Related Experiment Video

Updated: Apr 17, 2026

Induction of Diffuse Axonal Brain Injury in Rats Based on Rotational Acceleration
06:14

Induction of Diffuse Axonal Brain Injury in Rats Based on Rotational Acceleration

Published on: May 9, 2020

9.1K

Hypothalamic-amygdalar-brainstem volume reduction in a patient with narcolepsy secondary to diffuse axonal injury

Walid Yassin1, Genichi Sugihara1, Naoya Oishi2

  • 1Department of Psychiatry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Journal of Clinical Sleep Medicine : JCSM : Official Publication of the American Academy of Sleep Medicine
|February 11, 2015
PubMed

Keywords:
MRIamygdaladiffuse axonal injuryhypothalamusnarcolepsy

More Related Videos

Controlled Cortical Impact Model for Traumatic Brain Injury05:30

Controlled Cortical Impact Model for Traumatic Brain Injury

Published on: August 5, 2014

30.0K
Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury10:59

Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury

Published on: November 19, 2012

16.0K

Related Concept Videos

Narcolepsy01:07

Narcolepsy

Narcolepsy is a chronic sleep disorder characterized by pervasive, uncontrolled sleepiness and other sleep disturbances. One of its hallmark symptoms is an abrupt transition to REM sleep upon falling asleep, which causes symptoms typically associated with this phase to occur unexpectedly during wakefulness. These include the following symptoms, which typically last from a minute or two to half an hour.
822
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...
2
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this...
1
Sleep-Wake Cycles01:24

Sleep-Wake Cycles

Sleep is an essential physiological process vital to maintaining overall well-being. The reticular activating system (RAS), a network of neurons in the brainstem, regulates wakefulness and sleep. While it may seem passive, sleep consists of distinct cycles, each with its unique characteristics and functions. Two key sleep phases are non-rapid eye movement (NREM) and  rapid eye movement (REM).
NREM Sleep
NREM sleep comprises four progressive stages that seamlessly merge:
3.5K
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins...
2
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous...
1