422 Spinal Cord Injury
engage in a variety of health compromising behaviors,
and lack active coping skills (Yarkony, 1994). Yarkony
stressed the importance of considering the multifactorial eti-
ology and a person•s general medical condition, nutrition,
and social situation to achieve successful healing and prevent
recurrence. The emphasis of most studies has been on pre-
vention, stressing frequent repositioning, use of special beds,
mattresses, and wheelchair cushions. The need for surgical
closure tends to increase with the chronicity of the sore.
Spasticity and Contractures
Spasticity is a UMN disorder that refers to spasms, deep ten-
don re”exes, and clonus that occurs among persons with SCI
(Cardenas et al., 2000). When untreated and recurring, the
individual may experience weakness, fatigue, and loss of
dexterity over time. Urinary tract infections and pressure
sores can increase spasticity. Often spasticity is treated with
pharmacological agents such as baclofen or diazepam if
the spasms interfere with sleep, positioning, balance, skin
integrity, or if the spasms are painful.
Contractures may occur when patients and/or caregivers
do not provide adequate and continuous range of motion ex-
ercises. In their severe form, contractures cause permanent
limitation to joint movement and may require surgical inter-
vention. They can compromise sitting position and lead to
additional complications such as pressure sores and compro-
mised general quality of life because mobility, transfers,
bowel and bladder care, and so on, are adversely affected.
Urinary Tract Infections
Even though the incidence of renal failure, secondary to
chronic or recurrent UTI, in persons with SCI has decreased
markedly due to advances in diagnostic, preventive, and ther-
apeutic measures, UTI and its sequelae continue to be a major
problem regardless of bladder-emptying method. Bladder
management goals after SCI are to establish and maintain un-
restricted urine ”ow from the kidneys and maintain urine
sterility and bladder continence, thereby preserving renal
function. Neurologic damage that affects control of bladder
function, coupled with the need for catheters to facilitate
emptying, results in impairment of normal anatomic and
physiologic defense mechanisms responsible for eliminating
bacteria and maintaining urinary tract sterility. Normally, the
physical barrier of the urethra, urine ”ow, and toxic or anti-
adherence effects mediated by the bladder mucosa limit
spread and multiplication of bacteria in the urinary tract
(Stover, Lloyd, Waites, & Jackson, 1991). However, in the
neurogenic bladder, stagnant residual urine allows bacteria to
accumulate. Mucosal ischemia associated with obstructed
high-pressure voiding and poor bladder wall compliance
may also facilitate tissue invasion. Vesicoureteral re”ux
caused by elevated bladder pressures facilitates access of uri-
nary pathogens to the kidneys, leading to serious complica-
tions such as pyelonephritis, septicemia, and renal failure
(Stover et al., 1991).
Other UTI risk factors include structural abnormalities,
”uid intake, neurologic level, prior colonization of genital
skin by pathogenic bacteria, age, limited access to health care
providers, insurance coverage, social support systems, and
being female (National Institute on Disability and Rehabilita-
tion Research Consensus Statement, 1992; Stover et al.,
1991). Psychological variables, personal hygiene, care of uri-
nary drainage appliances, and drug abuse are the focus of in-
vestigation as they relate to development of UTI and pressure
ulcers following severe physical disability stemming from
the probability that inattention to self-care is one logical rea-
son these complications occur.DepressionDepression has received more attention from clinicians and
researchers than any other psychological issue among per-
sons with SCI (Elliott & Frank, 1996). For many years, clin-
ical lore maintained that depression was to be expected soon
after the onset of injury, and it was construed as a critical el-
ement in most stage models of adjustment, typically signal-
ing rational acceptance of the permanence of the injury. (For
a critique of these models, see Frank, Elliott, Corcoran, &
Wonderlich, 1987.) Empirical study has broadened our un-
derstanding of depression considerably. Studies relying on
DSM-III(American Psychiatric Association [APA], 1980)
criteria using small samples of recently injured persons and
conservative diagnostic interview techniques have found the
rate of major depressive episodes to range from 22.7% to
over 30% (Frank, Kashani, Wonderlich, Lising, & Visot,
1985; Fullerton, Harvey, Klein, & Howell, 1981). Lower
rates have been observed in studies using less stringent inter-
view methods (13.7%; Judd & Brown, 1992), and with self-
report measures based on DSM-III-R(APA, 1987) criteria
with a sample varying in time since the onset of injury (11%;
Frank et al., 1992). Other data indicate that among newly
injured persons who met criteria for major and minor depres-
sive disorders, many may remit within three months of in-
jury onset (Kishi, Robinson, & Forrester, 1994). Generally,
many report decreasing problems with depressive sympto-
mology over the “rst year of SCI (Richards, 1986).
The bulk of this research has relied on self-report
measures of depressive behavior that do not assess unique