Spinal cord injury (SCI) is a catastrophic condition for patients and their relatives. SCI does not lead only to motor and sensory dysfunctions, but also causes autonomic dysfunctions. Sympathetic preganglionic neurons in the spinal cord undergo some plastic changes in their morphology. Additionally, the sympathetic system shows some alterations at the level of the receptor and the mediator. After the acute period, exaggerated reflex responses and uncontrolled sympathetic outflow occur. Autonomic dysfunction has significant effects on cardiovascular and respiratory functions, thermoregulation, sweating, and sexual function. Some dysfunctions, especially cardiovascular, respiratory and thermoregulatory ones, may be life-threatening. Spinal cord injured patients with lesion above the level of the sixth thoracic segment may develop autonomic dysreflexia characterized by persistent peripheral vasoconstriction that is induced by afferent stimulation below the T6 level. Autonomic dysreflexia is an emergency condition because of its serious consequences such as intracranial hemorrhage and retinal detachment. Another autonomic dysfunction is orthostatic hypotension, which develops in two-thirds of all spinal cord injured patients within the acute or subacute period. Another disorder caused by loss of cardiac control mechanism is bradycardia. It occurs in 70% of subjects with SCI, being fatal in approximately 15% of them. Thermoregulatory mechanisms are impaired, particularly in tetraplegic patients. Accordingly, attacks of life-threatening hypothermia may be observed.