Murphy TK, Storch EA, Lewin AB, Edge PJ, Goodman WK
J Pediatr160p314-9(2012 Feb)
J Pediatr. 2012 Feb;160(2):314-9. Epub 2011 Aug 25. Clinical factors associated with pediatric autoimmuneA condition or disease thought to arise from an overactive immune response of the body against substances and tissues normally present in the body neuropsychiatric disorders associated with streptococcal infections. Murphy TK, Storch EA, Lewin AB, Edge PJ, Goodman WK. Source Department of Pediatrics, University of South Florida, St. Petersburg, FL 33701, USA. firstname.lastname@example.org Abstract OBJECTIVE: To explore associated clinical factors in children with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS). STUDY DESIGN: Children with tics, obsessive-compulsive disorder, or both (n=109) were examined with personal and family history, diagnostic interview, physical examination, medical record review, and measurement of baseline levels of streptococcal antibodies. RESULTS: Significant group differences were found on several variables, such that children in whom PANDAS (versus without PANDAS) were more likely to have had dramatic onset, definite remissions, remission of neuropsychiatric symptoms during antibiotic therapy, a history of tonsillectomies/adenoidectomies, evidence of group A streptococcal infection, and clumsiness. CONCLUSION: The identification of clinical features associated with PANDAS should assist in delineating risks for this subtype of obsessive-compulsive disorder/tics. Copyright © 2012 Mosby, Inc. All rights reserved. 1)
J Child Adolesc Psychopharmacol. 2011 Apr;21(2):177-82. Epub 2011 Apr 12. Pediatric autoimmune neuropsychiatric disorders associated with Streptococcus in identical siblings. Lewin AB, Storch EA, Murphy TK. Source Rothman Center for Neuropsychiatry, Department of Pediatrics, University of South Florida College of Medicine, St. Petersburg, Florida 33701, USA. email@example.com Abstract Termed pediatric autoimmune neuropsychiatric disorders associated with Streptococcus (PANDAS), these cases of childhood-onset obsessive compulsive disorder and tic disorders resemble the presentation of Sydenham chorea, in that they have an acute onset following a group A beta-hemolytic streptococcal infection (group A Streptococcus), with accompanying neurological signs, and an episodic or sawtooth course. Familial associations of this subgroup of patients remain understudied. This report provides phenotypic descriptions of three youth with PANDAS as well as their genetically identical siblings (in two cases of twins and one case of triplets). These cases highlight the potential for environmental influences for discordant presentations in genetically identical siblings. Despite identical genetics, presentations showed marked variation across siblings (from a full PANDAS presentation to asymptomatic). Further research into environmentally driven influences such as postinfectious molecular mimicry and epigenetic factors that may influence the manifestation of these pediatric neuropsychiatric disorders will promote our understanding of their prevention and treatment. 2)
All In The Mind
Interview with Julia Grier - sarcoidosis, OCD
Phobias and OCD help available in the UK
I think you've spoken to my twin sister Jean (also on the MP). I have been on the MP now for about 4 months. I developed Obsessive Compulsive Disorder last July after my doctor gave me three antibiotics for CFS. I could never have imagined the effect on my brain and the obsessive thoughts and handwashing rituals that resulted. I would never have understood the link between bacteria and the brain if it weren't for the MP and information from my doctor. It makes a lot of sense though.
I am still struggling with OCD but have much more perspective on it now so that I acknowledge its the bugs and that it will resolve if I carry on with the MP. I realise that this is a biological problem but decided to get some support from the National Phobic Society. They provided a counsellor who speaks to me over the phone on a weekly basis and is extremely helpful. He understands my position on the MP and provides a huge amount of encouragement as well as relaxation techniques and coping strategies to challenge the OCD.
I have just started the Modified Phase two and my OCD has become more exaggerated. However, I'm trying to stay focused and remain totally optimistic that the MP is the solution to this difficult situation I find myself in.
If you do take a break and I can understand why - please get back on the MP soon. Get in touch with the National Phobic Society and ask if you can get help from a counsellor. It's only £5 per session if you're on benefits and as well as providing help for OCD you'll get moral support in your fight for health. Their number is 0870 122 2325.
Stay strong and good luck. I can totally empathise with you and if you stay focused I know you'll get through.
MPers report OCD symptom resolution
My 15 yr.old daughter who also like myself, has neuro-lyme disease, was significantly affected with OCD, incapacitated as a matter of fact. Treatment with minocycline has been a godsend for her, she is doing 80% better, and we expect the improvement to continue as she introduces more/differing abx to kill the occult bacteria. It was suspected that she contracted PANDAS (pediatric autoimmune neuropsychiatric disorder associated with streptococcal infection) the year after becoming ill with Borreliosis, and this is what led to the increasing significant neuro-psychological difficulties she began having, in addition to her Borrelia symptoms.
The Benicar has been found to help with neuroses, as stated in papers by Dr. Marshall.
http://www.sciencedaily.com/releases/2009/08/090811143538.htm Yaddanapudi, K., M. Hornig, et al. (2009). “Passive transfer of streptococcus-induced antibodies reproduces behavioral disturbances in a mouse model of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection.” Mol Psychiatry. 3)
Streptococcal infections can induce obsessive-compulsive and tic disorders. In children, this syndrome, frequently associated with disturbances in attention, learning and mood, has been designated pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS). Autoantibodies recognizing central nervous system (CNS) epitopes are found in sera of most PANDAS subjects, but may not be unique to this neuropsychiatric subset. In support of a humoral immune mechanism, clinical improvement often follows plasmapheresis or intravenous immunoglobulin. We recently described a PANDAS mouse model wherein repetitive behaviors correlate with peripheral anti-CNS antibodies and immune deposits in brain following streptococcal immunization. These antibodies are directed against group A beta-hemolytic streptococcus matrix (M) protein and cross-react with molecular targets complement C4 protein and alpha-2-macroglobulin in brain. Here we show additional deficits in motor coordination, learning/memory and social interaction in PANDAS mice, replicating more complex aspects of human disease. Furthermore, we demonstrate for the first time that humoral immunity is necessary and sufficient to induce the syndrome through experiments wherein naive mice are transfused with immunoglobulin G (IgG) from PANDAS mice. Depletion of IgG from donor sera abrogates behavior changes. These functional disturbances link to the autoimmunity-related IgG1 subclass but are not attributable to differences in cytokineAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. profiles. The mode of disrupting blood-brain barrier integrity differentially affects the ultimate CNS distribution of these antibodies and is shown to be an additional important determinant of neuropsychiatric outcomes. This work provides insights into PANDAS pathogenesis and may lead to new strategies for identification and treatment of children at risk for autoimmune brain disorders.Molecular Psychiatry advance online publication, 11 August 2009; doi:10.1038/mp.2009.77.
See also Orbitofrontal-Cortex-Lesioned Rats: Possible Involvement of the Serotonergic System. 4) contains link to free article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055356/
— Sallie Q 02.26.2017 added Ref rat OCD responding to human psych drugs, rearranged content
High STREP antibodies is common in patients with OCD, interpreted as Strep inducing Antibodies cross reacting to Basal ganglia, governing learned behavours , like TIcs, , words etc seen in Tourette. www.ageofautism.com/2011/11/autism-and-pandas-.html#more www.scientificamerican.com/article.cfm?id=could-infection-cause-tourettes-like-symptoms-teenage-girls
Neuropsychopharmacology. 2012 Aug;37(9):2076-87. doi: 10.1038/npp.2012.56. Epub 2012 Apr 25. Behavioral, pharmacological, and immunological abnormalities after streptococcal exposure: a novel rat model of sydenham chorea and related neuropsychiatric disorders. Brimberg L, Benhar I, Mascaro-Blanco A, Alvarez K, Lotan D, Winter C, Klein J, Moses AE, Somnier FE, Leckman JF, Swedo SE, Cunningham MW, Joel D. Source School of Psychological Sciences, Tel Aviv University, Tel Aviv, Israel. Abstract Group A streptococcal (GAS) infections and autoimmunity are associated with the onset of a spectrum of neuropsychiatric disorders in children, with the prototypical disorder being Sydenham chorea (SC). Our aim was to develop an animal model that resembled the behavioral, pharmacological, and immunological abnormalities of SC and other streptococcal-related neuropsychiatric disorders. Male Lewis rats exposed to GAS antigen exhibited motor symptoms (impaired food manipulation and beam walking) and compulsive behavior (increased induced-grooming). These symptoms were alleviated by the D2 blocker haloperidol and the selective serotonin reuptake inhibitor paroxetine, respectively, drugs that are used to treat motor symptoms and compulsions in streptococcal-related neuropsychiatric disorders. Streptococcal exposure resulted in antibody deposition in the striatum, thalamus, and frontal cortex, and concomitant alterations in dopamine and glutamate levels in cortex and basal ganglia, consistent with the known pathophysiology of SC and related neuropsychiatric disorders. Autoantibodies (IgG) of GAS rats reacted with tubulin and caused elevated calcium/calmodulin-dependent protein kinase II signaling in SK-N-SH neuronal cells, as previously found with sera from SC and related neuropsychiatric disorders. Our new animal model translates directly to human disease and led us to discover autoantibodies targeted against dopamine D1 and D2 receptors in the rat model as well as in SC and other streptococcal-related neuropsychiatric disorders. 5)