Imaging of lumbar spondylosis

Low back pain is a common health problem and imaging is pivotal in its assessment. Most lesions can be diagnosed by MRI. The nomenclature of disc lesions is also presented.

1. Imaging of Disk Disease and Degenerative Spondylosis of the Lumbar Spine Dr. Hazem Abu Zeid Yousef Ass. Prof. Radiodiagnosis Assiut University Hospital

2. Introduction Low back pain is a common health problem. As one of the top five causes of doctor visits in the United States and it affects 85% of the population of the Western World at some time in their lives. Consequently, the lumbar spine is one of the most frequently imaged regions in the radiology practice. While there are numerous possible pathologies, degenerative change is the most common finding in people with low back pain or lower extremity radicular symptoms.

3. Normal Anatomy A “motion segment” refers to two adjacent vertebrae, the intervertebral disk, the facet joints, and the connecting ligaments. The normal intervertebral disk is composed of three different components. The first is the gelatinous center called the nucleus pulposus (90% of which is composed of water). Beginning in the teenage years a horizontal cleft of fibrous tissue containing collagenous, elastic, and reticular fibers gradually appears, seen well on T2-weighted magnetic resonance (MR) images as a low signal intensity horizontal band traversing the otherwise high signal intensity nucleus6 and is referred to as the nuclear cleft.

4. Intranuclear cleft. Sagittal fat-suppressed T2-weighted image of a normal lumbar spine shows well-hydrated, high signal intensity intervertebral disks with horizontal low signal intensity intranuclear clefts (arrows).

5. The nucleus is held in place by the second component of the disk called the annulus fibrosus, which is composed of 2 lamellae of collagen fibers. The inner collagen fibers blend with those of the nucleus pulposus. The outer fibers of the annulus fibrosus are bound to the adjacent vertebral endplates by Sharpey’s fibers. The purpose of the annulus is to contain the nucleus pulposus by withstanding the hoop stress of axial loading and the shearing forces of flexion and torsion. The third component of the disk is the hyaline cartilaginous endplate of the vertebral body above and below the nucleus pulposus, and across which diffusion of nutrients to the nucleus occurs. The cartilaginous endplate is usually not discernible with imaging.

6. The facet joints (also called the apophyseal joints) are true synovial joints, lined by hyaline cartilage and enclosed in a joint capsule. They are oriented approximately 40 degrees in the sagittal plane, and there may be mild tropism (asymmetry of orientation) between pairs of facets, most often at L4-5 and L5-S1.1.

7. Appearances and Terminology of Degenerative Disk Disease Intervertebral Osteochondrosis While degeneration of the disk usually affects both the nucleus pulposus and the annulus simultaneously, the imaging appearance of degeneration depends on which of the components is affected more. Degeneration of the nucleus pulposus is called “intervertebral osteochondrosis” and appears radiographically as narrowing of the disk space, with or without the “vacuum phenomenon” of intradiscal gas. The gas represents nitrogen that is pulled from the surrounding soft tissues into the nucleus pulposus by the negative pressure of the collapsing disk,. Calcification may also develop in the disk, but more often involves the annulus than the nucleus.

8. On MR imaging, the earliest appearance of degeneration of the nucleus is desiccation, manifest as low signal intensity on T2WI instead of the high signal intensity of normally hydrated disks. The disk will then narrow and may exhibit linear or patchy low signal intensity if gas or calcification is present. Occasionally, the vacuum created by the collapsing nucleus pulls in fluid instead of nitrogen, causing a paradoxical high signal intensity “white disk” appearance of degeneration on T2WI instead of the desiccated appearance. The clue is the associated disk narrowing and other features of degeneration such as endplate changes and osteophytes Similarly, intradiscal calcification, may cause paradoxical high signal intensity within the disk on T1- weighted images.

9. Disk desiccation. Sagittal fat-suppressed T2-weighted image shows a low signal intensity, desiccated disk (arrow) at the L2/3 level. Notice the other well-hydrated, high signal intensity disks with normal intranuclear clefts.

10. Degenerative changes may occur in the adjacent vertebral endplates, as described by Modic and colleagues. Type 1 change is vascular granulation tissue, demonstrated as low signal intensity on T1WI and high signal intensity on T2WI. These changes may occasionally mimic infection. Type 2 change is fatty infiltration of the endplates, demonstrated as high signal intensity on T1WI and low signal intensity on fat-suppressed sequences Type 3 change is sclerosis of the endplates, seen as low signal intensity on all pulse sequences. Types 1 and 2 are not radiographically visible, whereas type 3 appears radiographically as increased density of the endplate and is called “discogenic sclerosis.”

11. “White disk.” (A) Sagittal T1WI sequence shows degenerative disk disease at L5/S1 manifest by fatty endplate changes and anterior osteophyte formation at this level and the level above (arrows). The tiny focus of high signal intensity in the posterior aspect of the disk could be due to calcium. (B) Corresponding sagittal fat-suppressed T2WI sequence in this same patient shows linear high signal intensity indicating fluid that has been pulled into this degenerated disk (arrow). The presence of the endplate degeneration and osteophytes is the clue that this high signal intensity disk is actually degenerated.

12. Endplate changes. (A) Sagittal T1WI image shows low signal intensity type 1 granulation changes at L1/2 (solid arrows), which become high signal intensity on B. the fat suppressed T2WI sequence. In A, notice the type 2 fatty endplate changes at L5/S1 (dashed arrows), which become low signal intensity on the corresponding fat-suppressed sequences (B).

13. A Schmorl’s node is herniation of the nucleus pulposus through the cartilaginous endplate of the vertebra. Schmorl’s nodes are identified on radiographs and computed tomographic (CT) scans as focal depressions in the vertebral endplate, usually with a thin sclerotic rim, and on MR images as an extension of disk material into the vertebra. They are usually incidental findings on imaging studies performed for back pain or other reasons, but an acute intraosseous herniation can be painful. The typical chronic Schmorl’s node has normal surrounding marrow signal intensity, whereas an acute Schmorl’s node will have surrounding edema-like signal intensity.

14. Schmorl’s nodes. (A) Lateral radiograph shows multiple thin sclerotic indentations of the endplates (arrows). (B) Axial CT image of a different patient shows a round lucency with a thin sclerotic rim (arrow). (C) Sagittal reformatted CT image of the same patient in B shows the endplate invagination with the thin sclerotic rim (arrow). (D) Sagittal fat-suppressed T2-weighted sequence of a different patient shows small Schmorl’s nodes at the T12-L1 disk (arrows), as well as several smaller Schmorl’s nodes at other levels. Notice that the nuclear material fills the Schmorl’s nodes and that the surrounding marrow has normal signal intensity, indicating that these Schmorl’s nodes are chronic.

15. Spondylosis Deformans Degeneration of the annulus fibrosus renders it incompetent to withstand the hoop stress of axial loading, causing it to bulge outward against its anchors to the vertebral endplates. This outward bulging is well appreciated on sagittal MR images as extension of the low signal intensity annulus beyond the vertebral endplate. However, one must use caution in the interpretation of such extension, since a normal disk may extend beyond the confines of the endplate in some people, especially young ones due to normal physiologic turgor of the nucleus. Clues that the extension is in fact abnormal are if it is the only disk in the region that extends beyond the vertebral margin, or if there is associated desiccation of the nucleus.

16. Normal bulging. Sagittal T2-weighted image of a 9-yearold boy imaged for reasons other than back pain show normal extension of the annulus both anteriorly and posteriorly beyond the margins of the vertebral bodies. Notice that the disks are well hydrated but intranuclear clefts have not yet developed.

17. Eventually, the chronic pull of the annulus on the vertebral edge leads to the formation of osteophytes, an appearance called “spondylosis deformans.” These osteophytes can be small and horizontal (“traction” osteophytes) or can be large and curved (“claw” osteophytes) and occasionally bridging, and are well appreciated on radiographs, MR images, and CT images.

18. Annular tears, the degenerating annulus may develop frank tears. The tear may be characterized as concentric, transverse, or radial. Concentric tears run longitudinally along the plane of the collagen fibers, whereas transverse and radial tears are perpendicular to the annular lamellae; transverse tears are located peripherally and affect Sharpey’s fibers, whereas radial tears are “full thickness,” affecting the entire inner-to outer dimension of the annulus. Annular tears are usually well seen as high signal intensity on T2-weighted images and have been termed the “high intensity zone”.

19. Terminology of Disk Herniation Much variation exists in the use of terms to describe disk herniation, another feature of disk degeneration. To bring uniformity to the reporting of disk degeneration, the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology combined their committees on terminology, yielding a consensus paper on nomenclature. The task force recommends the term “herniated disk” to refer to localized extension of disk material beyond the vertebral margins. A disk herniation is considered “contained” if the overlying annulus and posterior longitudinal ligament are not ruptured, and “uncontained” if the overlying annulus and posterior longitudinal ligament are breached.

20. Based on the configuration of the herniation, the disk may be categorized as protruded (in which the base of the herniated material is broader than the herniation itself) or extruded (in which the base of the herniation is narrower than the herniation itself). Protrusion may be subcategorized as “focal” or “broad-based” depending on involvement of less than or more than 25%, respectively, of the circumference of the entire intervertebral disk. ,Extrusion may be subcategorized as “sequestrated” if the herniation no longer is in contact with the parent disk or “migrated” if the herniation is displaced away from the site of extrusion regardless if continuity with the parent disk is maintained.

21. The task force further states that a “disk bulge” is not a herniation and should not be used to describe the pathologic state of focal disk displacement; instead, they state that “bulge” is a term for describing extension of a disk beyond the confines of the vertebral endplate, must involve more than 50% of the circumference of the disk, and has several etiologies such as normal variation, disk degeneration, ligamentous laxity, vertebral body remodeling.

22. Apophyseal arthrosis This may range from mild narrowing of the facet joint space, and/or small osteophytes or hypertrophy of the articular processes, to the most severe involvement manifest as marked narrowing, large osteophytes, sclerosis, vacuum phenomenon, and subchondral cysts. The severe forms may be well seen on radiographs, whereas all levels of severity are seen equally well on CT and MR imaging. Focal outpouchings of the joint capsule, called synovial cysts, may also occur. cysts arising from the anterior surface are clinically important because they may contribute to central or foraminal stenosis. In addition, thickening of the ligamentum flavum often accompanies facet joint degeneration and contributes to central stenosis.

23. Epidural lipomatosis

24. Thank You