01 juin 2022

RENFORCEMENT MUSCULAIRE : 1 heure par semaine suffit à réduire de 20 % le risque de décès

Résumé :

Les exercices de renforcement musculaire doivent faire partie d’un programme d’exercice complet, bénéfique à la santé, ainsi, cette forme d'exercice ne doit pas être oubliée. 

C’est le rappel de cette méta-analyse des preuves disponibles dans la littérature, publiée dans le British Journal of Sports Medicine : 30 à 60 minutes d'activité de renforcement musculaire hebdomadaire s’avèrent liées à un risque de décès inférieur de 10 à 20 %, toutes causes confondues. 

Le principe donc, pour de meilleurs bénéfices : combiner les exercices de force à l'activité aérobie.

 

Extrait :

L'étude impliquant près de 4.000 participants, âgés de 18 à 97 ans, montre que :

  • les exercices de renforcement musculaire sont associés à une réduction du risque de décès de 10 à 17 % ;
  • à un risque également réduit de décès par maladie cardiaque et accident vasculaire cérébral, cancer, diabète et cancer du poumon ;
  • aucune association n’est identifiée entre le renforcement musculaire et un risque réduit de types spécifiques de cancer, notamment ceux de l'intestin, des reins, de la vessie ou du pancréas ;
  • l’association est en courbe en forme de J avec une réduction maximale du risque de 10 à 20 % avec environ 30 à 60 minutes/semaine d'activités de renforcement musculaire pour les décès toutes causes confondues, les maladies cardiovasculaires et tous les cancers ;
  • l’association est en forme de L cependant pour le diabète, avec une réduction importante du risque jusqu'à 60 minutes/semaine d'activités de renforcement musculaire, après quoi la diminution du bénéfice est progressive ;
  • la réduction du risque de décès toutes causes confondues, de maladies cardiovasculaires et de cancer est encore plus élevée lorsque les 2 types d'activités, renforcement musculaire et aérobie, sont combinées.

 

Lien vers l'article de SantéLog en français

Lien vers l'article complet du British Journal of Sports Medecine

10 avril 2022

Anhédonie et hyperhédonie dans l'autisme et les troubles neurodéveloppementaux associés

Aperçu: G.M.

Bien que le "trouble du spectre de l'autisme" (TSA) soit défini par une communication sociale altérée et des comportements et intérêts restreints et répétitifs, le TSA se caractérise également par des processus motivationnels altérés. La « théorie de la motivation sociale de l'autisme » décrit comment les perturbations de la motivation sociale dans les TSA dans la petite enfance peuvent entraver la volonté de s'engager dans des comportements sociaux réciproques et finalement interférer avec le développement de réseaux de neurones essentiels à la communication sociale (Chevallier et al., Trends Cogn Sci 16:231-239, 2012b). Il est important de noter que les études cliniques et la recherche préclinique utilisant des organismes modèles pour les TSA indiquent que les troubles de la motivation dans les TSA ne sont pas limités aux récompenses sociales, mais sont également évidents en réponse à une gamme de récompenses non sociales. De plus, des études translationnelles sur certains troubles neurodéveloppementaux génétiquement définis associés aux TSA indiquent que ces formes syndromiques de TSA sont également caractérisées par des déficits motivationnels et des troubles dopaminergiques mésolimbiques. 

Dans ce chapitre, nous résumons les recherches cliniques et précliniques pertinentes pour les troubles du traitement des récompenses dans les TSA et les troubles neurodéveloppementaux connexes. Nous proposons également une nosologie pour décrire les troubles du traitement des récompenses dans ces troubles qui utilise un modèle à trois axes.
Dans cette nosologie triaxiale, le premier axe définit la direction de la réponse de récompense (c'est-à-dire anhédonique, hyperhédonique); le deuxième axe définit la construction du processus de récompense (par exemple, aimer la récompense, vouloir la récompense); et le troisième axe définit le contexte de la réponse de récompense (par exemple, social, non social).
Une nosologie plus précise pour décrire les troubles du traitement des récompenses dans les TSA et les troubles neurodéveloppementaux connexes facilitera la traduction de la recherche préclinique en investigations cliniques qui contribueront finalement à accélérer le développement d'interventions ciblant les systèmes de motivation pour les TSA et les troubles neurodéveloppementaux connexes.

. 2022 Apr 10.
doi: 10.1007/7854_2022

Anhedonia and Hyperhedonia in Autism and Related Neurodevelopmental Disorders

Affiliations

Abstract

Although autism spectrum disorder (ASD) is defined by impaired social communication and restricted and repetitive behaviors and interests, ASD is also characterized by impaired motivational processes. The "social motivation theory of autism" describes how social motivation disruptions in ASD in early childhood may impede the drive to engage in reciprocal social behaviors and ultimately interfere with the development of neural networks critical for social communication (Chevallier et al., Trends Cogn Sci 16:231-239, 2012b). Importantly, clinical studies and preclinical research using model organisms for ASD indicate that motivational impairments in ASD are not constrained to social rewards but are evident in response to a range of nonsocial rewards as well. Additionally, translational studies on certain genetically defined neurodevelopmental disorders associated with ASD indicate that these syndromic forms of ASD are also characterized by motivational deficits and mesolimbic dopamine impairments. In this chapter we summarize clinical and preclinical research relevant to reward processing impairments in ASD and related neurodevelopmental disorders. We also propose a nosology to describe reward processing impairments in these disorders that uses a three-axes model. In this triaxial nosology, the first axis defines the direction of the reward response (i.e., anhedonic, hyperhedonic); the second axis defines the construct of the reward process (e.g., reward liking, reward wanting); and the third axis defines the context of the reward response (e.g., social, nonsocial). A more precise nosology for describing reward processing impairments in ASD and related neurodevelopmental disorders will aid in the translation of preclinical research to clinical investigations which will ultimately help to speed up the development of interventions that target motivational systems for ASD and related neurodevelopmental disorders.

Keywords: Autism; Dopamine; Preclinical; Reward; Social motivation.

References

    1. Alugubelly N, Mohammed AN, Edelmann MJ, Nanduri B, Sayed M, Park JW, Carr RL (2019) Adolescent rat social play: Amygdalar proteomic and transcriptomic data. Data Brief 27:104589
    1. American Psychiatric Association (2013) Desk reference to the diagnostic criteria from DSM-5. American Psychiatric Publishing, Washington
    1. APA (2013) Diagnostic and statistical manual of mental disorders: DSM-V, 5th edn. American Psychiatric Association, Washington
    1. Ashok AH, Marques TR, Jauhar S, Nour MM, Goodwin GM, Young AH, Howes OD (2017) The dopamine hypothesis of bipolar affective disorder: the state of the art and implications for treatment. Mol Psychiatry 22:666–679
    1. Atladottir HO, Thorsen P, Ostergaard L, Schendel DE, Lemcke S, Abdallah M, Parner ET (2010) Maternal infection requiring hospitalization during pregnancy and autism spectrum disorders. J Autism Dev Disord 40:1423–1430
    1. Atzil S, Touroutoglou A, Rudy T, Salcedo S, Feldman R, Hooker JM, Dickerson BC, Catana C, Barrett LF (2017) Dopamine in the medial amygdala network mediates human bonding. Proc Natl Acad Sci U S A 114:2361–2366
    1. Auerbach RP, Pagliaccio D, Pizzagalli DA (2019) Toward an improved understanding of anhedonia. JAMA Psychiatry 76:571–573
    1. Bale TL, Abel T, Akil H, Carlezon WA Jr, Moghaddam B, Nestler EJ, Ressler KJ, Thompson SM (2019) The critical importance of basic animal research for neuropsychiatric disorders. Neuropsychopharmacology 44:1349–1353
    1. Bariselli S, Tzanoulinou S, Glangetas C, Prevost-Solie C, Pucci L, Viguie J, Bezzi P, O'Connor EC, Georges F, Luscher C, Bellone C (2016) SHANK3 controls maturation of social reward circuits in the VTA. Nat Neurosci 19:926–934
    1. Berridge KC, Robinson TE, Aldridge JW (2009) Dissecting components of reward: ‘liking’, ‘wanting’, and learning. Curr Opin Pharmacol 9:65–73
    1. Berry Kravis E, Lewin F, Wuu J, Leehey M, Hagerman R, Hagerman P, Goetz CG (2003) Tremor and ataxia in fragile X premutation carriers: blinded videotape study. Ann Neurol 53:616–623
    1. Bishop SL, Farmer C, Bal V, Robinson EB, Willsey AJ, Werling DM, Havdahl KA, Sanders SJ, Thurm A (2017) Identification of developmental and behavioral markers associated with genetic abnormalities in autism spectrum disorder. Am J Psychiatry 174:576–585
    1. Bittel DC, Butler MG (2005) Prader-Willi syndrome: clinical genetics, cytogenetics and molecular biology. Expert Rev Mol Med 7:1–20
    1. Blundell J, Blaiss CA, Etherton MR, Espinosa F, Tabuchi K, Walz C, Bolliger MF, Sudhof TC, Powell CM (2010) Neuroligin-1 deletion results in impaired spatial memory and increased repetitive behavior. J Neurosci 30:2115–2129
    1. Bortolato M, Godar SC, Alzghoul L, Zhang J, Darling RD, Simpson KL, Bini V, Chen K, Wellman CL, Lin RC, Shih JC (2013) Monoamine oxidase A and A/B knockout mice display autistic-like features. Int J Neuropsychopharmacol 16:869–888
    1. Bottini S (2018) Social reward processing in individuals with autism spectrum disorder: a systematic review of the social motivation hypothesis. Res Autism Spectr Disord 45:9–26
    1. Bozarth MA (1990) Drug addiction as a psychobiological process. In: Warburto DM (ed) Addiction controversies. Harwood Academic Publishers, London, pp 112–134
    1. Bozdagi O, Sakurai T, Papapetrou D, Wang X, Dickstein DL, Takahashi N, Kajiwara Y, Yang M, Katz AM, Scattoni ML, Harris MJ, Saxena R, Silverman JL, Crawley JN, Zhou Q, Hof PR, Buxbaum JD (2010) Haploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication. Mol Autism 1:15
    1. Brielmaier J, Matteson PG, Silverman JL, Senerth JM, Kelly S, Genestine M, Millonig JH, DiCicco-Bloom E, Crawley JN (2012) Autism-relevant social abnormalities and cognitive deficits in engrailed-2 knockout mice. PLoS One 7:e40914
    1. Brodkin ES (2008) Social behavior phenotypes in fragile X syndrome, autism, and the Fmr1 knockout mouse: theoretical comment on McNaughton et al. (2008). Behav Neurosci 122:483–489
    1. Campbell LE, Daly E, Toal F, Stevens A, Azuma R, Catani M, Ng V, van Amelsvoort T, Chitnis X, Cutter W, Murphy DG, Murphy KC (2006) Brain and behaviour in children with 22q11.2 deletion syndrome: a volumetric and voxel-based morphometry MRI study. Brain 129:1218–1228
    1. Carlezon WA Jr, Kim W, Missig G, Finger BC, Landino SM, Alexander AJ, Mokler EL, Robbins JO, Li Y, Bolshakov VY, McDougle CJ, Kim KS (2019) Maternal and early postnatal immune activation produce sex-specific effects on autism-like behaviors and neuroimmune function in mice. Sci Rep 9:16928
    1. Carter RM, Jung H, Reaven J, Blakeley-Smith A, Dichter GS (2020) A nexus model of restricted interests in autism spectrum disorder. Front Hum Neurosci 14:212
    1. Ceravolo R, Antonini A, Volterrani D, Rossi C, Goldwurm S, Di Maria E, Kiferle L, Bonuccelli U, Murri L (2005) Dopamine transporter imaging study in parkinsonism occurring in fragile X premutation carriers. Neurology 65:1971–1973
    1. Chevallier C, Grezes J, Molesworth C, Berthoz S, Happe F (2012a) Brief report: selective social anhedonia in high functioning autism. J Autism Dev Disord 42:1504–1509
    1. Chevallier C, Kohls G, Troiani V, Brodkin ES, Schultz RT (2012b) The social motivation theory of autism. Trends Cogn Sci 16:231–239
    1. Clements CC, Zoltowski AR, Yankowitz LD, Yerys BE, Schultz RT, Herrington JD (2018) Evaluation of the social motivation hypothesis of autism: a systematic review and meta-analysis. JAMA Psychiatry 75:797–808
    1. Crawford DC, Acuna JM, Sherman SL (2001) FMR1 and the fragile X syndrome: human genome epidemiology review. Genet Med 3:359–371
    1. Dalton KM, Holsen L, Abbeduto L, Davidson RJ (2008) Brain function and gaze fixation during facial-emotion processing in fragile X and autism. Autism Res 1:231–239
    1. Dawson G, Webb SJ, McPartland J (2005) Understanding the nature of face processing impairment in autism: insights from behavioral and electrophysiological studies. Dev Neuropsychol 27:403–424
    1. de la Torre-Ubieta L, Won H, Stein JL, Geschwind DH (2016) Advancing the understanding of autism disease mechanisms through genetics. Nat Med 22:345–361
    1. Del Pino I, Rico B, Marin O (2018) Neural circuit dysfunction in mouse models of neurodevelopmental disorders. Curr Opin Neurobiol 48:174–182
    1. DeLorey TM, Sahbaie P, Hashemi E, Homanics GE, Clark JD (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. Behav Brain Res 187:207–220
    1. Devlin B, Scherer SW (2012) Genetic architecture in autism spectrum disorder. Curr Opin Genet Dev 22:229–237
    1. DiCarlo GE, Aguilar JI, Matthies HJ, Harrison FE, Bundschuh KE, West A, Hashemi P, Herborg F, Rickhag M, Chen H, Gether U, Wallace MT, Galli A (2019) Autism-linked dopamine transporter mutation alters striatal dopamine neurotransmission and dopamine-dependent behaviors. J Clin Invest 129:3407–3419
    1. Dichter GS, Damiano CA, Allen JA (2012) Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings. J Neurodev Disord 4:19
    1. Dolen G (2015) Autism: oxytocin, serotonin, and social reward. Soc Neurosci 10:450–465
    1. Dolen G, Darvishzadeh A, Huang KW, Malenka RC (2013) Social reward requires coordinated activity of nucleus accumbens oxytocin and serotonin. Nature 501:179–184
    1. Du L, Zhao G, Duan Z, Li F (2017) Behavioral improvements in a valproic acid rat model of autism following vitamin D supplementation. Psychiatry Res 253:28–32
    1. Dufour-Rainfray D, Vourc'h P, Le Guisquet AM, Garreau L, Ternant D, Bodard S, Jaumain E, Gulhan Z, Belzung C, Andres CR, Chalon S, Guilloteau D (2010) Behavior and serotonergic disorders in rats exposed prenatally to valproate: a model for autism. Neurosci Lett 470:55–59
    1. Ernst M, Zametkin AJ, Matochik JA, Pascualvaca D, Cohen RM (1997) Low medial prefrontal dopaminergic activity in autistic children. Lancet 350:638
    1. Estes ML, McAllister AK (2016) Maternal immune activation: implications for neuropsychiatric disorders. Science 353:772–777
    1. Etherton MR, Blaiss CA, Powell CM, Sudhof TC (2009) Mouse neurexin-1alpha deletion causes correlated electrophysiological and behavioral changes consistent with cognitive impairments. Proc Natl Acad Sci U S A 106:17998–18003
    1. Fallgatter AJ, Lesch KP (2007) 22q11.2 deletion syndrome as a natural model for COMT haploinsufficiency-related dopaminergic dysfunction in ADHD. Int J Neuropsychopharmacol 10:295–299
    1. Fiksinski AM, Schneider M, Zinkstok J, Baribeau D, Chawner S, Vorstman JAS (2021) Neurodevelopmental trajectories and psychiatric morbidity: lessons learned from the 22q11.2 deletion syndrome. Curr Psychiatry Rep 23:13
    1. Franchini M, Armstrong VL, Schaer M, Smith IM (2019) Initiation of joint attention and related visual attention processes in infants with autism spectrum disorder: literature review. Child Neuropsychol 25:287–317
    1. Gadow KD, Devincent CJ, Olvet DM, Pisarevskaya V, Hatchwell E (2010a) Association of DRD4 polymorphism with severity of oppositional defiant disorder, separation anxiety disorder and repetitive behaviors in children with autism spectrum disorder. Eur J Neurosci 32:1058–1065
    1. Gadow KD, DeVincent CJ, Pisarevskaya V, Olvet DM, Xu W, Mendell NR, Finch SJ, Hatchwell E (2010b) Parent-child DRD4 genotype as a potential biomarker for oppositional, anxiety, and repetitive behaviors in children with autism spectrum disorder. Prog Neuro-Psychopharmacol Biol Psychiatry 34:1208–1214
    1. Geschwind DH, State MW (2015) Gene hunting in autism spectrum disorder: on the path to precision medicine. Lancet Neurol 14:1109–1120
    1. Greene RK, Spanos M, Alderman C, Walsh E, Bizzell J, Mosner MG, Kinard JL, Stuber GD, Chandrasekhar T, Politte LC, Sikich L, Dichter GS (2018) The effects of intranasal oxytocin on reward circuitry responses in children with autism spectrum disorder. J Neurodev Disord 10:12
    1. Greene RK, Walsh E, Mosner MG, Dichter GS (2019) A potential mechanistic role for neuroinflammation in reward processing impairments in autism spectrum disorder. Biol Psychol 142:1–12
    1. Gunaydin LA, Deisseroth K (2014) Dopaminergic dynamics contributing to social behavior. Cold Spring Harb Symp Quant Biol 79:221–227
    1. Henske EP, Jozwiak S, Kingswood JC, Sampson JR, Thiele EA (2016) Tuberous sclerosis complex. Nat Rev Dis Primers 2:16035
    1. Hervas A (2016) One autism, several autisms. Phenotypical variability in autism spectrum disorders. Rev Neurol 62 Suppl 1:S9–S14
    1. Higashida H, Munesue T, Kosaka H, Yamasue H, Yokoyama S, Kikuchi M (2019) Social interaction improved by oxytocin in the subclass of autism with comorbid intellectual disabilities. Diseases 7:24
    1. Holsen L, Thompson T (2004) Compulsive behavior and eye blink in Prader-Willi syndrome: neurochemical implications. Am J Ment Retard 109:197–207
    1. Hung LW, Neuner S, Polepalli JS, Beier KT, Wright M, Walsh JJ, Lewis EM, Luo L, Deisseroth K, Dolen G, Malenka RC (2017) Gating of social reward by oxytocin in the ventral tegmental area. Science 357:1406–1411
    1. Insel T, Cuthbert B, Garvey M, Heinssen R, Pine DS, Quinn K, Sanislow C, Wang P (2010) Research domain criteria (RDoC): toward a new classification framework for research on mental disorders. Am J Psychiatry 167:748–751
    1. Johnson KP, Zarrinnegar P (2021) Autism spectrum disorder and sleep. Child Adolesc Psychiatr Clin N Am 30:195–208
    1. Johnson SA, Yechiam E, Murphy RR, Queller S, Stout JC (2006) Motivational processes and autonomic responsivity in Asperger’s disorder: evidence from the Iowa Gambling Task. J Int Neuropsychol Soc 12:668–676
    1. Joinson C, O'Callaghan FJ, Osborne JP, Martyn C, Harris T, Bolton PF (2003) Learning disability and epilepsy in an epidemiological sample of individuals with tuberous sclerosis complex. Psychol Med 33:335–344
    1. Kazdoba TM, Leach PT, Yang M, Silverman JL, Solomon M, Crawley JN (2016) Translational mouse models of autism: advancing toward pharmacological therapeutics. Curr Top Behav Neurosci 28:1–52
    1. Keifer CM, Day TC, Hauschild KM, Lerner MD (2021) Social and nonsocial reward anticipation in typical development and autism spectrum disorders: current status and future directions. Curr Psychiatry Rep 23:32
    1. Kenkel WM, Yee JR, Moore K, Madularu D, Kulkarni P, Gamber K, Nedelman M, Ferris CF (2016) Functional magnetic resonance imaging in awake transgenic fragile X rats: evidence of dysregulation in reward processing in the mesolimbic/habenular neural circuit. Transl Psychiatry 6:e763
    1. Klin A, Jones W, Schultz R, Volkmar F, Cohen D (2002) Visual fixation patterns during viewing of naturalistic social situations as predictors of social competence in individuals with autism. Arch Gen Psychiatry 59:809–816
    1. Klin A, Lin DJ, Gorrindo P, Ramsay G, Jones W (2009) Two-year-olds with autism orient to non-social contingencies rather than biological motion. Nature 459:257–261
    1. Kosillo P, Doig NM, Ahmed KM, Agopyan-Miu A, Wong CD, Conyers L, Threlfell S, Magill PJ, Bateup HS (2019) Tsc1-mTORC1 signaling controls striatal dopamine release and cognitive flexibility. Nat Commun 10:5426
    1. Kubota M, Fujino J, Tei S, Takahata K, Matsuoka K, Tagai K, Sano Y, Yamamoto Y, Shimada H, Takado Y, Seki C, Itahashi T, Aoki YY, Ohta H, Hashimoto RI, Zhang MR, Suhara T, Nakamura M, Takahashi H, Kato N, Higuchi M (2020) Binding of dopamine D1 receptor and noradrenaline transporter in individuals with autism spectrum disorder: a PET study. Cereb Cortex 30(12):6458–6468
    1. Kwon CH, Luikart BW, Powell CM, Zhou J, Matheny SA, Zhang W, Li Y, Baker SJ, Parada LF (2006) Pten regulates neuronal arborization and social interaction in mice. Neuron 50:377–388
    1. Lai MC, Lombardo MV, Baron-Cohen S (2014) Autism. Lancet 383:896–910
    1. Levy SE, Mandell DS, Schultz RT (2009) Autism. Lancet 374:1627–1638
    1. Lightbody AA, Reiss AL (2009) Gene, brain, and behavior relationships in fragile X syndrome: evidence from neuroimaging studies. Dev Disabil Res Rev 15:343–352
    1. Loas G, Krystkowiak P, Godefroy O (2012) Anhedonia in Parkinson’s disease: an overview. J Neuropsychiatry Clin Neurosci 24:444–451
    1. Luck C, Vitaterna MH, Wevrick R (2016) Dopamine pathway imbalance in mice lacking Magel2, a Prader-Willi syndrome candidate gene. Behav Neurosci 130:448–459
    1. Mabunga DF, Gonzales EL, Kim JW, Kim KC, Shin CY (2015) Exploring the validity of valproic acid animal model of autism. Exp Neurobiol 24:285–300
    1. Manduca A, Servadio M, Damsteegt R, Campolongo P, Vanderschuren LJ, Trezza V (2016) Dopaminergic neurotransmission in the nucleus accumbens modulates social play behavior in rats. Neuropsychopharmacology 41(9):2215–2223
    1. Markram K, Rinaldi T, La Mendola D, Sandi C, Markram H (2008) Abnormal fear conditioning and amygdala processing in an animal model of autism. Neuropsychopharmacology 33:901–912
    1. McDonald-McGinn DM, Sullivan KE, Marino B, Philip N, Swillen A, Vorstman JA, Zackai EH, Emanuel BS, Vermeesch JR, Morrow BE, Scambler PJ, Bassett AS (2015) 22q11.2 deletion syndrome. Nat Rev Dis Primers 1:15071
    1. Miles JH, Takahashi TN, Bagby S, Sahota PK, Vaslow DF, Wang CH, Hillman RE, Farmer JE (2005) Essential versus complex autism: definition of fundamental prognostic subtypes. Am J Med Genet A 135:171–180
    1. Miller JL, James GA, Goldstone AP, Couch JA, He G, Driscoll DJ, Liu Y (2007) Enhanced activation of reward mediating prefrontal regions in response to food stimuli in Prader-Willi syndrome. J Neurol Neurosurg Psychiatry 78:615–619
    1. Missig G, Robbins JO, Mokler EL, McCullough KM, Bilbo SD, McDougle CJ, Carlezon WA Jr (2020) Sex-dependent neurobiological features of prenatal immune activation via TLR7. Mol Psychiatry 25:2330–2341
    1. Molina J, Carmona-Mora P, Chrast J, Krall PM, Canales CP, Lupski JR, Reymond A, Walz K (2008) Abnormal social behaviors and altered gene expression rates in a mouse model for Potocki-Lupski syndrome. Hum Mol Genet 17:2486–2495
    1. Morales I, Berridge KC (2020) ‘Liking’ and ‘wanting’ in eating and food reward: brain mechanisms and clinical implications. Physiol Behav 227:113152
    1. Mosner MG, Kinard JL, McWeeny S, Shah JS, Markiewitz ND, Damiano-Goodwin CR, Burchinal MR, Rutherford HJV, Greene RK, Treadway MT, Dichter GS (2017) Vicarious effort-based decision-making in autism spectrum disorders. J Autism Dev Disord 47:2992–3006
    1. Nadler JJ, Moy SS, Dold G, Trang D, Simmons N, Perez A, Young NB, Barbaro RP, Piven J, Magnuson TR, Crawley JN (2004) Automated apparatus for quantitation of social approach behaviors in mice. Genes Brain Behav 3:303–314
    1. Nakasato A, Nakatani Y, Seki Y, Tsujino N, Umino M, Arita H (2008) Swim stress exaggerates the hyperactive mesocortical dopamine system in a rodent model of autism. Brain Res 1193:128–135
    1. Nakatani J, Tamada K, Hatanaka F, Ise S, Ohta H, Inoue K, Tomonaga S, Watanabe Y, Chung YJ, Banerjee R, Iwamoto K, Kato T, Okazawa M, Yamauchi K, Tanda K, Takao K, Miyakawa T, Bradley A, Takumi T (2009) Abnormal behavior in a chromosome-engineered mouse model for human 15q11-13 duplication seen in autism. Cell 137:1235–1246
    1. Narita N, Kato M, Tazoe M, Miyazaki K, Narita M, Okado N (2002) Increased monoamine concentration in the brain and blood of fetal thalidomide- and valproic acid-exposed rat: putative animal models for autism. Pediatr Res 52:576–579
    1. Neale BM, Kou Y, Liu L, Ma'ayan A, Samocha KE, Sabo A, Lin CF, Stevens C, Wang LS, Makarov V, Polak P, Yoon S, Maguire J, Crawford EL, Campbell NG, Geller ET, Valladares O, Schafer C, Liu H, Zhao T, Cai G, Lihm J, Dannenfelser R, Jabado O, Peralta Z, Nagaswamy U, Muzny D, Reid JG, Newsham I, Wu Y, Lewis L, Han Y, Voight BF, Lim E, Rossin E, Kirby A, Flannick J, Fromer M, Shakir K, Fennell T, Garimella K, Banks E, Poplin R, Gabriel S, DePristo M, Wimbish JR, Boone BE, Levy SE, Betancur C, Sunyaev S, Boerwinkle E, Buxbaum JD, Cook EH Jr, Devlin B, Gibbs RA, Roeder K, Schellenberg GD, Sutcliffe JS, Daly MJ (2012) Patterns and rates of exonic de novo mutations in autism spectrum disorders. Nature 485:242–245
    1. Numis AL, Major P, Montenegro MA, Muzykewicz DA, Pulsifer MB, Thiele EA (2011) Identification of risk factors for autism spectrum disorders in tuberous sclerosis complex. Neurology 76:981–987
    1. Ousley O, Rockers K, Dell ML, Coleman K, Cubells JF (2007) A review of neurocognitive and behavioral profiles associated with 22q11 deletion syndrome: implications for clinical evaluation and treatment. Curr Psychiatry Rep 9:148–158
    1. Ousley O, Evans AN, Fernandez-Carriba S, Smearman EL, Rockers K, Morrier MJ, Evans DW, Coleman K, Cubells J (2017) Examining the overlap between autism spectrum disorder and 22q11.2 deletion syndrome. Int J Mol Sci 18:1071
    1. Ozonoff S, Iosif AM, Baguio F, Cook IC, Hill MM, Hutman T, Rogers SJ, Rozga A, Sangha S, Sigman M, Steinfeld MB, Young GS (2010) A prospective study of the emergence of early behavioral signs of autism. J Am Acad Child Adolesc Psychiatry 49:256–266.e1–2
    1. Page DT, Kuti OJ, Prestia C, Sur M (2009) Haploinsufficiency for Pten and serotonin transporter cooperatively influences brain size and social behavior. Proc Natl Acad Sci U S A 106:1989–1994
    1. Parker KJ, Oztan O, Libove RA, Sumiyoshi RD, Jackson LP, Karhson DS, Summers JE, Hinman KE, Motonaga KS, Phillips JM, Carson DS, Garner JP, Hardan AY (2017) Intranasal oxytocin treatment for social deficits and biomarkers of response in children with autism. Proc Natl Acad Sci U S A 114:8119–8124
    1. Peca J, Feliciano C, Ting JT, Wang W, Wells MF, Venkatraman TN, Lascola CD, Fu Z, Feng G (2011) Shank3 mutant mice display autistic-like behaviours and striatal dysfunction. Nature 472:437–442
    1. Penagarikano O, Abrahams BS, Herman EI, Winden KD, Gdalyahu A, Dong H, Sonnenblick LI, Gruver R, Almajano J, Bragin A, Golshani P, Trachtenberg JT, Peles E, Geschwind DH (2011) Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities, and core autism-related deficits. Cell 147:235–246
    1. Phillips BU, Lopez-Cruz L, Saksida LM, Bussey TJ (2019) Translational tests involving non-reward: methodological considerations. Psychopharmacology 236:449–461
    1. Piantadosi PT, Halladay LR, Radke AK, Holmes A (2021) Advances in understanding meso-cortico-limbic-striatal systems mediating risky reward seeking. J Neurochem 157(5):1547–1571
    1. Pinto D, Delaby E, Merico D, Barbosa M, Merikangas A, Klei L, Thiruvahindrapuram B, Xu X, Ziman R, Wang Z, Vorstman JA, Thompson A, Regan R, Pilorge M, Pellecchia G, Pagnamenta AT, Oliveira B, Marshall CR, Magalhaes TR, Lowe JK, Howe JL, Griswold AJ, Gilbert J, Duketis E, Dombroski BA, De Jonge MV, Cuccaro M, Crawford EL, Correia CT, Conroy J, Conceicao IC, Chiocchetti AG, Casey JP, Cai G, Cabrol C, Bolshakova N, Bacchelli E, Anney R, Gallinger S, Cotterchio M, Casey G, Zwaigenbaum L, Wittemeyer K, Wing K, Wallace S, van Engeland H, Tryfon A, Thomson S, Soorya L, Roge B, Roberts W, Poustka F, Mouga S, Minshew N, McInnes LA, McGrew SG, Lord C, Leboyer M, Le Couteur AS, Kolevzon A, Jimenez Gonzalez P, Jacob S, Holt R, Guter S, Green J, Green A, Gillberg C, Fernandez BA, Duque F, Delorme R, Dawson G, Chaste P, Cafe C, Brennan S, Bourgeron T, Bolton PF, Bolte S, Bernier R, Baird G, Bailey AJ, Anagnostou E, Almeida J, Wijsman EM, Vieland VJ, Vicente AM, Schellenberg GD, Pericak-Vance M, Paterson AD, Parr JR, Oliveira G, Nurnberger JI, Monaco AP, Maestrini E, Klauck SM, Hakonarson H, Haines JL, Geschwind DH, Freitag CM, Folstein SE, Ennis S, Coon H, Battaglia A, Szatmari P, Sutcliffe JS, Hallmayer J, Gill M, Cook EH, Buxbaum JD, Devlin B, Gallagher L, Betancur C, Scherer SW (2014) Convergence of genes and cellular pathways dysregulated in autism spectrum disorders. Am J Hum Genet 94:677–694
    1. Pizzagalli DA, Goetz E, Ostacher M, Iosifescu DV, Perlis RH (2008) Euthymic patients with bipolar disorder show decreased reward learning in a probabilistic reward task. Biol Psychiatry 64:162–168
    1. Reith RM, McKenna J, Wu H, Hashmi SS, Cho SH, Dash PK, Gambello MJ (2013) Loss of Tsc2 in Purkinje cells is associated with autistic-like behavior in a mouse model of tuberous sclerosis complex. Neurobiol Dis 51:93–103
    1. Resendez SL, Namboodiri VMK, Otis JM, Eckman LEH, Rodriguez-Romaguera J, Ung RL, Basiri ML, Kosyk O, Rossi MA, Dichter GS, Stuber GD (2020) Social stimuli induce activation of oxytocin neurons within the paraventricular nucleus of the hypothalamus to promote social behavior in male mice. J Neurosci 40:2282–2295
    1. Roberts J, Symons F, Johnson AM, Hatton D, Boccia M (2005) Blink rate in boys with fragile X syndrome: preliminary evidence for altered dopamine function. J Intellect Disabil Res 49:647–656
    1. Rodriguez-Romaguera J, Namboodiri VMK, Basiri ML, Stamatakis AM, Stuber GD (2020) Developments from bulk optogenetics to single-cell strategies to dissect the neural circuits that underlie aberrant motivational states. Cold Spring Harb Perspect Med. https://doi.org/10.1101/cshperspect.a039792
    1. Salles J, Lacassagne E, Benvegnu G, Berthoumieu SC, Franchitto N, Tauber M (2020) The RDoC approach for translational psychiatry: could a genetic disorder with psychiatric symptoms help fill the matrix? The example of Prader-Willi syndrome. Transl Psychiatry 10:274
    1. Salussolia CL, Klonowska K, Kwiatkowski DJ, Sahin M (2019) Genetic etiologies, diagnosis, and treatment of tuberous sclerosis complex. Annu Rev Genomics Hum Genet 20:217–240
    1. Santini E, Huynh TN, MacAskill AF, Carter AG, Pierre P, Ruggero D, Kaphzan H, Klann E (2013) Exaggerated translation causes synaptic and behavioural aberrations associated with autism. Nature 493:411–415
    1. Schultz W (2019) Recent advances in understanding the role of phasic dopamine activity. F1000Res 8. https://doi.org/10.12688/f1000research.19793.1
    1. Semenova AA, Lopatina OL, Salmina AB (2020) Models of autism and methods for assessing autistic-like behavior in animals. Neurosci Behav Physiol 50:1024–1034
    1. Shapira NA, Lessig MC, He AG, James GA, Driscoll DJ, Liu Y (2005) Satiety dysfunction in Prader-Willi syndrome demonstrated by fMRI. J Neurol Neurosurg Psychiatry 76:260–262
    1. Shaywitz BA, Yager RD, Klopper JH (1976) Selective brain dopamine depletion in developing rats: an experimental model of minimal brain dysfunction. Science 191:305–308
    1. Sikich L, Kolevzon A, King BH, McDougle CJ, Sanders KB, Kim SJ, Spanos M, Chandrasekhar T, Trelles MDP, Rockhill CM, Palumbo ML, Witters Cundiff A, Montgomery A, Siper P, Minjarez M, Nowinski LA, Marler S, Shuffrey LC, Alderman C, Weissman J, Zappone B, Mullett JE, Crosson H, Hong N, Siecinski SK, Giamberardino SN, Luo S, She L, Bhapkar M, Dean R, Scheer A, Johnson JL, Gregory SG, Veenstra-VanderWeele J (2021) Intranasal oxytocin in children and adolescents with autism spectrum disorder. N Engl J Med 385(16):1462–1473. https://doi.org/10.1056/NEJMoa2103583 - DOI
    1. Smith SE, Zhou YD, Zhang G, Jin Z, Stoppel DC, Anderson MP (2011) Increased gene dosage of Ube3a results in autism traits and decreased glutamate synaptic transmission in mice. Sci Transl Med 3:103ra97
    1. Soderstrom H, Rastam M, Gillberg C (2002) Temperament and character in adults with Asperger syndrome. Autism 6:287–297
    1. Staal WG (2015) Autism, DRD3 and repetitive and stereotyped behavior, an overview of the current knowledge. Eur Neuropsychopharmacol 25:1421–1426
    1. Terranova ML, Laviola G (2005) Scoring of social interactions and play in mice during adolescence. Curr Protoc Toxicol Chapter 13:Unit13.10
    1. Thomas A, Burant A, Bui N, Graham D, Yuva-Paylor LA, Paylor R (2009) Marble burying reflects a repetitive and perseverative behavior more than novelty-induced anxiety. Psychopharmacology 204:361–373
    1. Trezza V, Damsteegt R, Achterberg EJ, Vanderschuren LJ (2011) Nucleus accumbens mu-opioid receptors mediate social reward. J Neurosci 31:6362–6370
    1. Tsai PT, Hull C, Chu Y, Greene-Colozzi E, Sadowski AR, Leech JM, Steinberg J, Crawley JN, Regehr WG, Sahin M (2012) Autistic-like behaviour and cerebellar dysfunction in Purkinje cell Tsc1 mutant mice. Nature 488:647–651
    1. Tschida JE, Yerys BE (2021) A systematic review of the positive valence system in autism spectrum disorder. Neuropsychol Rev 31:58–88
    1. Verkerk AJ, Pieretti M, Sutcliffe JS, Fu YH, Kuhl DP, Pizzuti A, Reiner O, Richards S, Victoria MF, Zhang FP et al (1991) Identification of a gene (FMR-1) containing a CGG repeat coincident with a breakpoint cluster region exhibiting length variation in fragile X syndrome. Cell 65:905–914
    1. Wang H, Wu LJ, Kim SS, Lee FJ, Gong B, Toyoda H, Ren M, Shang YZ, Xu H, Liu F, Zhao MG, Zhuo M (2008) FMRP acts as a key messenger for dopamine modulation in the forebrain. Neuron 59:634–647
    1. Weber-Stadlbauer U, Richetto J, Zwamborn RAJ, Slieker RC, Meyer U (2021) Transgenerational modification of dopaminergic dysfunctions induced by maternal immune activation. Neuropsychopharmacology 46(2):404–412
    1. Whitton AE, Kumar P, Treadway MT, Rutherford AV, Ironside ML, Foti D, Fitzmaurice G, Du F, Pizzagalli DA (2021) Mapping disease course across the mood disorder spectrum through a research domain criteria framework. Biol Psychiatry Cogn Neurosci Neuroimaging 6(7):706–715
    1. Wu HF, Chen PS, Hsu YT, Lee CW, Wang TF, Chen YJ, Lin HC (2018) D-Cycloserine ameliorates autism-like deficits by removing GluA2-containing AMPA receptors in a valproic acid-induced rat model. Mol Neurobiol 55:4811–4824
    1. Zurcher NR, Walsh EC, Phillips RD, Cernasov PM, Tseng CJ, Dharanikota A, Smith E, Li Z, Kinard JL, Bizzell JC, Greene RK, Dillon D, Pizzagalli DA, Izquierdo-Garcia D, Truong K, Lalush D, Hooker JM, Dichter GS (2021) A simultaneous [(11)C]raclopride positron emission tomography and functional magnetic resonance imaging investigation of striatal dopamine binding in autism. Transl Psychiatry 11:33

Comorbidité du trouble déficitaire de l'attention avec hyperactivité et des "troubles du spectre de l'autisme" : situation actuelle et orientations prometteuses

Aperçu: G.M.

Des taux élevés de troubles concomitants du déficit de l'attention avec hyperactivité (TDAH) et des "troubles du spectre de l'autisme" (TSA) suggèrent des voies causales communes, qui attendent d'être élucidées.
Ce qui est bien établi, cependant, est l'impact négatif du TDAH et du TSA comorbides sur les résultats de la vie quotidienne, en particulier dans l'interaction sociale et la communication et sur la psychopathologie plus large.
Les approches neurocognitives suggèrent que les corrélats de la comorbidité sont enracinés dans les réseaux de connectivité fonctionnelle associés au contrôle exécutif. Il existe un soutien pour les origines familiales, avec des études de génétique moléculaire suggérant un rôle causal des gènes pléiotropes. Des recherches plus approfondies sont nécessaires pour élucider pleinement comment le risque génétique de TDAH et de TSA affecte le développement neurologique et pour identifier les corrélats neuronaux structurels et fonctionnels et leurs séquelles comportementales.
L'identification des phénotypes intermédiaires est nécessaire pour faire progresser la compréhension, ce qui nécessite des études qui incluent le spectre complet de la gravité des symptômes de TSA et de TDAH, utilisent des conceptions longitudinales et des méthodes multivariées pour sonder de larges constructions, telles que la fonction exécutive et sociale, et prennent en compte d'autres sources d'hétérogénéité, tels que l'âge, le sexe et d'autres psychopathologies.
Des essais d'efficacité randomisés ciblant la symptomatologie comorbide sont nécessaires pour atténuer les résultats négatifs sur le développement.

doi: 10.1007/7854_2022_334. 

Comorbidity of Attention-Deficit Hyperactivity Disorder and Autism Spectrum Disorders: Current Status and Promising Directions

Affiliations

Abstract

High rates of co-occurring Attention-Deficit Hyperactivity Disorder (ADHD) and Autism Spectrum Disorders (ASD) suggest common causal pathways, which await elucidation. What is well-established, however, is the negative impact of comorbid ADHD and ASD on outcomes for everyday living, particularly in social interaction and communication and on broader psychopathology. Neurocognitive approaches suggest correlates of comorbidity are rooted in functional connectivity networks associated with executive control. There is support for familial origins, with molecular-genetic studies suggesting a causal role of pleiotropic genes. Further investigation is needed to elucidate fully how genetic risk for ADHD and ASD affects neurodevelopment and to identify structural and functional neural correlates and their behavioral sequelae. Identification of intermediate phenotypes is necessary to advance understanding, which requires studies that include the full spectrum of ASD and ADHD symptom severity, use longitudinal designs and multivariate methods to probe broad constructs, such as executive and social function, and consider other sources of heterogeneity, such as age, sex, and other psychopathology. Randomized efficacy trials targeting comorbid symptomatology are needed to mitigate negative developmental outcomes.

Keywords: Brain imaging; Executive control; Functional connectivity; Genetic.

Autisme : physiopathologie et plantes médicinales prometteuses

Aperçu: G.M.

L'autisme est une anomalie de croissance globale dans laquelle les compétences sociales, le langage, la communication et les compétences comportementales sont développées avec retard et comme diversion. Les causes de l'autisme ne sont pas claires, mais diverses théories sur la génétique, l'immunité, les facteurs biologiques et psychosociaux ont été proposées. En fait, l'autisme est un trouble complexe avec des causes distinctes qui coexistent généralement. Bien qu'aucun médicament n'ait été reconnu pour traiter ce trouble, les traitements pharmacologiques peuvent être efficaces pour réduire ses signes, tels que l'automutilation, l'agressivité, les comportements répétitifs et stéréotypés, l'inattention, l'hyperactivité et les troubles du sommeil. 

Récemment, des approches complémentaires et alternatives ont été envisagées pour traiter l'autisme. Le Ginkgo biloba est l'une des plantes les plus efficaces avec une longue histoire d'applications dans les troubles neuropsychologiques qui est récemment utilisée pour l'autisme. 

La présente revue traite des découvertes récentes, de la physiopathologie et de l'étiologie de l'autisme, puis aborde les résultats prometteurs des remèdes à base de plantes.

doi: 10.2174/1381612822666151112151529.

Autism: Pathophysiology and Promising Herbal Remedies

Affiliations

Abstract

Autism is a comprehensive growth abnormality in which social skills, language, communication, and behavioral skills are developed with delay and as diversionary. The reasons for autism are unclear, but various theories of genetics, immunity, biological, and psychosocial factors have been proffered. In fact, autism is a complex disorder with distinct causes that usually co-occur. Although no medicine has been recognized to treat this disorder, pharmacological treatments can be effective in reducing its signs, such as self-mutilation, aggression, repetitive and stereotyped behaviors, inattention, hyperactivity, and sleeping disorders. Recently, complementary and alternative approaches have been considered to treat autism. Ginkgo biloba is one of the most effective plants with an old history of applications in neuropsychological disorders which recently is used for autism. The present review discusses the recent findings, pathophysiology, and etiology of autism and thereafter addresses the promising results of herbal remedies.


29 juin 2021

Association entre les "troubles du spectre de l'autisme" et les changements dans le traitement auditif central chez les enfants

Aperçu: G.M.

Objectif :
Vérifier les preuves scientifiques sur l'association entre le "trouble du spectre de l'autisme" et le trouble du traitement auditif central chez les enfants, visant à répondre à la question de recherche suivante : quelle est l'association entre le "spectre de l'autisme" et l'altération du traitement auditif chez les enfants ?

Méthodes :
Les études ont été choisies grâce à la combinaison basée sur les termes de titre de sujet médical (MeSH) : [(traitement auditif) et (enfants) et (autisme) et (troubles neurologiques)]. Les bases de données MEDLINE (PubMed), LILACS et SciELO ont été utilisées. Les articles analysés couvraient une période de dix ans, de 2010 à 2020. Nous avons sélectionné des études descriptives, transversales, de cohorte et de cas. Nous avons évalué la qualité des articles, qui avaient un score minimum de six dans l'échelle modifiée de la littérature. 

Résultats :
126 articles ont été récupérés après la phase d'exclusion, et 17 d'entre eux ont suivi les critères d'inclusion. Seuls deux articles ont répondu à la question directrice avec des résultats audiologiques.

Conclusions :
Les patients diagnostiqués avec un "trouble du spectre de l'autisme" peuvent présenter des troubles du traitement auditif central, étant donné que des changements ont été trouvés à la fois dans les latences absolues et inter-pics dans l'audiométrie de réponse évoquée du tronc cérébral, ainsi que dans la latence et la latéralité de l'amplitude de l'onde N1c.
En outre, il y avait des changements dans le traitement auditif comportemental de l'évaluation. Ainsi, les troubles du traitement auditif central sont fréquents chez les enfants avec un diagnostic de "troubles du spectre de l'autisme".
 

. 2021 Jun 9;S0104-42302021005002209.  doi: 10.1590/1806-9282.67.01.20200588. 

Association between autism spectrum disorder and changes in the central auditory processing in children

Affiliations

Abstract

Objective: To verify the scientific evidence on the association between Autistic Spectrum Disorder and Central Auditory Processing Disorder in children, aiming to answer the following research question: What is the association between Autistic Spectrum and Alteration of Auditory Processing in Children?

Methods: Studies were chosen through the combination based on the Medical Subject Heading Terms (MeSH): [(auditory processing) and (children) and (autism) and (neurological disorders)]. The MEDLINE (PubMed), LILACS, and SciELO databases were used. The analyzed papers covered a ten-year period, from 2010 to 2020. We selected descriptive, cross-sectional, cohort, and case studies. We evaluated the quality of the papers, which had a minimum score of six in the modified scale of the literature.

Results: 126 papers were retrieved after the exclusion phase, and 17 of them followed the inclusion criteria. Only two papers answered the guiding question with audiological results.

Conclusions: Patients diagnosed with autistic spectrum disorder may have disturbance central auditory processing, considering that changes were found both in absolute and interpeak latencies in the brainstem evoked response audiometry, as well as in latency and laterality of the N1c wave amplitude. In addition, there were changes in the assessment behavioral auditory processing. Thus, disturbance central auditory processing is common in children with autistic spectrum disorder.

Similar articles

18 juin 2021

Une étude de validation de l'échelle LABIRINTO pour l'évaluation des "troubles du spectre de l'autisme" chez les enfants âgés de 2 à 4 ans

Aperçu: G.M.

Objectif :
Trouver des preuves du contenu, et de la validité des critères de l'échelle LABIRINTO pour le diagnostic des "troubles du spectre de l'autisme" (TSA) chez les enfants âgés de 24 à 59 mois. 

Méthodes :
L'échelle a été construite en quatre étapes : 

  1. les éléments ont été définis sur la base d'un examen approfondi de la littérature et de discussions avec des spécialistes de l'autisme et du développement de l'enfant ; 
  2. des spécialistes du développement de l'enfant ont évalué chaque élément ; 
  3. une version préliminaire de l'échelle a été appliquée aux enfants diagnostiqués avec un TSA pour permettre les ajustements nécessaires ; 
  4. l'échelle a ensuite été appliquée à 27 enfants avec un développement typique et sans trouble neurodéveloppemental et 48 enfants avec un diagnostic de TSA. Selon la 5e édition du Manuel diagnostique et statistique des troubles mentaux (DSM-5) et la Childhood Autism Rating Scale (CARS), le diagnostic clinique constitue l'étalon-or. 

Résultats :
Les indices psychométriques de l'échelle étaient appropriés pour la validité de construit, avec Kaiser-Meyer-Olkin = 0,94 et une erreur quadratique moyenne d'approximation = 0,000. Un seul facteur de l'échelle avait un alpha de Cronbach de 0,97. La courbe caractéristique de fonctionnement du récepteur indiquait un seuil de 12, avec une sensibilité de 100 % et une spécificité de 100 % pour distinguer les enfants ayant un développement autistique de ceux ayant un développement typique. 

Conclusion :
Cette étude a confirmé la validité de l'échelle LABIRINTO.

. 2021 Jun 15.  doi: 10.47626/2237-6089-2020-

A validation study of the LABIRINTO scale for the evaluation of autism spectrum disorder in children aged 2 to 4 years

Affiliations

Abstract

Objective: To find evidence of the content, construct, and criterion validity of the LABIRINTO scale for the diagnosis of autism spectrum disorder (ASD) in children aged 24-59 months.

Methods: The scale was constructed in four stages: 1) items were defined based on an extensive literature review and discussions with autism and child development specialists; 2) child development specialists evaluated each item; 3) a preliminary version of the scale was applied to children diagnosed with ASD to enable any necessary adjustments; 4) the scale was then applied to 27 children with typical development and no neurodevelopmental disorder and 48 children with ASD. According to the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and the Childhood Autism Rating Scale (CARS), clinical diagnosis constitutes the gold standard.

Results: The scale's psychometric indexes were appropriate for construct validity, with Kaiser-Meyer-Olkin = 0.94 and root mean square error of approximation = 0.000. Only one factor on the scale had a Cronbach alpha of 0.97. The receiver operating characteristic curve indicated a cutoff of 12, with a sensitivity of 100% and specificity of 100% for distinguishing children with ASD from those with typical development.

Conclusion: This study confirmed the validity of the LABIRINTO scale.

Keywords: Autism; diagnostic evaluation; psychometrics; validation.