C h a p t e r 3 6
Disorders of Neuromuscular Function
911
cause or stimulus. The person should be placed in an
upright position, and all support hose or binders should
be removed to promote venous pooling of blood and
reduce venous return, thereby decreasing blood pressure.
If the stimuli have been removed or the stimuli cannot be
identified and the upright position is established but the
blood pressure remains elevated, drugs that block auto-
nomic function are administered. Prevention of the type
of stimuli that trigger the dysreflexic event is advocated.
Postural Hypotension.
Postural, or orthostatic, hypo-
tension usually occurs in persons with injuries at T4
to T6 and above and is related to the interruption of
descending control of sympathetic outflow to blood ves-
sels in the extremities and abdomen.
62
Pooling of blood,
along with gravitational forces, impairs the return of
venous blood to the heart, causing a decrease in cardiac
output along with a drop in arterial blood pressure
when the person is placed in an upright position. The
disorder is characterized by dizziness, pallor, excessive
sweating above the level of the lesion, complaints of
blurred vision, and possible fainting. Postural hypoten-
sion usually is prevented by slow changes in position
and measures to promote venous return.
Disruption of Bladder, Bowel, and Sexual
Function
Among the most devastating consequences of SCI are
the loss of bladder, bowel, and sexual function.
18,64
Loss of bladder function results from disruption of
neural pathways between the bladder and the reflex
voiding center at the S2 to S4 level (i.e., a LMN lesion)
or between the reflex voiding center and higher brain
Baroreceptors
Pale, cool, moist skin
below level of injury
Piloerection
(goose bumps)
Bladder
Spinal cord
Sacral
Lumbar
Thoracic
Headache
Flushed skin
above level of injury
Visceral stimulus
(e.g., overdistended
bladder, visceral pain)
Spinal cord injury—
T6 or above with loss of CNS
control of sympathetic
reflexes below level of injury
Acute rise in
blood pressure
Vasoconstriction
below level of injury
Uncontrolled activation of
local sympathetic reflexes
below level of injury
f
Vasodilation and sweating
above the level of injury
FIGURE 36-18.
Mechanisms of
autonomic dysreflexia.
