Mapping the ‘Self’ in the Brain
Written by Brett Weiss
September 2019
What if the synchronous activation of a network of brain regions accounts for each individual’s sense of ‘self?’ Neuroscientists have identified such a network which activates both during ‘mind wandering’ and ‘unconstrained self-referential thought.’ Termed the ‘default mode network,’ this network of brain regions includes midline brain structures like the posterior cingulate cortex (a structure roughly toward the middle of the brain), the medial prefrontal cortex (a frontal region of the brain), and the inferior parietal lobes (two structures roughly on both sides of the brain). Neuroscientists study this network in order to answer ‘big questions’ regarding human self-consciousness. Moreover, studies have linked hyper activity in the ‘default mode network’ to psychopathologies such as depression, anxiety, and addiction. Interestingly, reports indicate that ingestion of psychedelic drugs reduces connectivity in the ‘default mode network’ and reduces network synchronization, which correlates “with a sense of dissolution of the self (Davey et al., 2016; Muthukumaraswamy et al., 2013).” Studies have also suggested that meditation may provide a means to reduce activation and synchronization of the ‘default mode network,’ which may also correlate with some sense of dissolution of the self. In order to explore how overactivity in the ‘default mode network’ may lead to pathology, the following will discuss activation and connectivity of the default mode network in major depressive disorder. A study on the potential changes in ‘default mode network’ activity from meditation will follow in order to illustrate how some people may benefit from this practice to reduce symptoms of brain pathology.
Major depressive disorder associates with self-focused rumination; and since previous research has implicated the ‘default mode network’ in self-referential thought patterns and rumination, interest has arisen to examine the role of the ‘default mode network’ in major depressive disorder. In fact, research has shown that ruminative thought patterns differentiate depressed individuals from never-depressed individuals (Hamilton et al., 2015). A review of studies, a meta-analysis, shows that increased ‘default mode network’ connectivity with the subgenual prefrontal cortex (an area toward the lower front of the brain) distinguishes major depressive disorder patients from healthy individuals (controls). Connectivity between the ‘default mode network’ and this region predicts higher levels of ruminative thought, also (Hamilton et al., 2015). Studies measuring connectivity of the ‘default mode network’ with other brain areas used regional cerebral blood flow as an indicator of synchronous brain activity. Of note, the review of studies showed no overactivity in the ‘default mode network’ alone when comparing major depressive disorder patients with healthy individuals (Hamilton et al., 2015). Hence, the group that performed this review of studies, Hamilton et al. (2015), generated a model to explain the regional cerebral blood flow findings with respect to the ‘default mode network’ and the subgenual prefrontal cortex (region toward the lower front of the brain).
The brain network model arises from studies on the function of the subgenual prefrontal cortex (toward lower front of the brain). In healthy individuals, research has found that elevated activity in this region associates with sad mood elicited through “elaboration of sad autobiographical scripts” (Hamilton et al, 2015). Other studies have shown that increased activity in the subgenual prefrontal cortex (lower frontal region of the brain) associates with feelings of guilt that results from behavior which runs counter to social norms and also associates with social withdrawal. Thus, elevated activity in this region results from peer rejection (Hamilton et al., 2015). Therefore, the increased functional connectivity between the ‘default mode network’ and the subgenual prefrontal cortex (lower frontal region of the brain) may very well represent a neural-level representation of depressive rumination. The increased functional connectivity between the ‘default mode network’ and the subgenual prefrontal cortex (lower frontal region of the brain) would also reflect a functional integration of the properties of the ‘default mode network’ and the subgenual prefrontal cortex (lower frontal region of the brain). Thus, in major depressive disorder, activity of the ‘default mode network’ would represent an egocentric frame of reference that would unite with processes of the subgenual prefrontal cortex (lower frontal region of the brain) to support behavioral withdrawal along with a ruminative and self-focused state of mind (Hamilton et al., 2015). The increased levels of functional connectivity of the ‘default mode network’ and the subgenual prefrontal cortex (lower frontal region of the brain) may serve as a ‘biomarker’ or measurable indicator of the presence of major depressive disorder. Hence, activity and connectivity patterns associated with the ‘default mode network’ facilitate states of brain pathology such as major depressive disorder. Practicing meditation may reduce levels of activity in the ‘default mode network,’ the purported seat of self-referential thought.
Another group, Garrison et al. (2015), performed a major study which explored reduced activity levels in the ‘default mode network’ in people who meditate. The study compared brain activity levels in healthy individuals focused on active cognitive tasks and healthy individuals that used any of three types of meditation. The three types of meditation incorporated in the study follow: focused concentration, loving kindness, and choiceless awareness. The study found that meditation associates with lower activity in regions of the ‘default mode network,’ which activates during self-referential thought. The study also found decreased activity in the ‘default mode networks’ of people who regularly meditate compared to those who do not (Garrison et al., 2015). Since ‘default mode network’ activity is linked to reduced cognitive performance, regular meditation practices may improve cognitive performance (Garrison et al., 2015). Increased ‘default mode network’ activity has also linked to depression, anxiety, and addiction, among other disorders (Garrison et al., 2015). Thus, regular practice of meditation has shown to curb symptoms associated with these illnesses (Garrison et al., 2015). Meditation, which appears to associate with reduced activity in the ‘default mode network’ has shown to improve attention and working memory (short-term memory) performance and to promote positive health outcomes as well (Garrison et al., 2015).
Studies of the ‘default mode network,’ a network of brain regions that interact and synchronize and which gives people a sense of selfhood, may give researchers an idea of how certain brain conditions such as depression, anxiety, and addiction come about. Increased activity in the ‘default mode network’ along with increased functional connectivity of this network with other brain regions associates with disease states such as major depressive disorder. Practicing meditation may alter brain connectivity patterns and reduce ‘default mode network’ activity, which can help allay these disease states of the brain.
References
Davey CG, Pujol J, & Harrison BJ (2016). “Mapping the self in the brain’s default mode network.” Neuroimage. 132: 390–397.
Garrison KA, Zeffiro TA, Scheinost D, Constable RT, & Brewer JA (2015). “Meditation leads to reduced default mode network activity beyond an active task.” Cogn Affect Behav Neurosci. 15(3): 712–720.
Hamilton JP, Farmer M, Fogelman P, & Gotlib IH (2015). “Depressive Rumination, the Default-Mode Network, and the Dark Matter of Clinical Neuroscience.” Biol Psychiatry. 78(4): 224–230.
Muthukumaraswamy SD, Carhart-Harris RL, Moran RJ, Brookes MJ, Williams TM, Errtizoe D, Sessa B, Papadopoulos A, Bolstridge M, Singh KD, Feilding A, Friston KJ, & Nutt DJ (2013). “Broadband cortical desynchronization underlies the human psychedelic state.” J Neurosci. 33: 15171–15183.
