Diffuse axonal injury

Diffuse axonal injury (DAI) is seen in closed head injuries and is potentially a difficult diagnosis to make on imaging (especially on CT), and can result in severe neurological impairment. 

Epidemiology

The patients at risk of diffuse axonal injury belong to the same cohort as those who suffer traumatic brain injury and as such young men are very much over-represented. 

Clinical presentation

Typically patients who are shown to have DAI, have loss of consciousness at the time of the accident. Post traumatic coma may last variable 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. 

Pathology

Diffuse axonal injury is the result of shearing forces, typically from rotational acceleration (although this is most often in the form of what laypeople would refer to as deceleration, from a physics point of view there is no such thing; all changes in velocity are acceleration).

Radiographic features

Diffuse axonal injury is characterised 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). 

CT

Non-contrast CT of the brain is routine in patients presenting with head injuries. Unfortunately it is not terribly sensitive to subtle diffuse axonal injury and as such some patients with relatively normal CT scans have significant unexplained neurological deficit ^4-5. 

The appearance depends on whether or not the lesions are overtly haemorrhagic. Haemorrhagic lesions will be hyperdense and range in size from a few millimetres to a few centimeters in diameter. Non-haemorrhagic lesions are hypodense. Both types are 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). They typically become more evident over the first few days as oedema develops around them. They may be associated with significant and disproportionate cerebral swelling. 

CT is particularly insensitive to non-haemorrhagic lesions (as defined by CT) only able to detect 19% of such lesions, compared to 92% using T2 weighted imaging ⁴. When lesions are haemorrhagic, and especially when they are large, then CT is quite sensitive. As such, it is usually a safe assumption that is a couple of small haemorrhagic lesions are visible on CT, the degree of damage is much greater and that MRI is likely to visualise a far greater number of lesions. 

MRI

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 blood products may demonstrate small regions of susceptibility artifact at the grey white matter junction, in the corpus callosum or the brain stem. Some lesions may be entirely non-haemorrhagic (even using high field strength SWI sequences). These will however be visible as regions of high FLAIR signal. 

Over the first few days the degree of surrounding oedema will typically increase. 

It should be noted, that even with high field strength modern scanners, absence of findings does not categorically exclude the presence of axonal injury. 

MR spectroscopy

MRS can be of benefit in identifying patients with grade I injury which may be inapparent on other sequence. Features typically demonstrate elevation of choline peak and reduction of NAA ³. 

Treatment and prognosis

Unfortunately little can be done for patients with diffuse axonal injury other than trying to minimise secondary damage caused by cerebral oedema, hypoxia etc.

Depending on the severity and distribution of injury  (see grading of diffuse axonal injury) patients can vary from minimally affected to being in a persistent vegetative state ^1-2. The amount of axonal injury in the brain stem is predictive of long term vegetative state, whereas supratentorial injury can result in focal neurological or neurophsychiatric deficits ¹.

Differential diagnosis

The main

• Cortical contusions: main differential in patients with head injuries are cortical contusions which are typically located superficially, involving the cortex (rather than at the grey-white matter junction) and are usually associated with variable amounts of extra-axial blood (sub-arachnoid and subdural). 
• Diffuse vascular injuries
• Particularly on T2* sequences:
  • Amyloid angiopathy
  • Chronic hypertensive encephalopathy
  • Cavernoma type VI