jean robert
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55 y.o. man is brought to his physician s office with a three month history of progressive mental deterioration in the form of memory loss, mood changes, and errors in judgment. His gait is unsteady and he requires assistance to prevent falling. He has no history of seizures, head trauma or incontinence. CT scan and lumbar puncture are unremarkable. PE reveals hypertonicity of all extremities, bilateral equivocal plantar response,ataxic gait and myoclonic jerks in the lower extremities. What is the mechanism by which this infectious agent causes its pathology?
a.- Amyloid deposition
b.-Autoimmune destruction
c. Chronic inflammation
d.-Embolization and infarction
e.-Toxin production
Edited by new_n_lost on 01/29/08 - 04:07 PM. Reason: Changed the Font
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| Tiff
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B. Autoimmune destruction
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| new_n_lost
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e.-Toxin production ?? or this could be a.- Amyloid deposition
Cos i m not sure abt anything which causes UMN and Mood changes with Ataxia within 3 months. With CT and LP negative it seriously reduces chances of anything being positive.My first initial thougt was Pick's Disease and Prion Disease. So not sure so going with A
Edited by new_n_lost on 01/29/08 - 05:58 PM
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| jean robert
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Correct Answer: A
This is the classic presentation of Creutzfeld- Jacob disease. Although the pathogenesis is incomplete understood, these patients develop extracellular deposition of abnormal fibrillar proteins in the brain, ie, amyloid.
Autoimmune destruction is not indicated because there is no immunologic response to the deposition of these extracellular proteins;thus there is no chronic inflammation.
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| Tiff
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Isn't this spongiform. Isn't spongiform an autoimmune process? But then again amyloid should be present.
Ok. have to go read....
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| Tiff
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Ok. I know I wasn't imaging it. 
http://iai.asm.org/cgi/reprint/67/12/6591.pdf
http://www.annalsnyas.org/cgi/content/abstract/10...
http://www.pubmedcentral.nih.gov/articlerender.fc...
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