Diffuse axonal injury

[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] DAI most commonly affects white matter in areas including the brain stem, the corpus callosum, and the cerebral hemispheres.

[25] When this swelling becomes large enough, it can tear the axon at the site of the cytoskeleton break, causing it to draw back toward the cell body and form a bulb.

[28] While sometimes only the cytoskeleton is disturbed, frequently disruption of the axolemma occurs as well, causing the influx of Ca2+ ions into the cell and unleashing a variety of degradational processes.

[21][26] Possible routes of Ca2+ entry include sodium channels, pores formed in the membrane during stretch, and failure of ATP-dependent transporters due to mechanical blockage or lack of available metabolic energy.

[31] About 15 minutes to half an hour after the onset of injury, a process called calpain-mediated spectrin proteolysis, or CMSP, begins to occur.

[32] Mitochondria, dendrites, and parts of the cytoskeleton damaged in the injury have a limited ability to heal and regenerate, a process which occurs over two or more weeks.

[35] 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.

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 like unconsciousness.

[9] MRI is more sensitive than CT scans, but is still liable to false negatives because DAI is identified by looking for signs of edema, which may not always be present.

[36] DAI currently lacks specific treatment beyond that for any type of head injury, which includes stabilizing the patient and trying to limit increases in intracranial pressure (ICP).

[citation needed] The idea of DAI first came about as a result of studies by Sabina Strich on lesions of the white matter of individuals who had sustained head trauma years before.

Immunoreactive axonal profiles are observed as either granular (B, G, H) or more elongated, fusiform (F) swellings in the corpus callosum and the brain stem (H) at 24h post traumatic brain injury . Example of APP immunoreactive neurons (arrow heads) observed in the cortex underneath the impact site (E, G). No APP staining was observed in healthy control animals (D). [ 23 ]
Diffuse axonal injury after a motorcycle accident. MRI after 3 days: on T1-weighted images the injury is barely visible. On the FLAIR , DWI and T2*-weighted images a small bleed is identifiable.