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.
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.
The research leads us to the idea that excess GAMMA needs a ‘hook’ or ‘handle’ to channel its connecting activity. In autism spectrum conditions (ASC) we see life powered by one interest at any one time. Some see this as obsession, I see this as opportunity. When we climb on board and utilize the facility of ‘interest’ (often an ASC’s individuals passion) we create a link or potential bridge to connection, and, therefore, to understanding. It’s a process, yes, but a journey worth taking. Some see the cup half empty, some see the cup half full, some don’t see the cup at all. To bring the cup into view we need connection. Interest is the common denominator.
That is a good thought to keep in mind. I think that there should be a common ground where we could provide treatment for seizures, hypersensitivities, and affective disorders without necessarily changing his/her pattern of thoughts or abilities.
Thanks Manuel. I’m extremely honoured!
It’s quite weird to see how many of the random ideas we threw out there in that paper seem to have stuck. That said, there are still huge holes in the “temporal binding deficit hypothesis” (if only we’d thought of a catchier name).
I think we over-emphasised the importance of gamma and it now seems more likely that lower frequency oscillations are key for long-distance connectivity. Though I think the findings of atypical gamma in autism are probably very informative about what’s going on at the local level.
We also weren’t really aware of the fact that the same ideas had been mooted in relation to schizophrenia. And still I think there’s a failure in the literature to recognise the fact that “underconnectivity” is not specific to autism.
Finally, the original idea as you note came from thinking about the neural correlates of weak central coherence – and while the neural level account has moved forward, in my view at least the evidence for weak central coherence at the cognitive level is a lot murkier than it was back in the early 2000s. So there’s still a lot of work to do in linking brain oscillations and connectivity back to cognition and behaviour.
Excellent observations. It is interesting that psychological theories, like weak central coherence, behave like moving targets. It is difficult to pin them down. Contradictory findings do not falsify the same but rather make them evolve and expand according to their originator’s whim.
I will come back sometime in the future with MRI data using anthropometrtic indices for corticocortical connectivity. As you said underconnectivity is not a defining characteristic of autistic individuals. Among other, a certain percentage of neurotypicals exhibit the same.
From my standpoint I would also like to add the possibility of using gamma as a severity dependent outcome measurement. Many of the behavioral assessment techniques are adequate screening tools but are otherwise useless for following how well patients are doing over time or after a particular intervention.
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