Neurosurgery notes/Trauma/Secondary head injury/Cortical spreading depression

Cortical spreading depression

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Secondary head injury

General

  • Occurs after
    • Severe head trauma and ischaemia
  • CSD and PID contribute to the increase of final infarct volume in a step- wise fashion as part of additional secondary insults and stress- induced changes in the penumbra of primary lesions.

Numbers

  • Occurs more frequently in the younger acutely injured patients
  • Occur in 50– 60% of TBI patients

Due to

  • Ionic homeostasis failure that transiently interrupts cortical function.

Characterized by

  • EEG depression,
    • Spontaneous peri-infarct depolarizations (PID) propagate to normal cerebral tissues and take on the characteristics of CSD.
    • Electrocorticographic (ECoG) recordings
      • Show spontaneous depressions accompanied by stereotyped CSDs spreading across the cortical mantle at 3.3 mm/ min;
      • ECoG background activity recovers spontaneously or 2 to 5 hours later
  • Pial vasodilation,
  • A slow negative potential shift

Propagating depolarization waves in neuronal and glial cells cause an increase in oxidative metabolism, compensated by increased CBF and metabolic activity;

  • CSD does not cause neuronal injury in the normal brain when flow- metabolism is intact.
  • Haemodynamic disruption and flow- metabolism decoupling are frequent phenomena after head injury, thus CSD may incur additional energy demand that cannot be metabolically compensated for by the injured brain.

CSD alters BBB permeability via matrix metalloproteinase (MMP) activity.

  • MMPs consists of neutral proteases implicated in wide range of processes:
    • The opening of the BBB;
    • Immune cell infiltration of neural tissue;
    • Shedding of cytokine and cytokine receptors;
    • Direct cellular damage;
    • Neuronal development and plasticity.
  • CSD increases MMP- 9 activity → leads to the breakdown of BBB → oedema formation.
  • Neuronal expression of MMP- 9 and MMP- 2 is implicated in
    • Neurotoxicity after ischaemia and trauma,
    • Increasing the susceptibility to cerebral haemorrhage.

Management

  • And may be attenuated with glutamate receptor inhibitors, specifically NMDA receptor antagonists.