Characteristics of an aging nervous system include diminished strength and reaction time (Fozard et al. 1994; Lynch et al. 1999), loss of vibratory sense (Knox 1994), reduced fine coordination and agility (Pathy 1985), slowing of motor unit recruitment patterns (Tax et al. 1990), declining function of basal ganglia (Roth & Joseph 1994) and cerebellar systems (Bickford et al. 1999), and deterioration of gait (Greenhouse 1994). A number of anatomical and functional changes occur with aging, including deficits in long-term potentiation (the normal enhancement in signal transmission between two neurons when stimulated together), decline in expression of neurotrophic factors which promote neuronal survival and dendritic branching, and reduction in brain volume in some regions due to a decrease in synaptic density (Mora 2013). With the exception of neurons from a few areas, there is no significant loss of neurons during the normal process of aging (Mora 2013). Aging also impacts the peripheral and autonomic systems, which respectively result in a progressive loss of nerve conduction velocity (Verdú et al. 2000), and impaired temperature regulation (Collins et al. 1977) and baroreceptor reflexes (Duke et al. 1976).
In SCI, there is a lack of longitudinal evidence regarding the nervous system other than studies that evaluate neurological complications such as chronic pain (see Table 8). Neuropathic chronic pain following SCI is a complex issue and results from the abnormal processing of sensory input due to damage to the nervous system (Cardenas & Rosenbluth 2001). It is often difficult to identify a specific stimulus or cause for neuropathic syndromes (Scadding 2003). Although this pain can be identified by site (region of sensory disturbance) and by features (sharp, shooting, electric, burning, stabbing), individuals may find it difficult to describe the quality of neuropathic pain (Scadding 2003). Typically, neuropathic pain is present at or below the level of lesion, and is constant but fluctuates in intensity depending on the individual’s emotional state or level of fatigue. SCI-related studies that have examined factors associated with the development of pain have yielded mixed results. With regards to age, some studies have found an association between chronological age and pain (e.g. Burke 1973; Anke et al. 1995; Stormer et al. 1997; Dalyan et al. 1999; Siddall et al. 1999; Putzke et al. 2000), whereas others have found none (e.g. Subbarao et al. 1995; Rintala et al. 1998; Curtis et al. 1999).
Overall, the dearth of literature on the nervous system is relatively surprising given the implications of how age may influence the recovery process following injury. New sensory and motor deficits in persons with SCI of more than 20 YPI (Whiteneck et al. 1992) may occur due to an age-related dropout of anterior horn cells and loss of myelinated tracts (Charlifue et al. 2002). As well, it is important to determine whether or not further deterioration in the autonomic nervous system occurs in the later decades of life, which hold implications for the gastrointestinal and genitourinary systems (Lammertse 1993).
In this section, 4 longitudinal studies on the nervous system after SCI are reviewed.