Canis ISSN: 2398-2942

Brain: cerebral concussion / contusion

Contributor(s): Laurent Garosi


  • See also brain trauma Brain: trauma.
  • Concussion is a transient loss of consciousness without structural pathology.
  • Contusion represents a bruising of the brain surface without rupture of the pia-arachnoid and/or interruption of the brain architecture.
  • Cause: usually traumatic injury.
  • Signs: neurological signs - often non-progressive after 48 hours and then regressive.
  • Diagnosis: signs.
  • Treatment: diuretics and steroids; occasionally surgery required.
  • Prognosis: guarded.



  • Fall, blow to the head, RTA (HBC).


  • Concussion is a reversible traumatic paralysis of the nervous system function and is immediate in onset. The effects of concussion on the brain function may last for a variable amount of time.
  • Contusion is a common result of severe head injury, often associated with a concussion. It represents a bruising of the brain surface without rupture of the pia-arachnoid and/or interruption of the brain architecture.
  • Contusions commonly occur in coup and contre-coup injuries. In coup injuries, the brain is injured directly under the area of impact, while in contre-coup injuries, it is injured on the side opposite the impact.
  • The response of the brain to most types of insult is swelling or edema. This may be made worse by a decrease in cerebral perfusion pressure due to hypovolemic shock or an increase in cerebral blood flow in response to hypocapnia secondary to hypoventilation.
    Ensure patency of airway is maintained.
  • The rigid cranium does not allow expansion of contents (blood, CSF and brain tissue), so brain edema causes an increase in intracranial pressure. Raised intracranial pressure usually leads to brain herniation Brain: tentorial herniation.

Types of brain herniation

  • Subfalcine.
  • Caudal transtentorial.
  • Foramen magnum (can cause respiratory depression).
  • Rostral transtentorial.
  • Intracranial disease processes may result in mechanical disruption of intracranial tissues from direct trauma and the forces applied to the brain at impact (primary injury). This primary injury may initiate a number of secondary pathophysiological sequelae such as:
    • Metabolic alterations in neuronal or glial cells.
    • Impairment of vascular supply to normal tissue (ischemia).
    • Impairment of cerebrovascular autoregulation.
    • Hemorrhage Intracranial hemorrhage (intraparenchymal, intraventricular, extradural or subdural).
    • Irritation (seizure generation).
    • Obstruction of the ventricular system.
    • Edema formation.
    • Production of physiologically active products.
    • Increased intracranial pressure (ICP).
  • See pathophysiology of brain trauma Brain: trauma.

Primary brain injury

  • Closed vs open head injury.
  • Hemorrhage.
  • Penetrating wound.
  • Axonal injury.

Secondary brain injury

  • After impact, a cascade of biomolecular events causing continued and progressive brain pathology. This secondary brain injury has a significant effect on outcome and can lead to continued death of neurons and glial cells.
  • The primary mediators involved in secondary brain injury include oxygen free radicals, excitatory amino acids (ie glutamate) and nitric acid.
  • Blood-flow:
    • Metabolism mismatch leads to brain 'suicide'.
    • High metabolic demand with poor perfusion or hypoxia.
  • Following trauma, neurons release excitatory amino acids, particularly glutamate → widespread neuronal depolarization and cellular influx of calcium intracellulary → cellular damage and promotes production of oxygen free radicals → stimulate production of nitric oxide → perpetuates oxygen free radical reactions and lipid peroxidation of cellular membranes → further release of excitatory amino acids.
  • This process results in a self-perpetuating vicious cycle leading to ischemia, infarction, brain edema and subsequent elevations in intracranial pressure.
  • Can be delayed (hours to days).
  • Edema develops after primary brain injury and continues to develop as secondary brain injury ensues. Typically, brain edema is most severe 24-48 hours after injury. There are two main types of edema: vasogenic and cytotoxic (intracellular).
  • Vasogenic edema occurs secondary to failure of the blood-brain barrier and vasodilation. Vasodilation is frequently secondary to hypercapnia Hypercapnia , which is often associated with head injury.
  • Cytotoxic edema occurs secondary to failure of cellular ion pumps and damage to cellular membranes.


  • Acute - usually within hours of injury.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Sande A, West C (2010) Traumatic brain injury: a review of pathophysiology and management. J Vet Emerg Crit Care 20, 177-190 PubMed.
  • Platt S R, Radaelli S T, McDonnell J J (2001) The prognostic value of the Modified Glasgow Coma Scale in head trauma in dogs. JVIM 15 (6), 581-584 PubMed.
  • Dewey C W (2000) Emergency management of the head trauma patient. Principles and practice. Vet Clin North Am Small Anim Pract 30, 207-225 PubMed.
  • Bagley R S (1996) Pathophysiologic sequelae of intracranial disease. Vet Clin North Am Smal Anim Pract 26 (4), 711-733 PubMed.
  • Dewey C W, Budsbery S C & Oliver J E Jr (1993) Principles of head trauma management in dogs and cat - Part II. Comp Cont Ed 15 (2), 177-193 VetMedResource.
  • Lobato R K, Sarabia R, Cordobes F, Rivas J J et al (1988) Post-traumatic cerebral hemispheric swelling. Analysis of 55 cases studied with computerized tomography.​ J Neurosurg 68 (3), 417-423 PubMed.
  • Schoenhuber R, Gentilini M & Orlando A (1988) Prognostic value of auditory brain-stem responses for late post-concussion symptoms following minor head injury. J Neurosurg 68 (5), 742-744 Journal of Neurosurgery.
  • Tornheim P A, McLaurin R L & Thorpe J F (1976) The edema of cerebral contusion. Surg Neurol 5 (3), 171-175 PubMed.
  • Kolata R J, Kraut N H, Johnston D L (1974) Patterns of trauma in urban dogs and cats - A study of 1000 cases. JAVMA 164 (5), 499-502 PubMed.

Other sources of information

  • Freeman A C, Platt S R (2012)Head trauma.In: Platt S R, Garosi L S (eds)Small Animal Neurological Emergencies.London, Manson. pp 363-382.
  • Brain trauma foundation (1996)The role of glucocorticoids in the treatment of severe head injury.J Neurotrauma13, 715-718.
  • Kornegay J N (1993)Pathogenesis of diseases of the central nervous system.In:Textbook of Small Animal Surgery. 2nd edn. Ed D Slatter. Philadelphia: W B Saunders. pp 1022-1037.
  • Shores A (1989)Craniocerebral trauma.In:Current Veterinary Therapy, 10th edn. Ed R W Kirk. Philadelphia: W B Saunders. pp 847-853.
  • Shores A (1989)Treatment and prognosis in head trauma.In:13th Anual Kal-Kan Symposium. Columbus OH. The Ohio State University.