Sensory Perception Deficits and Cortical Coherence in Children with Autism: A Study of the ‘Noisy Cortex’ Hypothesis
Autism is a behaviorally diagnosed disorder with defining impairments in socialization, interests, and communication abilities. Autism is also characterized by deficits in processing of simple visual and auditory information such as loudness discrimination or perception of moving dots, as well as complex visual and auditory information such as faces and language. Additionally, there is evidence of abnormal tactile sensitivity in autism. These functional findings are complemented by anatomical ones, the most robust of which is that the brains are large. Other neuroanatomical findings include neuroinflammation, and disrupted inhibitory circuitry. To date, no robust models have been formulated for either the neurobiological origin of the observed abnormalities, or the relationship between the pervasive anatomic abnormalities and the neural systems dysfunctions which are characteristic of autism. Furthermore, while the observed anatomical pathologies are distributed rather than localized, the vast majority of functional studies focus on localized features. The main objective of this project was to test the model that the neural substrates underlying the functional deficits of autism at the cortical level stem from a noisy cortex which has a poor signal to noise ratio. To this end, Dr. Kenet employed magnetoencephalograpy (MEG) to record functional activation in response to sensory stimuli in children with autism and age matched controls. The central hypotheses were: (1) that the cortex of individuals with autism is inherently and internally a “noisy” cortex, i.e. a cortex with a low signal to noise ratio; (2) that the “noisiness” of the cortex is widely distributed rather than localized, resulting in widespread functional abnormalities; and (3) that from this distributed “noisy” cortex emanates a network in which connectivity is disrupted, with ensuing functional abnormalities that include widespread perceptual deficits, and alterations in neural circuitry that may drive higher order cognitive and social impairments emanating at least in part from abnormal network properties.
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