Table 1.

Secondary ınjury mechanisms involved in the pathophysiology of spinal cord injury

Systemic effects

Heart rate - brief increase then prolonged bradycardia

Blood pressure - brief hypertension then prolonged hypotension

Peripheral resistance - decreased

Cardiac output - decreased

Local vascular damage of the cord microcirculation

Mechanical disruption of capillaries and venules

Hemorrhage - especially gray matter

Loss of microcirculation - mechanical, thrombosis, vasospasm

Biomechanical changes

Excitotoxicity - glutamate

Neurotransmitter accumulation

Catecholamines - noradrenaline, dopamine

Arachidonic acid release

Free radical production

Eicosanoid production

Prostaglandins

Lipid peroxidation

Endogenous opioids

Cytokines

Electrolyte shifts

Increased intracellular calcium

Increased intracellular potassium

Increased intracellular sodium

Inflammatory response

Free radical generation

Macrophages

Axonal breakdown, removal of myelin debris

Release of cytokines

Glial cell activation

Cytotoxic effects on oligodendrocytes

Wallerian degeneration

Edema

Apoptosis

Loss of energy Metabolism

Decreased ATP production

SCI: Spinal cord injury.