Abstract: The core scientific question addressed in this paper is: Through what mechanism do deficits in multisensory temporal integration in individuals with autism spectrum disorder (ASD) link low-level perceptual anomalies to high-level social dysfunction? To address this question, we propose a neurophysiological-cognitive-behavioral cascade model that delineates the causal pathway from biological disturbances to temporal processing deficits and, ultimately, to social interaction impairments. Based on this model, we derive mechanism-guided intervention principles. The main innovative contributions are as follows:
1. Establishing multisensory temporal integration as a mechanistic hub. Rather than merely cataloguing perceptual and social findings separately, this paper explicitly identifies dysfunction in multisensory temporal integration—specifically, a widened temporal binding window (TBW), impaired dynamic temporal coordination (unstable simultaneity judgments, increased sensorimotor asynchrony and variability), and disrupted integration of dynamic social cues (audiovisual speech, bodily synchrony)—as the critical mechanistic hub linking basic perception to complex social behavior.
2. Proposing a neurophysiological-cognitive-behavioral cascade model. Individuals with ASD exhibit atypical cross-sensory response patterns early in life (hyporesponsiveness, hyperresponsiveness, sensory seeking), which constitute the initial starting point of the cascade and directly affect the precision and stability of their perception of the world.
At the neurophysiological level, successful temporal alignment requires precise neural “alignment” of cross-modal signals. ASD is characterized by: (a) autonomic nervous system dysregulation (reduced heart rate variability, atypical electrodermal responses), which compromises the physiological baseline for processing dynamic temporal information; (b) neurotransmitter imbalances (dopamine, melatonin, oxytocin), which affect the perception and judgment of temporal rhythms; and (c) neural activation and connectivity deficits—reduced activation in the temporoparietal junction, inferior frontal gyrus, and superior temporal sulcus, coupled with diminished interregional functional connectivity, particularly reduced gamma-band (30-80 Hz) oscillatory synchrony critical for temporal binding. Together, these abnormalities constitute the biological foundation of temporal integration deficits.
At the cognitive level, neurophysiological anomalies are further mediated and amplified by cognitive processing. First, predictive coding impairments—characterized by “weak priors” and maladaptive precision weighting of prediction errors—prevent individuals with ASD from generating and updating precise internal models to predict upcoming sensory input. Second, atypical attention patterns (reduced social orienting, inappropriate attentional allocation) make it difficult for them to selectively bind temporally relevant information within a multisensory stream. These two mechanisms interact bidirectionally and, over the course of development, further impede neurophysiological maturation.
At the behavioral level, the convergence of neurophysiological and cognitive abnormalities produces three core features: (a) a widened TBW—an abnormally long temporal window for judging simultaneity, reflecting “blurriness” in the perception of temporal synchrony; (b) dynamic temporal coordination deficits—increased asynchrony and higher variability in sensorimotor synchronization tasks (e.g., finger-tapping to a beat), revealing instability in temporal perception and internal timing; and (c) impaired integration of social cues—difficulty integrating multisensory social signals (e.g., voice-lip movement, facial expression-prosody), leading to deficits in turn-taking, joint attention, and empathic responding.
Importantly, these behavioral deficits are modulated by task context (e.g., complexity, social relevance) and produce distal cascading effects: they directly impair the synchronous integration of social cues, erode episodic memory and social associative learning, and ultimately constitute a significant perceptual foundation of core social communication deficits in ASD. The model also highlights a negative feedback loop, whereby behavioral and cognitive difficulties further exacerbate neurophysiological dysregulation.
3.Intervention principles grounded in core deficits. Sensory integration therapy, by providing structured rhythmic vestibular, proprioceptive, and tactile inputs, optimizes arousal levels and neural synchronization, potentially narrowing the TBW and enhancing multisensory integration efficiency. Rhythm-based interpersonal synchrony interventions (e.g., joint drumming, coordinated movement games), by providing rhythmic cues, directly train temporal prediction and online error correction, strengthen internal timing models, and promote functional connectivity within sensorimotor and social brain networks. Theoretically, a combined approach that integrates low-level sensory regulation with high-level temporal prediction training may form a precise intervention pathway from basic perception to social coordination.
This paper offers a novel problem-solving framework that reframes social deficits in ASD as arising from fundamental abnormalities in multisensory temporal integration. By specifying a neurophysiological-cognitive-behavioral cascade and deriving testable, targeted intervention principles, it provides a more precise and dynamic theoretical perspective for understanding social interaction difficulties in autism and for developing precision interventions. Future research should employ rigorous randomized controlled trials that directly measure TBW and gamma-band synchrony to establish causal evidence for the effects of these interventions on improving temporal integration and social function.

Key words: autism spectrum disorder, multisensory temporal integration, temporal binding window, temporal synchrony, interpersonal synchrony