Geometry.Net - Health_Conditions: Corticobasal Degeneration

Corticobasal Ganglionic Degeneration
corticobasal Ganglionic degeneration. 13 January 2003. Age 5070.36% sensitivity for diagnosis. Best predictors for first visit limb
http://www.angelfire.com/retro/michaelpoon168/corticobasal ganglionic_degenerati

Extractions: Michael Poon's Shrine of Neurology HOME CONTENTS CONTACT US HOME ... CONTACT US Corticobasal Ganglionic Degeneration 13 January 2003 Age: 50-70 36% sensitivity for diagnosis Best predictors for first visit: limb dystonia, asymmetric Parkinsonism, ideomotor apraxia, absence of gait/balance disturbance, limb dystonia unresponsive to L-Dopa Best predictors in later stages: delayed onset of gait/balance disturbance, ideomotor apraxia, cognitive disturbance, focal myoclonus. Movement Disorders 100% Akinesia, rigidity 86% Postural instability 79% Postural, action tremor 57% Limb dystonia 54% Focal reflex myoclonus 18% Orolingual dyskinesia 18% Athetosis 7% Limb chorea 4% Rest tremor 4% Axial dystonia Cerebral cortical signs 71% Cortical sensory loss (neglect) 71% Apraxia 50% Alien limb 46% Frontal lobe reflexes 43% Dementia 21% Dysphasia Others 64% Hyperreflexia 46% Upgoing plantars 46% Impaired ocular motion 36% Dysarthria 21% Dysphagia 7% Dysphonia Investigations CT/MRI: asymmetry of sulci in parietal region HMPAO SPECT: perfusion asymmetry of parietal cortical regions IBZM SPECT: reduced basal ganglia uptake Oculography: abnormal horizontal saccades Abnormal SSEP or motor evoked potentials Autopsy: frontoparietal atrophy Swollen, achromatic neurons
Baylor Neurology Case Of The Month
Neurology. Diagnosis corticobasal ganglionic degeneration (CBGD). This month.A Review of corticobasal Ganglionic degeneration (CBGD). Clinical
http://www.bcm.tmc.edu/neurol/challeng/pat17/summary.html

Extractions: Corticobasal ganglionic degeneration (CBGD) This 73 year old man, with a history of hypertension and coronary artery disease, presented with a one-and-a-half year history of progressive inability to use his left arm, slurred speech, gait difficulty, and non-specific bladder complaints. On exam, he had slight postural hypotension, slight difficulties with arithmetic, impaired saccades, slurred speech, tremor, and dystonia, worse on the left than on the right. He also had apraxia and evidence of bilateral pyramidal tract dysfunction, again worse on the left. Pertinent negatives included lack of significant cognitive impairment, no clinical benefit to levodopa, no evidence of ataxia, and a negative family history. The differential diagnosis for progressive neurological decline in extrapyramidal, pyramidal, and cortical function, and a negative family history would include the "parkinsonism plus" syndromes. The following diseases or syndromes were considered in the differential for this patient: Hemiparkinsonism Idiopathic Parkinson's disease usually begins unilaterally and our patient's symptoms of predominantly left sided rigidity, cogwheeling, and shaking were consistent with this diagnosis. However, the additional signs and symptoms of postural hypotension and cortical apraxia, as well as the lack of a response to carbidopa/levodopa, suggested a different pathological process than that occurring in idiopathic Parkinson's disease.
(8[2]:355-365) Corticobasal Ganglionic Degeneration And Progressive Supranuclear
(82355365) corticobasal Ganglionic degeneration and ProgressiveSupranuclear Palsy Presenting with Cognitive Decline Catherine
http://brainpath.medsch.ucla.edu/abstracts/vol8/0802/82a9.htm

Extractions: Corticobasal Ganglionic Degeneration and Progressive Supranuclear Palsy Presenting with Cognitive Decline Catherine Bergeron, Andrea Davis, Anthony E. Lang Corticobasal ganglionic degeneration (CBGD) and progressive supranuclear palsy (PSP) were originally described in the sixties as predominantly motor syndromes. Over the years, the detailed study of additional cases of CBGD has shown that it is a distinctive histological entity which can often present as dementia or aphasia. Although some pathological features of CBGD overlap with those of other forms of non-Alzheimer non-Lewy body dementia, the distribution and relative number of these abnormalities and the distinctive pattern of tau immunodeposits allows the distinction of CBGD from Pick's disease and fronto-temporal dementia. In contrast, PSP only rarely presents with prominent dementia or behavioral changes. In these unusual PSP cases, care must be taken to exclude the diagnoses of CBGD and familial tangle-only dementia. (Download PDF:197KB)
My Wife, Barbara, Had CBGD: Corticobasal Ganglionic Degeneration
CBGD Network. Start Page Caregivers Case Histories Features and Glossary Network Support Groups From Alan G. McIlvaine, Scottsdale, AZ
http://www.tornadodesign.com/cbgd/mcilvaine.htm

Extractions: From Alan G. McIlvaine, Scottsdale, AZ This is a story of the small victories and distress that we experienced in caring for Barbara through the relentless assault of CBGD. It is not a guide on what to do but rather, since this disease treats everyone differently, different symptoms, how we coped with each new devastating symptom. Hopefully it will give others some ideas on what to expect and how to handle it. Some years before our introduction to CBGD, Barbara and I had decided that neither of us would be comfortable in a nursing home if we became ill enough to warrant it, and the other would do whatever was in his/her power to maintain the ill one at home. I know that Barbara would have felt deserted and would not have received the tender loving care in a nursing home that she did in our home. If you have a close family and there is any way possible to keep the patient at home with adequate care, I strongly urge you to do it. You will all feel better for it. I realize that sometimes it is not possible in which case the caregiver should devote as much time as possible to overseeing that the care being provided is appropriate, adequate and loving. I have also learned from letters received from others concerned with CBGD and from our own experience that this disease is very difficult to diagnose.
(8355-365) Corticobasal Ganglionic Degeneration And Progressive
corticobasal Ganglionic degeneration and Progressive Supranuclear Palsy Presentingwith Cognitive Decline Catherine Bergeron, Andrea Davis, Anthony E. Lang.
http://brainpathology.upmc.edu/vol8/0802/82a9.htm
Pathology Of Degenerative CNS Diseases
features of AD include neurofibrillary tangles, amyloid angiopathy, and granolovacuolar degeneration. there is lateral column degeneration with gliosis, the socalled "sclerosis"
http://www-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
Katalog - Wirtualna Polska
Serwis Katalog w Wirtualna Polska S.A. pierwszy portal w Polsce.
http://katalog.wp.pl/DMOZ/Health/Conditions_and_Diseases/Neurological_Disorders/
Feany Lab Publications
Feany MB, Dickson DW. Widespread cytoskeletal pathology characterizes corticobasaldegeneration. Am J Pathol 1995;14613881396. Feany MB.
http://feany-lab.bwh.harvard.edu/link3/
ÅßÌ_¶(2001/May/26)
Intracellular processing of aggregated tau differs between corticobasaldegeneration and progressive supranuclear palsy. Neuroreport.
http://ben.shiga-med.ac.jp/~hqmnrch/paper/paper2001-05-26.html

Extractions: Corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP) are sporadic neurodegenerative diseases with intracytoplasmic aggregates of the microtubule-associated protein, tau, in neurons and glial cells. Immunoblot analysis of detergent-insoluble brain extracts of patients with CBD and PSP shows distinctive patterns of tau fragments. These results suggest differing intracellular processing of aggregated tau in these two diseases despite an identical composition of tau isoforms. Such biochemical differences may be related to the neuropathological features of these diseases. Intracellular processing of aggregated tau differs between corticobasal degeneration and progressive supranuclear palsy. "Inflammatory responses to amyloidosis in a transgenic mouse model of Alzheimer's disease." Am J Pathol. 158(4): 1345-1354, 2001. Matsuoka Y , Picciano M, Malester B, LaFrancois J, Zehr C, Daeschner JM, Olschowka JA, Fonseca MI, O'Banion MK, Tenner AJ, Lemere CA, Duff K "Correlation of the Expression Level of C1q mRNA and the Number of C1q-Positive Plaques in the Alzheimer Disease Temporal Cortex. analysis of c1q mrna and its protein using adjacent or nearby sections." Dement Geriatr Cogn Disord. 12(4): 237-42, 2001
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http://www.neurology-jp.org/guideline/dementia/3_08c.html
Cdp-coline
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http://www.pileup.com/cbd/cdp-coline.htm

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(9681-693) Comparative Biochemistry Of Tau In Progressive
Comparative Biochemistry of Tau in Progressive Supranuclear Palsy, CorticobasalDegeneration, FTDP17 and Pick's Disease Luc Buée and André Delacourte
http://brainpathology.upmc.edu/vol9/0904/0904a6.htm

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