Brodmann and Cortical Maps Korbinian Brodmann: Cortical Maps and the Cytoarchitecture of the Brain
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Clinical Research
Clinical research The discovery of Alzheimer’s disease Hanns Hippius, MD; Gabriele Neundörfer, MD T he 37th Meeting of South-West German Psychiatrists (37 Versammlung Südwestdeutscher Irrenärzte) was held in Tübingen on November 3, 1906. At the meeting, Alois Alzheimer (Figure 1), who was a lecturer (Privatdozent) at the Munich University Hospital and a coworker of Emil Kraepelin, reported on an unusual case study involving a “peculiar severe disease process of the cerebral cortex” (Über einen eigenartigen, schweren Erkrankungsprozeß der Hirnrinde). Prelude On November 3, 1906, a clinical psychiatrist and neuro- anatomist, Alois Alzheimer, reported “A peculiar severe Alzheimer described the long-term study of the female disease process of the cerebral cortex” to the 37th patient Auguste D., whom he had observed and investi- Meeting of South-West German Psychiatrists in Tübingen. gated at the Frankfurt Psychiatric Hospital in November He described a 50-year-old woman whom he had fol- 1901, when he was a senior assistant there.Alzheimer had lowed from her admission for paranoia, progressive sleep been interested in the symptomatology, progression, and and memory disturbance, aggression, and confusion, until course of the illness of Auguste D. from the time of her her death 5 years later. His report noted distinctive admission, and he documented the development of her plaques and neurofibrillary tangles in the brain histology. unusual disease very precisely from the beginning. It excited little interest despite an enthusiastic response In March 1901, the husband of the 50-year-old woman had from Kraepelin, who promptly included “Alzheimer’s dis- noticed an untreatable paranoid symptomatology in his ease” in the 8th edition of his text Psychiatrie in 1910. -
Original Nicolás Achúcarro and the Histopathology of Rabies: A
Original Neurosciences and History 2019; 7(4): 122-136 Nicolás Achúcarro and the histopathology of rabies: a historical invitation from Nissl and Alzheimer D. Ezpeleta1, F. Morales2, S. Giménez-Roldán3 1Department of Neurology. Hospital Universitario Quirónsalud Madrid, Madrid, Spain. 2Department of Neurology. Hospital Clínico Universitario Lozano Blesa, Facultad de Medicina, Zaragoza, Spain. 3Department of Neurology. Hospital General Universitario Gregorio Marañón, Madrid, Spain. ABSTRACT Introduction. Nicolás Achúcarro (1880-1918), a brilliant disciple of Cajal, was invited by Nissl and Alzheimer to write on the subject of experimental rabies. The chapter, published in 1909 in German, has never previously been translated into Spanish. Material and methods. The study “On the understanding of the central nervous system histological pathology in rabies” was obtained from the University of Bonn, Germany, and translated into Spanish by one of the authors (FM). We researched the context of the study; its relevance to the epidemiology, diagnosis, and histopathology of rabies encephalitis; and its influence on Achúcarro’ s scientific career. Results. The study was conducted in rabbits, a dog, two hens, and a brain specimen from a man who died due to rabies. It was presented as a doctoral thesis in Madrid in December 1906. The German-language publication, from 1909, comprises 51 dense pages of text with 13 illustrations; a summary in Spanish was published in 1914. Achúcarro rejected the idea that Negri bodies were parasites, confirming Cajal’ s observations on Alzheimer neurofibrillary degeneration and argyrophilic fibres in rabies. He underlines the transformation of glial cells in the cornu ammonis into elongated elements (rod-like cells or Stäbchenzellen) to adapt to the parallel arrangement of pyramidal cells in the stratum radiatum. -
Bilateral Damage to Auditory Cortex
IS SPEECH A SPECIAL SOUND FOR THE BRAIN? Evidence from disorders How sound gets to the brain Outer ear Middle ear Inner ear Collects sound waves. The Transforms the energy of a Transform the energy of a configuration of the outer sound wave into the internal compressional wave within ear serves to amplify vibrations of the bone the inner ear fluid into structure of the middle ear sound, particularly at and transforms these nerve impulses which can 2000-5000 Hz, a vibrations into a be transmitted to the frequency range that is compressional wave in the brain. important for speech. inner ear. Auditory pathway • Auditory input reaches primary auditory cortex about 10–15 msec after stimulus onset (Liegeois-Chauvel, Musolino, & Chauvel 1991; Celesia, 1976). http://www.sis.pitt.edu/~is1042/html/audtrans.gif Auditory cortex in the superior temporal lobe Primary auditory cortex (A1): Brodmann areas 41 and 42 http://ist-socrates.berkeley.edu/ ~jmp/LO2/6.html Auditory cortex in the superior temporal lobe Primary auditory cortex (A1): Auditory-association cortex (A2): Brodmann areas 41 and 42 Brodmann area 22 http://ist-socrates.berkeley.edu/ ~jmp/LO2/6.html Disorders of auditory processing are rare • Signal from each ear is processed in both hemispheres (contra visual system). • Bilateral damage often necessary. • Generally requires two separate neurological events. DISORDER BEHAVIOR CHARACTERISTIC DAMAGE SITE Cortical Inability to hear sounds without Extensive bilateral damage to auditory deafness apparent damage to the hearing cortex (BAs 41 & 42). apparatus or brain stem abnormality. Auditory Inability to recognize auditorily Damage in auditory association cortex agnosia presented sounds (e.g., coughing, crying) (BAs 22 & 37). -
Normal Aging Associated Functional Alternations in Auditory
NORMAL AGING ASSOCIATED FUNCTIONAL ALTERNATIONS IN AUDITORY SENSORY AND WORKING MEMORY PROCESSING by YUAN GAO (Under the Direction of Brett A. Clementz) ABSTRACT The purpose of the present study was to determine normal aging associated changes in brain functions during auditory sensory and auditory working memory processing by magneto- encephalography (MEG) measurement. Old and young participants were recruited from data recording. It is found that though there are no significant age associated differences in behavioral performance; normal aging associated brain activations differ between age groups. For brain activations in auditory sensory processing, though both age groups activate the same cortical regions and show a habituation pattern on stimulus rate effects, old participants have larger response magnitude and faster response speed than young participants. For brain activations in auditory working memory, old participants’ brain responses are slower than young participants’ and different cortical areas of two age groups are activated in the same experiment task. The possible underlying mechanisms of these normal aging associated brain responses differences are discussed further. INDEX WORDS: Normal aging, Auditory, Sensory, Working memory, MEG NORMAL AGING ASSOCIATED FUNCTIONAL ALTERNATIONS IN AUDITORY SENSORY AND WORKING MEMORY PROCESSING by YUAN GAO B. S., Beijing Normal University, Beijing, China, 2003 A Thesis Submitted to the Graduate Faculty of The University of Georgia in Partial Fulfillment of the Requirements for the Degree MASTER OF SCIENCE ATHENS, GEORGIA 2006 © 2006 YUAN GAO All Rights Reserved NORMAL AGING ASSOCIATED FUNCTIONAL ALTERNATIONS IN AUDITORY SENSORY AND WORKING MEMORY PROCESSING by YUAN GAO Major Professor: Brett A. Clementz Committee: Jennifer E. McDowell Leonard W. -
Disrupted Functional Connectivity of the Pain Network in Fibromyalgia
Published Ahead of Print on December 30, 2011 as 10.1097/PSY.0b013e3182408f04 Disrupted Functional Connectivity of the Pain Network in Fibromyalgia IGNACIO CIFRE,PHD, CAROLINA SITGES,PHD, DANIEL FRAIMAN,PHD, MIGUEL A´ NGEL MUN˜ OZ,PHD, PABLO BALENZUELA,PHD, ANA GONZA´ LEZ-ROLDA´ N, MS, MERCEDES MARTI´NEZ-JAUAND, MS, NIELS BIRBAUMER,PHD, DANTE R. CHIALVO,MD, AND PEDRO MONTOYA,PHD Objective: To investigate the impact of chronic pain on brain dynamics at rest. Methods: Functional connectivity was examined in patients with fibromyalgia (FM) (n = 9) and healthy controls (n = 11) by calculating partial correlations between low-frequency blood oxygen levelYdependent fluctuations extracted from 15 brain regions. Results: Patients with FM had more positive and negative correlations within the pain network than healthy controls. Patients with FM displayed enhanced functional connectivity of the anterior cingulate cortex (ACC) with the insula (INS) and basal ganglia ( p values between .01 and .05), the secondary somatosensory area with the caudate (CAU) (p = .012), the primary motor cortex with the supplementary motor area (p = .007), the globus pallidus with the amygdala and superior temporal sulcus (both p values G .05), and the medial prefrontal cortex with the posterior cingulate cortex (PCC) and CAU (both p values G .05). Functional connectivity of the ACC with the amygdala and periaqueductal gray (PAG) matter (p values between .001 and .05), the thalamus with the INS and PAG (both p values G .01), the INS with the putamen (p = .038), the PAG with the CAU (p = .038), the secondary somatosensory area with the motor cortex and PCC (both p values G .05), and the PCC with the superior temporal sulcus (p = .002) was also reduced in FM. -
Function of Cerebral Cortex
FUNCTION OF CEREBRAL CORTEX Course: Neuropsychology CC-6 (M.A PSYCHOLOGY SEM II); Unit I By Dr. Priyanka Kumari Assistant Professor Institute of Psychological Research and Service Patna University Contact No.7654991023; E-mail- [email protected] The cerebral cortex—the thin outer covering of the brain-is the part of the brain responsible for our ability to reason, plan, remember, and imagine. Cerebral Cortex accounts for our impressive capacity to process and transform information. The cerebral cortex is only about one-eighth of an inch thick, but it contains billions of neurons, each connected to thousands of others. The predominance of cell bodies gives the cortex a brownish gray colour. Because of its appearance, the cortex is often referred to as gray matter. Beneath the cortex are myelin-sheathed axons connecting the neurons of the cortex with those of other parts of the brain. The large concentrations of myelin make this tissue look whitish and opaque, and hence it is often referred to as white matter. The cortex is divided into two nearly symmetrical halves, the cerebral hemispheres . Thus, many of the structures of the cerebral cortex appear in both the left and right cerebral hemispheres. The two hemispheres appear to be somewhat specialized in the functions they perform. The cerebral hemispheres are folded into many ridges and grooves, which greatly increase their surface area. Each hemisphere is usually described, on the basis of the largest of these grooves or fissures, as being divided into four distinct regions or lobes. The four lobes are: • Frontal, • Parietal, • Occipital, and • Temporal. -
High-Yield Neuroanatomy
LWBK110-3895G-FM[i-xviii].qxd 8/14/08 5:57 AM Page i Aptara Inc. High-Yield TM Neuroanatomy FOURTH EDITION LWBK110-3895G-FM[i-xviii].qxd 8/14/08 5:57 AM Page ii Aptara Inc. LWBK110-3895G-FM[i-xviii].qxd 8/14/08 5:57 AM Page iii Aptara Inc. High-Yield TM Neuroanatomy FOURTH EDITION James D. Fix, PhD Professor Emeritus of Anatomy Marshall University School of Medicine Huntington, West Virginia With Contributions by Jennifer K. Brueckner, PhD Associate Professor Assistant Dean for Student Affairs Department of Anatomy and Neurobiology University of Kentucky College of Medicine Lexington, Kentucky LWBK110-3895G-FM[i-xviii].qxd 8/14/08 5:57 AM Page iv Aptara Inc. Acquisitions Editor: Crystal Taylor Managing Editor: Kelley Squazzo Marketing Manager: Emilie Moyer Designer: Terry Mallon Compositor: Aptara Fourth Edition Copyright © 2009, 2005, 2000, 1995 Lippincott Williams & Wilkins, a Wolters Kluwer business. 351 West Camden Street 530 Walnut Street Baltimore, MD 21201 Philadelphia, PA 19106 Printed in the United States of America. All rights reserved. This book is protected by copyright. No part of this book may be reproduced or transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above-mentioned copyright. To request permission, please contact Lippincott Williams & Wilkins at 530 Walnut Street, Philadelphia, PA 19106, via email at [email protected], or via website at http://www.lww.com (products and services). -
Alzheimer's 100Th Anniversary of Death and His Contribution to A
DOI: 10.1590/0004-282X20140207 HISTORICAL NOTES Alzheimer’s 100th anniversary of death and his contribution to a better understanding of Senile dementia O 100o aniversário de morte de Alzheimer e sua contribuição para uma melhor compreensão da Demência senil Eliasz Engelhardt1,2, Marleide da Mota Gomes3 ABSTRACT Initially the trajectory of the historical forerunners and conceptions of senile dementia are briefly presented, being highlighted the name of Alois Alzheimer who provided clinical and neuropathological indicators to differentiate a group of patients with Senile dementia. Alzheimer’s examination of Auguste D’s case, studied by him with Bielschowsky’s silver impregnation technique, permitted to identify a pathological marker, the intraneuronal neurofibrillary tangles, characterizing a new disease later named after him by Kraepelin – Alzheimer’s disease. Over the time this disorder became one of the most important degenerative dementing disease, reaching nowadays a status that may be considered as epidemic. Keywords: dementia, Senile dementia, hystory of medicine, Alzheimer, Alzheimer’ disease. RESUMO Incialmente é apresentada brevemente a trajetória histórica dos precursores e dos conceitos da demência senil, sendo destacado o nome de Alois Alzheimer que forneceu indicadores clínicos e neuropatológicos para diferenciar um grupo de pacientes com Demência senil. O exame de Alzheimer do caso de Auguste D, estudado por ele com a técnica de impregnação argêntica de Bielschowsky, permitiu identificar um marcador patológico, os emaranhados neurofibrilares intraneuronais, caracterizando uma nova doença, mais tarde denominada com seu nome por Kraepelin – doença de Alzheimer. Com o passar do tempo esta desordem tornou-se uma das mais importantes doenças demenciante degenerativa, alcançando, na atualidade, um status que pode ser considerado como epidêmico. -
History of Alzheimer's Disease
Print ISSN 1738-1495 / On-line ISSN 2384-0757 Dement Neurocogn Disord 2016;15(4):115-121 / https://doi.org/10.12779/dnd.2016.15.4.115 DND REVIEW History of Alzheimer’s Disease Hyun Duk Yang,1,2 Do Han Kim,1 Sang Bong Lee,3 Linn Derg Young,2,4,5 1Harvard Neurology Clinic, Yongin, Korea 2Brainwise Co. Ltd., Yongin, Korea 3Barun Lab Inc., Yongin, Korea 4Department of Business Administration, Cheongju University, Cheongju, Korea 5Boston Research Institute for Medical Policy, Yongin, Korea As modern society ages rapidly, the number of people with dementia is sharply increasing. Direct medical costs and indirect social costs for dementia patients are also increasing exponentially. However, the lack of social awareness about dementia results in difficulties to dementia patients and their families. So, understanding dementia is the first step to remove or reduce the stigma of dementia patients and promote the health of our community. Alzheimer’s disease is the most common form of dementia. The term, ‘Alzheimer’s disease’ has been used for over 100 years since first used in 1910. With the remarkable growth of science and medical technologies, the techniques for diagnosis and treat- ment of dementia have also improved. Although the effects of the current symptomatic therapy are still limited, dramatic improvement is ex- pected in the future through the continued research on disease modifying strategies at the earlier stage of disease. It is important to look at the past to understand the present and obtain an insight into the future. In this article, we review the etymology and history of dementia and pre- vious modes of recognizing dementia. -
High-Yield Neuroanatomy, FOURTH EDITION
LWBK110-3895G-FM[i-xviii].qxd 8/14/08 5:57 AM Page i Aptara Inc. High-Yield TM Neuroanatomy FOURTH EDITION LWBK110-3895G-FM[i-xviii].qxd 8/14/08 5:57 AM Page ii Aptara Inc. LWBK110-3895G-FM[i-xviii].qxd 8/14/08 5:57 AM Page iii Aptara Inc. High-Yield TM Neuroanatomy FOURTH EDITION James D. Fix, PhD Professor Emeritus of Anatomy Marshall University School of Medicine Huntington, West Virginia With Contributions by Jennifer K. Brueckner, PhD Associate Professor Assistant Dean for Student Affairs Department of Anatomy and Neurobiology University of Kentucky College of Medicine Lexington, Kentucky LWBK110-3895G-FM[i-xviii].qxd 8/14/08 5:57 AM Page iv Aptara Inc. Acquisitions Editor: Crystal Taylor Managing Editor: Kelley Squazzo Marketing Manager: Emilie Moyer Designer: Terry Mallon Compositor: Aptara Fourth Edition Copyright © 2009, 2005, 2000, 1995 Lippincott Williams & Wilkins, a Wolters Kluwer business. 351 West Camden Street 530 Walnut Street Baltimore, MD 21201 Philadelphia, PA 19106 Printed in the United States of America. All rights reserved. This book is protected by copyright. No part of this book may be reproduced or transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above-mentioned copyright. To request permission, please contact Lippincott Williams & Wilkins at 530 Walnut Street, Philadelphia, PA 19106, via email at [email protected], or via website at http://www.lww.com (products and services). -
1 Korbinian Brodmann's Scientific Profile, and Academic Works
BRAIN and NERVE 69 (4):301-312,2017 Topics Korbinian Brodmann’s scientific profile, and academic works Mitsuru Kawamura Honorary Director, Okusawa Hospital & Clinics, 2-11-11, Okusawa, Setagaya-ku, Tokyo, 1580083, Japan E-mail: [email protected] Abstract Brodmann’s classic maps of localisation in cerebral cortex are both well known and of current value. However, his original 1909 monograph is not widely read by neurologists. Furthermore, he reproduced his maps in 1910 and 1914 with a number of important changes. The 1914 version also excludes areas 12-16 and 48-51 in human brain while areas 1-52 are described in animal brain. Here, we provide a detailed explanation of the different versions, and review Brodmann's academic profile and work. Key words: Brodmann’s map; missing numbers; Brodmann’s profile; Brodmann’s works; infographics Introduction The following paper is based on a Japanese language version (BRAIN and NERVE, April 2017) by MK. Recently I developed a passion for the design of charts and diagrams and enjoy looking through books on infographics. The design of visual information has made remarkable progress in recent years. Furthermore, figures, tables, and graphic records are on the agenda at every editorial meeting of Brain And Nerve. The maps of Korbinian Brodmann (1868-1918) were first published in German in 19091, and I believe they rightly belongs to infographics since they localise neuroanatomical information onto human and animal brain – monkey, for example – using the techniques of histology and comparative anatomy. Unlike the cerebellar cortex, which has a generally uniform three-layer structure throughout, most of the cerebral cortex has a six-layer structure of regionally diverse patterns. -
The Tangled Story of Alois Alzheimer
Bratisl Lek Listy 2006; 107 (910): 343345 343 TOPICAL REVIEW The tangled story of Alois Alzheimer Zilka N, Novak M Institute of Neuroimmunology, AD Centre of Excellence, Slovak Academy of Sciences, Bratislava, Slovakia. [email protected] Abstract In 1907, Bavarian psychiatrist Alois Alzheimer, who is considered to be a founding father of neuropa- thology, was first to describe the main neuropathologic characteristics of the peculiar disease in the brain of a woman showing progressive dementia when she was in her early 50s. Using a newly deve- loped Bielschowskys silver staining method, Alzheimer observed degenerating neurons with bundles of fibrils (neurofibrillary tangles) and miliary foci of silver-staining deposits scattered over the cortex (senile plaques). In 1910 Emil Kraepelin (Alois Alzheimers superior) coined the term Alzheimers disease to distinguish the presenile form of dementia from the more common senile variant. Alzheimers findings were followed up, and soon a number of reports of similar cases appeared in the literature. During the time, both pathological hallmarks of Alzheimers disease became the gold standard for post-mortem diagnosis of the disease. One hundred years later, dementia of Alzheimers type is con- sidered to be one of the most devastating illnesses of old age. Despite intensive research the cause of the disease still remains elusive (Fig. 2, Ref. 17). Key words: Alzheimers disease, Alois Alzheimer, Augusta D, neurofibrillary tangles, senile plaques. Alois Alzheimer was born in June 14, 1864 in Markbreit am pathology of the nervous system, studying in particular the nor- Main in Southern Germany. He commenced the study of medi- mal and pathological anatomy of the cerebral cortex.