cell death in Korsakoff syndrome

F. Frank LeFever flefever at ix.netcom.com
Mon Nov 16 22:07:38 EST 1998


In <365026CB.99A507D5 at mail.rz.uni-duesseldorf.de> Tobias Kalenscher
<kalensch at mail.rz.uni-duesseldorf.de> writes: 
>
>Can anybody give me useful information about the onset of the cell
death
>in Korsakoff patients. Precisely, my question is if the neurons die in
a
>short period after the critical level of  thiamin deficiency or if
their
>death is progressive in terms of long-term atrophy until the first
>functional symptoms are measurable. Is the amount of atrophy
correlated
>with the functional deficits?
>
>Thanks,
>Tobi
>

I'll hazard a guess.

  First, by way of analogy, careful neuropsychological testing is
beginning to show in a number of conditions (e.g. Parkinsonism,
Huntington's Disease, HIV infection, having the wrong APOE allele--I
can never remenber which one) cognitive changes long before frank
symptoms.  

In the case of HD (just happened to pick up a copy of Journal of the
Internat. Neuropsych. Soc. with a relevant article, yesterday) some
damage may have occured, inasmuch as caudate volumes were inversely
correlated with scores on some of the tests. 

 In the case of HIV infection, soome evidence suggests that functional
changes can develop before brain cells are destroyed, perhaps even
before the relevant cells are infected.

The latter case probably illustrates the effects of neuroimmune
interactions which can be detrimental to cognitive function with or
without cell damage or death.

Unfortunately, I took my copy of Society for Neuroscience abstracts for
its recent annual meeting (I was there, along with 24,000 other
neuroscientists--including at least two other readers of this
newsgroup), so I must be fuzzy on the details, but I believe there was
one poster presentation on lesions due to thiamine deficiency, and I
believe it reported proliferation of mast cells in the affected
regions.

 Caught my attention because 3 years ago I presented a paper at the INS
meeting in Australia suggesting that proliferation of mast cells in the
brain after mild head injury might be a fruitful dimension to explore. 
All my subsequent research (bibliographical) has strengthened my belief
in the importance of neuroimmune reactions (with or without mast cells)
in a wide variety of conditions with functional changes but no obvious
signs of cell loss.

Bottom line: my guess is "probably progressive"--much depends on what
you mean by "a short period".


F. Frank LeFever, Ph.D.
New York Neuropsychology Group



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