A propos Dr. Wheatley's speculation: the flood of excitatory amino
acids and subsequent/concurrent (yes) "cytokine cascade" is quite
similar for any kind of brain insult, so traumatic injury and stroke
have much in common right at the outset, i.e. in the acute reaction.
For several years, I have been exploring possibilities for chronic
alterations in some of the neuroimmune components--e.g. IL-1, NO, NOS,
and (rarely considered) mast cells. I have addressed these
possibilities in the context mainly of mild traumatic brain injury, in
papers presented at meetings of the International Neuropsychological
Society, Society for Neuroscience, and at a conference I organized for
NYNG, at NYU Med Ctr last year.
There has been much research on the acute events Dr. Wheatley
describes, but pathetically little on chronic activity or reactivity of
Almost a "P.S.": (reread his post and took special note of his
reference to "secondary brain damage") Yes, not instantaneous damage,
such as an inert mechanism would suffer (e.g. hitting computer with a
hammer), but a process which can cause further damage--BUT we are
talking here of seconds, minutes, and (a very few) hours. This is the
window of opportunity for interventions aimed at moderating this
cascade, and this is the time-frame of the most intense investigation.
MOST such studies suggest return to baseline values, with or without
treatment, within a matter of hours or perhaps 2-3 days. At the SFN
1996 meeting, one woman presented a paper showing elevated IL-1
concentrations in the brain 30 days after traumatic injury, but it is
RARE for anyone to keep animals alive this long after injury and even
rarer for anyone to look at this level of analysis (there are a few
"chronic" behavioral studies).
I think the answer to subtle chronic sequelae are in this domain, but
nobody is looking; I'm not looking (directly) because I do not have a
F. Frank LeFever, Ph.D.
New York Neuropsychology Group
In <rawheatley-2303991907490001 at canadalane.demon.co.uk>
rawheatley at canadalane.demon.co.uk (Dr. Alan Wheatley) writes:
>>>flefever at ix.netcom.com(F. Frank LeFever) wrote (7227) on 20 Mar 1999:
>>>One month is VERY early in the recovery process.
>>>>To some extent, it appears "nonspecific" complaints of fatigue and
>>impaired concentration, very much like in some cases of mild
>>brian injury (post-concussion syndrome) may be common after stroke,
>>although traditionally not given so much attention as specific
>>(aphasia, apraxia, unilateral neglect, etc.), and may persist beyond
>>acute recovery. <--snip-->
>>I'm afraid I have no wisdom to offer on the rehabilitation of the
>patient except to say that Frank's comments sound very reasonable.
>However, I have come across the concept of secondary brain damage
>by arachidonic acid (AA) following head injury. AA is released by
>brain tissue and its peroxidation by specific forms of lipoxygenase
>cyclo-oxygenase leads to the formation of leukotrienes, prostaglandins
>oxygen-derived free radicals. These active species have been shown to
>capable of neurotoxicity and of damage to the blood-brain barrier.
>(Unterberg A, Maier-Hauff K, Dautermann C, Hack U, Schürer L &
>A, in Baethmann A, Go K G & Unterberg A, eds., Mechanisms of
>Secondary Brain Damage. Plenum, 1984, p139). Could the "nonspecific"
>complaints of fatigue and impaired concentration be associated with
>phenomenon, I wonder? I should be very interested to learn of
>and/or opinions about this.
>>Dr. Alan Wheatley at http://www.canadalane.demon.co.uk