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      Desorden Neuropsiquiátrico Pediátrico Asociado con Infecciones Estreptocócicas Translated title: Pediatric Neuropsiquiatric Dissorder Associated with Streptococca Infections

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          Abstract

          El síndrome PANDAS pone en manifiesto la explicación para una serie de trastornos neuropsiquiátricos, basándose en un modelo de afección autoinmune explicando como un agente causal de un cuadro infeccioso como es el estreptococo beta hemolítico del grupo A, aunque se consideran a otros agentes posibles causantes, sea el desencadenante de una reacción con serias consecuencias en el desenvolver de la persona.Viendo un nuevo enfoque de ciertas afecciones neuropsiquiátricas como el trastorno de déficit de atención por hiperactividad o el trastorno autista. Siendo un modelo de posibilidades innumerables para futuros estudios.

          Translated abstract

          PANDAS syndrome puts on a attend explanation for a sort of neuropsiquiatric affections, based on an autoimmune model affection explaining how a casual agent like Streptococci B-Hemolitic of the A group, or others infection possibilities, being the triggering factor of some serious consequences in persons development. Showing a new perspective of some neuropsiquiatric illness such as the attention déficit by hyperactivity or the autism disorder. Being a model of countless searches possibilities in the future.

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          Most cited references29

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          Cerebral glucose metabolism in adults with hyperactivity of childhood onset.

          W E Semple, S Hamburger, Andrew Gross … (1990)
          The cause of childhood hyperactivity (attention deficit-hyperactivity disorder) is unknown. We investigated the hypothesis that cerebral glucose metabolism might differ between normal adults (controls) and adults with histories of hyperactivity in childhood who continued to have symptoms. Each patient was also the biologic parent of a hyperactive child. None of the adults had ever been treated with stimulant medication. To measure cerebral glucose metabolism, we administered 148 to 185 MBq (4 to 5 mCi) of [18F]fluoro-2-deoxy-D-glucose intravenously to 50 normal adults and 25 hyperactive adults while they performed an auditory-attention task. Images were obtained for 30 minutes with a Scanditronix positron-emission tomograph with a resolution of 5 to 6 mm. Whole-brain and regional rates of glucose metabolism were measured with computer assistance by two trained research assistants, working independently, who were blinded to the subjects' status (control or hyperactive). Global cerebral glucose metabolism was 8.1 percent lower in the adults with hyperactivity than in the normal controls (mean +/- SD, 9.05 +/- 1.20 mg per minute per 100 g vs. 9.85 +/- 1.68 mg per minute per 100 g; P = 0.034). In the adults with hyperactivity, glucose metabolism was significantly reduced, as compared with the values for the controls, in 30 of 60 specific regions of the brain (P less than 0.05). Among the regions of the brain with the greatest reductions in glucose metabolism were the premotor cortex and the superior prefrontal cortex. When the seven women with hyperactivity or the six patients with learning disabilities were omitted from the analysis, the results were similar. Glucose metabolism, both global and regional, was reduced in adults who had been hyperactive since childhood. The largest reductions were in the premotor cortex and the superior prefrontal cortex--areas earlier shown to be involved in the control of attention and motor activity.
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            A genomewide scan for loci involved in attention-deficit/hyperactivity disorder.

            James T. McCracken, M Del'Homme, Anthony Monaco … (2002)
            Attention deficit/hyperactivity disorder (ADHD) is a common heritable disorder with a childhood onset. Molecular genetic studies of ADHD have previously focused on examining the roles of specific candidate genes, primarily those involved in dopaminergic pathways. We have performed the first systematic genomewide linkage scan for loci influencing ADHD in 126 affected sib pairs, using a approximately 10-cM grid of microsatellite markers. Allele-sharing linkage methods enabled us to exclude any loci with a lambda(s) of > or =3 from 96% of the genome and those with a lambda(s) of > or =2.5 from 91%, indicating that there is unlikely to be a major gene involved in ADHD susceptibility in our sample. Under a strict diagnostic scheme we could exclude all screened regions of the X chromosome for a locus-specific lambda(s) of >/=2 in brother-brother pairs, demonstrating that the excess of affected males with ADHD is probably not attributable to a major X-linked effect. Qualitative trait maximum LOD score analyses pointed to a number of chromosomal sites that may contain genetic risk factors of moderate effect. None exceeded genomewide significance thresholds, but LOD scores were >1.5 for regions on 5p12, 10q26, 12q23, and 16p13. Quantitative-trait analysis of ADHD symptom counts implicated a region on 12p13 (maximum LOD 2.6) that also yielded a LOD >1 when qualitative methods were used. A survey of regions containing 36 genes that have been proposed as candidates for ADHD indicated that 29 of these genes, including DRD4 and DAT1, could be excluded for a lambda(s) of 2. Only three of the candidates-DRD5, 5HTT, and CALCYON-coincided with sites of positive linkage identified by our screen. Two of the regions highlighted in the present study, 2q24 and 16p13, coincided with the top linkage peaks reported by a recent genome-scan study of autistic sib pairs.
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              The pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS) subgroup: separating fact from fiction.

              Phoebe H. Leonard, J L Rapoport, Susan E Swedo (2004)
              Article 0 comments Cited 28 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Octavio Chavez Herbas: Role: ND
                Karol Paola Crespo Vargas: Role: ND
                Rafael de Acha Torrez: Role: ND
                Aríane Nataly Flores Mercado: Role: ND
                Journal
                Journal ID (publisher-id): rccm
                Title: Revista Científica Ciencia Médica
                Abbreviated Title: Rev Cient Cienc Méd
                Publisher: Facultad de Medicina, Universidad Mayor de San Simón. (Cochabamba, Cochabamba, Bolivia )
                ISSN (Print): 2077-3323
                Publication date (Print and electronic): December 2010
                Volume: 13
                Issue: 2
                Pages: 86-89
                Affiliations
                [01] Cochabamba orgnameUniversidad Mayor de San Simón Bolivia
                Article
                Publisher ID: S1817-74332010000200008
                SO-VID: 39f96beb-651b-42b2-b565-dab0c5b5890d
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                Date accepted : 26 November 2010
                Date received : 01 September 2010
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 18, Pages: 4
                Product

                SciELO Bolivia


                Keywords: Desórdenes neuropsiquiátricos,Pediátrico,Streptococcus,Autoinmune,Neuropsychiatric disorders,Pediatric,Streptoccocus,Autoimmune
                Data availability:
                Keywords: Desórdenes neuropsiquiátricos, Pediátrico, Streptococcus, Autoinmune, Neuropsychiatric disorders, Pediatric, Streptoccocus, Autoimmune

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