Traumatic brain injury: can the consequences be stopped?

CMAJ. 2008 Apr 22;178(9):1163-70. doi: 10.1503/cmaj.080282.

Abstract

Traumatic brain injury is a leading cause of morbidity and death in both industrialized and developing countries. To date, there is no targeted pharmacological treatment that effectively limits the progression of secondary injury. The delayed progression of deterioration of grey and white matter gives hope that a meaningful intervention can be applied in a realistic timeframe following initial trauma. In this review we discuss new insights into the subcellular mechanisms of secondary injury that have highlighted numerous potential targets for intervention.

Publication types

  • Review

MeSH terms

  • Animals
  • Axons / metabolism
  • Biomarkers / metabolism
  • Brain Edema / physiopathology
  • Brain Injuries / metabolism*
  • Brain Injuries / physiopathology*
  • Calcium / metabolism
  • Calpain / metabolism
  • Diffuse Axonal Injury / physiopathology
  • Glutamic Acid / metabolism
  • Humans
  • Intracranial Hypertension / physiopathology
  • Receptors, AMPA / metabolism
  • Receptors, N-Methyl-D-Aspartate / metabolism

Substances

  • Biomarkers
  • Receptors, AMPA
  • Receptors, N-Methyl-D-Aspartate
  • Glutamic Acid
  • Calpain
  • Calcium