Geometry.Net - Health_Conditions: Corticobasal Degeneration

POSTER NUMERO 12
Translate this page corticobasal degeneration. A clinical study of 36 cases. Accuracy of the clinicaldiagnosis of corticobasal degeneration a clinicopathologic study.
http://neurologia.rediris.es/congreso-1/posters/p-12.html

Extractions: La degeneración cortico-basal (DCB) es una enfermedad neurodegenerativa poco frecuente caracterizada por una afectación asimétrica de corteza y ganglios basales. Se han descrito recientemente trastornos del sueño asociados a esta enfermedad, aunque no movimientos periódicos de las piernas (MPP). Varón de 65 años, con distonía en mano derecha de 5 años de evolución y afasia motora progresiva a lo largo de tres años. La exploración demostró además un síndrome rígido-acinético en miembros derechos, hiperreflexia derecha, apraxia gestual y deterioro cognitivo córtico-subcortical. Una PET cerebral mostró hipometabolismo en corteza asociativa y ganglios basales del lado izquierdo. La RM cerebral únicamente mostró atrofia difusa.
Pick's Disease And Other Frontotemporal Dementias - Geriatrics And Aging, Pick's
Because corticobasal degeneration is also characterized by ballooned neurons (butin a frontalparietal distribution) and can present with FTD and PA, some
http://www.pdsg.org.uk/articles/GaA-1.htm

Extractions: The prevalence of dementia in Canada has been estimated at 8%, after the age of 65 years. Alzheimer disease (AD) accounts for approximately 60% of cases, while other conditions accounting for the remaining 40% include, among others, vascular dementia, dementia with Lewy bodies (DLB) and frontotemporal lobar degeneration (FTLD). Differences in prognosis and symptomatic treatment, as well as eventually disease-modifying therapy underline the importance of the differential diagnosis of dementia. The use of clinical criteria for diagnosis of degenerative and vascular dementias can increase the level of clinical diagnosis accuracy and should, therefore, be known by physicians dealing with dementia. Advances in the understanding of FTLD have been made over the past 15 years. We will review the clinical manifestations of FTLD and highlight the differences with AD.
Pick's Disease And Other Frontotemporal Dementias - Geriatrics & Aging, Pick's D
Neurology 1994;44206572. Kertesz A. Frontotemporal degeneration,Pick disease, and corticobasal degeneration. One entity or 3? 1
http://www.pdsg.org.uk/articles/GaA-3.htm

Extractions: There is no impairment of the cholinergic system in FTLD, rendering the use of anticholinesterase inhibitors unnecessary. Furthermore, cholinergic boosting compounds are reported to exacerbate psychiatric symptoms in these patients. However, serotonin binding is decreased in the frontal cortex of patients with FTLD and use of selective serotonin reuptake inhibitors has provided temporary symptomatic relief of affective and behavioural manifestations. Caregivers need to be educated and supported (e.g. emotional support, respite care) early.
Corticobasal Degeneration
Translate this page English version corticobasal degeneration. Aspects cliniques Hyperphosphorylatedtau proteins differentiate corticobasal degeneration and Pick's disease.
http://home.nordnet.fr/~adelacourte/CBD.html

Extractions: This site is devoted to Alzheimer's disease, neurodegenerative disorders and cerebral aging, as well as neuroendocrinolgy. English version Publications VCDN Autres pathologies Equipe VCDN ... English version: Corticobasal degeneration Aspects cliniques: tremblement d'attitude, syndrome pseudo-bulbaire avec dysarthrie, dysphagie, troubles oculomoteurs Neuropathologie: Hyperphosphorylated tau proteins differentiate corticobasal degeneration and Pick's disease. Buee Scherrer V, Hof PR, Buee L, Leveugle B, Vermersch P, Perl DP, Olanow CW, Delacourte A Acta Neuropathol (Berl) 1996;91(4):351-359 PMID: 8928611, UI: 96254284 J Neurochem 1999 Mar;72(3):1243-9 Neurofibrillary degeneration in progressive supranuclear palsy and corticobasal degeneration: tau pathologies with exclusively "exon 10" isoforms. Sergeant N, Wattez A, Delacourte A INSERM Unite 422, Lille, France. English version Publications VCDN Autres pathologies Equipe VCDN ... DERNIERES NOUVELLES
SpringerLink: Neuroradiology - Abstract Volume 37 Issue 8 (1995) Pp 642-644
Focal cortical hypoperfusion in corticobasal degeneration demonstrated by threedimensionalsurface display with 123 I-IMP a possible cause of apraxia.
http://link.springer-ny.com/link/service/journals/00234/bibs/5037008/50370642.ht

Extractions: Received: 4 April 1994 Accepted: 12 July 1994 Abstract To clarify cortical lesions responsible for apraxia in corticobasal degeneration (CBD), we reconstructed three-dimensional surface images from single-photon emission computed tomography (SPECT) data with N -isopropyl- p [I-123]-iodoamphetamine in two patients with CBD. Both had limb-kinetic apraxia (LKA) and one also had constructional apraxia (CA). Both showed asymmetrical cortical hypoperfusion in the perirolandic area. The patient with CA had unilateral hypoperfusion in the posterior parietal area. Thus, cortical hypoperfusion in the perirolandic area corresponded to LKA, and that in the posterior parietal area to CA. Key words Article not available online Online publication: December 2, 1997
SpringerLink: Acta Neuropathologica - Abstract Volume 92 Issue 5 (1996) Pp 534-5
corticobasal degeneration with primary progressive aphasia and accentuatedcortical lesion in superior temporal gyrus case report and review.
http://link.springer-ny.com/link/service/journals/00401/bibs/6092005/60920534.ht
Pathology Of Degenerative CNS Diseases
CNS degenerative diseases by the Internet Pathology Laboratory.Category Health Conditions and Diseases Neurodegenerative Diseases corticobasal degeneration (CBD) is classified as an akinetic rigid movement disorderclassically consisting of progessive asymmetric rigidity and apraxia with
http://medlib.med.utah.edu/WebPath/TUTORIAL/CNS/CNSDG.html

Extractions: Return to the tutorial menu. Senile dementia of the Alzheimer's type (SDAT), or Alzheimer's disease (AD) is becoming more common in developed nations as the population includes more and more older persons. There is no known cause for the disease. It is not known why some people present as early as 30 or 40 years of age with dementia while others do not present until their late 70's or 80's. Familial cases with a defined inheritance pattern account for only 5 to 10% of Alzheimer's disease. Familial cases tend to have an earlier age at onset. Genetic defects in familial cases have been identified on chromosomes 21, 19, 14, 12 and 1. The so-called "early onset" cases of AD in persons in their 30's, 40's, and 50's may have a genetic basis. Less than 1% of early onset AD cases are linked to a genetic defect on chromosome 21 (which may explain the appearance of Alzheimer's disease in persons with Down syndrome surviving to middle age) which affects amyloid precursor protein (APP), resulting in fibrillar aggregates of beta-amyloid that is toxic to neurons. About half of early onset AD cases are linked to mutations in the presenilin 1 gene on chromosome 14. A presenilin 2 gene has been discovered on chromosome 1, but this defect accounts for less than 1% of cases. The more typical "late onset" cases of AD occurring after age 60 may have underlying genetic defects. A genetic locus on chromosome 19 encodes for a cholesterol transporter called apolipoprotein E (apoE). The E4 variant of apoE, which increases deposition of fibrillar beta-amyloid, can be found in 40% of AD cases. However, the presence of apoE4 is neither necessary nor sufficient for development of AD, so testing for it is not warranted. A genetic locus on chromosome 12 that encodes for alpha-2-macroglobulin may be found in 30% of AD cases. Mutations in the tau gene which codes for
ECR 2001 - Presentation C-0591
C0591. M. Ukmar, R. Moretti, P. Torre, RM Antonello, R. Longo, R. Pozzi Mucelli;Trieste/IT. fMRI evaluation of motor skills in corticobasal degeneration.
http://www.ecr.org/T/ECR01/sciprg/abs/pc0591.htm

Extractions: Materials and methods: We propose three cases presenting clinically with asymmetric rigidity, bradykinesia, astereognosis, tactile extinction and dystonic postures of the left hemisoma. It can also be detected an ideomotor apraxia, a mild to discrete impairment of frontal executive and attention functions. All subjects undergone an MR examination by using an 1.5 T magnet. A morfological and functional study was performed. The functional study was performed with a GE T2* sequence by using BOLD contrast. The patient were asked to execute a finger opposition task with both left and right hand. Results: Conventional MRI demonstrate an important atrophy of the perirolandic and in particular postrolandic cortex, associated with a discrete atrophy of the parietal area and the omolateral basal ganglia. Movements executed with the healthy hand revealed a good activation of the rolandic region with extension to the supplementary motor area and in part of parietal area. There is an hypoactivation of the rolandic area and no activation of the supplementary motor and parietal cortex during the movement of the affected hand.
EMedicine - Cortical Basal Ganglionic Degeneration : Article By Anna M Barrett,
Synonyms and related keywords corticobasal degeneration, corticodentatonigral degenerationwith neuronal achromasia, corticonigral degeneration with neuronal
http://www.emedicine.com/NEURO/topic77.htm

Extractions: document.write(''); (advertisement) Home Specialties CME PDA ... Patient Education Articles Images CME Patient Education Advanced Search Link to this site Back to: eMedicine Specialties Neurology Movement And Neurodegenerative Diseases Last Updated: February 8, 2002 Rate this Article Email to a Colleague Synonyms and related keywords: corticobasal degeneration, corticodentatonigral degeneration with neuronal achromasia, corticonigral degeneration with neuronal achromasia, extrapyramidal apractic syndrome, Pick complex disorders, Rebeiz disease, apraxia AUTHOR INFORMATION Section 1 of 10 Author Information Introduction Clinical Differentials ... Bibliography Author: Anna M Barrett, MD , Assistant Professor, Division of Neurology, Pennsylvania State University College of Medicine Anna M Barrett, MD, is a member of the following medical societies: American Academy of Neurology, American Society of Neurorehabilitation, and Society for Neuroscience Editor(s): Stephen T Gancher, MD
CBU Bibliography
68(3), 304312 Year 2000 Key Words corticobasal degeneration, Frontotemporaldementia; frontotemporal lobar degeneration; non-Alzheimer dementias Abstract
http://www.mrc-cbu.cam.ac.uk/cgi-bin/biblio.cgi?author=Bak T&abstract=on
SpringerLink: Journal Of Neurology - Abstract Volume 246 Issue 12 (1999) Pp 1151
Abstract Volume 246 Issue 12 (1999) pp 11511158. original communication Fluorodopauptake and glucose metabolism in early stages of corticobasal degeneration.
http://link.springer.de/link/service/journals/00415/bibs/9246012/92461151.htm
Fiche Document :Inter Brain CD-ROM â¢ Academusâ¢ WEB
http://catalogue.iugm.qc.ca/Document.htm&numrec=031906613918840
Parkinson's Disease With Additional Symptoms
Drugs may be used to increase blood pressure, but should be used with care dueto a decrease in the body's ability to compensate. corticobasal degeneration.
http://www.mayo.edu/fpd/pd-info/parkplus.htm

Extractions: 'Parkinson's Plus' is a name given to a group of disorders with parkinsonian symptoms, but with additional features. While the clinical symptoms of these disorders overlap with Parkinson's disease, the underlying neuropathology is often different and individuals may require alternate treatments. We've tried to provide an informative passage on each of these disorders, but for further information, please see our links for other sources. Cortical Lewy bodies of dementia with Lewy bodies (DLB) are noticeably smaller and different in appearance, both with a standard H+E stain, and with an anti-synuclein staining (see figure). Prior to the identification of Lewy bodies in demented patients, the 50% (approx.) of dementia cases not attributable to pure Alzheimer's disease were assumed the result of vascular dementia. The discovery of Lewy bodies in the brains of demented patients by Kosaka and coleagues (1984) prompted a variety of new diagnoses i.e. dementia with Lewy bodies, diffuse Lewy body disease, Lewy body variant of Alzheimer's disease and others. More recently, the umbrella term 'Dementia with Lewy bodies' has been used - distinctions between different Lewy dementias were probably due to the variable bias between research groups. As a result, today's DLB is probably the second most common form of dementia after Alzheimer's disease. In DLB, patients usually initially develop Alzheimer's like dementia symptoms or parkinsonian signs and subsequently progress to symptoms of the other condition. McKeith and colleagues (1996) defined the features of possible or probable DLB diagnoses. These are (2 needed for a probable, 1 for a possible diagnosis):
Listings Of The World Health Conditions And Diseases
Listings World Health Conditions and Diseases Neurological Disorders BrainDiseases corticobasal degeneration. Listings World,
http://listingsworld.com/Health/Conditions_and_Diseases/Neurological_Disorders/B
IRCS/CCN Brain & Language Series: Halpern Abstract
Casey Halpern University of Pennsylvania. Dissociation of number knowledgeand object naming in corticobasal degeneration and semantic dementia.
http://www.ldc.upenn.edu/brainlang/halpern.html
TIP - Psychogeriatrics - Archives
McGeer PL Distinct isoforms of tau dggregated in neurons and glial cells in brainsof patients with Pick's disease, corticobasal degeneration and progressive
http://www.prit.go.jp/En/Pgeriat/works.html
National Parkinson Foundation, Inc.
Group 1 would now be viewed as classic Pick's disease, and a number of those withinGroup 2 would probably be diagnosed as cases of corticobasal degeneration.
http://www.parkinson.org/ftd.htm

Extractions: Frontotemporal dementia (FTD) has become recognized as a common cause of progressive cognitive and behavioral decline in adults. Estimates indicate that as many as 20% of adults presenting to a memory disorders clinic with impaired language, cognition, and behavior may suffer from FTD. (The number of suffers from FTD is less than people with Alzheimer Disease or Lewy Body Dementia). Patients with FTD are generally younger than people with Alzheimer Disease (AD) , but this feature is not sufficient to distinguish FTD from AD. Routine neuropsychologic investigations have not discriminated between FTD and AD with any reliability: both FTD and AD patients have difficulty with "executive functions" such as planning, mental organization, and working memory. One subgroup of patients with FTD presents with Progressive Nonfluent Aphasia. These patients have effortful, telegraphic (compressed) speech with reasonably good comprehension. Another subgroup of patients with FTD presents with Semantic Dementia. The core feature of these patients is poor single-word comprehension despite a fluent and melodic speech pattern. Both subgroups also show social and behavioral abnormalities including financial recklessness, sexual deviance, and criminal behavior.
CBGD
Corticalbasal ganglionic degeneration (CBGD), or corticobasal degeneration typicallybegins from 50 70 years of age. Mean survival is about 8 years.
http://www.cmdg.org/Movement_/Parkinsons_Plus/CBGD/cbgd.htm

Extractions: Cortical Basal Ganglionic Degeneration (CBGD) See also www.wemove.org/cbd.html Cortical-basal ganglionic degeneration (CBGD), or corticobasal degeneration typically begins from 50 70 years of age. Mean survival is about 8 years. Its distinctive features are an asymmetric levodopa-resistant akinetic-rigid syndrome associated with "cortical" features such as apraxia, cortical sensory loss, and alien limb phenomenon. General cognitive function had been thought to be preserved. This "classical" description emphasizing a parietal/perceptual-motor presentation may be biased because the cases mainly originate from movement disorder centers. Features of speech disturbances or dementia had been thought to represent the minority of cases. In a recent review by Grimes et al. only 4 of 13 pathologically proven patients had a prior clinical diagnosis of CBGD. It appears now that dementia can be a prominent feature of advanced disease and may be the most common feature. Aphasia can be seen in over 50% of patients. Depression is common. Apathy, social withdrawal, bizarre behavior, hypersexuality irritability, and anarthria have been described. Parkinsonian signs including unilateral limb rigidity (79%), bradykinesia (71%), postural instability (45%) and apraxia are found in almost all patients. Dystonic posturing of the arm and hand is common (43%). Tremor when present is typically an action tremor that improves at rest. It frequently has a myoclonic (jerky) component. Stimulus sensitive myoclonus can be seen. The rigidity may be extreme and associated pain is common.
Case Records Of The Massachusetts General Hospital -- NEJM 1997; 337: 549-556
Because of the considerable overlap of the neuropathological findings among progressivesupranuclear palsy, corticobasal degeneration, and Pick's disease, (38
http://med.hallym.ac.kr/~medline/public/1997/0337/0008/0549/5.htm

Extractions: NEJM Home Table of Contents Previous Article Next Article The New England Journal of Medicine August 21, 1997 Volume 337, Number 8 Pathological Discussion Dr. M. Joe Ma: At autopsy the brain weighed 1283 g. Coronal sections revealed marked atrophy and brown discoloration of the subthalamic nucleus ( Figure 2 ) and moderate-to-marked depigmentation of the substantia nigra. The globus pallidus was slightly brown but not visibly atrophic. Moderate ventricular dilatation and diffuse reduction of cerebral white matter were evident. The remainder of the brain appeared normal. The selective degeneration of the subthalamic nucleus, the substantia nigra, and possibly the pallidum is a specific feature of progressive supranuclear palsy. ( Microscopical examination of the substantia nigra showed a marked loss of pigmented neurons, many globose neurofibrillary tangles, severe gliosis, which was more marked in the pars compacta than in the pars reticularis, a few grumose bodies, and numerous pigment-laden macrophages. The globose neurofibrillary tangles were moderately argyrophilic and strongly immunoreactive to a monoclonal antibody (AT8) against phosphorylated tau ( Figure 3A ), a microtubule-associated phosphoprotein found in neurofibrillary tangles. The subthalamic nucleus was also severely degenerated, with marked gliosis, vacuolization, neuronal loss, and numerous globose neurofibrillary tangles (
Corticobasal Ganglionic Degeneration
corticobasal Ganglionic degeneration This is a webforum to discuss and comment on corticobasal Ganglionic degeneration. This Web Forum is not moderated in any sense.
http://neuro-www.mgh.harvard.edu/forum/Cortico.Gang.Deg.Menu.html

Extractions: This is a webforum to discuss and comment on Corticobasal Ganglionic Degeneration. Click here to Enter a new Neurology WebForum article... This Web Forum is not moderated in any sense. Anyone on the Internet can post articles or reply to previously posted articles, and they may do so anonymously. Therefore, the opinions and statements made in all articles and replies do not represent the official opinions of MGH and MGH Neurology. Neither is MGH or MGH Neurology responsible for the content of any articles or replies. No messages are screened for content. - Very Important Message! - Please Click Here to Read Current Posts: Dec 3, 1997 to Present Useful Websites can be found and posted here! IMPORTANT: If this page seems to be missing recently added documents, click the "Reload Page" button on your Web Browser to update the menu. Return to the main Neurology WebForum Page.

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