Diffuse axonal injury

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Diffuse axonal injury ( DAI ) is a brain injury in which extensive lesions of the white matter tract occur over a large area. DAI is one of the most common and powerful types of traumatic brain injury, and is the leading cause of unconscious and persistent vegetative state after severe head trauma. This occurs in about half of all cases of severe head trauma and may be the major damage that occurs in concussions. The result is often comatose, with over 90% of patients with severe DAI never regaining consciousness. Those who wake up often remain significantly impaired.

DAI can occur at any level of severity from very mild or moderate to very severe. A concussion may be a milder type of axial axial injury

Video Diffuse axonal injury

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DAI is the result of a traumatic shear force that occurs when the head is rapidly accelerated or slowed, as can occur in car accidents, falls, and attacks. Vehicle accidents are the most common cause of DAI; it can also occur as a result of child abuse as in the shaken baby syndrome.

Termination of axons may soon be observed in severe brain injury, but the main deterioration of DAI is the delay in secondary axon termination which gradually develops for extended periods. The axon marks, which appear white due to myelin, are referred to as white matter. Lesions in gray and white matter are found in the postmortem brain in CT and MRI.

In addition to the axonal mechanical termination of the cytoskeleton, the pathology of DAI also includes secondary physiological changes such as axonal transport disturbances, progressive swelling, and degeneration. Recent studies have linked these changes to rotate and miss the damaged axon microtubules, as well as tap and APP deposition.

Maps Diffuse axonal injury

Characteristics

Lesions are usually present in white matter brain injured by DAI; The lesion varies in size from about 1-15 mm and is distributed in a typical way. DAI most often affects white matter in areas including the brainstem, corpus callosum, and cerebral hemispheres.

The most likely brain lobes are the frontal and temporal lobes. Other common locations for DAI include white matter in the cerebral cortex, cerebral superior cerebral, basal ganglia, thalamus, and deep hemispheric nuclei. These areas may be more easily damaged by differences in the density between them and the rest of the brain.

Histological Characteristics

DAI is characterized by axonal separation, in which the axon is torn at the stretch site and distal to the teardrop. While it was once thought that the main cause of axonal separation was torn due to mechanical forces during trauma, it is now understood that axons are not normally torn at impact; In contrast, a secondary biochemical cascade, which occurs in response to a primary injury (which occurs as a result of mechanical strength at the time of trauma) and lasts several hours to the day after the initial injury, is largely responsible for axon damage.

Although the processes involved in secondary brain injury are still poorly understood, it is now accepted that stretching axon during injury causes physical disturbance and proteolytic degradation of the cytoskeleton. It also opens the sodium channel in the axolemma, which causes the voltage-gated calcium channel to open and Ca ² to flow into the cell. The presence of intracellular Ca ² releases several different pathways, including activating phospholipase and proteolytic enzymes, destroying mitochondria and cytoskeleton, and activating secondary messengers, which can lead to the separation of axons and cell death.

Disruption of cytoskeleton

Axons are usually elastic, but when rapidly stretched they become brittle, and axonal cytoskeleton can be damaged. Cytoskeletal element misalignment after stretch injury can lead to axon rupture and neuron death. The axonal transport continues to the point of rest in the cytoskeleton, but no farther, leading to a buildup of local transport and swelling products at the time. When it becomes quite large, the swelling can tear the axon at the resting location in the cytoskeleton, causing it to pull back towards the body cell and form the bulb. These light bulbs are called retracting balls, characteristic of diffuse axonal injury.

When the axons are transmitted, the degrees of Wallerian, where the axon portion is distal to the degraded break, takes place within one to two days after injury. Axolemma is destroyed, myelin is damaged and begins to detach from the cells in the anterograde direction (from the body of the cell to the end of the axon), and nearby cells begin phagocytic activity, swallowing debris.

The entry of calcium

While sometimes only the cytoskeleton is disturbed, frequent disturbances from axolemma occur as well, causing the entry of Ca ² into the cells and releasing various degrading processes. Increased levels of Ca ² and Na and decreased levels of K were found in the axon immediately after the injury. Possible routes of Ca ² entry include sodium channels, torn pores within the membrane during stretching, and ATP-dependent carrier failure due to mechanical blockage or lack of energy. High levels of intracellular Ca ² , a major cause of post-injury cell damage, destroys the mitochondria, and triggers phospholipase and proteolytic enzymes that damage Na channels and decrease or alter cytoskeleton and axoplasma. Excess Ca ² can also cause damage to the blood brain barrier and brain swelling.

One of the proteins activated by the presence of calcium in the cells is calpain, a non-lysosomic non-lysosome Ca ² protein. About 15 minutes to half an hour after the onset of injury, a process called calpain-mediated spectrum mediolysis, or CMSP, begins. Calpain breaks up a molecule called spectrin, which holds the membrane to the cytoskeleton, leading to the formation of blebs and the breakdown of the cytoskeleton and membrane, and finally cell death. Other molecules that can be degraded by calpains are the microtubule subunits, microtubule-related proteins, and neurofilaments.

Generally occurring one to six hours into the post-stretch injury process, the presence of calcium in cells begins the caspase cascade, a process in which cell injury usually leads to apoptosis, or "cell suicide".

Mitochondria, dendrites, and injury-damaged cytoskeleton parts have limited ability to heal and regenerate, a process that occurs more than 2 weeks or more. After an injury, astrocytes can shrink, causing the brain to have atrophy.

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Diagnosis

DAI is difficult to detect because it does not appear well on CT scans or with other macroscopic imaging techniques, although it appears microscopically. However, there are typical characteristics of DAI that may or may not appear on CT scan. Diffuse injuries have more microscopic injuries than macroscopic injuries and are difficult to detect with CT and MRI, but their presence can be inferred when small bleeding is seen in the corpus callosum or cerebral cortex. MRI is more useful than CT to detect diffuse axonal injury characteristics in subacute and chronic time frames. New studies such as Diffusion Tensor Imaging are able to show a level of white fiber tract injury even when standard MRI is negative. Because axonal damage in DAI is largely the result of a secondary biochemical cascade, it has a delayed onset, so someone with a initially good looking DAI may worsen later. Thus, injuries are often more severe than are conscious, and medical professionals should suspect DAI in patients whose CT scans appear normal but who have symptoms such as unconsciousness.

MRI is more sensitive than CT scans, but MRI may also lose DAI, as it identifies injuries using signs of edema, which may not be present.

DAI is classified into a value based on the severity of the injury. In Grade I, extensive axonal damage is present but no focal abnormality is observed. In Grade II, damage found in Grade I is present in addition to focal abnormalities, especially in the corpus callosum. Grade III damage includes Grades I and II plus rostral brain stem injuries and often tears in the tissues.

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Treatment

DAI currently has no specific treatment beyond what is done for all types of head injuries, including stabilizing the patient and trying to limit the increase in intracranial pressure (ICP).

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History

The idea of ​​DAI first emerged as a result of a study by Sabina Strich on lesions on white matter of individuals who had experienced head trauma several years earlier. Strich first proposed the idea in 1956, calling it degeneration diffused from white matter, but the more concise term "Diffuse Axonal Injury" was finally preferred. Strich was examining the relationship between dementia and head trauma and asserted in 1956 that DAI plays an integral role in the development of dementia due to head trauma. The term DAI was introduced in the early 1980s.

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Important example

• Top Gear presenter Richard Hammond suffered DAI as a result of Vampire Dragster Crash in 2006.
• Champ Car World Series racer Roberto Guerrero suffered DAI from an accident while performing tests at Indianapolis Motor Speedway in 1987.
• Formula 1 rider Jules Bianchi suffered DAI from an accident at the 2014 Japanese Grand Prix and died, unknowingly returning, 9 months later on July 17, 2015.
• The audiobook actor and narrator Frank Muller, famous for his reading of Stephen King's The Dark Tower, suffered a DAI due to a motorcycle accident in 2001. He died in 2008.

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See also

• Brain injury
• Axoplasma Transport

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References

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External links

• Image of Nerve Injury and MRI Axis Diffusion

Source of the article : Wikipedia