Diffuse axonal injury

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Diffuse axonal injury

Classification and external resources

Susceptibility weighted image (SWI) of diffuse axonal injury in trauma at 1.5 teslas (right)

eMedicine

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MeSH

D020833

Diffuse axonal injury (DAI) is one of the most common and devastating types oftraumatic brain injury,[1] meaning that damage occurs over a more widespread area than in focal brain injury. DAI, which refers to extensive lesions in white matter tracts, is one of the major causes of unconsciousness and persistent vegetative state after head trauma.[2] It occurs in about half of all cases of severe head trauma and also occurs in moderate and mild brain injury.[3] The outcome is frequently coma, with over 90% of patients with severe DAI never regaining consciousness.[2] Those who do wake up often remain significantly impaired.[4] Nowadays, other authors state that DAI can occur in every degree of severity from (very) mild or moderate to (very) severe.[5][6] Concussion may be a milder type of diffuse axonal injury.[7]

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 [8] in auto accidents, falls, and assaults. It usually results from rotational forces or [9][10] severe deceleration. Vehicle accidents are the most frequent cause of DAI; it can also occur as the [11] [12] result ofchild abuse such as in shaken baby syndrome.

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 [2] density, especially at junctions between white and grey matter. Two thirds of DAI lesions occur in areas [2] where grey and white matter meet. [edit]Characteristics Lesions typically exist in the white matter of brains injured by DAI; these lesions vary in size from about [2] 115 mm and are distributed in a characteristic way. DAI most commonly affects white matter in areas [3] including the brain stem, the corpus callosum, and thecerebral hemispheres. The lobes of the [13] brain most likely to be injured are the frontal and temporal lobes. Other common locations for DAI include the white matter in the cerebral cortex, the corpus callosum, the superior cerebral [12] [14] peduncles, basal ganglia,thalamus, and deep hemispheric nuclei. These areas may be more easily [14] damaged because of the difference in density between them and the rest of the brain. [edit]Histological

characteristics

DAI is characterized by axonal separation, in which the axon is torn at the site of stretch and the part distal to the tear degrades. While it was once thought that the main cause of axonal separation was tearing due to mechanical forces during the trauma, it is now understood that axons are not typically torn upon impact; rather, secondary biochemical cascades, which occur in response to theprimary injury (which occurs as the result of mechanical forces at the moment of trauma) and take place hours to [3][8][15] days after the initial injury, are largely responsible for the damage to axons. 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 [1] the cytoskeleton. It also opens sodium channels in the axolemma, which causes voltage-gated calcium 2+ [1] 2+ channels to open and Ca to flow into the cell. The intracellular presence of Ca unleashes several different pathways, including activating phospholipases and proteolytic enzymes, damaging mitochondria and the cytoskeleton, and activating secondary messengers, which can lead to [8] separation of the axon and death of the cell.

Diagnosis and treatment

DAI is difficult to detect since it does not show up well on CT scans or with other macroscopic imaging [2] techniques, though it shows up microscopically. However, there are characteristics typical of DAI that [3] may or may not show up on a CT scan. Diffuse injury has more microscopic injury than macroscopic injury and is difficult to detect with CT and MRI, but its presence can be inferred when small bleeds are [27] visible in the corpus callosum or the cerebral cortex. MRI is more useful than CT for detecting [28] characteristics of diffuse axonal injury in the subacute and chronic time frames. Newer studies such as Diffusion Tensor Imaging are 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 [2] like unconsciousness. MRI is more sensitive than CT scans, but MRI may also miss DAI, because it identifies the injury using [26] signs of edema, which may not be present. DAI is classified into grades based on severity of the injury. In Grade I, widespread axonal damage is present but no focal abnormalities are seen. In Grade II, damage found in Grade I is present in addition to focal abnormalities, especially in the corpus callosum. Grade III damage encompasses both Grades I and [29] II plus rostral brain stem injury and often tears in the tissue. 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). [edit]Potential
[3]

Treatments

Polyethylene glycol acts as a membrane sealant, and may serve to prevent the aforementioned devastating calcium influx. Rats treated with polyethylene glycol immediately following DAI induction [30] showed no cytotoxic edema on diffusion weighted MRI 7 days later unlike controls.