But I recall that there is a growing body of research linking "illness
behaviors" (i.e. fever, decreased socialization, etc.) with immune system
cytokines acting directly on the brain. I don't recall the exact authors
right now, try L. Watkins [?] or keywords: IL1, fever, vagus, if you have
access to medline.
One belief is that peripheral nerves, but especially the vagus nerve, have
receptors for cytokines, such as IL1, TNF-b, and IL6. So when you have an
infection, local cytokines activate the vagus nerve, which in turn
mediates illness responses in the central nervous system via the
hypothalamus.
Perhaps, with ADHD, this response is altered. Or maybe the illness
response in the hypothalamus counteracts the neurochemical pathways
involved in ADHD...
-----------------------------------------------------------------------------
-Neal Prakash
Department of Psychobiology, College of Medicine
http://meded.med.uci.edu:80/~nprakash/neal.html
lab:714-824-5031
fax:714-824-2447
re Neal Prakash's commentary: my reply to the original query (reply is
header #16908, at least via my server) discussed the IL-1 angle. In
addition to Linda Watkins re vagus, check out Robert Dantzer re
exploratory behavior, operant behavior, etc.
In my earlier comment, I speculated re IL-1 effect on Ne
(noradrenaline), the target most prominent in theories of ritalin
(etc.) action in ADD (although dopamine should not be ignored). I did,
indeed find a very good review of IL-1 effects on classsical
neurotransmitters, including increasing Ne activity--but left it at
work! will try to bring it home tomorrow. Believe it was in
Neuroimmunology, 1996 or possibly 1995.
Frank LeFever
New York Neuropsychology Group
In <Pine.GSO.3.95.970202...@taurus.oac.uci.edu> Neal
Dunn, AJ & Wang, J. Cytokine effects on CNS biogenic amines.
Neuroimmunomodulation, 1995, vol.2, 319-328.
Their discussion focused on the hypothalamic-pituitary-adrenocortical
axis and the possible relevance of IL-1-induced noradrenaline activity
to activation of the HPA axis, but they also cite a study reporting
increased prefrontal cortical dopamine activity, which would make sense
in terms of the "frontal/intentional" sort of interpretation of ADD I
have alluded to previously.
That study is:
Zalcman S, Green-Johnson JM, Murray L et al. (incl. H. Anisman)
Cytokine-specific central monoamine alterations induced by
interleukin-1, -2, and -6. Brain Research 1994, 643, 40-49.
Thus, there is a plausible rationale for such an effect.
NOW, the remaining question is: how much evidence is there that this
phenomenon (reduced ADD symptoms during fever) exists?
>------