Related Experiment Video
Updated: May 13, 2026
09:41
Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
[Local demyelination in amyotrophic lateral sclerosis].
N Kvirkvelia1, R Shakarishvili
1Iv. Javakhishvili Tbilisi State University, Department of Neurology&Neurosurgery, Faculty of Medicine, Georgia.
Georgian Medical News
|March 14, 2013
Summary
This study presents three amyotrophic lateral sclerosis (ALS) cases with conduction block, challenging the exclusion criteria for ALS. It explores the pathogenetic mechanisms of conduction block in ALS and multifocal motor neuropathy (MMN).
Area of Science:
- Neuroscience
- Neurology
Context:
- Demyelination in peripheral nerves can be diffuse or local.
- Diffuse demyelination underlies inflammatory demyelinating polyneuropathies.
- Local demyelination, characterized by conduction block, is typical of multifocal motor neuropathy (MMN).
Purpose:
- To describe three cases of amyotrophic lateral sclerosis (ALS) with confirmed conduction block.
- To investigate the pathogenetic mechanisms of conduction block in ALS and MMN.
- To discuss differential diagnosis between ALS and MMN.
Summary:
- Electroneuromyographic (ENMG) research revealed conduction block in three patients diagnosed with ALS.
- This finding contrasts with the general understanding that conduction block excludes an ALS diagnosis.
- The study examines the underlying mechanisms of conduction block in both ALS and MMN.
Impact:
- Challenges the established diagnostic criteria for ALS.
- Highlights the importance of ENMG in diagnosing complex neurological conditions.
- Provides insights into the differential diagnosis between ALS and MMN, improving patient management.
Related Concept Videos
01:19Multiple 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...
01:26Cross-bridge Cycle
As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.
01:25Secondary 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...
01:22Myasthenia 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...