BACKGROUND:Limbic encephalitis is a rare syndrome that specifically affects the limbic system. Magnetic resonance imaging(MRI) has been typically used to detect brain changes in this disease. However,the mechanisms of limbic encephalitis-related white matter damage remain poorly understood. OBJECTIVE:To characterize white matter connectivity changes secondary to injuries of the limbic system in limbic encephalitis through combined application of diffusion tensor imaging(DTI) and voxel-based morphometry. DESIGN,TIME AND SETTING:A non-randomized,controlled,clinical,neuroimaging,DTI study was performed at the Department of Radiology,West China Hospital in December 2008. PARTICIPANTS:A male,46-year-old,limbic encephalitis patient,as well as 11 age- and gender-matched healthy volunteers,were enrolled in the present study. METHODS:MRI was performed on the limbic encephalitis patient using a 3.0T MR scanner. Three-dimensional SPGR T1-weighted images and DTI were acquired in the patient and controls. Data were analyzed using Matlab 7.0 and SPM2 software. MAIN OUTCOME MEASURES:Results from routine MRI scan with contrast enhancement of patient,as well as fractional anisotropy and mean diffusivity value map differences between patient and controls. RESULTS:Significant symmetric MRI signal intensity abnormalities were observed with routine MRI. Affected bilateral hippocampi and amygdala exhibited hypointense signals in T1WI and hyperintense signals in T2 images.The DTI study revealed decreased fractional anisotropy values in the bilateral alveus and fimbria of the hippocampus,bilateral internal and external capsules,white matter of the right prefrontal area,and left corona radiate in the patient compared with normal controls(P<0.001). Significantly increased fractional anisotropy,mean diffusivity,or decreased mean diffusivity were not observed in the patient,compared with controls. CONCLUSION:Secondary white matter damage to the hippocampal alveus and fimbria was apparent in the limbic encephalitis patient.In addition,other white matter fiber injuries surrounded the limbic structures,which were not attributed to secondary limbic system injuries. BACKGROUND: Limbic encephalitis is a rare syndrome that specifically affects the limbic system. Magnetic resonance imaging (MRI) has been typically used to detect brain changes in this disease. However, the mechanisms of limbic encephalitis-related white matter damage remain poorly understood. OBJECTIVE : To characterize white matter connectivity changes secondary to injuries of the limbic system in limbic encephalitis through combined application of diffusion tensor imaging (DTI) and voxel-based morphometry. DESIGN, TIME AND SETTING: A non-randomized, controlled, clinical, neuroimaging, DTI study was performed at the Department of Radiology, West China Hospital in December 2008. PARTICIPANTS: A male, 46-year-old, limbic encephalitis patient, as well as 11 age- and gender-matched healthy volunteers, were enrolled in the present study. METHODS: MRI was performed on the limbic encephalitis patient using a 3.0T MR scanner. Three-dimensional SPGR T1-weighted images and DTI were acquired in the patient and co MAIN OUTCOME MEASURES: Results from routine MRI scan with contrast enhancement of patient, as well as fractional anisotropy and mean diffusivity value map differences between patient and controls. RESULTS: Significant symmetric MRI signal intensity Affected bilateral hippocampi and amygdalaUTION hypointense signals in T1WI and hyperintense signals in T2 images. DTI study revealed decreased fractional anisotropy values ​​in the bilateral alveus and fimbria of the hippocampus, bilateral internal and external capsules, white matter of the right prefrontal area, and left corona radiate in the patient compared with normal controls (P <0.001). Significantly increased fractional anisotropy, mean diffusivity, or decreased mean diffusivity were not observed in the patient, compared with controls. matter damage to the hippocampal alveus and fimbria was apparent in the limbic encephalitis patient. addition, other white matter fiber injuries surrounded the limbic structures, which were not attributed to secondary limbic system injuries.