Diffuse axonal injury

Diffuse axonal injury (DAI) is a brain injury in which scattered lesions occur over a widespread area in white matter tracts as well as grey matter. DAI is one of the most common and devastating types of traumatic brain injury and is a major cause of unconsciousness and persistent vegetative state after severe head trauma. It occurs in about half of all cases of severe head trauma and may be the primary damage that occurs in concussion. The outcome is frequently coma, with over 90% of patients with severe DAI never regaining consciousness.

DAI can occur across the spectrum of traumatic brain injury (TBI) severity, wherein the burden of injury increases from mild to severe. Concussion may be a milder type of diffuse axonal injury.

Mechanism

DAI is the result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated, as may occur in car accidents, falls, and assaults. Vehicle accidents are the most frequent cause of DAI; it can also occur as the result of child abuse

Immediate disconnection of axons may be observed in severe brain injury, but the major damage of DAI is delayed secondary axon disconnections, slowly developed over an extended time course. Recent studies have linked these changes to twisting and misalignment of broken axon microtubules, as well as tau protein and amyloid precursor protein (APP) deposition.

Characteristics

Lesions typically are found in the white matter of brains injured by DAI; these lesions vary in size from about 1–15 mm and are distributed in a characteristic pattern. Other common locations for DAI include the white matter in the cerebral cortex, the superior cerebral peduncles, These areas may be more easily damaged because of the difference in density between them and the other regions of the brain.

Though the processes involved in secondary brain injury are still poorly understood, it is now accepted that stretching of axons during injury causes physical disruption to and proteolytic degradation of the cytoskeleton. It also opens sodium channels in the axolemma, which causes voltage-gated calcium channels to open and Ca2+ to flow into the cell. When this swelling becomes large enough, it can tear the axon at the site of the cytoskeleton break, causing it to draw back toward the cell body and form a bulb. The axolemma disintegrates, and nearby cells begin phagocytic activity, engulfing the cellular debris.

Calcium influx

While sometimes only the cytoskeleton is disturbed, frequently disruption of the axolemma occurs as well, causing the influx of Ca2+ ions into the cell and unleashing a variety of degradational processes. An increase in Ca2+ and Na+ levels and a drop in K+ levels are found within the axon immediately 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. MRI is more useful than CT for detecting characteristics of diffuse axonal injury in the subacute and chronic time frames. Newer technology, such as diffusion tensor imaging, is able to demonstrate the degree of white matter fiber tract injury even when the standard MRI is negative. Since axonal damage in DAI is largely a result of secondary biochemical cascades, it has a delayed onset, so a person with DAI who initially appears well may deteriorate later. Thus, injury is frequently more severe than is realized, and medical professionals should suspect DAI in any patients whose CT scans appear normal but who have symptoms like unconsciousness.

Treatment

There is no treatment that reverses the primary axonal shearing once it has occurred; management is therefore primarily supportive and follows neurocritical-care principles used for moderate-to-severe traumatic brain injury, with the goal of preventing secondary brain injury from hypoxia, hypotension and intracranial hypertension.

Severe diffuse axonal injury may require intensive care with airway protection and mechanical ventilation when indicated to reduce secondary injury.

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 sustained head trauma years before. Strich first proposed the idea in 1956, calling it diffuse degeneration of white matter; however, the more concise term "diffuse axonal injury" came to be preferred. Strich was researching the relationship between dementia and head trauma The term DAI was introduced in the early 1980s.

Notable examples

Top Gear presenter Richard Hammond sustained a DAI as a result of the Vampire dragster crash in 2006.
Champ Car World Series driver Roberto Guerrero suffered a DAI as a result of a crash during testing at the Indianapolis Motor Speedway in 1987.
Formula 1 driver Jules Bianchi suffered a DAI as a result of an accident at the 2014 Japanese Grand Prix and died without regaining consciousness 9 months later.
Actor and audiobook narrator Frank Muller, who read Stephen King's The Dark Tower, suffered a DAI in 2001 due to a motorcycle accident. He died in 2008.
NASCAR driver Adam Petty, grandson of seven time Cup Series champion Richard Petty, sustained a diffuse axonal injury secondary to a fatal basilar skull fracture in May 2000 at New Hampshire Motor Speedway during practice for the upcoming race.

References

External links

Diffuse Axonal Injury MRI and CT Images