Abstract
Limbic encephalitis is an autoimmune disease. A variety of autoantibodies have been associated with different subtypes of limbic encephalitis, whereas its MR imaging signature is uniformly characterized by mesiotemporal abnormalities across subtypes. Here, we hypothesized that patients with limbic encephalitis would show subtype-specific mesiotemporal structural correlates, which could be classified by supervised machine learning on an individual level. T1WI MPRAGE scans from 46 patients with antibodies against glutamic acid decarboxylase and 34 patients with antibodies against the voltage-gated potassium channel complex (including 10 patients with leucine-rich glioma-inactivated 1 autoantibodies) and 48 healthy controls were retrospectively ascertained. Parcellation of the amygdala, hippocampus, and hippocampal subfields was performed using FreeSurfer. Volumes were extracted and compared between groups using unpaired, 2-tailed t tests. The volumes of hippocampal subfields were analyzed using a multivariate linear model and a binary decision tree classifier. Temporomesial volume alterations were most pronounced in an early stage and in the affected hemispheric side of patients. Statistical analysis revealed antibody-specific hippocampal fingerprints with a higher volume of CA1 in patients with glutamic acid decarboxylase-associated limbic encephalitis (P = .02), compared with controls, whereas CA1 did not differ from that in controls in patients with voltage-gated potassium channel complex autoantibodies. The classifier could successfully distinguish between patients with autoantibodies against leucine-rich glioma-inactivated 1 and glutamic acid decarboxylase with a specificity of 87% and a sensitivity of 80%. Our results suggest stage-, side- and antibody-specific structural correlates of limbic encephalitis; thus, they create a perspective toward an MR imaging-based diagnosis.
Highlights
BACKGROUND AND PURPOSELimbic encephalitis is an autoimmune disease
Statistical analysis revealed antibody-specific hippocampal fingerprints with a higher volume of CA1 in patients with glutamic acid decarboxylase–associated limbic encephalitis (P = .02), compared with controls, whereas CA1 did not differ from that in controls in patients with voltage-gated potassium channel complex autoantibodies
Our results suggest stage, side- and antibody-specific structural correlates of limbic encephalitis; they create a perspective toward an MR imaging–based diagnosis
Summary
T1WI MPRAGE scans from 46 patients with antibodies against glutamic acid decarboxylase and 34 patients with antibodies against the voltage-gated potassium channel complex (including 10 patients with leucine-rich glioma-inactivated 1 autoantibodies) and 48 healthy controls were retrospectively ascertained. We retrospectively ascertained clinical and MR imaging data from patients with LE who were treated the Department of Epileptology at University of Bonn Medical Center between April 2006 and June 2017 and met the following inclusion criteria: 1) 18 years of age or older, 2) having a diagnosis of a limbic syndrome (with at least 1 of the following symptoms: temporal lobe seizures, episodic memory disturbance, or psychiatric symptoms with affective disturbance), 3) serologically proved autoantibodies against the VGKC complex (or, if tests were available, against its antigenic components LGI1 or CASPR2) or GAD, and 4) availability of at least one 3D T1-weighted MPRAGE MR imaging scan. The late group included the most recent available T1WI scans acquired at least 24 months after the onset of epilepsy and is referred to as late GAD group (33 patients in total, 10 men; age at MR imaging, 33.9 6 12.3 years) or late VGKC group Ten patients from the GAD group and 13 patients from the VGKC group were included in both the early and the late groups because they were scanned repeatedly less than and more than 24 months after the onset of the first LE-related symptom
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