Thermodysregulation is a well-recognized clinical phenomena after SCI, first described in 1878 by Pfluger (see Colachis and Otis and Schmidt and Chan [58–59]). It occurs in the acute phase of SCI and can potentially last a lifetime. Although thermoregulation is recognized as an autonomic function, the precise mechanisms of dysregula- tion have not been fully elucidated. The degree of dysregu- lation appears related to injury level and perhaps to degree of completeness of SCI, similar to the pattern of AD . However, completeness of SCI has not yet been well cor- related and is not precisely correlated with the degree of thermodysregulation in individuals with SCI. Nonetheless, temperature is easy to measure and classify, even in the very early stages postinjury. Therefore, thermodysregula- tion may be a useful means of early assessment of auto- nomic function, although further research will be needed.
Thermodysregulation falls into three categories based on the available literature. The first is the well-known poikilothermia, often called an “environmental fever,” that also relates to hypothermia from prolonged cold exposure. The second is termed “quad fever” and relates to a fever without an infectious source occurring in the first several weeks to months after SCI. The third, increas- ingly studied in the exercise literature, is exercise-induced fever.
Body temperature is under direct autonomic control via hypothalamic regulation. Peripheral cold and warm receptors project to the hypothalamus via the spinal cord, although deep temperature sensors are also present . When core temperature decreases, sympathetic (noradrenergic) mechanisms induce piloerection, shiver- ing, and vasoconstriction to produce body heat and shunt blood away from the cool surface. Areas lacking connec- tion between the hypothalamus and the sympathetic sys- tem do not mount this response. Given a large enough surface area lacking these mechanisms, core temperature will decline. In practical terms, individuals with lesions at T6 and above exhibit the problem, since a loss of descending sympathetic control of more than half of the body is present. Although individuals with lower injury levels exhibit no response to cold in the legs, this does not result in a clinically significant alteration in core temperature. Individuals with tetraplegia usually exhibit a more marked manifestation than individuals with para- plegia, both from the standpoint of lack of hypothalamic connection to the spinal sympathetic circuits and from the standpoint of reduced surface area that can respond.
Quad fever was described by Sugarman et al. in 1982 . Although clinically recognized, it is not widely dis- cussed in the literature and deserves considerable investi- gation into the possible controlling mechanism. Quad fever occurs in individuals with tetraplegia and occasion- ally those with high paraplegia. Patients present with fever, often exceeding 40 °C (101.5 °F), although only a mild elevation in core temperature may be present. This is a diagnosis of exclusion because infection, throm- boembolic disease, inflammation, and atelectasis must be ruled out as sources of fever before quad fever can be diagnosed. Blood pressure and pulse alterations are not a component, since they would suggest a noxious source. No existing theories explain this early phenomena, and since patients are in the hospital in an environmentally controlled setting, poikilothermia also does not explain it. Alterations in the hypothalamic axis can be suspected, particularly in light of changes in hypothalamic afferents, but have not been explored. As with poikilothermia, the role of completeness has not been correlated. The inabil- ity of patients to get rid of excess heat by sweating may play a role.
Exercise-induced hyperthermia has been more widely studied in recent years. This fever is again more common in persons with tetraplegia, since they display greater dif- ficulty in dispersing endogenously produced heat . Persons with tetraplegia have a greater increase in body temperature with exercise than persons with paraplegia, even at equal peak oxygen consumption. A prolonged period of increased body temperature is also noted in tetra- plegia, with delay in normalization of core temperature. However, neither persons with paraplegia nor those with tetraplegia show any alteration in thigh skin temperature, which confirms the absence of temperature regulation in all levels of complete SCI. Again, degree of completeness of SCI h as not been adequately studied. High core tem- perature can be combated by cool- water foot baths before and during exercise . As has been observed in other forms of temperature dysregulation, environmental tech- niques are successful in restoring normal body tempera- ture. Mechanisms of temperature dysregulation need further study, particularly with regard to incomplete lesions. Differentiating between those with and without temperature dysregulation may be helpful in discerning those with autonomic incompleteness, even in the pres- ence of motor and sensory completeness.
Core temperatures (oral, rectal, or tympanic) should be regularly and accurately assessed, along with ambient temperature, amount of activity, and recent exposure to an alternate environment. In the acute phase of SCI, tem- perature may be the easiest parameter to test and measure for autonomic function. Both core body temperature and skin temperature above and below the level of injury are helpful in assessing temperature and autonomic function.