Axonal injury as demonstrated immunohistochemically is increasingly being r
ecognized at post-mortem in patients who have been unconscious, and in some
cases the cause of the coma may not be immediately apparent. Consideration
s include microscopical diffuse traumatic axonal injury and axonal injury a
ssociated with a range of metabolic encephalopathies. In this study, extens
ive neurohistological examination was undertaken in 13 patients in whom com
a was attributed to hypoglycaemia and in whom neurohistological examination
had revealed varying degrees of widely distributed neuronal necrosis: in f
ive of these cases there was also evidence that the intracranial pressure h
ad been high with internal hernation. It is concluded that a significant am
ount of axonal injury found in these 13 cases can be attributed to hypoglyc
aemia per se although the amount and distribution of the axonal damage is a
ltered in the presence of raised intracranial pressure. However, in some ca
ses axonal damage is seen in the absence of an elevated intracranial pressu
re and in one case its distribution closely mimicked that seen in microscop
ical diffuse traumatic axonal injury. This further demonstrates that not al
l axonal pathology is traumatic, and that adequate sampling and care in int
erpretation of A beta-PP staining is required in forensic practice.