MEG revealed new functional hub of atypical brain network in autism spectrum disorders
Autism spectrum disorders (ASD) are neurodevelopmental disorders with continuous disturbance of cognitive flexibility and social communication, restricted, repetitive patterns of interests and behavior (O'Connor, 2012; Schelinski et al. 2016) Emerging evidence has been almost proving the idea that ASD is a condition of altered brain functional connectivity, especially in resting state. Previous brain connectivity studies using functional magnetic resonance imaging (fMRI) in young adults with ASD showed reduction of resting state connectivity at the medial prefrontal cortex (mPFC) the anterior hub of the default mode network (DMN) and the posterior cingulate cortex (PCC) the posterior hub of the DMN (Kennedy and Courchesne, 2008; Di Martino et al. 2009) Electroencephalography (EEG) and magnetoencephalography (MEG) resting state connectivity studies have demonstrated decreased long range connectivity, such as in fronto occipital connections, and increased short range connectivity affecting lateralfrontal connections, which correlated with ASD symptom severity (Barttfeld et al. 2011; Kikuchi et al. 2015) It has been repeatedly suggested that ASD might have some atypical networks with enhanced local connections of short range networks and lack typical central nodes and hubs and a more modular structure of long range networks (Barttfeld et al. 2011) ASD are also characterized by abnormalities in various aspects of language functions, varying from semantic or/and pragmatic deficits to the absence of speech. Although many previous structural and functional imaging studies, using MRI, EEG or MEG, have tried to reveal its pathophysiology, it remains unclear which surface based morphometry parameters or physiological activities are most closely associated with altered brain language networks in ASD (Matsuzaki et al. 2012; Kikuchi et al. 2013, 2015; Xiang et al. 2016; Takahashi et al. 2017) This might be attributed to the experimental designs of those studies, focusing on the anatomical localization rather than on the functional connectivity, or on the resting state activity but not on evoked responses, or on the primary evoked response to pure tone stimuli but not on the higher cognitive response to real voice stimuli. A very few researchers have challenged this by using real spoken language stimuli in patients with ASD and suggested an association between poor language scores and atypical left hemisphere brain responses (Yau et al. 2016) and the lower synchronization between the right and left hemispheres (Kurita et al. 2016) but these results were still not fully consistent to each other. In this issue of Clinical Neurophysiology, Tanigawa et al. (2018) assessed the language abilities of adolescents with ASD and typically developing (TD) adolescents, analyzed the surface based morphometric structure between the groups using MRI, measured cortical responses to an auditory word comprehension task with MEG, and performed network based statistics using the phase locking value (PLV) Although they observed no structural differences between the groups in MRI, they found a significant correlation between the volume of the left ventral central sulcus (vCS) and linguistic scores in ASD. With respect to PLV, they found a weaker cortical activation in the left vCS and superior temporal sulcus (STS) in ASD, which showed differential correlations with linguistic scores between the groups. Moreover, the ASD group had an atypical gamma band (25 40 Hz) network centered on the left vCS. They concluded that adolescents with ASD showed atypical responses on the auditory word comprehension task and functional brain differences. Their data provide new evidence that atypical activity in the left vCS and gamma band network activity play an important role in the pathophysiology of impaired auditory language processing in adolescents with ASD. By applying multimodal analysis which combined MRI to detect surface based morphometry abnormalities, and MEG PLV to visualize the electrophysiological characteristics during the auditory language task, as opposed to pure tones or single vowels, Tanigawa et al. (2018) succeeded to elucidate vCS as a possible functional hub of atypical brain network of auditory language processing in adolescents with ASD, not found among the TD control subjects. We can speculate that this newly discovered functional hub centered at vCS might be one of the enhanced local connections of atypical networks also found by Barttfeld et al. (2011) in ASD. It would be prudent not to call this new atypical functional hub an abnormal network. Instead, this hub and network activity, observed only in ASD, could be interpreted as a compensation of absence of central nodes and hubs and a more modular structure of long range networks in ASD. Of course, these findings need to be verified by large scale studies with a longitudinal design in multiple languages to clarify the mechanisms underlying impaired comprehensive auditory language processing in ASD. Further
Clinical Neurophysiology