Literature DB >> 21596814

Reversible changes in brain glucose metabolism following thyroid function normalization in hyperthyroidism.

Q Miao1, S Zhang, Y H Guan, H Y Ye, Z Y Zhang, Q Y Zhang, R D Xue, M F Zeng, C T Zuo, Y M Li.   

Abstract

BACKGROUND AND
PURPOSE: Patients with hyperthyroidism frequently present with regional cerebral metabolic changes, but the consequences of endocrine-induced brain changes after thyroid function normalization are unclear. We hypothesized that the changes of regional cerebral glucose metabolism are related to thyroid hormone levels in patients with hyperthyroid, and some of these changes can be reversed with antithyroid therapy.
MATERIALS AND METHODS: Relative regional cerebral glucose metabolism was compared between 10 new-onset untreated patients with hyperthyroidism and 20 healthy control participants by using brain FDG-PET scans. Levels of emotional distress were evaluated by using the SAS and SDS. Patients were treated with methimazole. A follow-up PET scan was performed to assess metabolic changes of the brain when thyroid functions normalized.
RESULTS: Compared with controls, patients exhibited lower activity in the limbic system, frontal lobes, and temporal lobes before antithyroid treatment. There were positive correlations between scores of depression and regional metabolism in the cingulate and paracentral lobule. The severity of depression and anxiety covaried negatively with pretreatment activity in the inferior temporal and inferior parietal gyri respectively. Compared with the hyperthyroid status, patients with normalized thyroid functions showed an increased metabolism in the left parahippocampal, fusiform, and right superior frontal gyri. The decrease in both FT3 and FT4 was associated with increased activity in the left parahippocampal and right superior frontal gyri.
CONCLUSIONS: The changes of regional cerebral glucose metabolism are related to thyroid hormone levels in patients with hyperthyroidism, and some cerebral hypometabolism can be improved after antithyroid therapy.

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Year:  2011        PMID: 21596814      PMCID: PMC8013137          DOI: 10.3174/ajnr.A2449

Source DB:  PubMed          Journal:  AJNR Am J Neuroradiol        ISSN: 0195-6108            Impact factor:   3.825


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