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The Thyroid Gland01:23

The Thyroid Gland

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The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
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Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
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Hyperthyroidism II: Pathophysiology01:27

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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...
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Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

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Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence...
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Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

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Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor,...
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Hypothyroidism II: Pathophysiology01:23

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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...
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Computer-Aided Three-Dimensional Visualization in the Treatment of Locally Advanced Thyroid Cancer
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Specific static and dynamic functional network connectivity changes in thyroid-associated ophthalmopathy and it

Hao Liu1, Yu-Lin Zhong2, Xin Huang2

  • 1School of Ophthalmology and Optometry, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.

Frontiers in Neuroscience
|September 9, 2024
PubMed
Summary
This summary is machine-generated.

Thyroid-associated ophthalmopathy (TAO) alters brain connectivity, particularly in visual and cognitive networks. These findings highlight potential neural targets for understanding and treating central nervous system effects in TAO.

Keywords:
functional connectivityfunctional network connectivityindependent component analysisresting-state networkthyroid-associated ophthalmopathy

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Area of Science:

  • Neuroimaging
  • Neuroscience
  • Autoimmune Diseases

Background:

  • Thyroid-associated ophthalmopathy (TAO) is an autoimmune condition causing ocular and central nervous system symptoms, including cognitive deficits.
  • Previous research indicates brain abnormalities in TAO patients, but static and dynamic functional network connectivity changes remain unexplored.

Purpose of the Study:

  • To investigate alterations in static functional network connectivity (sFNC) and dynamic functional network connectivity (dFNC) in patients with TAO.
  • To identify potential neuroimaging biomarkers for TAO using independent component analysis (ICA).

Main Methods:

  • Resting-state functional magnetic resonance imaging (rs-fMRI) was performed on 32 TAO patients and 30 healthy controls (HCs).
  • Independent component analysis (ICA) was employed to analyze sFNC and dFNC patterns.

Main Results:

  • TAO patients showed altered intra-network connectivity in visual and cognitive networks, with decreased connectivity in dorsal attentional (DAN), default mode (DMN), and executive control networks (ECN).
  • Reduced inter-network connectivity was observed between visual (VN), cerebellum (CN), and high-level cognitive networks in TAO patients.
  • Dynamic functional network connectivity (dFNC) analysis revealed widespread abnormalities, with compensatory increased connectivity between DMN and low-level networks.
  • Support vector machine (SVM) models based on functional connectivity (FC) effectively distinguished TAO patients from HCs.

Conclusions:

  • Significant alterations in visual and high-level cognitive networks are characteristic of TAO.
  • These findings enhance understanding of the neural mechanisms underlying TAO and suggest potential targets for future research into central nervous system manifestations.