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Spinocerebellar Degenerations: more detail

Spinocerebellar degenerations: Proceedings of the International Symposium on Spinocerebellar Degenerations held October 12-14, 1978, Tokyo

Trh and Spinocerebellar Degeneration

Spinocerebellar Degenerations: The Ataxias and Spastic Paraplegias: Blue Books of Neurology Series, Volume 31 by Alexis Brice MD, Stefan-M. Pulst MD, 2007-05-23

Hereditary Neuropathies and Spinocerebellar Atrophies

The Spino-Cerebellar Degenerations by J G Greenfield, 1954-01-01

Advances in Research on Neurodegeneration.: Volume 7 (Journal of Neural Transmission Supplementum)

Handbook of Ataxia Disorders (Neurological Disease and Therapy)

lists with details

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palsy Corticobasal degeneration ShyDrager syndrome Olivopontocerebellar atrophyHuntington disease spinocerebellar degenerations Spinocerebellar ataxias
http://www.ncku.edu.tw/~nckmpat/teacher/paper-chang.htm
WebGuest - Open Directory : Health : Conditions And Diseases : Neurological Diso
Myelitis@ (6). Spinal Muscular Atrophy@ (11); spinocerebellar degenerations (5);StiffPerson Syndrome@ (4); Syringomyelia@ (4); Tabes Dorsalis (2). See also
http://directory.webguest.com/index.cgi/Health/Conditions_and_Diseases/Neurologi
Differential Diagnosis Of PD And Parkinsonism Plus Syndromes
Extensive article by Mark Stacy, MD Conditions and Diseases Neurodegenerative Diseases parkinsonism Huntington's disease Wilson's disease HallervordenSpatz disease Olivopontocerebellarand spinocerebellar degenerations Familial basal ganglia
http://www.parkinsons-information-exchange-network-online.com/archive/091.html

Extractions: Drug Database Index Select a Focus Topic Allergy Alternative Medicine Arthritis Asthma Beyond Dieting Body Aches and Pains Breast Cancer Cancer Awareness Cardio Health Children's Health Colon Cancer Contraception COPD/Emphysema Dental Health Diabetes Elder Care Emergency Room Epilepsy Erectile Dysfunction Eye Care Fertility Fitness Gastrointestinal Health Glands and Hormones Gynecologic Health Hair Loss Headache Health care Today Healthy Aging HIV and AIDS Infectious Diseases Kidney Health Leukemia Liver Health Lung Cancer Lymphoma Overview Multiple Sclerosis Men's Health Mental Health Nutrition Osteoporosis Parkinson's Disease Sexual Health Skin Health Sleep Disorders Special Events Stroke Surgeries and Procedures Teen Health Thyroid Health Urologic Health Vascular Health Women's Health Workplace Health Parkinsn Current Topics DIFFERENTIAL DIAGNOSIS OF PARKINSON'S DISEASE AND THE PARKINSONISM PLUS SYNDROMES Table 1. ETlOLOGIC CATEGORIES OF PARKINSONISM*
Ataxia Resource Updates
by Patricia Birdsong Hamilton The Clumsy Child A Study of Developmental Apraxicand Agnostic Ataxia by Sasson S. Gubbay spinocerebellar degenerations by Tokyo
http://www.health.xq23.com/inst/Research_Updates/Ataxia.html
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?( Electrophysiological Studiesin spinocerebellar degenerations ), ? 0000297982 ?(JPN).
http://www.nii.ac.jp/sokuho/articles/ncid/AN10402438/19920000_18.html
DEMENTIA (I): INTRODUCTION, CLASSIFICATION
Translate this page diseases, as well as in rarer extrapyramidal syndromes, eg, progressive supranuclearpalsy, striatonigral degeneration, spinocerebellar degenerations, and a
http://www.fonendo.com/noticias/7/2001/02/2.shtml

Extractions: DEMENTIA (I): INTRODUCTION, CLASSIFICATION www.fonendo.com 18/02/2001 INTRODUCTION Dementia is a clinical syndrome characterized by acquired persistent disturbances in multiple areas of neuropsychologic function (including memory impairment) that are due to the direct physiological effects of a general medical condition, to the persisting effects of a substance, or to multiple etiologies. Dementing illnesses become increasingly common in old age but should not be regarded as an expected component of the normal aging process. Regardless of the patient's age, a thorough search for the cause of dementia is warranted. Many of the problems affecting aged individuals should be viewed as syndromes (i.e., collections of signs and symptoms with several potential etiologies). Just as the clinical presentation of heart failure and anemia trigger a differential diagnosis of pathogenetic entities, so should the major geriatric syndromes of dementia, depression, falling, and incontinence. Investigations of established syndromes in other medical subspecialties have led to the understanding of disease mechanisms and effective therapies for the underlying conditions. Compared with delirium, dementia has a less abrupt onset, lasts longer, exhibits less impairment of arousal, and has less fluctuation in the level of consciousness. Dementia is distinguished from mental retardation by its late occurrence and a decline from a higher level of intellectual functioning. Dementia is differentiated from monosymptomatic neuropsychologic syndromes, such as aphasia and amnesia, by the simultaneous occurrence of deficits that involve several cognitive functions. While the syndrome must have been present for several months or more to be labeled as a dementia, the decline in intellectual ability is not necessarily irreversible, and appropriate diagnosis and treatment may produce improvement in cognitive function.
Home Objectives Schedule Lectures �
Other progressive diseases (eg, Parkinsons disease, HallervordenSpatz disease,spinocerebellar degenerations, progressive supranuclear palsy).
http://umed.med.utah.edu/neuronet/lectures/2002/cognitive testing in dementia.ht

Extractions: To know the diagnostic criteria for the diagnosis of dementia To list five causes of dementia To understand the importance of age-based norms when evaluating cognition in the elderly To recognize that there are reversible causes of dementia To name three basic tests used in the evaluation of possible dementia DEMENTIA DEFINITION A progressive loss of intellectual abilities of sufficient severity to interfere with social and/or occupational functioning. Dementia is a descriptive term, not a specific disease or condition. There are dozens of pathophysiologic causes of dementia. Because dementia is seen in the context of so many conditions, dementia is one of the most common findings encountered by neurologists who see adult patients. A. MAGNITUDE OF THE PROBLEM The population over 65 years of age is increasing rapidlyfrom 23 million in 1978 (11% of the population) to 51 million by 2030 (about 19% of the population). If life expectancy continues to rise, and the mean age of onset of dementia does not, some authors have projected that about 45% of the population would develop dementia at some point during their lives (with life expectancy extending into the late 90s).
UNIT 7 MULTIPLE SCLEROSIS
These include vasculitides (SLE, Sjögrens), AIDS, Lyme disease, some of theinherited spinocerebellar degenerations, adrenoleukodystrophy, or CNS mass
http://www.neurology.arizona.edu/unit7.htm

Extractions: 1. Basic Science Discuss why CNS demyelination produces the signs and symptoms commonly seen in MS. Describe the basic immunopathologic mechanism(s) thought to be responsible for CNS demyelination. 2. Clinical Aspects a. List at least six common symptoms and/or clinical presentations of MS. Describe the criteria for making a clinical diagnosis of MS. List the paraclinical tests that are used to help make a diagnosis of MS. List a short differential for other conditions that may mimic MS. 3. Treatment Discuss treatment for an acute exacerbation of MS. Discuss the pharmacologic or other treatment modalities that are used in the management of common symptoms of MS. Name the three agents that are currently (early 1998) FDA approved for prophylactic treatment of MS, the rationale for their use, and assumed mechanism of action. Describe their major clinical effects and side effects.
Bibliographic Information About Parkinson's Disease And Movement Disorders
Palsy 229 Mark Stacy, MD 17 Multiple System Atrophy 235 James H. Bower, MD 18 FamilialAdultOnset spinocerebellar degenerations 243 James H. Bower, MD 19
http://www2.utsouthwestern.edu/cfdocs/library/facultypubs/bib_cite.cfm?titleID=5
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SUTUDY OF SOMATOSENSORY EVOKED POTENTIALS IN spinocerebellar degenerations.M.sahara, A.Kanno, M.Watanabe, M.Tachiya, N.Okita and S.Takase.
http://homepage1.nifty.com/masakisahara/masaro.htm

Extractions: 88NÈãÌàÌ@s¯ CN:95156494 TI:Ò¬]Ï«ÇÉ¨¯é®«]²½Ì¢ Õ°a^¨æÑ¸²ÇóÆABRÌär AU:ì²(Lìa@),§Ôüaq,²´³N JN:ãw¸ CI :26C KW : UdÊ ]²®o ff l AB:SCDÌe¾³QÉÂ¢ÄABRÆÕ°ÇóÌÖAð¢µ½BABRÌÙíÍ,ÙÚSáÉ¨¢Ä 3gÌö·àµÍÁ¸ð¦µ½Bµ©µ,Õ°ÇóÆABRÙíÉÖÍ©o¹È©Á½ CN:96200284 TI:ÒáQ¥óªFßçêÈ©Á½èò½`äPèîÌdí JN:Õ°_ow(0009-918X) 35ª 11 Page 1235-1240 (1995.11) CI: KW: _oäPî CK: l ¬l j ð¦µ½.Ó¯áQÆ½«Ì]_o¥Ò_oªáQªXÉisµ,Soß11TÅSµ ª`o³ê,À¿àaÏÍºèòÉÌÝ¦´³ê½.]ÌUÅ½`äPèîÌdíÆ ff³ê½ª,]À¿àÉÍ´Æzè³êéaÏªÈ,Òª´Æl¦çê½(TR ³M) CN:96090550 TI:â`qffªLpÅ Á½ÇáÆl¦çê½ójÔjWÙ²ÌÞkÇ(DRPLA)Ì JN:Õ°_ow(0009-918X) 35ª 2 Page 201-203 (1995.02) CI: KW:; â`qff ójÔjWÙ²ÌÞkÇ ff CK: l N CN :97157527 TI: å®¬ð£Éæéêß«ÒÌ1á JN:Õ°_ow(0009-918X) 36ª 10 Page 1197 (1996.10)
COGNITIVE TESTING IN PATIENTS WITH SUSPECTED DEMENTIA
Other progressive diseases (eg, Parkinsons disease, HallervordenSpatzdisease, spinocerebellar degenerations, progressive supranuclear palsy).
http://medlib.med.utah.edu/neuronet/cogtest/

Extractions: COGNITIVE TESTING IN PATIENTS WITH SUSPECTED DEMENTIA T. Schenkenberg, Ph.D. DEFINITION A loss of intellectual abilities of sufficient severity to interfere with social and/or occupational functioning. MAGNITUDE OF THE PROBLEM Population over 65 years of age is increasing rapidly (from 23 million, 11% of the population in 1978, to 51 million, about 19% of the population by 2030). If life expectancy continues to rise, and the mean age of onset of dementia does not, some authors have projected that about 45% of the population would develop dementia at some point during their lives (with life expectancy extending into the late 90s). Close to 3 million people are in nursing homes in the USA now. About two-thirds of them suffer from dementia. Annual cost of formal and informal care is in the neighborhood of $75,000 per year per patient. Estimates suggest that there might be 4 million people in the USA with Alzheimers. Some estimates are that there will be 12 million by 2050. B. DIAGNOSTIC CRITERIA Demonstrable impairment in short-term and long-term memory At least one of the following: impairment of abstract thinking impaired judgement other disturbances of higher cortical functioning (e.g., apraxia, acalculia, agnosia, language dysfunction)
Indian Pediatrics - Case Reports
Biol Chem 1999; 12 13451354. 6. Brett EM. spinocerebellar degenerations andsome related disorders. In Pediatric Neuro-logy, 2nd edn. Ed Brett EM.
http://www.indianpediatrics.net/sept2001/sept-1056-1058.htm

Extractions: Rajiv Mittal, Jatinder S. Goraya Srikanta Basu From the Department of Pediatrics, Government Medical College Hospital, Sector 32 B, Chandigarh 160 047, India. Correspondence to: Dr. Jatinder S. Goraya, Reader, Department of Pediatrics, Government Medical College Hospital, Sector 32 B, Chandigarh 160 047, India. E-mail: goraya@glide.net.in Manuscript received: November 7, 2000; Initial review completed: December 12, 2000; Revision accepted: January 30, 2001. Dopa-responsive dystonia (DRD) also known as hereditary progressive dystonia with diurnal variations or Segawas syndrome was first described by Segawa et al. in 1976(1). The dystonia characteristically worsens throughout the day and there is marked benefit from sleep. Another equally important feature is the complete relief of symptoms from small doses of L-dopa(2). Because of lack of awareness, it is not unusual for this uncommon disorder to be mis-diagnosed as hysteria, hereditary spastic para-paresis or cerebral palsy(2-4). Since an effective therapy for DRD is available, implication of wrong diagnosis can be enor-mous. We report one such case to highlight these aspects. Case Report Discussion Dopa-responsive dystonia represents about 5-10% of primary childhood dystonia(2). Age of onset is usually between 4-8 years but may be as early as infancy. The disorder is more common in females. It is inherited in an autosomal dominant fashion. Occasionally, the condition may occur sporadically(2,3). The causative gene for the disorder has been localized to chromosome 14q and it encodes for enzyme GTP-Cyclohydrolase 1(5).
Spinocerebellar Degenerations Information Sites
Reviewed spinocerebellar degenerations sites, by people who know SpinocerebellarDegenerations and work with spinocerebellar degenerations. HEALTHorgs.com.
http://www.healthorgs.com/ConditionsandDiseases/NeurologicalDisorders/SpinalCord
1Up Health > Health Links Directory >Conditions And Diseases:Neurological Disord
degenerations Friedreich_Ataxia. An autosomal recessive disease, usually of childhood onset, characterized pathologically by degeneration of the spinocerebellar
http://www.1uphealth.com/links/desc-559.html

Extractions: The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed physician should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only they do not constitute endorsements of those other sites. Home Contact Us Privacy Links Directory
1Up Health > Health Links Directory > Conditions And Diseases: Neurological Diso
See Related Categories. Health Conditions and Diseases Genetic Disorders(510) Health Conditions and Diseases Rare Disorders (128). Sites.
http://www.1uphealth.com/links/spinocerebellar-degenerations-friedreich-ataxia.h
Spinocerebellar Ataxia
feasible that within the next decade, we may be able to determine the gene that isdamaged in most inherited cerebellar degenerations. spinocerebellar ATAXIAS
http://www.tchain.com/otoneurology/disorders/central/cerebellar/sca.htm

Extractions: Return to Education Index Last update: Feb 20, 2000 The main goal of this page is to serve as a repository for recent information about inherited cerebellar degenerations. It is not comprehensive, but we hope that it might be of some use to individuals searching for information about these rare conditions on the web. We highly recommend also using the OMIM database , which can be accessed on the web. A large number of the genetic ataxias can be tested for using contemporary methodology. An example of a lab that does this is Athena Most of the information here concerns inherited conditions, as there is considerable new data derived from researchers using a nearly complete map of the human genome (your tax dollar is doing some good !), and improvements in the technology of molecular biology. It seems quite feasible that within the next decade, we may be able to determine the gene that is damaged in most inherited cerebellar degenerations. As these data become known, it may also be possible to target specific therapies, probably over the next 2 decades. In other words, stay tuned, but we aren't there yet. There are numerous non-genetic causes of cerebellar disease.
Spinocerebellar Ataxia Type 1
repeat and phenotypic variability of spinocerebellar ataxia type 1. Ann Neurol395006 Medline; Greenfield JG (1954) The Spino-cerebellar degenerations.
http://www.geneclinics.org/profiles/sca1/details.html

Extractions: 29 January 2001 Disease characteristics. SCA1 is characterized by progressive cerebellar ataxia, dysarthria, and eventual bulbar dysfunction. Diagnosis/testing. The diagnosis of SCA1 rests upon the results of DNA-based testing to detect an abnormal CAG trinucleotide repeat expansion of the gene (chromosomal locus 6p23). Affected individuals have alleles with 39-81 CAG trinucleotide repeats. Such testing detects 100% of cases and is available in clinical laboratories. Genetic counseling. SCA1 is inherited in an autosomal dominant manner. It is necessary to confirm the diagnosis in an affected family member using molecular genetic testing of the gene to determine the size of the CAG trinucleotide repeat prior to genetic counseling and testing of asymptomatic at-risk family members. Offspring of an affected individual have a 50% chance of inheriting the gene mutation. Prenatal diagnosis by molecular genetic testing is possible for fetuses at 50% risk, but prenatal testing of typically adult-onset diseases requires careful genetic counseling. The diagnosis of SCA1 rests upon molecular genetic testing to detect a CAG trinucleotide repeat expansion in the gene (chromosomal locus 6p23) in a patient with cerebellar ataxia. Such testing detects 100% of cases and is available in clinical laboratories.
Therapy Information Services - Neuroscience
cord; spinocerebellar atrophy (Friedreich's ataxia); distinctive pattern of spinalcord tract degenerations (posterior columns, spinocerebellar tracts and
http://www.therapyedu.com/neuro/chap10.htm

Extractions: TIS Chapter 10 Degenerative and Metabolic Disorders DEGENERATIVE DISEASES OF GRAY MATTER 1. Characteristics: a. Clinical: steady progression of signs and symptoms b. Pathology: loss of neurons in stereotyped patterns, generally within functionally related neuronal systems, and atrophy of tracts that originate from the lost neurons. c. Etiology: often genetically determined; several were originally considered to be simply accelerated aging. d. Gene defects, gene products, and genotype risk factors have been identified for many disorders 2. Macroscopic abnormalities a. Atrophy of involved gray matter structures with decreased brain weight. b. Color changes: 1. light brown discoloration of shrunken gray matter 2. loss of normal pigment (e.g., pale substantia nigra in Parkinson's disease) c. Secondary atrophy of cerebral white matter and fiber tracts leading from the atrophic gray matter region d. Enlargement of ventricles due to shrinkage of white matter (e.g., in Alzheimer's disease); called "hydrocephalus ex vacuo". 3. Microscopic Abnormalities
THE LIGHTNING HYPERTEXT OF DISEASE.
olivopontocerebellar atrophy with retinaldegeneration) Fd spinocerebellar ataxia7 degenerationdegeneration, olivo-ponto-cerebellar degenerations, olivo-ponto
http://www.pathinfo.com/cgi-bin/lh.cgi?tx=opc
Revista Nº 4
Spinal muscular atrophy. Hereditary degenerations. Idiopathic cerebellar, spinocerebellardegenerations. Bands are not found when complicating cases are excluded
http://www.fedem.org/revista/n4/liquido2ing.html

Extractions: London Diagnosis CSF and MRI are complementary tests in the diagnosis of multiple sclerosis, since the sensitivity of both tests is very high (abnormalities found in almost all patients). However, CSF has the advantage of greater specificity since immunoglobulin abnormalities are rarely found in the normal population. The same cannot be said for MRI abnormalities, especially after the 4 th decade of life. The most important technique for analysis of intrathecally-synthesised immunoglobulins is the separation of IgG by isoelectric focusing followed by the detection of the banding pattern using visualisation with immuno-specific staining for IgG molecules. We see in Figure 5 that there are two basic types of pattern in comparing CSF with parallel serum: identical versus discordant. The latter is pathognomonic of local synthesis of IgG within the central nervous system. There are 5 types of CSF/serum banding patterns: Type 1 is normal with a polyclonal response in both CSF and serum;

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