Adaptive sports are organized sporting activities that are practiced by individuals with disabilities. In addition to promoting chronic disease prevention and health maintenance, the psychological and social benefits of adaptive sports participation have been well established and include increased community and social integration, reduced anxiety and depression, improved life satisfaction, greater functional independence, and heightened self-esteem (1). However, adaptive athletes present with a unique set of circumstances that influence their relationship with sport, including the nature of their underlying disability as well as the mechanics and equipment involved in their sport. Such factors yield distinct risks related to sports participation. A fundamental understanding of such risks is paramount to uphold safe participation in sport as well as overall health. The consequences of injury for an adaptive athlete may extend well beyond exclusion from sport, potentially limiting functional independence and the ability to carry out routine daily activities. The present review aims to summarize some of the more common medical and orthopedic conditions encountered by adaptive athletes participating in wheelchair sports specifically, emphasizing current evidence and recommendations for the prevention of such disorders.
Prevalence rates of medical illness appear to be about twice as high in Paralympic athletes when compared with Olympic athletes (2). Certain illnesses may be particularly more common in wheelchair athletes, due to distinctive factors related to their underlying disability. Individuals with spinal cord injury (SCI), for example, can have impairment of the autonomic nervous system yielding unique changes in cardiorespiratory, thermoregulatory, as well as gastrointestinal and genitourinary function that in turn predispose to various health risks. As SCI represents one of the most common disabilities observed in wheelchair athletes (3), the ensuing discussion will focus largely on medical conditions common to the athlete with SCI. Specifically, the conditions of autonomic dysreflexia (AD), impaired thermoregulation, neurogenic bladder, and pressure injuries will be reviewed (see Table).
AD refers to a syndrome of imbalanced sympathetic discharge and may be observed in individuals with SCI. Specifically, AD may affect individuals above the level of the major splanchnic outflow, most typically an SCI at or above the T6 level (4). AD arises in the setting of a noxious stimulus below the level of injury, which in turn stimulates a sudden, unopposed reflex sympathetic activity with profound vasoconstriction and other autonomic responses (5). Included among the most common triggers for AD is bladder distention, urinary tract infection (UTI), or constipation (5). However, other important causes to consider, particularly in the athlete, include pressure sores, blisters, tight-fitting clothes/straps, and ingrown toenails (5). Clinically, AD can present with headache, hypertension, diaphoresis, flushing, nasal congestion, hypertension, and/or bradycardia. The hypertension may be significant and can result in cerebral hemorrhage, seizures, and even death, such that AD should be regarded seriously and treated swiftly. Principles of management include positioning the patient upright, removing tight or constrictive garments, and identifying and reversing the underlying precipitant. Blood pressures should be monitored closely, every 2 to 5 min. Should hypertension persist (systolic blood pressure ≥150 mm Hg) despite the aforementioned efforts, treatment with an antihypertensive, such as nitroglycerin or nifedipine, is indicated (4).
Despite the potential risks associated with AD, some athletes may attempt to intentionally induce a dysreflexic state in an effort to increase cardiovascular output and in turn enhance performance; a practice commonly termed “boosting” (6). This may be accomplished through self-infliction of a nociceptive stimulus, most commonly by overdistending the bladder, sitting on a sharp object, or applying a tight leg strap, and is typically performed 1 or 2 h prior to competition to maximize the response (7). The precise incidence of boosting among wheelchair athletes has not been clearly established. One relatively small study comprising 99 athletes across a variety of sports found that 16.7% self-reported a history of boosting (8). The study also suggested a higher preponderance of boosting among male athletes and perhaps, not surprisingly, higher rates of boosting in sports that particularly stress the cardiovascular system including wheelchair rugby as well as marathon and long-distance racing. Interestingly, over one quarter of the athletes polled believed boosting to be common in their sport (8).
While research regarding the performance effects of boosting is overall limited, increases in catecholamine release, heart rate, oxygen update, and peak performance have been demonstrated (9,10). Moreover, one study suggested a nearly 10% improvement in race times among wheelchair racers in a boosted state (9). Regardless, as was previously mentioned, AD may be highly dangerous and potentially life-threatening. In fact, the International Paralympic Committee (IPC) has prohibited athletes from competing in a dysreflexic state as much for the ethical implications as to protect the health of athletes (6,11). The IPC Position Statement on Autonomic Dysreflexia and Boosting stipulates that:
- A hazardous dysreflexic state is reflected by a systolic blood pressure of 180 mm Hg or higher;
- an athlete with a systolic blood pressure of 180 mm Hg or above should be reexamined 10 min after the first examination. If on the second examination the systolic blood pressure remains above 180 mm Hg, the athlete should be withdrawn from competition;
- any deliberate attempt to induce AD is expressly forbidden and should prompt immediate disqualification from competition (12).
When evaluating and counseling patients, it is important to be aware that both the performance enhancing as well as health hazardous effects of AD have been demonstrated at notably lower blood pressure thresholds (systolic blood pressure, 140-160 mm Hg) (6). It is the author’s recommendation that all athletes with a history of cervical or thoracic SCI be screened for a history of AD. Athletes must be advised regarding the signs, symptoms, and common precipitants because prevention and rapid treatment are vital. Of particular importance is education in relation to proper bladder and bowel maintenance as well as skin care. In individuals with a known history of AD, consideration for an antihypertensive prescription (such as nitropaste) to be used pro re nata for emergent blood pressure reversal is warranted. The risks of AD, including possible death, cannot be overemphasized.
Under usual circumstances, core temperature is maintained by the thermoregulatory center of the hypothalamus in the brain (13). Increases in temperature are sensed by the hypothalamus and in turn yield sympathetic inhibition characterized by vasodilation, increased circulation to skin blood vessels, and stimulation of sweat glands (7,14). As was previously mentioned, SCI may disrupt afferent and efferent pathways with consequent loss of supraspinal control of the sympathetic nervous system. This can result in deficient vasomotor control and sweating capacity below the level of injury, posing a greater risk for heat-related illness (13,14). This is particularly so in athletes with SCI at or above the T6 level (15). Griggs et al. (16) compared core temperature in 16 wheelchair athletes engaging in an intermittent sprint protocol: eight athletes with tetraplegia and eight with paraplegia. In this study, athletes with tetraplegia demonstrated significant increases in core temperature despite similar levels of external work (16). While commonly regarded in individuals with SCI, it is worth noting that impaired thermoregulation may be observed in those with a history of multiple sclerosis or brain injury as well (17,18).
Given the increased risk of heat-related illness as well as the known detrimental effects of heat on performance, cooling has been an area of active research in athletes with SCI. However, an optimal cooling strategy for such athletes remains a matter of debate. A variety of factors ought to be considered, including both the method and timing of cooling. Commonly used methods include cold air exposure, application of ice vests, whole or partial body water emersion, and ingestion of ice slurries (19). Meanwhile, these techniques may be implemented either prior to (so-called precooling) or during exercise (19). Both precooling and cooling during exercise have demonstrated benefit, although some combination of the two is likely ideal (20). Webborn et al. (21) compared no cooling with cooling with an ice vest either before or during intermittent sprint exercise in a group of male athletes with tetraplegia. Lower core temperatures were demonstrated in the groups cooled before or during exercise when compared with no cooling. More recently, Griggs et al. (20) evaluated the effect of an intermittent sprint protocol on temperature in tetraplegic athletes under three conditions: no cooling, precooling with an ice vest, and precooling with an ice vest combined with water sprays between quarters. The latter (combined) method of cooling yielded the smallest increase in both core and skin temperatures (20). In terms of methods for cooling, as was previously stated, few studies to date have undertaken a comparison of cooling techniques in adaptive athletes specifically. One recent study investigated precooling through cold water immersion, cold liquid ingestion, and cold liquid ingestion augmented with application of iced towels (22). In this study, the most significant reduction in core temperature was observed after cold water immersion; however, cold liquid ingestion combined with iced towels also demonstrated a statistically significant reduction in core temperature (22). Further studies are certainly needed to clarify the most effective method and timing of cooling in wheelchair athletes with impaired thermoregulation. At this time, it is recommended that preventive cooling strategies be implemented and customized to the athlete based on risk, logistics, and comfort (19). Other practical recommendations for preventing heat-related illness in at-risk individuals include assurance of adequate hydration and sleep (19). A period of heat acclimation also has been proposed, although current literature does not support this strategy in isolation (23).
Finally, it is worth noting that while less studied, wheelchair athletes (namely those with high-level SCI, multiple sclerosis, and possibly brain injury) may be at higher risk for systemic cold injury (hypothermia), by a similar mechanism that results in impaired vasoconstriction and shivering in cold environments (14). Thus, it is critical that coaches and medical support staff be properly educated regarding environmental illness including the signs, symptoms, and risk factors for both heat- and cold-related illness. A fundamental awareness of training and competition conditions is essential, with appropriate provisions in place for rapid cooling and/or heating should the need arise.
Neurogenic bladder is another common problem, affecting up to 84% of patients with SCI (24), but also may arise in the setting of multiple sclerosis, cerebral palsy, spina bifida, and brain injury (24,25). Neurogenic bladder is important to recognize because it can predispose to a variety of ailments, including infection, stones, and obstruction (26). While the literature regarding neurogenic bladder in athletes is explicitly relatively lacking, several factors unique to the adaptive athlete may rationally increase one’s risk in such conditions, and thus warrants further discussion here. Specifically, dehydration as well as inadequate coordination of bladder management (e.g., around practice, competition, and/or travel schedules) can be problematic (27). Epidemiologic studies evaluating illness rates in recent Paralympic games suggest that 7% to 11% of athletes suffer genitourinary illness (2).
It is worth noting that asymptomatic bacteriuria is a frequent finding in those with neurogenic bladder; and in the absence of signs or symptoms to suggest a secondary illness, treatment is not indicated. However, the symptoms of UTI in individuals with SCI can be variable and ill-defined. Indicators that should raise concern for infection include fever, rigors, malaise, nausea and vomiting, worsening spasticity, new or increased urinary incontinence, and AD (28,29).
Consensus guidelines for the prevention of UTI in spinal cord injured athletes were recently proposed by the Australian Institute of Sport and the Australian Paralympic Committee (29). Education regarding proper bladder management is critical. Preventative measures should include adequate perineal hygiene, regular bladder emptying, and appropriate use of catheters (29). Krassioukov et al. (30) evaluated catheterization practices of elite athletes with SCI and found that individuals who reused catheters experienced more frequent UTI. Therefore, catheter reuse should be strongly discouraged. Other important preventative measures comprise regular hand washing and ample hydration (29). Although a variety of home remedies, including cranberry products, methenamine salts, and acidification/alkalinization agents, have been proposed in UTI prevention, their efficacy is currently not supported (29). Routine antibiotic prophylaxis also is not recommended. Antibiotic prophylaxis may be considered on a case-by-case basis for individuals at particular risk or who suffer frequent, recurrent UTI, but must be heavily weighed against the serious risk of engendering resistant bacteria (29).
Pressure injuries represent areas of localized tissue damage due to intense or prolonged pressure or pressure in combination with shear forces (31). In particular, pressure forces over soft tissue that exceed those of the blood vessels supplying the area can result in ischemia and edema, and ultimately tissue breakdown (32). Pressure injuries most typically occur over bony prominences, but may alternatively arise from pressure related to an external device (31). Areas of particular concern include the sacrum, ischium, greater trochanters, and calcanei (33). Individuals with impaired mobility and insensitivity are at especially high risk (32); however, other common risk factors include moisture, poor nutrition, spasticity, incontinence, low life satisfaction, medical comorbidities, male sex, and history of pressure injuries (4,34).
The epidemiology of pressure-related injuries in wheelchair athletes is poorly defined, although skin injuries, in general (including blisters, lacerations/abrasions, and pressure injuries), appear to represent one of the most common injury types among wheelchair athletes (35–37). Moreover, while higher levels of activity are generally considered protective, several factors specific to the athlete may actually augment pressure injury development, including repetitive movement(s) related to sport, increased moisture exposure due to sweating, and/or environmental conditions, as well as equipment designs that increase hip and knee flexion angle (38). Indeed, recent studies have demonstrated rather striking rates (45% to 62%) of deep tissue injury by ultrasonography in wheelchair basketball players (39,40), while another study indicated average seated pressures that consistently exceeded clinically accepted thresholds for skin ulceration among a cohort of ice sledge hockey players (38).
Implementation of pressure injury prevention strategies is critical to minimize the risk of associated complications such as infection while in the case of wheelchair athletes also upholding regular participation in sport. Pressure relief represents the mainstay of pressure injury prevention. Methods include self-repositioning and seated pressure reliefs, as well as pressure-relieving support surfaces. While data supporting an ideal frequency for performing seated pressure reliefs are overall limited, and recommendations should be tailored based on an individual’s risk factor profile, regular weight shifts performed at least every 15 to 30 min are typically recommended for individuals with SCI (41). Common pressure relief techniques include push-ups, leaning, tilting, and reaching for manual wheelchair users, as well as tilting and reclining for power wheelchair users (42).
In addition, high-risk individuals must be counseled regarding skin maintenance including vigilant inspection and prompt offloading for any evidence of an early pressure injury (e.g., erythema) or abrasion to pressure-sensitive areas (41). An educational program aimed at enhancing self-efficacy through organized counseling, demonstration, and feedback may be especially effective in promoting knowledge and compliance with pressure injury prevention (43). Other strategies that may further support self-management and prevention include computer-based educational technologies and telemedicine programs, as well as implementation of interface pressure mapping equipment (44). Interface pressure mapping enables direct measurement of skin-surface pressures and aims to identify areas under unacceptably high pressures and may be coupled with feedback (audio or tactile) systems that alert users to high-risk situations (44). Pressure mapping data also may be used to direct the use of specific pressure-relieving support surfaces.
Research regarding the potential role for specialized support surfaces in adaptive sports is notably limited (45). One study demonstrated no significant difference in seated pressures between a standard sledge hockey seating system and one fitted with a pressure-relieving activity cushion (38). More recently, Anderson et al. (45) likewise failed to establish a consistent offloading effect with the application of cushioned shorts in wheelchair athletes. Nonetheless, this study did suggest that cushioned shorts had varying influences based on the athletes’ movement condition (static versus dynamic), type of sports equipment used, and brand of short (45), supporting the need for further investigation into various styles of cushioning and their role in individual sports or equipment types.
In addition to the medical considerations aforementioned, there are a variety of musculoskeletal conditions to which wheelchair athletes are uniquely predisposed. Manual wheelchair users in general are largely dependent on their upper body for day-to-day function, placing significant and repetitive strain on the upper extremity. Perhaps, not surprisingly then, the upper extremity represents the most common anatomic site of injury reported among wheelchair athletes (36). In addition, individuals with disability are at increased risk for developing osteoporosis, raising concern for fracture potential (46). Shoulder injuries, upper-extremity entrapment neuropathies, and osteoporotic fractures will thus be reviewed here (see Table).
Shoulder pain is perhaps the most common musculoskeletal complaint observed in wheelchair athletes (47,48). Frequently identified etiologies include rotator cuff impingement or tear, biceps tendon pathology, and acromioclavicular joint pathology (48). The rotator cuff is particularly vulnerable to injury among wheelchair athletes. One study of wheelchair athletes engaging in overhead sports demonstrated evidence of rotator cuff tears in 76% of participants, a rate far exceeding those observed in nonathletes (36%) (49). The high rates of shoulder injury, and especially of the rotator cuff, are believed to be related to a variety of factors specific to the adaptive athlete including unfavorable sitting posture, impaired shoulder mechanics, and repetitive use for propulsion (50). In particular, wheelchair positioning may predispose to an unfavorable posture characterized by posterior pelvic tilt, increased thoracic kyphosis, and forward head position, in turn yielding anterior displacement of the shoulder girdle (50). Moreover, wheelchair athletes, and particularly those with underlying SCI, are prone to muscle imbalance and selective muscle weakness with consequent scapular dyskinesis (51). Other risk factors for the development of shoulder pain in the wheelchair athlete include poor trunk control (48,52), longer duration since injury (48,49), advancing age (48,49), increased BMI (48,49,53), and more frequent transfers (53).
Unfortunately, directed interventions in the prevention of shoulder injuries for wheelchair athletes specifically have not been well studied. General guidelines may be inferred based on universal ergonomic recommendations for wheelchair users and knowledge of effective prevention strategies for able-bodied athletes. Given the multifactorial nature of shoulder pain in the wheelchair athlete, a comprehensive intake that evaluates all of an individual’s relevant risk factors is advised to promote successful injury prevention. This should include first an assessment of seated posture. Providing posterior pelvic support can reduce thoracic kyphosis and in turn improve shoulder positioning (51). If the kyphosis is fixed (i.e., does not reduce significantly with dynamic movement), a contoured back rest with a degree of seat tilt may be effective (51). Next, wheelchair users should be educated to minimize the frequency and force of repetitive upper-extremity tasks. Limiting the number of transfers required per day and maintaining an ideal body weight is suggested (51,53). Efficiency of movement may be achieved through long, smooth propulsive strokes (51). As well, extremes of position and especially those that predispose to impingement (namely extremes of internal rotation with abduction or forward flexion) ought be avoided when possible (51).
Finally, preventative physical therapy programs have been advocated to avert shoulder injuries (50,51,54). Exercise programs to address range of motion as well as dyskinesis and scapular stabilization have been reasonably proposed (50). Currently, few studies have actually confirmed the efficacy of such programs on shoulder injury prevention in wheelchair athletes. A recent study described the effect of a 6-wk shoulder exercise program in a group of wheelchair basketball players, reporting overall improvements in shoulder range of motion (54). While the authors did not evaluate injury risk specifically, given a previously established association between restricted range of motion and shoulder pain and injury (55,56), they concluded that the program may have utility for injury prevention in wheelchair athletes (54). Certainly, further research is needed; however, at present, expert experience supports the recommendation for a directed therapy program aimed at shoulder range of motion and scapular stabilization to promote overall function and injury prevention in wheelchair athletes.
Upper-extremity entrapment neuropathies represent another common injury in wheelchair users. Clinical findings of upper-extremity entrapment neuropathies have been reported in 23% of wheelchair athletes (57), while a much higher proportion demonstrate electrodiagnostic findings of nerve compression (57–59). This is believed to be the result of repetitive trauma, particularly about the wrist, from the repeated flexion and extension motions as well as direct pressure required for wheelchair propulsion and transfers (58,60). This idea is supported by a recent study that found higher median nerve cross-sectional areas at the wrist by ultrasound following a wheelchair propulsion exercise (59). Moreover, high pushrim forces and push frequency have been associated with reduced median nerve conduction at the wrist (61). It follows that the most common entrapment neuropathies observed in wheelchair athletes are carpal tunnel syndrome and ulnar neuropathy at the wrist, followed thereafter by ulnar neuropathy at the elbow (57).
As with shoulder injuries, studies regarding the prevention of entrapment neuropathies in adaptive athletes are lacking. The strategies that follow reflect consensus recommendations for wheelchair users at large (51,62). Given the previously demonstrated relationship between pushrim force and frequency and median nerve function, individuals should be trained in economical wheelchair propulsion techniques (61). As aforementioned, a long, smooth propulsive stroke is linked to reduced peak forces (51). The importance of maintaining an ideal body weight is again emphasized (51). Cadence may be enhanced through a semicircular stroke pattern whereby the user’s hand drifts below the pushrim during the recovery phase can reduce peak forces and stroke frequency (51). In addition, increased range of motion in wrist flexion and extension has been implicated in reduced force and frequency of propulsion as well as better nerve function (63). It is plausible, then, that wheelchair athletes may benefit from a regular stretching program to promote wrist range of motion and propulsion efficiency, and in turn reduce upper-extremity injury risk; however, further investigation is necessary to confirm this notion. Then again, extremes of wrist position should be avoided during routine daily activities, such as transfers (51). It is recommended that transfers be performed along a level or downward trajectory when feasible (51). Additionally, alternating the leading arm and varying transfer techniques may be beneficial (51). Closed fist transfers are likely to reduce pressures through the carpal tunnel (51). Finally, padded gloves are commonly used by wheelchair athletes for hand and wrist protection. One study evaluated the effect of such gloves on median nerve conduction specifically and concluded no significant influence (64). Regardless, padded gloves represent a low risk, relatively low-cost intervention that may portend worthwhile support and comfort, such that their prescription to wheelchair athletes warrants consideration.
Osteoporosis and Fractures
Persons with disability, in general, are at high risk for developing low bone mineral density (BMD) (46). Studies investigating populations with a variety of disabilities have indicated rates of osteopenia or osteoporosis exceeding 60% (65,66). Reduced ambulatory status and/or wheelchair dependence represents a particularly important risk factor for low BMD (46). Indeed, it has been suggested that most individuals with SCI will develop some degree of low BMD over time due, at least in part, to reduced skeletal loading (67). Among patients with SCI, patterns of bone demineralization most prominently affect the long bones of the lower limbs from distal (i.e., tibia) to proximal (i.e., femur), although the upper extremities also may be involved in patients with tetraplegia (68). Meanwhile, in individuals with acquired brain injury, disproportionate reductions in BMD involving the paretic side have been demonstrated (65,69).
Low BMD is associated with an increased risk for fracture (70). Given the higher rates of low BMD noted in individuals with disability, fracture risk is of particular concern for adaptive athletes. According to one study that evaluated 139 elite-level athletes with physical disabilities, 13 (9.4%) reported a history of sports-related fracture (35). It follows that interventions aimed at management and prevention of osteoporosis may help reduce the risk of fracture among disabled athletes. Of note, BMD in individuals with SCI appears to reach fracture thresholds within 1 to 9 years postinjury, supporting the notion that interventions aimed at prevention should be implemented as early as possible (71).
The role of physical activity, particularly weight-bearing activity, in the prevention of osteoporosis has been well established in able-bodied individuals, although its influence in persons with physical disability is less clear (72). While several studies have reported mixed effects of weight-bearing and sports activity on BMD in patients with SCI (72–74), congruent with the timing of bone loss following injury, earlier implementation of activity appears to portend greater preservation of BMD (72,74). Both regular loading exercise (tilt table or standing) during the early phases of rehabilitation (74) as well as timely return to sport (72) have been implicated as potential interventions to help attenuate bone loss. Nevertheless, particulars regarding the optimal type, frequency, and duration of exercise in the prevention of osteoporosis for adaptive athletes remain poorly defined, and more studies are needed in this regard (75).
Functional electrical stimulation (FES) also has been examined for its effect on BMD in individuals with SCI, with the majority of studies indicating some benefit (75). FES utilizes electrical stimulation applied through surface electrodes to activate paralyzed musculature. As an exercise modality, FES aims to reduce muscle atrophy and enhance musculoskeletal health (76). Common forms of FES exercise include cycling and rowing. Most of the studies investigating FES and BMD to date have used FES cycling specifically, typically executed over 30- to 60-min sessions, three to five times per week (75). A meta-analysis summarizing this literature upheld a positive effect of FES on BMD, but suggested greater efficacy in programs using FES ≥5 d wk−1 (77). A more recent case report purported significant benefits following a 1-year FES training program beginning with 3 months of knee extensor strengthening and followed by 9 months of rowing performed three times per week (78). The patient presented exhibited significant increases in measures of muscle strength as well as a 19% improvement in bone density (78). Regardless, as with other forms of exercise, further investigation is necessary to clarify an ideal modality, frequency, and duration of FES to optimize bone health. Furthermore, the role of FES as an adjunct in adaptive athletes specifically remains unstudied.
The importance of adequate nutrition, including both macronutrient and micronutrient intake, to preserve bone health is well recognized. Despite this, several studies have indicated nutrient inadequacies in wheelchair athletes (79–82). Vitamin D and calcium are especially relevant to BMD, yet vitamin D deficiency is ubiquitous in patients with SCI and brain injury alike (83,84). Moreover, insufficient intake of both calcium and vitamin D has been consistently demonstrated in wheelchair athletes (80,82). Maintaining sufficient calcium and vitamin D is recommended as a safe and inexpensive means to reduce fracture risk for all individuals (85). It follows that wheelchair athletes should be regularly screened and treated for nutritional deficits, including calcium and vitamin D, in an effort to promote bone health and lower fracture risk.
Lastly bisphosphonates, a class of medication that inhibits bone resorption and is commonly used in the treatment of osteoporosis, have been studied for their role in osteoporosis prevention for individuals with SCI. A meta-analysis in 2013 concluded that early administration of bisphosphonates following SCI may effectively attenuate bone loss (77). Two more recent studies similarly demonstrated reduced BMD loss at the hip in patients with SCI treated with IV zoledronic acid within 12 wk of injury (86,87). However, both studies failed to demonstrate statistically significant attenuation in bone loss about the knee (86,87). As the knee more closely reflects the sites of greatest demineralization and fracture risk after SCI, this finding calls into question the utility of bisphosphonates to reduce fractures in this population. At present, no definitive recommendation exists for the use of bisphosphonates as a preventative measure for osteoporosis after SCI, and further studies are needed to clarify the influence, if any, of bisphosphonates on fracture risk in athletes and nonathletes with disability alike.
Regular participation in physical activity, including organized sports, is strongly encouraged for individuals with disability to promote health maintenance and quality of life. Adaptive athletes display distinct patterns of injury and illness as a consequence of their underlying disability as well as the mechanics and equipment involved in their sport. It is imperative that health care providers recognize these patterns and implement appropriate screening and prevention protocols to uphold safe participation in sport. Current evidence supports comprehensive patient education as the cornerstone of prevention. As well, promotion of adequate hydration, nutrition, and personal hygiene are important to avert a variety of medical complications. Finally, an emphasis on proper wheelchair positioning, posture, and biomechanics is likely to reduce the risk of pressure-related and musculoskeletal injuries. Nevertheless, there is a significant need for continued research on the subject of injury and illness prevention in the wheelchair athlete.
The author declares no conflict of interest and does not have any financial disclosures.
1. Sahlin KB, Lexell J. Impact of organized sports on activity, participation, and quality of life in people with neurologic disabilities. PMR
. 2015; 7:1081–8.
2. Janse Van Rensburg DC, Schwellnus M, Derman W, Webborn N. Illness among Paralympic athletes: epidemiology, risk markers, and preventative strategies. Phys. Med. Rehabil. Clin. N. Am
. 2018; 29:185–203.
3. Klenck C, Gebke K. Practical management: common medical problems in disabled athletes. Clin. J. Sport Med
. 2007; 17:55–60.
4. Braddom RL, Chan L, Harrast MA, editors. Physical Medicine and Rehabilitation
. 4th ed. Philadelphia (PA): Saunders/Elsevier; 2011. 1506 p.
5. Milligan J, Lee J, McMillan C, Klassen H. Autonomic dysreflexia: recognizing a common serious condition in patients with spinal cord injury. Can. Fam. Physician
. 2012; 58:831–5.
6. Gee CM, West CR, Krassioukov AV. Boosting in elite athletes with spinal cord injury: a critical review of physiology and testing procedures. Sports Med
. 2015; 45:1133–42.
7. Bhambhani Y. Physiology of wheelchair racing in athletes with spinal cord injury. Sports Med
. 2002; 32:23–51.
8. Bhambhani Y, Mactavish J, Warren S, et al. Boosting in athletes with high-level spinal cord injury: knowledge, incidence and attitudes of athletes in Paralympic sport. Disabil. Rehabil
. 2010; 32:2172–90.
9. Burnham R, Wheeler G, Bhambhani Y, et al. Intentional induction of autonomic dysreflexia among quadriplegic athletes for performance enhancement: efficacy, safety, and mechanism of action. Clin. J. Sport Med
. 1994; 4:1–10.
10. Schmid A, Schmidt-Trucksäss A, Huonker M, et al. Catecholamines response of high performance wheelchair athletes at rest and during exercise with autonomic dysreflexia. Int. J. Sports Med
. 2001; 22:2–7.
11. Mazzeo F, Santamaria S, Iavarone A. “Boosting” in Paralympic athletes with spinal cord injury: doping without drugs. Funct. Neurol
. 2015; 30:91–8.
13. Price MJ. Thermoregulation during exercise in individuals with spinal cord injuries. Sports Med
. 2006; 36:863–79.
14. Schmidt K, Chan C. Thermoregulation and fever in normal persons and in those with spinal cord injury. Mayo Clin. Proc
. 1992; 67:469–75.
15. Chester R, Smith TO, Sweeting D, et al. The relative timing of VMO and VL in the aetiology of anterior knee pain: a systematic review and meta-analysis. BMC Musculoskelet. Disord
. 2008; 9:64.
16. Griggs KE, Leicht CA, Price MJ, Goosey-Tolfrey VL. Thermoregulation during intermittent exercise in athletes with a spinal-cord injury. Int. J. Sports Physiol. Perform
. 2015; 10:469–75.
17. Huang M, Jay O, Davis SL. Autonomic dysfunction in multiple sclerosis: implications for exercise. Auton Neurosci Basic Clin
. 2015; 188:82–5.
18. Al-Qudah ZA, Yacoub HA, Souayah N. Disorders of the autonomic nervous system after hemispheric cerebrovascular disorders: an update. J. Vasc. Interv. Neurol
. 2015; 8:43–52.
19. Griggs KE, Price MJ, Goosey-Tolfrey VL. Cooling athletes with a spinal cord injury. Sports Med
. 2015; 45:9–21.
20. Griggs KE, Havenith G, Paulson TAW, et al. Effects of cooling before and during simulated match play on thermoregulatory responses of athletes with tetraplegia. J. Sci. Med. Sport
. 2017; 20:819–24.
21. Webborn N, Price MJ, Castle P, Goosey-Tolfrey VL. Cooling strategies improve intermittent sprint performance in the heat of athletes with tetraplegia. Br. J. Sports Med
. 2010; 44:455–60.
22. Forsyth P, Pumpa K, Knight E, Miller J. Physiological and perceptual effects of precooling in wheelchair basketball athletes. J. Spinal Cord Med
. 2016; 39:671–8.
23. Trbovich MB, Kiratli JB, Price MJ. The effects of a heat acclimation protocol in persons with spinal cord injury. J. Therm. Biol
. 2016; 62:56–62.
24. Ginsberg D. The epidemiology and pathophysiology of neurogenic bladder. Am. J. Manag. Care
. 2013; 19:s191–6.
25. McKibben MJ, Seed P, Ross SS, Borawski KM. Urinary tract infection and neurogenic bladder. Urol. Clin. North Am
. 2015; 42:527–36.
26. Gormley EA. Urologic complications of the neurogenic bladder. Urol. Clin. North Am
. 2010; 37:601–7.
27. Walter M, Krassioukov AV. Autonomic nervous system in Paralympic athletes with spinal cord injury. Phys. Med. Rehabil. Clin. N. Am
. 2018; 29:245–66.
28. Goetz LL, Klausner AP. Strategies for prevention of urinary tract infections in neurogenic bladder dysfunction. Phys. Med. Rehabil. Clin. N. Am
. 2014; 25:605–18.
29. Compton S, Trease L, Cunningham C, Hughes D. Australian Institute of Sport and the Australian Paralympic Committee position statement: urinary tract infection in spinal cord injured athletes. Br. J. Sports Med
. 2015; 49:1236–40.
30. Krassioukov A, Cragg JJ, West C, et al. The good, the bad and the ugly of catheterization practices among elite athletes with spinal cord injury: a global perspective. Spinal Cord
. 2015; 53:78–82.
31. Edsberg LE, Black JM, Goldberg M, et al. Revised National Pressure Ulcer Advisory Panel pressure injury staging system: revised pressure injury staging system. J. Wound Ostomy Cont. Nurs
. 2016; 43:585–97.
32. Ricci JA, Bayer LR, Orgill DP. Evidence-based medicine: the evaluation and treatment of pressure injuries. Plast. Reconstr. Surg
. 2017; 139:275e–86.
33. Kruger EA, Pires M, Ngann Y, et al. Comprehensive management of pressure ulcers in spinal cord injury: current concepts and future trends. J. Spinal Cord Med
. 2013; 36:572–85.
34. Gélis A, Dupeyron A, Legros P, et al. Pressure ulcer risk factors in persons with spinal cord injury part 2: the chronic stage. Spinal Cord
. 2009; 47:651–61.
36. McCormack D, Reid D, Steadward R, Syrotuik D. Injury profiles in wheelchair athletes: results of a retrospective survey. Clin. J. Sport Med
. 1991; 1:35–40.
37. Curtis K, Dillon D. Survey of wheelchair athletic injuries—common patterns and prevention. Olymp Sci Congr Proc Sport Disabl Athletes
. 1986; 9:211–6.
38. Berthold J, Dicianno BE, Cooper RA. Pressure mapping to assess seated pressure distributions and the potential risk for skin ulceration in a population of sledge hockey players and control subjects. Disabil. Rehabil. Assist. Technol
. 2013; 8:387–91.
39. Shimizu Y, Mutsuzaki H, Tachibana K, et al. A survey of deep tissue injury in elite female wheelchair basketball players. J. Back Musculoskelet. Rehabil
. 2017; 30:427–34.
40. Mutsuzaki H, Tachibana K, Shimizu Y, et al. Factors associated with deep tissue injury in male wheelchair basketball players of a Japanese national team. Asia-Pac J Sports Med Arthrosc Rehabil Technol
. 2014; 1:72–6.
41. Consortium for Spinal Cord Medicine, Paralyzed Veterans of America. Pressure ulcer prevention and treatment following spinal cord injury: a clinical practice guideline for health-care providers
. Washington, DC: Consortium for Spinal Cord Medicine; 2014.
42. Groah SL, Schladen M, Pineda CG, Hsieh C-HJ. Prevention of pressure ulcers among people with spinal cord injury: a systematic review. PMR
. 2015; 7:613–36.
43. Kim JY, Cho E. Evaluation of a self-efficacy enhancement program to prevent pressure ulcers in patients with a spinal cord injury: self-efficacy enhancement program. Jpn. J. Nurs. Sci
. 2017; 14:76–86.
44. Tung JY, Stead B, Mann W, et al. Assistive technologies for self-managed pressure ulcer prevention in spinal cord injury: a scoping review. J. Rehabil. Res. Dev
. 2015; 52:131–46.
45. Anderson TM, McKirgan KL, Hastings JD. Seated pressures in daily wheelchair and sports equipment: investigating the protective effects of cushioned shorts. Spinal Cord Ser Cases
. 2018; 4:47. Available from: http://www.nature.com/articles/s41394-018-0084-5
46. Smith ÉM, Comiskey CM, Carroll ÁM. A study of bone mineral density in adults with disability. Arch. Phys. Med. Rehabil
. 2009; 90:1127–35.
47. Fagher K, Lexell J. Sports-related injuries in athletes with disabilities. Scand. J. Med. Sci. Sports
. 2014; 24:e320–31.
48. Heyward OW, Vegter RJK, de Groot S, van der Woude LHV. Shoulder complaints in wheelchair athletes: a systematic review. PLoS One
. 2017; 12:e0188410.
49. Akbar M, Brunner M, Ewerbeck V, et al. Do overhead sports increase risk for rotator cuff tears in wheelchair users? Arch. Phys. Med. Rehabil
. 2015; 96:484–8.
50. Aytar A, Zeybek A, Pekyavas NO, et al. Scapular resting position, shoulder pain and function in disabled athletes. Prosthetics Orthot. Int
. 2015; 39:390–6.
52. Fairbairn JR, Bliven KC. Incidence of shoulder injury in elite wheelchair athletes differ between sports: a critically appraised topic. J. Sport Rehabil
. 2018; 6:1–14.
53. Ferrero G, Mijno E, Actis MV, et al. Risk factors for shoulder pain in patients with spinal cord injury: a multicenter study. Musculoskelet. Surg
. 2015; 99:53–6.
54. Wilroy J, Hibberd E. Evaluation of a shoulder injury prevention program in wheelchair basketball. J. Sport Rehabil
. 2017; 15:1–21.
55. Waring WP, Maynard FM. Shoulder pain in acute traumatic quadriplegia. Paraplegia
. 1991; 29:37–42.
56. Ballinger DA, Rintala DH, Hart KA. The relation of shoulder pain and range-of-motion problems to functional limitations, disability, and perceived health of men with spinal cord injury: a multifaceted longitudinal study. Arch. Phys. Med. Rehabil
. 2000; 81:1575–81.
57. Burnham RS, Steadward RD. Upper extremity peripheral nerve entrapments among wheelchair athletes: prevalence, location, and risk factors. Arch. Phys. Med. Rehabil
. 1994; 75:519–24.
58. Boninger ML, Robertson RN, Wolff M, Cooper RA. Upper limb nerve entrapments in elite wheelchair racers. Am. J. Phys. Med. Rehabil
. 1996; 75:170–6.
59. Kim DK, Kim BS, Kim MJ, et al. Electrophysiologic and ultrasonographic assessment of carpal tunnel syndrome in wheelchair basketball athletes. Ann. Rehabil. Med
. 2017; 41:58.
60. Goodman CM, Steadman AK, Meade RA, et al. Comparison of carpal canal pressure in paraplegic and nonparaplegic subjects: clinical implications. Plast. Reconstr. Surg
. 2001; 107:1464–71; discussion 1472.
61. Boninger ML, Cooper RA, Baldwin MA, et al. Wheelchair pushrim kinetics: body weight and median nerve function. Arch. Phys. Med. Rehabil
. 1999; 80:910–5.
62. Boninger ML, Koontz AM, Sisto SA, et al. Pushrim biomechanics and injury prevention in spinal cord injury: recommendations based on CULP-SCI investigations. J. Rehabil. Res. Dev
. 2004; 42(3sup1):9.
63. Boninger ML, Impink BG, Cooper RA, Koontz AM. Relation between median and ulnar nerve function and wrist kinematics during wheelchair propulsion. Arch. Phys. Med. Rehabil
. 2004; 85:1141–5.
64. Burnham R, Chan M, Hazlett C, et al. Acute median nerve dysfunction from wheelchair propulsion: the development of a model and study of the effect of hand protection. Arch. Phys. Med. Rehabil
. 1994; 75:513–8.
65. Smith É, Comiskey C, Carroll Á. Prevalence of and risk factors for osteoporosis in adults with acquired brain injury. Ir. J. Med. Sci
. 2016; 185:473–81.
66. Shinchuk LM, Morse L, Huancahuari N, et al. Vitamin D deficiency and osteoporosis in rehabilitation inpatients. Arch. Phys. Med. Rehabil
. 2006; 87:904–8.
67. Blauwet CA, Brook EM, Tenforde AS, et al. Low energy availability, menstrual dysfunction, and low bone mineral density in individuals with a disability: implications for the Para athlete population. Sports Med
. 2017; 47:1697–708.
68. Jiang S-D, Dai L-Y, Jiang L-S. Osteoporosis after spinal cord injury. Osteoporos. Int
. 2006; 17:180–92.
69. Demirbag D, Ozdemir F, Kokino S, Berkarda S. The relationship between bone mineral density and immobilization duration in hemiplegic limbs. Ann. Nucl. Med
. 2005; 19:695–700.
70. Goolsby MA, Boniquit N. Bone health in athletes: the role of exercise, nutrition, and hormones. Sports Health Multidiscip Approach
. 2017; 9:108–17.
71. Szollar SM, Martin EM, Sartoris DJ, et al. Bone mineral density and indexes of bone metabolism in spinal cord injury. Am. J. Phys. Med. Rehabil
. 1998; 77:28–35.
72. Miyahara K, Wang D-H, Mori K, et al. Effect of sports activity on bone mineral density in wheelchair athletes. J. Bone Miner. Metab
. 2008; 26:101–6.
73. Goktepe AS, Yilmaz B, Alaca R, et al. Bone density loss after spinal cord injury: elite paraplegic basketball players vs. paraplegic sedentary persons. Am. J. Phys. Med. Rehabil
. 2004; 83:279–83.
74. Frey-Rindova P, de Bruin ED, Stüssi E, et al. Bone mineral density in upper and lower extremities during 12 months after spinal cord injury measured by peripheral quantitative computed tomography. Spinal Cord
. 2000; 38:26–32.
75. Zleik N, Weaver F, Harmon RL, et al. Prevention and management of osteoporosis and osteoporotic fractures in persons with a spinal cord injury or disorder: a systematic scoping review. J. Spinal Cord Med
. 2018; 10:1–25.
76. Gater DR, Dolbow D, Tsui B, Gorgey AS. Functional electrical stimulation therapies after spinal cord injury. NeuroRehabilitation
. 2011; 28:231–48.
77. Chang K-V, Hung C-Y, Chen W-S, et al. Effectiveness of bisphosphonate analogues and functional electrical stimulation on attenuating post-injury osteoporosis in spinal cord injury patients—a systematic review and meta-analysis. PLoS One
. 2013; 8:e81124.
78. Deley G, Denuziller J, Casillas J-M, Babault N. One year of training with FES has impressive beneficial effects in a 36-year-old woman with spinal cord injury. J. Spinal Cord Med
. 2017; 40:107–12.
79. Rastmanesh R, Taleban FA, Kimiagar M, et al. Nutritional knowledge and attitudes in athletes with physical disabilities. J. Athl. Train
. 2007; 42:99–105.
80. Krempien JL, Barr SI. Risk of nutrient inadequacies in elite Canadian athletes with spinal cord injury. Int. J. Sport Nutr. Exerc. Metab
. 2011; 21:417–25.
81. Krempien JL, Barr SI. Eating attitudes and behaviours in elite Canadian athletes with a spinal cord injury. Eat. Behav
. 2012; 13:36–41.
82. Gerrish HR, Broad E, Lacroix M, et al. Nutrient intake of elite Canadian and American athletes with spinal cord injury. Int. J. Exerc. Sci
. 2017; 10:1018–28.
83. Nemunaitis GA, Mejia M, Nagy JA, et al. A descriptive study on vitamin D levels in individuals with spinal cord injury in an acute inpatient rehabilitation setting. PM R
. 2010; 2:202–8.
84. Coskun Benlidayi I, Basaran S, Seydaoglu G, Guzel R. Vitamin D profile of patients with spinal cord injury and post-stroke hemiplegia: all in the same boat. J. Back Musculoskelet. Rehabil
. 2016; 29:205–10.
85. Cosman F, de Beur SJ, LeBoff MS, et al. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos. Int
. 2014; 25:2359–81.
86. Bauman WA, Cirnigliaro CM, La Fountaine MF, et al. Zoledronic acid administration failed to prevent bone loss at the knee in persons with acute spinal cord injury: an observational cohort study. J. Bone Miner. Metab
. 2015; 33:410–21.
87. Schnitzer TJ, Kim K, Marks J, et al. Zoledronic acid treatment after acute spinal cord injury: results of a randomized, placebo-controlled pilot trial. PMR
. 2016; 8:833–43.