Diffuse Axonal Injury, Causes, Signs and Symptoms, Diagnosis and Treatment.

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Chapters

0:00 Introduction
1:59 Causes of Diffuse axonal injury
2:30 Symptoms of Diffuse axonal injury
2:56 Diagnosis of Diffuse axonal injury
3:23 Treatment of 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.[1][2][3][4][5][6][7] DAI is one of the most common and devastating types of traumatic brain injury[8] and is a major cause of unconsciousness and persistent vegetative state after severe head trauma.[9] 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.[9] Those who do wake up often remain significantly impaired.[10]


DAI can occur across the spectrum of traumatic brain injury (TBI) severity, wherein the burden of injury increases from mild to severe.[11][12] Concussion may be a milder type of diffuse axonal injury.[12][13]


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.[14] Vehicle accidents are the most frequent cause of DAI; it can also occur as the result of child abuse[15] such as in shaken baby syndrome.[16]

Immediate disconnection of axons could be observed in severe brain injury, but the major damage of DAI is delayed secondary axon disconnections slowly developed over an extended time course.[2] Tracts of axons, which appear white due to myelination, are referred to as white matter. Lesions in both grey and white matters are found in postmortem brains in CT and MRI exams.[9]

Besides mechanical breaking of the axonal cytoskeleton, DAI pathology also includes secondary physiological changes such as interrupted axonal transport, progressive swellings and degeneration.[17] 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.[17][18]