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[[image:Robert_Bransfield.JPG|Robert Bransfield le 3 mai 2014 à un séminaire de patients à Ridgefield (Connecticut)<br>Capture d'écran sur une vidéo youtube <ref>https://www.youtube.com/watch?v=7BbEBb-SzIE Vidéo mise en ligne le 16 juillet 2014 par Lyme Connection / Ridgefield Lyme Disease Taske (Groupe de travail Maladie de Lyme de Ridgefield)</ref>|450px|thumb]]

[[image:Robert_Bransfield.JPG|Robert Bransfield le 3 mai 2014 à un séminaire de patients à Ridgefield (Connecticut)<br>Capture d'écran sur une vidéo youtube <ref>https://www.youtube.com/watch?v=7BbEBb-SzIE Vidéo mise en ligne le 16 juillet 2014 par Lyme Connection / Ridgefield Lyme Disease Taske (Groupe de travail Maladie de Lyme de Ridgefield)</ref>|450px|thumb]]

'''Robert Bransfield''' ou '''Robert C Bransfield''' est un médecin psychiatre exerçant au Riverview Medical Center à Red Bank dans le New Jersey, ancien président de l'[[ILADS]] (de 2009 à 2011) et ancien président de L'ILADEF (International Lyme and Associated Diseases Educational Foundation). Il est également l'un des membres du Scientific & Professional Advisory Board (Conseil consultatif scientifique et professionnel) de la Lyme Disease Association<ref>https://lymediseaseassociation.org/about-us/lda-boards/professional-a-scientific-advisory-board/</ref>, une association qui, bien qu'ayant son siège dans le New Jersey, a des activités qui dépassent cet État des USA.

'''Robert Bransfield''' ou '''Robert C Bransfield''' est un médecin psychiatre exerçant au Riverview Medical Center à Red Bank dans le New Jersey, ancien président de l'[[ILADS]] (de 2009 à 2011) et ancien président de L'ILADEF (International Lyme and Associated Diseases Educational Foundation). Il est également l'un des membres du Scientific & Professional Advisory Board (Conseil consultatif scientifique et professionnel) de la Lyme Disease Association<ref>https://lymediseaseassociation.org/about-us/lda-boards/professional-a-scientific-advisory-board/</ref>, une association qui, bien qu'ayant son siège dans le New Jersey, a des activités qui dépassent cet État des USA.<ref>https://lymediseaseassociation.org/about-us/about-the-lyme-disease-association/mission-statement-a-history/</ref>

Robert C. Bransfield (avec ses co-auteurs Jeffrey S. Wulfman, William T. Harvey et [[Anju Usman|Anju I. Usman]]) a publié en 2008 un article "The association between tick-borne infections, Lyme borreliosis and autism spectrum disorders" (L'association entre les infections transmises par les tiques, la [[maladie de Lyme|borréliose de Lyme]] et les Troubles du Spectre autistique) dans le Journal [[Medical Hypotheses]].<ref>https://www.ncbi.nlm.nih.gov/pubmed/17980971 Article "The association between tick-borne infections, Lyme borreliosis and autism spectrum disorders", auteurs: Bransfield RC, Wulfman JS, Harvey WT, Usman AI, publié en 2008 dans le journal [[Medical Hypotheses]].<br>Abstract<br>Chronic infectious diseases, including tick-borne infections such as Borrelia burgdorferi may have direct effects, promote other infections and create a weakened, sensitized and immunologically vulnerable state during fetal development and infancy leading to increased vulnerability for developing autism spectrum disorders. A dysfunctional synergism with other predisposing and contributing factors may contribute to autism spectrum disorders by provoking innate and adaptive immune reactions to cause and perpetuate effects in susceptible individuals that result in inflammation, molecular mimicry, kynurenine pathway changes, increased quinolinic acid and decreased serotonin, oxidative stress, mitochondrial dysfunction and excitotoxicity that impair the development of the amygdala and other neural structures and neural networks resulting in a partial Klüver-Bucy Syndrome and other deficits resulting in autism spectrum disorders and/or exacerbating autism spectrum disorders from other causes throughout life. Support for this hypothesis includes multiple cases of mothers with [[maladie de Lyme|Lyme disease]] and children with autism spectrum disorders; fetal neurological abnormalities associated with tick-borne diseases; similarities between tick-borne diseases and autism spectrum disorder regarding symptoms, pathophysiology, immune reactivity, temporal lobe pathology, and brain imaging data; positive reactivity in several studies with autistic spectrum disorder patients for Borrelia burgdorferi (22%, 26% and 20-30%) and 58% for mycoplasma; similar geographic distribution and improvement in autistic symptoms from antibiotic treatment. It is imperative to research these and all possible causes of autism spectrum disorders in order to prevent every preventable case and treat every treatable case until this disease has been eliminated from humanity.</ref><ref>http://www.medical-hypotheses.com/article/S0306-9877(07)00578-6/fulltext</ref>

Robert C. Bransfield (avec ses co-auteurs Jeffrey S. Wulfman, William T. Harvey et [[Anju Usman|Anju I. Usman]]) a publié en 2008 un article "The association between tick-borne infections, Lyme borreliosis and autism spectrum disorders" (L'association entre les infections transmises par les tiques, la [[maladie de Lyme|borréliose de Lyme]] et les Troubles du Spectre autistique) dans le Journal [[Medical Hypotheses]].<ref>https://www.ncbi.nlm.nih.gov/pubmed/17980971 Article "The association between tick-borne infections, Lyme borreliosis and autism spectrum disorders", auteurs: Bransfield RC, Wulfman JS, Harvey WT, Usman AI, publié en 2008 dans le journal [[Medical Hypotheses]].<br>Abstract<br>Chronic infectious diseases, including tick-borne infections such as Borrelia burgdorferi may have direct effects, promote other infections and create a weakened, sensitized and immunologically vulnerable state during fetal development and infancy leading to increased vulnerability for developing autism spectrum disorders. A dysfunctional synergism with other predisposing and contributing factors may contribute to autism spectrum disorders by provoking innate and adaptive immune reactions to cause and perpetuate effects in susceptible individuals that result in inflammation, molecular mimicry, kynurenine pathway changes, increased quinolinic acid and decreased serotonin, oxidative stress, mitochondrial dysfunction and excitotoxicity that impair the development of the amygdala and other neural structures and neural networks resulting in a partial Klüver-Bucy Syndrome and other deficits resulting in autism spectrum disorders and/or exacerbating autism spectrum disorders from other causes throughout life. Support for this hypothesis includes multiple cases of mothers with [[maladie de Lyme|Lyme disease]] and children with autism spectrum disorders; fetal neurological abnormalities associated with tick-borne diseases; similarities between tick-borne diseases and autism spectrum disorder regarding symptoms, pathophysiology, immune reactivity, temporal lobe pathology, and brain imaging data; positive reactivity in several studies with autistic spectrum disorder patients for Borrelia burgdorferi (22%, 26% and 20-30%) and 58% for mycoplasma; similar geographic distribution and improvement in autistic symptoms from antibiotic treatment. It is imperative to research these and all possible causes of autism spectrum disorders in order to prevent every preventable case and treat every treatable case until this disease has been eliminated from humanity.</ref><ref>http://www.medical-hypotheses.com/article/S0306-9877(07)00578-6/fulltext</ref>