| Abstract|| |
Background : Schmorl's node or intraosseous disc prolapse is herniation of the nucleus pulposus material through the vertebral end plates. Presence of Schmorl's nodes as end plate lesions following trauma, tumours and osteoporosis further complicates diagnosis. The present study was done to understand diagnosis and approach to management of symptomatic Schmorl's nodes.
Methods : During a period of three years we came across 14 patients who presented with severe back pain. Conventional radiographs, CT Scans and MRI showed the presence of end plate lesions with varied radiological appearance. The first group, comprising of seven patients had lytic lesions without any sclerosis on only one side of the intervertebral disc as seen on the CT scan. The second group comprising of five patients had sclerotic lesions with new bone formation associated with disc space reduction. The two patients in the third group showed a combined lytic and sclerotic lesion without any soft tissue changes. MRI of eleven patients revealed hypointense lesion on T 1 and T 2 weighted images with surrounding zone of hyper intensity on T 2 weighted images. The remaining three patients, did not have this hyper intense zone on T 2 weighted images . In five patients multiple Schmorl's nodes were observed. Diagnosis of symptomatic Schmorl's nodes was mainly done by exclusion. All patients were given rest and anti-inflammatory drugs followed by exercises.
Results : The first two groups of patients responded to the treatment and had complete relief of symptoms but both the patients in third group had persistent symptoms. MRI repeated after eight weeks showed an enhancing lesion with prevertebral soft tissue. A transpedicular core biopsy proved the lesion to be tuberculosis in one patient. Anti Koch's therapy was promptly started and follow up study showed resolution of the lesions. At the end of the study period all the patients were asymptomatic and returned to their active profession.
Conclusion : The difficulty in diagnosis is attributed to the fact that every person with Schmorl's node is not symptomatic. For accurate diagnosis it is necessary to have high index of suspicion, close follow up and exclusion of other associated conditions. In case of poor response to conservative treatment an alternative diagnosis has to be considered and if required it should be proved or disproved by a biopsy of the lesion (percutaneous or open).
Keywords: Schmorl′s Nodes; Intraosseous disc prolapse; Diagnosis; Classification; Prognosis.
|How to cite this article:|
Parasnis R, Talawadekar GD, Sancheti K H, Bhojraj S. Intraosseous disc prolapse: A diagnostic puzzle. Indian J Orthop 2006;40:168-72
| Introduction|| |
Schmorl's nodes or intraosseous disc herniations or superior and inferior disc herniations or vertical disc displacements have received less attention  . Though Schmorl's nodes are seen in as many as 19% of the population  , its clinical significance is still controversial. Radiological appearance of Schmorl's nodes may sometimes be confused with initial stage of infective lesions. Only up to 30% of Schmorl's nodes can be detected by conventional radiographs  . It is considered that discal prolapse occurs through the areas of weakness in the end plates resulting from ossification of gaps or scarred vascular channels during the first two decades of life. After the third decade of life, Schmorl's nodes are seen to be associated with conditions like trauma, tumours and osteoporosis. It is also suggested that avascular necrosis of the underlying vertebral bone may be the cause for development of Schmorl's nodes  . It is reported that as many as 38% patients presenting with low back pain may have Schmorl's nodes  . Only one third of these lesions are seen on plain X-rays. The clinical significance of these lesions is controversial and usually the diagnosis of symptomatic Schmorl's nodes is done after excluding other conditions. Some reports suggest that the MRI appearance of the symptomatic and asymptomatic Schmorl's nodes may be different.
Hyperintense signal from the bone surrounding the Schmorl's nodes on T 2 weighted images is seen in many cases in symptomatic Schmorl's nodes, suggesting inflammatory edema.
We came across 14 patients with Schmorl's nodes who presented with severe backache. These patients were thoroughly investigated and followed regularly to study this condition in detail.
| Materials and methods|| |
In a 3 year period 14 patients presented with severe back pain. Only three patients had history of trauma in the past and two other patients were involved in vigorous sporting activity. Plain radiographs, CT scans and MRI scans were done in all patients. A total of 22 Schmorl's nodes were found in these patients's MRI and only eight nodes were seen on plain X-Rays. Nine patients had single large lesion and the remaining had multiple nodes. There were eleven females and three males in this study, whose average age was thirty four years and six months. Depending upon the similarity in X-ray, CT and MRI appearance, these patients were classified into three groups.
Group-1: Seven patients in this group presented with pain in lower thoracic and/or upper lumbar lesion, associated with morning stiffness. Physical examination revealed tenderness over the involved area of spine and para-spinal muscle spasm. The forward bending of the spine was restricted due to pain. There was no neurological localizing sign or any other positive finding. The patient's X-rays showed marginal reduction in the disc space with appearance of a single lytic end plate lesion in only two patients. In five patients, no lesion was seen on the X-ray. Routine laboratory investigations were within normal limits. The CT scan revealed lytic lesion in the adjacent end plates near the involved disc in four patients. In three patients the lytic lesion was seen only in one vertebral end plate (inferior to the disc space).
There was moderate reduction in the disc space without any other abnormality. MRI revealed hypo-intense lesions in T 1 weighted images. Small zone of hyper intensity surrounding this lesion was seen on T 2 weighted images in some patients. Associated mild posterior disc protrusions were seen in three patients without significant neurological compression. The patients were advised conservative treatment in the form of rest and antiinflammatory drugs followed by back exercises. Mainly spinal extension exercises and core stabilization exercises were advised.
Group-2: Four patients presented with back pain in the thoraco-lumbar and lumbar region associated with restriction of activity and flank pain. On examination there was tenderness and para-spinal muscle spasm. Spinal flexion was painful and restricted. Reduced disc space was seen in plain X-rays of three patients. Sclerotic end plate lesion was seen in four patients. CT scan showed a sclerotic lesion in the end plates superior to the involved disc space. There was reduction in the disc space with mild protrusion in three cases. The sclerosis was eccentric without any associated lytic lesion and the adjacent end plate was normal. MRI showed degeneration of the involved disc with hypointensity in both T 1 And T 2 weighted images. Gadolinium enhanced contrast study in one patient revealed vascularisation of the lesion.
The patients were advised conservative treatment in the form of rest and antiinflammatory drugs along with muscle relaxants followed by back exercises. Mainly spinal extension exercises and core stabilization exercises were advised.
Group-3: Two patients presented with severe lumbar back pain resulting in restriction of activity and disability.
There was no history of neurological and constitutional symptoms. Physical examination revealed tenderness with para-spinal muscle spasm. Forward flexion was painful and restricted. There was no history of any constitutional symptoms. Plain radiographs indicated minimal disc space reduction associated with a lytic and sclerotic lesion. CT scan showed lesions in both the adjacent end plates with sclerosis and lysis. In one case there was an additional sclerotic lesion in the inferior part of adjacent vertebra. MRI revealed hypointense lesion surrounded by zone of hyperintense lesions on T 2 weighted images in both the adjacent vertebrae. All investigations including the blood count, ESR, chest X-rays etc were within normal limits. Patients were treated with rest and anti-inflammatory drugs, but the symptoms persisted. MRI was repeated after eight weeks of treatment. This MRI showed an enhancing destructive lesion involving adjacent vertebrae with prevertebral soft tissue, characteristic of vertebral tuberculosis [Figure - 3]b. The patients blood counts were still normal with marginal increase in the ESR. Mantoux test was positive and the IgG, IgM antibody tests were negative.
As the prevertebral soft tissue was very small in amount and not easily assessable by percutaneous technique, it was thought that it would be extremely difficult to perform a CT guided biopsy. Percutaneous trans-pedicular core biopsy was done in one patient and diagnosis of tuberculosis was confirmed on histo-pathological examination. The other patient refused the procedure and hence was empirically started on anti - TB therapy. Both patients were advised rest for six weeks along with anti-Kochs therapy including four drugs. After six weeks both the patients improved symptomatically and were mobilized with a hyper-extension orthoses. Follow up MRI repeated after six months of treatment showed resolution of the lesion [Figure - 3]c.
| Results|| |
After an average follow up of two years and four months it was seen that all the patients in Groups 1 and 2 had complete pain relief and were asymptomatic. None of the patient required medicines more than three months. Three patients had recurrence of the symptoms within one and half years. But the symptoms resolved with two weeks of medication and resuming back exercises. All the patients went back to their work. There was no residual disability.
Both the patients in the third group required repeat MRI and the diagnosis was revised as vertebral tuberculosis. Anti-Kochs therapy inclusive of four drugs for three months followed by three drugs for six months & bed rest was advised. After first six weeks of therapy, both the patients improved symptomatically and were mobilized with a hyperextension orthosis. Follow up MRI repeated after six months of treatment showed resolution of the lesion [Figure - 3]c. Eventually, both the patients had complete symptomatic relief and went back to their active profession.
Follow-up examination of patients in the first two groups showed restoration of complete range of movement of the spine. However patients in group three had restriction of forward bending terminally.
| Discussion|| |
Coventry suggested that the ossification gaps and vascular channels in the cartilaginous plates form areas of weakness through which intraspongy extrusion of disc material may occur in the first two decades of life  . Degenerative changes form similar weakness in the cartilaginous plates beginning in the third decade of life. Schmorl's nodes could be due to trauma, tumour or various metabolic bone diseases but in many cases these factors are absent and the cause remains speculative. Peng et al found that the CT changes in cystic Schmorl's nodes were similar to the typical changes of osteonecrosis. They suggested that Schmorl's nodes are end result of ischaemic necrosis beneath the cartilaginous end plate and that herniation into the body of the vertebrae is secondary  .
Stabler et al reported 38% incidence of intraosseous disc herniations in patients with backache  . Hilton et al reported 36-79% incidence in various studies in human cadavers  . Schmorl's nodes are the most common non intervertebral disc abnormalities in persons without backache and are found in 19% of the population on MR imaging. However the clinical importance of intraosseous disc herniations is controversial. Most Schmorl's nodes are detected incidentally on spinal radiographs. Few Schmorl's nodes become symptomatic. Stabler et al considered the size of the enhancing nodes and the degree of concomitant edema in the surrounding bone marrow as the factors correlating with the probability of localizing symptoms 5 . These changes are seen only on the MR imaging and plain X-rays can detect only 5-35% of all Schmorl's nodes 3 . Martel also recognized that large Schmorl's nodes (>3 mm in size) are frequently symptomatic 8 . Bobechko suggested that back pain in a Schmorl's node could be due to an auto immune response to the nucleus pulposus which may result in increasing vascularity and bone marrow edema  .
In all the fourteen cases we observed large Schmorl's nodes (more than three mm in size) associated with surrounding bone marrow edema. In the absence of any other detectable pathology, it was accepted that these lesions were the cause of the patient's symptoms. The patients in first two groups responded favorably with conservative methods confirming the diagnosis. However the two patients in the third group remained symptomatic inspite of similar treatment. The repeated MR imaging showed progressive destructive lesion due to tuberculous infection. This forced us to reconsider our diagnosis and highlighted the need to differentiate the various types of end plate lesions.
Martel  divided the vertebral end plate lesions into three types: (i) primarily lytic group, (ii) sclerotic group and (iii) lytic and sclerotic group (6). In the lytic group usually the upper portion of the vertebral body is involved and the adjacent disc space is spared. There is no new bone formation with minimal disc space reduction. These lesions are never associated with infection and do not progress. In Group 1 there were lytic lesions in the adjacent end plates of involved vertebrae with moderate disc space reduction. This type of lesion is differentiated from infective lesions by the absence of paravertebral soft tissue mass. It is possible that Myeloma or metastatic neoplasm can weaken the end plates leading to secondary intrabody disc herniations, but such destruction is usually not limited to the end plate.
In some cases, the adjacent end plate was spared which is also a rare feature in infective pathology. MRI in some cases also showed posterior protrusion of the disc suggesting degenerative changes as the cause for the intraosseous herniation. The configuration and sites of vertebral osteolysis usually distinguishes these cases from those with infective lesions. All the cases in Group 1 responded well to conservative treatment and the lesions did not increase in size.
In Group 2 the lesion was sclerotic with disc space reduction. This sclerosis was eccentric involving a broad area. Martel has suggested that these lesions be compared to osteitis pubis or osteitis condensans ileii as these are thought to be secondary to mechanical stress. These lesions may be mistaken for metastasis or spinal neuroarthropathy; however, progressive vertebral fragmentation or bony overgrowth, which characterize these conditions, are never observed in sclerotic intraosseous disc lesions. These sclerotic lesions also respond well to conservative treatment and a transition to mixed type is not reported.
In Group 3 the first MR imaging showed lytic and sclerotic lesions in the adjacent end plates of the involved vertebrae. These were irregular lesions with surrounding bone marrow edema. In the absence of clinical signs of infection and evidence of paraspinal soft tissue mass, it is difficult to differentiate from infection. Williams et al termed several cases with similar appearance as "pseudoinfections of the intervertebral disc" as the cultures for these lesions proved sterile  . Our patients did not respond to the treatment and MRI, repeated after eight weeks showed progressive destruction indicating vertebral tuberculosis.
Transpedicular core biopsy in one patient provided histopathological confirmation of tuberculosis but second patient refused biopsy procedure. Anti Koch's therapy was started immediately to which they responded and subsequent imaging showed resolution of the lesion.
The radiographic appearance of lytic and sclerotic lesions is sufficiently characteristic for reliable diagnosis. These cases require conservative management with periodic clinicoradiological re-evaluation. It is the group of lesions with lytic and sclerotic appearance, which presents a diagnostic challenge. In these cases one requires high index of suspicion along with close observation and regular follow-ups. Repeated MR imaging may be required and in case of poor response to conservative treatment an alternative diagnosis has to be considered, proved or disproved by a biopsy of the lesion (percutaneous or open).
| References|| |
|1.||Schmorl G, Junghans H. The human spine in health and disease. New York: Grune and Stratton.1971. |
|2.||Jensen MC, Brant-Zavidzki MN, Obuchowski Nimodic MT, Malkasian D, Ross JS. Magnetic resonance imaging of the lumbar spine in people without backache. N Engl J Med. 1994; 331: 69-73. |
|3.||Hamanishi C, Kawabata T. Schmorl's nodes on magnetic resonance imaging. Spine. 1994; 19 4: 450-453. |
|4.||Peng B, Wu W, Hou S, Whang X, Yang Y. The Pathogenesis of Schmorl's nodes. J Bone Joint Surg (Br). 2003; 85-B, No.6: 879-882. |
|5.||Stabler A, Bellan M, Weiss M, Gartner C, Brossmann J, Reisr J. MR imaging of enhancing intraosseous disc herniations. Am J Roengenol. 1997; 168: 933-938. |
|6.||Coventry MB, Ghoumley RK, Kernohan JW. The intervertebral disc: its microscopic anatomy and pathology. Part II. Changes in the intervertebral disc concomitant with age. J Bone Joint Surg. 1945;27:233-47. |
|7.||Hilton RC, Ball J, Benn RT. Vertebral end plate lesions in the dorso lumbar spine. Ann Rheumat Dis. 1976; 35: 127-132. |
|8.||Martel W, Seeger JF, Wicks JD, Washburn RL. Traumatic lesions of the discovertebral junction in the lumbar spine. Am J Roentgenol. 1976; 27: 457-464. |
|9.||Bobechko WP, Hirsch C. Auto immune response to nucleus pulposus in rabbit. J Bone Joint Surg (Br). 1965; 47: 574-580. |
|10.||Williams Jl, Moller GA, O'Rourke TL. Pseudoinfections of the intervertebral disc and adjacent vertebrae? Am J Roentgenol. 1968; 103: 611-615. |
Consultant Spine Surgeon, Archis Bunglow, 35/98, Bhusari Colony, Paud Road, Kothrud, Pune-411038
Source of Support: None, Conflict of Interest: None
[Figure - 1], [Figure - 2], [Figure - 3]