Diffuse axonal injury
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Diffuse axonal injury (DAI), also known as traumatic axonal injury (TAI), is a severe form of traumatic brain injury due to shearing forces. It is a potentially difficult diagnosis to make on imaging alone, especially on CT as the finding can be subtle, but it has the potential to result in severe neurological impairment.
The diagnosis is best made on MRI where it is characterized by several small regions of susceptibility artifact at the grey-white matter junction, in the corpus callosum, and in more severe cases in the brainstem, surrounded by FLAIR hyperintensity.
The patients at risk of diffuse axonal injury are the same cohort who suffer traumatic brain injury; young men are over-represented.
Typically, patients who are shown to have diffuse axonal injury have loss of consciousness at the time of the accident. Post-traumatic coma may last a considerable time and is often attributed to coexistent more visible injury (e.g. cerebral contusions). As such the diagnosis is often not suspected until later when patients fail to recover neurologically as expected.
Diffuse axonal injury is the result of shearing forces, typically from rotational acceleration (most often a deceleration). Due to the slightly different specific gravities (relative mass per unit volume) of white and grey matter, shearing due to change in velocity has a predilection for axons at the grey-white matter junction. In the majority of cases these forces damage cells and result in edema. Complete tearing of the axons is only seen in severe cases. Neurons may undergo degeneration in the weeks or months after trauma (secondary axonotmesis).
Diffuse axonal injury is characterized by multiple focal lesions with a characteristic distribution: typically located at the grey-white matter junction, in the corpus callosum, and in more severe cases in the brainstem (see: grading of diffuse axonal injury).
Non-contrast CT of the brain is routine in patients presenting with head injuries. Unfortunately, it is not sensitive to subtle diffuse axonal injury and as such, some patients with relatively normal CT scans may have significant unexplained neurological deficit 4,5.
CT findings depend on whether the lesions are overtly hemorrhagic, in which case they will be hyperdense, ranging in size from a few millimeters to a few centimeters in diameter. Non-hemorrhagic lesions are hypodense. They typically become more evident over the first few days as edema develops around them. They may be associated with significant and disproportionate cerebral swelling.
CT is particularly insensitive to non-hemorrhagic lesions, where only 19% are detected, compared to 92% with MR T2 weighted imaging 4. CT is sensitive to larger hemorrhagic lesions, so if these are visible on CT, the degree of damage is likely much greater.
Traumatic midline subarachnoid hemorrhage on initial CT is associated with severe diffuse axonal injury, with 60.8% sensitivity and 81.7% specificity for grade 2 or 3 injury 9.
MRI is the modality of choice for assessing suspected diffuse axonal injury even in patients with entirely normal CT of the brain 5,6. MRI, especially SWI or GRE sequences, exquisitely sensitive to paramagnetic blood products may demonstrate small regions of susceptibility artefact at the grey-white matter junction, in the corpus callosum or the brainstem. Some lesions may be entirely non-hemorrhagic (even using high field strength SWI sequences). These will, however, be visible as regions of high FLAIR signal.
Over the first few days post-injury, the degree of surrounding edema will typically increase, although by 3-months FLAIR changes will have largely resolved 7. In contrast, SWI changes usually take longer to resolve, with substantial resolution by 12-months post-injury 7. This makes sense as edema is faster to resolve than hemorrhage.
In the months that follow the trauma, there is accelerated brain volume reduction, which can sometimes be detected by visual inspection, but sometimes only by volumetric studies 8.
Importantly, even with high field strength modern scanners, the absence of findings does not categorically exclude axonal injury.
Treatment and prognosis
Unfortunately little can be done for patients with diffuse axonal injury other than providing supportive care trying to minimize secondary damage caused by cerebral edema, hypoxia, seizures, etc. Management involves the early recognition and treatment of neurosurgical complications such as herniation and hydrocephalus.
Depending on the severity and distribution of injury (see: grading of diffuse axonal injury) patients can vary from minimally affected to be in a persistent vegetative state 1,2. The amount of axonal injury in the brainstem is predictive of long-term vegetative state, whereas supratentorial injury can result in focal neurological or neuropsychiatric deficits 1.
On imaging consider:
particularly on T2* sequences
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