Neuroprotective actions of thyroid hormones and low-T3 syndrome as a biomarker in acute cerebrovascular disorders

Abstract

Acute cerebrovascular disorders are common causes of death and disability worldwide. Prognostication of stroke victims rests mainly on admission clinical and radiological indexes of disease severity. Preclinical studies strongly suggest that thyroid hormones have a capacity to exert neuroprotective actions in the central nervous system under ischemic conditions via genomic and nongenomic actions. Low triiodothyronine (T3) syndrome affects 32-62% of patients following acute cerebrovascular events. Lower serum T3 concentrations are associated with greater stroke severity, more complicated clinical course, greater mortality rates and elevated risk for poor functional outcomes at discharge and long term. Further studies should address whether T3 can improve clinical stroke prognostication models. Studies investigating the neuroprotective role of thyroid hormone administration in acute cerebrovascular disease victims are encouraged.

Keywords: biomarker; hemorrhagic stroke; ischemic stroke; low T3 syndrome; outcome; subarachnoid hemorrhage; triiodothyronine.