2) TRANSECTION OF THE CORD
Transection most frequently results from trauma but it can be associated with vascular infarction or hemorrhage, compression, demyelinating or inflammatory lesions. Shearing or compressing the cord produces destruction of the gray and white matter. Pathologic changes are maximal at the level of the lesion but injury extends above and below the lesion for a segment or two. The final clinical outcome is a result of the irreversible structural damage and functional disorders created.
A Sample Case: A healthy man of 50 years of age was thrown from his horse. He was immediately rendered quadriplegic (paralyzed in all four extremities) and described a numb feeling from the neck on down. He never lost consciousness.
The immediate neurologic exam revealed flaccid paralysis of all four extremities and no deep tendon reflexes could be demonstrated. All sensation was absent bilaterally from his arms on down. Some weeks after the accident the limbs showed signs of spastic paralysis with markedly increased deep tendon reflexes but there was no return of sensory function. Bowel and bladder control were lost.
X-ray examination showed severe fractures and displacement of the C5,6 vertebrae.
"Spinal shock". As a result of a rapid and complete transection there is complete loss of voluntary movement and sensation from levels below the cord lesion and loss of all reflexes in the isolated cord segments. This is called "spinal shock" and its duration can vary, 1 to 6 weeks is common. As this phenomenon fades it may be replaced by heightened flexor reflex activity in which exaggerated deep tendon reflexes occur in response to noxious or even trivial stimuli. A mass reflex may develop in which slight stimuli elicit severe bilateral flexor spasms of the arms and legs accompanied by evacuation of the bowel and bladder, profuse sweating and even priapism (a sustained reflexogenic erection). Reflex emptying of the bowel and bladder may also begin at this time. Autonomic reflex activity is also heightened and so filling of the bladder or rectum may result in increased sweating, flushing of the face, piloerection, shivering, slowing of the pulse, elevation of blood pressure, etc. After 6 -12 months many of the exaggerated reflex responses wane. The mechanisms underlying all of the phenomena of spinal shock are not completely understood. In general, the initial loss of all reflexes is thought to be due to the effect of the sudden withdrawal of all supraspinal influences on the segments of the cord below the lesion. After a period of time the segmental reflex arcs reappear and become supersensitive to segmental sensory information, the effects of which easily spread to adjacent cord levels. The reflex responses are now operating without the usual controls imparted by the now absent descending pathways.
Spastic paralysis follows the period of spinal shock. At first only a positive Babinski sign occurs; later the other signs appear, e.g., increased muscle tone, heightened deep tendon reflexes, disuse (slow) atrophy of muscle, and loss of superficial (abdominal and cremasteric) reflexes below the level of the lesion.
There is loss of all sensation bilaterally below the level of the lesion: loss of proprioception, vibratory sense, tactile discrimination, pain, temperature, light touch, and visceral sensibility. All sensory tracts are immediately severed and if the lesion is in fact complete there is no recovery.
Autonomic disturbances include bowel and bladder functions. Initially, there is retention of urine and feces, which are no longer under voluntary control. Since ascending sensory pathways are interrupted there is no awareness of bowel or bladder fullness. After several weeks hypertrophy of the smooth muscle overcomes sphincter resistance so emptying occurs when eventually those organs become overfilled (overflow incontinence). Even if there was an awareness, the absence of the descending tracts would preclude volitional control. Eventually, the bowel and bladder empty on a segmental automatic basis reflexly, when they become full. Cutaneous blood vessels in the areas below the lesion do not respond to hot or cold stimuli. Horner's syndrome (ptosis, miosis, anhydrosis) also is likely, due to the loss of the descending autonomics which are scattered among the lateral corticospinal tract fibers in the cord.
A careful sensory evaluation may reveal that at the dermatomal level of the lesion there is a bilateral loss of pain and temperature sensation. Since the second order neurons from both sides cross in the midline below the central canal, a hemisection of the cord may interrupt the crossing fibers from both sides and produce this limited bilateral deficit.
The pain in the left breast was the result of the pressure of the tumor on the dorsal root.