This blog is a continuation of my previous one: “How do we put our thoughts together?”. It is meant to emphasize the importance of gamma oscillation abnormalities in autism. The idea was probably initiated by Brock (2002) who suggested that the different brain regions of autistic individuals worked well as single entities but did not worked equally well when integrating together the functions of disparate brain regions. This neural explanation offered a pathological correlate to the weak central coherence idea of autism previously proposed by Frith. Visual and auditory perception anomalies as well as some features of language processing and social communication deficits, and executive dysfunctions associated with “weak central coherence” in autism may be attributed to reduced gamma-frequency synchronization and decreased temporal binding of activity between networks processing local features. Some of the information given below is taken out of 3 chapters that I wrote for an upcoming book to be published by Springer (2013) entitled “Imaging the Brain in Autism” (Casanova et al., 2013).
Electroencephalography (EEG) has been used to decompose oscillatory patterns into several frequency bands: delta (0.5 Hz–4 Hz), theta (4 Hz–8 Hz), alpha (8 Hz–13 Hz), beta (13 Hz–30 Hz), and gamma (30 Hz–80 Hz), each of which operates over various spatiotemporal scales to control cortical activity. Different mental states and cognitive functions have been presumably ascribed to each of these brain frequencies. Brain oscillations in the gamma frequency range are closely associated with sensory processing, working memory, attention and many other cognitive domains. The brain’s limited long-range wiring cannot directly sustain coordinated activity across arbitrary cortical locations, but it can convey patterns of synchronous activity as oscillatory neuronal fluxes, represented by local field potentials measured by EEG. Coordination of oscillations at varying interacting frequencies allows for relatively efficient and unconstrained segregation in varying forms and across hierarchical cortical levels. Disrupted patterns of coordinated oscillatory output in distributed minicolumnar networks might be associated with cortical “disconnection” in autism. More specifically, altered oscillatory activity in developing cortical circuits may contribute to impaired development of intra-areal and transcortical connections giving rise to a bias in short (e.g. arcuate) vs. long corticortical projections (e.g., commisural fibers). The pervasive nature of abnormalities ingrained in this oscillatory activity bears significant analogy to the cognitive deficits observed in autism. It is therefore unsurprising that gamma oscillations have been claimed to be directly related to the pathophysiology of autism. To my knowledge every study on gamma frequencies in autism has been abnormal.
It has been proposed that “weak central coherence” in autism could result from a reduction in the integration of specialized local networks in the brain caused by a deficit in temporal binding (Brock et al. 2002). Audio-visual perception anomalies associated with weak central coherence may be attributed to a reduction in synchronization of gamma activity between networks processing local features and can explain some of the features of language deficits, executive dysfunctions, and other impairments in social communication in autism. Excessive but not synchronized gamma can be linked to a reduction in the ability to focus attention. In autism, uninhibited gamma activity suggests that none of the circuits in the brain can come to dominance because too many of them are active simultaneously. A proposed “temporal binding deficit” hypothesis of autism suggests that many features of autism, such as superiority in processing of detail (local processing) and disadvantage in global processing, necessitating integration of information either over space, time, or context can be explained by a failure of binding between cortical areas. Abnormal gamma activation would suggest disrupted neural signaling and would support the hypothesis of abnormal regional activation patterns.
References
Brock J, Brown CC, Boucher J, Rippon G. The temporal binding deficit hypothesis of autism. Development and Psychopathology 14:209-224, 2002.
Casanova MF, Baruth J, El-Baz AS, Sokhadze GE, Hensley M, Sokhadze EM. Evoked and induced gamma frequency oscillations in autism. In Casanova MF(ed) Imaging the Brain in Autism, Springer, 2013, in press.