¹⁸ F‐ FDG PET Reveals a Nucleus Accumbens‐Centered Metabolic Network Correlating With Clinical Severity in Anti‐LGI1 Encephalitis

The metabolic signature of anti-leucine-rich glioma-inactivated 1 (anti-LGI1) autoimmune encephalitis remains poorly defined. We sought to delineate disease-specific ¹⁸F-FDG PET patterns and assess their relationships with clinical severity and cognition. Forty-seven patients with anti-LGI1 encephalitis and 25 healthy controls underwent ¹⁸F-FDG PET/CT, and voxel-wise comprised to identify regional metabolic alterations. A disease-specific metabolic pattern was derived with fivefold cross-validation, and a metabolic covariance network was mapped using the Brainnetome atlas. Pattern expression scores were correlated with clinical assessments. Compared to controls, patients demonstrated hypermetabolism in the hippocampal rostal, nucleus accumbens (NAc), and hypothalamus, alongside hypometabolism in the dorsolateral prefrontal cortex and posterior cingulate cortex (PCC). We identified a robust metabolic pattern centered on the NAc with extensions to the hippocampus, prefrontal cortex, and PCC; expression of this pattern correlated positively with both clinical severity and cognitive impairment. Subgroup analyses showed no significant differences in basal ganglia metabolism between patients with and without faciobrachial dystonic seizures (FBDS), or in hypothalamic metabolism between those with and without hyponatremia. Overall, ¹⁸F-FDG PET uncovers a NAc-centered metabolic network that parallels disease severity in anti-LGI1 encephalitis. Our study offers potential biomarker for clinical evaluation and provides valuable insights into the underlying pathogenesis of clinical manifestations.