“Central” dysesthesia or “deafferentation” pain is the most common type of pain experienced below the level of SCI and is generally characterized as a burning, aching and/or tingling sensation. In many cases this dysesthetic or deafferentation pain has defied a pathophysiological explanation (Britell 1991) although most researchers firmly support a central nervous system origin for this pain. Nashold (1991) goes as far as stating that except for radicular pain, all other pains of paraplegia are central or deafferentation in origin. This pain is most often perceived in a generalized manner below the level of the lesion, often a diffuse burning type of pain (Britell 1991; Tunks 1986). Burning pain is reportedly most common with lesions at the lumbar levels, although it may be found with SCI at thoracic and cervical levels (Tunks 1986). Nashold (1991) reported this pain occurred almost immediately after SCI and persisted.
Beric (1997) refers to this pain as central dysesthetic pain (CDP) and found dissociative sensory loss and absence of spinothalamic-anterolateral functions, with different degrees of dorsal column function preservation present almost exclusively in incomplete SCI patients. CDP takes weeks or months to appear and is often associated with recovery of some spinal cord function. Paradoxically CDP is often characterized by complete loss of temperature, pinprick, and pain perception below the level of the lesion. It rarely occurs in spinal cord Injuries with complete sensory loss or loss of both sensory and motor functions below the level of the lesion. Davidoff et al. (1987a) concurred and further noted dysesthetic pain was more likely to be found in incomplete paraplegia resulting from penetrating wounds of the spinal cord, and in spinal fractures treated with conservative management.
A number of factors may contribute to exacerbations of these “central” pain syndromes; these include visceral diseases or disturbances, movement, smoking or alcohol, emotional factors, fatigue, and even weather changes (Botterell et al. 1953; Davis & Martin 1947; Davis 1975; Tunks 1986). Pressure sores, particularly if infected, or an occult injury such as a fracture, may result in an increase in burning, dysesthetic pain. These stimuli often provoke autonomic dysreflexic-like symptoms and simultaneously also may aggravate this “burning” pain.