Sensorimotor abnormalities are common in autism spectrum disorder (ASD) and among the earliest manifestations of the disorder. They have been studied far less than the social-communication and cognitive deficits that define ASD, but a mechanistic understanding of sensorimotor abnormalities in ASD may provide key insights into the neural underpinnings of the disorder. In this human study, we examined rapid, precision grip force contractions to determine whether feedforward mechanisms supporting initial motor output before sensory feedback can be processed are disrupted in ASD. Sustained force contractions also were examined to determine whether reactive adjustments to ongoing motor behavior based on visual feedback are altered. Sustained force was studied across multiple force levels and visual gains to assess motor and visuomotor mechanisms, respectively. Primary force contractions of individuals with ASD showed greater peak rate of force increases and large transient overshoots. Individuals with ASD also showed increased sustained force variability that scaled with force level and was more severe when visual gain was highly amplified or highly degraded. When sustaining a constant force level, their reactive adjustments were more periodic than controls, and they showed increased reliance on slower feedback mechanisms. Feedforward and feedback mechanism alterations each were associated with more severe social-communication impairments in ASD. These findings implicate anterior cerebellar circuits involved in feedforward motor control and posterior cerebellar circuits involved in transforming visual feedback into precise motor adjustments in ASD.

The purpose of this study was to consider the effects of valence, motoric direction (i.e., approach/withdrawal), and arousal on the perception of facial emotion in patients with unilateral cortical lesions. We also examined the influence of lesion side, site, and size on emotional perception. Subjects were 30 right-hemisphere-damaged (RHD) and 30 left-hemisphere-damaged (LHD) male patients with focal lesions restricted primarily to the frontal, temporal, or parietal lobe. Patient groups were comparable on demographic and clinical neurological variables. Subjects were tested for their ability to match photographs of four facial emotional expressions: happiness, sadness, fear, and anger. Overall, RHD patients were significantly more impaired than LHD patients in perceiving facial emotion. Lesion side, but not site, was associated with motoric direction and valence dimensions. RHD patients had specific deficits relative to LHD patients in processing negative and withdrawal emotions; there were no group differences for positive/approach emotions. Lesion size was not significantly correlated with accuracy of emotional perception.

Sensorimotor abnormalities are common in individuals with autism spectrum disorder (ASD); however, the processes underlying these deficits remain unclear. This study examined force production with and without visual feedback to determine if individuals with ASD can utilize internal representations to guide sustained force. Individuals with ASD showed a faster rate of force decay in the absence of visual feedback. Comparison of force output and tests of social and verbal abilities demonstrated a link between motor memory impairment and social and verbal deficits in individuals with ASD. This finding suggests that deficits in storage or retrieval of motor memories contribute to sensorimotor deficits and implicates frontoparietal networks involved in short-term consolidation of action dynamics used to optimize ongoing motor output.

Focal brain-damaged patients (left hemisphere damage, right hemisphere damage) and hospitalized general medical patients were asked to sort test photographs into target expressions of four facial emotions, happy, sad, fear and anger. In a second task, patients were asked to match neutral photographs with these target emotion expressions in a forced-choice format. Patients were also asked to rate their mood state on a two-dimensional affect grid. Right hemisphere-damaged patients were significantly inaccurate in matching the test-target expressions of facial emotions in comparison to left hemisphere-damaged or general medical patients. Analysis of error scores indicated a bias toward negative emotions by left hemisphere-damaged patients. Congruent to their mood state, left hemisphere-damaged patients also attributed "sadness" on neutral state of expression significantly more often than in right hemisphere-damaged patients.

Force control deficits have been repeatedly documented in autism spectrum disorder (ASD). They are associated with worse social and daily living skill impairments in patients suggesting that developing a more mechanistic understanding of the central and peripheral processes that cause them may help guide the development of treatments that improve multiple outcomes in ASD. The neuromuscular mechanisms underlying force control deficits are not yet understood. Seventeen individuals with ASD and 14 matched healthy controls completed an isometric index finger abduction test at 60% of their maximum voluntary contraction (MVC) during recording of the first dorsal interosseous (FDI) muscle to determine the neuromuscular processes associated with sustained force variability. Central modulation of the motorneuron pool activation of the FDI muscle was evaluated at delta (0–4 Hz), alpha (4–10 Hz), beta (10–35 Hz) and gamma (35–60 Hz) frequency bands. ASD patients showed greater force variability than controls when attempting to maintain a constant force. Relative to controls, patients also showed increased central modulation of the motorneuron pool at beta and gamma bands. For controls, reduced force variability was associated with reduced delta frequency modulation of the motorneuron pool activity of the FDI muscle and increased modulation at beta and gamma bands. In contrast, delta, beta, and gamma frequency oscillations were not associated with force variability in ASD. These findings suggest that alterations of central mechanisms that control motorneuron pool firing may underlie the common and often impairing symptoms of ASD.