Neuronal correlates of overt hypothyroidism measured by FDG PET

Abstract

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Objectives: Despite the frequent clinical finding of hypothyroidism being associated with mood changes like depression or loss of efficiency, the underlying cerebral processes are still unclear. Aim of this study was to investigate the cerebral neuronal correlates of hypothyroidism using positron emission tomography. Methods: In this prospective study, 10 patients (19-64 years, median 53 yrs) with overt hypothyroidism underwent a cerebral 18-FDG PET examination. 7 patients (39-64 yrs, median 56 yrs) underwent a second scan after getting euthyroid by thyroxin substitution. All PET scans were performed at the same day time (a.m.) in order to minimize influences of circadian hormonal variability. PET images were spatially normalized to the MNI space using the FDG template and statistics were calculated on voxelwise basis using SPM2 (paired t-test, categorical comparison to gender and age matched controls). Results: Compared to the normal controls, the hypothyroid patients showed a significantly decreased metabolism in large parts of the bilateral thalamus and in the bilateral posterior insula (p<0.001). Under euthyroidism, we still found deactivation of thalamic areas (p<0.001), however, in the posterior insula no significant clusters were detectable. In the paired t-test for the longitudinal study (n=7), the patients showed after remission to euthyroidism compared to their hypothyroid state an activation in the primary visual cortex bilaterally and in parts of the sensory association cortex (p<0.005) whereas no significant deactivations were found. Conclusions: Hypothyroidism-associated psychopathological symptoms are correlated to regional metabolic changes in main structures of the thalamus and in the functionally connected insular cortex. Compared to controls, the deactivation in thalamic areas still remains detectable under euthyroid conditions. The activation of visual and secondary sensory cortex in the patients’ course is surprising and might be the correlate of compensatory neuronal processes after metabolic remission.