Thermodysregulation is a well-recognized clinical phenomenon after SCI (Colachis & Otis 1995; Schmidt & Chan 1992). It typically occurs in the acute phase of SCI and can potentially last a lifetime. Although thermoregulation is at least in part regulated by autonomic function, the precise mechanisms of thermodysregulation after SCI are not yet fully understood. The degree of dysregulation appears to be related to injury level and perhaps to degree of completeness of SCI, similar to the pattern of AD (Guttman 1976). Body temperature is under direct autonomic control via hypothalamic regulation; peripheral cold and warm receptors and sensors send messages to the hypothalamus via the spinal cord (Downey 1973). Temperature is easy to measure and classify, even in the early stages post-injury, and therefore, tracking thermodysregulation may be a useful means of early assessment of autonomic function.
Under normal conditions (when the environment is temperature controlled, i.e. not too hot or too cold), people with SCI can have difficulty regulating their body temperature. Individuals with tetraplegia and those with lesions at T6 and above usually exhibit more marked differences in thermoregulation than individuals with paraplegia, most likely due to a lack of hypothalamic connection to the spinal sympathetic circuits and from the standpoint of reduced surface area that can respond (Krassioukov et al. 2007).
Data suggests that patients with tetraplegia after SCI have episodes of subnormal body temperature in a normal ambient environment, and that cold temperatures have a greater negative impact on personal comfort and ability in people with tetraplegia than that of non-SCI controls (Khan et al. 2007; Handrakis et al. 2016). There is a clinically recognized, though not widely studied, phenomenon known as “quad fever” where people with tetraplegia or high paraplegia present with a fever exceeding 40 °C (101.5 °F) without a significant rise in core body temperature or an infectious source (Krassioukov et al. 2007).