Diffuse axonal injury

Changed by Henry Knipe, 17 Mar 2016

Updates to Article Attributes

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

It is best approached on MRI where it is characterised by small regions of susceptibility artifact at the grey-white matter junction, in the corpus callosum, and, in more severe cases, in the brainstem.

Epidemiology

The patients at risk of diffuse axonal injuryDAI 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). 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, as the name implies. In majority of cases these forces result in damage to the cells in a way that cause cell oedema. Actual tear of the axons is rare and only seen in very severe cases. 

Associations

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 centimetres in diameter. Non-haemorrhagic lesions are hypodense. 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 if a couple of small haemorrhagic lesions are visible on CT, the degree of damage is much greater. 

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 paramagnetic blood products may demonstrate small regions of susceptibility artefact 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, the 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 sequences. 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: (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 neuropsychiatric deficits 1.

Differential diagnosis

On imaging consider:

  • -<p><strong>Diffuse axonal injury (DAI)</strong> is a severe parenchymal traumatic insult seen in closed head injuries and is potentially a difficult diagnosis to make on imaging (especially on CT). It can result in severe neurological impairment. </p><p>It is best approached on MRI where it is characterised by small regions of susceptibility artifact at the grey-white matter junction, in the <a href="/articles/corpus-callosum">corpus callosum</a> and, in more severe cases, in the brainstem.</p><h4>Epidemiology</h4><p>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. </p><h4>Clinical presentation</h4><p>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. <a href="/articles/cerebral-haemorrhagic-contusion">cerebral contusions</a>). As such the diagnosis is often not suspected until later when patients fail to recover neurologically as expected. </p><h4>Pathology</h4><p>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). 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, as the name implies. In majority of cases these forces result in damage to the cells in a way that cause cell oedema. Actual tear of the axons is rare and only seen in very severe cases. </p><h5>Associations</h5><ul><li><a href="/articles/intermediary-injury">intermediary injuries</a></li></ul><h4>Radiographic features</h4><p>Diffuse axonal injury is characterised by multiple focal lesions with a characteristic distribution: typically located at the grey-white matter junction, in the <a href="/articles/corpus-callosum">corpus callosum</a> and in more severe cases in the brainstem (see: <a href="/articles/grading-of-diffuse-axonal-injury">grading of diffuse axonal injury</a>). </p><h5>CT</h5><p>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 <sup>4-5</sup>. </p><p>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 centimetres in diameter. Non-haemorrhagic lesions are hypodense. 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. </p><p>CT is particularly insensitive to non-haemorrhagic lesions (as defined by CT) only able to detect 19% of such lesions, compared to 92% using <a href="/articles/t2-weighted-image">T2 weighted imaging</a> <sup>4</sup>. When lesions are haemorrhagic, and especially when they are large, then CT is quite sensitive. As such, it is usually a safe assumption that if a couple of small haemorrhagic lesions are visible on CT, the degree of damage is much greater. </p><h5>MRI</h5><p>MRI is the modality of choice for assessing suspected diffuse axonal injury even in patients with entirely normal CT of the brain <sup>5-6</sup>. MRI, especially <a href="/articles/susceptibility-weighted-imaging-1">SWI</a> or <a href="/articles/gradient-echo-sequences-1">GRE</a> 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 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 <a href="/articles/fluid-attenuation-inversion-recovery">FLAIR</a> signal. </p><p>Over the first few days, the degree of surrounding oedema will typically increase. </p><p>It should be noted, that even with high field strength modern scanners, the absence of findings does not categorically exclude the presence of axonal injury. </p><h6>MR spectroscopy</h6><p>MRS can be of benefit in identifying patients with grade I injury which may be inapparent on other sequences. Features typically demonstrate elevation of choline peak and reduction of NAA <sup>3</sup>. </p><h4>Treatment and prognosis</h4><p>Unfortunately little can be done for patients with diffuse axonal injury other than trying to minimise secondary damage caused by cerebral oedema, hypoxia, etc.</p><p>Depending on the severity and distribution of injury  (see <a href="/articles/grading-of-diffuse-axonal-injury">grading of diffuse axonal injury</a>) patients can vary from minimally affected to being in a persistent vegetative state <sup>1-2</sup>. 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 neuropsychiatric deficits <sup>1</sup>.</p><h4>Differential diagnosis</h4><p>On imaging consider:</p><ul>
  • +<p><strong>Diffuse axonal injury (DAI)</strong> is a severe parenchymal traumatic insult seen in closed head injuries and is potentially a difficult diagnosis to make on imaging (especially on CT). It can result in severe neurological impairment. </p><p>It is best approached on MRI where it is characterised by small regions of susceptibility artifact at the grey-white matter junction, in the <a href="/articles/corpus-callosum">corpus callosum</a>, and in more severe cases in the brainstem.</p><h4>Epidemiology</h4><p>The patients at risk of DAI belong to the same cohort as those who suffer traumatic brain injury and as such young men are very much over-represented. </p><h4>Clinical presentation</h4><p>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. <a href="/articles/cerebral-haemorrhagic-contusion">cerebral contusions</a>). As such the diagnosis is often not suspected until later when patients fail to recover neurologically as expected. </p><h4>Pathology</h4><p>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). 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, as the name implies. In majority of cases these forces result in damage to the cells in a way that cause cell oedema. Actual tear of the axons is rare and only seen in very severe cases. </p><h5>Associations</h5><ul><li><a href="/articles/intermediary-injury">intermediary injuries</a></li></ul><h4>Radiographic features</h4><p>Diffuse axonal injury is characterised by multiple focal lesions with a characteristic distribution: typically located at the grey-white matter junction, in the <a href="/articles/corpus-callosum">corpus callosum</a> and in more severe cases in the brainstem (see: <a href="/articles/grading-of-diffuse-axonal-injury">grading of diffuse axonal injury</a>). </p><h5>CT</h5><p>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 <sup>4-5</sup>. </p><p>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 centimetres in diameter. Non-haemorrhagic lesions are hypodense. 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. </p><p>CT is particularly insensitive to non-haemorrhagic lesions (as defined by CT) only able to detect 19% of such lesions, compared to 92% using <a href="/articles/t2-weighted-image">T2 weighted imaging</a> <sup>4</sup>. When lesions are haemorrhagic, and especially when they are large, then CT is quite sensitive. As such, it is usually a safe assumption that if a couple of small haemorrhagic lesions are visible on CT, the degree of damage is much greater. </p><h5>MRI</h5><p>MRI is the modality of choice for assessing suspected diffuse axonal injury even in patients with entirely normal CT of the brain <sup>5-6</sup>. MRI, especially <a href="/articles/susceptibility-weighted-imaging-1">SWI</a> or <a href="/articles/gradient-echo-sequences-1">GRE</a> 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 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 <a href="/articles/fluid-attenuation-inversion-recovery">FLAIR</a> signal. </p><p>Over the first few days, the degree of surrounding oedema will typically increase. </p><p>It should be noted, that even with high field strength modern scanners, the absence of findings does not categorically exclude the presence of axonal injury. </p><h6>MR spectroscopy</h6><p>MRS can be of benefit in identifying patients with grade I injury which may be inapparent on other sequences. Features typically demonstrate elevation of choline peak and reduction of NAA <sup>3</sup>. </p><h4>Treatment and prognosis</h4><p>Unfortunately little can be done for patients with diffuse axonal injury other than trying to minimise secondary damage caused by cerebral oedema, hypoxia, etc.</p><p>Depending on the severity and distribution of injury (see: <a href="/articles/grading-of-diffuse-axonal-injury">grading of diffuse axonal injury</a>) patients can vary from minimally affected to being in a persistent vegetative state <sup>1-2</sup>. 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 neuropsychiatric deficits <sup>1</sup>.</p><h4>Differential diagnosis</h4><p>On imaging consider:</p><ul>
  • -<a href="/articles/cortical-contusions">c</a><a href="/articles/cerebral-haemorrhagic-contusion">ortical contusions</a>: <ul>
  • +<a href="/articles/cortical-contusions">c</a><a href="/articles/cerebral-haemorrhagic-contusion">ortical contusions</a><ul>

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