Numerous studies have found the life expectancy after spinal cord injury (SCI) has increased steadily in the past few decades, and is now comparable to that of the able-bodied population (Geisler et al. 1983; Whiteneck et al. 1992; Hartkopp et al. 1997; McColl et al. 1997; Frankel et al. 1998; DeVivo et al. 1999; Yeo et al. 2000; Krause et al. 2004). Due to advances in emergency, acute, and rehabilitation treatments, persons are now living many decades post-injury. Although still relatively small, there are increasing numbers of persons who have long-term SCI and who are over the age of 55 years of age (Adkins 2001), which has allowed for some appreciation and perspective on the types of changes that occur for an individual with SCI over time.
By definition, aging is a multi-dimensional process of physical, psychological, and social change, and gaining an understanding of aging is extremely complex (Aldwin & Gilmer 2004). Even in the general population, the study of aging is still a relatively new area that has experienced an upsurge in research, but is in the process of gaining consensus on many theoretical and methodological issues (Aldwin & Gilmer 2004). Initially, SCI was considered a relatively static condition, and that persons with SCI would be able to maintain their functional level for most of their lives (Trieschmann 1987). However, we now understand that the superimposition of impairment, such as SCI, further complicates the assessment of aging effects (Adkins 2004).
McColl and colleagues (2002) list five changes that persons with SCI undergo as they age: 1) the effects of living with SCI long-term (e.g. shoulder pain, chronic bladder infections); 2) secondary health conditions of the original lesion (e.g. post-traumatic syringomyelia); 3) pathological processes unrelated to the SCI (e.g. cardiovascular disease); 4) degenerative changes associated with aging (e.g. joint problems); and 5) environmental factors (e.g. societal, cultural) that may potentially complicate the experience of aging with a SCI. All of these factors have the potential to compromise a person with SCI’s ability to sustain independence and ability to participate in their communities at later stages in life.
Chronological Age, Years Post-Injury, and Age at Injury
A problem with aging research after SCI is that the relationship between age at injury, current chronological age, and years post-injury (YPI) are all linearly dependent, which limits the ability to assess the influence of all three factors at the same time statistically (Adkins 2001). Hence, investigators are limited to examine only three possible combinations of factors, which include: 1) current age and YPI; 2) current age and age at injury; and 3) age at injury and YPI. Despite this issue, the field continues to strive to attribute changes in health and well-being to these aging variables. Thompson and Yakura (2001) comment that “developing an understanding of the effect of advancing age versus longer durations of injury on the incidence and type of changes can help in the prediction of when people with SCI might be susceptible to changes in function” (p. 73). Doing so may lead to better health promotion strategies to avoid declines in health and well-being since even slight changes in functioning after SCI can adversely affect a person’s level of independence.
SCI: A Model of Premature Aging?
A growing body of evidence in the literature is suggesting that SCI represents a model for premature aging (Bauman & Spungen 1994). The premature aging of certain body systems may occur because of additional stresses that extend some physical systems beyond their ability to repair themselves, which then become systematic (Charlifue & Lammertse 2002). Although the aging process occurs at varying rates and at different ages for each individual (Charlifue 1993), it is generally accepted that our bodily functions reach a maximum capacity prior to or during early adulthood, and then begin to experience a gradual decline. This decline is thought to commence at approximately 25 years of age when the developmental process plateaus and biological capacity has peaked (Capoor & Stein 2005). At this point, the reserve capacity of our organ systems begins to drop at a rate of 1% of their function per year in able-bodied persons. This physical peak can be measured by examining the functioning of individual organ sytems. For example, we can assess cardiovascular capcity by how well the heart can pump blood. Similarly, we can assess the individual's maximum functional capacities (eg. how much weight an individual can lift). Hence, the average person at age 70 has approximately 50% of his/her capacity remaining in each organ system, which does not necessarily impact negatively on health or functioning since all organ systems have an 'excess reserve' (i.e. more cells, structure and supportive tissue than is required to meet daily life needs; Adkins 2004).
When the reserve capacity declines below 40% of original functioning, there is greater chance of becoming injured, and/or more susceptible to infection or disease (Kemp & Thompson 2002). With the occurrence of an SCI, there is disruption to the system. This disruption to physiological and functional changes potentially accelerates bodily declines for a period of time or capacity is reduced at approximately the time of injury, after which the effect of aging is said to proceed at a normal rate (Adkins 2004).
Age of injury may have important consequences on different aspects of health. Because there are increasing numbers of seniors incurring a SCI due to falls, a bi-modal age-of-onset distribution exists, with the prevalence of SCI peaking among individuals who are 30 and 60 years of age (Pickett et al. 2006). As a result, researchers have been able to investigate and compare age-related outcomes after SCI. For example, there are a number of studies showing that persons who incur a SCI at later ages have poorer functional outcomes than those injured at younger ages (DeVivo et al. 1990; Alander et al. 1997; Scivoletto et al. 2004), although in some instances, the impact of SCI may be minimized in older persons.
Within a reserve capacity model of biological aging that is disrupted by SCI, Adkins (2004) theorizes that the impact of injury “decreases the further out on the age continuum the injury occurs” (p. 5). However, if the injury occurs far enough along the continuum, then even a minimal change in rate will lower reserve capacity below 40% soon after injury since capacity is already low. Further, adults with older ages of SCI-onset may have other pre-existing or vulnerabilities to co-morbidities that affect outcomes compared to younger adults (Furlan et al. 2009).
Given the increasing mean age of SCI onset, along with increased life expectancy, we may be able to clarify which changes to systems are attributed to the SCI, those which are related to chronological age and the aging process, and those which result from their interaction. Adkins (2004), however, suggests that it may be prudent to establish age of onset exclusion criteria when studying biological aging with SCI. In addition, completeness and neurological level of SCI must also be taken into account since a person with a complete lesion may experience aging in a different manner than someone with an incomplete lesion (Charlifue 1993).
Aging and Quality of Life
In addition to issues of biological aging, the interaction of environmental and psychological factors with aging must be taken into account. Unlike physical aging, it may be that these aspects of a person’s life may actually improve, and may be more amenable to intervention to either delay, modify or eliminate their potential negative impact (Charlifue & Lammertse 2001). There are a multitude of individual factors that may affect, or be affected, by physiologic aging, which must be considered when evaluating how people age with SCI. This may include economic factors, environmental barriers and facilitators, cultural issues, and social networks (intimate and remote; Charlifue & Lammertse 2001). As a result of this complex phenomenon, there are issues that remain unclear with quality of life and aging with SCI, as some studies report contradictory findings, with life satisfaction and community integration decreasing with age, but increasing with years post-injury (YPI; i.e., Eisenberg & Saltz 1991; Krause & Crewe 1991; McColl & Rosenthal 1994; Pentland et al. 1995; Westgren & Levi 1998; Dowler et al. 2001; Tonack et al. 2008). Hence, it is imperative that we identify which factors lead to high levels of quality of life in order to ensure that people with SCI are not only living long, but that they are also living well.
Chapter Purpose
The chapter summarizes some key issues in the SCI aging literature, and evaluates the level of evidence provided by selected studies on aging with SCI. The selected research for evaluation includes longitudinal studies (duration of at least 2 years or more), case-control and cross-sectional comparative studies. As longitudinal studies inherently include at least a baseline and follow-up evaluation, these studies were graded with a level of evidence of 4 (at least equivalent to pre-post studies). Prospective longitudinal studies that also included a control group (e.g., able-bodied group) were graded with a level of evidence of 2 as they are considered cohort studies where one group is exposed to a particular condition (in this case, a spinal cord injury). Longitudinal studies which included historical controls (from chart review or database) were graded with a level of evidence of 3. Cross-sectional studies (or comparative studies) utilizing both individuals with SCI and able-bodied controls at one point in time were graded with a level of evidence of 5. Studies involving mixed populations in which < 50% of the subjects had a SCI were excluded as were articles not in English. As well, studies with small sample sizes (less than 5 SCI participants) and/or with limited age ranges (i.e. only persons in their twenties and/or early thirties, etc.) were excluded. Longitudinal studies that only reported cross-sectional analysis were also excluded from evaluation. The results presented from each study primarily focus on the analyses relevant to aging, and the p-values reported are those reported in the original articles.
Although the use of longitudinal designs are preferred, comparison studies with age-matched able-bodied (AB) controls is a useful approach for studying aging after SCI because it provides some awareness of the factors associated with the typical aging process (Charlifue 1993), while helping to illuminate whether changes are due to YPI rather than current age per se. After sustaining a SCI, age and YPI increase at the same pace, and so using age-matched AB controls allows us to determine the effects that might have occurred without SCI and those that occurred with SCI (Adkins 2004). This approach may offer some insight on whether changes after SCI are unique and/or accelerated in persons with SCI or if they are typical of the aging process.
The issues related to aging are described as mortality and life expectancy (see Table 1), physiological aging, which include the cardiovascular and endocrine systems (see Table 2), immune system (see Table 3), musculoskeletal system (see Table 4), respiratory system (see Table 5), nervous system (see Table 6), skin and subcutaneous tissues (see Table 7), and the genitourinary and gastrointestinal systems (see Table 8), and community reintegration and quality of life (see Table 9).
Survival rates for individuals with SCI have made steady improvements over the past five decades. Prior to World War II, however, life expectancy for individuals with SCI was quite poor (Geisler et al. 1983). Leading causes of death were those resulting from renal failure and infection (Lammertse 2001). Since the introduction of antibiotics, improved emergency transportation, advances in long-term health interventions, and the availability of preventative care at specialized treatment centers, mortality rates have been steadily decreasing, and the causes of death have begun to mirror those of the general population (Whiteneck et al. 1992; DeVivo et al. 1999). However, the life expectancy is still diminished compared to the general population (Geisler et al. 1983; Whiteneck et al. 1992; Hartkopp et al. 1997; McColl et al. 1997; Frankel et al. 1998; DeVivo et al. 1999; Yeo et al. 2000; Krause et al. 2004).
In 2008, the two leading causes of death in high- and middle- income countries for the general population included ischemic heart disease, and stroke and other cerebrovascular diseases (WHO 2008). Other common causes were chronic obstrructive pulmonary disease, trachea, bronchus, lung cancers, lower respiratory infections, and Alzheimer and other dementias (WHO 2008). Similarly, two leading causes of death in the SCI population are respiratory complications and heart disease (Hartkopp et al.1997; Frankel et al.1998; DeVivo et al. 1999; Soden et al. 2000; Zeilig et al. 2000; Garshick et al. 2005). In addition, the latest report from the National Spinal Cord Injury Database (NSCIDB), which has yielded information on the aging SCI population in the United States, indicates the main causes of death are pneumonia, and septicemia (NSCISC 2011). The high rates of cardiovascular disease in the SCI population may be partly due to physiological and functional changes following injury (Bauman et al. 1992a; Dearwater et al. 1986; Gupta 2006; Yekutiel et al. 1989; Bauman et al. 1992b). Interestingly, cancer is a growing cause of death in persons with SCI (DeVivo et al. 1999; Zeilig et al. 2000; Imai et al. 2004).
In general, it appears that as individuals with SCI age, the causes of death become more closely associated with the typical age-related causes of death rather than those associated with the SCI itself (Capoor & Stein 2005). However, some causes may be occurring prematurely (e.g. cardiovascular disease; Yekutiel et al. 1995), and there are some notable differences in mortality patterns between the SCI and the general populations.
In this section, the evidence reviewed (see Table 1) is consistent with the general findings on mortality and life expectancy in the SCI literature.
Table 1: Mortality and Life-Expectancy
The data from Pickelsimer and colleagues (2010) showed a shockingly higher rate of death (15.5%) compared to other studies (7-9%) examining people with SCI over a 10-year period that did not meet the inclusion criteria for the chapter (e.g. less than 2 years of follow-up) (O'Connor 2005; Dorsett & Ceraghty 2008; Bloemen-Vrencken et al. 2005). Similarly, Frisbie (2010) found a death rate of 25.8% in a retrospective analysis of a cohort of persons aging with SCI. Among the individuals in this study with anemia and/or hypoalbuminemia, the leading cause of death were sepsis, cancer, and pulmonary failure. Comparable findings were noted by Savic et al. (2010), with the mortality rate jumping up to 35.6% after 16 years of follow-up.
Although Samsa et al. (1993) found that neurologic impairment was not a significant predictor for mortality, they noted a moderate effect (p < 0.06) for persons with complete cervical injuries. A few studies have shown a lack of association between impairment and mortality (e.g. Liang et al. 2001; Imai et al. 2004; Garshick et al. 2005), whereas several studies have highlighted the importance of impairment as a prognostic factor (Whiteneck et al. 1992; McColl et al. 1997; Coll et al. 1998; DeVivo et al. 1998; Soden et al. 2000; Yeo et al. 2000; Strauss et al. 2006). Samsa and colleagues (1993) found age of onset to be a significant predictor of long-term survival, which is consistent with other important longitudinal studies (i.e. Whiteneck et al. 1992; Frankel et al. 1998) that did not meet our systematic review criteria (e.g. less than 2 year follow-up).
With regards to causes of mortality, Samsa et al. (1993) found that diseases of the genitourinary system (i.e. renal failure, septicemia) disproportionately accounted for death in their SCI sample and the patterns of death began to approach that of the general population by 20 years post-injury. For instance, the rates of circulatory disease and neoplasms steadily increased across time points. Interestingly, the causes of death due to injury and poisoning, and external conditions were the highest at 3-months to 5 years post-SCI, and steadily decreased across time points. Although not discussed, their findings on these causes of death may have included suicides. Regardless, the findings of lower levels of evidence highlighting the high rates of suicide as a cause of death (i.e. Imai et al. 2004) reinforces the need to provide psycho-social services to help minimize the occurrence of suicide in persons with SCI.
An acknowledged limitation of the study by Samsa et al. (1993) is the reliance on secondary data sources for case identification, control selection, and mortality assessment. The study was also only on male veterans that did not include women or persons who did not survive acute SCI (i.e. less than 3 months post-SCI). As well, the causes of death were not reported by Pickelsimer et al. (2010) or by Savic et al. (2010).
There is Level 4 evidence (Picklesimer et al. 2010; Frisbie et al. 2010; Savic et al. 2010) that the mortality rate post-SCI over a 10-year period may be 15.5% to 25.8%.
There is Level 4 evidence (Frisbie 2010) and Level 5 evidence (Samsa et al. 1993) that the causes of death post-SCI are beginning to approximate those of the general population.
Even at the biological level, aging is a highly complex phenomenon that can be examined at the genetic, cellular, organ-system, and even the psycho-social level(Aldwin & Gilmer 2004). Although there are some conflicting findings on where declines occur, for the most part persons aging with SCI exhibit decreases in health status and physical functioning over time (see Table 2), which serve as markers of premature aging.
Table 2: Health Status and Physical Functioning
To address physiological aging after SCI, the identified studies were separated into different body systems, which include the cardiovascular and endocrine systems (see Table 3), immune system (see Table 4), musculoskeletal system (see Table 5), respiratory system (see Table 6), nervous system (see Table 7), skin and subcutaneous tissues (see Table 8), and the genitourinary and gastrointestinal systems (see Table 9).
There is Level 3 (Mitchell et al. 2010) and Level 4 evidence (Hitzig et al. 2010) that health declines over time, while there is Level 4 evidence (Savic et al. 2010) that health may remain stable.
Similar to the general population, cardiovascular disease has become one of the leading causes of death in the SCI population (DeVivo et al. 1989; DeVivo et al. 1993; Frankel et al. 1998). There are multiple risk factors for its premature development due to physiological and functional changes following SCI (Bauman et al. 1994; Bauman & Spungen 2001a; Bauman & Spungen, 2001b). For instance, many age-associated disorders such as carbohydrate intolerance, insulin resistance (Duckworth et al. 1980; Duckworth et al. 1983; Bauman et al. 1992; Karlsson et al. 1991) and lipid abnormalities (LaPorte et al. 1983; Brenes et al. 1986; Bauman et al. 1992; Bauman & Spungen 2001) are known to occur prematurely in persons with SCI. Some have hypothesized that a marked decreased in physical activity (Myers et al. 2007), along with injury-related changes in metabolic function, lead to an increased risk and premature development of cardiovascular disease (Bravo et al. 2004) and diabetes mellitus (Bauman 1993).
Related to the metabolic changes noted above, there is a high prevalence of muscle weakness in persons with SCI attributed to a loss of lean body mass (Thompson & Yakura 2006), that is possibly linked to reduced activity, and abnormally low levels of endogenous anabolic hormones (i.e. human growth hormone and testosterone; Bauman et al. 1994). In the general population, age-related declines in the endocrine systems also lead to decreases in lean muscle mass and an increase in fat (Tenover 1999). However, these declines have been shown to be greater in persons with SCI (Bauman & Spungen 2001b). Similarly, the noted changes in insulin resistance are thought to account for the high rates of diabetes mellitus in persons with SCI (Yekutiel et al. 1989) This in turn leads to an increased risk for cardiovascular disease since the development of diabetes impairs the circulatory system (Halter 1999). As such, it may be that alterations in body composition, which occur early following SCI, contribute to premature development of these disorders as compared to the AB population (Bauman et al. 1994).
Table 2: Cardiovascular and Endocrine Systems
Cardiovascular System
In this section, the evidence reviewedappears to support the notion that the cardiovascular system is prematurely aging. With regard to risk factors for cardiovascular disease, Bauman and colleagues (2001) found that regardless of age or sex, persons with SCI had significantly higher levels of plasma homocysteine than able bodied (AB) controls, and that older persons with SCI (>50 years) had higher levels than younger persons with SCI. Plasma homocysteine is thought to promote coagulation and to decrease the resistance of the endothelium to thrombosis (Malinow 1994), and is a clear independent mark for the prediction of vascular disease (Clarke et al. 1991; Stampfer et al. 1992). The findings regarding lipid profiles also support an increased risk for the development of cardiovascular disease. Several studies (Demirel et al. 1991; Zlotolow et al. 1992; Bauman and Spungen, 1994; Bauman et al. 1995; Bauman et al. 1999; Liang et al. 2007; Wang et al. 2007) found that serum high-density lipoprotein cholesterol (HDL-c) are depressed in persons with SCI compared to AB controls, which is associated with an increased risk for developing coronary heart disease (Goldbour and Medalie 1979; Castelli 1984).
An important factor influencing these variables might be lifestyle. For instance, one longitudinal study (Shiba et al. 2010) on athletes with SCI (N=7) found that physical capacity was maintained over a span of two decades. Regardless, this study involved persons who continued strenuous wheelchair sport activities, which is likely not representative of the general SCI population, which is predominantly characterized as being sedentary (Maki et al. 1995). Although no blood pressure changes were noted, the sample did have a significantly (p< 0.05) higher BMI from baseline to 20 year follow-up. Unfortunately, data on lipid profiles were not collected in this study. Further work on the role of diet and physical activity is needed to help clarify their impact on aging with SCI.
One study provides evidence that C-reactive protein levels were higher in men with SCI (n = 62) compared to AB controls (n=29), which could also account for the decreases in total cholesterol, low-density lipoprotein and high-density lipoprotein. At the same time, increases in C-reactive protein levels may also partly explain why persons with SCI are nonetheless at increased risk for accelerated atherogenesis (Wang et al. 2007). A risk factor for vascular disease in both symptomatic (Budoff 2005) and asymptomatic (Raggi 2000) populations is coronary artery calcification (CAC), which is a component of artherosclerotic plaque. Orakzai and colleagues (2007) found higher (p < 0.05) levels of CAC in persons with SCI (N = 82) compared to AB controls (N = 273), and that this risk is higher for males, and for persons with tetraplegia.
Sustaining a SCI also affects blood pressure by altering the sympathetic activity to blood vessels. There is evidence that men with tetraplegia (Yamamoto et al. 1999) and paraplegia (Petrofsky & Laymon 2002) have increased blood pressure responses during exercise compared to AB controls. As well, Petrofsky and Laymon (2002) found that their group with paraplegia had a larger change in blood pressure both at rest and during exercise and was more associated with aging than for the controls. Disturbingly, static exercise has been found to cause tachycardia in AB controls, but not in persons with SCI (Petrofsky & Laymon 2002; Orakzai et al. 2007) when paralyzed muscles were engaged. Several studies highlight that irregular blood pressure responses post-SCI hold significant implications for cardiovascular health (Bluvshtein et al. 2011; Groothuis et al. 2010a ; Groothuis et al. 2010b; LaFountaine et al. 2010; Yasar et al. 2010).Overall, these findings are indicative of altered autonomic control, but not of aging per se. Further work is needed to determine the long-term implications for cardiovascular health.
Decreases in physical activity may contribute to the development of cardiovascular disease, which may be reflected in body composition changes following SCI. One longitudinal study (DeGroote et al. 2010) found that over a five year period, BMI increased in their SCI sample (N = 184), which significantly increased the year after discharge from in-patient rehabilitation (p < 0.001). Similar findings are reported by Crane and colleagues (Crane et al. 2011).
Assessing body composition, however, should not solely rely on body mass index (BMI). One study (Spungen et al. 2000) found greater BMI levels in persons with SCI compared to AB controls, whereas others found the opposite (Bauman et al. 1999; Bauman et al. 2004) or no differences at all (Zlotolow et al. 1992; Bauman & Spungen 1994; Bauman et al. 1994; Tsitouras et al. 1995; Bauman et al. 1996; Liang et al. 2007). Given these contradictory findings, BMI may not be an appropriate measure for SCI since studies (Bauman et al. 1996; Bauman et al. 1999; Spungen et al. 2000; Bauman et al. 2004; Jones et al. 2004) that also examined lean and fat mass tissue found that persons with SCI had significantly higher levels of fat mass tissue and lower levels of lean tissue than AB controls. These differences in lean and fat mass tissue appear to be attributable to YPI, and not age. For instance, Spungen et al. (2000) found lower lean mass and higher fat mass in persons with SCI who were matched with their AB monozygotic twin, which was directly related to YPI. As well, Bauman and colleagues (2004) concluded from their monozygotic SCI twin study that reductions in lean muscle tissue lead to reduced energy expenditure, which appear to be related, albeit not significantly, to YPI. These findings are congruent with SCI-only cross-sectional studies examining body composition (Cardus & McTaggart 1985; Shizgal et al. 1986; Rossier et al. 1991).
Endocrine System
Metabolic changes after SCI may also be associated with changes in body composition, and may increase the risk of developing diabetes mellitus. Tsitouras and colleagues (1995) posited that impaired hGH secretion may be partially responsible for SCI- and aging-associated lean body and muscle mass depletion. Several identified studies (Shetty et al. 1993; Bauman et al. 1994; Tsitouras et al. 1995) provide evidence that serum IGF-I levels are lower in persons with SCI compared to age-matched controls, and that this depletion is associated with impaired hGH. Bauman et al. (1994) found that the average IGF-I was significantly lower (p < 0.05) in younger individuals with SCI than that in younger AB controls, but not in those greater than 45 years of age. As such, this pattern of IGF-I levels in younger males with SCI appears to be similar to those of elderly AB individuals (Bauman et al. 1994).
Related to this, Bauman and Spungen (1994) found that persons with SCI (N = 100) had an abnormality in carbohydrate tolerance, with the SCI group having higher mean glucose and insulin levels (p < 0.05), and lower mean fasting plasma glucose levels than the AB control group (N = 50). This intolerance was found to be present in two-thirds of their group with tetraplegia, and in half their group with paraplegia. Further, 22% of the persons with SCI met the diagnostic criteria for having diabetes mellitus, whereas only 6% of the AB controls were found to be diabtetic. Since these adverse clinical features occurred at younger ages in their SCI sample, Bauman and Spungen (1994) interpreted their findings as being a model of premature aging. The findings of Jones and colleagues (2004), and LaVela and colleagues (2006) appear to confirm this hypothesis as they both found higher rates of metabolic syndrome and diabetes in their SCI samples compared to the AB population.
In a follow-up study by Lewis and colleagues (2010), using the same cohort of men with SCI as Jones et al. (2004), they found that that their SCI sample (n = 20) had significantly slower plasma-free cortisol responses than AB controls (n = 20), which may signify a mechanism for the induction of heightened insulin and glucose responses and abdominal obesity in persons with SCI. Conversely, Liang et al. (2007) found that males with SCI (N = 185) were not a higher risk for metabolic syndrome compared to AB controls (N = 185). This discrepancy may be due to some of the study’s limitations (i.e., reliance on self-report height and weight to calculate BMI), and because they used a standard, rather than a modified, criteria for the syndrome which is not appropriate for persons with SCI.
The predisposition to carbohydrate and lipid abnormalities is thought to be largely a consequence of extreme inactivity, and the constellation of metabolic findings (i.e. hormone growth hormone deficiency, testosterone deficiency) appears to be occurring prematurely in persons with SCI (Bauman & Spungen 1994). As well, studies (Wang et al. 1992; Huang et al. 1993; Cheville et al. 1995) showing evidence of thyroid impairment after SCI compared to the AB population. All of these findings suggest that persons with SCI may be frequently physiologically comprised, and more susceptible to minor pathologic insults. Along with associated changes in body composition, an increased risk for the development of cardiovascular disease, diabetes mellitus, and infection is higher following SCI (Bauman & Spungen 2001b).
There is Level 5 evidence (Lewis et al. 2004) that men with SCI have slower plasma-free cortisol responses than AB controls.
There is Level 4 evidence (DeGroote et al. 2010; Crane et al. 2011) that BMI increases over time in persons with SCI.
Although the immune system is affected by a number of factors, including nutritional status, stress, exercise, neuroendcorine change, and disease, there is consensus that immune functioning undergoes some age-related declines (Miller 1996; Burns & Leventhal 2000; Rabin 2000). There is limited evidence on the effects of SCI on the immune system with aging, although several studies (i.e. Lyons 1987; Nash 1994; Kliesch et al. 1996; Campagnolo et al. 1999; Cruse et al. 2000) suggest deficits in immune functioning. Hence, there is greater likelihood of immune impairment in the aging SCI population compared to the non-disabled population (Charlifue & Lammertse 2002).
One study provides level 4 evidence (Frisbie 2010) that persons with SCI have a high prevalence of anemia and hypoalbuminemia, which might serve as markers for infection. As well, two studies provide level 5 evidence that this system is compromised at the acute and chronic stages of SCI compared with AB controls.Persons with acute and chronic SCI who have complete injuries (N = 5) demonstrated altered immune function compared to AB controls (Campagnolo et al. 1994). As well, Campagnolo et al. (1999) compared persons with SCI (N = 18) to AB controls (N = 18), which suggests that persons with SCI have higher levels of cortisol (p = 0.06) and dehydroepiandrosterone sulfate (DS; p = 0.05), but comparable levels of dehydroepiandrosterone, adrenocorticotropin, and prolactin. Further, they found that DS (p = 0.05) and dehydroepiandrosterone (p = 0.07) were higher in persons with tetraplegia compared to controls, but no differences between persons with paraplegia and controls. Campagnolo et al. (1999) concluded that immune functioning is altered after SCI, but may be mediated by level of injury. Thus, persons with tetraplegia may have a greater degree of alteration to the immune system compared to persons with paraplegia. Unfortunately, the sample sizes in both studies were quite small.
Further research related to the immune system need to be investigated since older age of SCI-onset leads to poorer outcomes (Prusmack et al. 2006) and SCI of long duration results in increased infection (Whiteneck et al. 1992). Given that persons with SCI are treated with antiobiotics throughout their lives, there are a number of important questions regarding the long-term effects on the immune system (Adkins 2004).
There is Level 4 evidence that persons with SCI have a prevalence of anemia and hypoalbuminemia (Frisbie 2010), which might serve as markers for infection.
The musculoskeletal (MSK) system provides the most obvious external signs of aging, and is especially impacted by aging as most people have some wear and tear in this area as they age (Aldwin & Gilmer 2004). Declines in the MSK system after long-term SCI often include upper extremity pain (Waters et al. 1993), reduced strength due to muscle atrophy (Giangregorio & McCartney 2006), and an increased risk for fractures (Lazo et al. 2001). Hence, the complications associated with a degenerating MSK system hold serious implications in terms of functionality for the person aging with SCI.
In terms of bone health, peak bone mass is achieved by the age of 30 in the general population and then declines, but the rate of decline is impacted by a number of factors such as age, gender, and lifestyle (e.g. smoking). Although the risk for osteoporosis and fracture are greater among post-menopausal women over the age of 65 in the general community (Goddard & Kleerekoper1998), there is evidence for increased risk in the SCI population (Ingram et al. 1989; Garland et al. 1992; Lazo et al. 2001). After sustaining a SCI, there are several reports of bone loss occurring in the early months following injury (Garland et al. 1992). These losses are regional; areas rich in trabecular bone are demineralized to the greatest degree, with the distal femur and proximal tibia bones being the most affected, followed by the pelvis and arms (Garland et al. 2001a). However, there is some evidence that there is a continual loss of bone mass with time since injury (Demirel et al. 1998; Bauman et al. 1999), which suggests that a steady-state of lower extremity bone mineral homeostasis is not reached (Ashe et al. 2010). Assuming that the rate of bone loss in the aging SCI-population is similar to that of the non-disabled population, it is likely that the degree of osteoporosis will be much more severe since they will have less skeletal mass at the onset of typical age-related declines in bone mass (Waters et al. 1993).
As a result of bone loss associated with SCI, there is an increased risk for fracture (Garland et al. 2001a; Ashe et al. 2010). In the general population, fracture of the hip is one of the few skeletal disorders associated with significant mortality (Aldwin & Gilmer 2004). Approximately 20% of older persons who sustain a hip fracture die with in a year, which are thought due to secondary causes or the person was debilitated (Pottenger 1997; Cooney 1999). After SCI, the most common areas at risk for fracture include the distal femur and proximal tibia, and are consistent with site-specific decreases in bone mineral density around the knee (Ashe et al. 2010). The majority of fragility fractures occur following transfers or activities that involve minimal or no trauma (Ragnarsson & Sell 1981). With regards to age, there are studies of lower evidence levels (i.e. Lazo et al. 2001) that individuals with SCI with osteoporosis are older, and who have longer durations of SCI than those who have normal BMD. However, it is BMD, and not age per se, that is the significant predictor for risk of fracture (Lazo et al. 2001). Interestingly, the BMD of the spine is often maintained or actually increases (Garland et al. 2001a; Sabo et al. 2001).
Although BMD of the spine after SCI does not appear to be affected by aging, other age-related changes to the spine do occur. As one ages, the spine undergoes degeneration, which may lead to symptoms of pain radiating into the extremities, deformity, or loss of sensation and/or motor function due to nerve root compression (Waters et al. 1993). Age-related degenerative changes in the spine could severely impact individuals with SCI whose functional capacities are already limited (Waters et al. 1993). Long-term SCI is associated with scoliosis and/or Charcot spine (Sobel et al. 1985; Park et al. 1994; Krause 2000; Vogel et al. 2002; Abel et al. 2003). Age at injury, however, may also play a role as there is some lower level evidence that the odds of developing curvature of the spine is lower in persons who were older when injured (Krause 2000).
In the general population, there is degeneration in the joints of the upper and lower extremities, and common sites include the shoulder, knee, and hip (Waters et al. 1993). As well, muscle atrophy is inevitable with age, although the rate of decline varies from person to person (Loeser & Delbono 1999). These age-related changes may lead to joint pain, stiffness, restricted range of motion, or trauma (i.e. fracture) that would not typically occur in a younger person. As a result, independence when performing daily activities may be compromised due to restricted activities of daily living, mobility, and even the ability to maintain body temperature (Aldwin & Gilmer 2004).
In addition to bone loss (see section 2.2.1), persons with SCI experience muscle atrophy Giangregorio & McCartney 2006), especially those denervated from complete SCI (Lam et al. 2006). In the lower extremities, muscle degeneration typically occurs at the knee in persons who are capable of ambulation but have persisting gait abnormalities, which in turn generate pathologic forces at the knee (Waters et al. 1993). Although persons who primarily utilize wheelchairs rarely develop clinically significant degenerative problems in the lower extremities, they are more likely to have problems in the upper extremities due to increased reliance on the upper extremities to push their wheelchairs, to transfer, and perform weight-shift maneuvers to prevent pressure ulcers (Waters et al. 1993).
Upper extremity pain is common in persons with long-term SCI, and most frequently affects the shoulder and wrist (Sie et al. 1992; Thompson & Yakura 2001; Waters & Sie 2001), and typically increases with duration of injury (Sie et al. 1992; Ballinger et al. 2000; Waters & Sie, 2001). The prevalence of shoulder pain in SCI individuals ranges between 30-100% (Curtis et al. 1999) and is a consequence of increased physical demands and overuse (Nichols et al. 1979; Pentland & Twomey 1991). It is unclear, however, if these findings are independent of treatment era effects or are affected by environmental changes in mobility technology, accessibility, and rehabilitation practices (Adkins 2004).
Losses in strength and diminished joint capacity along with joint degeneration due to overuse can negatively impact functional ability, which makes maintaining high levels of independence difficult. Since persons with SCI are operating at a near-maximum capacity but have a low reserve capacity, these declines in functionality may occur prematurely (Thompson & Yakura 2001).
Table 4: Musculoskeletal System
In general, the evidence (see Table 4) supports the notion that the musculoskeletal system undergoes obvious external signs of premature aging except for a few areas. Several studies find that there is rapid bone loss, and particularly so for the pelvis and lower limbs within the acute stage post-SCI (Garland et al. 1992; Biering-Sorenson et al. 1990; Wilmet et al. 1995; Dauty et al. 2000; de Bruin et al. 2000; Frey-Rindova et al. 2000; Garland et al. 2004; Frotzler et al. 2008; Dudley-Javoroski & Shields 2010; Dionyssiotis et al. 2011). Further, this loss may be greater for older persons (Chow et al. 1996), and females with SCI (Garland et al. 2001b) and is evident in both bone mineral density (BMD; amount of matter per cubic centimeter of bones) and content (BMC; bone mass). Similarly, there are bone geometric changes (Finsen et al. 1992; de Bruin et al. 2000; Giangregorio et al. 2005) that occur, which may be independent of chronological age and YPI (Slade et al. 2005).
Some of the findings are mixed with regards to the duration of decline, with some suggesting that bone mass continues to decline throughout the chronic phase (Finsen et al. 1992), with one reporting a rapid loss with stabilization after approximately 2 years (Dudley-Javorski & Shields 2010). However, a cross-sectional study with AB controls (Eser et al. 2004) and a longitudinal analysis of the same cohort of persons with complete SCI (Frotzler et al. 2008) found that tibial and femoral bone geometry and density properties reach a new steady-state within 3-8 YPI, with the time frame depending on bone parameter and skeletal site. The use of peripheral quantitative computed tomography (pQCT) is viewed as a superior approach for investigating changes in BMD and BMC compared to dual energy X-ray absorptiometry, DXA), but there are some unresolved issues with the use of this technology in people with SCI (Dudley-Javorski & Shields 2010). A mixed cross-sectional and longitudinal study by Dudley-Javorski & Shields (2010) who used two approaches for studying declines in BMD via pQCT found BMD values of their SCI subjects (n = 15) fell below the lowest range of control values (n = 10), suggesting that subjects lost an average of 1.7% BMD per month within the first two years post-SCI. However, their subjects (N=4) who were followed longitudinally starting at approximately 2 years demonstrated no BMD decline over time. Based on their results, a percentage peel approach was suggested as being more appropriate when special sensitivity is required to detect BMD adaptations while threshold-based methods may be more appropriate when asymmetric adaptations (such as in persons with chronic SCI) are observed. As well, there is a need to better understand anatomical variations related to bone adaptive processes in order to account for SCI-related bone losses (Rittweger et al. 2010). As such, further refinement into pQCT assessment and discrepancies in bone anatomical features are needed to help clarify some of the mixed findings noted in the literature.
There are also a number of other factors that contribute to bone loss post-SCI. For instance, endocrine changes may be contributing to the losses in bone density (Dauty et al. 2000; Szollar et al. 1998; Finsen et al. 1992; Vaziri et al. 1994; Bauman et al. 1995). It is thought that altered bone structure and microarchitecture due to SCI (de Bruin et al. 2000; Eser et al. 2004; Giangregorio et al. 2005; Kiratli et al. 2000; Slade et al. 2005; Frotzler et al. 2008) leads to impaired calcium and phosphate metabolism and the parathyroid hormone (PTH)-vitamin D axis (Finsen et al. 1992; Vaziri et al. 1994; Bauman et al. 1995; Szollar et al. 1998; Dauty et al. 2000). For instance, Bauman and colleagues (1995) noted that the reduction in the bioavailabilty of vitamin D in persons with SCI is similar to that found in AB elderly persons. These changes have been shown to contribute to premature onset of osteoporosis and increased risk for fracture in total and regional sites following SCI when compared to the AB population (Garland et al. 1992; Szollar et al. 1997a; Szollar et al. 1997b; Dauty et al. 2000; Kiratli et al. 2000; Garland et al. 2001b; Vlychou et al. 2003; Eser et al. 2004; Giangregorio et al. 2005; Frotzler et al. 2008, Dudley-Javoroski & Shields, 2010), which may be more related to YPI than chronological age (Bauman et al. 1999; Garland et al. 2001b).
Age of SCI onset, however, may be an influential factor on the extent of the decline in bone loss (Garland et al. 2001b; Kiratli et al. 2000; Szollar et al. 1997a). For instance, the findings by Szollar and colleagues (1997a) provides evidence that the BMD of persons with SCI are significantly lower than the AB population, but that YPI may be more influential on BMD changes in specific areas (i.e. femoral and trochanter regions), although older males may not be as severely impacted. Persons who were 60 years or older had comparable levels to their age-matched AB controls in their BMD in all four regions (irrespective of YPI) whereas persons in the younger age categories had significant differences in their femoral regions at different intervals. For instance, younger adults with SCI (20-39 year olds) had significantly lower BMD at 1-5 YPI and at 10-19 YPI in the femoral regions of their neck and trochanter when compared to their AB controls, and the mid-age group (40-59 year olds) only had lower BMD at 10-19 YPI in the femoral neck and trochanter regions. These findings possibly allude to premature aging occurring at specific intervals post-injury, most notably in the first year, in the femoral region in younger persons with SCI, and are consistent with the other identified studies (Garland et al. 1992; Biering-Sorenson et al. 1990; de Bruin et al. 2005; Frey-Rindova et al. 2000; Wilmet et al. 1995; Chow et al. 1996; Szollar et al. 1997a; Szollar et al. 1997b; de Bruin et al. 2000; Kiratli et al. 2000; Eser et al. 2004; Frotzler et al. 2008). It may be that age-related factors become less important on changes in bone mass when an individual reaches a certain chronological age threshold (i.e. 60 years). At this point, other factors (i.e., immobilization) affecting bone mass may become more prominent. In general,all of these changes provide additional support that premature aging is occurring
Gender also is an influential factor on bone loss. Garland and colleagues (2001b) provide evidence that women with a complete SCI incur a rapid bone loss in the knee, resulting in a BMD that is approximately 40% to 45% of the AB population, and that this loss is greater than the loss seen in males with comparable injuries. Unlike the findings by Szollar and colleagues (1997a), the pattern of bone loss of the hip was linear regardless of the age at the time of injury. The findings by Bauman and colleagues (1999), which used a cross-sectional monozygotic twin design, also shows evidence that duration of injury may be more closely associated to bone loss than current age. Although lifestyle habits such as smoking and alcohol intake were examined and found not to be significant, the sample in Bauman et al. (1999) study was quite small, and relatively young.
As well, a study by Slade and colleagues (2005) who compared bone loss at the knee between AB and SCI women who were pre- and post-menopausal concluded that although age and estrogen effects could not be independently discerned, it was unloading (lack of weight bearing) that resulted in the deterioration of trabeculae that occurs early post-injury. Given that SCI is uncommon in women, further studies are needed to further our understanding of the interaction between gender, SCI, and aging plays on bone loss.
Interestingly, the lumbar spine BMD of persons with SCI appears to increase with age regardless of YPI. Szollar and colleagues (1997a) interpreted this finding as either being representative of the lumbar spine becoming the primary weight bearing region or that neuropathic osetorarthropathy (i.e. spectrum of bone andjoint destructive processes associated with neurosensory deficit) may have caused diffused increased radiodensity of the spinal column. The finding that BMD and BMC of the spine remains unaffected or increases is consistent with several other of the identified studies (Biering-Sorensen et al. 1990; Dauty et al. 2000; Chow et al. 1996; Garland et al. 2001b; Szollar et al. 1997b; Szollar et al. 1998), and are complementary to the findings by Catz and colleagues (1992). Based on their findings, Catz et al. (1992) concluded that paraparesis does not accelerate the aging process of the lumbar spine, and that it may even prevent some expected spinal bone changes since no significant differences were detected between their group with SCI and their AB matched control group. However, they noted that a limitation of their study was that 10 years may be too short a duration to detect any significant effects. As well, the sample size was small, and consisted of a heterogeneous group of spinal cord etiologies (i.e. non-traumatic). Finally, one study (Amsters & Nitz, 2006) found that postural changes, such as thoracic kyphosis, may also be independent of age and YPI.
With regard to the upper extremities, the musculoskeletal system appears to decline with YPI (Siddall et al. 2003; Jensen et al. 2005, Akbar et al. 2010), with the incidence of shoulder pain increasing over time. However, the role of chronological age may also be influential (Lal et al. 1998; Kivimäki et al. 2008). The incidence of degenerative shoulder changes (Lal 1998) may be higher in persons with advanced age (older than 30 years) who are less than 10 YPI, suggesting that degenerative changes may occur earlier than previously thought in persons with SCI.
In addition to the lumbar spine, there are other areas of the musculoskeletal system that are not negatively impacted by aging. For instance, handgrip strength may increase with YPI in males with paraplegia relative to AB controls (Petrofsky &Laymon 2002). This may be due to the use of manual wheelchairs, as well as to age-related changes in muscle fiber composition, and/or to a reduction in intramuscular pressure (Petrofsky &Laymon 2002). As well, older males with paraplegia (45 years and older) may have comparable levels of upper extremity strength to AB controls whereas younger adults do not (Pentland & Twomey 1994).
As a consequence of SCI, especially injury to the cervical and upper thoracic parts of the spinal cord, functioning of the respiratory muscles is disrupted, and leads to lowered lung volume parameters (Linn et al. 2000), in addition to other respiratory complications, such as decreases in compliance of the chest wall, changes in breathing patterns, sleep-disordered breathing (SBD), and ventilator dependency.
For individuals with SCI who have impaired autonomic function and impaired inspiratory muscle weakness, SDB may occur (Bonekat et al. 1990). In general, the incidence of SDB, characterized by sleep apnea, is estimated to be at least twice that reported in the general population (Schilero et al. 2009). Respiratory complications lead to significant morbidity and mortality in people with SCI (DeVivo et al. 1993; Cotton et al. 2005).
Among the general population, age associated changes in the respiratory system involve loss of elastic recoil of the lung, and similar to SCI, yet for different reasons, decreases in the compliance of the chest wall, and strength of the respiratory muscles are observed (Janssens et al. 1999; Janssens 2005). Complications resulting from SCI may therefore hold important respiratory implications as individuals’ age.
Several of the identified studies highlight that SDB and other respiratory complications are higher in persons with SCI than in the general population (see Table 5). In a five-year longitudinal study to assess changes in SDB, Bach and Wang (1994) measured oxygen desaturation, which is characteristic of sleep apnea, in 10 individuals with tetraplegia; six individuals had oxygen desaturation below 90%. At the five-year follow-up, 5 of the 10 individuals had increased patterns of oxygen desaturation, leading to the conclusion that oxygen desaturation is common among people with tetraplegia and increases with age. Cahan and colleagues (1993) produced similar findings in a case-control study. Oxygen desaturation in 6 of 16 persons with tetraplegia was found to be outside the normative range of AB controls, and indicative of SDB. In another longitudinal study (Berlowitz et al. 2005) sleep apnea, defined as an apnea-hypopnea index (AHI) of >10 events per hour, was found in 62% of the sample in the first month, peaking at 83% at 13 weeks, and falling to 68% and 62% at weeks 26 and 52 respectively.
Snoring is another important indicator of sleep apnea and appears to be more prevalent among SCI populations. In a large case-control study, 29% of men (N = 331) and 21% of women with SCI (N = 77) snored daily or almost daily compared to 18.2% of the control group (N = 339) representing the normal population of Denmark (Biering-Sorenson & Biering-Sorenson 2001). Further, those with SCI snored louder and had been snoring for more years than those in the control group. In addition, those who snored daily or almost daily in the SCI group were significantly older than those with SCI who snored less frequently.
After SCI, there are temporal changes in pulmonary functioning. Forced vital capacity (FVC), inspiratory capacity (IC), and maximum inspiratory mouth pressure (Pimax) are lowered in the acute stage of SCI, and then gradually improve over time. Loveridge and colleagues (1992) showed that seated positioning imposes greater stress on the respiratory system in the acute stages of SCI than the supine position. While breathing patterns in the supine position at all measured time points one-YPI were comparable to the controls (N = 18), breathing patterns in the seated position had to be adjusted in order to maintain minute ventilation. Over time, however, improved breathing patterns were observed in the seated position, so much so that differences initially observed between the seated and supine positions became insignificant. Such improved breathing pattern is speculated to be due to increased accessory muscle function, improved chest wall stability, thoraco-abdominal coupling, or a combination of these factors over time. Loveridge et al. (1992) also determined that persons with tetraplegia (N = 6) retain the ability to take deep breaths but do not do so as frequently in the sitting position as they do while supinated.
An increasing shallow breathing pattern resulting from a lack of deep breaths, and other factors associated with SCI, such as obesity and decreased chest wall compliance, may lead to hypercapnia, or excessive amounts of carbon dioxide in the blood, and possibly ventilatory failure(Bach & Wang 1994). Despite these results from this prospective longitudinal study, it is unclear if breathing patterns change as a result of the injury or due to aging with SCI. The former may be the case as the study followed adjustments only during the first YPI. No data are available on breathing patterns after individuals have adjusted long-term to their injury except for one study that did not meet the inclusion criteria for this chapter (Stolzmann et al. 2010), which found that chest illness resulting in time spent away from typical activities was related to reduced pulmonary function, wheeze, chronic obstructive pulmonary disease, a history of pneumonia and bronchitis, and smoking. Interestingly, level or completeness of SCI were not associated factors.
It should also be noted that several level 5 studies (Ovechkin et al. 2010; Radulovic et al. 2010; Tamplin et al. 2011) support the studies with higher levels of evidence (Bach & Wang, 1994; Loveridge et al. 1992) that persons with SCI have impaired respiratory function compared to AB controls, with one study highlighting persons with cervical injuries having similar patterns of responses to mild asthmatics with regard to airway inflammatory response (Radulovic et al. 2010).
Sustaining a SCI often leads to an initial respiratory insufficiency and necessitates a need for mechanical ventilation. In some instances, individuals may be weaned from the ventilator. Wicks et al. (1986) conducted a 10-year retrospective study of ventilator-dependent patients with tetraplegia (N = 134) to determine factors associated with weaning and long-term survival rate. Despite similar levels of injury, patients over 50 years of age had a 20% mortality rate compared to 6% for those younger than 50, and that ventilator weaning is less successful for those over the age of 50. This suggests that ventilator-dependency among SCI individuals who are older than 50 possess a much greater risk of negative health outcomes (Wicks & Menter 1986).
Although there are additional factors that can affect respiratory health long-term for the individual with SCI (i.e. level and completeness), there are several preventative activities that can be done to minimize the aging of the respiratory system, such as not smoking, minimizing exposure to polluted air, and controlling body weight (Wilmot & Hall 1993). Further work is required but the evidence that SDB is higher in persons with SCI may have implications for cardiovascular health for the aging SCI population and should be monitored.
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 cerebellarsystems (Bickford et al. 1999), and deterioration of station and gait (Greenhouse 1994). Whether these normative changes occur in the morphology or structure of the brain is controversial (Aldwin & Gilmer 2004), but it is “generally felt to be the result of a loss of neurons, a diminuition of neuronal dendritic processes, and accompanying gliosis (Lammertse 1993, p. 129). 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 of 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 6). 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. It may be that reported sensory and motor deficits in persons with SCI of more than 20 YPI (Whiteneck et al. 1992) occur due to a presumed 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).
The most robust finding was that presence of pain at an earlier time point appears to be the best predictor of future pain, and that it likely does not change significantly over time (Jensen et al. 2005; Siddall et al. 2003; Putzke et al. 2002a; Rintala et al. 2004). A limitation of most studies was the lack of clear assessments of the type and characteristics of pain being experienced by participants. For instance, Putzke and colleagues (2002a) do not report on the quality (e.g. frequency, intensity, duration) or pain type (e.g. neuropathic, nociceptive, etc.) of their sample. Although their findings suggested that age of onset may be an important factor, pain is a complex issue that involves the interaction of biological, psycho-social, and environmental factors.
In general, there are considerable gaps in knowledge regarding how the nervous system changes with aging with an SCI. Although identified as an issue of importance more than a decade ago (Lammertse 1993), research on the nervous system still remains incomplete and speculative at best.
Skin undergoes structural and physiological changes resulting from both the natural aging process and being exposed to damaging environmental elements. Over a lifetime, skin is observed to progressively degenerate. Most notable are the changes and deterioration in the structure of the skin which are due to losses and/or a disordering of collagen, the protein primarily responsible for the tensile strength of skin, and elastin fibres (Farage et al. 2009). The elderly, therefore, have an increased susceptibility to skin injuries such as pressure ulcers, and a decreased healing response.
Pressure ulcers are common among individuals with SCI, which typically occur over boney prominences, such as the ischial tuberosities and malleoli. Damage to the skin and underlying tissue caused by pressure, shearing, and/or friction due to continuous sitting are the primary causes of developing a pressure ulcer, but as it has also been reported that collagen metabolism increases as a result of SCI. People with SCI are therefore more susceptible to pressure ulcers than non-SCI individuals (Claus-Walker &Halstead 1982a; Claus-Walker &Halstead 1982b). As a result of the combined effects of pressure, from sitting, and reduced skin integrity, due to collagen degradation, it is estimated that 85% of individuals with SCI will experience a pressure ulcer in their lifetime (Gunnewicht 1995). Given that the mean cost of healing a wound is approximately $50,000, which translates into an annual cost of 3.6 billion dollars (Beckrich &Aronovitch 1999), there is a strong need to understand age-related changes to the skin following SCI in order to help minimize the occurrence of wounds.
Table 7: Skin and Subcutaneous Tissues
The presence of glu-gal Hyl, a collagen metabolite, in large concentrations in urine is indicative of the degradation of skin collagen. Although there is no evidence suggesting that glu-gal Hyl excretions increase with age after SCI (Rodriguez & Garber 1994), there is evidence that these levels are higher (but not statistically significant) in persons with SCI (N = 10) compared to the AB population (N = 5; Rodriguez & Claus-Walker 1984). Understanding how skin changes post-SCI is important, not only because of the implication of pressure ulcers, but because of other non-life threatening skin complications that commonly occur after SCI, which include local fungal infection, seborrheic dermatitis, and chronic acne vulgaris (Rubin-Asher et al. 2005; Stover et al. 1994). As well, attenuated immune response following SCI facilitates skin infections and lack of cutaneous sensation increases the incidence of pressure ulcers.
Park and colleagues (2011) found that the biomechanical skin properties were significantly altered following SCI in men, and these changes were directly influenced by regional sympathetic denervation rather than somatic sensory denervation. They found that age significantly correlated with all biomechanical skin parameters in their AB controls. However, in men with motor and sensory complete SCI, YPI, rather than age, was shown to be the most important factor influencing skin changes. Since the amount of dermal thickening is positively correlated with YPI, Park et al. (2011) hypothesized that the thickening process following SCI may be strong enough to overwhelm the impact of aging on biomechanical skin properties.
There is Level 2 evidence indicating that males with SCI have higher levels of a collagen metabolite, glu-gal Hyl, than AB controls (Rodriguez & Claus-Walker 1984).
There is Level 5 evidence that the biomechanical skin properties are significantly influenced by sympathetic paralysis rather than somatic sensory paralysis. Furthermore, in men with complete SCI, YPI may be the influential factor on the biomechanical properties of the skin (Park et al. 2011).
There are several normative age-related changes of the genitourinary and gastrointestinal systems that can lead to serious health problems for the elderly. With regard to the genitourinary system, there is a progressive and structural breakdown of the kidneys with age, and problems with urinary continence that results from decreased bladder capacity and compliance, and an increase in involuntary bladder contractions (Aldwin & Gilmer 2004). In males, enlargement of the prostate also contributes to incontinence (Dubeau 1997), and prostate cancer is one of the primary causes of death (McClain & Gray 2000). Although urinary tract infections (UTIs) increase with age, women are at greater risk, with the incidence in males only approaching that of women when they are 60 years or older (Foxman 2002). Unlike the genitourinary system, the gastrointestinal system retains much of its regular function, and it is unclear whether the few normal changes do affect the health of the older population. Some potential issues include slowing in large intestine motility, and diminished gut motility, with an increase in water resorption in the colon, which contributes to hard stool and increased risk of constipation, rectal fissures, hemorrhoids, and diverticular diseases (Wilson et al. 1997).
In persons with SCI, the effects of neurogenic bladder may compound the effects of aging in persons with SCI (Madersbacher & Oberwalder 1987) since bladder management techniques, such as the use of indwelling catheters, may contribute to the occurrence of common complications such as UTIs (Charlifue et al. 1999) and for a higher risk of developing bladder cancer (Groah et al. 2002). Similarly, neurogenic bowel may also compound aging after SCI given that persons with SCI often have higher rates of bowel-related complications compared to the general population (Cosman et al. 1993).
Table 8: Genitourinary and Gastrointestinal Systems
From the list of identified studies on the genitourinary system (see Table 8), there are four longitudinal studies (Viera et al. 1986; DeWire et al. 1992; MacDiarmid et al. 1995; Sekar et al. 1997) suggesting there are no differences in renal function over time among persons using various bladder management techniques. However, the samples of these studies did incur typical SCI-related complications such as UTIs and bladder stones, and there were some indications of renal decline. For instance, Lamid (1988) found that after 4 YPI, the number of vesicoureteral refluxes increased and progressed to grades II and IV, which caused kidney damage with caliectasis in 27 of 32 patients with SCI followed over 12 YPI. Finally, Sekar and colleagues (1997) reported that renal function (as measured by total and individual kidney effective renal plasma flow; ERPF) decreased over time in their SCI sample (N = 1,114) with a slight reversal occurring at 10 YPI. A methodological strength of the study was the assessment of ERPF, which is thought to be a more sensitive measure of kidney function than serum creatinine (Kuhlemeier et al. 1984a). Based on the findings of the identified studies, it may be that significant declines in renal function occur approximately at 5 YPI.
Work regarding age of onset and the genitourinary system is also needed as the findings of a cross-sectional study by Kuhlemeier and colleagues (1984b) suggests that persons with acute SCI (N = 160) who were younger than 20 or older than 50 had comparable levels of individual and global kidney effective plasma flows compared to AB controls (N = 287), whereas persons with between 21-51 had impaired renal function.
Although six cross-sectional studies found there were no differences in serum prostate specific antigen (PSA) between persons with SCI and AB controls (Konety et al. 2000; Pramjudi et al. 2002; Pannek et al. 2003; Scott Sr et al. 2003; Alexandrino et al. 2004; Shim et al. 2008), one study (Scott Sr et al. 2003) did find elevated levels in persons with SCI (n = 7; 63.6%) at the time of cancer diagnosis compared to AB controls (n = 267; 29.1%) with prostate cancer, and that the cancer in individuals with SCI was more advanced or metastatic (p = 0.012). Further, a study by Alexandrino et al. (2011) found in a case-control comparing men with SCI (n = 24) to AB controls (n =24) that mean seminal zinc concentration was significantly lower in men with SCI. Mean seminal zinc may serve as a marker of function of the prostate, which means lower levels may negatively impact fertility, and may make men with SCI more susceptible to more aggressive prostatic tumors.
Overall, the risk for prostate cancer appears to be lower in persons with SCI due to impaired testosterone levels, but prostate cancer screening should be encouraged given the possibility that males with SCI who do develop prostate cancer may have poorer outcomes than AB males (Scott Sr et al. 2003).
With regard to women with SCI (n = 62), Kalpakjian and colleagues (2010) found that they experience greater symptom bother in certain areas related to menopause compared to AB controls (n = 66). Specifically, women with SCI reported greater bother of somatic symptoms, bladder infections, and diminished sexual arousal. However, the patterns of symptoms, transitioning through menopause, and age at final menstrual period transitions were comparable between groups. Overall, the authors concluded that in important ways, women with SCI appear to experience menopause similarly to their peers.
Although bowel function is clearly impaired in persons with SCI compared to AB controls, one study (Lynch et al. 2000) demonstrated that continence deteriorates with increasing age in an AB population (N = 467) but does not change with increasing age in persons with SCI (N = 467).This supports a Level 4 study that found that gastrointestinal transit times and colonic dimensions do not change during the first decade, nor within the second decade, post-SCI (Faaborg et al. 2011). However, a 10 year longitudinal study (Faaborg et al. 2008) suggests persons with SCI do incur an increase in constipation-related symptoms over time. One possible reason for this occurrence is due to the evidence that high amplitude propagating contractions (HAPC) are absent in persons with SCI compared to AB controls (Ancha et al. 2010). HAPC are often associated with colonic mass movements and are thought to be a precursor of bowel evacuation. Thus it is an important factor in the occurrence of difficulty with evacuation post-SCI. Conversely, the need for assistance from medications or persons does not change, while fecal incontinence decreases. It may be that bowel dysfunction worsens over time for persons with SCI but three studies (Menardo et al. 1987; Krogh et al. 2000; Emmanuel et al. 2009) provide evidence that level of injury plays a primary role in the extent of bowel dysfunction. At this time, the SCI evidence on aging and the gastrointestinal system is limited, but attention to bowel symptoms should be incorporated into routine follow-up procedures and education (Charlifue et al. 2002).
In the general population, advancing into older adulthood is a period when individuals are faced with a unique array of physical, functional, and environmental stressors. This is no different for individuals aging with a traumatic SCI, who are now living an average of 30 to 40 years post-injury (YPI) (Samsa et al. 1993). As more persons survive into their second, third, and even later decades, living with a disability becomes a life-long process for persons with SCI (Hallin et al. 2001).
Given the evidence in the previous sections of this chapter indicating that SCI represents a model for premature aging in some body systems (e.g. cardiovascular and endocrine, musculoskeletal, immune, and respiratory systems), the physical and functional declines associated with natural aging are likely to present more quickly among individuals with SCI. Such knowledge of these effects of aging however is insufficient for rehabilitation purposes without any indication of how individuals perceive the aging-related changes and how they adapt their lifestyles in response to such changes (Charlifue et al. 2010).
In attempts to gain more perspective, the evaluation of community reintegration and QoL are often used to contextualize the quality of a person’s life. As a result, a key goal of rehabilitation is to maximize functionality and independence to allow for successful community reintegration and high QoL. QoL describes the well-being and life satisfaction of an individual, and is a multi-factorial construct, which includes but is not limited to, interpersonal relationships and social support, physical and mental health, environmental comfort, and a host of psycho-social factors (Kaplan &Erickson 2000). Community reintegration is an important constructs shown to be predictive of life satisfaction in persons with SCI (e.g., Pierce et al. 1999; Richards et al. 1999; Putzke et al. 2002b; Tonack et al. 2008; Kemp &Bateham 2010). The term community reintegration is used to refer to returning to the mainstream of family and community life, engaging in normal roles and responsibilities, actively contributing to one‟s social groups and of society as a whole (Dijkers 1998). Thus successful reintegration means resuming occupations or activities deemed important to the individual (i.e., self-care, employment, leisure, etc.; Yasui &Berven 2008). The environment (e.g., social, institutional, cultural or physical), can either create barriers or facilitate access to the community at large. Without exception successful reintegration can lead to improved QoL (Anderson 2004).
In the general population, older adults may face limitations with activities of daily living (e.g., Hoyer et al. 1999), and experience functional declines in the physical domain (e.g., Branch &Jette 1983), which can negatively impact community reintegration and QoL. Similarly, both physical and mental health factors influence quality of life in persons with SCI. For instance, issues with poor physical health, secondary health conditions (e.g., pressure ulcers, pain, etc.), depression and stress, and have all been shown to negatively impact on QoL.
With regards to aging, however, there are some mixed findings in relation to community reintegration and QoL, even within the same studies. For instance, there are some reports that life satisfaction and community reintegration (at least in some domains) improve with years post-SCI (e.g. Zarb et al. 1990; Tonack et al. 2008), whereas older age is associated with poorer community reintegration and quality of life (e.g. Krause &Crewe 1990; Eisenberg &Saltz 1991; Whiteneck et al. 1992; Tonack et al. 2008).
As well, some reports provide evidence that QoL improves with increasing age (e.g. Pentland et al. 1995; Westgren &Levi, 1998; Dijkers 1999). However, discrepancies with aging and quality of life tend to be more evident in cross-sectional analyses whereas longitudinal studies “mostly show relatively high and stable levels of QoL over long periods of time” (Kemp &Ettelson 2001, p. 119; Savic et al. 2010). As well, these differences may arise due to the use of different instruments, which may not all assess the same underlying QoL construct.
In this section (see Table 10), twenty-one longitudinal studies and two cross-sectional studies on community reintegration and QoL after SCI are reviewed.
Table 9: Quality of Life and Community Reintegration
Aging is a complex process that not only encompasses biology. Environmental factors also change over time, which may be particularly critical to persons with SCI, because they not only face physical limitations associated with their SCI, but also social and economic changes that result from injury (Krause &Coker 2006). For example, in a series of papers reporting on the same cohort at different time points over a period of 30 years, there were significant improvements with satisfaction with employment and finances over time (Crewe &Krause 1990; Krause 1992; Krause 1998; Krause &Broderick 2005; Krause &Coker 2006), whereas satisfaction with both social and sex lives decreased (Krause 1997; Krause &Broderick 2005; Krause &Coker 2006). Similarly, Bushnik and Charlifue (2005) observed changes related to economics and technology, but not related to SCI or aging per se. For example, letter writing, which probably included emails, increased in the sample over time because home computing had likely become more common. Although not significant, the high percentage of persons who switched to a portable ventilator or pneumobelt from a fixed ventilator may have improved community reintegration for these individuals. As well, the finding that economic self-sufficiency steadily improved with time (e.g. Charlifue &Gerhart 2004a; Krause &Broderick 2005; Krause &Coker 2006) supports Bushnik’s (2002) speculation that increased economic standing may improve community reintegration. In the case of Bushnik’s (2002) sample, improved financial status enabled access to adaptive equipment (e.g. modified van).
Conversely, level of community reintegration for Charlifue and Gerhart’s (2004a) sample did not significantly change over time, but this may have been due to sample differences between the studies (i.e. high level tetraplegia versus homogeneous impairment groups), and that the time between data collection intervals in the other studies reviewed were further apart. As well, the individuals in Gerhart and Charlifue‟s (2004a) study were at least 20 years post-injury when they entered the study. At 20 years post-injury, it is likely that routines and strategies for community participation have been well-established, and are not likely to dramatically change over 3 year periods. However, an understanding of environmental factors is important for assessing quality of life since there is evidence that an individual‟s adjustment over time is influenced by corresponding environmental changes (Krause &Sternberg 1997).
With regards to change in activity patterns, Bushnik and Charlifue (2005) attributed the changes to the natural progression of time utilization from external social activities associated with youth (e.g. card games with friends) to other activities not captured by the study (e.g. spending time with family). Further, the reported declines in activity by the SCI cohorts as they aged (Bushnik’s (2002), Charlifue and Gerhart’s (2004a), and Krause and Broderick’s (2005) might be similar to declines in activity patterns in the general population (Christensen et al. 1996; Bukov et al. 2002).
One of the main strengths of the studies by Krause (1997), Krause and Broderick (2005), and Krause and Coker (2006) is they assessed whether there were any differences between their current sample and those who were lost to follow-up. Based on these analyses, clear survivor effects emerged in both studies as the characteristics of respondents (persons who participated in both data collection periods) at Time 1 were younger, younger at age of SCI-onset, were less years post-injury, had higher levels of education, more likely to have cervical injuries, greater sitting tolerance, and had more social outings than non-respondents (persons who only participated in the first data collection period). These findings highlight that some care should be taken when interpreting the findings from these studies as it may only reflect survivors.
Although having a SCI inevitably does place some form of activity limitation from the onset of injury, aging “may magnify issues of dependency as needs, ability, and limitation change over time” (Charlifue &Lammertse 2001, p. 415). As with the general population (Roy 1986; Gaston-Johansson et al. 1996; Poluri et al. 2005), issues of fatigue and pain can limit the independence of a person with SCI. Fatigue can be defined as an overwhelming sense of tiredness, lack of energy and often a feeling of total exhaustion (Herlofson & Larsen, 2002). Fatigue after SCI is a prevalent issue (Gerhart et al. 1999; McColl et al. 2003; McColl et al. 2004; Fawkes-Kirby et al. 2008). The findings on the associations between age and fatigue after SCI have been somewhat conflicting. For example, one study found that males with SCI reported an increased fatigue with increasing age (Pentland et al., 1995), whereas some have found greater reports of fatigue in younger persons with SCI with short durations of injury (McColl et al. 2003).
Both pain and fatigue have been both found to negatively impact on several domains of function and QoL (Rintala et al. 1998; Ingles et al. 1999; Herlofson &Larsen 2002). As well, there is some evidence of a relationship between fatigue and pain after SCI (Fawkes-Kirby et al. 2008). When examined together, the study by Charlifue and colleagues (1999) and by Putzke and colleagues (2002a) highlight chronological age as a factor that mediates the expression and/or onset of change. In the study by Charlifue et al. (1999), the youngest and oldest group reported no significant changes in fatigue between Time 1 and Time 2. Similarly, in the study by Putzke et al. (2002a) the youngest and oldest group reported the least amount of pain interference between Year 1 and Year 2, however, overall, older individuals were significantly (p<0.01) more likely to report pain in both years than younger individuals with SCI. In terms of the influence of pain and the interference of pain on QoL over time, Putzke et al. (2002a) found that those individuals who experienced increased interference over time had decreased life satisfaction scores, whereas those whose interference subsided had increased life satisfaction. Similarly, Stensman (1994) observed over 5 years that individuals with variable pain experienced fluctuating global QoL, those with constant pain experience consistently low QoL, and those with no or little pain had consistently high or improvements to an initially low QoL over time.
The finding by Charlifue and colleagues (1999) that increasing age is associated with increased fatigue and additional physical assistance is congruent with other studies examining the effects of long-term SCI (e.g. Gerhart et al. 1993; Thompson, 1999; Liem et al. 2004). A limitation noted by Charlifue et al. (1999) was that their sample was a relatively ‘young’ age (M = 37.1 years), and none having lived with their SCI for more than 20 years (M = 9.3), and may not have been impacted by the aging process to significantly impact overall health and functional status. However, the consistent findings for increased fatigue between Time 1 and Time 2 do highlight that there is a consistent physical decline occurring. Charlifue and colleagues (1999) recognized the systematic changes in their sample (i.e., improved health but declining functionality) but attributed them to external factors such as less contact with the healthcare system, funding changes, which lead to fewer participants reporting particular outcomes. As well, they noted the need for increased physical assistance over time in their sample may have reflected attitude changes in rehabilitation practice where maintaining functionality is preferred over complete physical independence. Although the strength of the study is its provision of several perspectives to aging with a SCI, an alternative analysis strategy might have helped to provide a more cohesive model of how the factors assessed related to one another. For instance, the increases in physical assistance between Time 1 and Time 2 were often accompanied with improvements in health but also with increases in fatigue. Reporting on associations (or lack of) between these variables may have provided additional support for their conclusions.
The studies reviewed provide some interesting findings regarding living long-term with SCI, but do highlight some of the challenges associated with assessing quality of life in relation to aging.
The findings appear to provide some conflicting evidence where in some cases QoL/life satisfaction remained stable over time (i.e. Charlifue et al. 1998; Charlifue et al. 1999; Charlifue &Gerhart 2004b; Savic et al. 2010), decreased with time (i.e. Krause 1997; Charlifue et al. 1998), or improved with time (Stensman 1994; Kemp &Krause 1999; Bushnik 2002; Putzke et al. 2002; Bushnik &Charlifue 2005; Krause &Coker 2006; van Koppenhagen et al. 2009; DeVivo &Chen 2011; Kalpakjian et al. 2011; van Leeuwen et al. 2011). The discrepancies in these studies are partly due to theoretical and methodological differences. For instance, the study by Charlifue et al. (1998) was the only study that explicitly provided a theoretical model for assessing life satisfaction. Specifically, Charlifue and colleagues (1998) framed aging with SCI within a global thesis of function, which took into account physical, psychological, and environmental factors. Several studies with lower levels of evidence predicting life satisfaction have used other models that incorporate a variety of domains thought to impact on QoL (i.e. Pierce et al. 1999; Richards et al. 1999; Tonack et al. 2008). Unfortunately, Charlifue et al. (1998) did not provide a clear rationale for including specific predictor variables in their models. A larger theoretical concern is the issue of response shift (also known as recalibration, reprioritization, and reconceptualization; Schwartz &Spangers 2000), which refers to a dynamic process where an individual undergoes simultaneous changes in their internal standards, values, and conceptulizations of QoL in response to health and physical functioning changes (Tate et al. 2002). Ambiguous or paradoxical findings can occur because of differences among people or changes within people regarding internal standards, values, or conceptualization of health-related QoL (Schwartz et al. 2007). As a result, the psychometric properties (e.g. validity and reliability) of measurement tools can be affected (Schwartz et al. 2007). Hence, issues of response shift should be considered when assessing QoL in persons with SCI, and several recommendations are put forth by Schwartz and colleagues (2007) on how to address them.
In terms of methodological differences, because the samples in each of the studies had different mean ages and YPI it is not surprising that there are discrepancies in reported QoL. However, when examining the QoL results by an aging parameter, YPI for example, a common finding was that regardless of age, individuals with relatively new SCI (i.e.≤5 YPI) are more likely to experience improvements to their QoL (Stensman 1994; Kemp &Krause 1999; Bushnik 2002; Putzke et al. 2002; Bushnik &Charlifue 2005; Krause &Coker 2006; van Koppenhagen et al. 2009; DeVivo &Chen 2011; Kalpakjian et al. 2011; van Leeuwen et al. 2011) than individuals with longer term SCI (i.e. ≥6 YPI). who consistently report high and stable QoL levels (i.e. Charlifue et al. 1998; Charlifue et al. 1999; Charlifue &Gerhart 2004b; Savic et al. 2010). That is, after sustaining a traumatic SCI, the QoL of these individuals may be low and have more room to improve than those individuals with longer term SCI. In fact, Dijkers (2005) notes that the well-being after SCI reaches a plateau at the end of the adjustment period, which is estimated to last from two to five years (Dijkers 2005). Similarly, Whalley-Hammell (2007) reports that after a four year adjustment period, individuals with SCI feel as though as they live a normal life, and have the same problems as everyone else (Whalley-Hammell 2007). In this review, there one study however that observed no changes in QoL among individuals with ≤5 YPI (Mortenson et al. 2010). Mortenson et al. (2010) argued that the individuals may have already adjusted and experienced a response shift prior to the baseline assessment.
Although age of SCI onset does not appear to preclude high QoL, there are likely age related factors that potentially influence QoL. For example, in studies with samples with mean ages in the 20s, individuals were found to have greater improvements in life satisfaction and QoL if they were students, lived independently, had a lower level injury, had overcome past medical problems, and if they had accessible vans for transportation. Among individuals in their 30s, both Putzke et al. (2002) and Stensman (1994) found QoL to be influenced by amount of pain and interference with pain (Putzke et al. 2002; Stensman 1994), and Kalpakjian et al. (2011) found the relationship between life satisfaction and YPI to vary depending on marital status and sex (Kalpakjian et al. 2011).
Furthermore, when considering research design, comparing persons with SCI to control groups will also likely provide a different picture on QoL in different domains. A strength of Kemp and Krause‟s (1999) was the use of an able-bodied, and a disabled (i.e. polio) comparison group when examining issues of QoL after SCI as it provides some context to the extent of some problems for persons post-SCI (i.e. levels of depression). However, the characteristics of the control groups were significantly different to the group with SCI on some key factors. For instance, the able-bodied and polio groups were significantly older (p< 0.01) and had higher levels of education than the group with SCI (p< 0.05). As well, the polio group was comprised mostly of females, had a mean pediatric age of onset, was 50.9 years post-polio, and 90% were Caucasian, whereas the SCI group was comprised of mostly males from culturally diverse backgrounds, and who had an adult age of onset, and were only 14.5 years post-injury. This limitation was addressed in the study, but highlights that the findings should be interpreted with caution since many socio-demographic and historical factors may have influenced levels of depression and life satisfaction. Nonetheless, the finding that persons with SCI have lower QoL compared to the able-bodied population is consistent with other studies that did not meet the chapter‟s inclusion criteria (Kemp &Ettelson 2001).
Finally, although a couple of studies reported declines in QoL over time (Krause 1997; Charlifue et al. 1998), subsequent papers focusing on the same cohorts at longer lengths of follow-up reported different results. For example, Charlifue et al. (1998) first reported that after 3 years of observation 76% of the sample consistently rated their overall QoL as either good or excellent, but that there were significant decreases in life satisfaction, as measured by the life satisfaction index (LSI), among older individuals, those with <30 YPI and >40 YPI, and those with complete paraplegia (Charlifue et al. 1998). At a follow up thirteen years later, Savic et al. (2010) similarly reported that 76% of the sample consistently reported overall QoL as good or excellent, and that there were significant differences in LSI scores at 6 different time points over the course of 16 years, with the highest life satisfaction reported at the last time point (Savic et al. 2010). Similarly, over two time points 9 years apart, Krause (1997) reported diminished satisfaction related to social and sex lives, as measured by the life situation questionnaire (LSQ)* (Krause 1997). Such lower satisfaction is corroborated in papers by Krause and Broderick (2005), and Krause and Coker (2006) that used observations from the same cohort at different lengths of follow-up (Krause &Broderick 2005; Krause &Coker 2006). However, these two papers in addition to Crewe and Krause (1990), Krause (1992), and Krause (1998), all reported significant increases in satisfaction related to employment among the same cohort over various lengths of time (Crewe &Krause 1990; Krause 1992;Krause 1998). In general, the overall and common finding from studies that followed the same cohorts over time is that global QoL tends to remain high and stable over time but when considering specific areas of QoL, fluctuations exist with some domains increasing in importance (e.g. employment) and other decreasing (e.g. social and sex lives).
*Note: Krause (1997) used a modified version of the LSQ. Using this version, the authors also observed significant declines in satisfaction related to family relationships, emotional adjustment and control over life.
There is Level 4 evidence from a longitudinal study (Charlifue et al. 1999) that fatigue and the need for physical assistance increases over time with SCI.
There is level 4 evidence from ten longitudinal studies that individuals with ≤5 YPI have the potential to improve their QoL (Stensman 1994; Kemp &Krause 1999; Bushnik 2002; Putzke et al. 2002; Bushnik &Charlifue 2005; Krause &Coker 2006; van Koppenhagen et al. 2009; DeVivo &Chen 2011; Kalpakjian et al. 2011; van Leeuwen et al. 2011).
There is level 4 evidence from four longitudinal studies that individuals with longer term SCI (i.e. ≥6 YPI) consistently report high and stable QoL level (Charlifue et al. 1998; Charlifue et al. 1999; Charlifue & Gerhart 2004b; Savic et al. 2010).
The majority of studies for all the systems provide some important findings regarding the role of chronological age (including age of SCI onset) and YPI, but there is still lack of clarity on how all of these factors affect (individually and in combination) the individual living with SCI over time, and further work is needed to determine if SCI is indeed a model for premature aging. It appears that the field of aging with SCI has yet to make significant advances since many of the issues and questions raised over 15 years ago (Whiteneck et al. 1993) are still relevant today.
In general, longitudinal designs are the preferred method for investigating aging, but a number of longitudinal aging-related studies of SCI are limited in scope and quality due to several methodological issues (Krause 2007). One limitation with longitudinal research designs are problems with retaining sufficient sample size over many years to observe long term changes with aging. Problems with attrition lead to another type of cohort effect, namely survivor effects. Survivor effects describe those individuals who may have outlived other members in their cohort due to some unusual advantage (e.g. environmental, physiological, Adkins 2001). Persons who remain in longitudinal studies often represent those who are healthier, wealthier, and better educated whereas persons with poorer functioning drop-out or have died. Another limitation of longitudinal designs is the possibility that data collected at an earlier time point may become obsolete due to advances or changes in measurement. Longitudinal research is also considerably more resource intensive than cross-sectional studies in terms of cost and time.
Despite the challenges associated with longitudinal research, gaining an understanding of what changes a person with SCI may undergo over time is important to identify potential problems that can be anticipated and perhaps prevented in some cases. This in turn may contribute to continued levels of maximum independence and overall well-being. The field of aging with SCI has made some tremendous strides forward, but the dearth of knowledge in some areas highlights research opportunities that will help to resolve current challenges and more importantly provide information to fill many existing gaps.
There is Level 4 evidence (Picklesimer et al. 2010; Frisbie et al. 2010; Savic et al. 2010) that the mortality rate post-SCI over a 10-year period may be 15.5% to 25.8%.
There is Level 4 evidence (Frisbie 2010) and Level 5 evidence (Samsa et al. 1993) that the causes of death post-SCI are beginning to approximate those of the general population.
There is Level 5 evidence (Lewis et al. 2004) that men with SCI have slower plasma-free cortisol responses than AB controls.
There is Level 4 evidence (DeGroote et al. 2010; Crane et al. 2011) that BMI increases over time in persons with SCI.
There is Level 4 evidence that persons with SCI have a prevalence of anemia and hypoalbuminemia (Frisbie 2010), which might serve as markers for infection.
There is Level 5 evidence that respiratory function is impaired compared to AB controls (Ovechkin et al. 2010; Tamplin et al. 2011), and that persons with cervical SCI have similar airway inflammatory responses as mild asthmatics (Radulovic et al. 2010).
There is Level 5 evidence that the biomechanical skin properties are significantly influenced by sympathetic paralysis rather than somatic sensory paralysis. Furthermore, in men with complete SCI, YPI may be the influential factor on the biomechanical properties of the skin (Park et al. 2011).
There is Level 5 evidence (Alexandrino et al. 2011) that men with SCI have lower seminal zinc concentrations, as an indicator of prostate function, than AB controls.
There is Level 3 evidence (Kalpakjian et al. 2010) that women with SCI experience menopause similarly to AB controls.
There is Level 5 evidence that high amplitude propagating contractions (HAPC) are absent in persons with SCI compared to AB controls (Ancha et al. 2010).
There is Level 4 evidence (Faaborg et al. 2011) that gastrointestinal transit times and colonic dimensions do not change over time in persons with SCI.
There is Level 4 evidence from 6 longitudinal studies (Crewe &Krause 1990; Krause 1992; Krause 1997; Krause 1998; Krause &Broderick 2005; Krause &Coker 2006) that selected domains of life satisfaction change (i.e., social life and sex life decrease, and employment and finances increase) as one ages with an SCI. It may be that these changes in satisfaction of certain domains are comparable to changes in the general population.
There is level 4 evidence from 10 longitudinal studies that individuals with ≤5 YPI have the potential to improve their QoL (Stensman 1994; Kemp &Krause 1999; Bushnik 2002; Putzke et al. 2002; Bushnik &Charlifue 2005; Krause &Coker 2006; van Koppenhagen et al. 2009; DeVivo &Chen 2011; Kalpakjian et al. 2011; van Leeuwen et al. 2011).
There is level 4 evidence from 4 longitudinal studies that individuals with longer term SCI (i.e., ≥6 YPI) consistently report high and stable QoL level (Charlifue et al. 1998; Charlifue et al. 1999; Charlifue &Gerhart 2004b; Savic et al. 2010).