The salience network (SN), also known anatomically as the midcingulo-insular network (M-CIN) or ventral attention network, is a large scale network of the human brain that is primarily composed of the anterior insula (AI) and dorsal anterior cingulate cortex (dACC). It is involved in detecting and filtering salient stimuli, as well as in recruiting relevant functional networks.[3][4] Together with its interconnected brain networks, the SN contributes to a variety of complex functions, including communication, social behavior, and self-awareness through the integration of sensory, emotional, and cognitive information.[5]
Interaction between the ventral (salience) and dorsal attention networks enables dynamic control of attention in relation to top-down goals and bottom-up sensory stimulation.[8]
While the function of the salience network is not exactly known, it has been implicated in the detection and integration of emotional and sensory stimuli,[9] as well as in modulating the switch between the internally directed cognition of the default mode network and the externally directed cognition of the central executive network.[7] Evidence that the salience network mediates a switch between the DMN and CEN comes from Granger causality analysis and studies utilizing transcranial magnetic stimulation.[10] The timing of electrophysiological responses during the oddball task is consistent with interaction, as after the initial mismatch negativity response is transmitted "bottom-up" from sensory regions, a "top-down" signal localized to the AI and dACC occurs before a widespread evoked potential that corresponds to attentional shifting.[3] It has also been hypothesized that the AI receives multimodal sensory input and the ACC and the associated dorsomedial prefrontal cortex sends motor output.[3]
Clinical significance
Dysfunction in the salience network have been observed in various psychiatric disorders, including anxiety disorders, post-traumatic stress disorder, schizophrenia, frontotemporal dementia, and Alzheimer's disease. The AI node of the salience network has been observed to be hyperactive in anxiety disorders, which is thought to reflect predictions of aversive bodily states leading to worrisome thoughts and anxious behaviors. In schizophrenia, both structural and functional abnormalities have been observed, thought to reflect excessive salience being ascribed to internally generated stimuli.[11] In individuals with autism, the relative salience of social stimuli, such as face, eyes, and gaze, may be diminished, leading to poor social skills.[5]
Nomenclature
The cingulo-opercular network (CO) has generally been equated with the salience network, but it may represent a distinct but adjacent network[12] or a part of the SN.[13] The CO may involve more dorsal areas, while the SN involves more ventral and rostral areas of the anterior insula and medial frontal cortex containing von Economo neurons.[12] The CO is sometimes also referred to as the cingulo-insular network.[12]
The ventral attention network (VAN), also known as the ventral frontoparietal network (VFN) or ventral attention system (VAS), has also been equated with the SN. The VAN is commonly defined as a right-hemisphere-dominant network involving the temporoparietal junction and the ventral frontal cortex that responds to unexpected salient stimuli.[14][15] Some have defined it as a larger, bilateral network that is a combination of the SN and CO,[16] while others have described it as a part of the salience network involving the more dorsal anterior insular cortex.[17]
In 2019, Uddin et al. proposed that midcingulo-insular network (M-CIN) be used as a standard anatomical name for the network that includes the SN, CO, and VAN.[6]
^Downar, J.; Crawley, A. P.; Mikulis, D. J.; Davis, K. D. (2000). "A multimodal cortical network for the detection of changes in the sensory environment". Nature Neuroscience. 3 (3): 277–283. doi:10.1038/72991. PMID10700261. S2CID8807081.
^Uddin, Lucina Q. (19 November 2014). "Salience processing and insular cortical function and dysfunction". Nature Reviews Neuroscience. 16 (1): 55–61. doi:10.1038/nrn3857. PMID25406711. S2CID7786680.
