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THE NERVOUS SYSTEM

Spinal Cord Injury

A 19-year-old man hyperextended his neck in a car accident. He lost consciousness for a short time, and
when he awoke he could not move any of his limbs, nor could he feel any sensations in his trunk or limbs.
After a month he could move his shoulders to some extent, but otherwise, all four extremities remained
paralyzed. At this time he developed increased muscle tone and hyperactive stretch reflexes in both arms
and legs. Also, when either foot was sharply dorsiflexed, sustained clonus of the ankle occurred. Signs of
Babinski could readily be elicited bilaterally. Stimulation of one foot caused withdrawal of that foot and
also flexion of the other leg. He had to be catheterized to allow drainage of the urinary bladder.

1. At what level was the spinal cord functionally transected?

2. Why was the patient unable to move his extremities?

3. Why was all sensation lost in the trunk and extremities?

4. Would the phasic or the tonic stretch reflexes be more affected? What causes clonus?

5. Why do flexion reflexes become more active?

6. How did urinary bladder function change?

1. The trauma of the car accident functionally transected the spinal cord at the level of the neck. The
segmental level of the spinal injury is suggested by the pattern of loss of voluntary motor control.
The patient eventually had some motor function in the shoulder. Shoulder muscles receive a motor
supply from the C5 spinal segment. The muscles that receive motor axons from the remainder of the
cervical enlargement, C6-Tl, are paralyzed; therefore the transection must have been at the C5-C6
level.

2. The patient could not move his extremities voluntarily because the descending motor pathways,
including the corticospinal tracts, had been severed.

3. The patient could not feel anything below the level of transection because the somatosensory
pathways, including the dorsal columns and the spinothalamic tracts, had been interrupted.

4. The type of paralysis that results from the interruption of the corticospinal and associated motor tracts
is known as a spastic paralysis. In normal individuals, phasic stretch reflexes can be elicited by
tapping the tendon of a muscle, such as the quadriceps, to stretch the muscle and activate group la
muscle spindle afferent fibers. The burst discharges of these stretch receptors cause synchronous
discharges of alpha motoneurons that supply the same and synergistic muscles. Hence a tendon tap
results in a contraction of the muscle whose tendon is tapped. In spastic paralysis, the motor control
circuits in the spinal cord are altered (this is poorly understood). Therefore, gamma motoneurons
become hyperactive, and their activity results in a greater sensitivity of muscle spindles to muscle
stretches, especially to phasic stretches. Thus the phasic stretch reflexes become more active.
Although muscle tone is increased, the most prominent change in spastic paralysis is the increase in
phasic stretch reflexes. This change accounts for the appearance of clonus. When a muscle, such as
the triceps surae, is stretched briskly by dorsiflexion of the foot, the contraction of this muscle causes
plantar flexion of the ankle. This in turn stretches the pretibial flexors and elicits their contraction.
This contraction stretches the triceps surae muscles once more (or the continued upward pressure on
the foot by the examiner causes another stretch of the triceps surae), and causes another
contraction. The result is a continued series of alternating contractions of antagonistic muscle groups
and the consequent alternating movements of the ankle.

5. The flexor withdrawal reflex becomes exaggerated below the level of a spinal cord transection because
of interruption of pathways that descend from the brain and that normally tend to suppress the
flexion reflex. These descending control systems include a pathway that originates in the medulla.

6. After a spinal cord transection, the bladder initially becomes flaccid. At this time, urine retention
becomes a major problem, and bladder infections are common. As spasticity develops, the bladder
wall develops excessive tone, the bladder contracts reflexly or at irregular intervals, and incontinence
develops. Evacuation of the bladder is still incomplete, and the bladder remains susceptible to
infections.