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Related Concept Videos

Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...

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Transient Middle Cerebral Artery Occlusion Model of Stroke
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Subclinical hyperthyroidism is a risk factor for poor functional outcome after ischemic stroke.

Frank Arne Wollenweber1, Vera Zietemann, Andreas Gschwendtner

  • 1Institute for Stroke and Dementia Research, Klinikum der Universität München, Ludwig-Maximilians-University, Marchioninistr. 15, 81377 Munich, Germany.

Stroke
|March 14, 2013
PubMed
Summary

Subclinical hyperthyroidism increases the risk of poor functional outcomes after ischemic stroke. This condition is linked to greater disability and dependency three months post-stroke.

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Published on: August 18, 2015

Area of Science:

  • Endocrinology
  • Neurology
  • Cardiovascular Medicine

Background:

  • Subclinical hyperthyroidism is linked to adverse cardiovascular events like stroke.
  • The impact of subclinical hyperthyroidism on stroke functional outcomes is not well understood.

Purpose of the Study:

  • To investigate the association between subclinical thyroid dysfunction and functional outcomes after ischemic stroke.
  • To determine if subclinical hyperthyroidism is a risk factor for poor recovery post-stroke.

Main Methods:

  • 165 ischemic stroke patients were prospectively studied.
  • Patients were categorized into subclinical hyperthyroidism, subclinical hypothyroidism, and euthyroid groups based on thyroid-stimulating hormone levels.
  • Functional outcomes (modified Rankin Scale, Barthel Index) were assessed at 3 months post-stroke.

Main Results:

  • Subclinical hyperthyroidism was present in 11.5% of patients.
  • Patients with subclinical hyperthyroidism showed a significantly increased risk of functional disability (OR, 3.95) and dependency (OR, 9.12) at 3 months.
  • These associations remained significant after adjusting for multiple confounders.

Conclusions:

  • Subclinical hyperthyroidism is an independent risk factor for poor functional outcomes following ischemic stroke.
  • Early detection and management of subclinical thyroid dysfunction may be crucial for stroke recovery.