Acute cerebral blood flow and its connectivity in patients with anti-LGI1 autoimmune encephalitis: an arterial spin labeling study

PURPOSE: Pseudocontinuous arterial spin labeling (PCASL) is an innovative technique for measuring cerebral blood flow (CBF). The aim of this study was to investigate alterations in CBF and connectivity in anti-leucine-rich glioma-inactivated 1 autoimmune encephalitis (anti-LGI1-AE). METHODS: CBF was analyzed in 27 acute anti-LGI1-AE patients and 81 healthy controls using arterial spin labeling. Regions with altered CBF were designated as regions of interest (ROIs)，followed by between-group CBF connectivity comparisons. RESULTS: Patients exhibited increased CBF in the bilateral putamen, bilateral amygdala (Amygdala_Bi), bilateral hippocampus (Hippocampus_Bi), bilateral parahippocampus, and right insula (Insula_R) (P = 0.001, cluster-level familywise error [FWE] corrected). The following regions showed decreased CBF connectivity (P < 0.05, FWE-corrected): the right hippocampus demonstrated decreased connectivity with the right superior temporal gyrus (STG_R), right Rolandic operculum (RO_R), right caudate nucleus (Caudate_R), right superior temporal pole (STP_R), right middle cingulate gyrus (MCG_R), and right anterior cingulate gyrus; the right amygdala displayed decreased connectivity with the STG_R, RO_R, STP_R, right putamen, Caudate_R, MCG_R, and right supplementary motor area; the Insula_R exhibited reduced connectivity with the right middle temporal gyrus and STG_R; the right parahippocampal gyrus presented weakened connectivity with the STP_R, RO_R, Insula_R, MCG_R, and left MTG; the left hippocampus showed decreased connectivity with the left STG and insula; the left parahippocampal gyrus manifested impaired connectivity with the left lingual gyrus and left precuneus. Increased CBF connectivity was observed between Amygdala_Bi and Hippocampus_Bi (P = 0.001, FWE-corrected). CONCLUSION: PCASL imaging revealed increased CBF in subcortical regions and widespread disruption of CBF connectivity in patients with anti-LGI1 AE, which may offer valuable insights into the neural mechanisms underlying the clinical manifestations of this condition.