The human brain (and most primates), in all its dizzying glory of 8600000000 neurons, a few billion neuroglia and that one amul milk jingle, can be functionally grouped into 2 classes of anticorrelated networks – The task positive network (for all things cognitive and intentional) and the task negative network (for all things hippie). In the resting brain, this anticorrelation can be interpreted as evidence that the resting brain rhythmically shifts between these two modes of computation. This cycle of anticorrelation may be the brains way of separating competing processes/representations of data and is thought to be foundational in the development of integrative long-term memory.
The Task positive network/Executive Control Network(ECN) spans the vast expanse of the outer cortical grey matter regions like the anterior insula, supplementary motor area, lateral premotor cortex ,anterior middle frontal gyrus, superior parietal lobule/anterior inferior parietal lobule and the lateral inferior posterior temporal gyrus.
The ECN is associated with most voluntary thoughts or actions and serves as the seat for rationality, impulse control, allocentric thought and sensitivity to external stimuli. And more importantly, as an inhibitor of the more dominant Task negative/default mode network (DMN).
The DMN(task negative/auto pilot/emotional mind), primarily mediates a state of conscious but unfocused/non-goal directed processing of data, with a heavy bias towards internal stimuli, self-reflection, egocentric thought and emotional regulation. The mind stays in the default mode unless inhibited by ECN.
A key player between the cycling of DMN and ECN is the Salience network, which represents a group of structures involved in perceiving/consolidating sensory and emotional stimuli and in recruiting either the DMN or ECN to compute and act on the incident data based on its nature. (not doing stuff – DMN, doing stuff – ECN)
The DMN and ECN, along with the Salience Network (SN) are the delicately balanced game of Jenga that define our perception of self, the world around us, and our place in it all.
A deeper look at the DMN –
The DMN can be classified into its constitutive components based on their anatomical locations and the overarching purpose they serve-
Posterior cingulate cortex – Autobiographical thinking, wandering
Medial temporal lobe – retrieving associations and inferences from memories
Orbitofrontal cortex – Reward from sensory stimuli
A broader classification would be to divide the structures into
Anterior group – involved in emotion regulation and sensitivity to internal stimuli
Posterior group – involved in self-referential thought, egocentric behaviour, expectations on self and rumination/wandering of thoughts and memories - mostly negative :(
Although the Amygdala isn’t formally thought of as a part of the default mode network, it shares extensive connectivity with the posterior part of the DMN and is functionally linked to the workings of the DMN in initiating a fear response to internal stimuli and anxiety.
Role of DMN in chronic trauma
Trauma can be defined as a psychological, emotional response to an event or an experience that is deeply distressing or disturbing
In the setting of conditions induced by chronic trauma (PTSD, DV, etc), the Hypothalamo-pituitary-axis is hyperfunctioning, with increased levels of Cortisol, that cause the hippocampus to shrink (emotion regulation) and strengthen the connectivity between the SN, DMN and amygdala. Thereby mapping the self-referential intrusive thoughts polled by the DMN to a physical fear reaction from the amygdala.
This hyperconnectivity between the DMN and amygdala creates a recursive loop that amplifies the fear reaction by repeated negative reinforcement through self-reference and fear response, further strengthening the connection and instilling a sense of powerlessness.
Anxiety and Major Depressive disorder(MDD)
An increase in amygdala and DMN connectivity creates an environment of hyper vigilance and stimulus over-generalization (gross overestimation of risk), which are further amplified by the fear reaction to an unstable internal state.
MDD is characterized by reduced ECN-SEN connectivity and a reduction in the inhibitory effect of the ECN on DMN, along with greater amygdala connections. This creates a state of heightened surveillance of self, hypervigilance to intrusive thoughts and a reduced ability to terminate the loop to focus on external stimuli, as demonstrated by an increased frequency and duration of mind wandering in people with MDD.
A key modality in the treatment of MDD involves dampening norepinephrine, serotonin and dopamine signalling in the DMN
DMN in Alzheimers and other degenerative Tau-pathies
Consistent alterations in connectivity were found in the default mode, salience, and limbic networks in patients with AD dementia, especially between posterior (precuneus and posterior cingulate cortex) and anterior (anterior cingulate cortex and medial prefrontal cortex) regions
AD neurodegeneration interrupts rhythmic cycling between the DMN and ECN and causes discontinuous high frequency firing of the DMN in the early stages and later causes substantial cell loss and cessation of function
Increased DMN activity characteristically presents as paranoia, outbursts, rapid alterations in mood and loss of inhibition.
Further along the course of the disease, lack of function affects episodic memory(hippocampus), emotional dysregulation(hippocampus), incoherence of speech (dominant parietal lobe), loss of empathy (medial prefrontal cortex), hemineglect (non - dominant parietal lobe), impaired interpretation facial expressions, etc
Temporal Lobe Epilepsy
In patients with TLE, the amplitude of the BOLD signal is increased in the mesial temporal lobe, but decreased in the DMN during interictal discharges (periods between seizure episodes)
Patients with TLE have less anterograde connectivity (from the anterior DMN to the posterior DMN) and retrograde connectivity (from the posterior DMN to the anterior DMN) when compared to healthy controls. Especially in the hippocampus, cingulum, medial occipital cortex and left lateral temporal cortex
Parkinson’s Disease
Chronic neurodegenerative movement disorder characterized by loss of dopaminergic neurons in the nigro-striatal pathway of the basal ganglia.
Reduced functional connectivity across DMN regions in PD patients has been observed during both cognitively demanding tasks and when they are at rest. The functional coupling between the DMN and the central executive network (CEN), which consists of the dorsolateral prefrontal cortex and the parietal cortex and has been linked to cognitive functions such as reasoning, attention, inhibition, and working memory, has also been suggested to be impacted by disease-related network disruptions.
The way out
Limiting the reach of the DMN by inhibiting neurotransmitter release in depression, PTSD, chronic pain syndrome, etc
Psychedelics like LSD, MDMA, ecstasy, fivestar and PCP show highly significant results in treating MDD/Anxiety/PTSD by modulating and repurposing the connectome of the DMN.
Cognitive Behavioural Therapy encouraging the use of ECN pathways and weakening of the DMN-amygdala connection
Backward chaining
Hampson M, Driesen N, Roth JK, Gore JC, Constable RT. Functional connectivity between task-positive and task-negative brain areas and its relation to working memory performance. Magn Reson Imaging. 2010 Oct;28(8):1051-7. doi: 10.1016/j.mri.2010.03.021. Epub 2010 Apr 21. PMID: 20409665; PMCID: PMC2936669.
Xu, X., Yuan, H. & Lei, X. Activation and Connectivity within the Default Mode Network Contribute Independently to Future-Oriented Thought. Sci Rep 6, 21001 (2016). https://doi.org/10.1038/srep21001
Daniels JK, Frewen P, McKinnon MC, Lanius RA. Default mode alterations in posttraumatic stress disorder related to early-life trauma: a developmental perspective. J Psychiatry Neurosci. 2011 Jan;36(1):56-9. doi: 10.1503/jpn.100050. PMID: 20964955; PMCID: PMC3004976.
Wackerhagen C, Veer IM, Erk S, Mohnke S, Lett TA, Wüstenberg T, Romanczuk-Seiferth NY, Schwarz K, Schweiger JI, Tost H, Meyer-Lindenberg A, Heinz A, Walter H. Amygdala functional connectivity in major depression - disentangling markers of pathology, risk and resilience. Psychol Med. 2020 Dec;50(16):2740-2750. doi: 10.1017/S0033291719002885. Epub 2019 Oct 22. PMID: 31637983.
van Eimeren T, Monchi O, Ballanger B, Strafella AP. Dysfunction of the default mode network in Parkinson disease: a functional magnetic resonance imaging study. Arch Neurol. 2009 Jul;66(7):877-83. doi: 10.1001/archneurol.2009.97. PMID: 19597090; PMCID: PMC2972248.
Комментарии