Acute cerebral blood flow and its connectivity in patients with anti-LGI1 autoimmune encephalitis: an arterial spin labeling study
摘要
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).
MethodsCBF 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.
ResultsPatients 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).
ConclusionPCASL 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.