Global hypoxia per se is an unusual cause of axonal injury

Irreversible hypoxic brain damage and axonal injury are present in over 90% of fatal blunt head injuries. Given the frequency each, difficulties arise as to whether or not they are due to different mechanisms and, as such, ca n be separately recognised and quantified. Recent literature has raised the possible role of hypoxia in the formation of axonal bulbs. The present stu dy of 17 cases of cardio-respiratory arrest, 12 of status epilepticus, 3 of carbon monoxide poisoning and 12 controls was designed to test the relatio nship between hypoxia and axonal injury and to test the hypothesis whether or not the two entities can be separated into primary and secondary forms o f traumatic brain injury. Axonal damage was seen in 9/17 and 7/12 of the ca ses with cardiac arrest and status epilepticus, respectively, in most of wh om there was also evidence of raised intracranial pressure (ICP). All 3 cas es of carbon monoxide poisoning had evidence of white matter damage in keep ing with the classical pattern of selective vulnerability. It is concluded that the great majority of axonal damage identified in cases dying after ca rdiac arrest and status epilepticus can be attributed to raised ICP and the vascular complications of internal herniation. However, in some cases, axo nal damage was seen in the absence of an elevated ICP, although its amount and distribution were different from diffuse axonal injury. In many cases t here was an increase in expression of neuronal beta amyloid precursor prote in.