Diffuse axonal injury Totally Explained

Everything about Diffuse Axonal Injury totally explained

Diffuse axonal injury (DAI) is one of the most common and devastating types of traumatic brain injury, occurring in about half of all cases of severe head trauma and also occurring in moderate and mild brain injury.
Though diffuse axonal injury seldom kills, the outcome is frequently coma, with over 90% of patients with severe DAI never regaining consciousness.
Nowadays, other authors state that DAI can occur in every degree of severity from (very) mild or moderate to (very) severe. Concussion is thought to be a milder type of diffuse axonal injury.

Mechanism

Unlike brain trauma that occurs due to direct impact and deformation of the brain, DAI is the result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated, as may occur in auto accidents, falls, and assaults. It usually results from rotational forces or severe deceleration. Vehicle accidents are the most frequent cause of DAI; other common causes include falls, assaults, and child abuse
   The major cause of damage in DAI is the disruption of axons, the neural processes that allow one neuron to communicate with another. Tracts of axons, which appear white due to myelination, are referred to as white matter. Acceleration causes shearing injury, which refers to damage inflicted as tissue slides over other tissue. When the brain is accelerated, parts of differing densities and distances from the axis of rotation slide over one another, stretching axons that traverse junctions between areas of different density, especially at junctions between white and grey matter. Other common locations for DAI include the white matter in the cerebral cortex, the corpus callosum, the superior cerebral peduncles, These areas may be more easily damaged because of the difference in density between them and the rest of the brain. Axons are not typically torn at the time of injury; rather they usually become separated hours or days after the injury.
   Though the processes involved in secondary brain injury are still poorly understood, it's now accepted that stretching of axons during injury causes physical disruption to and proteolytic degradation of the cytoskeleton.
   Misalignment of cytoskeletal elements after stretch injury can lead to tearing of the axon and death of the neuron. Axonal transport continues up to the point of the break in the cytoskeleton, but no further, leading to a buildup of transport products and local swelling at that point. When it becomes large enough, swelling can tear the axon at the site of the break in the cytoskeleton, causing it to draw back toward the cell body and form a bulb. The axolemma disintegrates, and nearby cells begin phagocytic activity, engulfing debris.

Calcium influx

While sometimes only the cytoskeleton is disturbed, frequently disruption of the axolemma occurs as well, causing the influx of Ca²⁺ into the cell and unleashing a variety of degrading processes. An increase in Ca²⁺ and Na⁺ levels and a drop in K⁺ levels is found within the axon directly after injury. destroy mitochondria, Calpain breaks down a molecule called spectrin, which holds the membrane onto the cytoskeleton, causing the formation of blebs and the breakdown of the cytoskeleton and the membrane, and ultimately the death of the cell. After the injury, astrocytes can shrink, causing parts of the brain to atrophy.
DAI currently lacks a specific treatment beyond what is done for any type of head injury, including stabilizing the patient and trying to limit increases in intracranial pressure (ICP).

History

The idea of DAI first came about as a result of studies by Sabina Strich on lesions of the white matter of individuals who had suffered head trauma years before. She was researching the relationship between dementia and head trauma

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