Default Mode Network is a network of interacting brain regions known to have activity highly correlated with each other and distinct from other networks in the brain. The existence of a default mode network (DMN) in the brain is well established. Converging evidence suggests a fundamental role for the default mode network (DMN) in the working of the brain; however its function remains controversial.
Post-stroke depression (PSD) is the severe emotional and expressive disorder following stroke, affecting one-third of all stroke survivors. Depression is associated with reduced temporary recovery and long-lasting rehabilitation outcomes, extra incapacity, cognitive deficiency, and mortality in stroke fightors. The neuroanatomical model of PSD remains vague despite decade’s research. A new model recommends that grey and white matter lesions/ischemia in PSD disturbs the brain’s affective regulation network, leading to hyperactivation of the limbic system and following depressive symptoms.
The default mode network (DMN) is such a network that contains brain regions evolving in emotion regulation: ventromedial prefrontal cortex, ventral anterior cingulate cortex, the posterior cingulate, precuneus, inferior lateral parietal lobes, and parts of the temporal lobe. These brain regions present synchronic activation when the individual is in a state of wakeful rest and deactivation when observant to the external world. Thus the temporal correlation between the BOLD signal in DMN brain regions (measured by functional connectivity magnetic resonance imaging, FCMRI) at rest is thought to reflect important interrelationships among their structures with related functions.
The DMN theory of depression is proposed by Northoff et al. in 2011. According to the theory, depressive phenomenology is associated with specific subcortico-cortical systems, and neural hyperactivity during rest is one of the endophenotype for unipolar mood disorder.
Many evidences support this theory. For instance, abnormal resting DMN FC contributes to the patho-physiology of mid-life and late life depression. Increased FC in anterior regions but reduced FC in posterior regions of the DMN has been found in mid-life depression. DMN hyperactivity is related to various depressive symptoms and psychopathology, including negative rumination, over general autobiographical memory, negativity bias, sustained negative mood, and hopelessness.
FC abnormalities happen in stroke. Local structural damage due to stroke can result in dysfunction in remote regions connected to the lesion. It is plausible that grey and white matter lesions/ischemia in PSD disrupts the brain mechanisms of affective regulation, thus leading to limbic hyper activation and subsequent depressive symptoms. In fact, in one study, yet so far, DMN FC at 10-days post-stroke has been associated with depressive symptoms in 24 stroke survivors at 3-month follow up.
PSD is a complex disorder, and a host of imaging and non-imaging factors contribute to its development. This may partly account for the contrary findings yielding by substantial studies about the relationship between lesion location and PSD. The study on DMN FC have shed light on underlie neuroanatomical mechanisms of PSD. Study on brain network functional connectivity including DMN FC in PSD is in incipient stage and plenty of work is needed to clarify the role of brain functional connectivity in development, treatment response and outcome of PSD.