Stimulation du nerf vague comme traitement de la peur et de l'anxiété chez les personnes avec un diagnostic de troubles du spectre de l'autisme

Aperçu: G.M.

Les troubles anxieux touchent un grand pourcentage de personnes avec un diagnostic de trouble du spectre de l'autisme (dTSA). Chez les enfants avec un dTSA, une anxiété excessive est également liée à des problèmes gastro-intestinaux, à des comportements d'automutilation et à des symptômes dépressifs. Les thérapies cognitivo-comportementales basées sur l'exposition sont des traitements efficaces pour les troubles anxieux chez les enfants avec un dTSA, mais des taux de rechute élevés indiquent la nécessité de stratégies de traitement supplémentaires. 

Cette perspective discute des preuves issues de la recherche préclinique, qui indiquent que la stimulation du nerf vague (SNV) associée à l'exposition à des stimuli et à des situations provoquant la peur pourrait offrir des avantages en tant que traitement adjuvant des troubles anxieux qui coexistent avec les TSA. 

La stimulation du nerf vague est approuvée pour une utilisation dans le traitement de l'épilepsie, de la dépression et, plus récemment, comme adjuvant dans l'entraînement de réadaptation après un AVC. 

Dans les modèles précliniques, la SNV semble prometteuse pour améliorer simultanément la consolidation des souvenirs d'extinction et réduire l'anxiété. Dans cette revue, nous présenterons les mécanismes potentiels par lesquels la SNV pourrait traiter la peur et l'anxiété dans les TSA. 

Nous discutons également des utilisations potentielles de la SNV pour traiter la dépression et l'épilepsie dans le contexte des TSA, et des méthodes non invasives pour stimuler le nerf vague.

 

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. 2022;7(4):e220007.

doi: 10.20900/jpbs.20220007. Epub 2022 Sep 23.

Vagus Nerve Stimulation as a Treatment for Fear and Anxiety in Individuals with Autism Spectrum Disorder

Tanushree Shivaswamy  ¹ , Rimenez R Souza  ¹ , Crystal T Engineer  ¹ , Christa K McIntyre  ¹

Affiliations

• PMID: 36303861
• PMCID: PMC9600938
• DOI: 10.20900/jpbs.20220007

Abstract

Anxiety disorders affect a large percentage of individuals who have an autism spectrum disorder (ASD). In children with ASD, excessive anxiety is also linked to gastrointestinal problems, self-injurious behaviors, and depressive symptoms. Exposure-based cognitive behavioral therapies are effective treatments for anxiety disorders in children with ASD, but high relapse rates indicate the need for additional treatment strategies. This perspective discusses evidence from preclinical research, which indicates that vagus nerve stimulation (VNS) paired with exposure to fear-provoking stimuli and situations could offer benefits as an adjuvant treatment for anxiety disorders that coexist with ASD. Vagus nerve stimulation is approved for use in the treatment of epilepsy, depression, and more recently as an adjuvant in rehabilitative training following stroke. In preclinical models, VNS shows promise in simultaneously enhancing consolidation of extinction memories and reducing anxiety. In this review, we will present potential mechanisms by which VNS could treat fear and anxiety in ASD. We also discuss potential uses of VNS to treat depression and epilepsy in the context of ASD, and noninvasive methods to stimulate the vagus nerve.

Keywords: behavioral therapy; exposure therapy; neurodevelopmental disorders; neuromodulation; rehabilitation.

Conflict of interest statement

CONFLICTS OF INTEREST CT Engineer is married to an employee of MicroTransponder, Inc. CK McIntyre is an author of a patent entitled “Methods for Enhancing Exposure Therapy using Vagus Nerve Stimulation”.

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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.

 

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

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

Gabriel S Dichter  ^{1   2   3} , Jose Rodriguez-Romaguera  ^{4   5   6}

Affiliations

• PMID: 35397066
• DOI: 10.1007/7854_2022_312

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.

© 2022. The Author(s), under exclusive license to Springer Nature Switzerland AG.

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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.

2022 Apr 10.

doi: 10.1007/7854_2022_334. 

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

Chandan J Vaidya  ^{1   2} , Christoph Klein  ^{3   4   5}

Affiliations

• PMID: 35397063
• DOI: 10.1007/7854_2022_334

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.

2016;22(3):277-85.

doi: 10.2174/1381612822666151112151529.

Autism: Pathophysiology and Promising Herbal Remedies

Mahmoud Bahmani, Amir Sarrafchi, Hedayatollah Shirzad, Mahmoud Rafieian-Kopaei  ¹

Affiliations

• PMID: 26561063
• DOI: 10.2174/1381612822666151112151529

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.