Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies01:22

Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies

The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
Rheumatic Heart Disease I: Introduction01:23

Rheumatic Heart Disease I: Introduction

Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Rheumatic Heart Disease III: Medical Management01:21

Rheumatic Heart Disease III: Medical Management

Rheumatic heart disease (RHD) management can be divided into two main strategies: prevention and long-term management.Primary PreventionPrimary prevention focuses on timely diagnosis and management of group A streptococcal pharyngitis to prevent acute rheumatic fever. The most widely used antibiotic for treating this condition is intramuscular benzathine penicillin G.Acute Rheumatic Fever TreatmentThe primary treatment goal for a patient diagnosed with acute rheumatic fever is to suppress the...
Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which leads...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Therapeutic Outcomes in VEXAS Syndrome: A Multicenter Comparative Cohort of Allogeneic Hematopoietic Stem Cell Transplantation and Hypomethylating Agents.

American journal of hematology·2026
Same author

Treatment strategies in giant cell arteritis and polymyalgia rheumatica: beyond glucocorticoids.

Nature reviews. Rheumatology·2026
Same author

Giant Cell Arteritis.

Annals of internal medicine·2026
Same author

Significance of positive rheumatoid factor in ANCA-associated vasculitis.

Clinical and experimental rheumatology·2026
Same author

Structured Vascular Segment Analysis for Giant Cell Arteritis: A Proposed Scoring System for CT Angiography-Based Diagnosis.

AJNR. American journal of neuroradiology·2026
Same author

A Delphi exercise informing the development of criteria to measure response to treatment in giant cell arteritis.

Seminars in arthritis and rheumatism·2026
Same journal

Medical compartmentalisation: a patient with chromosome 22q11.2 deletion syndrome in Japan.

Lancet (London, England)·2026
Same journal

[<sup>177</sup>Lu]Lu-edotreotide versus everolimus for gastroenteropancreatic neuroendocrine tumours (COMPETE): a phase 3, multicentre, randomised, open-label, superiority trial.

Lancet (London, England)·2026
Same journal

Research priorities for characterising Bundibugyo virus.

Lancet (London, England)·2026
Same journal

Rethinking treatment sequence in advanced gastroenteropancreatic neuroendocrine tumours.

Lancet (London, England)·2026
Same journal

Dual mobility total hip replacement in fractures: stability promotes patient confidence.

Lancet (London, England)·2026
Same journal

Dual mobility versus standard cups in total hip replacement for displaced femoral neck fractures (Duality): an international, multicentre, randomised, controlled, superiority trial.

Lancet (London, England)·2026
See all related articles

Related Experiment Videos

Polymyalgia rheumatica.

Tanaz A Kermani1, Kenneth J Warrington

  • 1Division of Rheumatology, Department of Internal Medicine, Mayo Clinic, Rochester, MN 55905, USA.

Lancet (London, England)
|October 12, 2012
PubMed
Summary
This summary is machine-generated.

Polymyalgia rheumatica is an inflammatory disorder causing pain and stiffness in older adults. Diagnosis relies on clinical assessment, and while glucocorticoids help, relapses and side effects are common, necessitating better treatments.

Related Experiment Videos

Area of Science:

  • Rheumatology
  • Immunology
  • Internal Medicine

Background:

  • Polymyalgia rheumatica (PMR) is a chronic inflammatory condition affecting individuals over 50.
  • Characterized by pain and morning stiffness in the neck, shoulders, hips, and thighs.
  • Diagnosis is clinical, as no specific laboratory test exists, though inflammation markers may be elevated.

Purpose of the Study:

  • To summarize the key aspects of polymyalgia rheumatica.
  • To highlight diagnostic challenges and current treatment approaches.
  • To underscore the need for improved understanding of disease pathogenesis.

Main Methods:

  • Clinical assessment and provisional classification criteria (2012 EULAR/ACR).
  • Review of imaging studies (ultrasonography, MRI) showing periarticular inflammation.
  • Association with large artery vasculopathy (giant cell arteritis) in a subset of patients.

Main Results:

  • PMR symptoms often mimic other inflammatory arthropathies like spondyloarthritis and rheumatoid arthritis.
  • Imaging reveals a predominantly periarticular inflammatory process.
  • Glucocorticoid therapy offers symptomatic relief but is linked to frequent relapses and significant morbidity.

Conclusions:

  • Polymyalgia rheumatica diagnosis remains clinically based, with challenges in differentiating it from other inflammatory conditions.
  • Current standard treatment with glucocorticoids is effective for symptom management but has limitations.
  • Further research into PMR pathogenesis is crucial for developing more targeted immunotherapies.