J. Neurol. Neurosurg. Psychiat., 1968, 31, 61-66

Protrusion of the posterior longitudinal ligamentsimulating herniated lumbar intervertebral discROBERT A. BEATTY, OSCAR SUGAR, AND THEODORE A. FOX

From the Departments of Neurological Surgery and Orthopedic Surgery,University of Illinois College of Medicine, and Illinois Masonic Hospital,

Chicago, Illinois, U.S.A.

The most common cause of lumbar or sacral nerve-root compression probably is herniation of thenucleus pulposus. There are some patients withtypical clinical-and even radiological-evidence of

ne'rVe root compression, however, in whom noherniation is found at operation; instead the nerveroot is compressed by a fold in the posterior longi-tudinal ligament, and, when this is excised, there is

TABLE ICLINICAL SUMMARY OF 13 PATIENTS

Age Sex Occupation Signs and symptoms Operation Length of Late resultsfollow-up

37 F Housewife Pain in right hip radiating to lateralaspect right ankle. Absent right anklejerk. Hypaesthesia lateral aspect rightfoot

53 M Carpenter Pain left calf and foot. Atrophic leftcalf

19 M Student Weakness and numbness right calf.Weak right plantar flexion. Hypaes-thesia lateral aspect right foot

48 F Housewife Low back pain into left leg. Decreasedleft ankle jerk. Hypaesthesia lateralleft foot

34 F Factory Low back pain. Left paraspinal spasm.worker Hypaesthesia dorsum left foot

33 M Steel worker Low back pain. Straight leg raising 30'on right

35 M

30 M

Newspaper- Low back pain into left leg. Leftman straight leg raising limited

Dock Low back pain into left leg. Weakworker dorsiflexion left foot

L5-S1 laminotomy right. 6 yrFusion

Left L4-5 laminotomy and 5 yrforaminotomy

Right L5-S1 laminotomy 4 yr

Left laminotomy, L4-5, -

L5-Sl. Foraminotomy L4-5

Bilateral laminotomy L4-5, 4 yrL5-S1

Right laminotomy L4-5, 3 yrL5-Sl. Transdural approachto L4-5. Fusion

Left laminotomy L4-5, 3 yrL5-Sl. FusionLeft laminotomy L4-5, 3 yrL5-S1 Fusion

37 F Housewife Low back pain into right leg. Absent Bilateral L4-5 laminotom:right ankle jerk. Bilateral weak foot Fusiondorsiflexors

40 F Housewife Low back pain into right leg. Hypaes- Bilateral L5-Sl laminotonthesia lateral right foot Fusion

41 M Businessman Low back pain into right leg. Decreased Bilateral laminotomy L4-'right ankle jerk. Limited right straight- L5-Sl. Fusionleg raising

15 M Student Low back pain into right foot. Weak Right laminotomy L4-5,right foot dorsiflexors L5-S1

44 M Dairy Low back pain into left leg. Absent Left laminotomy L5-Slworker left ankle jerk. Hypaesthesia lateral

left thigh61

iy. 2yr

my. I yr

Asymptomatic. Activehousewife

Still has burning dysaes-thesias in leg; noimpairment of bending

Mild back pain withactivity

Lost to follow up

No back pain

Less strenuous job. Painin leg and low backimproved

Back at work; no leg pain;occasional mild backache

Working as dockhand.Mild leg and lumbar pain.No weakness

Occasional mild leg andlow back pain. Noweakness

Asymptomatic; no straight-leg raising impairment

*5, 11 months No impairment of bend-ing; straight-leg raisingnormal

8 months No list, bends well, nopain, no muscle spasm;straight-leg raising normal

8 months No back or leg pain

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Robert A. Beatty, Oscar Sugar, and Theodore A. Fox

FIG. 1. Drawing of operative exposure showing protruded

posterior longitudinal ligament over which the nerve root

is stretched. Inset shows redundant ligament when disc

space is narrowed.

FIG. 3. Myelogram of same patientdefect at the L 4-5 interspace.

showing filling

little or no intervertebral disc material to be foundin the interspace. We are reporting a series of 13such patients.

CLINICAL MATERIAL

PREOPERATIVE EVALUATION Thirteen patients were drawnfrom both neurosurgical and orthopaedic practices(Table I). The duration of symptoms before operationvaried from two months to 13 years, with the majorityat three years. Ten patients related the onset of theirsymptoms to a specific episode of trauma, usually,bending or lifting. Low back pain radiating into one legwas present in 10, and into both legs in two. In three,the initial complaint was calf or hip pain. There wereobjective signs of nerve-root compression (hypaesthesia,depressed stretch reflex, weakness) in 11 patients, whiletwo showed only limitation of straight leg raising on theaffected side, in addition to persisting complaints ofsciatica.Narrowing of the appropriate intervertebral disc space

corresponding to the radicular signs was demonstratedon plain radiographs of the lumbosacral area in seven of12 patients (one set of films was inadvertently destroyed).Myelography was performed in six patients, five ofwhomhad abnormalities. In three of-these, there were unilateral

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FIG. 2. Lateral view of lumbar spine showing whatappears to be a normal L 45 interspace. Note the over-riding Sacers narrowing the nerve-root foramen.

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Protrusion of the posterior longitudinal ligament simulating herniated lumbar intervertebral disc

FIG. 5. Cadaver lumbar canal after removal of laminaeandpedicles on one side.

FIG. 4. Posterior-anterior view of same myelogram.

filling defects in the column of contrast medium, while,in two, bilateral defects were found. Electromyography(EMG) carried out in 11 patients showed evidence oflower lumbar or first sacral radiculopathy in nine.When the nerve root indicated by EMG corresponded tothe clinical picture, Pantopaque myelography was notalways done, for it is our opinion that one does notoperate because of a positive or negative myelogram.

OPERATION This was carried out with the patient prone,sometimes with the legs dropped into a kneeling position,and under general endotracheal anaesthesia. After re-moval of the ligamentum flavum and as much laminaredge as was needed for exposure, the dural sac wasretracted and the nerve root visualized, mobilized, andretracted (Fig. 1). The bulging posterior longitudinalligament was incised and the disc space entered. Theamount of cartilaginous material (disc and cartilageplate) was always scant and never protruding. The nu-cleus pulposus was practically non-existent. In somepatients, the interspace was so narrowed that only asmall curette (No. 0 or 1) could be inserted. Thoroughcurettage was always carried out. The part of the bulg-ing ligament, over which the nerve root was stretched,was exised. If the level explored was between the fourthand fifth lumbar vertebral bodies, the next lower level

was also explored (and vice versa), to assure the absenceof a typical herniated nucleus with false localization. Inseven patients, spinal fusion was carried out by the ortho-paedist with an H-shaped iliac graft interposed betweenthe spinous processes of the fourth lumbar and firstsacral vertebrae. The material removed from the discspace was usually degenerated cartilage, compatiblewith degenerated intervertebral disc.We have followed cases as long as six years post-

operatively. In 1966, five patients in the series were re-examined, and a questionnaire was sent to the others.One was lost to follow-up. All patients reported thatthey were improved and were either asymptomatic orwere experiencing only mild backaches. None of thepatients examined demonstrated limitation of straight-leg raising or paraspinal muscle spasm. Hypaesthesiaand depressed stretch reflexes tended to persist, however.

CASE REPORT

The syndrome is illustrated in the following typical casereport. T.T., a 30-year-old dock worker, developed lowback pain with radiation into the left leg following anautomobile accident two years previously. Persistence ofpain and weakness of the left foot led to hospitalization.The most striking finding was weakness of the dorsi-flexors of the left foot. Plain radiographs of thespine (Fig. 2) showed straightening of the normal lum-bar lordotic curve, retained height of the intervertebral

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FIG. 6. Same specimen as Fig. S after removal of onenucleus pulposus and application of longitudinal com-pression. Note marked bulge of posterior longitudinalligament (arrow), slight bulge of ligamentum flavum, andnarrowing ofnerve-root foramen.

FIG. 7. Radiographs of lateral view of cadaver lumbarspine after removal of nucleus pulposus (from in front, atarrow).

FIG. 8. Same specimen as in Fig. 7 with longitudinalcompression applied. Note narrowing of intervertebraldisc space.

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Protrusion of the posterior longitudinal ligament simulating herniated lumbar intervertebral disc

spaces, but overriding of the facets at the L 4-5 inter-space, with narrowing of the intervertebral foramen.Myelography (Figs. 3 and 4) demonstrated filling defectsat this interspace, especially on the left; EMG was notdone. Operation revealed nerve-root compression at theL 4-5 interspace by a bulging posterior longitudinalligament under which there was scant disc material.This was removed, and the bulging ligament excised;the spine was fused because of the apparent instabilityof the facet joints. When last seen, three years later,the patient was working as a dock hand and experiencingonly minimal low back pain and no weakness of the leftankle.

ANATOMICAL STUDIES In an attempt to reproduce in acadaver what occurs clinically, we removed the lowerthree lumbar vertebrae intact and, through the anteriorlongitudinal ligament, removed the nucleus pulposus ofthe intervertebral disc. Photographs and radiographswere taken before and after longitudinal compres-sion was applied to the vertebrae by an ordinary wood-working 'C' clamp.There was marked bulging of the posterior longi-

tudinal ligament, narrowing of the nerve root foramen,and slight bulging of the ligamentum flavum into thespinal canal (Figs. 5 and 6). Radiographs (Figs. 7 and 8)showed narrowing of the affected interspace and slightoverriding of the facets when compression was applied.

DISCUSSION

The anatomy of the intervertebral disc and itssurrounding structures has been discussed in otherpublications (Larmon, 1944; Coventry, Ghormley,and Kernohan, 1945). Several related featuresshould be emphasized. The posterior longitudinalligament is attached only at the disc and passesloosely over the vertebral body. It is thickest mediallyand thins as it fans out laterally to blend with theannulus fibrosus (Hanraets, 1959; Hadley, 1964);some physicians even doubt its presence laterally.We have observed it laterally, where, along with theannulus fibrosus, it forms the anterior border of theintervertebral foramen. We have referred here tothis fused structure as the posterior longitudinalligament.The mechanism of the degenerative disc has been

reviewed by Saunders and Inman (1940), Hanraets(1959), and by Rabinovitch (1961). Briefly, thenucleus pulposus dessicates with age, allowing thedisc space to narrow and causing the surroundingligaments to become lax. In the herniated discsyndrome, the laxity of the ligaments places stresson the annulus fibrosus, which tears and causes thenucleus pulposus to herniate through the weakestpoint (posterolaterally where the foetal vessels tothe disc originally travelled).On the other hand, in the degenerative disc

syndrome, a different mechanism must be at work.To account for the negligible disc material one mustsuppose an extreme degree of dessication, herniationof material through fissures in the cartilage platesinto the vertebral bodies, or a congenital lack ofdisc material. The last two possibilities seem unlikely,first, because we saw no Schmorl's nodes and, sec-ondly, because redundant ligaments could hardlybe expected in congenitally narrowed discs. More-over, it would be difficult for such a disc to herniatethrough the annulus fibrosus (Hanraets, 1959).

Various explanations have been proposed toaccount for radicular symptoms in the absence of aprotruded disc. Most explanations have blamedstructures which might narrow the nerve rootforamen. Elsberg (1913) and Love and Walsh (1940)emphasized the significance of a thickened liga-mentum flavum as it encroaches on the foramenposteriorly. With narrowing of the disc space, it isnot inconceivable that the ligament could fold intothe lumbar canal and the intervertebral foramen;here, for all practical purposes, it would becomepart of the posterior wall and cause nerve rootcompression (Fig. 8).Hadley (1938, 1964) has shown that narrowing of

the disc may cause subluxation of the facet jointsand narrowing of the intervertebral foramen(Fig. 6). In fact, this may be the earliest radiologicalfinding before narrowing of the disc space is appa-rent (Harris and Macnab, 1954).

Friberg (1941), on the other hand, contends thatsimple narrowing of the disc space cannot producenerve root compression because the bony frame istoo large to permit it. He has shown that the twolowest lumbar foramina are the smallest, while thecorresponding nerves are the largest and are theonly ones that pass directly over the disc. Narrowingmay cause retropulsion of one vertebral body onits neighbour, thus decreasing the intervertebralforamen. In general, the interlumbar facets are in asagittal plane, and the lumbo-sacral facets are in acoronal plane. However, these lower facets areoften asymmetrical or are in a sagittal plane whichmay allow retropulsion (Armstrong, 1965). Theseanatomical facts may account for radicular symp-toms in the face of slight changes in the inter-vertebral foramina.Dandy described the 'concealed disc' in which

there is a small amount of disc material and noprotrusion of the disc. Adhesions between thenerve root and the posterior ligaments are said toaccount for the symptoms (Dandy, 1941; O'Connell,1943). We did not encounter this condition in ourpatients.

Others have reported protrusion of the annulusfibrosus in patients with narrowed intervertebral

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discs. Mixter (1937) described both a unilateral anda general bulging of the whole edge of the disc,causing radicular symptoms which he treated byfacetectomy or by 'trimming' where it seemed tocompress the nerve root.

Bradford and Spurling (1945) doubted that ageneralized protrusion was a frequent cause of thecharacteristic clinical picture of ruptured annulusfibrosus. They felt that facetectomy is preferable toattacking an intact annulus. However, it is unlikelythat facetectomy in our patients could correct thebulging ligament lying anterior to the nerve andover which the nerve is stretched rather thancompressed.

Friberg (1941) described a series of patients quitesimilar to ours. Of 58 patients undergoing explo-ration for symptoms of herniated disc, seven hadonly protrusion of the annulus fibrosus. Five ofthese had narrow disc spaces and abnormal myelo-grams. Two had filling defects in the midline, whilethree had filling defects laterally. Although there isa semantic difference between this series and ours,it is likely that they are pathologically identical.For several years, we have performed spinal

fusions in addition to resecting the redundantposterior longitudinal ligaments. The fundamentalproblem is an unstable back with narrowed inter-spaces, overriding facets, tilted vertebrae causinglaminae to 'shingle' under one another, and buckledinterlaminar and posterior longitudinal ligaments.Instability of the back sufficient to require fusion isdefined by a long history of back pain with orwithout sciatica, aggravated by bending, and usuallyrelieved temporarily by a lumbo-sacral support. Inall patients in this series in whom fusion was per-formed, instability was demonstrated when, at thetime of operation, the spinous process below thedisc concerned was grasped and moved up anddown and from side to side.Narrowing of the disc space and overriding facets

on the plain films before operation were consideredin the decision to fuse the spine. However, asBegg and Falconer (1949) have shown, narroweddisc spaces on plain films are difficult to identifyunless the diverging x-rays are parallel to the oppo-sing vertebral surfaces. This special technique wasnot carried out in our patients, so the actual inci-dence of narrowed interspaces is not known. Anarrowed interspace alone is no indication forfusion. When it is present with other clinical andoperative evidence of instability, it is further argu-ment for fusion.

There is insufficient material to warrant a validcomparison of the diagnostic value of a myelo-gram versus an electromyogram in this condition.The significant point is that either test may showresults that are indistinguishable from those com-monly associated with patients who have protrudedintervertebral discs.

SUMMARY

We have reported 13 patients with clinical syn-dromes of lumbar or sacral nerve-root compression,in whom operation failed to reveal herniated inter-vertebral discs but whose clinical, radiological,and electromyographical changes could have beencaused by folding of the posterior longitudinalligament into the lumbar canal compressing thenerve root. Excision of the redundant ligament,with or without fusion, resulted in significant reliefof symptoms in all cases. We believe that thispathological process may be one of several causativefactors to be considered in the group of patients whoshould have protruded discs, but do not.

REFERENCES

Armstrong, J. R. (1965). Lumbar Disc Lesions, 3rd ed., p. 74. Living-stone, Edinburgh.

Begg, A. C., and Falconer, M. A. (1949). Plain radiography inintraspinal protrusion of lumbar intervertebral disks: a corre-lation with operative findings. Brit. J. Surg., 36, 225-239.

Bradford, F. K., and Spurling, R. G. (1945). The Intervertebral Disc,2nd ed., p. 98. Thomas, Springfield, Ill.

Coventry, M. B., Ghormley, R. K., and Kernohan, J. W. (1945).The intervertebral disc; its microscopic anatomy and pathology.J. Bone Jt Surg., 27, 233-247.

Dandy, W. E. (1941). Concealed ruptured intervertebral disks. J.Amer. med. Ass., 117, 821-823.

Elsberg, C. A. (1913). Experiences in spinal surgery. Observationsupon 60 laminectomies for spinal disease. Surg. Gynec. Obstet.,16, 117-132.

Friberg, S. (1941). Low back and sciatic pain caused by intervertebraldisc herniation. Acta chir. scand., 85, Suppl. 64.

Hadley, L. A. (1938). Pathologic conditions of the spine. J. Amer.Med. Ass., 110, 275-278.

Hadley, L. A. (1964). Anatomico-Roentgenographic Studies of theSpine, pp. 9, 174-178. Thomas, Springfield, Ill.

Hanraets, P. R. M. G. (1959). The Degenerative Back and Its Diffe-rential Diagnosis, pp. 137, 167, 175. Elsevier, Amsterdam.

Harris, R. I., and Macnab, I. (1954). Structural changes in the lumbarintervertebral discs. J. Bone. Jt Surg., 36B, 304-322.

Larmon, W. A. (1944). An anatomic study of the lumbosacral regionin relation to low back pain and sciatica. Ann. Surg., 119,892-896.

Love, J. G., and Walsh, M. N. (1940). Intraspinal protrusion of inter-vertebral disks. Arch. Surg. (Chic.), 40, 454484.

Mixter, W. J. (1937). Rupture of the lumbar intervertebral disk. Ann.Surg., 106, 777-787.

O'Connell, J. E. A. (1943). Sciatica and the mechanism of the pro-duction of the clinical syndrome in protrusions of the lumbarintervertebral discs. Brit. J. Surg., 30, 315-327.

Rabinovitch, R. (1961). Diseases of the Intervertebral Disc and its Sur-rounding Tissues. Thomas, Springfield, Ill.

Saunders, J. B. deC. M., and Inman, V. T. (1940) Pathology of theintervertebral disk. Arch Surg. (Chic.), 40, 389-416.

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