Systemic effects of spinal cord injury

The traumatic insult causing the spinal cord injury is associated with an immediate stimulation of central and peripheral sympathetic tone. Initially, the elevated sympathetic activity increases systemic arterial blood pressure and induces cardiac arrhythmias. At the stage of spinal shock with loss of neuronal conduction, the sympathetic excitation is closely followed by decreases in systemic vascular resistance, arterial hypotension, and venous pooling. Lesions above the level of T5 additionally present with severe bradycardia and cardiac dysfunction. The decreases in cardiac output combined with systemic hypotension further aggravate spinal cord ischemia in tissues with defective autoregulation.

Spinal cord injury may produce respiratory failure. The extent of respiratory complications is related to the level of the injured segments. Injuries above the level of C4 to C5 produce complete paralysis of the diaphragm with substantial decreases in tidal volume and consecutive hypoxia. With lesions below C6, the function of the diaphragm is maintained and there is incomplete respiratory failure due to paralyzed intercostal and abdominal musculature. As a consequence, arterial hypoxia and hypercapnia occur, both of which promote neuronal and glial acidosis, edema, and neuroexcitation. In summary, primary spinal cord injury creates a cascade of pathophysiological events which eventually induce secondary insults and determine outcome. Spinal cord ischemia and disruption of the blood-cerebrospinal fluid barrier are the most important complications following the initial impact. Acute systemic hypotension and respiratory failure with spinal shock further reduce spinal cord perfusion and oxygen delivery. The mechanical stress of the primary impact and the reduced tissue perfusion lead to accumulation of lactic acid, terminal membrane depolarization, ATP depletion, and release of excitatory neurotransmitters. The subsequent postsynaptic receptor stimulation triggers Ca 2+ and Na+ influx, which in turn activates catabolic enzyme reactions and finally leads to cellular necrosis.

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