Question:
I'm afraid I have no wisdom to offer on the rehabilitation of the stroke patient except to say that Frank's comments sound very reasonable. However, I have come across the concept of secondary brain damage mediated by arachidonic acid (AA) following head injury. AA is released by damaged brain tissue and its peroxidation by specific forms of lipoxygenase and cyclo-oxygenase leads to the formation of leukotrienes, prostaglandins and oxygen-derived free radicals. These active species have been shown to be capable of neurotoxicity and of damage to the blood-brain barrier. (Unterberg A, Maier-Hauff K, Dautermann C, Hack U, Schьrer L & Baethmann 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 this phenomenon, I wonder? I should be very interested to learn of evidence and/or opinions about this.

Answer: 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 neuroimmune mechanisms.

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