“SCIATICA” CAUSED BY INTERVERTEBRAL DISC LESIONS

Abstract

A review of the literature reveals that much is known of the normal anatomy and physiology of the intervertebral disc and that, chiefly due to Schmorl's work, the pathological changes which may occur are fairly well elucidated. The entity of posterior prolapse into the spinal canal is of great clinical significance, as it may cause disability and even death from pressure on the cord or on the cauda equina. The lesion known as chondroma or ecchondrosis of the intervertebral disc is apparently the same as the posterior prolapses. The cases in which the lesion is in the low lumbar spine may show symptoms and signs indistinguishable from those of sacro-iliac or lumbosacral strain and so are seen primarily by orthopaedic surgeons. Unless the specialists in this field are aware of the entity and take the proper steps to arrive at the correct diagnosis, useless orthopaedic treatment will be instituted. A careful neurological examination, in addition to the orthopaedic examination, is indicated in every case of strain. If the symptoms remain intractible after adequate conservative treatment, lumbar puncture should be performed and the total protein content of the spinal fluid should be determined. If it is over 50 milligrams per 100 cubic centimeters, the evidence is in favor of an intraspinal lesion rather than mechanical joint or ligamentous strain, and, therefore, sacro-iliac or lumbosacral fusion is contra-indicated until cord or root pressure is ruled out by careful lipiodol roentgenographic examination. Even if the total protein is within so called normal limits, there may be present a ruptured disc which is responsible for the patient's symptoms. Forty cases of proved rupture of the intervertebral disc into the lumbar spinal canal with involvement of one or more roots of the cauda equina by direct pressure have been reported in this paper. Twelve were in the lumbosacral disc, twenty-six in the disc between the fourth and fifth lumbar vertebrae, one between the second and third lumbar, and one between the third and fourth lumbar. There were thirty-five males and five females. The average age was thirty-seven years. A history of trauma was present in 77.5 per cent. of the cases. Pain was the major presenting symptom. Its character was that of the familiar sciatica, always radiating down the posterior thigh and usually the posterolateral calf. Orthopaedic examination revealed the classical signs of low-back strain,—muscle spasm, list, limitation of motion, limitation of straight-leg raising, tender areas, etc. Fixed lumbar kyphosis or an abnormally flat back was present in over half of the cases. Neurological examination revealed definite peripheral sensory changes in seventeen cases. There was an absent ankle jerk in 50 per cent. of the cases. Muscle weakness, paralysis, cramps, and loss of urinary and rectal control were less frequent, but they occurred. Lumbar puncture revealed an elevated total protein in all but five cases. The average was 60 to 100 milligrams per 100 cubic centimeters. Roentgenograms showed local hypertrophic changes or disc narrowing in less than half the cases. Lipiodol examination localized the lesion in thirty-six of the forty cases. The end-result study showed one death due to the lesion (paraplegia). There was essentially complete relief from pain in all cases but one. In that one the continued pain seems to be due to other pathology. Sufficient time has not elapsed to permit determination of the amount of permanent disability following the operative removal of a ruptured disc. Our experience indicates that the back is stronger if fusion is combined with the laminectomy. There seems to be no doubt that a clinical entity with a proved pathological etiology is being removed from the vague classification of lumbosacral and sacro-iliac strains. It is not excessively rare and should be thought of in every case of back strain and sciatica.