Repetitive Behaviours in Autistic and Non-Autistic Adults: Associations with Sensory Sensitivity and Impact on Self-Efficacy

Nwaordu, Gabrielle; Charlton, Rebecca A.

doi:10.1007/s10803-023-06133-0

Cited by 5 publications

(5 citation statements)

References 34 publications

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“…A recent human study showed that reductions in repetitive behaviors in individuals are associated with an increase in other autism phenotypes like anxiety and social difficulties and vice versa, suggesting that some repetitive behaviors may be a self-regulation mechanism rather than a primary phenotype in autism 275 . Given the close correlations that have been found between repetitive behaviors and sensory sensitivity and the beneficial effects of repetitive behaviors 276 , our finding that sensory dysregulation is the more dominant brain phenotype in rsfMRI of MIR mice with SOR, supports the idea of an emergence of repetitive behaviors as coping mechanism rather than being a cause of dysfunction. The acute rapamycin treatment in MIR mice reduced FC towards control levels in the cortex but curiously caused even greater FC differences in subcortical structures.…”

Section: Discussionsupporting

confidence: 74%

Acute rapamycin treatment reveals novel mechanisms of behavioral, physiological, and functional dysfunction in a maternal inflammation mouse model of autism and sensory over-responsivity

Le Belle,

Condro,

Cepeda

et al. 2024

Preprint

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Maternal inflammatory response (MIR) during early gestation in mice induces a cascade of physiological and behavioral changes that have been associated with autism spectrum disorder (ASD). In a prior study and the current one, we find that mild MIR results in chronic systemic and neuro-inflammation, mTOR pathway activation, mild brain overgrowth followed by regionally specific volumetric changes, sensory processing dysregulation, and social and repetitive behavior abnormalities. Prior studies of rapamycin treatment in autism models have focused on chronic treatments that might be expected to alter or prevent physical brain changes. Here, we have focused on the acute effects of rapamycin to uncover novel mechanisms of dysfunction and related to mTOR pathway signaling. We find that within 2 hours, rapamycin treatment could rapidly rescue neuronal hyper-excitability, seizure susceptibility, functional network connectivity and brain community structure, and repetitive behaviors and sensory over-responsivity in adult offspring with persistent brain overgrowth. These CNS-mediated effects are also associated with alteration of the expression of several ASD-,ion channel-, and epilepsy-associated genes, in the same time frame. Our findings suggest that mTOR dysregulation in MIR offspring is a key contributor to various levels of brain dysfunction, including neuronal excitability, altered gene expression in multiple cell types, sensory functional network connectivity, and modulation of information flow. However, we demonstrate that the adult MIR brain is also amenable to rapid normalization of these functional changes which results in the rescue of both core and comorbid ASD behaviors in adult animals without requiring long-term physical alterations to the brain. Thus, restoring excitatory/inhibitory imbalance and sensory functional network modularity may be important targets for therapeutically addressing both primary sensory and social behavior phenotypes, and compensatory repetitive behavior phenotypes.

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Section: Discussionsupporting

confidence: 74%

Acute rapamycin treatment reveals novel mechanisms of behavioral, physiological, and functional dysfunction in a maternal inflammation mouse model of autism and sensory over-responsivity

Le Belle,

Condro,

Cepeda

et al. 2024

Preprint

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“…More precisely, we hold that the propensity to tic within certain contexts serves to resolve ambiguity about the status of the inferred, agentive self by disambiguating the outcomes of self-generated action and worldly events (Clarke, 1996). This crucially involves both information gain about the agent 'that I am' and the fulfilment of a supervening pragmatic imperative, which draws me to act so that 'I will be able to observe the sensations that I cause'-perhaps the most overt expression of self-evidencing (see e.g., self-stimming behaviour in severe autism (Nwaordu & Charlton, 2023). This need to buttress my belief-about the type of thing that I am-stems from the failure of sensory attenuation outlined above.…”

Section: Section 2: Tics As Epistemic Foragingmentioning

confidence: 99%

“…In fact, we suggest that our four-tiered model may provide explanatory power beyond TS and OCD, especially since it is unclear to what degree tics (or at least tic-like movements) are exclusive to TS. Indeed, certain aspects of our model might be able to generate insights into the neurocognitive processes relevant to the expression of motoric phenomena that resemble tics within both hypo-and (especially) hyper-kinesias, including self-stimming in autism spectrum disorder ASD (Nwaordu & Charlton, 2023), but also stimulus utilisation behaviours (Janik et al, 2018), functional tics (Cavanna et al, 2023), and attention deficit hyperactivity disorder (ADHD). For example, in ASD, individuals may produce self-initiated (rhythmic) actions to regulate sensory input (e.g., to ameliorate symptoms of hypersensitivity), otherwise known as self-stimming.…”

Section: Empirical Predictions Limitations and Future Directionsmentioning

confidence: 99%

When the interoceptive and conceptual clash: the case of oppositional phenomenal self-modelling in Tourette Syndrome

Parvizi-Wayne,

Severs

2024

Preprint

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Tourette syndrome (TS) has been associated with a rich set of symptoms that are said to be uncomfortable, unwilled, and effortful to manage. Furthermore, tics, the canonical characteristic of TS, are multifaceted and their onset and maintenance is complex. A formal account that integrates these features of TS symptomatology within a plausible theoretical framework is currently absent from the field. In this paper, we assess the explanatory power of hierarchical generative modelling in accounting for TS symptomatology from the perspective of active inference. We propose a fourfold analysis of sensory, motor, and cognitive phenomena associated with TS. In section 1, we characterise tics as a form of action aimed at sensory attenuation. In section 2, we introduce the notion of epistemic ticcing and describe such behaviour as the search for evidence that there is an agent (i.e., self) at the heart of the generative hierarchy. In section 3, we characterise both epistemic (sensation-free) and non-epistemic (sensational) tics as habitual behaviour. Finally, in section 4 we propose that ticcing behaviour involves an inevitable conflict between distinguishable aspects of selfhood; namely, between the minimal phenomenal sense of self—which is putatively underwritten by interoceptive inference—and the explicit preferences that constitute the agent’s narrative sense of self. In sum, we aim to provide an empirically informed analysis of TS symptomatology under active inference, revealing a continuity between covert and overt features of the condition.

show abstract

“…More precisely, we hold that the propensity to tic within certain contexts serves to resolve ambiguity about the status of the inferred, agentive self by disambiguating the outcomes of self-generated action and worldly events (Clarke, 1996). This crucially involves both information gain about the agent "that I am" and the fulfilment of a supervening pragmatic imperative, which draws me to act so that "I will be able to observe the sensations that I cause"-perhaps the most overt expression of self-evidencing (see e.g., selfstimming behaviour in severe autism (Nwaordu & Charlton, 2023). This need to buttress my belief-about the type of agent that I am-stems from the failure of sensory attenuation outlined above.…”

Section: Section 2: Tics As Epistemic Foragingmentioning

confidence: 99%

“…In fact, we suggest that our four-tiered model may provide explanatory power beyond TS and OCD, especially because it is unclear to what degree tics (or at least tic-like movements) are exclusive to TS. Indeed, certain aspects of our model might be able to generate insights into the neurocognitive processes relevant to the expression of motoric phenomena that resemble tics within both hypoand (especially) hyper-kinesias, including self-stimming in autism spectrum disorder ASD (Nwaordu & Charlton, 2023) but also stimulus utilisation behaviours (Janik et al, 2018), functional tics (Cavanna et al, 2023), and attention deficit hyperactivity disorder (ADHD). For example, in ASD, individuals may produce self-initiated (rhythmic) actions to regulate sensory input (e.g., to ameliorate symptoms of hypersensitivity), otherwise known as selfstimming.…”

Section: Empirical Predictions Limitations and Future Directionsmentioning

confidence: 99%

When the interoceptive and conceptual clash: The case of oppositional phenomenal self-modelling in Tourette syndrome

Parvizi-Wayne,

Severs

2024

Cogn Affect Behav Neurosci

View full text Add to dashboard Cite

Tourette syndrome (TS) has been associated with a rich set of symptoms that are said to be uncomfortable, unwilled, and effortful to manage. Furthermore, tics, the canonical characteristic of TS, are multifaceted, and their onset and maintenance is complex. A formal account that integrates these features of TS symptomatology within a plausible theoretical framework is currently absent from the field. In this paper, we assess the explanatory power of hierarchical generative modelling in accounting for TS symptomatology from the perspective of active inference. We propose a fourfold analysis of sensory, motor, and cognitive phenomena associated with TS. In Section 1, we characterise tics as a form of action aimed at sensory attenuation. In Section 2, we introduce the notion of epistemic ticcing and describe such behaviour as the search for evidence that there is an agent (i.e., self) at the heart of the generative hierarchy. In Section 3, we characterise both epistemic (sensation-free) and nonepistemic (sensational) tics as habitual behaviour. Finally, in Section 4, we propose that ticcing behaviour involves an inevitable conflict between distinguishable aspects of selfhood; namely, between the minimal phenomenal sense of self—which is putatively underwritten by interoceptive inference—and the explicit preferences that constitute the individual’s conceptual sense of self. In sum, we aim to provide an empirically informed analysis of TS symptomatology under active inference, revealing a continuity between covert and overt features of the condition.

show abstract

Repetitive Behaviours in Autistic and Non-Autistic Adults: Associations with Sensory Sensitivity and Impact on Self-Efficacy

Cited by 5 publications

References 34 publications

Acute rapamycin treatment reveals novel mechanisms of behavioral, physiological, and functional dysfunction in a maternal inflammation mouse model of autism and sensory over-responsivity

Acute rapamycin treatment reveals novel mechanisms of behavioral, physiological, and functional dysfunction in a maternal inflammation mouse model of autism and sensory over-responsivity

When the interoceptive and conceptual clash: the case of oppositional phenomenal self-modelling in Tourette Syndrome

When the interoceptive and conceptual clash: The case of oppositional phenomenal self-modelling in Tourette syndrome

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