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N E U R O P a T H O L O G Y 2009 N E U R O P A T H O L O G Y 2009 COLLEGE OF PHYSICIANS & SURGEONS COLUMBIA UNIVERSITY New York, New York 1 NEUROPATHOLOGY SYLLABUS CONTENTS PAGE Message from the Course Director 3 Neuropathology small-Group Schedule 4 Faculty 5 Cellular Neuropathology 6 Cerebral Edema, Intracranial Shifts & Herniations 12 Cerebrovascular Diseases 20 Infectious Diseases of Central Nervous System 30 Neuro-Radiology 44 Degenerative Diseases and Dementia 49 Metabolic Diseases 79 Developmental Disorders 89 Brain Tumors 99 Seizures and Epilepsy 108 Diseases of Myelin 113 Neuromuscular Diseases 126 Ophthalmology 144 Trauma 154 Image Guideline 167 Clinical Exercises 195 2 MESSAGE FROM THE COURSE DIRECTOR Welcome to the Neuropathology Course. We hope that you will find this to be a pleasurable and challenging introduction to diseases of the nervous system. During this phase of your medical school experience, you are expected to become familiar with the vocabulary, basic pathologic concepts and morphologic aspects of neurologic diseases. Traditionally, diseases of the nervous system have been classified or divided etiologically into vascular, metabolic, neoplastic, infectious, degenerative, demyelinative, traumatic and developmental categories. Diseases of the neuromuscular system have been segregated somewhat, but can be divided similarly. This approach is still considered to be the most effective and understandable way to present this myriad of afflictions, but it often seems disjointed to the novice. So, be patient and we believe that things will fall into place by the end of the course. We shall try to emphasize common entities in the lectures, the small groups and images reviews, but prototypes of rare diseases also will be presented to provide you with an overview and perspective. The main purpose of the formal lectures is the presentation of conceptual, nosological, or pathogenetic aspects of neuropathology. In the small groups, we will reinforce material from lectures largely through review of images. Additionally, we will illustrate the application of basic neuropathologic principles to problem solving and analysis in the clinical setting. To this end, we will discuss a series of clinical cases in the group sessions. We will enlist your help in generating differential diagnoses to give you a feel for how we approach neurological diseases. We have included a lecture on Neuroimaging since this area is currently expanding tremendously and a basic appreciation of techniques and the value, and limitations, of those techniques will assist you in many areas of your clinical training. The Course Syllabus will be used in lieu of the textbook. We have intentionally listed somewhat extensive chapters, too much to be used in a short course. These readings are for those of you who wish to explore material in more detail. Images for the small group sessions are online at the following website: www.columbia.edu/itc/hs/medical/pathology/pathoatlas. This will lead you to the site that contains images for all pathology courses (topic bar will say ‘General Pathology’). Scroll down to the ‘Neuropathology’ section to access images for this course. Access to this site is possible both on and off campus. A large number of additional websites are available that may enhance your learning, if you wish to investigate them. At www.neuropat.dote.hu/ you will find a large online resource with links to Neuroanatomy, Neuropathology and Neuroradiology. The website at University of Rochester (www.urmc.rochester.edu/neuroslides) is useful and contains neuroradiology along with pathologic images. If you want to review some normal neurohistology, there is an interesting “virtual slide box of histology” at www.medicine.uiowa.edu/pathology/nlm_histology. There are many others to explore. Finally, constructive criticism and comments are welcome and should be referred to the course director. Phone and office numbers are given for the preceptors and we encourage you to make use of this resource outside of our formal teaching plan. We hope and expect that this will be a good learning experience for you. 3 NEUROPATHOLOGY SMALL GROUP SCHEDULE - 2008-2009 Tues., 12/8 11:00-12:50 Prec.Rms. Introduction to Cellular Neuropathology/Cerebral Edema Cerebrovascular Diseases Review Weds., 12/9 11:00-12:50 Prec.Rms. Infectious Diseases Review Case 1: Cerebrovascular Diseases Thurs., 12/10 11:00-12:50 Prec.Rms. Dementia and Degenerative Diseases & Metabolic Diseases Review Case 2: Dementia Fri., 12/11 11:00-12:50 Prec.Rms. Developmental Disorders & Brain Tumors Review Case 3: Brain tumors Mon., 12/14 11:00-12:50 Prec.Rms. Diseases of Myelin Review Case 4: Myelin Tues., 12/15 11:00-12:50 Prec.Rms Diseases of Nerve & Muscle Review Case 5: Nerve/Muscle Weds., 12/16 11:00-12:50 Prec. Rms Trauma Review Review Session for exam 4 NEUROPATHOLOGY COURSE FACULTY Neuropathology Faculty Phyllis L. Faust, M.D., Ph.D. PH 15-124 5-7345 Andrew Dwork, M.D. New PI Bldg.Rm.2913 212 543-5563 James E. Goldman, M.D., Ph.D. P&S 15-420 5-3554 Arthur P. Hays, M.D. PH 15-124 2-3034 Jean Paul Vonsattel BHS T-8 5-5161 Peter Canoll, M.D. ICRC 10-01 212 851-4632 Kurenai Tanji, M.D. PH 15-124 2-3035 John Crary, M.D., Ph.D. PH 15-124 5-7012 Andrew Teich, M.D., Ph.D. PH 15-124 5-7012 Neuroradiology Faculty Angela Lignelli. MH 3-101 5-2511 Neurology Faculty Hyunmi Choi, M.D. NI 1402 5-3049 Ophthalmology Faculty Steven Kane, M.D, Ph.D. EI Box 3 5/5400 or 212 927-8722 5 CELLULAR NEUROPATHOLOGY James E. Goldman, M.D., Ph.D. 6 CELLULAR NEUROPATHOLOGY At the beginning of this course, it is useful to consider each class of cells in the nervous system separately and to examine the diverse pathologies that may affect each of them. You will discover that these alterations are common to a variety of neuropathological disorders. NEURONS A. Cell body 1. Acute ischemic or hypoxic damage produces a shrinkage of the cell body and a hypereosinophilia. The nucleus becomes pyknotic. These are thought to be irreversible and lethal changes [CN-1]. 2. Atrophy, a non-eosinophilic shrinkage of the cell body [CN-2], is the hallmark of many neurodegenerative disorders (eg. Alzheimer, Parkinson, and Huntington diseases). The neuron may be involved directly or indirectly, through retrograde (via efferents) or anterograde (via afferents) transneuronal or transynaptic degeneration. 3. Chromatolysis results from axon damage (including axon transection). The cell body becomes hypertrophic and loses its Nissl substance (rough ER) [CN-3]. Chromatolysis may be followed by regrowth of the axon from the point of damage, a phenomenon more often seen in the peripheral than in the central nervous system. 4. In neuronal storage diseases, excessive amounts of lipids, carbohydrates, glycosaminoglycans, or glycoproteins accumulate within neurons, enlarging and distorting the normal geometry of the cell body and proximal processes. These are usually seen in the context of inherited disorders of lipid or glycosaminoglycan catabolism (eg. Tay Sachs disease, mucopolysaccharidoses). In many of these diseases, similar storage material accumulates in glial cells. 5. Inclusions represent abnormal nuclear or cytoplasmic structures. Some reflect the focal storage of metabolites, some the presence of viral proteins or nucleoproteins, and some the abnormal accumulation of structural proteins (eg. neurofibrillary tangles, Lewy bodies). 6. Lipofuscin is an insoluble mix of proteins, lipids, and minerals that accumulates in neurons and astrocytes during the normal aging process. 7. Neuronophagia is the phagocytosis of degenerating neurons, usually by macrophages. This is commonly seen after hypoxic or ischemic insults or during viral infections. 7 B. Axon 1. Wallerian degeneration is the loss of the axon (and its myelin sheath) distal to the point of axonal damage [CN-4]. 2. Dying back degeneration, a degeneration of the most distal axon, followed by the progressive loss of more and more proximal regions, is often seen in toxic peripheral neuropathies. 3. Demyelination refers to the primary loss of myelin with relative preservation of the axon (eg. as in multiple sclerosis) [CN-5]. 4. A spheroid is a focal enlargement of an axon due to damage, regardless of cause [CN-6]: trauma, local areas of necrosis, or toxic-metabolic insults. Spheroids contain mixtures of lysosomes, mitochondria, neurofilaments, and other cytoplasmic constituents. Slowing or cessation of axoplasmic transport at sites of damage presumably account for spheroids. C. Dendrite 1. Hypoplasia refers to an inadequate development of dendritic branches. This is seen in many types of mental retardation, including congenital hypothyroidism (cretinism). 2. Atrophy is a reduction in the volume and surface area of dendritic branches, commonly seen in neurodegenerative diseases. D. Neuropil 1. Neuritic plaques are collections of degenerating axons and dendrites, mixed with microglia and astrocytes and associated with the extracellular deposition of amyloid (beta-amyloid, see lecture on Neurodegenerative diseases). 2. Status spongiosis refers to a spongy state of the neuropil, the formation of fine to medium sized vacuoles representing swollen neuronal and astrocytic processes. This change is typical of transmissible spongiform encephalopathies, such as Creutzfeldt- Jacob disease. ASTROCYTES Astrocytes are found in all brain regions. They contact blood vessels, pial surfaces, and enfold synapses in their functions to maintain the concentration of ions, neurotransmitters, and other metabolites within normal levels in the extracellular space. They also play a fundamental role in inducing blood brain barrier functions in cerebral vessels [CN-7]. 8 1. Astrocytes undergo hypertrophy (enlargement) and hyperplasia (proliferation) in response to a great many pathological processes, including hypoxic-ischemic damage and trauma. Astrocytes form the majority of scars in the CNS (unlike other organs, in which scars are typically collagenous, formed by fibroblasts). Astrocytes develop abundant pink cytoplasm, either due to imbibing plasma proteins and fluid in the short-term (when the blood-brain-barrier is broken) or filling up with intermediate filaments (in long-term scarring).
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