Department Of Neuropathology Research Articles

Eduardo Tolosa: from Spain to the USA and back again

Eduardo Tolosa: from Spain to the USA and back again

Frontotemporal dementia and Parkinsonism linked to chromosome 17 in a young Australian patient with the G389R Tau mutation

Neuropathology and Applied NeurobiologyVolume 34, Issue 3 p. 366-370 Frontotemporal dementia and Parkinsonism linked to chromosome 17 in a young Australian patient with the G389R Tau mutation N. Bermingham, N. Bermingham Department of Neuropathology, Cork University Hospital, Ireland,Search for more papers by this authorT. F. Cowie, T. F. Cowie Department of Pathology, The University of Melbourne,Search for more papers by this authorM. Paine, M. Paine Department of Neurology, St. Vincent's Hospital,Search for more papers by this authorE. Storey, E. Storey Department of Neurosciences, The Alfred Hospital, andSearch for more papers by this authorC. McLean, C. McLean Department of Anatomical Pathology, The Alfred Hospital, Melbourne, AustraliaSearch for more papers by this author N. Bermingham, N. Bermingham Department of Neuropathology, Cork University Hospital, Ireland,Search for more papers by this authorT. F. Cowie, T. F. Cowie Department of Pathology, The University of Melbourne,Search for more papers by this authorM. Paine, M. Paine Department of Neurology, St. Vincent's Hospital,Search for more papers by this authorE. Storey, E. Storey Department of Neurosciences, The Alfred Hospital, andSearch for more papers by this authorC. McLean, C. McLean Department of Anatomical Pathology, The Alfred Hospital, Melbourne, AustraliaSearch for more papers by this author First published: 07 December 2007 https://doi.org/10.1111/j.1365-2990.2007.00918.xCitations: 14Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume34, Issue3June 2008Pages 366-370 RelatedInformation

147th ENMC International Workshop: Guideline on processing and evaluation of sural nerve biopsies, 15–17 December 2006, Naarden, The Netherlands

a Department of Neurology, University of Wurzburg, Wurzburg, Josef-Schneider-Str. 11, 97080 Wurzburg, Germany b Department of Neuropathology, Institute of Neurology, London, United Kingdom c Department of Neurology, Mayo Clinic and Mayo Foundation, Rochester, United States d Department of Neurology, CHRU Dupuytren, Limoges, France e Department of Neurology, University of Tromso, Tromso, Norway f IRCCS Foundation Neurological Institute ‘‘Carlo Besta’’, Milan, Italy g Department of Neurosciences, Ophthalmology and Genetics, Universita degli Studi, Genova, Italy h Department of Neurology, Hacettepe University, Ankara, Turkey i Department of Neuropathology, University of Aachen, Aachen, Germany

Ultrastructural Heterogeneity of Gangliogliomas

Gangliogliomas are rare brain tumors, composed of neuronal and glial cells mixed in a different proportion. The basic histopathological pattern of gangliogliomas is well recognized but the variable microscopic appearance still can pose a challenge to the neuropathologist. The authors reanalyzed their series of gangliogliomas in the files of two departments of neuropathology. All analyzed tumors fulfilled the WHO histological criteria of ganglioglioma. Seven tumors were examined by electron microscopy. The following ultrastructural features were graded: presence of dense-cored vesicles, synaptic vesicles, synapses and intermediate filaments, abundant basal membranes, dystrophic neurites, autophagic vacuoles, and multivesicular bodies. Most of the neoplastic neurons were large, polyglonal or oval with well-developed subcellular organelles, round nuclei, and prominent nucleoli. In most cases there were abundant dense core vesicles, observed in both the tumor cell bodies as well as in their processes. Synapses were typically observed. Intermediate filaments were abundant in all tumors. The most intriguing ultrastructural finding was abundant presence of autophagic vacuoles. In 4 cases, multivesicular bodies were observed. All of the tumors with multivesicular bodies also contained abundant autophagic vacuoles.

Tuesday July 4, 2006 15:00-17:00 Hall 3D Discussion Group Session Large scale mRNA and protein expression profiling in epilepsy-where we are and where we are going

Abstract 1 M. Majores ( 1 Department of Neuropathology, University of Bonn Medical Center, Germany )

A 52‐year‐old man with hypohidrosis

NeuropathologyVolume 26, Issue 6 p. 592-594 A 52-year-old man with hypohidrosis Jun Shimizu, Corresponding Author Jun Shimizu Department of Neurology, Graduate School of Medicine, University of Tokyo, andJun Shimizu, md. PhD, Department of Neurology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. Email: [email protected]Search for more papers by this authorMeiko Hashimoto, Meiko Hashimoto Department of Neurology, Graduate School of Medicine, University of Tokyo, andSearch for more papers by this authorShigeo Murayama, Shigeo Murayama Department of Neuropathology, Tokyo Metropolitan Institute of Gerontology, Tokyo, JapanSearch for more papers by this authorShoji Tsuji, Shoji Tsuji Department of Neurology, Graduate School of Medicine, University of Tokyo, andSearch for more papers by this author Jun Shimizu, Corresponding Author Jun Shimizu Department of Neurology, Graduate School of Medicine, University of Tokyo, andJun Shimizu, md. PhD, Department of Neurology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. Email: [email protected]Search for more papers by this authorMeiko Hashimoto, Meiko Hashimoto Department of Neurology, Graduate School of Medicine, University of Tokyo, andSearch for more papers by this authorShigeo Murayama, Shigeo Murayama Department of Neuropathology, Tokyo Metropolitan Institute of Gerontology, Tokyo, JapanSearch for more papers by this authorShoji Tsuji, Shoji Tsuji Department of Neurology, Graduate School of Medicine, University of Tokyo, andSearch for more papers by this author First published: 24 November 2006 https://doi.org/10.1111/j.1440-1789.2006.00716.xCitations: 1Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume26, Issue6December 2006Pages 592-594 RelatedInformation

Neuropathological Reference Centre for Epilepsy Surgery: update 2006

For more than 10 years, many neuroscience centres in Germany established surgical strategies for the treatment of focal, refractory epilepsies. According to our estimation, major centers in Germany (i.e. Aachen, Berlin, Bielefeld-Bethel, Bonn, Erlangen, Freiburg/Kehl-Kork, Greifswald, Marburg, Munich, Ulm, Vogtareuth,) have already carried out a total of 5,000 operations. In each patient, extensive presurgical monitoring has been performed to identify a structural lesion within the epileptogenic area and to predict postoperative seizure relief and cognitive performance. The histopathological examination of surgical specimens, however, represents a particular challenge for neuropathologists. The spectrum of lesions is variable, detailed clinical-neuropathological follow-up studies are hardly available and no international classification system and evaluation criteria have been established. In May 2003, we have founded a neuropathological reference centre for epilepsy surgery at the Department of Neuropathology at the University of Erlangen in order to support the clinico-pathological evaluation and scientific studies of human focal epilepsies. The following issues are particularly addressed by the consultant and reference center for epilepsy surgery: (1) A data bank is settled intending to include all patients undergoing epilepsy surgery in Germany, Austria and Switzerland. (2) Colleagues examining epilepsy-surgical specimens can request for a second, consultant opinion. (3) A standardized neuropathological examination (i.e. cell counting, immunohistochemical analyses, etc.) is provided to support clinical studies (i.e. with respect to operation strategies, pharmacoresistance, cognitive outcome, etc.). (4) The neuropathological epilepsy register can be instrumental to support international committees (e.g. establishment of data- and tissue banks, classification schemes, etc.). So far, 3160 surgical specimens were microscopically evaluated representing the following lesions: Hippocampal sclerosis: 1043 cases; dual pathology: 149; epilepsy-associated tumors (LEAT): 898; Malformations of cortical development: 393; encephalitis: 50; glial scars/ischemia: 146; vascular lesions: 184; head trauma: 15; 239 cases remain to be further specified. The neuropathological reference center for epilepsy surgery is recommended by the executive board of the “Arbeitsgemeinschaft für prächirurgische Epilepsiediagnostik und operative Epilepsietherapie e.V.“.

Non-traumatic forensic neuropathology

The practicing Forensic Pathologist is likely to encounter case material in which either the cause of death or a major contribution to the cause of death is underlying damage to or disease of the central nervous system. While it is good practice in many instances to have a working relationship with a Department of Neuropathology, from which advice and practical help can be sought, there may be instances when the Forensic Pathologist needs to proceed on a basis of a working knowledge of Forensic Neuropathology up to and including how to examine the specimen and take tissue blocks for processing and subsequent histological examination. Some of the more common conditions of the central nervous system such as damage consequent to hypoxia-ischaemia, hypoglycemia and epilepsy, the encephalopathies associated with altered sodium concentration, deficiency due to Vitamin B 1 and various neurodegenerative diseases that manifest as dementia and include Alzheimer's disease, cortical Lewy body disease and the prion disorders, are outlined in this article.

Introduction

Brain PathologyVolume 14, Issue 1 p. 59-60 Free to Read Introduction Hans H. Goebel, Corresponding Author Hans H. Goebel Department of Neuropathology, Johannes Gutenberg University, Mainz, Germany.Hans H. Goebel, MD, Department of Neuropathology, Johannes Gutenberg University, Langenbeckstrasse 1,55131 Mainz, Germany. (E-mail: [email protected])Search for more papers by this author Hans H. Goebel, Corresponding Author Hans H. Goebel Department of Neuropathology, Johannes Gutenberg University, Mainz, Germany.Hans H. Goebel, MD, Department of Neuropathology, Johannes Gutenberg University, Langenbeckstrasse 1,55131 Mainz, Germany. (E-mail: [email protected])Search for more papers by this author First published: 05 April 2006 https://doi.org/10.1111/j.1750-3639.2004.tb00498.xCitations: 5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume14, Issue1January 2004Pages 59-60 RelatedInformation

AANP award for meritorious contributions to neuropathology presented to Fusahiro Ikuta, MD. American Association of Neuropathologists.

Figure. No caption available. It is my pleasure to make introductory remarks to the presentation of the Association's Award for Meritorious Contribution to Neuropathology to Dr. Fusahiro Ikuta. Dr. Ikuta graduated from Niigata University School of Medicine in Japan in 1955. After his internship, he joined the Neurosurgical Department of Niigata University established by Dr. Mizuho Nakata. He soon became more interested in neuropathology than neurosurgery. He came to America to receive training in neuropathology from Dr. Zimmerman's Neuropathology Department at Montefiore Hospital in 1960. Dr. Ikuta has been an active member of AANP since 1964 and his first presentation at the annual meeting of AANP received the Weil Award in 1964. …

Gangliogliomas: an intriguing tumor entity associated with focal epilepsies.

Gangliogliomas represent the most frequent tumor entity in young patients suffering from chronic focal epilepsies. In a series of 326 gangliogliomas collected from the University of Bonn Epilepsy Surgery Program and other departments of neuropathology in Germany, Austria, and Switzerland, epidemiological findings and histopathological hallmarks of gangliogliomas are systematically reviewed. The majority of these tumors occur within the temporal lobe and reveal a biphasic histological architecture characterized by a combination of dysplastic neurons and neoplastic glial cell elements. However, gangliogliomas exhibit a considerable variability in their histopathological appearance. Immunohistochemical studies are an important tool to discriminate these neoplasms from other tumor entities. Almost 80% of gangliogliomas reveal immunoreactivity for CD34, a stem cell epitope not expressed in normal brain. Immunohistochemical reactions for MAP2 or NeuN can be employed to characterize the dysplastic nature of neurons in those areas difficult to discriminate from pre-existing brain parenchyma. Less than 50% of the cases display binucleated neurons. With the frequent finding of "satellite" tumor clusters in adjacent brain regions, gangliogliomas are microscopically less circumscribed than previously assumed. The distinction from diffusely infiltrating gliomas is of considerable importance since tumor recurrence or malignant progression are rare events in gangliogliomas. Only little is known about the molecular pathogenesis of these glioneuronal tumors. Our findings support a dysontogenic origin from a glioneuronal precursor lesion with neoplastic, clonal proliferation of the glial cell population. Candidate genes appear to associate with neurodevelopmental signaling cascades rather than cell cycle control or DNA repair mechanisms. The reelin signaling and tuberin/insulin growth receptor pathways have recently been implicated in ganglioglioma development. Powerful new molecular genetic and biological tools can now be employed to unravel the pathogenesis of these intriguing lesions.

Third ventricular chordoid glioma: clinicopathological features of two cases

Introduction: Primary brain tumours occupying the third ventricle form a heterogenous group of uncommon lesions including colloid cysts, choroid plexus tumours, ependymoma, pilocytic astrocytoma, germinoma and pineal parenchymal tumours. Recently Brat et al. (J Neuropathol Exp Neurol 1998; 57: 238) described a tumour of the third ventricle composed of epithelioid cells with eosinophilic cytoplasm, extracellular mucin as well as a lymphoplasmacytic infiltrate. Although they resembled chordoma and chordoid meningioma histologically, immunohistochemistry demonstrated that these tumours were in fact glial in nature. These tumours have therefore been termed third ventricular chordoid glioma. They characteristically lack the chromosomal and genetic alterations commonly found in other types of gliomas or meningiomas (Reifenberger et al. Brain Pathol 1999; 9: 617). We describe the clinicopathological features of two recent cases of chordoid glioma that presented to the Department of Neuropathology, Western General Hospital, Edinburgh.Results: Case 1 (238/01) Case 2 (474/01) Sex Female Female Age 32 years 37 years Presentation Mild but progressive Acute hydrocephalus visual failure, weight increase of 25.5 kg over 4 years headache, memory problems, collapse Imaging Lower lateral third Third ventricular ventricle/ Hypothalamic lesion lesion Immuno. Ki67 <1% <1% GFAP +++ +++ VIM +++ +++ EMA ++ ++ Conclusions: The two cases of chordoid glioma we describe have slightly different clinical presentations and different appearances on histology. Understanding these variations will aid diagnosis of this unusual tumour.

Association of APOE polymorphisms and pathological features in traumatic brain injury

Introduction: Previous studies have found that polymorphisms of the apolipoprotein E gene (APOE) influences the outcome from head injury, with possession of APOE ε4 being associated with an unfavourable outcome (Teasdale et al. Lancet 1997; 350: 1069–1071). In this study we correlated the pathological features of traumatic brain injury with the presence or absence of APOE ε4. Materials and methods: During the 13-year period 1987–99, 238 brains were examined from cases of traumatic brain injury (TBI) in the Department of Neuropathology, Glasgow. APOE genotype was determined by PCR. For each case a number of pathological features were recorded ‘blind’ to the APOE ε4 status. Results: Of the 238 cases examined, 83 (35%) had the APOE ε4 allele, while 155 (65%) did not. Possession of APOE ε4 was associated with a greater incidence of severe hypoxic brain damage (ε4+ 54%, ε4– 42%) and with a greater incidence of moderate or severe contusion index (ε4+ 42%, ε4– 30%). No significant differences were noted between the other pathological features examined. Conclusions: Possession of APOE ε4 is associated with a greater incidence of moderate/severe contusional injury and severe hypoxic brain damage in fatal cases of TBI. This may be relevant to the relatively poor outcome from TBI in patients with an APOE ε4 allele identified in clinical studies.

Pleomorphic xanthoastrocytoma with predominantly exophytic growth: case report

Yasushi Miyagi, M.D., Ph.D.,* Satoshi O. Suzuki, M.D., Ph.D.,‡ Toru Iwaki, M.D., Ph.D.,‡ Fumio Shima, M.D., Ph.D.,§ Katsuya Ishido, M.D.,* Takehisa Araki, M.D., Ph.D.† and Kazufumi Kamikaseda, M.D., Ph.D.* *Departments of Neurosurgery and †Neurology, Kaizuka Hospital, Fukuoka, Japan; ‡Departments of Neuropathology and §Clinical Neurophysiology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan

Activity-Induced Expression of Common Reference Genes in Individual CNS Neurons

T he quantitative study of gene expression in neurons under physiological and pathophysiological conditions has gained considerable importance. Consequently, a variety of different techniques to quantify gene expression have evolved. Generally, such approaches can be subdivided into strategies that provide absolute versus relative quantitation of a target transcript. Quantitative procedures such as quantitative Northern blots or conventional quantitative reverse transcription polymerase chain reaction (RT-PCR) methods have several disadvantages. For instance, Northern blots require substantial amounts of RNA, rendering investigation of mRNA levels from single cells impossible. Comparability of results is extremely dependent upon identical amounts of starting mRNA used in different samples, a condition that cannot usually be achieved with small cell numbers or minute amounts of tissue. To circumvent these obstacles, various techniques have been developed to quantify gene expression relative to a reference gene (Fink et al, 1998; Waha et al, 1998). This obviates the need to perform an accurate determination of initial mRNA concentrations. On the other hand, a suitable reference gene is essential as an internal control for relative mRNA quantitation. This internal control is crucial for a quantitative comparison of gene expression between different tissue types, at various developmental stages, and between control and disease tissue. Ideally, internal control transcripts should show constant, highlevel expression independent of experimental conditions. The genes for glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and b-actin have been commonly used as reference genes. In recent years, cyclophilin A and hypoxanthine phosphoribosyl-transferase (HPRT) have also been adopted for this purpose. However, several classical reference genes may exhibit considerable changes in expression in cell types or under disease conditions (Suzuki et al, 2000). Here, we have analyzed several of these genes as reference transcripts for activity-dependent chronic changes in central nervous system (CNS) gene expression. Pilocarpine-induced epilepsy in rats was employed as experimental paradigm. We find that GAPDH is not suitable for this purpose, whereas the neuron-specific gene synaptophysin appears remarkably stable following intense neuronal activity. To study activity-dependent alterations in reference gene expression, seizure activity was induced in vivo by applying a single dose of the convulsant pilocarpine (male Wistar rats 150–200 g, 300–380 mg/kg, ip) after prior administration of methyl-scopolamine (1 mg/kg, sc, 30 minutes before pilocarpine, ip). Seizures were terminated after 2 hours by application of diazepam (0.1 mg/kg, sc). Age-matched rats, injected with saline served only as controls. Thirty days after pilocarpine/saline injection, the brains of pilocarpinetreated and control animals (n 5 5 each) were removed. One hippocampus was immediately frozen in liquid nitrogen for in situ hybridization, whereas the contralateral hippocampus was used for preparation of 400-mm transverse vibratome slices. From these slices, single CA1 neurons were harvested with a glass pipette in less than 10 ml of extracellular solution (Beck et al, 1999). mRNA was isolated using the Dynabead mRNA Direct Micro Kit (Dynal, Hamburg, Germany) according to the manufacturer’s protocol. For real-time RT-PCR fluorescent hybridization, oligonucleotides and primers were chosen for the five putative reference genes: GAPDH, b-actin, cyclophilin A, HPRT, and synaptophysin (Eurogentec, Seraing, Received March 9, 2001. This work is supported by the Deutsche Forschungsgemeinschaft (SFB 400), the BONFOR program of the University of Bonn Medical Center, and the German-Israel Program of the Bundesministerium fur Bildung und Fors and Ministry of Science. Address reprint requests to: Dr. Albert J. Becker, Department of Neuropathology, University of Bonn Medical Center, Sigmund-Freud Str. 25, 53105 Bonn, Germany. E-mail: albert_becker@uni-bonn.de 0023-6837/01/8106-913$03.00/0 LABORATORY INVESTIGATION Vol. 81, No. 6, p. 913, 2001 Copyright © 2001 by The United States and Canadian Academy of Pathology, Inc. Printed in U.S.A.

Analysis of cardiovascular and respiratory nuclei in sudden infant death syndrome infants

Ambulatory Child HealthVolume 6, Issue s1 p. 4-6 Analysis of cardiovascular and respiratory nuclei in sudden infant death syndrome infants T. Ansari, T. Ansari Department of Surgical Research, Northwick Park Institute for Medical Research, Northwick Park Hospital, Watford Road, Harrow, UK,Search for more papers by this authorP.D. Sibbons, P.D. Sibbons Department of Surgical Research, Northwick Park Institute for Medical Research, Northwick Park Hospital, Watford Road, Harrow, Uk,Search for more papers by this authorM.L. Rossi, M.L. Rossi Department of Neuropathology, Walton Centre for Neurology and Neurosurgery, Fazakerely Hospital, Liverpool, UKSearch for more papers by this author T. Ansari, T. Ansari Department of Surgical Research, Northwick Park Institute for Medical Research, Northwick Park Hospital, Watford Road, Harrow, UK,Search for more papers by this authorP.D. Sibbons, P.D. Sibbons Department of Surgical Research, Northwick Park Institute for Medical Research, Northwick Park Hospital, Watford Road, Harrow, Uk,Search for more papers by this authorM.L. Rossi, M.L. Rossi Department of Neuropathology, Walton Centre for Neurology and Neurosurgery, Fazakerely Hospital, Liverpool, UKSearch for more papers by this author First published: 03 May 2002 https://doi.org/10.1046/j.1467-0658.2000.00002.xCitations: 2 Dr. Tahera Ansari Department of Surgical Research, Northwick Park Institute for Medical Research, Northwick Park Hospital, Watford Road, Harrow HA1 3UJ, UK. Tel: +44 (0)20 8869 2099; Fax: +44 (0)20 8869 3270; e-mail:t.i.ansari@ic.ac.uk Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume6, Issues1June 2000Pages 4-6 RelatedInformation

The vesicular forebrain (pseudo-aprosencephaly): a missing link in the teratogenetic spectrum of the defective brain anlage and its discrimination from aprosencephaly.

Two cases out of a sample of 41 fetuses and infants with prosencephalic malformation, observed at the Institute of Pathology and Department of Neuropathology of the University of Heidelberg, are described here in detail. These cases presented grossly with microcephaly and missing forebrain, appearing to be cases of aprosencephaly. However, in one of these cases glio-mesenchymal membranes with an ependymal outline, consistent with the microscopic appearance of the dorsal sac membrane in holoprosencephaly and obviously representing remnants of a collapsed primitive prosencephalic vesicle, could be demonstrated. In the other case only hindbrain structures, with the exception of the cerebellum, were present without any demonstrable remnants of a prosencephalon. We propose that the microscopic specification of a primitive prosencephalic vesicle in the first case and similar cases does not justify the diagnosis of atelencephaly/aprosencephaly because the prosencephalon was not really missing (pseudo-aprosencephaly). The prosencephalic anlage had been formed but remained vesicular without further differentiation of a holospheric brain mantle as in common holoprosencephaly ('vesicular forebrain'). We believe that pseudo-aprosencephaly represents the most primitive form of holoprosencephaly, in which the forebrain remains as a complete sac, linking classical holoprosencephaly with 'true' aprosencephaly, i.e., defective prosencephalic anlage due to developmental arrest. The 'vesicular forebrain' allows one to extend the classification of Probst by an additional category which might be termed complete sac category, intercalated between the dorsal sac category and 'true' atelencephaly/aprosencephaly.

The neuropathology of the vegetative state after head injury.

The technologies of resuscitation and intensive care have reduced mortality after acute brain damage, but some of those rescued are left with permanent brain damage, the most severely aVected being...

The Danish Multiple Sclerosis Registry: a 50-year follow-up.

The Danish Multiple Sclerosis Registry was established in 1948 in continuation with a nationwide survey of the prevalence of Multiple Sclerosis (MS) in Denmark. The register has since collected information on MS patients from all Danish departments of neurology, practising neurologists, MS rehabilitation centres, the National Patient Registry, the Danish MS Society, and departments of neuropathology. The registry is linked with the Danish Central Population Registry. The completeness has been estimated at more than 90%. All cases are reclassified by two neurologists as to diagnosis and year of onset. 12 070 cases with a confirmed diagnosis of MS are kept in the databases. They were prevalent in 1949 or have had onset in the period 1948 - 1993. The registry is continuously updated with new information on registered cases and new cases. The crude average annual incidence rate 1980 - 89 was 4.99/105; the prevalence rate was 112/105 by 1 January 1990. Cross-linking with other registers have enabled analytical prospective epidemiological studies, and the registry has provided population based unbiased samples of patients for a number of clinical studies.

The Danish Multiple Sclerosis Registry: a 50-year follow-up

The Danish Multiple Sclerosis Registry was established in 1948 in continuation with a nationwide survey of the prevalence of Multiple Sclerosis (MS) in Denmark The register has since collected information on MS patients from all Danish departments of neurology, practising neurologists, MS rehabilitation centres, the Notional Patient Registry, the Danish MS Society, and departments of neuropathology. The registry is linked with the Danish Central Population Registry. The completeness has been estimated at more than 90%. All cases are reclassified by two neurologists as to diagnosis and year of onset 12 070 cases with a confirmed diagnosis of MS are kept in the databases. They were prevalent in 1949 or have had onset in the period 1948 - 1993. The registry is continuously updated with new information on registered cases and new cases. The crude average annual incidence rate 1980-89 was 4.99/10 5 ; the prevalence rate was 112/10 5 by I January 1990. Cross-linking with other registers have enabled analytical prospective epidemiological studies, and the registry has provided population based unbiassed samples of patients for a number of clinical studies.