After my recent lecture on infections of the CNS, Southern Illinois University medical student Mike Sinha came up to the podium to ask why the herpes virus had a predilection for attacking the temporal lobes. I passed Mike's question on to Dr. Tom Smith, the neuropathologist who provided the photographs (see above) of herpes encephalitis for Robbins and Cotran Pathologic Basis of Disease (7th edition). Dr. Smith wrote that the question is not completely resolved, but he directed me to a 2002 review article which addressed the issue (Journal of Neurology Neurosurgery and Psychiatry 2002;73:237-238). I quote from that article:
"Regarding the site specificity of herpes simplex encephalitis (HSE), the pathway of viral spread is probably more important than cell-type viral susceptibility. The unique anatomical localisation has been thought to result from entry of the virus via the olfactory pathway with spread along the base of the brain to the temporal lobes, a view that is supported by the immunocytochemical evidence of HSV antigens in the olfactory tract and cortex, as well as temporal lobes, hippocampus, amygdaloid nucleus, insula, and cingulate gyrus in patients dying from HSE. Another suggestion is that HSE may result from viral spread from the trigeminal ganglia to the temporal and frontal cortex, a view that is consistent with this known site of HSV latency."
Thanks to Mike Sinha for a provocative question and to Tom Smith for researching the response.
4 comments:
Not related to this post, but related to a twitter you had a few days/weeks ago: Sen. Kennedy was diagnosed with a malignant glioma, but do we know which specific entity he is battling (e.g. glioblastoma, WHO grade III tumor, etc.)?
The New York Times reports Sen. Kennedy as having a "malignant glioma", but is no more specific than that. Statistically, the most likely diagnosis is glioblastoma, but we cannot be certain.
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