Fig. 2: Anatomical characterization of contributions to sevoflurane-induced loss of functional identifiability.
a, Edge-level difference in ICC between awake versus recovery and awake versus sevoflurane. b, The anaesthetic-induced loss of ICC is significantly more pronounced for functional connections within the transmodal cortex than those involving unimodal regions. For edges within the transmodal cortex, mean = 0.44 and s.d. = 0.34; for other edges, mean = 0.22 and s.d. = 0.35; t(39,998) = 55.93; P < 0.001; effect size (Hedge’s g) = 0.63; CI = [0.60, 0.65]; two-sided t-test). The ICC ranges between −1 and +1. n = 5,580 edges within the transmodal cortex and n = 34,420 unimodal–transmodal and unimodal–unimodal edges. In the box plot, the central lines indicate median values, the bounds of the boxes indicate the 25th and 75th percentiles and the whiskers indicate 1.5× the interquartile range. c, Regional distribution of anaesthetic-induced loss of ICC, projected onto the cortical surface. d, The anaesthetic-induced regional loss of ICC is significantly spatially aligned with the archetypal sensory–association axis of cortical organization (Spearman’s ρ = 0.67; pspin < 0.001; n = 200 regions), the regional distribution of inter-individual variability of FC (Spearman’s ρ = 0.63; pspin < 0.001; n = 200 regions), the regional distribution of cortical expansion between macaque and human brains (Spearman’s ρ = 0.35; pspin < 0.001; n = 200 regions) and the regional expression of human-accelerated genes pertaining to brain function and development (that is, HAR–brain genes) (Spearman’s ρ = 0.42; pspin < 0.001; n = 200 regions). For each brain map, the range of values spanned by the colour bar is displayed on the y axis of the scatter plot directly underneath. Source data are provided.
