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U N I T 1 0
Nervous System
centers that coordinate sphincter control (i.e., a UMN
lesion). Persons with UMN lesions or spastic bladders
lack awareness of bladder filling (i.e., storage) and vol-
untary control of urination. In LMN lesions or flaccid
bladder dysfunction, lack of awareness of bladder fill-
ing and lack of bladder tone render the person unable
to urinate voluntarily or involuntarily (see Chapter 27).
Bowel elimination is a coordinated function involv-
ing the enteric nervous system, the autonomic nervous
system, and the CNS. Persons with SCI above S2 to S4
develop spastic functioning of the defecation reflex and
loss of voluntary control of the external anal sphincter.
Damage to the cord at the S2 to S4 level causes flac-
cid functioning of the defecation reflex and loss of anal
sphincter tone. Even though the enteric nervous system
innervation of the bowel remains intact, without the
defecation reflex, peristaltic movements are ineffective
in evacuating stool.
Sexual function, like bladder and bowel control, is
mediated by the S2 to S4 segments of the spinal cord.
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The genital sexual response in SCI, which is mani-
fested by an erection in men and vaginal lubrication in
women, may be initiated by mental or touch stimuli,
depending on the level of injury. The T11 to L2 cord
segments have been identified as the mental-stimulus,
or psychogenic, sexual response area, where autonomic
nerve pathways in communication with the forebrain
leave the cord and innervate the genitalia. The S2 to S4
cord segments have been identified as the sexual-touch
reflex center. In T10 or higher injuries, reflex sexual
response to genital touch may occur freely. However, a
sexual response to mental stimuli (T11 to L2) does not
occur because of the spinal lesion blocking the com-
munication pathway. In an injury at T12 or below, the
sexual reflex center may be damaged, and there may be
no response to touch.
In men, the lack of erectile ability or inability to
experience penile sensations or orgasm is not a reliable
indicator of fertility, which should be evaluated by an
expert. In women, fertility is normally reestablished
with the return of menses, which usually occurs at about
3 to 5 months after injury. There are hazards to preg-
nancy, labor, and use of birth control devices relative to
SCI that require the services of knowledgeable health
care providers.
Disruption of Other Functions
Temperature Regulation.
The central mechanisms for
thermoregulation are located in the hypothalamus. In
response to cold, the hypothalamus stimulates vaso-
constrictor responses in peripheral blood vessels, par-
ticularly those of the skin. This results in decreased loss
of body heat. Heat production results from increased
metabolism, voluntary activity, or shivering. To reduce
heat, hypothalamus-stimulated mechanisms produce
vasodilation of skin blood vessels to dissipate heat, and
sweating to increase evaporative heat losses.
After SCI, the communication between the ther-
moregulatory centers in the hypothalamus and the
sympathetic effector responses below the level of injury
is disrupted; the ability to control blood vessel responses
that conserve or dissipate heat is lost, as are the abili-
ties to sweat and shiver. Higher levels of injury tend to
produce greater disturbances in thermoregulation. In
tetraplegia and high paraplegia, there are few defenses
against changes in the environmental temperature, and
body temperature tends to assume the temperature of
the external environment, a condition known as
poiki-
lothermy.
Persons with lower-level injuries have various
degrees of thermoregulation. Disturbances in thermo-
regulation are chronic and may cause continual loss of
body heat. Treatment consists of education in the adjust-
ment of clothing and awareness of how environmental
temperatures affect the person’s ability to accommodate
to these changes.
DeepVeinThrombosis and Edema.
Persons with SCI
are at high risk for development of deep vein thrombo-
sis (DVT) and pulmonary embolism, particularly dur-
ing the first 2 to 3 weeks after injury.
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The high risk
for DVT in patients with acute SCI is due to immobil-
ity, decreased vasomotor tone below the level of injury,
and hypercoagulability and stasis of blood flow. Current
preventative interventions include mechanical and phar-
macological methods.
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Mechanical methods of pre-
vention include intermittent pneumatic compression,
thigh-high graduated elastic compression stockings, and
neuromuscular electrical stimulation. Pharmacologic
methods include oral anticoagulants and low–molecu-
lar-weight heparin. Local pain, a common symptom of
DVT, is often absent because of sensory deficits. Thus,
a regular schedule of visual inspection for local signs of
DVT (e.g., swelling) is important. Testing of persons at
high risk for DVT includes plethysmography and duplex
ultrasonography.
Edema is also a common problem in persons with
SCI. The development of edema is related to decreased
peripheral vascular resistance, decreased muscle tone in
the paralyzed limbs, and immobility that causes increased
venous pressure and abnormal pooling of blood in the
abdomen, lower limbs, and upper extremities. Edema in
the dependent body parts usually is relieved by position-
ing to minimize gravitational forces or by using com-
pression devices (e.g., support stockings, binders) that
encourage venous return.
Skin Integrity.
The entire surface of the skin is inner-
vated by cranial or spinal nerves organized into derma-
tomes that show cutaneous distribution. The CNS and
autonomic nervous system also play a vital role in skin
function. The sympathetic nervous system, through con-
trol of vasomotor and sweat gland activity, influences
the health of the skin by providing adequate circulation,
excretion of body fluids, and temperature regulation.
The lack of sensory warning mechanisms and voluntary
motor ability below the level of injury, coupled with cir-
culatory changes, place the spinal cord–injured person at
major risk for disruption of skin integrity (see Chapter
46). Significant factors associated with disruption of
