Individuals with SCI frequently experience a band of pain and hyperalgesia at the border zone between diminished or abnormal and preserved sensation (Botterell et al. 1953; Davis 1975; Heliporn 1978; Kaplan et al. 1962; Maury 1978; Melzack & Loeser 1978; Michaelis 1970; Tunks 1986). In the more recent literature, this segmental pain is further described as occurring at or just above the level of sensory loss in the cutaneous transition zone from the area of impaired/lost sensation to areas of normal sensation, involving at least one to three dermatomes (Friedman & Rosenblum 1989; Nashold 1991; Ragnarsson 1997) and is often associated with spontaneous painful tingling or burning sensations in the same area. Ragnarsson (1997) also noted that in an individual with a cervical cord injury, segmental pain may be described as tingling, burning or numbing pain in the shoulders, arms or hands, those with a thoracic cord injury frequently describe a circumferential, feeling of tightness and pain around the chest and abdomen while lumbar lesions tend to be localized to the groins and different parts of the lower extremities. According to Nashold (1991) paraplegics often complain that touching the skin in the pain region activates the pain causing it to radiate into the lower parts of the body, especially the legs. Pain can be triggered by stroking and/or touching the skin in adjacent painful dermatomes (Nashold 1991). Even light touch or the pressure of clothing or bed sheets over this region may provoke marked discomfort (Tunks 1986). It may be accompanied by sweating or vasodilation at or below the level of hyperalgesia. Segmental pain is generally symmetrical although a partial spinal cord injury with asymmetrical neurological involvement will produce asymmetries (Nashold 1991).
This pain has also been described as “neuropathic at level pain” (Siddall et al. 1997)
Although several theories have been proposed (Levitt 1983; Matthew & Osterholm 1972; Melzack & Loeser 1978; Nashold & Bullitt 1981; Pollock et al. 1951; Tunks 1986) the neurological mechanism responsible for this area of hyperalgesia after spinal injury is not well understood (Farkash & Portenoy 1986). Although radicular pain is most severe in incomplete SCI lesions, it is also seen in transected cauda equina lesions which are, by definition, radicular types of pain (Heaton & Coates 1965; Siddall et al. 1997). It may also be secondary to spinal cord instability by facet or disc material, or to direct damage to the nerve root during the initial injury (Burke 1973; Nashold 1991). This “radicular” pain is associated with sensory change in the involved painful dermatome (Nashold 1991) and is most common to cervical or lumbosacral nerve roots. Non-neural structures, such as the dura mater, have also been suggested as a source of radicular pain (Cyriax 1969; Farkash & Portenoy 1986). In addition, it has been suggested that central borderzone pain may be generated in the damaged spinal cord just proximal to the spinal cord injury (Nashold 1991; Pollock et al. 1951). Unfortunately, unless there is definitive evidence on imaging of nerve root damage, it is difficult to distinguish between these various mechanisms of pain.
To reflect this uncertainty Siddall et al. (1997) in their proposed classification of SCI pain note that this “neuropathic at level pain” is divided into radicular and central pain. Radicular pain is due to nerve root pathology while central pain is due to changes within the spinal cord or possibly supraspinal structures. Pain attributable to nerve root damage is suggested by features of neuropathic pain (i.e. burning, stabbing, shooting, electric-like pain, allodynia) and increased pain with spinal movement. Sjolund (2002) notes that this pain is thought to occur from nerve root entrapment and may occasionally benefit from decompression.
However, pain, which appears radicular in nature, may occur in the absence of nerve root damage. This leads to the second grouping of borderzone pain, namely central pain or that which is due to pathology within the spinal cord thought to be the result of damage to the gray matter of the dorsal horn of the spinal cord (Ragnassaron 1997; Woolsey 1995). According to Ragnassaron (1997), such an injury “has been said to result in hyperactivity of the nociceptor cells within the dorsal horn (Nashold & Bullitt 1981; Nashold & Ostdahl 1979) which can be electrically recorded (Nashold & Alexander 1989).” Sojlund (2002) notes that this second type of at level neuropathic pain is experienced as a girdle pain uni- or bilaterally in two to four segments of the transitional region. This pain is described as stimulus independent, often accompanied by troublesome allodynia or hyperalgesia and thought to arise from segmental deafferentation (Sjolund 2002).