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» LymeNet Flash » Questions and Discussion » Medical Questions » Advances in Understanding Illness Anxiety article, neuroimmunology

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Author Topic: Advances in Understanding Illness Anxiety article, neuroimmunology
danielb
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Member # 8522

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( http://www.ncbi.nlm.nih.gov/pubmed/18627669 )

Curr Psychiatry Rep. 2008 Aug;10(4):311-7.Links
Advances in understanding illness anxiety.
Harding KJ, Skritskaya N, Doherty E, Fallon BA.

Department of Psychiatry, Columbia University Medical Center, 1051 Riverside Drive, Unit 69, New York, NY 10032, USA. [email protected]

Illness anxiety, also known in its more severe form as hypochondriasis, is a debilitating and chronic condition in which normal bodily symptoms are misinterpreted as signs of serious medical illness. Patients suffer with the fear that they are ill despite reassurance to the contrary and often overuse medical services in the process. This article critically evaluates the recent literature on illness anxiety and related, medically unexplained symptoms, highlighting new and interesting findings in the areas of prevalence, classification/diagnosis, management, and evidence-based treatment and new frontiers in understanding illness anxiety, such as brain imaging, neuroimmunology, and cyberchondria.

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taking from neuroimmunology:

( http://www.ncbi.nlm.nih.gov/pubmed/15652419 )

J Neuroimmunol. 2005 Feb;159(1-2):192-5. Epub 2004 Nov 26.Click here to read Links
Antibodies against OspA epitopes of Borrelia burgdorferi cross-react with neural tissue.
Alaedini A, Latov N.

Department of Neurology and Neuroscience, Cornell University, 1300 York Ave., New York, NY 10021, USA. [email protected]

Neurological sequela of chronic Lyme disease include encephalopathy, myelopathy and peripheral neuropathy. These have generally been attributed to either persistent infection or pathogen-induced autoimmunity. In this study, we investigated the presence of cross-reactive human neural epitopes that share amino acid sequences with Borrelia burgdorferi OspA protein. Sequence similarity analysis was carried out by searching known cDNA sequences from brain tissue. The cDNA database search yielded three sequences that were identical to sequences in OspA. Corresponding peptides were synthesized and antibodies were generated against them in rabbits. Antibodies against two of the homologous OspA peptides were found to react with neurons in human brain, spinal cord and dorsal root ganglia by immunohistochemistry.

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taking from random wikipedia discussion:

( http://en.wikipedia.org/wiki/Talk:Lyme_disease/Archive_2 )

I don't have a dog in this fight, but from a medical point of view...The OspA protein is produced while the B. burgdorferi is residing in the tick, but rapidly diminshes (even extinguishes) once the tick is exposed to warm mammalian blood. This produces a couple of problems, the first being that the vaccine is only useful for a short time (perhaps less than a few weeks) after administration. Secondly, because OspA is rapidly downregulated once inside a human host, it would not be useful for determining if there is a current infection in an animal host. (ref: Sherris 4ed. pp434-435). The only caveat to this, is that Anti-OspA antibodies do have some cross reactivity to human HLAs. Current guidelines say that the presence of EM is diagnostic, but can be followed up with IgM blot(2of3 presumptive) followed by a IgG blot(5of10 diagnostic), but the proteins that show up on these tests are also proteins found in other bacteria. I hope that helps a little. BruceD270 00:48, 9 October 2007 (UTC)

An important point that should be stressed about the vaccine is that the OspA antibody kills B. burgdorferi within the tick midgut as it feeds on the vaccinated individual's blood, before transmission of the bacteria from the tick to the human occurs (see Sherris p. 437, 4th ed). NighthawkJ 07:55, 9 October 2007 (UTC)

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taking from the fact that Lymerix vaccine many people got sick for longer than the "few weeks" Lymerix is apparently effective for, is there a separate illness from active infection, where someone has an immune system that can perpetuate OspA antibody production indefinitely?

is the presence of "OspA" antibodies a pathology in and of itself? additionally, i think it has been discussed before: can the antibodies can be generated not only from lyme infection, but other infections or sources, or inappropriate autoimmune response to human cells?

can "OspA" antibodies, from whichever possible source, interact with or attack nerve cells or tissues to cause CFS and neuropsychiatric symptoms that most people sympathize with as much as they sympathize with panhandlers, and other people they don't care about?

is it known if any of the antibodies attributed to lyme interact with neurotransmitter receptors? (like, for example, the antibodies in this article below.)

( http://www.ncbi.nlm.nih.gov/pubmed/12851722 )

Autoantibodies against muscarinic cholinergic receptor in chronic fatigue syndrome.

(cannot insert whole article due to error messages over less-than symbols)

[ 02. August 2008, 04:28 PM: Message edited by: danielb ]

Posts: 244 | From Ottawa | Registered: Dec 2005  |  IP: Logged | Report this post to a Moderator
Melanie Reber
Frequent Contributor (5K+ posts)
Member # 3707

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'Cyberchondria'?

For some reason, it is really disturbing to me to see Fallon associated with any article that speaks to this terminology.

Wish I could read it in its entirety.

Posts: 7052 | From Colorado | Registered: Mar 2003  |  IP: Logged | Report this post to a Moderator
   

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