Christina Bankston

Objective Epilepsy and depression share neurobiological origins, and evidence suggests a possible bidirectional relationship that remains poorly understood. This exploratory, cross‐sectional study aimed to investigate this relationship by employing magnetic resonance spectroscopic imaging (MRSI) and thermometry (MRSI‐t) in patients with temporal lobe epilepsy (TLE) with comorbid depressive symptoms and control participants. This is the first study to combine MRSI and MRSI‐t to examine brain temperature and choline abnormalities in regions implicated in seizure onset and depression. Methods Twenty‐six patients with TLE and 26 controls completed questionnaires and underwent imaging at 3T. Volumetric echo‐planar MRSI/MRSI‐t data were processed within the M etabolite I maging and D ata A nalysis S ystem (MIDAS). Choline (CHO) was quantified as a ratio over creatine (CRE; CHO/CRE). Brain temperature (T CRE ) was calculated based on the chemical shift difference of H 2 O relative to CRE's stable location on the ppm spectrum. The Hospital Anxiety and Depression Scale measured anxiety and depressive symptoms. The Chalfont Seizure Severity Scale measured seizure severity in patients with TLE. Two sets of voxelwise independent sample t tests examined group differences in CHO/CRE and T CRE maps. Voxel‐based multimodal canonical correlation analysis (mCCA) linked both datasets to investigate if, how, and where CHO/CRE and T CRE abnormalities were correlated in TLE participants and controls. Results Compared to controls, patients with TLE reported more depressive symptoms ( P = 0.04) and showed CHO/CRE and T CRE elevations in left temporal and bilateral frontal regions implicated in seizure onset and depressive disorders ( p FWE < 0.05). For the TLE group, CHO/CRE levels in temporal and frontal cortices were associated with elevated T CRE in bilateral frontal and temporal gyri ( r = 0.96), and decreased T CRE in bilateral fronto‐parietal regions ( r = −0.95). Significance Abnormalities in T CRE and CHO/CRE were observed in seizure‐producing areas and in regions implicated in depression. These preliminary findings suggest that common metabolic changes may underlie TLE and depression. Our results suggest further investigations into the proposed bidirectional mechanisms underlying this relationship are warranted.

This observational study aimed to determine whether individuals with fibromyalgia (FM) exhibit higher levels of neuroinflammation than healthy controls (HCs), as measured with positron emission tomography using [ 18 F]DPA-714, a second-generation radioligand for the translocator protein (TSPO). Fifteen women with FM and 10 HCs underwent neuroimaging. Distribution volume (V T ) was calculated for in 28 regions of interest (ROIs) using Logan graphical analysis and compared between groups using multiple linear regressions. Group (FM vs HC) was the main predictor of interest and TSPO binding status (high- vs mixed-affinity) was added as a covariate. The FM group had higher V T in the right postcentral gyrus ( b = 0.477, P = 0.033), right occipital gray matter (GM; b = 0.438, P = 0.039), and the right temporal GM ( b = 0.466, P = 0.042). The FM group also had lower V T than HCs in the left isthmus of the cingulate gyrus ( b = −0.553, P = 0.014). In the subgroup of high-affinity binders, the FM group had higher V T in the bilateral precuneus, postcentral gyrus, parietal GM, occipital GM, and supramarginal gyrus. Group differences in the right parietal GM were associated with decreased quality of life, higher pain severity and interference, and cognitive problems. In support of our hypothesis, we found increased radioligand binding (V T ) in the FM group compared with HCs in several brain regions regardless of participants' TSPO binding status. The ROIs overlapped with prior reports of increased TSPO binding in FM. Overall, increasing evidence supports the hypothesis that FM involves microglia-mediated neuroinflammation in the brain.