Canada Spinal cord injury (SCI) results not only in a devastating paralysis but is also associated with a myriad of secondary conditions including autonomic dysfunctions [1]. For example cardiovascular responses to orthostatic challenge and exercise following SCI are significantly altered. When able-bodied individual assumes standing position a typical blood pressure response associated with redistribution of blood within the body and approximately 500 ml transfers caudally to the abdominal and lower extremities vasculature. This typically associated with central baroreceptors activation, decreasing vagal tone to the heart, and increasing in peripheral sympathetic activity. The increase in sympathetic tone with standing result in increased heart rate and peripheral vasoconstriction that responsible in maintenance of stable level of arterial blood pressure. After SCI, although the baroreceptors certainly detect reductions in central blood volume during orthostatic stress, disrupted descending spinal sympathetic pathways precludes the capacity for the peripheral vasoconstriction, often resulting in abnormal fluctuation in blood pressure with changing position by individuals with SCI. Latest evidence from preclinical studies and clinical evaluations of individuals with SCI demonstrated that disruption of autonomic spinal pathways and plastic alterations within the spinal cord and periphery that occur after SCI are among the leading causes for the dysfunctional cardiovascular control affecting both: 1) the heart, and 2) the systemic vasculature. Cardiac function is under the combined control of sympathetic (SPNs from T1-T5 levels) and parasympathetic vagal divisions of autonomic nervous systems. After a cervical SCI, sympathetic tonic control is disrupted, while vagal control is intact. Alternatively, when the SCI is below the T6 level, both sympathetic and vagal control of the heart is intact. These divergent scenarios of cardiac autonomic control lead to quite different cardiovascular responses in various physiological circumstances such as rest, exercise, or orthostatic challenge [2]. It is not just the heart that can have these differing autonomic effects (i.e., disrupted sympathetic control yet intact parasympathetic pathways). These same considerations have important outcomes for a variety of essential functions including the cerebrovasculature, urinary bladder, bowel, temperature and sweat glands control. We are just beginning to unravel the mechanisms underlying abnormal cardiovascular function after SCI. The morphological changes within the spinal autonomic circuits after SCI have been established relatively recently. [3] Furthermore, the role these changes are playing in the development of autonomic dysfunction has only just been solidified. A variety of autonomic circuits have been highlighted that possibly contribute to abnormal cardiovascular control after SCI. The disruption of descending spinal cardiovascular pathways leads to a minimum of six neuroanatomical changes that influence autonomic cardiovascular control: