Background
SCIs are classified as primary or secondary. Primary SCIs are caused by mechanical disruption, transection, extradural pathology (spinal epidural hematomas or abscesses), or distraction of neural elements. This usually occurs with fracture and/or dislocation of the spine. However, primary SCI may occur in the absence of spinal fracture or dislocation. Penetrating injuries due to bullets or weapons may also cause primary SCI. More commonly, displaced bony fragments cause penetrating spinal cord or segmental spinal nerve injuries.
Vascular injury to the spinal cord can be caused by arterial disruption, arterial thrombosis, or hypoperfusion due to shock. These are the major causes of secondary SCI; anoxic or hypoxic effects compound the extent of the injury. The science behind vascular performance or blood flow is that perfusion pressure and vascular resistance govern blood flow to tissue. Because mean arterial pressure and venous pressure are normally maintained within narrow limits, blood flow control is accomplished in large part by variation in vascular resistance.
Vascular resistance is essentially under dual control, through systemic control via the autonomic nervous system and humoral factors and by local control via the conditions in the immediate vicinity of the blood vessels. The importance of sympathetic innervation for vascular resistance has been demonstrated by studies that examined the effect of sympathetic blocking or sympathetic denervation on vascular resistance.
After spinal cord injury, the centrally mediated sympathetic control of the circulation may be lacking in the lower part of the body as a result of the disrupted spinal cord. This would lead to vasodilatation of peripheral vessels and, therefore, to a decrease in vascular resistance below the lesion. However, the part of the body below the spinal lesion is paralyzed and extremely inactive, which may affect the vascular properties in this part of the body as well.
Previous studies reported a lower blood flow to the paralyzed legs in SCI individuals than in controls as measured by echo Doppler ultrasound. However, no blood pressure data were given in these studies, and, with the knowledge that especially tetraplegic individuals often have low blood pressure levels, it is impossible to speculate about changes in vascular resistance in these SCI individuals.
Researchers have hypothesized that vascular resistance in the legs of long-term SCI individuals will be increased. This belief stems from the fact that (1) animal research findings that endothelial function changes after long-term sympathectomy with a predominance of endothelin-1 release and a decrease in nitric oxide release; (2) after deconditioning of the leg muscles, oxygen demand will be low, and oxygen delivery will be geared accordingly, which would lead, most likely via flow-dependent mechanisms, to vascular atrophy; and (3) in long-term SCI patients, the clinically obvious cold and blue-colored legs and the reported poor wound healing are suggestive of a reduced leg blood flow and possibly of increased vascular resistance.
A New Study
This apparent conflict between reported data on blood flow and vascular resistance in SCI vs. clinical observations and physiological references urged a team of Dutch physiologists to assess leg and arm vascular resistance in SCI individuals.
The authors of "Increased Vascular Resistance in Paralyzed Legs After Spinal Cord Injury is Reversible by Training," are Maria T. E. Hopman, Jan T. Groothuis, Marcel Flendrie, Karin H. L. Gerrits, and Sibrand Houtman, all from the Department of Physiology, University Medical Centre Nijmegen, The Netherlands. Their findings are published in the December 2002 edition of the Journal of Applied Physiology, one of 14 scientific journals published each month by the American Physiological Society (APS).
Methodology
To accomplish their goal, the researchers measured resting blood flow in the legs and arms and blood pressure in patients with SCI and compared these values with data obtained in a healthy control group.
In addition, leg blood flow and blood pressure were measured in a group of SCI patients before and after six weeks of electrically stimulated leg muscle training to gain insight into the plasticity of the peripheral vascular system and to distinguish between the effect of loss of central neural control vs. deconditioning on changes in leg vascular resistance. They hypothesized that, in contrast to previously reported results, vascular resistance in the legs of long-term SCI patients has been increased and will decrease by leg muscle training. The researchers measured blood pressure and resting flow above and below the spinal cord lesion in 11 patients with SCI and in ten healthy controls. Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue.
Results
The investigators found increased vascular resistance in the paralyzed legs of humans with long-term SCI. Although animal research supports and provides explanations for the findings of the present study, the results seem to be in contrast with previous studies in humans.
In addition, this is the first study to show that only a short period of training of the previously deconditioned legs leads to a marked decrease in vascular resistance, which suggests that the increase in vascular resistance as observed in SCI patients results primarily in deconditioning. CV, representing the reproducibility of the used protocol and measuring technique, varied between 9.5 percent (legs) and 14.5 percent (arms) in this study, which is comparable with other blood-flow studies that reported CVs ranging from 9 to 24.9 percent.
A second major difference found between the control and SCI patients is that the former have normal voluntary motor control of the affected limb, whereas the sympathetic deprived limbs of SCI patients are paralyzed. As a result of the inactivity and atrophy of the paralyzed muscles below the level of the lesion, oxygen demand is low, and oxygen delivery will be geared accordingly, as has been demonstrated by vascular atrophy in the legs of SCI individuals.
Within the SCI group, arterial blood flow was significantly higher and vascular resistance was profoundly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control versus deconditioning, a group of nine SCI patients was trained for six weeks and showed a 30 percent increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance.
Conclusions
The researchers conclude that leg vascular resistance is dramatically enhanced in SCI individuals. This may be caused by structural as well as by functional changes. The increased leg vascular resistance is reversible toward normal values by training the paralyzed legs with electrical stimulation of the muscle.
These findings will provide new insight to those offering rehabilitative treatment to spinal cord patients, while a quest for a cure continues.
Source: December 2002 edition of the Journal of Applied Physiology.
The American Physiological Society (APS) was founded in 1887 to foster basic and applied science, much of it relating to human health. The Bethesda, MD-based Society has more than 10,000 members and publishes 3,800 articles in its 14 peer-reviewed journals every year.
Journal
Journal of Neurophysiology