Andrea Legati, Anna Ardissone, Daniele Ghezzi, Luisa Chiapparini, Barbara Garavaglia, Simona Orcesi, Eleonora Lamantea, Laura Farina, Davide Tonduti, Marco Maggioni, Ardissone, A, Tonduti, D, Legati, A, Lamantea, E, Barone, R, Dorboz, I, Boespflug-Tanguy, O, Nebbia, G, Maggioni, M, Garavaglia, B, Moroni, I, Farina, L, Pichiecchio, A, Orcesi, S, Chiapparini, L, and Ghezzi, D

Subjects
Lysine-tRNA Ligase, 0301 basic medicine, Microcephaly, Pathology, medicine.medical_specialty, Mitochondrial disease, Encephalopathy, lcsh:Medicine, Calcification, Leukoencephalopathy, 03 medical and health sciences, 0302 clinical medicine, Leukoencephalopathies, KARS, medicine, Humans, Genetic Predisposition to Disease, Pharmacology (medical), Calcifications, Genetics (clinical), Progressive leukoencephalopathy, business.industry, Research, lcsh:R, Calcinosis, General Medicine, medicine.disease, Spinal cord, 3. Good health, 030104 developmental biology, medicine.anatomical_structure, Peripheral neuropathy, Spinal Cord, Brainstem, business, 030217 neurology & neurosurgery, Brain Stem
Abstract

Background KARS encodes lysyl- transfer ribonucleic acid (tRNA) synthetase, which catalyzes the aminoacylation of tRNA-Lys in the cytoplasm and mitochondria. Eleven families/sporadic patients and 16 different mutations in KARS have been reported to date. The associated clinical phenotype is heterogeneous ranging from early onset encephalopathy to isolated peripheral neuropathy or nonsyndromic hearing impairment. Recently additional presentations including leukoencephalopathy as predominant cerebral involvement or cardiomyopathy, isolated or associated with muscular and cerebral involvement, have been reported. A progressive Leukoencephalopathy with brainstem and spinal cord calcifications was previously described in a singleton patient and in two siblings, without the identification of the genetic cause. We reported here about a new severe phenotype associated with biallelic KARS mutations and sharing some common points with the other already reported phenotypes, but with a distinct clinical and neuroimaging picture. Review of KARS mutant patients published to date will be also discussed. Results Herein, we report the clinical, biochemical and molecular findings of 2 unreported Italian patients affected by developmental delay, acquired microcephaly, spastic tetraparesis, epilepsy, sensory-neural hypoacusia, visual impairment, microcytic hypochromic anaemia and signs of hepatic dysfunction. MRI pattern in our patients was characterized by progressive diffuse leukoencephalopathy and calcifications extending in cerebral, brainstem and cerebellar white matter, with spinal cord involvement. Genetic analysis performed on these 2 patients and in one subject previously described with similar MRI pattern revealed the presence of biallelic mutations in KARS in all 3 subjects. Conclusions With our report we define the molecular basis of the previously described Leukoencephalopathy with Brainstem and Spinal cord Calcification widening the spectrum of KARS related disorders, particularly in childhood onset disease suggestive for mitochondrial impairment. The review of previous cases does not suggest a strict and univocal genotype/phenotype correlation for this highly heterogeneous entity. Moreover, our cases confirm the usefulness of search for common brain and spine MR imaging pattern and of broad genetic screening, in syndromes clinically resembling mitochondrial disorders in spite of normal biochemical assay. Electronic supplementary material The online version of this article (10.1186/s13023-018-0788-4) contains supplementary material, which is available to authorized users.

Published
2018

6. Redefining phenotypes associated with mitochondrial DNA single deletion

Author

Carlo Minetti, Enrico Bertini, Elena Cardaioli, Elena Pegoraro, Filippo M. Santorelli, Liliana Vercelli, Donato Sauchelli, Michelangelo Mancuso, Paola Da Pozzo, Giacomo P. Comi, Maurizio Moggio, Daniele Orsucci, Mauro Scarpelli, Valerio Carelli, M. Sciacco, Serenella Servidei, Elena Caldarazzo Ienco, Corrado Angelini, Massimiliano Filosto, Paola Tonin, Isabella Moroni, Massimo Zeviani, Gabriele Siciliano, Claudio Bruno, Maria Lucia Valentino, Costanza Lamperti, Tiziana Mongini, Maria Alice Donati, Michela Catteruccia, Dario Ronchi, Luca Bello, Antonio Toscano, Olimpia Musumeci, Antonio Federico, Mancuso, M., Orsucci, D., Angelini, C., Bertini, E., Carelli, V., Comi, G.P., Donati, M.A., Federico, A., Minetti, C., Moggio, M., Mongini, T., Santorelli, F.M., Servidei, S., Tonin, P., Toscano, A., Bruno, C., Bello, L., Caldarazzo Ienco, E., Cardaioli, E., Catteruccia, M., Da Pozzo, P., Filosto, M., Lamperti, C., Moroni, I., Musumeci, O., Pegoraro, E., Ronchi, D., Sauchelli, D., Scarpelli, M., Sciacco, M., Valentino, M.L., Vercelli, L., Zeviani, M., and Siciliano, G.

Subjects
Male, Ophthalmoplegia, Chronic Progressive External, Mitochondrial Diseases, Databases, Factual, Kearns-Sayre Syndrome, mitochondrial DNA, Disease, CPEO, KSS, Mitochondrial disorders, mtDNA, Pearson syndrome, Single deletion, Neurology (clinical), Neurology, Bioinformatics, Acyl-CoA Dehydrogenase, Kearns–Sayre syndrome, Congenital Bone Marrow Failure Syndromes, Genetics, Ophthalmoplegia, Inborn Errors, Medicine (all), Acyl-CoA Dehydrogenase, Long-Chain, Middle Aged, Heteroplasmy, Mitochondrial, Settore MED/26 - NEUROLOGIA, Phenotype, Female, Cohort study, Adult, musculoskeletal diseases, Mitochondrial DNA, Mitochondrial disease, Biology, DNA, Mitochondrial, Lipid Metabolism, Inborn Errors, Databases, Young Adult, Muscular Diseases, medicine, Humans, Factual, Retrospective Studies, Retrospective cohort study, DNA, Lipid Metabolism, medicine.disease, progressive external ophthalmoplegia, PEO, Chronic Progressive External, Long-Chain, Gene Deletion
Abstract

Progressive external ophthalmoplegia (PEO), Kearns–Sayre syndrome (KSS) and Pearson syndrome are the three sporadic clinical syndromes classically associated with single large-scale deletions of mitochondrial DNA (mtDNA). PEO plus is a term frequently utilized in the clinical setting to identify patients with PEO and some degree of multisystem involvement, but a precise definition is not available. The purpose of the present study is to better define the clinical phenotypes associated with a single mtDNA deletion, by a retrospective study on a large cohort of 228 patients from the database of the “Nation-wide Italian Collaborative Network of Mitochondrial Diseases”. In our database, single deletions account for about a third of all patients with mtDNA-related disease, more than previously recognized. We elaborated new criteria for the definition of PEO and “KSS spectrum” (a category of which classic KSS represents the most severe extreme). The criteria for “KSS spectrum” include the resulting multisystem clinical features associated with the KSS features, and which therefore can predict their presence or subsequent development. With the new criteria, we were able to classify nearly all our single-deletion patients: 64.5% PEO, 31.6% KSS spectrum (including classic KSS 6.6%) and 2.6% Pearson syndrome. The deletion length was greater in KSS spectrum than in PEO, whereas heteroplasmy was inversely related with age at onset. We believe that the new phenotype definitions implemented here may contribute to a more homogeneous patient categorization, which will be useful in future cohort studies of natural history and clinical trials. © 2015, Springer-Verlag Berlin Heidelberg.

Published
2015

7. Neurological Disorders Associated with Striatal Lesions: Classification and Diagnostic Approach

Author

Celeste Panteghini, Anna Ardissone, Luisa Chiapparini, Davide Tonduti, Barbara Garavaglia, Sergio Raspante, Federica Zibordi, Giovanna Zorzi, Isabella Moroni, and Nardo Nardocci

Subjects
0301 basic medicine, medicine.medical_specialty, Pathology, Neurology, Movement disorders, Striatal lesions, Degeneration (medical), Infections, Necrosis, 03 medical and health sciences, 0302 clinical medicine, Basal ganglia, medicine, Humans, Thiamine, Movement Disorders, General Neuroscience, Putamen, Biological Transport, 030104 developmental biology, Etiology, Neurology (clinical), Nervous System Diseases, medicine.symptom, Differential diagnosis, Psychology, 030217 neurology & neurosurgery
Abstract

Neostriatal abnormalities can be observed in a very large number of neurological conditions clinically dominated by the presence of movement disorders. The neuroradiological picture in some cases has been described as "bilateral striatal necrosis" (BSN). BSN represents a condition histo-pathologically defined by the involvement of the neostriata and characterized by initial swelling of putamina and caudates followed by degeneration and cellular necrosis. After the first description in 1975, numerous acquired and hereditary conditions have been associated with the presence of BSN. At the same time, a large number of disorders involving neostriata have been described as BSN, in some cases irrespective of the presence of signs of cavitation on MRI. As a consequence, the etiological spectrum and the nosographic boundaries of the syndrome have progressively become less clear. In this study, we review the clinical and radiological features of the conditions associated with MRI evidence of bilateral striatal lesions. Based on MRI findings, we have distinguished two groups of disorders: BSN and other neostriatal lesions (SL). This distinction is extremely helpful in narrowing the differential diagnosis to a small group of known conditions. The clinical picture and complementary exams will finally lead to the diagnosis. We provide an update on the etiological spectrum of BSN and propose a diagnostic flowchart for clinicians.

Published
2016

8. Ataxia with oculomotor apraxia type1 (AOA1): novel and recurrent aprataxin mutations, coenzyme Q10 analyses, and clinical findings in Italian patients

Author

Davide Pareyson, Roberto Fancellu, Massimo Plumari, Daniela Di Bella, Caterina Mariotti, Graziella Uziel, Nardo Nardocci, Marco Rimoldi, Stefano Di Donato, Sara Caimi, Franco Taroni, Barbara Castellotti, Cinzia Gellera, Giovanna Zorzi, and Isabella Moroni

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Ataxia, Adolescent, Apraxias, Ubiquinone, DNA Mutational Analysis, aptX, Gene mutation, Biology, Cohort Studies, Young Adult, Cellular and Molecular Neuroscience, Gene Frequency, Oculomotor Nerve, Oculomotor Nerve Diseases, Genetics, medicine, Humans, Abnormalities, Multiple, Cognitive decline, Oculomotor apraxia, Child, Genetic Association Studies, Genetics (clinical), Aprataxin, Cerebellar ataxia, Nuclear Proteins, Chorea, Middle Aged, medicine.disease, DNA-Binding Proteins, Italy, Mutation, Female, medicine.symptom
Abstract

Ataxia with oculomotor apraxia type1 (AOA1, MIM 208920) is a rare autosomal recessive disease caused by mutations in the APTX gene. We screened a cohort of 204 patients with cerebellar ataxia and 52 patients with early-onset isolated chorea. APTX gene mutations were found in 13 ataxic patients (6%). Eleven patients were homozygous for the known p.W279X, p.W279R, and p.P206L mutations. Three novel APTX mutations were identified: c.477delC (p.I159fsX171), c.C541T (p.Q181X), and c.C916T (p.R306X). Expression of mutated proteins in lymphocytes from these patients was greatly decreased. No mutations were identified in subjects with isolated chorea. Two heterozygous APTX sequence variants (p.L248M and p.D185E) were found in six families with ataxic phenotype. Analyses of coenzyme Q10 in muscle, fibroblasts, and plasma demonstrated normal levels of coenzyme in five of six mutated subjects. The clinical phenotype was homogeneous, irrespectively of the type and location of the APTX mutation, and it was mainly characterized by early-onset cerebellar signs, sensory neuropathy, cognitive decline, and oculomotor deficits. Three cases had slightly raised alpha-fetoprotein. Our survey describes one of the largest series of AOA1 patients and contributes in defining clinical, molecular, and biochemical characteristics of this rare hereditary neurological condition.

Published
2011

9. Clinical, biochemical and neuroradiological findings in L -2-hydroxyglutaric aciduria

Author

Ludovico D'Incerti, Isabella Moroni, Laura Farina, Marco Rimoldi, and G. Uziel

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Neurology, Adolescent, Neural Conduction, Dermatology, Glutarates, Epilepsy, Cerebrospinal fluid, Prenatal Diagnosis, medicine, Humans, Neuroradiology, medicine.diagnostic_test, business.industry, Leukodystrophy, Brain, Magnetic resonance imaging, Syndrome, General Medicine, medicine.disease, Binswanger's disease, Magnetic Resonance Imaging, Psychiatry and Mental health, Inborn error of metabolism, Child, Preschool, Female, Neurology (clinical), Nervous System Diseases, business
Abstract

L-2-Hydroxyglutaric aciduria is a rare inborn error of metabolism, marked by a large and persistent increase of L-2-hydroxyglutaric acid in urine, blood and cerebrospinal fluid (CSF). We present clinical, biochemical and neuroradiological findings of seven Italian patients aged 4-19 years presenting at different stages of the disease. The disorder was characterized by a progressive neurological syndrome with cerebellar and pyramidal signs, mental deterioration, epilepsy and subcortical leukoencephalopathy on magnetic resonance imaging (MRI). We observed a good correlation between the severity of the disease and the extent of lesions on MRI. We report the result of the first positive prenatal diagnosis.

Published
2000

10. Congenital muscular dystrophy with merosin deficiency: MRI findings in five patients

Author

Marina Mora, M. Savoiardo, Isabella Moroni, Chiara Pantaleoni, Elisa Ciceri, Lucia Morandi, I. Milanesi, and Laura Farina

Subjects
Adult, Male, medicine.medical_specialty, Pathology, Neurology, Central nervous system, Muscular Dystrophies, White matter, medicine, Humans, Radiology, Nuclear Medicine and imaging, Muscular dystrophy, Child, Creatine Kinase, Neuroradiology, medicine.diagnostic_test, business.industry, Magnetic resonance imaging, medicine.disease, Magnetic Resonance Imaging, medicine.anatomical_structure, Child, Preschool, Congenital muscular dystrophy, Female, Laminin, Neurology (clinical), Neurosurgery, Cardiology and Cardiovascular Medicine, business
Abstract

We present the MRI findings in five patients with congenital muscular dystrophy (CMD) and merosin (laminin alpha2) deficiency, which was total in one and partial in four. In one patient with partial merosin deficiency, MRI was normal. The other four patients had supratentorial white matter abnormalities. In three, T2-weighted images revealed subcortical, deep lobar and periventricular high signal in white matter, while in the other there were only small peritrigonal areas of increased signal. On T1-weighted images, there was slightly low signal. Cortical abnormalities were absent. None of these changes were accompanied by symptoms or signs of central nervous system involvement. White matter abnormalities in a patient with CMD should prompt investigation of merosin.

Published
1998

11. SETX mutations are a frequent genetic cause of juvenile and adult onset cerebellar ataxia with neuropathy and elevated serum alpha-fetoprotein

Author

Isabella Moroni, Davide Pareyson, Alfredo Brusco, Giovanna Zorzi, Viviana Pensato, Carlo Antozzi, Lorenzo Nanetti, Simona Cavalieri, Cinzia Gellera, Alessandra Erbetta, Marta Panzeri, and Caterina Mariotti

Subjects
Male, Pathology, Recessive ataxia, Genetics(clinical), Pharmacology (medical), Age of Onset, Oculomotor apraxia, Genetics (clinical), Medicine(all), Genetics, education.field_of_study, SETX, Ataxia with Oculomotor Apraxia type 2, AOA2, ATM, Alpha-fetoprotein, Ataxia telangiectasia, General Medicine, Middle Aged, Pedigree, Phenotype, Italy, Recessive ataxias, Female, alpha-Fetoproteins, medicine.symptom, RNA Helicases, Adult, medicine.medical_specialty, Ataxia, Adolescent, Cerebellar Ataxia, Apraxias, Population, aptX, Biology, Ataxia Telangiectasia, Young Adult, medicine, Humans, Family, education, Aged, Cerebellar ataxia, Research, DNA Helicases, medicine.disease, Multifunctional Enzymes, Mutation, Ataxia-telangiectasia, Gait Ataxia, Age of onset, Hypoalbuminemia
Abstract

Objectives/backgroundAtaxia with oculomotor apraxia defines a group of genetically distinct recessive ataxias including ataxia-telangectasia (A-T,ATMgene), ataxia with oculomotor apraxia type 1 (AOA1,APTXgene) and type 2 (AOA2,SETXgene). Although, a few unique clinical features differentiate each of these forms, the patients also share common clinical signs, such as the presence of cerebellar atrophy, sensorimotor axonal neuropathy, and elevated alpha-fetoprotein (AFP) serum level.Materials and methodsWe selected 22 Italian patients from 21 families, presenting progressive cerebellar ataxia, axonal neuropathy, and elevated serum AFP. We screened the coding regions ofATM,APTXandSETXgenes for point mutations by direct sequencing or DHPLC, and searched genomic rearrangements inSETXby MLPA analysis. In selected cases, quantification of ATM and senataxin proteins was performed by Western blot. Clinical, neurophysiological, and neuroimaging data were collected.ResultsThirteen patients (12 families) carriedSETXmutations (AOA2, 57%), two were mutated inATM(A-T), and three inAPTX(AOA1). In three remaining patients, we could not find pathogenic mutations, and in one case we found, in homozygosis, theSETXp.K992R polymorphism (population frequency 1-2%). In AOA2 cases, we identified 14 novel and three reportedSETXmutations. Signs at onset were gait ataxia and facial dyskinesia, and the age ranged between 11 and 18 years. None had obvious oculomotor apraxia at the latest examination (age 14–45 years). The patient carrying the p.K992RSETXpolymorphism had a phenotype similar to that of the diagnosed AOA2 patients, while the other three undiagnosed subjects had a very late onset and a few distinguishing clinical features.Discussion and conclusionsWe describe a large series of 13 AOA2 Italian patients. The phenotype was consistent with previous descriptions of AOA2, except for a higher frequency of strabism, and for the absence of oculomotor apraxia. In our survey ~60% of juvenile-to-adult cases with cerebellar ataxia, sensorimotor neuropathy and increased AFP are due to mutations in theSETXgene, and a smaller percentage toAPTXandATMgene mutations.

Published
2013

12. 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. Zucconl, Javier Muruzabal, R. R. Allen, R. Rivolta, K. Haugaard, A. Nespolo, K. Hoang-Xuang, G. Bussone, T. Avramidis, E. Corsini, Christiana Franke, T. Vinogradova, H. Boot, K. Vestergaard, G. H. Jansen, N. Argentino, M. Raltzig, W. Linssen, Mark B. Pepys, P. Roblot, L. Lauritzen, E. Fainardi, D. Morin, T. X. Arbizu Urdiain, J. Wollenhaupt, S. Bostantjopoulou, G. Pavesi, A. D. Forman, Giovanni Fabbrini, D. Jean, J. J. Archelos, M. I. Blanchs, M. Del Gobbo, Anna Carla Turconi, Ch. Derouesné, Elio Scarpini, A. Visbeck, P. Castejon, J. P. Renou, F. Mounier-Vehier, G. Potagas, Ch. Duyckaerts, A. Filla, R. Schneider, G. Ronen, K. Nagata, J. P. Vedel, A. Henneberg, G. van Melle, C. Baratti, H. Knott, M. C. Prevett, A. Bes, B. Metin, Jos V. Reempts, L. Martorell, Mefkure Eraksoy, H. O. Handwerker, D. S. Younger, O. Oktem, D. Frongillo, C. Soriano-Soriano, L. Niehaus, F. Zipp, A. Tartaro, S Newman, R. H. Browne, P. Davous, R. Sanchez, M. Muros, M. E. Kornhuber, A. Lavarone, M. Mohr, M. R. Garcia, S. Russell, H. Kellar-Wood, M. R. Tola, B. Ostermeyer, Ch. Tzekov, K. Sartor, E. B. Ringelstein, P. P. Gazzaniga, Paul Krack, H. Fidaner, H. Rico, T. Dbaiss, F. Alameda, E. Torchiana, L. Rumbach, I. Charques, J. M. Bogaard, C. D. Frith, L. J. Rappelle, R. Brenner, A. Joutel, K. Fuxe, G. HÄcker, M. J. Blaser, J. Valls-SolÇ, G. Ulm, M. Alberdi, A. Bock, F. W. Bertelsmann, U. Wieshmann, J. Visa, J. R. Lupski, D. D'Amico, L. M. P. Ramos, A. A. Vanderbark, R. Horn, M. Warmuth, Dietmar Kühne, Mark S. Palmer, C. Ehrenheim, E. Canga, S. Viola, O. Scarpino, P. Naldi, R. Almeida, A. A. Raymond, J. Gamez, Stephan Arnold, A. DiGiovanni, J. Dalmau, C. C. Chari, H. F. Beer, J. C. Koetsier, J. Iriarte, E. Yunis, J. Casadevall, E. Le Guern, E. Stenager, S. R. Benbadis, J. M. Warter, F. Burklin, I. Theodorou, L. Johannesen, G. A. Graveland, X. Leclerc, I. Vecchio, L. Ozelius, G. Nicoletti, R. K. Gherardi, E. Esperet, M. L. Delodovici, F. Cattin, F. Paiau, Giorgio Sacilotto, C. A. J. Broere, D. Chavdarov, J. P. Willmer, C. H. Hawkes, Th. Naegele, E. Ellie, E. Dartigues, M. J. Guardiola, S. Hesse, Z. Levic, Marco Rovaris, P. Saugeir-Veber, B. A. Yaqub, H. F. Durwen, R. Larumbe, J. Ballabrina, M. Sendtner, J. Röther, M. Horstink, C. Kluglein, M.P. Montesi, H. Apaydin, J. Montoya, E. Waubant, Ch. Verellen-Dunoulin, A. Nicolai, J. Lopez-Delval, R. Lemon, G. Cantinho, E. Granieri, A. Zeviani, Wolfgang H. Oertel, U. Ficola, V. Di Piero, V. Fragola, K. Sabev, M. V. Guitera, I. Turki, F. Bolgert, P. Ingrand, J. M. Gobernado, L. M. E. Grimaldi, S. Baybas, B. Eymard, Y. Rolland, Y. Robitaille, Ta. Pampols, P. J. Koehler, A. Carroacedo, J. Vilchez, S. Di Vittorio, I. R. Rise, T. Nagy, M. Kuffner, E. Palazzini, A. Ott, J. Pruim, T. X. Arbizu, E. Manetti, C. Cervera, S. Felber, G. Gursoy, J. Scholz, G. A. Buscaino, M. S. Chen, A. Pascual, J. Hazan, J. U. Gajda, J. G. Cea, G. Bottini, G. Damalik, F. Le Doze, G. Bonaldi, J. M. Hew, C. Messina, A. M. Kennedy, J. M. Carney, N. M. F. Murray, M. Parent, M. Koepp, V. Dimova, D. De Leo, K. Jellinger, G. Salemi, S. Mientus, M. L. Hansen, F. Mazzucchelli, J. Vieth, M. Mauri, E. Bartels, L. Johannsen, C. Humphreys, J. Emile, D. N. Landon, E. Kansu, R. Sanchez-Pernaute, Rsj Frackowiak, M. Gonzalez Torres, L. Oller, C. Machedo, J. Kother, M. Billiard, H. Durak, T. Schindler, A. Frank, A. Uncini, A. Sbriccoli, C. Farinas, D. W. Paty, N. Fast, A. T. Zangaladze, A. Kerkhofs, J. M. Pino Garcia, I. De la Fuente, B. Marini, L. Gomez, I. Rubio, Alessandra Bardoni, C. Brodie, P. Acin, U. Sliwka, S. A. Hawkins, S. Tardieu, F. Vitullo, J. M. Pereira Monteino, R. Gagliardi, T. Jezewski, A. Cano, T. Lempert, F. Abad Alegria, G. Rotondo, D. Ince, C. Martinez Parra, Y. Huang, H. Luders, Y. Steinvil, F. G. A. Van Der Meche, R. Bianchi, A. Sanchez, T. Sevilla, J. M. Ketelslegers, A. Domzal-Stryga, M. Pandolfo, M. O. Josse, K. W. Neff, I. Blanco, G. W. Bruyn, O. W. Witte, J. L. Thibault, G. Andersen, J. Pariset, A. Marcone, R. J. M. 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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. 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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

Catalog

Books, media, physical & digital resources
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