re: hippocampus damage & immune cell infiltration
2006-10-31 22:24:20Trina, here is a citation that doesn't address your question about
how to increase perfusion but may provide clues regarding possible
etiology specific to hippocampal regions and what the SPECT may be
indicating. I can't help but wonder if an immune infiltration headed for the
hippocampus at some point, then the portion of the bbb adjoining the hippocampi
might have been affected in ways leading to hypoperfusion. The following offers
a *possible* etiology, but whether or not the article's information applies to
your son is not known.
The following citation describes how inflammatory response to
intracerebral HSV can damage subcortical structures including the
hippocampus, while sparing the cerebral cortex, including cortical areas
positive for HSV. Furthermore, an entry route from corneal scarification
(scratching the cornea) led to more neuronal damage (from lymphocyte
infiltration) that did intracerebral injection of HSV.
Song GY, Jia W.
The heterogeneity in the immune response and efficiency of viral
dissemination in brain infected with herpes simplex virus type 1 through
peripheral or central route.
Acta Neuropathological 97.649-56 1999
From the abstract:
...we studied the correlation between the dissemination of the virus, the
inflammatory responses and the expression of major histocompatibility
complex (MHC) proteins in rat brain infection with herpes simplex virus
(HSV-1) F strain by either corneal scarification or intracerebral
injection.
Our results showed that the mortality of the corneally infected rats
was much higher than that of the intracerebrally infected rats, due to a
more extensive dissemination of the virus in the brain, particularly in
the brain stem.
The inflammatory responses were similar in brains infected through
either route, as demonstrated by the expression of MHCI/II antigens on
infiltrating lymphocytes, leukocytes and macrophage/microglia cells.
While there was strong immunoreactivity for HSV-1 antigens in the
cerebral cortex, the [immune cell] infiltrates were only located in
subcortical areas, especially the hippocampus.
Therefore, the distribution of these immune cells did not always
overlap with the regions of viral infection.
These results suggest that HSV-1 disseminate more efficiently from
the peripheral to the central nervous system (CNS) than from the CNS to
CNS, which is independent of the immune responses, and that the cerebral
cortex may immunologically respond to HSV-1 infection differently from
other brain regions.
From the article:
[a] "...the inflammatory response [to HSV] may not depend on viral
replication, since infection with a replication-defective mutant virus
could also induce a similar immune response..."
[b] "...in the corneally infected rats...numerous neurons with positive
staining for HSV-1 [monoclonal] antibodies [a lab tool] were located in
the in the sensory cortex... Columns of infected cells through all
cortical layers were occasionally seen... the number of infected neurons
in the brain stem was substantially higher in cornea-scarified than in
cortically injected animals."
[c] Citing Kennedy PGE et al 1983, the authors write: "...cortical
neurons were the least permissive cell types... the difference in the
efficiency of viral dissemination in the brain lies in the distribution
of the receptors on the cytoplasmic membrane of different cells and
terminals. In the cornea scarification model, the virus infected the CNS
retrogradely through the synapses of sensory projecting afferents, while
the intracerebrally injected virus may infect mainly cortical cell bodies
and the synapses of local circuits [other cites]. In has been shown that
attachment of HSV-1 to neuronal cell bodies is much less efficient than
to their terminals [cite]. In addition, specific tropism by HSV for
monoaminergic circuits has also been reported..."
[d] It is clear that [immune cell] infiltrates and MHC class II
expression were restricted to subcortical regions, the hippocampus, and,
to a much lesser extent, the pyriform area. Some of the inflammatory
cells may respond directly to [focal] viral encephalitis, as these
[inflammatory] cells were found immediately surrounding the necrotic
areas shown in the hippocampus..."
[e] "...neurons in the CNS have been reported not to express MHC
molecules [cite] or the espression was only induced by interferon gamma,
which is also neuronal-activity dependent [cites]"
{ for a discussion of MMR vaccination-induced interferon gamma
and its effect on infected cells within the CNS, see:
http://www.jorsm.com/~binstock/mmr-v-g.htm }
[f] "...infiltration of T lymphocytes or other immune cells may
contribute to CNS damage as much as the virus does [cite]. The mismatch
in locations of viral infection and MHC-expressing immune cells in the
present study suggests that an inflammatory response to HSV-1 infection
in the brain may have a range of consequences much broader than
eliminating viral infection..."
<<< On Saturday, July 17, 1999, Trina Montgomery had written:
I am back from California where we took our son to see Dr. Susan Fosnot, Dr.
Goldberg, and had the neuro spec scan. The scan showed that our son has
decreased perfusion to the hippocampus and central white matter of his
brain. Ironically, his temporal lobes did not show decreased perfusion. I
did not have access to the internet while there and just walked in from the
airport. So, who out there can shed some light on this? Goldberg is
adjusting some of our meds and we are going to start some new ideas from
Fosnot. But, are there some over the counter things I can do to increase
the bloodflow to these areas of his brain (MSM, DMG, CoQ10, etc. )? We
already do transdermal secretin and SSRI's.
Trina