Concordance between focal brain temperature elevations and focal edema in temporal lobe epilepsy

Objective: Neuroinflammation (NI) is a pathophysiological factor in many neurological disorders, including epilepsy. Because NI causes microstructural tissue damage that worsens with increasing brain temperature, abnormally elevated brain temperatures may be a surrogate measure of the biochemical consequences of NI. This study investigated whether patients with temporal lobe epilepsy (TLE) have abnormal brain temperature elevations (T-CRE) in seizure-producing regions that show evidence of edema and/or microstructural damage.Methods: Twenty adults with TLE and 20 healthy controls (HCs) were scanned at 3-Tesla. T-CRE in each voxel was calculated (T-CRE = -102.61(& UDelta;(H20-CRE)) + 206.1 & DEG;C) by non-invasive volumetric magnetic resonance spectroscopic imaging and thermometry (MRSI-t). Multi-shell diffusion images were processed by neurite orientation and density imaging (NODDI). Voxel wise two-sample t tests computed group differences in imaging data. Multimodal data fusion (joint independent component analysis [ICA]) determined the spatial coupling of T-CRE with NODDI.Results: T-CRE analyses showed that, compared to HCs, TLEs had higher T-CRE (p < .001). NODDI analyses showed increased extracellular free water (p(FWE) < 0.05) in the medial temporal lobes, with the most pronounced increases ipsilateral to seizure onset. TLEs also had increased angular dispersion of neurites (p < .001) and decreased neurite density (p(FWE) < 0.05) in the ictal-onset medial temporal lobe, as well as more widespread, bilateral patterns of abnormalities. Focal increases in T-CRE were spatially concordant with increased free water in the left inferior and middle temporal gyri and the associated cortex. In TLE, ICA loadings extracted from this region of overlap were associated with greater mood disturbance (r = .34, p = .02) and higher depression scores (r = .37, p = .009).Significance: The spatial concordance between focal T-CRE elevations and edema in TLE supports the notion that brain thermometry visualizes the correlates of focal NI. MRSI-t-based T-CRE elevations may, therefore, be a useful biomarker for identifying seizure-producing tissue in patients with focal epilepsy caused by brain damage.