• Muscles remain biochemically active after the death of an animal
  • Following a period of relaxation, contraction and stiffening occurs
  • Due to deficiency of ATP releasing myosin heads from their binding sites at end of power stroke
  • Onset faster in ATP deprived animals (starvation, hunting, tetanus...)
  • May be absent in cachetic animals
  • Disappears due to autolysis or putrefaction
  • See general pathology


    • Damage occured at one time, e.g. trauma or one toxin exposure
  • Multiphasic lesions - different stages as described above
    • Ongoing damage, e.g. vitamin E - selenium deficiency, continuous exposure to toxin