A specific regulatory mechanism underlying classical trigeminal neuralgia (cTN) remains unknown. The present study posits that the initiation and advancement of cTN may be attributed to a self-regulatory and compensatory mechanism within the brain's limbic system. A sample size of thirty-three patients diagnosed with cTN and twenty-one normal controls were recruited for this investigation. Functional magnetic resonance imaging data were collected from all participants. Graph-theoretic analysis was employed to identify abnormal nodes induced by cTN in the brain atlas, followed by determining the brain network function in conjunction with the outcomes of regional homogeneity (ReHo) and functional connectivity (FC). During data processing, relatively strict thresholds were set for all corrections. The findings indicated that the discrepancy in small-worldness characteristics between the two cohorts primarily stemmed from the characteristic path length. Additionally, there was an overlap between brain regions exhibiting markedly reduced node efficiency in cTN patients and those exhibiting markedly reduced ReHo signal. The FC analysis of the whole brain revealed nine brain regions with reduced connectivity in the cTN group, corresponding to brain regions with diminished node efficiency. Notably, most of these abnormal brain regions were located in the limbic system, providing evidence of the compensatory mechanism of the limbic system.Graphical abstractWhole brain FC analysis showed reduced connectivity in nine brain regions in the cTN group compared to the NC group. Notably, most of these abnormal brain regions belong to the limbic system.