Related Experiment Video
Updated: May 4, 2026
09:41
Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
12.4K
Disease course heterogeneity and OCT in multiple sclerosis
L J Balk1, P Tewarie2, J Killestein2
1Department of Neurology, VU University Medical Centre, the Netherlands L.balk@vumc.nl.
Multiple Sclerosis (Houndmills, Basingstoke, England)
|January 10, 2014
Summary
Retinal layer thinning, especially in the inner layers (RNFL, GCC), correlates with multiple sclerosis (MS) disease heterogeneity. Benign MS shows preserved retinal layers, suggesting limited neurodegeneration relevant for future trials.
Area of Science:
- Ophthalmology
- Neurology
- Medical Imaging
Background:
- Multiple sclerosis (MS) disease course heterogeneity poses challenges for patient management and clinical trials.
- Understanding factors influencing MS progression is crucial for effective treatment strategies.
Purpose of the Study:
- To investigate the association between the heterogeneous course of multiple sclerosis and retinal layer thicknesses.
- To determine if retinal layer measurements can differentiate between benign and typical MS disease courses.
Main Methods:
- Spectral-domain optical coherence tomography (OCT) was used to scan the peripapillary and macular regions of 230 MS patients and 63 controls.
- Automated eight-layer segmentation and generalized estimation equations were applied for analysis.
- Receiver operating characteristic (ROC) curves were calculated to assess diagnostic capabilities.
Main Results:
- Primary progressive MS patients exhibited relative preservation of inner retinal layers compared to relapsing-onset MS.
- In MS eyes without optic neuritis, typical disease courses showed significant thinning of inner retinal layers (RNFL to INL) compared to benign courses, even after 20 years.
- Retinal layer thicknesses, particularly RNFL and GCC, were significantly linked to MS disease heterogeneity.
Conclusions:
- Inner retinal layer thickness is a significant indicator of MS disease course heterogeneity.
- Preserved retinal layers in benign and primary progressive MS suggest lower retinal neurodegeneration susceptibility.
- OCT measurements of retinal layers may serve as a valuable secondary outcome in future neurodegenerative treatment trials for primary progressive MS.
Related Concept Videos
01:19Multiple Sclerosis l: Introduction
20
Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
20
01:24Parkinson Disease ll: Pathophysiology
28
Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
28
01:21Huntington Disease l: Introduction
110
Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show...
110
01:23Alzheimer Disease ll: Pathophysiology
35
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
35
01:22Myasthenia Gravis ll: Pathophysiology
53
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...
53
01:21EPS and iPS Cells in Disease Research
3.2K
Embryonic and induced pluripotent stem cells are excellent models for disease research because of their ability to self-renew and differentiate into most cell types. Somatic cells from a patient are isolated and reprogrammed into induced pluripotent stem cells or iPSCs. These iPSCs are later differentiated into the desired cell type, which mirrors the diseased cell of the patient. In this way, disease models have been created for investigating diseases such as Down syndrome, type I diabetes,...
3.2K