Related Experiment Video

Updated: May 6, 2026

Induction and Clinical Scoring of Chronic-Relapsing Experimental Autoimmune Encephalomyelitis
26:48

Induction and Clinical Scoring of Chronic-Relapsing Experimental Autoimmune Encephalomyelitis

Published on: July 4, 2007

18.3K

Definition of delayed-onset neurologic sequelae: A review article

Alik Dakessian1,2, Zachary Hagen1, Eugenio R Rocksmith3

  • 1Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD, United States of America.

Undersea & Hyperbaric Medicine : Journal of the Undersea and Hyperbaric Medical Society, Inc
|August 17, 2025
PubMed
Abstract

Keywords:
carbon monoxidecarbon monoxide poisoningdelayed encephalopathydelayed encephalopathy after acute carbon monoxide poisoningdelayed-onset neurologic sequelae

More Related Videos

Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients12:23

Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients

Published on: April 14, 2014

14.2K
The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage: Technical Aspects09:00

The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage: Technical Aspects

Published on: October 2, 2014

13.8K

Related Concept Videos

Long-term Depression01:05

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
27.3K
Long-term Depression01:03

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over...
2.6K
Toxic Reactions: Overview01:26

Toxic Reactions: Overview

When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
4.3K
Introduction to Language of Pathophysiology ll01:17

Introduction to Language of Pathophysiology ll

This lesson explores key terms that describe how diseases progress, their outcomes, and their distribution in populations.Diagnostic tests identify diseases and monitor treatment. These include blood and urine tests, biopsies, imaging (X-ray, MRI), and detection of infectious agents.Remission is a reduction or disappearance of symptoms.Exacerbation refers to the worsening of symptoms, such as increased wheezing during an asthma attack.A precipitating factor triggers an acute episode, while a...
69
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
32
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...
72