Autismo: entre a alta sistematização e a baixa empatia. Um estudo sobre a hipótese de hiper masculinização do cérebro no espectro autista

Autores/as

  • Thiago Perez Bernardes de Moraes Universidad John Fitzgerald Kennedy

Palabras clave:

Autismo, Sistematização, Empatia, Psicologia evolucionista.

Resumen

Na década de 1940, Hans Asperger promulgou que o autismo era uma espécie de “exacerbada” masculinização do cérebro. Na década de 1980 embasado na psicobiologia, Baron-Cohen lança a ideia de que o autismo seria um estado de alto déficit de teoria da mente. A posteriori ele refinou os conceitos criando a ideia de hiper sistematização e mais recentemente tal arcabouço teórico deu revitalidade à teoria de Asperger, com a consolidação teórica do autismo como um estado de hiper masculinização do cérebro (extreme male brain). Nesse artigo, revisamos as evidências da neurobiologia, da genética e da psicologia evolucionista a respeito das evidências de uma possível hiper masculinização do cérebro. Para tanto em um primeiro momento apresentamos as principais singularidades neurofuncionais nos cérebros autistas e revisamos os principais genes candidatos ao autismo. Em outro momento, apresentamos a teoria de Baron-Cohen, junto com as definições sobre dimorfismo sexual e os conceitos de mentes empáticas (femininas), mentes sistemáticas (masculinas) e mentes hiper sistemáticas (“exacerbadamente” masculinas). Mesmo que algumas das evidências apontadas ainda estejam em estágio incipiente, a maior parte delas corrobora a aderência da tese de Baron-Cohen e os primeiros preceitos de Asperger.

Descargas

Los datos de descargas todavía no están disponibles.

Citas

Abdolmaleky, H. M., Cheng, K. H., Russo, A., Smith, C. L., Faraone, S. V., Wilcox, M., . & Tsuang, M. T. (2005). “Hypermethylation of the reelin (RELN) promoter in the brain of schizophrenic patients: a preliminary report”. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 134(1), 60-66.

Abrahams, B. S., & Geschwind, D. H. (2008). “Advances in autism genetics: on the threshold of a new neurobiology”. Nature Reviews Genetics, 9(5), 341-355.

Alvarez-Dolado, M., Pardal, R., Garcia-Verdugo, J. M., Fike, J. R., Lee, H. O., Pfeffer, K., .& Alvarez-Buylla, A. (2003). “Fusion of bone-marrow-derived cells with Purkinje neurons, cardiomyocytes and hepatocytes”. Nature, 425(6961), 968-973.

Amaral, D. G., & Corbett, B. A. (2003, June). “The amygdala, autism and anxiety” inn Novartis Found Symp (Vol. 251, pp. 177-187).

Armstrong, E. (1986). “Enlarged limbic structures in the human brain: the anterior thalamus and medial mamillary body”. Brain Research, 362(2), 394-397.

Bailey, A., Palferman, S., Heavey, L., & Le Couteur, A. (1998). “Autism: the phenotype in relatives”. Journal of autism and developmental disorders, 28(5), 369-392.

Baron-Cohen, S. (2002). “The extreme male brain theory of autism”. Trends in cognitive sciences, 6(6), 248-254.

Baron-Cohen, S. (2004). “The cognitive neuroscience of autism”. Journal of Neurology, Neurosurgery & Psychiatry, 75(7), 945-948.

Baron-Cohen, S. (2006). “The hyper-systemizing, assortative mating theory of autism”. Progress in Neuro-Psychopharmacology and Biological Psychiatry,30(5), 865-872.

Baron‐Cohen, S. (2009). “Autism: The Empathizing–Systemizing (E‐S) Theory”. Annals of the New York Academy of Sciences, 1156(1), 68-80.

Baron-Cohen, S., & Hammer, J. (1997). “Is autism an extreme form of the "male brain"?”. Advances in Infancy Research, 11, 193-218.

Baron-Cohen, S., & Wheelwright, S. (2004). “The empathy quotient: an investigation of adults with Asperger syndrome or high functioning autism, and normal sex differences”. Journal of autism and developmental disorders, 34 (2), 163-175.

Baron-Cohen, S., Ashwin, E., Ashwin, C., Tavassoli, T., & Chakrabarti, B. (2009). “Talent in autism: hyper-systemizing, hyper-attention to detail and sensory hypersensitivity”. Philosophical Transactions of the Royal Society B: Biological Sciences, 364 (1522), 1377-1383.

Baron-Cohen, S., Lutchmaya, S., & Knickmeyer, R. (2004). Prenatal testosterone in mind [electronic resource]: amniotic fluid studies. The MIT Press.

Baron-Cohen, S., Wheelwright, S., Skinner, R., Martin, J., & Clubley, E. (2001). “The autism-spectrum quotient (AQ): Evidence from asperger syndrome/high-functioning autism, malesand females, scientists and mathematicians”. Journal of autism and developmental disorders, 31(1), 5-17.

Bauman, M. L. (1991). “Microscopic neuroanatomic abnormalities in autism”. Pediatrics, 87(5), 791-796.

Beacher, F. D., Minati, L., Baron-Cohen, S., Lombardo, M. V., Lai, M. C., Gray, M. A., & Critchley, H. D. (2012). “Autism attenuates sex differences in brain structure: a combined voxel-based morphometry and diffusion tensor imaging study”. American Journal of Neuroradiology, 33(1), 83-89.

Benayed, R., Gharani, N., Rossman, I., Mancuso, V., Lazar, G., Kamdar, S., . & Millonig, J. H. (2005). “Support for the Homeobox Transcription Factor Gene as an Autism Spectrum Disorder Susceptibility Locus”. The American Journal of Human Genetics, 77(5), 851-868.

Blatt, G. J., Fitzgerald, C. M., Guptill, J. T., Booker, A. B., Kemper, T. L., & Bauman, M. L. (2001). “Density and distribution of hippocampal neurotransmitter receptors in autism: an autoradiographic study”. Journal of autism and developmental disorders, 31(6), 537-543.

Campbell, D. B., Sutcliffe, J. S., Ebert, P. J., Militerni, R., Bravaccio, C., Trillo, S., . & Levitt, P. (2006). “A genetic variant that disrupts MET transcription is associated with autism”. Proceedings of the National Academy of Sciences, 103(45), 16834-16839.

Castelli, F., Frith, C., Happé, F., & Frith, U. (2002). “Autism, Asperger syndrome and brain mechanisms for the attribution of mental states to animated shapes”. Brain, 125(8), 1839-1849.

Connellan, J., Baron-Cohen, S., Wheelwright, S., Batki, A., & Ahluwalia, J. (2000). “Sex differences in human neonatal social perception”. Infant Behavior and Development, 23(1), 113-118.

Conroy, J., Meally, E., Kearney, G., Fitzgerald, M., Gill, M., & Gallagher, L. (2004). “Serotonin transporter gene and autism: a haplotype analysis in an Irish autistic population”. Molecular psychiatry, 9(6), 587-593.

DeLorey, T. M., Sahbaie, P., Hashemi, E., Homanics, G. E., & Clark, J. D. (2008). “Gabrb3 gene deficient mice exhibit impaired social and exploratory behaviors, deficits in non-selective attention and hypoplasia of cerebellar vermal lobules: a potential model of autism spectrum disorder”. Behavioural brain research, 187(2), 207-220.

Duong, T., Robinson, H., BA, D. G., & Ritvo, A. (1986). “Lower Purkinje cell counts in the cerebella of four autistic subjects: initial findings of the UCLA-NSAC Autopsy Research Report”. Am J Psychiatry, 143(7), 862-866.

Durand, C. M., Betancur, C., Boeckers, T. M., Bockmann, J., Chaste, P., Fauchereau, F. & Bourgeron, T. (2006). “Mutations in the gene encoding the synaptic scaffolding protein SHANK3 are associated with autism spectrum disorders”. Nature genetics, 39(1), 25-27.

El-Fishawy, P. (2010). “The Genetics of Autism: Key Issues, Recent Findings and Clinical Implications”. The Psychiatric clinics of North America, 33(1), 83.

Fatemi, S. H., Halt, A. R., Realmuto, G., Earle, J., Kist, D. A., Thuras, P., & Merz, A. (2002). “Purkinje cell size is reduced in cerebellum of patients with autism”. Cellular and molecular neurobiology, 22(2), 171-175.

Fuster, J. (2008). The prefrontal cortex. Access Online via Elsevier.

Gadia, C. A., Tuchman, R., & Rotta, N. T. (2004). “Autism and pervasive developmental disorders”. Jornal de Pediatria, 80(2), 83-94.

García-Peñas, J. J. (2009). “Autismo, epilepsia y patología del lóbulo temporal”. Rev Neurol, 48(Supl 2), S35-45.

Goldman, J. G., Stebbins, G. T., Bernard, B., Stoub, T. R., Goetz, C. G., & Toledo‐Morrell, L. (2012). “Entorhinal cortex atrophy differentiates Parkinson's disease patients with and without dementia”. Movement Disorders, 27(6), 727-734.

Grace, A. A. (2010). “Dopamine system dysregulation by the ventral subiculum as the common pathophysiological basis for schizophrenia psychosis, psychostimulant abuse, and stress”. Neurotoxicity research, 18(3-4), 367-376.

Gregory, S., Connelly, J., Towers, A., Johnson, J., Biscocho, D., Markunas, C. & Pericak-Vance, M. (2009). “Genomic and epigenetic evidence for oxytocin receptor deficiency in autism”. BMC medicine, 7(1), 62.

Hafting, T., Fyhn, M., Molden, S., Moser, M. B., & Moser, E. I. (2005). “Microstructure of a spatial map in the entorhinal cortex”. Nature, 436(7052), 801-806.

Hill, E. L., & Frith, U. (2003). “Understanding autism: insights from mind and brain”. Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences, 358(1430), 281-289.

Hollander, E., Kaplan, A., Cartwright, C., & Reichman, D. (2000). “Venlafaxine in children, adolescents, and young adults with autism spectrum disorders: an open retrospective clinical report”. Journal of child neurology, 15(2), 132-135.

Kanwisher, N., McDermott, J., & Chun, M. M. (1997). “The fusiform face area: a module in human extrastriate cortex specialized for face perception”. The Journal of Neuroscience, 17(11), 4302-4311.

Kim, S. J., Young, L. J., Gonen, D., Veenstra-VanderWeele, J., Courchesne, R., Courchesne, E. & Insel, T. R. (2002). “Transmission disequilibrium testing of arginine vasopressin receptor 1A (AVPR1A) polymorphisms in autism”. Molecular psychiatry, 7(5), 503-507.

Kumar, R., Woo, M. A., Birrer, B. V., Macey, P. M., Fonarow, G. C., Hamilton, M. A., & Harper, R. M. (2009). “Mammillary bodies and fornix fibers are injured in heart failure”. Neurobiology of disease, 33(2), 236-242.

Laumonnier, F., Shoubridge, C., Antar, C., Nguyen, L. S., Van Esch, H., Kleefstra, T., & Raynaud, M. (2009). “Mutations of the UPF3B gene, which encodes a protein widely expressed in neurons, are associated with nonspecific mental retardation with or without autism”. Molecular psychiatry,15(7), 767-776.

Lawson-Yuen, A., Saldivar, J. S., Sommer, S., & Picker, J. (2008). “Familial deletion within NLGN4 associated with autism and Tourette syndrome”. European Journal of Human Genetics, 16(5), 614-618.

Mandy, W. P., & Skuse, D. H. (2008). “Research Review: What is the association between the social‐communication element of autism and repetitive interests, behaviours and activities?” Journal of Child Psychology and Psychiatry, 49(8), 795-808.

Mutter, J., Naumann, J., Schneider, R., Walach, H., & Haley, B. (2005). “Mercury and autism: accelerating evidence”. Neuroendocrinol Lett, 26(5), 439-446.

Nacewicz, B. M., Dalton, K. M., Johnstone, T., Long, M. T., McAuliff, E. M., Oakes, T. R., & Davidson, R. J. (2006). “Amygdala volume and nonverbal social impairment in adolescent and adult males with autism”. Archives of general psychiatry, 63(12), 1417.

Nelson, K. B., & Bauman, M. L. (2003). “Thimerosal and autism?. Pediatrics,111(3), 674-679.

Nguyen, A., Rauch, T. A., Pfeifer, G. P., & Hu, V. W. (2010). “Global methylation profiling of lymphoblastoid cell lines reveals epigenetic contributions to autism spectrum disorders and a novel autism candidate gene, RORA, whose protein product is reduced in autistic brain”. The FASEB Journal, 24(8), 3036-3051.

Parker, S. K., Schwartz, B., Todd, J., & Pickering, L. K. (2004). “Thimerosal-containing vaccines and autistic spectrum disorder: a critical review of published original data”. Pediatrics, 114(3), 793-804.

Peça, J., Feliciano, C., Ting, J. T., Wang, W., Wells, M. F., Venkatraman, T. N. & Feng, G. (2011). “Shank3 mutant mice display autistic-like behaviours and striatal dysfunction”. Nature, 472(7344), 437-442.

Pfaff, D. W., Rapin, I., & Goldman, S. (2011). “Male predominance in autism: neuroendocrine influences on arousal and social anxiety”. Autism Research,4(3), 163-176.

Pierce, K., Müller, R. A., Ambrose, J., Allen, G., & Courchesne, E. (2001). “Face processing occurs outside the fusiformface area'in autism: evidence from functional MRI”. Brain, 124(10), 2059-2073.

Polšek, D., Jagatic, T., Cepanec, M., Hof, P. R., & Šimić, G. (2011). “Recent developments in neuropathology of autism spectrum disorders”. Translational neuroscience, 2(3), 256-264.

Purcell, A. E., Jeon, O. H., Zimmerman, A. W., Blue, M. E., & Pevsner, J. (2001). “Postmortem brain abnormalities of the glutamate neurotransmitter system in autism”. Neurology, 57(9), 1618-1628.

Rippon, G., Brock, J., Brown, C., & Boucher, J. (2007). “Disordered connectivity in the autistic brain: Challenges for the ‘new psychophysiology’”. International Journal of Psychophysiology, 63(2), 164-172.

Robinson, P. D., Schutz, C. K., Macciardi, F., White, B. N., & Holden, J. J. (2001). “Genetically determined low maternal serum dopamine β‐hydroxylase levels and the etiology of autism spectrum disorders”. American Journal of Medical Genetics, 100(1), 30-36.

Ronald, A., Happe, F., Bolton, P., Butcher, L. M., Price, T. S., Wheelwright, S. & Plomin, R. (2006). “Genetic heterogeneity between the three components of the autism spectrum: a twin study”. Journal of the American Academy of Child & Adolescent Psychiatry, 45(6), 691-699.

Rubenstein, J. L. R., & Merzenich, M. M. (2003). “Model of autism: increased ratio of excitation/inhibition in key neural systems”. Genes, Brain and Behavior, 2(5), 255-267.

Saitoh, O., Karns, C. M., & Courchesne, E. (2001). “Development of the hippocampal formation from 2 to 42 years MRI evidence of smaller area dentata in autism”. Brain, 124(7), 1317-1324.

Schanen, N. C. (2006). “Epigenetics of autism spectrum disorders”. Human molecular genetics, 15 (suppl 2), R138-R150.

Stephan, H. (1983). “Evolutionary trends in limbic structures”. Neuroscience & Biobehavioral Reviews, 7(3), 367-374.

Teicher, M. H., Anderson, C. M., & Polcari, A. (2012). “Childhood maltreatment is associated with reduced volume in the hippocampal subfields CA3, dentate gyrus, and subiculum”. Proceedings of the National Academy of Sciences, 109(9), E563-E572.

Wassink, T. H., Piven, J., Vieland, V. J., Pietila, J., Goedken, R. J., Folstein, S. E., & Sheffield, V. C. (2002). “Evaluation of FOXP2 as an autism susceptibility gene”. American journal of medical genetics, 114(5), 566-569.

Whitney, E. R., Kemper, T. L., Bauman, M. L., Rosene, D. L., & Blatt, G. J. (2008). “Cerebellar Purkinje cells are reduced in a subpopulation of autistic brains: a stereological experiment using calbindin-D28k”. The Cerebellum, 7(3), 406-416.

Witter, M. P., & Groenewegen, H. J. (1990). “The subiculum: cytoarchitectonically a simple structure, but hodologically complex”. Progress in brain research, 83, 47-58.

Yang, S. Y., Cho, S. C., Yoo, H. J., Cho, I. H., Park, M., Yoe, J. & Kim, S. (2010). “Family-based association study of microsatellites in the 5′ flanking region of< i> AVPR1A with autism spectrum disorder in the Korean population”. Psychiatry research, 178(1), 199-201.

Young, L. J., Pitkow, L. J., & Ferguson, J. N. (2001). “Neuropeptides and social behavior: animal models relevant to autism”. Molecular psychiatry, 7, S38-9.

Zhang, Y., Schuff, N., Jahng, G. H., Bayne, W., Mori, S., Schad, L. & Weiner, M. W. (2007). “Diffusion tensor imaging of cingulum fibers in mild cognitive impairment and Alzheimer disease”. Neurology, 68(1), 13-19.

Zilbovicius, M., Garreau, B., Samson, Y., Remy, P., Barthelemy, C., Syrota, A. & Lelord, G. (1995). “Delayed maturation of the frontal cortex in childhood autism”. American Journal of Psychiatry, 152(2), 248-252.

Descargas

Publicado

30-12-2023

Cómo citar

Perez Bernardes de Moraes, T. (2018). Autismo: entre a alta sistematização e a baixa empatia. Um estudo sobre a hipótese de hiper masculinização do cérebro no espectro autista. Revista Pilquen. Sección Psicopedagogía, 11(1), 1–19. Recuperado a partir de https://revele.uncoma.edu.ar/index.php/psico/article/view/2094