Letter to Medscape on "Bipolar" in children
kathleen
This sounds identical to neurologic Lyme borreliosis in children (ADD
plus "bipolar"):
http://mp.medscape.com/cgi-bin1/DM/y/hofU0KhFuR0D2W0Ga6q0Ev
In case you are not aware of it, there is a new initiative by the
combined National Institutes to (finally) look at actual physiological
markers of CNS disease:
http://intramural.nimh.nih.gov/inip/call4proposals.htm
Notice that they classify Lyme as a central nervous system infection,
in the class with neuroAIDS.
It is actually malpractice to not rule out an organic brain syndrome,
and the NIH has announced that tranquilizers worsen dementia (Lyme).
Borrelia and brain- 167 citations:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=PureSearch&db=pubmed&details_term=%28%22borrelia%22%5BMeSH%20Terms%5D%20OR%20borrelia%5BText%20Word%5D%29%20AND%20%28%22brain%22%5BMeSH%20Terms%5D%20OR%20brain%5BText%20Word%5D%29
The American Psychiatric Association's Guidelines on the treatment of
delirium state that the medical cause of delirium must be treated
first. Their own guidelines declare any other practice than the
determination of the presence of valid brain disease to be medical
negligence.
Recommended sites:
http://www.columbia-lyme.org
http://www.mentalhealthandillness.com
http://www.ILADS.org
Allen Steere, who has said to the press that we have "some psychiatric
illness" rather than this permanent brain infection, previously made
this observation on Lyme brain:
J Infect Dis. 1994 May;169(5):1014-22. Related Articles, Links
Borrelia burgdorferi and Escherichia coli lipopolysaccharides induce
nitric oxide and interleukin-6 production in cultured rat brain cells.
Tatro JB, Romero LI, Beasley D, Steere AC, Reichlin S.
Division of Endocrinology, New England Medical Center Hospitals,
Boston, MA 02111.
Borrelia burgdorferi, the spirochetal agent of Lyme disease, infects
the central nervous system (CNS), but the factors that mediate
inflammation and neurologic dysfunction are not known. Sonicated B.
burgdorferi stimulated in a concentration-dependent manner the
production of nitric oxide (NO) in glial-enriched primary cultures of
neonatal rat brain cells via induction of NO synthase activity.
Lipopolysaccharide (LPS) of Escherichia coli also stimulated nitrite
accumulation in a concentration-dependent manner. Stimulation of NO
production by B. burgdorferi sonicate and E. coli LPS was associated
with increased levels of mRNA coding for the cytokine-inducible form of
NO synthase. B. burgdorferi sonicate also stimulated release of
interleukin-6, with a concentration-response relationship similar to
that for its stimulation of nitrite production, as did E. coli LPS. A
competitive antagonist of E. coli LPS, Rhodopseudomonas sphaeroides
lipid A, inhibited LPS-induced stimulation of NO synthase activity but
markedly potentiated that of B. burgdorferi, indicating that the
initial triggering mechanism of B. burgdorferi is distinct from that of
E. coli LPS. Induction of NO synthase by bacterial agents within the
brain may represent a common pathway of CNS inflammation and
neurotoxicity.
PMID: 7513330 [PubMed - indexed for MEDLINE]
Unfortunately we can't get the CDC to coordinate their announcements on
Lyme:
Here we have CDC's Paul Mead stating that the "bogus" Dressler/Steere
method for detection
of early Lyme is just for surveillance purposes (and is NOT on the
CDC's website), and
"there is no substitute for sound clinical judgment"
http://www.hhs.gov/asl/testify/t040129.html
While on the CDC's website, they clearly assert that the "bogus"
Dressler/Steere
criteria is a criteria for treatment:
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5405a6.htm
I don't recommend giving CME credits for people who complete this
"course" on bipolar in children. ClinicalTrials.gov recently ran a
clinical trial on "Rapid-Cycling Bipolar in Children" and one of the
rule-outs was Lyme disease.
There is a Chapter in the 2002 Sadock's Comprehensive Textbook on
Psychiatry by Dr. Brian Fallon at New York State Psychiatric Hospital
and Columbia (www.columbia-lyme.org) which I highly recommend reading.
Perhaps that Fallon chapter should be republished on the CDC's, NIHs,
NINDS', and espeically on the APA's website, since there is nothing on
the APA's website about Lyme disease, and Lyme is a permanent brain
infection- The New Great Imitator.
We have to start somewhere, demanding accountability. Since we already
know all psychotropics are brain damaging, I find it ridiculous to see
yet another article on the misdiagnosis and mistreatment of children.
"Abilify" is a dopamine *agonist*, giving new meaning to the term
"DOPE-amine." The Psych/Pharmaceuticals industry has already stated
that they do not know what the drug targets are- That is because
receptor or transporter blockade (anesthesia) is the wrong mechanism
entirely for neuroprotection and recovery.
The only thing we have that is clearly neuroprotective is lithium, but
let's face it- Lithium is unpatentable, and would cost about 5 dollars
a month. (This would not make BigPharma very happy.)
Unfortunately, we have no central medical intelligence agency. You
would think that would start with brain chemistry. APA would probably
lobby against it.
Most hilarious:
Am J Psychiatry. 2005 Mar;162(3):433-40. Related Articles, Links
Toward a philosophical structure for psychiatry.
Kendler KS.
Department of Psychiatry, Medical College of Virginia, Virginia
Commonwealth University, Richmond, VA, USA. ken...@hsc.vcu.edu
This article, which seeks to sketch a coherent conceptual and
philosophical framework for psychiatry, confronts two major questions:
how do mind and brain interrelate, and how can we integrate the
multiple explanatory perspectives of psychiatric illness? Eight
propositions are proposed and defended: 1) psychiatry is irrevocably
grounded in mental, first-person experiences; 2) Cartesian substance
dualism is false; 3) epiphenomenalism is false; 4) both brain-->mind
and mind-->brain causality are real; 5) psychiatric disorders are
etiologically complex, and *** no more "spirochete-like" discoveries
will be made*** that explain their origins in simple terms; 6)
explanatory pluralism is preferable to monistic explanatory approaches,
especially biological reductionism; 7) psychiatry must move beyond a
prescientific "battle of paradigms" to embrace complexity and support
empirically rigorous and pluralistic explanatory models; 8) psychiatry
should strive for "patchy reductionism" with the goal of "piecemeal
integration" in trying to explain complex etiological pathways to
illness bit by bit.
PMID: 15741457 [PubMed - indexed for MEDLINE]
Thanks,
Kathleen M. Dickson
Greatcod
people with FMS have a Nitrous Oxide problem. I don't pretend to
understand the biochemistry of the 94 Steere article, but it apppears
to be a fit.
kathleen
near-free radical, which lyses the cell
membrane of an infecting bacterium.
This results in other activated intermediates
and so forth.
You have heard of superoxide dismutase?
Quinolinic acid is produced by macrophages
and we are subject to the toxic effects of that.
Neurology. 1992 Jan;42(1):43-50. Related Articles, Links
Neuroactive kynurenines in Lyme borreliosis.
Halperin JJ, Heyes MP.
Department of Neurology, SUNY, Stony Brook.
Although neurologic dysfunction occurs frequently in patients with Lyme
borreliosis, it is rarely possible to demonstrate the causative
organism within the neuraxis. This discordance could arise if
neurologic symptoms were actually due to soluble neuromodulators
produced in response to infection. Since immune stimulation is
associated with the production of quinolinic acid (QUIN), an
excitotoxin and N-methyl-D-aspartate (NMDA) agonist, we measured levels
of CSF and serum QUIN, and lymphokines. Samples were obtained from 16
patients with CNS Borrelia burgdorferi infection, eight patients with
Lyme encephalopathy (confusion without intra-CNS inflammation), and 45
controls. CSF QUIN was substantially elevated in patients with CNS Lyme
and correlated strongly with CSF leukocytosis. In patients with
encephalopathy, serum QUIN was elevated with corresponding increments
in CSF QUIN. Lymphokine concentrations were not consistently elevated.
We conclude that CSF QUIN is significantly elevated in B burgdorferi
infection--dramatically in patients with CNS inflammation, less in
encephalopathy. The presence of this known agonist of NMDA synaptic
function--a receptor involved in learning, memory, and synaptic
plasticity--may contribute to the neurologic and cognitive deficits
seen in many Lyme disease patients.
PMID: 1531156 [PubMed - indexed for MEDLINE]
(We know these people actually
have Munchausen's, hypochondria,
and/or this could simply be a
psychogenic response.)
Kathleen