Thyroid Disorders and Movement Disorders—A Systematic Review

Abstract

Background There is overlap between movement disorders and neuroendocrine abnormalities. Objectives and methods To provide a systematic review on the association of thyroid dysfunction and movement disorders. Thyroid physiological function and classical thyroid disorders highlighting typical and atypical manifestations including movement disorders, as well as diagnostic procedures, and treatments are discussed. Results Hypothyroidism may be associated with hypokinetic and hyperkinetic disorders. There is debate whether their concomitance reflects a causal link, is coincidence, or the result of one unmasking the other. Hypothyroidism‐associated parkinsonism may resemble idiopathic Parkinson's disease. Hypothyroidism‐associated hyperkinetic disorders mainly occur in the context of steroid‐responsive encephalopathy with autoimmune thyroiditis, that is, Hashimoto disease, mostly manifesting with tremor, myoclonus, and ataxia present in 28–80%, 42–65% and 33–65% in larger series. Congenital hypothyroidism manifesting with movement disorders, mostly chorea and dystonia, due to Mendelian genetic disease are rare. Hyperthyroidism on the other hand mostly manifests with hyperkinetic movement disorders, typically tremor (present in three quarters of patients). Chorea (present in about 2% of hyperthyroid patients), dystonia, myoclonus, ataxia and paroxysmal movement disorders, as well as parkinsonism have also been reported, with correlation between movement intensity and thyroid hormone levels. On a group level, studies on the role of thyroid dysfunction as a risk factor for the development of PD remain non‐conclusive. Conclusions In view of the treatability of movement disorders associated with thyroid disease, accurate diagnosis is important. The pathophysiology remains poorly understood. More detailed case documentation and systematic studies, along with experimental studies are needed.

Blood-brain barrier on-a-chip and its application

“…MCT8-deficient BBB-Chips showed significantly lower permeability for T3, which is a thyroid precursor. The results of this study confirmed the necessity of MCT8 protein for T3 transport across BBB, and given that loss of thyroid hormone-binding proteins increases the vulnerability of striatal neurons in Huntington's Disease [11], the model confirmed the contribution of MCT8 deficiency to the disorder. Similarly, Pediaditakis et al 2021 showed that abnormal accumulation of alpha-synuclein aggregates led to phosphorylation of αSyn localized in the endothelial cells in the vascular channel and therefore BBB damage in Parkinson's Disease [12]; Shin et al 2019 showed that in Alzheimer's Disease there is increased BBB permeability induced by reduced expression of tight junction and adherens proteins [13].…”

Rare Neurologic Presentation of Thyrotoxicosis

“…1 Since then, there have been various case reports of the condition, but it still remains a rare occurrence. 2 In our country, this is the first reported case in literature.…”

The First Indian Patient With Benign Hereditary Chorea due to a De Novo Mutation in the NKX2-1 Gene

“…1 Thyroid involvement may manifest as congenital hypothyroidism 2 or compensated hypothyroidism in childhood or even adulthood. 6 Our patient had well-controlled hypothyroidism with onset in early childhood and motor delay. This presentation contrasted with that of the patient with the same variant reported by Li et al, 2 who had congenital hypothyroidism and marked motor and language developmental delay.…”