Regulation and Integration of the Body
Spinal Cord Trauma and Disorders
Distinguish between flaccid and spastic paralysis, and
between paralysis and paresthesia.
Spinal Cord Trauma
Te spinal cord is elastic, stretching with every turn of the head
or bend of the trunk, but it is exquisitely sensitive to direct pres-
sure. Any localized damage to the spinal cord or its roots leads
to some functional loss, either
(loss of motor function)
ze-ahz) (abnormal sensations).
Severe damage to ventral root or ventral horn cells results in
flaccid paralysis
sid) of the skeletal muscles served. Nerve
impulses do not reach these muscles, which consequently can-
not move either voluntarily or involuntarily. Without stimula-
tion, the muscles atrophy.
When only the upper motor neurons of the primary mo-
tor cortex are damaged,
spastic paralysis
occurs. In this case,
the spinal motor neurons remain intact and spinal reflex activ-
ity continues to stimulate the muscles irregularly. As a result,
the muscles remain healthy longer, but their movements are no
longer subject to voluntary control. In many cases, the muscles
shorten permanently.
±ransection (cross sectioning) of the spinal cord at any level
results in total motor and sensory loss in body regions inferior
to the site of damage.
If the transection occurs between ±
and L
, both lower limbs
are affected, resulting in
a blow).
If the injury occurs in the cervical region, all four limbs are
affected and the result is
, paralysis of one side of the body, usually reflects
brain injury rather than spinal cord injury.
Anyone with a spinal cord transection must be watched for
symptoms of
spinal shock
, a transient period of functional loss that
follows the injury. Spinal shock immediately depresses all reflex
activity caudal to the lesion site. Bowel and bladder reflexes stop,
blood pressure falls, and all muscles (somatic and visceral alike) be-
low the injury are paralyzed and insensitive. Neural function usu-
ally returns within a few hours following injury. If function does
not resume within 48 hours, paralysis is permanent in most cases.
gray matter;
inflammation of the spinal cord) results from the poliovi-
rus, which typically enters the body in feces-contaminated wa-
ter and destroys ventral horn motor neurons. Early symptoms
include fever, headache, muscle pain and weakness, and loss of
certain somatic reflexes. Later, paralysis develops and the mus-
cles served atrophy. Te victim may die from paralyzed respira-
tory muscles or from cardiac arrest. Fortunately, vaccines have
nearly eliminated this disease and a global effort is ongoing to
eradicate it completely.
However, many survivors of the great polio epidemic of the
late 1940s and 1950s have begun to experience extreme lethargy,
sharp burning pains in their muscles, and progressive muscle
weakness and atrophy. Tese disturbing symptoms are referred
to as
postpolio syndrome
. Te cause of postpolio syndrome
is not known, but a likely explanation is that its victims, like
the rest of us, continue to lose neurons throughout life. While
a healthy nervous system can recruit nearby neurons to com-
pensate, polio survivors have already drawn on that “pool” and
have few neurons le² to take over. Ironically, those who worked
hardest to overcome their disease are its newest victims.
Amyotrophic Lateral Sclerosis (ALS)
Amyotrophic lateral sclerosis
) (ah-mi
ik), also called
Lou Gehrig’s disease, is a devastating neuromuscular condition
that progressively destroys ventral horn motor neurons and
fibers of the pyramidal tracts. As the disease progresses, the
sufferer loses the ability to speak, swallow, and breathe. Death
typically occurs within five years.
Environmental and genetic factors interact to cause ALS. In
10% of cases mutations are inherited; spontaneous mutations
are probably involved in the rest. Recently, the mutations have
been localized to genes that are involved in RNA processing.
While the exact mechanism is not clear, the presence of excess
extracellular glutamate suggests that excitotoxic cell death is in-
volved. Riluzole, a drug that interferes with glutamate signaling,
is the only available life-prolonging treatment.
Diagnostic Procedures for
Assessing CNS Dysfunction
List and explain several techniques used to diagnose brain
If you have had a routine physical examination, you are familiar
with the reflex tests done to assess neural function. A tap with
a reflex hammer stretches your quadriceps tendon and your
anterior thigh muscles contract. Tis produces the knee-jerk
response, which shows that your spinal cord and upper brain
centers are functioning normally.
Abnormal responses to a reflex test may indicate such serious
disorders as intracranial hemorrhage, multiple sclerosis, or hy-
drocephalus. Tey indicate that more sophisticated neurologi-
cal tests are needed to identify the problem.
New imaging techniques have revolutionized the diagnosis
of brain lesions (see
A Closer Look
, pp. 18–19). ±ogether, vari-
MRI scanning techniques
allow quick identification
of most tumors, intracranial lesions, multiple sclerosis plaques,
and areas of dead brain tissue (infarcts). PE± scans can local-
ize brain lesions that generate seizures (epileptic tissue), and
new radiotracer dyes that bind to beta-amyloid promise earlier,
more reliable diagnosis of Alzheimer’s disease.
±ake, for example, a patient arriving in the emergency room
with a stroke. A race against time begins to save the affected area
of the patient’s brain. Te first step is to determine if the stroke
is due to a clot or a bleed by imaging the brain, most o²en with
C±. If the stroke is due to a clot, the clot-busting drug tPA can
be used, but only within the first hours. tPA is usually given
intravenously, but a longer time window is possible if tPA is ap-
plied directly to the clot using a catheter guided into position.
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