ArticleJournal of movement disorders2026
Clinical Significance of Thyroid 123I- Meta-Iodobenzylguanidine Uptake in Parkinson's Disease.
Article in Journal of movement disorders, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThe thyroid gland receives sympathetic innervation. 123I-meta-iodobenzylguanidine (123I-MIBG) is a noradrenaline analog taken up by adrenergic nerve terminals. Although thyroid uptake can be detected on 123I-MIBG scintigraphy, its quantitative value is poorly understood. This study examined the clinical relevance of thyroid 123I-MIBG uptake in Parkinson's disease (PD).
methodsA total of 233 de novo patients were enrolled in a longitudinal cohort and underwent 123I-MIBG scintigraphy. Early and late heart-to-mediastinum ratios (HMRs) and early thyroid-to-mediastinum ratios (TMRs) were calculated. Baseline TMRs were estimated using a mixed model after verifying the empirical linear decline over time. Observed and model-implied uptake ratios were analyzed in relation to adrenergic blood pressure (BP) control, motor and nonmotor burdens, and quality of life (QoL). Baseline thyroid uptake was further assessed for its influence on longitudinal disease progression.
resultsPatients were assessed for early PD (mean age, 68.7±8.7 years; median disease duration, 1.0 years). The mean follow-up was 57.3±22.1 months. A lower baseline HMR correlated with greater changes in orthostatic BP, greater autonomic symptom burden, and worse motor and nonmotor functions and QoL. Overall, the TMR was not significantly correlated; however, it was associated with a greater occurrence of supine hypertension, orthostatic hypotension, and nondipper or nocturnal hypertension. Thyroid uptake did not influence longitudinal changes in motor, nonmotor, cognitive, or QoL measures, although higher uptake tended to be associated with slower cognitive decline and better QoL.
conclusionThyroid 123I-MIBG uptake did not predict disease progression but may indicate early blood pressure dysregulation and could reflect nonmotor vulnerability in PD patients.
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