In the 25 years or so after the first clinicopathological descriptions of d
iffuse axonal injury (DAI), the criterion for diagnosing recent traumatic w
hite matter damage was the identification of swollen axons ('bulbs') on rou
tine or silver stains, in the appropriate clinical setting. In the last dec
ade, however, experimental work has given us greater understanding of the c
ellular events initiated by trauma to axons, and this in turn has led to th
e adoption of immunocytochemical methods to detect markers of axonal damage
in both routine and experimental work. These methods have shown that traum
atic axonal injury (TAI) is much more common than previously realized, and
that what was originally described as DAI occupies only the most severe end
of a spectrum of diffuse trauma-induced brain injury. They have also revea
led a whole field of previously unrecognized white matter pathology, in whi
ch axons are diffusely damaged by processes other than head injury; this in
turn has led to some terminological confusion in the literature. Neuropath
ologists are often asked to assess head injuries in a forensic setting: the
diagnostic challenge is to sort out whether the axonal damage detected in
a brain is indeed traumatic, and if so, to decide what - if anything - can
be inferred from it. The lack of correlation between well-documented histor
ies and neuropathological findings means that in the interpretation of assa
ult cases at least, a diagnosis of 'TAI' or 'DAI' is likely to be of limite
d use for medicolegal purposes.