Basal ganglia and autism – a translational perspective

Subramanian, Krishna; Brandenburg, Cheryl; Orsati, Fernanda Tebexreni; Soghomonian, Jean‐Jacques; Hussman, John P.; Blatt, Gene J.

doi:10.1002/aur.1837

Cited by 68 publications

(51 citation statements)

References 204 publications

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“…Multiple motor control mechanisms used to maintain stability and initiate movements have been implicated in ASD, including sensory feedback, motor coordination, and feedforward processes. In order to ensure precision and minimize variability during ongoing motor behaviors (e.g., maintaining a steady posture during standing), sensory feedback inputs are used to continuously adjust behavioral output [10][11][12][13][14]. Control of continuous motor behaviors also involves the coordination of distinct joint movements [10].…”

Section: Introductionmentioning

confidence: 99%

Postural control processes during standing and step initiation in autism spectrum disorder

Bojanek

Wang

White

et al. 2020

J Neurodevelop Disord

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Background: Individuals with autism spectrum disorder (ASD) show a reduced ability to maintain postural stability, though motor control mechanisms contributing to these issues and the extent to which they are associated with other gross motor activities (e.g., stepping) are not yet known. Methods: Seventeen individuals with ASD and 20 typically developing (TD) controls (ages 6-19 years) completed three tests of postural control during standing. During the neutral stance, individuals stood with their feet shoulder width apart. During the Romberg one stance, they stood with feet close together. During the circular sway, participants stood with feet shoulder width apart and swayed in a circular motion. The standard deviation (SD) of their center of pressure (COP) in the mediolateral (ML) and anteroposterior (AP) directions and the COP trajectory length were examined for each stance. We also assessed mutual information (MI), or the shared dependencies between COP in the ML and AP directions. Participants also completed a stepping task in which they stepped forward from one force platform to an adjacent platform. The amplitude and duration of anticipatory postural adjustments (APAs) were examined, as were the maximum lateral sway, duration, and velocity of COP adjustments following the initial step. We examined stepping variables using separate one-way ANCOVAs with height as a covariate. The relationships between postural control and stepping measures and ASD symptom severity were assessed using Spearman correlations with scores on the Autism Diagnostic Observation Schedule-Second Edition (ADOS-2) and the Autism Diagnostic Interview-Revised (ADI-R). Results: Individuals with ASD showed increased COP trajectory length across stance conditions (p = 0.05) and reduced MI during circular sway relative to TD controls (p = 0.02). During stepping, groups did not differ on APA amplitude (p = 0.97) or duration (p = 0.41), but during their initial step, individuals with ASD showed reduced ML sway (p = 0.06), reduced body transfer duration (p < 0.01), and increased body transfer velocity (p = 0.02) compared to controls. Greater neutral stance COP ML variability (r = 0.55, p = 0.02) and decreased lateral sway (r = − 0.55, p = 0.02) when stepping were associated with more severe restricted and repetitive behaviors in participants with ASD. Conclusions: We found that individuals with ASD showed reduced MI during circular sway suggesting a reduced ability to effectively coordinate joint movements during dynamic postural adjustments. Additionally, individuals with ASD showed reduced lateral sway when stepping indicating that motor rigidity may interfere with balance and gait. Postural control and stepping deficits were related to repetitive behaviors in individuals with ASD indicating that motor rigidity and key clinical issues in ASD may represent overlapping pathological processes.

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Section: Introductionmentioning

confidence: 99%

Postural control processes during standing and step initiation in autism spectrum disorder

Bojanek

Wang

White

et al. 2020

J Neurodevelop Disord

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“…But, during development activity in many regions is likely to be influenced by any deficit, making it unlikely that a developmental atypicality will be consistently associated with one specific brain structure. Indeed, both the basal ganglia and the cerebellum display functional and anatomical abnormalities in autism spectrum disorders (Gowen & Miall, 2005;Fatemi et al, 2012;Subramanian et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Impaired online error-correction disrupts synchronization to external events in autism

Vishne¹,

Jacoby

Malinovitch³

et al. 2020

Preprint

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Autism is a developmental disorder characterized by impaired social skills and accompanied by motor and perceptual atypicalities. Its etiology is an open question, partly due to the diverse range of associated difficulties. Based on recent observations that individuals with autism are slow in updating perceptual priors, we now hypothesized that motor updating is also slow. Slow motor updating is expected to hamper the ability to synchronize to external events, since asynchronies are corrected sluggishly. Since sensorimotor synchronization is important for social bonding and cooperation, its impairment is expected to impair social skills. To test this hypothesis, we measured paced finger tapping to a metronome in neurotypical, ASD, and dyslexia groups. Dyslexia was assessed as a control group with a non-social neurodevelopmental atypicality. Only the ASD group showed reduced sensorimotor synchronization. Trial-by-trial computational modelling revealed that their ability to form controlled motor responses and to maintain reliable temporal representations was adequate. Only their rate of error-correction was slow and was correlated with the severity of their social difficulties. Taken together, these findings suggest that slow updating in autism contributes to both sloppy sensorimotor performance and difficulties in forming social bonds.SignificanceThe prevalence of autism diagnosis has increased immensely is the last decades. Yet its etiology remains a challenge, partly since the functional relations between characteristic social difficulties, perceptual and motor atypicalities are not understood. Using trial-by-trial computational modelling, we show that a single deficit underlies the poor synchronization of individuals with autism in both static and changing environments. Slow updating, leading to slow online error correction of motor plans, has an immense explanatory power explaining both difficulties in sensorimotor synchronization, and social impairments.

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“…The complex inhibitory structure of the basal ganglia may be altered in autism since inhibitory neurons are often impaired in ASD. Indeed, volumetric changes and alterations in cell densities in the basal ganglia nuclei have been found in autism; see, e.g., (Subramanian et al, 2017) and the references therein. In autism, the basal ganglia operate differently; the sizes of the substructures, e.g., the putamen, caudate nucleus, globus pallidus can change, and the information flow between these units and to and from the neocortex also changes.…”

Section: Potential Side Effects Of Impairments Of Component Formationmentioning

confidence: 99%

“…In autism, the basal ganglia operate differently; the sizes of the substructures, e.g., the putamen, caudate nucleus, globus pallidus can change, and the information flow between these units and to and from the neocortex also changes. According to suggestions in the literature reviewed by Subramanian et al, (2017), repetitive behavior is related to these structures. We believe that a restricted motor repertoire and stereotypic behaviors may also originate from impaired component formation.…”

Section: Potential Side Effects Of Impairments Of Component Formationmentioning

confidence: 99%

Colors of Autism Spectrum: A Single Paradigm Explains the Heterogeneity in Autism Spectrum Disorder

Lörincz¹

2018

Preprint

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We propose a theory of ASD as a condition of comorbid cognitive impairments that corrupt the learning, encoding, and manipulation of episodic and semantic memories. We consider (i) episodic and semantic memory functions of the entorhinal-hippocampal complex, (ii) constraints on the transfer and encoding of these memory components into neocortical areas, and (iii) the demands of cognitively manipulating memories in distributed computations being necessary for goaloriented interactions. In ASD, learning and cognitive challenges manifest in diverse ways but especially in high-complexity-model predictive control tasks with latent variables. ASD impairments in social interactions represent a prototypical example. Social interactions are at the high end of complexity and require processes (i) -(iii) to work in a concerted fashion due to the need for the learning and estimation of many, sometimes latent, parameters, including emotions, intention, physical and mental capabilities as well as the predictive modeling of these parameters for decision making and timed-action series. We put forth the idea that autism is a result of an arbitrary combination of otherwise not prominent corruptions in processes (i)-(iii). Together, these corruptions may severely impair intelligence and slow down learning, especially in highcomplexity learning tasks. Over time, slow learning may spare the spontaneous learning-by-doing method -namely, repetitive behavioral patterns, whereas behavioral failures related to complex tasks can restrict interest in such task, thus inducing a fear of novelty; conversely, the fear of novelty restricts interest and can slow learning down. We embed our thoughts into a predictive autoencoding, goal-oriented model of a deterministic world. We compare this model to others, such as the noisy brain model, the Bayesian prior theory, the mirror neuron theory and the weak central coherence theory. We argue that the predictive autoencoder model of the deterministic world harmonizes with these other models and embraces them in a straightforward way. AUTHOR SUMMARYThe core of our arguments is based on the autoencoder model of the entorhinal-hippocampal complex and its role in forming declarative memories. We argue that social behavior and language usage are highly complex cognitive tasks involving the encoding, learning, and manipulation of declarative memories with latent variables. All these processes can be corrupted in many ways. Corruptions may manifest as epilepsy, schizophrenia, attention deficit, and depression, among other disorders. However, if these symptoms are weak but co-occur, then the most strongly affected behavioral feature is the ability to solve complex cognitive tasks. This condition can be brought about by diverse combinations of impairments that sum up in corrupted social behavior the most.

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Basal ganglia and autism – a translational perspective

Cited by 68 publications

References 204 publications

Postural control processes during standing and step initiation in autism spectrum disorder

Postural control processes during standing and step initiation in autism spectrum disorder

Impaired online error-correction disrupts synchronization to external events in autism

Colors of Autism Spectrum: A Single Paradigm Explains the Heterogeneity in Autism Spectrum Disorder

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Basal ganglia and autism – a translational perspective

Cited by 68 publications

References 204 publications

Postural control processes during standing and step initiation in autism spectrum disorder

Postural control processes during standing and step initiation in autism spectrum disorder

Impaired online error-correction disrupts synchronization to external events in autism

Colors of Autism Spectrum: A Single Paradigm Explains the Heterogeneity&nbsp;in Autism Spectrum Disorder

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Colors of Autism Spectrum: A Single Paradigm Explains the Heterogeneity in Autism Spectrum Disorder