Related Experiment Video

Updated: Apr 26, 2026

The Multiple Sclerosis Performance Test MSPT: An iPad-Based Disability Assessment Tool
11:35

The Multiple Sclerosis Performance Test MSPT: An iPad-Based Disability Assessment Tool

Published on: June 30, 2014

58.9K

The natural history of early versus late disability accumulation in primary progressive MS

Marcus W Koch1, Jamie Greenfield2, Omid Javizian2

  • 1Department of Clinical Neurosciences and Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada Department of Community Health Sciences, University of Calgary, Calgary, Alberta, Canada.

Journal of Neurology, Neurosurgery, and Psychiatry
|August 6, 2014
PubMed
Abstract

Insights

Age at disease onset is key for disability progression in primary progressive multiple sclerosis (PPMS). Bilateral motor onset symptoms also accelerate PPMS progression, unlike in relapsing-remitting MS.

Area of Science:

  • Neurology
  • Neuroimmunology
  • Clinical Neuroscience

Background:

  • Primary progressive multiple sclerosis (PPMS) is a less common and more severe form of MS.
  • Understanding disability accumulation patterns in PPMS is crucial for prognosis.
  • Distinct disability phases seen in relapsing-remitting MS (RRMS) are not well-characterized in PPMS.

Purpose of the Study:

  • To investigate factors influencing disability progression in PPMS.
  • To determine if PPMS exhibits distinct early and late disability accumulation phases.
  • To identify predictors of disability milestones (EDSS 4 and 6) in PPMS patients.

Main Methods:

  • Kaplan-Meier survival analyses and Cox regression were employed.
  • Investigated influence of sex, age at onset, and onset symptoms.
  • Analyzed time to and age at Expanded Disability Status Scale (EDSS) 4 and 6, and time between these milestones.

Main Results:

  • Older age at onset and bilateral motor onset symptoms predicted faster progression to EDSS 4 and 6.
  • Median time to EDSS 4 was 5 years; median time to EDSS 6 was 9 years.
  • Only age at onset influenced the time between EDSS 4 and 6.

Conclusions:

  • Age at disease onset is the primary predictor of disability accumulation in PPMS.
  • Bilateral motor onset symptoms are associated with accelerated disease progression.
  • No evidence of distinct disability accumulation phases was found in PPMS, unlike in RRMS.
Keywords:
EPIDEMIOLOGYMULTIPLE SCLEROSIS

More Related Videos

Measuring Progressive Neurological Disability in a Mouse Model of Multiple Sclerosis08:11

Measuring Progressive Neurological Disability in a Mouse Model of Multiple Sclerosis

Published on: November 14, 2016

10.6K
A Method of Trigonometric Modelling of Seasonal Variation Demonstrated with Multiple Sclerosis Relapse Data10:46

A Method of Trigonometric Modelling of Seasonal Variation Demonstrated with Multiple Sclerosis Relapse Data

Published on: December 9, 2015

10.3K

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...
16
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...
19
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
39
Huntington Disease l: Introduction01:21

Huntington Disease l: Introduction

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...
68
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...
21
Long-term Potentiation01:35

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
51.5K