Related Experiment Video

Updated: Aug 24, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

Grey and white matter atrophy in early clinical stages of primary progressive multiple sclerosis

Jaume Sastre-Garriga1, Gordon T Ingle, Declan T Chard

  • 1Institute of Neurology, UCL, 23 Queen Square, London WC1N 3BG, UK.

Neuroimage
|April 28, 2004
PubMed
Abstract

Insights

Brain atrophy, affecting both grey and white matter (GM and WM), is evident early in primary progressive multiple sclerosis (PPMS). White matter atrophy correlates more strongly with clinical outcomes and focal damage in PPMS patients.

Area of Science:

  • Neuroimaging
  • Neurology
  • Neuroscience

Background:

  • Limited data exists on grey and white matter (GM and WM) atrophy in primary progressive multiple sclerosis (PPMS).
  • Understanding atrophy patterns and their clinical relevance in early PPMS is crucial for disease management.

Purpose of the Study:

  • To assess early disease progression in PPMS using volumetric MRI.
  • To investigate axonal loss via WM and GM atrophy.
  • To correlate MRI findings with clinical outcomes and lesion load.

Main Methods:

  • Studied 43 PPMS patients (within 5 years of onset) and 45 controls.
  • Used 3D MRI scans segmented for WM, GM, and CSF.
  • Calculated brain parenchymal fraction (BPF), WM fraction (WMF), and GM fraction (GMF).
  • Assessed T2 and enhancing lesion loads, EDSS, and MSFC scores.

Main Results:

  • Significant differences in BPF, WMF, and GMF between PPMS patients and controls.
  • BPF and WMF correlated with Expanded Disability Status Scale (EDSS) scores.
  • BPF, WMF, and GMF correlated with Multiple Sclerosis Functional Composite (MSFC) scores.
  • Correlations with lesion load were significant for BPF and WMF.

Conclusions:

  • Brain atrophy, impacting both GM and WM, is present in early PPMS stages.
  • WM atrophy shows a stronger association with clinical outcomes and focal WM damage in PPMS.

More Related Videos

Automated Segmentation of Cortical Grey Matter from T1-Weighted MRI Images06:48

Automated Segmentation of Cortical Grey Matter from T1-Weighted MRI Images

Published on: January 7, 2019

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines09:46

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines

Published on: September 21, 2021

Related Concept Videos

Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

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...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

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 microglia. Abnormal...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
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...
Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...