Hypoglycaemia is a cause of axonal injury

D Dolinak, C Smith, D I Graham

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Axonal injury as demonstrated immunohistochemically is increasingly being recognized at post-mortem in patients who have been unconscious, and in some cases the cause of the coma may not be immediately apparent. Considerations include microscopical diffuse traumatic axonal injury and axonal injury associated with a range of metabolic encephalopathies. In this study, extensive neurohistological examination was undertaken in 13 patients in whom coma was attributed to hypoglycaemia and in whom neurohistological examination had revealed varying degrees of widely distributed neuronal necrosis: in five of these cases there was also evidence that the intracranial pressure had been high with internal hernation. It is concluded that a significant amount of axonal injury found in these 13 cases can be attributed to hypoglycaemia per se although the amount and distribution of the axonal damage is altered in the presence of raised intracranial pressure. However, in some cases axonal damage is seen in the absence of an elevated intracranial pressure and in one case its distribution closely mimicked that seen in microscopical diffuse traumatic axonal injury. This further demonstrates that not all axonal pathology is traumatic, and that adequate sampling and care in interpretation of Abeta-PP staining is required in forensic practice.
Original languageEnglish
Pages (from-to)448-53
Number of pages6
JournalNeuropathology and Applied Neurobiology
Issue number5
Publication statusPublished - Oct 2000

Keywords / Materials (for Non-textual outputs)

  • Adolescent
  • Adult
  • Aged
  • Amyloid beta-Protein Precursor
  • Axons
  • Brain
  • Brain Damage, Chronic
  • Cerebral Infarction
  • Child
  • Coma
  • Encephalocele
  • Female
  • Humans
  • Hypoglycemia
  • Intracranial Pressure
  • Male
  • Middle Aged
  • Necrosis
  • Neurons


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