ABCs of the degenerative spine
Degenerative changes in the spine have high medical and socioeconomic significance. Imaging of the degenerative spine is a frequent challenge in radiology. The pathogenesis of this degenerative process represents a biomechanically related continuum of alterations, which can be identified with different imaging modalities. The aim of this article is to review radiological findings involving the intervertebral discs, end plates, bone marrow changes, facet joints and the spinal canal in relation to the pathogenesis of degenerative changes in the spine. Findings are described in association with the clinical symptoms they may cause, with a brief review of the possible treatment options. The article provides an illustrated review on the topic for radiology residents.
• The adjacent vertebrae, intervertebral disc, ligaments and facet joints constitute a spinal unit.
• Degenerative change is a response to insults, such as mechanical or metabolic injury.
• Spine degeneration is a biomechanically related continuum of alterations evolving over time.
KeywordsDegenerative spine Intervertebral disc herniation Spondylosis Modic changes Spinal canal stenosis
Degenerative change is considered a response to insults, such as mechanical or metabolic injury, rather than a disease . The aetiology of the degenerative changes may be mechanical micro-insults or damage secondary to macro-insults, such as spinal fractures, spinal surgery not related to degenerative disc disease or significant metabolic processes, such as ochondrosis or mucoplysaccharidoses. All elements of the spine, including the intervertebral discs, joints, ligaments and bony structures, may undergo morphological changes that can be classified as degenerative.
Accurate and comprehensive interpretation of imaging findings relating to the degenerative spine can be challenging and sometimes even confusing because the word “degeneration” means different things to radiologists, neurologists, neurosurgeons and pathologists . The pathogenesis of these changes in the spine is a biomechanically related continuum of alterations that evolve over time . Therefore, understanding the pathophysiology of these biomechanical changes in the spine is essential for radiologists to characterise radiological abnormalities. The pathophysiology-based approach in assessing imaging findings in the degenerative spine can: (1) accurately characterise the process in the involved segment; (2) identify the sequence of degenerative changes and predict further abnormalities; (3) identify hidden or subtle abnormalities based on indirect signs; (4) assist clinicians in finding the source of pain or neurological symptoms; (5) identify the best treatment options for patients. No degenerative change should be considered an isolated event or reported as a random finding.
A-changes: nucleous pulposus
Abnormal mechanical axial stress owing to the combined effects of an unfavourable inheritance, age, inadequate metabolite transport and trauma impairs chondrocytes and can cause an nucleous pulposus to degenerate . As degeneration progresses, the nucleous pulposus becomes desiccated resulting in reduced intradiscal pressure , thus passing the mechanical load on to the annulus fibrosus . Because it has to hold greater weight, the annulus fibrosus undergoes changes to reflect the increasing strain it bears. Most of the annulus fibrosus then acts like a fibrous solid to resist compression (Fig. 5) [3, 11]. Increased stress on the annulus fibrosus can lead to development of cracks and cavities, subsequently progressing to clefts and fissures . This loss of annulus fibrosus structural integrity may result in disc herniation. Structural weakness of the annulus fibrosus may also lead to the inability of the disc to maintain anatomical alignment and position progressing to instability and/or spondylolisthesis. All these structural changes are irreversible because adult discs have limited healing potential .
Novel functional imaging techniques, such as T2/T2* mapping, T1ρ calculation, T2 relaxation time measurement, diffusion quantitative imaging, chemical exchange saturation transfer, delayed contrast-enhanced MRI of cartilage, sodium-MRI and MR spectroscopy, are promising tools that allow the evaluation of early disc degeneration based on the chemical composition of a disc, mainly by evaluating the proteoglycan content . These novel MRI techniques might be useful in the assessment of progression of disc degeneration and have potential applications in clinical trials to evaluate the efficacy of disc restoration therapies.
As disc degeneration progresses, nitrogen accumulates within the disc. This is a very rapid process and appears to be posture-dependent and often associated with segmental instability [16, 17]. On MRI, the vacuum phenomenon manifests as a signal void on both T1- and T2-WI  (Fig. 7a).
Intradiscal fluid accumulation
Fluid in the disc is highly associated with the presence of the vacuum phenomenon, type 1 bone marrow changes (Modic 1) and severe end plate abnormalities. Fluid shows high signal on T2-WI and in the presence of type 1 Modic changes can mimic early spondylodiscitis  (Fig. 7b).
B-changes: annulus fibrosus, end plates and bone marrow
Displacement of disc material beyond the limits of the intervertebral disc space may be diffuse (bulging) or focal herniation (protrusion, extrusion and extrusion with sequestration)  (Fig. 9). On the axial plane, it may be anterior or posterior. Herniation can be classified as: central, paracentral, foraminal or extraforaminal [21, 22, 23, 24]. The herniation may migrate superiorly or inferiorly  (Fig. 10).
Disc bulging. This occurs when intradiscal pressure remains high and the annulus fibrosus is intact and the height of the disc preserved. A rapid increase in intradiscal pressure in the setting of bulging may lead to the development of annular fissures and eventually result in herniation. Bulging is very often seen in asymptomatic individuals (Fig. 11a, b).
Annular bulging (folding). Degeneration of the nucleous pulposus eventually leads to a marked drop in intradiscal pressure resulting in disc space narrowing or collapse with the vertebral bodies moving closer to one another. Increased vertical loading on the annulus fibrosus causes it to bulge or fold radially outward [25, 26, 27]. Annular bulging (folding) may be symptomatic as severe disc space narrowing also results in decreased size of the intervertebral foraminae, which is further exacerbated by bulging annulus fibrosus (Fig. 11c). Annular bulging (folding) has never been identified as a separate entity; however, it is an important finding from the clinical point of view, since the surgical treatment aims to restore the intervertebral disc space rather than microdiscectomy.
Protrusion is described as localised (more than 25% of the circumference of the disc) displacement of disc material and the distance between the corresponding edges of the displaced portion must not be greater than the distance between the edges of the base of the displaced disc material at the disc space of origin . Anatomically, protrusion is a focal displacement of disc material with no or minimal disruption of the fibres of the overlying annulus fibrosus and intact posterior longitudinal ligament (Fig. 12).
Extrusion is a herniated disc in which, in at least one plane, any one distance between the edges of the disc material beyond the disc space is greater than the distance between the edges of the base of the disc material beyond the disc space in the same plane or when no continuity exists between the disc material beyond the disc space and that within the disc space . Anatomically, the extrusion is the displacement of disc material with a full-thickness disruption of the annulus fibrosus fibres; usually the posterior longitudinal ligament however remains intact (Fig. 13). The posterior aspect of the extrusion may be larger than its base in the sagittal plane causing the posterior longitudinal ligament to tent, which often causes neurological symptoms and pain.
Extrusion with sequestration is a focal disc displacement when extruded disc material that has no continuity with the disc of origin . A subligamentous sequestration is a variant of an extrusion with sequestration, which occurs when the nucleous pulposus material splays along the posterior longitudinal ligament . It appears spindle shaped on imaging. A transligamentous sequestration is when the disc material displacement results in full-thickness disruption of the annulus fibrosus fibres and posterior longitudinal ligament . A fragment may stay at the level of the disc or may migrate superiorly or inferiorly. Pain and neurological symptoms may fluctuate with the migration of the free fragment within the spinal canal. The acute displacement of a free fragment from the disc into the spinal canal may cause acute cauda equina syndrome (Fig. 14).
Herniation directed posteriorly toward the spinal canal may have clinical significance as it can cause neuronal or spinal cord compression. However, annular fissures and acute disc herniation involving the anterior aspect of the disc can also be responsible for back pain. These are frequently are overlooked and underestimated.
Acute herniations occur in the early stage of degenerative disease when intradiscal pressure is still relatively high. Acute increases in intradiscal pressure in the setting of trauma or lifting heavy weights lead to the displacement of the nucleous pulposus through the compromised fibres of the annulus fibrosus, causing the annulus fibrosus fibres to rupture. Injured tissues show increased levels of catabolic cytokines and an acute focal inflammatory reaction . Every episode of acute disc displacement leads to further migration of the nucleous pulposus posteriorly and worsening of the annulus fibrosus tear. Herniation without disc degeneration is rarely seen and typically occurs secondary to an acute traumatic event (Fig. 15a).
Subacute disc herniation is associated with classically described back pain that worsens with standing and is better when the patient is lying down . It arises only when disc material migrates peripherally as the intradiscal pressure increases (for example, in the standing position), but improves when intradiscal pressure drops (in the horizontal position) and the remaining intact fibres of the annulus fibrosus recoil to bring the extruded material back into the disc space. Since the majority of MRI and CT studies are performed in the prone position when the intradiscal pressure decreases, imaging findings may underestimate the extent of fluctuating nucleous pulposus displacement (Fig. 15b).
Chronic nucleous pulposus displacement represents the stable displacement of the disc material outside the disc. In its early stage, chronic protrusions persist because of high intradiscal pressure pushing the nucleous pulposus material out of the disc; however, annulus fibrosus fibres later undergo advanced degenerative changes and lose the ability to recoil (Fig. 15c). Excessive axial stresses may lead to further migration of the intradiscal nucleous pulposus fragment, and additional tearing of the annulus fibrosus fibres results in the repetition of the acute stage. Extrusion occurs when the intradiscal fragment tears apart all the annulus fibrosus layers. Further migration of the extrusion leads to posterior longitudinal ligament tearing and free disc fragments (sequester) floating freely in the spinal canal.
Complications of disc displacement may be neurological, vascular or focal. Neurological complications are related to nerve root and spinal cord compression, which are the most common complications of disc herniation. At any spinal level, an acute persistent neurological deficit from disc herniation is a medical emergency, which may require surgical decompression. Vascular complications develop secondary to acute or chronic compression of the vertebral artery or medullary segmental arteries feeding the spinal cord (large cervical radiculomedullary at level C5–C7; dominant radiculomedullary artery at T4–T5; the artery of Adamkiewicz located at T10 and the additional radiculomedullary artery of Deproges-Gotteron arises at the L4–L5 level), which may cause a severe neurological deficit and also may require intervention. Focal complications occur because of long-standing inflammatory changes secondary to persistent fluctuating or chronic hernia, which eventually may lead to extensive epidural scarring (without surgical intervention). Normally, the nerve roots freely move in the foraminae with body movements. Epidural scarring limits nerve root passage through foraminae and may cause nerve root tethering. This process is virtually impossible to identify at imaging. Acute disc sequestration in the settings of adhesions between the ventral wall of the dura and the posterior longitudinal ligament may lead to dural perforation and developing intradural herniation. This is a very rare complication, comprising only 0.27% of all herniated discs and mostly occurring on the lumbar spine [31, 32]. Epidural vein varicosis, enlargement of epidural veins secondary to disc herniation usually on the lumbar spine, can mimic the clinical signs of disc herniation or spinal stenosis. MRI has been reported to be of high value in demonstrating the dilated epidural vein but the findings might be misinterpreted as herniated nucleus pulposus material .
Many studies have reported the spontaneous regression or disappearance of disc herniations without surgical management. Sequestrations have the highest likelihood of regressing radiographically in the shortest timeframe in comparison to the other subtypes of disc herniation. Although the exact mechanism of this phenomenon is unknown, dehydration and shrinkage appear to play a primary role and can be clearly demonstrated using MRI because of the decreasing water content over time . After disc material sequestrates into the epidural space, it is recognised as a foreign body, and autoimmune and inflammatory responses lead to neovascularisation, enzymatic degradation and macrophage phagocytosis .
End plate changes
Degenerative marrow changes
Although the exact causes of degenerative changes of the bone marrow (so-called Modic changes) are not clear, their occurrence may be closely related to mechanical stress . The abnormal load and stress will affect vertebral end plates and the microenvironment of adjacent vertebral bone marrow, resulting in histological changes, which exhibit signal intensity change on MRI . There are three main forms of degenerative change involving the bone marrow of the adjacent vertebral bodies. These may also occur in the pedicles .
Type 2 changes (increased on T1-WI and iso/hyperintense on T2-WI without contrast enhancement) reflect the presence of yellow marrow in the vertebral bodies (Fig. 17d–f).
Type 3 changes (decreased on both T1- and T2-WI) represent dense woven bone and the absence of marrow. These changes are potentially stable and almost always asymptomatic (Fig. 17g–i).
Degenerative intervertebral instability
Clinically, instability presents with intermittent nonspecific back pain that worsens with movement. A variety of imaging modalities are currently used to assess spinal instability. Conventional MRI and CT performed in the prone position provide limited information on the functional status of the affected segment as spondylolisthesis with instability may “self-reduce” without a normal axial load. These techniques can demonstrate indirect signs of instability, such as the presence of traction spurs, intradiscal vacuum phenomenon or ligamentum flavum hypertrophy. Functional modalities, such as kinetic MRI and flexion and extension radiographs, are effective ways to evaluate abnormal motions in the involved segment. For the lumbar spine, on flexion-extension radiographs values of 10° for sagittal rotation and 4 mm for sagittal translation are typically used to infer instability . Specific criteria for the diagnosis of instability of the cervical spine have not yet been established: transitions from 1 mm to 3.5 mm on functional radiographs have been proposed in the literature , and a 3-mm slippage appears to be a reliable cut-off. The CT twist test is obtained through the facet joint while the patient twists his/her body and the pelvis is tightly strapped to the CT table. The clinical significance of the twist test is not well established.
C-changes: facet joints, figamentum flavum and spinal canal
Degenerative changes in the facet joints
Bulging of the synovium through the facet joint capsule, especially in the presence of instability, may result in synovial cysts . The majority (about 90%) of synovial cysts are found at the L4–L5 level and present clinically with lumbar radiculopathy. On MRI, synovial cysts are hyperintense on T2-WI if there is direct communication with the facet joint and hyperintense on T1-WI if there is a haemorrhagic or proteinaceous component. If clinically significant, a synovial cyst may require percutaneous fenestration or open surgery (Fig. 25).
Ligamentum flavum hypertrophy
Spinal canal stenosis
Cervical spinal canal stenosis
Lumbar spinal canal stenosis
Lumbar lateral canal stenosis can be classified as: grade 0, no stenosis; grade 1, mild stenosis, where there is narrowing of the lateral recess without root flattening or compression; grade 2, moderate stenosis, where further narrowing of the lateral recess occurs with root flattening but there is some preservation of the space lateral to the root in the lateral recess; grade 3, severe stenosis in which there is severe root compression with severe narrowing and complete obliteration of the CSF space surrounding or lateral to the nerve root (Fig. 29) .
Lumbar foraminal stenosis can be absent (grade 0), mild (grade 1, with deformity of the epidural fat while the remaining fat still completely surrounds the existing nerve root), moderate (grade 2, with marked foraminal stenosis where epidural fat only partially surrounds the nerve root) and severe (grade 3 or advanced stenosis, with complete obliteration of the foraminal epidural fat) (Fig. 29) .
Other findings of the degenerative spine
Lateral atlanto-axial joints
The incidence of lateral atlanto-axial osteoarthritis in the elderly population varies from 4% to 18% . Patients with atlanto-axial arthritis may suffer from suboccipital pain that is exacerbated by head rotation and distinct from other types of cervicalgia and headaches. The severity of the osteoarthritis is graded as none, mild, moderate and severe in each joint  (Fig. 30).
The atlanto-odontoid joint contributes between 40% and 70% to total cervical spine rotation . The incidence of degenerative changes in this joint in the normal population is quite high, with 42% in the 7th decade and 61% in the 8th decade . The severity of the osteoarthritis can be graded as none, mild, moderate and severe . Rarely atlanto-dental OA complicated with hypertrophic changes is the cause of cervical myelopathy  (Fig. 30).
Diffuse idiopathic skeletal hyperostosis (DISH) of the spine or Forestier disease
The condition is characterised by continuous ossification of ligaments and enthuses of the spine. The coarse and thick bony spinal bridges form along the anterior longitudinal ligament in a more horizontal orientation and mainly on the right side . The commonly accepted Resnick and Niwayama classification criteria for the spine require flowing osteophytes over four vertebral bodies and in addition the preservation of the intervertebral disc space . Ankylosis of the spine in patients with DISH increases the risk of spinal fracture four-fold; fractures may occur even after relatively low-energy trauma and often display highly unstable fracture configurations .
DTI/tractography and the degenerative spine
Senescence of the spine
Senescence of the spine is a normal part of ageing . It resembles changes in other ageing collagenous tissues and is unassociated with pain . With age the intervertebral discs become drier, more fibrous and stiffer secondary to decreased water-binding power, which makes them less able to recover from deformation. Nevertheless, the boundary between physiological disc ageing and early degenerative changes is not always clear since in most cases ageing and degenerative changes do not substantially differ on imaging. The imaging findings that are not associated with senescence and should be considered as degenerative include annular fissures, disc herniations, end plate changes, degenerative bone marrow changes, instability/spondylolisthesis and spinal canal stenosis.
Metabolic causes of degenerative changes
Clinical aspects of degenerative spine disease and reporting
The role of imaging is to provide accurate morphological information and influence therapeutic decision-making . The presence of degenerative change is not itself an indicator of symptoms. In the majority of cases, when patients with degenerative spine diseases are referred for imaging, clinicians are looking for answers to two simple questions: what is the cause of the patient’s pain or neurological symptoms, and what treatment option should be primarily considered in this particular situation? Therefore, these imaging findings must be interpreted in the context of the patient’s clinical condition. In the majority of cases, even in advanced cases of degenerative spine disease with multilevel involvement, it is possible to identify one leading cause of the patient’s problem or to provide a list of potential choices or culprits so that the referring physician can select the right answer based on the presentation, clinical symptoms and physical examination of the patient.
We would like to express our gratitude to Irina Nefedova, a Ukrainian artist, for drawing the amazing illustrations.
- 1.Oxland TR (2015) Fundamental biomechanics of the spine—what we have learned in the past 25 years and future directions. J BiomechGoogle Scholar
- 2.Dupre DA et al (2016) Disc nucleus fortification for lumbar degenerative disc disease: a biomechanical study. J Neurosurg Spine 1–7Google Scholar
- 22.Cousins MJ, Bridenbaugh PO (1998) Neural Blockade in Clinical Anesthesia and Management of Pain. Lippincott-RavenGoogle Scholar
- 23.Mandell J (2013) Core Radiology. Cambridge University PressGoogle Scholar
- 24.Herkowitz HN et al (2011) Rothman-Simeone The Spine: Expert Consult. Elsevier Health SciencesGoogle Scholar
- 25.Bogduk N (2003) Functional anatomy of the disc and lumbar spine. In: Karin Büttner-Janz SHH, McAfee PC (eds) The artificial disc. Springer-Verlag, Berlin-HeidelbergGoogle Scholar
- 26.Shen FH, Samartzis D, Fessler RG (2014) Textbook of the Cervical Spine. Elsevier Health SciencesGoogle Scholar
- 27.Büttner-Janz K, Hochschuler SH, McAfee PC (2003) The Artificial Disc. SpringerGoogle Scholar
- 30.Tandon PN, Ramamurthi R (2012) Textbook of Neurosurgery, Third Edition, Three Volume Set. Jaypee Brothers, Medical Publishers Pvt. LimitedGoogle Scholar
- 44.Denis F (1984) Spinal instability as defined by the three-column spine concept in acute spinal trauma. Clin Orthop Relat Res 189:65–76Google Scholar
- 45.(2015) Spinal instability. Springer Berlin Heidelberg, New York. pages cmGoogle Scholar
- 53.McCrory DC et al (2006) Spinal fusion for treatment of degenerative disease affecting the lumbar spine. Agency for Healthcare Research and Quality (US), RockvilleGoogle Scholar
- 72.Choi JM et al (2012) Cerebellar infarction originating from vertebral artery stenosis caused by a hypertrophied uncovertebral joint. J Stroke Cerebrovasc Dis 21(8):908 e7–908 e9Google Scholar
Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.