nondual awakening and autism...the battle of the "blah, blah" and "tasking" networks..

Q.  Hi Gary,  i study nonduality and have a young son who has been diagnosed with Autism Spectrum Disorder (ASD), particularly for delays in his speaking.  

I saw you on YouTube speaking on using fMRI and EEG to detect the brain activity that leads to Selfing.  (See videos "No Thoughts, No Time - Part I".) Could my son's brain be studied to understand if those tools could give an insight into understanding the source of autism?   I am not sure if this makes sense, but a thought came across that you will be the right person for me to get in touch with on this issue from a perspective on non-duality.  

G.  Great to hear from you.  i have a relative who also may have ASD.

Yijuan Liu
fMRI imaging lab
U of Florida

As far as fMRI and EEG research on autism, there is much  being done in this area.  In most major cities there are facilities specializing in ASD.  In San Diego, there is a program at UC San Diego School of Medicine.  In San Francisco, at UC San Francisco there is the Autism and Neurodevelopment Program.  In the NYC region there is GRASP.  In Chicago, there is the Autism Resource Center.  In Dallas there is the Callier Center for ASD.

Q.  My husband and I have no issues in getting an MRI or EEG done at one of the institutions.  My interest is in studying the images from a non-dualistic perspective on how the child perceives the world vs just a disorder, just as how you studied the Selfing process through images. 

Mingzhou Ding
U of Florida

G.  As the Universe would have it, there is a excellent new paper in the Journal of Neuroscience, "Top-Down Regulation of Default Model Activity in Spatial Visual Attention", by Xiaotong Wen, Yijun Liu, Li Yao,and Mingzhou Ding from the Univ of Florida, Peking University, Beijing Normal University and Univ of Florida, respectively, which gives some new understanding on how the default mode network (DMN), the "selfing network", operates and how that might pertain to ASD, and other attention-deficit disorders.    

As discussed in earlier blogs ("What is the Default Mode Network?..."), there are two major networks, a) the "task positive, or task control network" (TCN) which initiates and maintains task level control, selects motor responses to stimuli, and suppresses irrelevant distracting information, and b) the default mode network (DMN) which is responsible for our sense of "self and other" and "self in time" (Is "time" all in the mind?...), self-reflection and related emotions and is the core of the "blah, blah" self-referential narrative.  

The DMN typically is activated when folk are not doing a task.  Deenergizing the DMN with either long-term meditation or with psychedelics (esp. psilocybin) has been demonstrated in studies in leading journals to produce the classical mystical experiences of "all is One" and living "now, now, now".  (See "Persistent meditative states - how? psychedelics - how?...", "Seeing everything as 'One'?  What is 'mystical'? What is really 'real'?...", and "the latest psychedelic research...").

Long Term Meditators Shut Down PCC
and Activate ACC and LPFC
Even When NOT Meditating 

The work of Brewer, et al. @ Yale (See "Folk Who Meditate Decrease Mind Wandering") in which i have been a subject and collaborator, showed that the DMN could be deactivated in long term meditators, whether they were meditating or not, which is my experience.  

Brewer, et al. also found that the anterior cingulate cortex (ACC) and the lateral prefrontal cortex (LPFC) shown @ left, were apparently "up activated" in long term meditators when the DMN was shut down, apparently as a "monitoring and control" network.  However, Brewer et al. showed only a correlation, not causation between these two regions and their presumed linkage/effect.  The old adage is that "correlation does not prove causation", i.e. things can happen at the same time but may be unrelated.

The current Wen, et al., paper described above moves that correlation into causation.  These scientists used fMRI and biostatistical methods, particularly the Granger causality technique, in their work.  The Granger technique makes it possible to examine how one variable affects another variable, in this case, how the TCN and DMN might influence each other by looking at the different directions of their interactions and their impacts.  

As one of the authors, Ding, said, "We knew that the default mode network decreases in activity when a task is being performed, but we didn’t know why or how.  We also wanted to know what is driving that activity decrease.  For a long time, the questions we are asking could not be answered.”

TCN
cross slice

DMN
longitudinal slice

In Wen, et al., the TCN was represented by the dorsal anterior cingulate cortex (dACC) and the left and right anterior insula (AI).  The DMN was represented by the posterior cingulate cortex (PCC), ventral and dorsal medial prefrontal cortex (MPFC), and (not shown) left and right inferior parietal lobe (IPL), and lateral temporal cortex; the main focus was on the PCC and MPFC.

This study examined the fMRI scans of folk who were performing a visual task requiring concentration, and when they were not.  They then looked at how successful they were in performing that task and how that correlated to what regions of the brain were active.  

Increased accuracy and response
when TCN suppresses DMN

“People have hypothesized different functions for signals going in different directions,” Ding says. “We show that when the task control network (TCN) suppresses the default mode network (DMN), the person can do the task better and faster. The better the default mode network (DMN) is shut down, the better a person performs.”

Decreased accuracy and response
when DMN interferes w/TCN

The study also showed that when the DMN is not sufficiently suppressed, it distracts and interferes with the TCN by sending it signals; this causes performance to drop.  This demonstrates that, as Ding says, "Your brain is a constant seesaw back and forth.” 

The Granger causality technique is helping researchers understand how neurological disorders operate.  The DMN has been found to remain unchanged in folk with autism spectrum disorders (ASDs) whether they are performing a task or not, which as we have seen, is not how it operates in most folk.  These confusing signals from the DMN to the TCN , as shown above in the graph above, could explain symptoms such as difficulty reading social cues or being easily overwhelmed by sensory stimulation. Similar findings have been observed with depression and mild cognitive impairment.

Behavior enhancing and
Behavior degrading actions

The Granger causality technique may be useful in unravelling many causative linkages between brain centers, in everything from meditation and  psychedelics to how different psychopathologies manifest, develop and operate.

This work makes clearer what may be happening with longer meditation times as the DMN is "shut down" and maintained that way with a "monitoring and control" network while a new network comprised of an expanded version of this paper's TCN is stabilized and maintained as the "new normal" replacement, default operating system.  

It does appear, IME, that with increased numbers and duration of events of the "new normal" state, i.e. stillness and "now, now, now" replacing confusion, anxiety and suffering, that the brain, which "prefers" this "new normal", is able to refine and improve the replacement network.  This new network/operating system becomes less "noisy", more stable, and natural in the sense that it doesn't require a "doer" w/a technique to keep it "in place".  The "new normal" operating system has as a key feature the persistent loss of the self-referential narrative, and w/it, the loss of self-referential fears and desires.