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Inflammatory and Infectious Disordersof the Spine

Imaging Approach

Marcel Wolf and Marc-André Weber

ContentsInflammatory and Infectious Disorders of the Spine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Seronegative Spondylarthropaties . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3Definition of Entity and Clinical Highlights . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3Basic Epidemiology and Demographics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3Clinical Scenario and Indications for Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4Imaging Technique and Recommended Protocol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9Interpretation Checklist and Structured Reporting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11Treatment Monitoring: Follow-up Scheme and Findings/Pitfalls . . . . . . . . . . . . . . . . . . . . . . . 12Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

Noninflammatory Ankylosis of the Spine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12Diffuse Idiopathic Skeletal Hyperostosis (DISH), and Ossification of the Posterior

Longitudinal Ligament (OPLL) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

Spondylodiscitis (Pyogenic Vertebral Osteomyelitis) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17Definition of Entity and Clinical Highlights . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18Basic Epidemiology and Demographics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19Clinical Scenario and Indications for Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

This publication is endorsed by: European Society ofNeuroradiology (www.esnr.org).

M. Wolf (*)Department of Neuroradiology, University of Heidelberg,Heidelberg, Germanye-mail: [email protected]

M.-A. WeberInstitute of Diagnostic and Interventional Radiology,University Medical Center Rostock, Rostock, Germanye-mail: [email protected]

© Springer Nature Switzerland AG 2019F. Barkhof et al. (eds.), Clinical Neuroradiology,https://doi.org/10.1007/978-3-319-61423-6_80-1

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Imaging Technique and Recommended Protocol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20Interpretation Checklist and Structured Reporting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22Treatment Monitoring: Follow-up Scheme and Findings/Pitfalls . . . . . . . . . . . . . . . . . . . . . . . 24Differential Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

Differential Diagnostic Considerations in Imaging of Inflammatory Diseasesof the Spine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28

AbstractSpondylarthropathies are a heterogeneousgroup of chronic inflammatory diseases affect-ing the spine and sacroiliac joints. They displaya negative serostatus for rheumatoid factor, thustermed seronegative spondylarthritides, but arestrongly associated with HLA-B27. Spondylar-thropathies can be classified in ankylosing spon-dylitis (Bechterew disease), the most frequentseronegative spondylarthropathy, or as psoriaticspondylarthritis, reactive arthritis (formerlytermed Reiter syndrome), enteropathicspondylarthritis (associated with inflammatorybowel disease), and undifferentiatedspondylarthritis. As each category does not rep-resent a distinctive entity, clinical, laboratory,and also imaging findings may overlap, clinicalneuroradiology may not lead to a definitivediagnosis, but to certain imaging patterns, andpossible differential diagnoses.

Noninflammatory conditions with ossifica-tions of the paravertebral ligaments may resultin ankylosis of the spine as well. The mostfrequent entities of noninflammatory ankylosisare diffuse idiopathic skeletal hyperostosis(DISH), and ossification of the posterior longi-tudinal ligament (OPLL), but exclusive ossifi-cation of the flava ligaments (OFL) may occuras well.

Spondylodiscitis is an infectious disorder ofthe spine found mostly in elderly, immobile,and immune suppressed patients, in particularafter trauma or surgery. As clinical symptomsand laboratory tests are unspecific, imagingplays a pivotal role in its diagnosis. In certaincases, image-guided acquisition of tissue formicrobiological tests may be useful for diag-nosis, targeted antibiotic therapy, or evaluationof suspicious imaging findings. In early stagesof the disease, radiography and CT may be

normal, or at least unspecific, in case of pre-existing degenerative conditions. MRI is theradiological technique of choice; as it showspathological findings even in early stages ofthe disease and potential involvement of theparaspinal tissue.

KeywordsSeronegative spondylarthropathy · Ankylosingspondylitis · Bechterew disease ·Spondylodiscitis · Pyogenic vertebralosteomyelitis · Diffuse idiopathic skeletalhyperostosis · DISH · ossification of theposterior longitudinal ligament · OPLL ·Imaging · Radiology · MRI

AbbreviationsCRP C-reactive proteinDISH Diffuse idiopathic skeletal

hyperostosisDMARD Disease modifying anti-rheumatic

drugESR Erythrocyte sedimentation rateHLA Human leukocyte antigenNSAID Non-steroidal anti-inflammatory

drugOFL Ossification of flava ligamentOPLL Ossification of the posterior longi-

tudinal ligamentSTIR Short tau inversion recoveryTNF Tumor necrosis factor

Inflammatory and Infectious Disordersof the Spine

The spinemay be involved in various inflammatorydiseases. The twomajor categories of inflammatorydisease of the spine are infectious and non-infectious. Infectious disease can be located in thespine itself, or the surrounding structures.

2 M. Wolf and M.-A. Weber

Hematogenous seeding is the most common causeof pyogenic and nonpyogenic infection, but directinoculation is possible as well. Noninfectiousinflammatory conditions of the spine are systemicdiseases that can be divided into two main catego-ries, rheumatoid disorders including rheumatoidarthritis, and seronegative spondylarthropathies.

Entheses, the bony insertions of ligaments andtendons, are target structures in certain non-pyogenic inflammatory diseases. Spinal enthesitiscan be caused by a seronegative spondylar-thropathy, like ankylosing spondylitis, and leadto calcifications of the ligaments, and finally anky-losis of the spine and sacroiliac joints.

Early diagnosis is crucial for initiation of ade-quate anti-inflammatory therapy. As no singlespecific diagnostic test is available, and evenimaging findings may overlap, the diagnosis ofseronegative spondylarthropathies is based onclinical, laboratory, and radiological examina-tions. Thus, clinical neuroradiology alone maynot be capable to lead to a definitive diagnosis,but certain imaging patterns may contribute topossible differential diagnoses.

Noninflammatory conditions may result inossification of spinal ligaments as well, involvingthe anterior longitudinal ligament in diffuse idio-pathic skeletal hyperostosis (DISH), the posteriorlongitudinal ligament (OPLL), or the flava liga-ment (OFL), that can be reliably diagnosed byimaging methods. Although they may be an inci-dental finding in radiological studies, radiologicwork-up is mandatory, when symptoms of spinalcanal stenosis, and myelopathy (OPLL and OFL),or fractures occur.

Seronegative Spondylarthropaties

Definition of Entity and ClinicalHighlights

Spondylarthropathies can be classified in ankylos-ing spondylitis (Bechterew disease), the most fre-quent seronegative spondylarthropathy, or aspsoriatic spondylarthritis, reactive arthritis (formerlytermed Reiter syndrome), enteropathicspondylarthritis (associated with inflammatorybowel disease), and undifferentiated

spondylarthritis. Among all entities of seronegativespondylarthropathies, ankylosing spondylitis orBechterew disease is by far the most frequent one.As imaging findings are similar, and nonspecific fordifferent spondylarthropathies, this chapter willfocus on the most frequent seronegative spondylar-thropathy. Ankylosing spondylitis or Bechterew dis-ease is an HLA-B27 associated chronicinflammatory disease of the axial skeleton,manifested by back pain, and resulting in ankylos-ing of the affected joints, with progressive stiffnessof the spine and sacroiliac joints. Besides stiffeningof the spine and sacroiliac joints, decrease of lumbarand cervical lordosis and accentuation of thoracickyphosis occurs, which can be compensated to acertain extent by hip extension, but may lead to lossof sagittal balance and loss of straight vision. Theprogressive rigidity of the spine, and the accompa-nying osteopenia, predispose for fractures, evencaused by minor trauma.

Basic Epidemiology and Demographics

The incidence of Bechterew disease varies amongdifferent ethnic groups. The prevalence ofBechterew disease in a given population is corre-lated with the prevalence of human leukocyteantigen (HLA)-B27 in that group. Approximately5–6% of HLA-B27-positive individuals sufferfrom ankylosing spondylitis. The mean preva-lence of ankylosing spondylitis per 10,000 isabout 23.8 in Europe, 31.9 in North America,10.2 in Latin America, 16.7 in Asia, and 7.4 inAfrica (Dean et al. 2014).

Relatives of an affected patient have anincreased risk for ankylosing spondylitis them-selves: monozygotic twins – 63%; first-degreerelatives – 8.2%; second-degree relatives –1.0%; third-degree relatives – 0.7%; and parent-child – 7.9% (Brown et al. 2000). The male-female ratio is approximately 2:1 to 3:1.

Pathophysiology

Typical clinical symptoms of ankylosing spondy-litis are back pain and progressive stiffening of thespine. The sacroiliac joints are frequently

Inflammatory and Infectious Disorders of the Spine 3

involved as well, even in early stages of the dis-ease. The primary targets of the autoimmuneinflammatory processes in ankylosing spondylitisare the entheses, fibrous and fibrocartilaginoustissue, providing anchorage of ligaments and ten-dons to bones. The enthesitis is accompanied bysmall erosions of the cortical bone, and reactivesubcortical osteosclerosis (osteitis) and bonereabsorption. With progression of the disease,osteoproliferation may result in ossification ofligaments, tendons, joint capsules, and eventuallyankylosis. Sacroiliitis may cause erosions andlater ossification of the sacroiliac joints. The spinalstiffness is caused by calcified syndesmophytes,ossifications of the paraspinous ligaments, bridgingadjacent vertebral bodies. Furthermore, a range ofextraskeletal manifestations, as uveitis, inflamma-tory bowel disease, psoriasis, cardiovascular, orpulmonary disease may occur. The most commonextraarticular symptom is unilateral uveitis, affect-ing 25–40% of patients (Stolwijk et al. 2015).About 50% of cases with acute uveitis are associ-atedwith ankylosing spondylitis. As uveitis may bethe first symptom requiring medical evaluation, itshould alert the treating physician to the possibilityof ankylosing spondylitis. Histological examina-tions of the mucosa of the ileum and colon showulcerations in about 50–60% of cases with anky-losing spondylitis, while only relatively few ofthese patients develop a clinically manifest inflam-matory bowel disease, whether Crohn’s disease orulcerative colitis. Up to 10% of patients suffer frompsoriasis (Stolwijk et al. 2015; El Maghraoui2011). An additional psoriasis predisposes tohigher frequency of peripheral joint involvementand a more severe course of the ankylosing spon-dylitis (Pérez Alamino et al. 2011).

Clinical Scenario and Indicationsfor Imaging

Lower back pain caused by sacroiliitis is often oneof the first symptoms, those may already occur inchildhood or early adulthood, usually prior to45 years of age. In most cases, involvement of thespine occurs in later stages of the disease. As there

exists no single, specific diagnostic test, the diag-nosis of ankylosing spondylitis, and the other sero-negative spondylarthropathies, is based on thecombination of clinical symptoms, physical exam,laboratory tests (HLA-B27 serostatus andC-reactive protein), and imaging. Thus, whenspondylarthropathy is suspected, imaging is indi-cated (Schueller-Weidekamm et al. 2014; Sudoł-Szopińska et al. 2015).

MRIMRI is the method of choice in early stages of thedisease (Fig. 1). MRI is able to diagnose bonemarrow edema of the sacrum and ilium adjacentto the sacroiliac joints (Rudwaleit et al. 2009).Synovial gadolinium enhancement correlateswith disease activity, as measured by laboratoryinflammation markers. Erosions, with loss andirregular margins of subchondral bone of thejoints of the sacroiliac joints, can also be diag-nosed in MRI, but occur in later stages of thedisease. In spinal MRI, edema in the anteriorcorners of the vertebral bodies (termed “Romanuslesions”) might be seen, indicating inflammationof the entheses that might result in formation ofbridging syndesmophytes (Fig. 2). The facetjoints may also exhibit edema. As syn-desmophytes are thin and have low signal inten-sity on all pulse sequences, ankylosis of the spinemay only be poorly visualized on MRI. Disc-related signal intensity abnormalities, in particularhyperintensities on STIR-weighted images, of thecentral portion and sparing of the anterior andposterior part of the endplates, and latercorresponding erosions and irregularities arereferred to as “Andersson lesions.”

Radiography and CTUsually radiographs are recommended as the firstimaging modality. Especially in young patientswithout relevant degeneration of the joints, radi-ography and even CT may not show pathologicalfindings when initial symptoms of the sacroiliacjoints occur. While radiography and even CT arestill normal, MRI might already reveal pathologicfindings. Radiography and CT show pathologicalfindings in later stages of the disease. Compared


to radiography, the sensitivity of CT is muchhigher, because of its higher spatial resolution,even small structural changes of cortical andspongious bone can be detected. Sacroiliac jointsmay show bilateral erosions (Fig. 3), then sclero-sis occurs, which may result in the endstageof complete fusion of the joints (Fig. 4).A widespread radiographic scoring system con-sists of the modified New York criteria (Table 1),although already proposed in 1984 (Van der Lin-den et al. 1984). In relatively early stages of thedisease, erosions and later adjacent sclerosis of the

anterior corners of the vertebral bodies occur,designated the “shiny corners” sign on radio-graphs. Squaring of the vertebral bodies is rela-tively characteristic for ankylosing spondylitis,most frequently seen in the lumbar spine. Withprogression of the disease, ossified syn-desmophytes, bridging adjacent vertebral bodies,may result in extended ankylosis of the spine, inthe endstage with involvement of the whole spine(“bamboo spine”). Involvement of the facet anduncovertebral joints can lead to erosions and laterfusion as well. During the course of the disease,

Fig. 1 In early stage of sacroiliitis, MRI is the mostsensitive imaging modality, and thus method of choice.Adjacent to the joint, the sacrum and ilium show bonemarrow edema (arrow in a) and contrast-enhancement(arrow in c). In later stages of the disease, erosions (e),sclerosis (d and e), and finally fusion of the joints (f) occur,

which can be detected on plain radiography (d) and moresensitively on CT (e and f) as well. (a) Axial fat-suppressedproton density-weighted MRI. (b) Axial unenhancedT1-weighted MRI. (c) Axial gadolinium-enhancedT1-weighted MRI. (d) a.p. radiograph. (d and e) AxialCT bone window


Fig. 2 In early stage of HLA-B27 associatedspondylarthritis, MRI (a, b and c) is the method of choice,able to detect enthesitis at the ventral corners of the verte-bral bodies. These often subtle findings, referred to as“Romanus lesions,” are hypointense on T1-weighted(arrows in a), and hyperintense on T2-weighted (arrowsin b) images, with fluid-sensitive sequences (arrows in c)being most sensitive. In MRI, “Romanus lesions” may bevisible, before syndesmophytes can be detected inCT. With progression of the disease, syndesmophytes,calcification of the syndesmophytes, the interspinous

ligaments and finally fusion of facet, and uncovertebraljoints occur. These changes subsequently result in ankylo-sis of the spine, visible on radiographs (f), and more sen-sitively on CT (d, e, and g). As syndesmophytes andcalcifications are hypointense, they can be difficult to diag-nose in MRI. Severe ankylosis of the spine results inbamboo-like appearance (e to g) and predisposes to highlyinstable fractures, even caused by minor trauma (g). (a)Sagittal T1-weighted MRI. (b) Sagittal T2-weighted MRI.(c) Sagittal fat-saturated T2-weighted MRI. (d, e, and g)Sagittal CT reformats bone window. (f) Lateral radiograph.


osteopenia occurs and can be seen on radiographsand CT. Localized vertebral or discovertebrallesions of the spine, with erosions, and irregular-ities of the central portion, and sparing of theanterior and posterior aspect of the endplates, are

referred to as “Andersson lesions” that regularlyoccur in patients with ankylosing spondylitis. Onradiographs and CT these osseous erosions andirregularities of the endplates can be depicted,while MRI is more sensitive for earlier stages by

Fig. 3 Ankylosing spondylitis. Case 1: 79-year-oldwoman with ankylosing spondylitis. Lateral radiograph(a) and sagittal CT (b) show squaring of the lumbar verte-bral bodies. While the lumbar spine does at least showsubtle syndesmophytes (a and b), the thoracic spineshows bridging syndesmophytes and hyperkyphosis (c).

Furthermore, CT of the sacroiliac joints shows erosionswith subtle adjacent sclerosis (c). (a) Lateral radiograph ofthe lumbar spine. (b) Sagittal CT reformat bone window ofthe lumbar spine. (c) Lateral radiograph of the thoracicspine. (d) Axial CT bone window of the sacroiliac joints


Fig. 4 Ankylosing spondylitis. Case 2: 68-year-oldwoman with severe ankylosing spondylitis. Spinal CTshows bridging syndesmophytes (a, b and c), fusion ofthe uncovertebral und facet joints (d and e), and thoracichyperkyphosis (b). Squaring of the vertebral bodies, accen-tuated on the lumbar spine (c). The sacroiliac joints arefused as well (e). Note osteopenia of the whole axial

skeleton (a–e). (a) Sagittally reformatted postmyelographyCT of the cervical spine. (b) Sagittal CT reformat of thethoracic spine. (c) Sagittal CT reformat of the lumbar spine.(d) Coronal reformat of postmyelography CT of the cervi-cal spine. (e) Coronal CT reformat of the lumbar spine andsacroiliac joints


detecting disc-related signal intensity abnormali-ties, in particular hyperintensities on STIR-weighted images.

In patients with severe ankylosing of the spine,even minor trauma may cause highly instable

fractures (Figs. 5 and 6). MRI can be helpful todiagnose occult fractures, which may be hard todiagnose using CT or radiography, due toosteopenia. Even if no fracture is directly seen,MRI may reveal the bone marrow edema. Further-more, MRI is optimal for evaluation of the spinalcanal and neural structures.

Imaging Technique and RecommendedProtocol

In early stages of the disease, MRI is the methodof choice. The sequence protocol for the sacroil-iac joints should include axial and or coronalfluid-sensitive sequences (e.g., STIR-weighted,fat-saturated T2-weighted, or fat-saturated pro-ton density-weighted), axial and/or coronal non-enhanced and fat-saturated gadolinium-

Table 1 Modified New York criteria for scoring ofsacroiliitis

Grade Radiographic findings

0 No abnormalities

1 Suspicious changes

2 Minimal abnormalities: Small localized areaswith erosions or sclerosis without alteration inthe joint width

3 Unequivocal abnormality, with one or more ofthe following: Erosions, evidence of sclerosis,widening, narrowing or partial ankylosis

4 Severe abnormality: Complete ankylosis

Fig. 5 Ankylosing spondylitis. Case 3: 50-year-oldwomanwith severe ankylosing spondylitis and instable fracture ofT9 and T10 caused byminor fall. Besides typical findings ofprogressed ankylosing spondylitis, like bridging syn-desmophytes, fusion of facet and uncovertebral joints,osteopenia, and “bamboo spine,” sagittal CT (a) showsinstable, displaced fracture of T9 and T10. This instable

fracture was stabilized by internal fixation from T8 to T12,displayed on sagittal CT (b), a.p. (c) and lateral (d) radio-graphs. (a) Sagittal CTreformat after trauma. (b) Sagittal CTreformat bone window after surgery and dorsal stabilizationwith internal fixation. (c) Postoperative a.p. radiograph. (d)Postoperative lateral radiograph


enhanced T1-weighted sequences (Fig. 7). AnMRI of the sacroiliac joints should includescans of the lumbar spine as well. A sequenceprotocol for spinal MRI should include sagittal

fluid-sensitive sequences (e.g., STIR-weighted,or fat-saturated T2-weighted), T2-weighted,nonenhanced, and fat-saturated gadolinium-enhanced T1-weighted, and axial T2-weighted

Fig. 6 Ankylosing spondylitis. Case 4: 68-year-oldwomanwith severe ankylosing spondylitis. Radiography (a) of thecervical spine prior to trauma shows progressed ankylosingspondylitis, with bridging syndesmophytes and fusion ofuncovertebral and facet joints. After a minor fall, sagittalCT (b) revealed instable, displaced fracture of the cervicalspine at C5/C6, besides bamboo-like appearance of thewhole spine. This fracture was initially stabilized by ventraland dorsal fixation of only this segment (c and d), leading to

increased biomechanical stress to the adjacent segments andafter another minor trauma, finally instable fracture directlycranially adjacent to this spondylodesis (c and d). Thus,dorsal stabilization extending from craniocervical junctionto mid-thoracic level was performed (e). (a) Lateral radio-graph of the cervical spine. (b) Sagittal CT reformat of thewhole spine bone window. (c and d) Sagittal CT reformatsof cervical spine bone window. (e) Lateral localizer ofintraoperatively acquired CT


and fat-saturated gadolinium-enhancedT1-weighted sequences (Schueller-Weidekammet al. 2014; Sudoł-Szopińska et al. 2015). InTable 2, a suggestion for an MRI pulse sequenceprotocol is shown.

Interpretation Checklist and StructuredReporting

Always evaluate alignment and potential degen-eration of the spine.

Radiography and CTSacroiliac joints:

– Bilateral erosions, later sclerosis, and finallyfusion of the sacroiliac joints, highly sug-gestive for ankylosing spondylitis

– Osteopenia, often present but unspecificSpine:

– Erosions, later sclerosis (shiny corner sign)of the anterior corners of the vertebral bod-ies, highly suggestive for ankylosingspondylitis

Fig. 7 Ankylosing spondylitis. Case 5: Sacroiliitis in a13 year-old, HLA-B27 positive boy with lower back pain.While unenhanced T1-weighted MRI appears nearly nor-mal, fat-suppressed proton density-weighted MRI showsbone marrow edema of the sacrum and ilium adjacent tothe left sacroiliac joint (arrows in b). Gadolinium-enhancedT1-weighted images and subtraction of gadolinium-

enhanced and nonenhanced T1-weighted images exhibitcorresponding enhancement (arrows in c and d). (a) Axialunenhanced T1-weighted MRI. (b) Axial, fat-saturated pro-ton density-weighted MRI. (c) Gadolinium-enhancedT1-weighted MRI. (d) subtraction of gadolinium-enhancedand nonenhanced T1-weighted MRI

Table 2 Suggested MRI pulse sequence protocol

Pulse sequence Orientation

Slicethickness(mm)

STIRw Sagittal orcoronal

3

T1w Sagittal 3

T2w Sagittal andaxial

3

Contrast-enhanced,fat-saturated T1w

Sagittal andaxial

3


– Andersson lesions, disc-related erosionsand irregularities of the central potion withsparing of the anterior and posterior part ofthe endplates

– Squaring of vertebral bodies– First subtle, later bridging syndesmophytes,

finally, and very specific for ankylosingspondylitis

– In later stages fusion of facet anduncovertebral joints

– Endstage of ankylosing of the spine (“bam-boo spine”) with decreased lumbar and cer-vical lordosis and accentuated thoracichyperkyphosis, and consecutive loss of sag-ittal balance

– Osteopenia, often present but unspecific

MRISacroiliac Joints:

• Bilateral sacroiliitis highly suggestive forankylosing spondylitis: First bone marrowedema, later erosions, and finally fusion ofthe joints

Spine:• If present, synovial gadolinium enhance-

ment indicates on-going inflammatoryactivity

• Contrary to CT and radiography, syn-desmophytes, and fusion of facet anduncovertebral joints are difficult to diagnosein MRI

• Andersson lesions• Romanus lesions

Treatment Monitoring: Follow-upScheme and Findings/Pitfalls

In young patients with back pain, and withouthistory of malignancy or trauma, MRI is themethod of choice when ankylosing spondylitisor any other spondylarthropathy is suspected.MRI may detect pathologic findings in earlystages of the disease, when radiography andeven CT may still be normal. Radiography is themost important imaging technique for follow-upof patients with already confirmed ankylosingspondylitis. After trauma, CT and in certain

cases additional MRI is indicated, as patientswith severe ankylosing spondylitis have anincreased risk for instable fracture.

Therapy

Therapeutic options for ankylosing spondylosiscomprise physical therapy, medication, and sur-gery. There is no cure for ankylosing spondylitis,the aim of the therapy is to stop, or at leastdecelerate progression of the disease. Physicaltherapy includes exercises that are supposed topreserve the flexibility. Nonsteroidal anti-inflammatory drugs (NSAIDs) reduce pain andinflammation activity. Disease modifying anti-rheumatic drugs (DMARDs) are beneficial forpatients with peripheral arthritis in particular,but less in axial manifestation. Tumor necrosisfactor (TNF)-alpha blockers (antagonists) havebeen demonstrated to reduce clinical and labora-tory disease activity. In patients with inadequateresponse to TNF alpha antagonists, Interleukin-17A inhibitors are an option.

Noninflammatory Ankylosisof the Spine

Noninflammatory conditions with ossifications ofthe paravertebral ligaments may result in ankylo-sis of the spine as well. The most frequent entitiesof noninflammatory ankylosis are diffuse idio-pathic skeletal hyperostosis (DISH), and ossifica-tion of the posterior longitudinal ligament(OPLL), but exclusive ossification of the flavaligaments (OFL) may occur as well. Involvementof different paraspinal ligaments may be associ-ated with each other, or with other ossifications ofentheses, tendons, and ligaments. Usually elderlypeople are affected, and some ethnical predispo-sitions were shown. For instance, the highest inci-dence of OPLL is observed in Japan. Thepathophysiology remains still undetermined.Although DISH and OPLL are relatively frequentincidental findings in imaging studies, and areoften asymptomatic, these conditions inherit thepotential for causing symptoms. When OPLL


leads to relevant spinal canal stenosis, and con-secutive myelopathy, surgical decompression ofthe spinal cord is indicated. DISH with extendedprevertebral hyperostosis may cause unspecificsymptoms as well, like dysphagia.

Diffuse Idiopathic SkeletalHyperostosis (DISH), and Ossificationof the Posterior Longitudinal Ligament(OPLL)

SynonymsAsymmetrical skeletal hyperostosis; Forestierdisease; Senile ankylosing hyperostosis

Definition of Entity and ClinicalHighlightsSpinal manifestation of diffuse idiopathic skeletalhyperostosis are flowing anterior vertebral ossifi-cations of more than four contiguous levels, lackof significant degenerative disc disease, and lackof arthritis of facet and sacroiliac joints (Resnickand Niwayama 1976). The cervical spine is mostoften affected, followed by thoracic spine. Thesespinal hyperostoses are usually accentuated on theright side. DISH is most often an incidental find-ing in radiologic studies, but extended hyperosto-sis may become symptomatic.

In OPLL, flowing ossifications are localized pos-teriorly to multiple vertebral bodies, caused by ossi-fication of the posterior longitudinal ligament, withrelatively minimal degeneration of the vertebraldiscs, and without ankylosis of the facet joints. Theformation of ectopic new bone can result in signif-icant narrowing of the a.p.-diameter of the spinalcanal, and thus may cause compression of the spinalcord. Most often, the cervical spine is affected,especially on mid-cervical level. Less frequent,OPLL may also occur in mid-thoracic and lumbarspine. Cervical myelopathy with spastic paresis andfurther progression to paralysis may occur.

Basic Epidemiology and DemographicsDISH usually occurs in middle-aged and olderpatients, and rarely before the age of 50. Themale-female-ratio is about 2:1. The incidence dif-fers among ethnic groups, with Caucasians being

most often affected. The reported incidence variesnotably.

The highest prevalence of OPLL is observed inJapan, and other Asian countries ranging from 2%to 4%, everywhere else being much lower. Themale-female-ratio is about 2:1. OPLL usuallyaffects patients older than 50 years and rarelyoccurs under the age of 30.

PathophysiologyThe definitive causes of DISH-related exagger-ated bone proliferation are still undetermined.Associations with diabetes mellitus, dyslipidemia,hyperuricemia, osteoarthritis, rheumatoid arthri-tis, gout, or calcium pyrophosphate depositiondisease have been postulated, and severalinvolved genes have been identified.

The etiology of OPLL is still undetermined, aswell, but mechanical stress to ligaments cellsseems to be among the contributing factors,up-regulating signaling pathways to promoteosteoblastic differentiation (Chen et al. 2017).Linkage of several genes has been identified(He et al. 2014; Furushima et al. 2002; Kogaet al. 1998).

Clinical Scenario and Indicationsfor ImagingDISH often is an incidental finding on imagingstudies, but extended hyperostosis may becomesymptomatic. For instance, large ossificationsventrally to the cervical spine may cause dyspha-gia, and after trauma may lead to instable frac-tures. If asymptomatic, no imaging studies areindicated.

In cases without relevant stenosis of the spinalcanal, OPLL often is an incidental finding inasymptomatic patients. With increasingnarrowing of the spinal canal, and consecutivecompression of the spinal cord, OPLL maybecome symptomatic, due to progressive myelop-athy with neurologic symptoms of tetra- or para-paresis. When OPLL is already known or inpatients with clinical symptoms suggestive forspinal cord compression, MRI is the method ofchoice for evaluation of compressive myelopathy.When MRI is contraindicated, postmyelographyCT with multiplanar reformats is an alternative.


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For determining the extent of ossifications andprior to surgical decompression, CT with multi-planar reformats is indicated (Figs. 8, 9, and 10).


DISHRadiography or CT is sufficient fordiagnosing DISH.

OPLLDue to its localization ventrally inside the spinalcanal, OPLL is superimposed over facet joints onlateral radiographs and thus findings may be sub-tle and easily overlooked using radiography.Therefore, CT with multiplanar reformats is thebest imaging tool for detecting the full extent of

ossifications and spinal stenosis (Fig. 11). AxialCT images reveal characteristic ossifications mid-line or laterally deviated along the posterior sur-face of the vertebral bodies, so called “upside-down T” or “bowtie.” The compression of thespinal cord can be visualized by MRI and post-myelography CT, but in case of myelopathy, theintramedullary edema can only be diagnosed byMRI. OPLL typically shows low signal intensityon all pulse sequences, but extended ossificationsmay exhibit central bone marrow with signal-hyperintensities on T1- and T2-weighted sequences.On T2�-weighted gradient echo sequences, theextent of ossifications and spinal stenosis can beexaggerated by susceptibility effects (Figs. 12 and13). Although MRI reliably shows relevant spinalstenosis and is the best imaging tool to evaluate

Fig. 8 Lateral radiographs are sufficient for diagnosingDISH, with extended bridging ossifications ventrallylocated to the spine. DISH usually affects the cervicalspine (a), while thoracic (b) and especially lumbar spineshow no or at least less ossifications. On MRI, in particularon sagittal images these ossifications can easily be over-looked, as they usually have low signal intensity in all

pulse sequence. Note the relatively minimal degenerationof the discs that is typical for DISH. (a) Lateral radiographof the cervical spine. (b) Lateral radiograph of the thoracicspine. (c) Sagittal CT reformat bone window. (d) Axial CTbone window. (e) Sagittal T1-weighted MRI. (f) AxialT1-weighted MRI. (g) Sagittal T2-weighted MRI. (h)Axial T2-weighted MRI


the spinal cord, CT is usually recommended prior tosurgical decompression (Fig. 14).


DISHRadiography:

– Sufficient for diagnosis– Flowing ossifications ventrally located at

the vertebral bodies

– Relatively minimal degeneration of thediscs

CT:– Flowing ossifications ventrally located at

the vertebral bodies– Axial CT shows right-lateral accentuation

of these ossifications– Indicated for complications, for example,

after traumaMRI:

Fig. 9 DISH. Case 1: Spinal DISH in an 81-year-oldwoman. Lateral radiograph reveal extended ventrallylocated spondylophytes, bridging more than four cervicalvertebral bodies (a), without significant decrease of discspace height. On thoracic spine, these changes are typicallyless severe and thus may only be subtle on radiographs (b)but obvious on CT (c). On MRI (d–h), the signal intensityof these flowing spondylophytes are hypointense or if

present equivalent to bone marrow. Thus, on MRI DISHcan be easily overlooked, especially if a saturator is posi-tioned ventrally to the vertebral bodies. (a and b) Lateralradiograph. (c) Sagittal CT reformat bone window. (d)Sagittal T1-weighted MRI. (e) Sagittal T2-weighted MRI.(f) Sagittal STIR-weighted MRI. (g) Axial T1-weightedMRI. (h) Axial T2-weighted MRI


– Not necessary for diagnosis, but indicatedfor imaging of complications or trauma

– Early, small ossifications have low signalintensity in all pulse sequences

– Extended, bulky ossifications may containbone marrow, with bone marrow-equivalentsignal intensity (increased signal intensityon T1- and T2-weighted sequences)

OPLLRadiography:

– Flowing multilevel ossification posterior tovertebral bodies: may easily be overlooked,as these OPLL is superimposed by facetjoints on lateral radiographs, and vertebral

bodies, laminae, and spinal processes ona.p. radiographs.

– No ankylosis of facet joints.– Relatively minimal degeneration of

intervertebral discs.CT:

– Axial images: “upside down T” or “bowtie”– Sagittal reformats: flowing multilevel ossi-

fications of the posterior longitudinalligament

Postmyelography CT:– Compression of the spinal cord can be bet-

ter visualized than on plain CT scansMRI:

– Flowing multilevel ossification posterior tovertebral bodies

Fig. 10 DISH. Case 2: Spinal DISH in an 86-year-oldman. CT shows flowing ossification of the anterior longi-tudinal ligament, bridging more than four vertebral bodies.

The extended spondylophytes ventrally to C3 to C6 causemoderate displacement of the larynx. (a) Sagittal CTreformat bone window. (b and c) Axial CT bone window


– “upside down T” or “bowtie” on axialimage

– Ossifications have low signal intensity onall pulse sequences, but extended ossifica-tions may contain bone marrow, displayingfat equivalent high signal intensity on T1-and T2-weighted sequences

– Intramedullary edema on T2-weightedimages

– CAVE: the extent of spinal canal stenosismay be exaggerated on T2�-weighted gra-dient echo sequences

Treatment Monitoring: Follow-upScheme and Findings/PitfallsIncidental OPLL can be observed, as long as stillasymptomatic. In case of high grade spinal canal

stenosis or symptomatic compressive myelopathy,decompressive surgery is indicated. Two surgicalstrategies are possible, anterior decompressionwith fusion and posterior decompression withlaminectomy.

Spondylodiscitis (Pyogenic VertebralOsteomyelitis)

The risk for spondylodiscitis is increased inelderly, immobile, and immune-suppressedpatients, in particular after trauma or surgery.As clinical symptoms and laboratory tests areunspecific, imaging plays a pivotal role in itsdiagnosis. In certain cases, image-guided acqui-sition of tissue for microbiological tests may beuseful for diagnosis, targeted antibiotic therapy,

Fig. 11 OPLL may easily be overlooked on radiography,as the flowing multilevel ossification of the posterior lon-gitudinal ligament is superimposed by the facet joints. CT(a–d) is the best imaging tool for visualizing the extent ofthe ossifications, but narrowing of the spinal canal and ofcourse cord compression is best seen on MRI (e–h). Cordcompression and potential intramedullary edema can bedetected using T2-weighted sequences. Gradient echo

sequences are the most sensitive pulse sequences fordetecting calcifications, but may exaggerate the extent ofspinal canal stenosis. Note the “upside-down T” or“bowtie” on axial CT (b and d) and gradient echo MRI(h). (a and c) Sagittal CT reformats bone window. (b and d)Axial CT bone window. (e) Sagittal T1-weighted MRI. (f)Axial T2-weighted MRI. (g) Sagittal T2-weighted MRI.(h) Axial T2�-weighted sequence


or evaluation of suspicious imaging findings. Inearly stages of the disease, radiography and CTmay be normal, or at least unspecific, in case ofpreexisting degenerative conditions. MRI is theimaging method of choice, as it shows patho-logical findings even in early stages of the dis-ease and potential involvement of the paraspinaltissue (Fig. 15). CT and radiography are helpfulfor evaluating spinal stability. Thus, clinicalneuroradiology is essential in the diagnostic

workup of suspected or confirmedspondylodiscitis.

Definition of Entity and ClinicalHighlights

Spondylodiscitis (Synonym: pyogenic vertebralosteomyelitis) comprises pyogenic infection of

Fig. 12 OPLL Case 1: OPLL in a 42-year-old male. InMRI (a–c) narrowing of the spinal canal and compressionof the spinal cord is clearly displayed, but the flowingmultilevel ossification of the posterior longitudinal liga-ment has low signal intensity on all pulse sequences andthus is better visualized on CT (d–g). CT is usually neededfor surgical planning. As the extent of OPLL caused symp-tomatic myelopathy, surgical decompression by

laminectomy C3 to C6 and implantation of dorsalspondylodesis was performed. (a) Sagittal T1-weightedMRI. (b) Sagittal T2-weighted MRI. (c) AxialT2-weighted MRI. (d) Sagittal CT reformat bone window.(e) Axial CT bone window. (f) Sagittal CT reformat bonewindow. (g) Axial CT bone window. (h) Lateral radio-graph. (a–e) prior and (f–h) postsurgery


the vertebral disc (discitis) and adjacent vertebralbodies (spondylitis).

Basic Epidemiology and Demographics

The overall incidence is about 2.4 cases per100,000. The incidence increases with age. Inpersons older than 70 years, the incidence isabout 6.5 per 100,000, in persons younger than20 years only about 0.3 per 100,000 (Zimmerli

2010). A predominance of males is observed, withan approximate ratio of 2:1.

Pathophysiology

Most often it is caused by hematogenous seeding,followed by direct inoculation in spinal surgery, orcontiguous spread of an infection of adjacent tis-sue. Staphylococcus aureus is by far the mostcommon microorganism being responsible for

Fig. 13 OPLL Case 2: OPLL in a 65-year-old male. InMRI (a–e) the flowing multilevel ossification of the poste-rior longitudinal ligament shows low signal intensity on allpulse sequences. Compression of the spinal cord andpotential intramedullary edema are best displayed onT2-weighted images. Gradient echo sequences are themost sensitive MRI pulse sequences for detection of calci-fications. However, when using MRI, gradient echo

sequences (e) can visualize the ossifications best, but mayexaggerate the extent of spinal canal stenosis. CT bettershows the exact extent of ossifications than MRI. (a) Sag-ittal T1-weighted MRI. (b) Sagittal T2-weighted MRI. (c)Axial T1-weighted MRI. (d) Axial T2-weighted MRI. (e)Axial gradient echo sequence. (f) Sagittal CT reformatbone window. (g) Axial CT bone window


about 50% of cases, followed by Escherichia coli,Pseudomonas aeruginosa, and Candida albicans.

In adults, the vertebral discs are rather avascu-lar, in children they are relatively wellvascularized (Ratcliffe 1985). Thus, primaryhematogenous discitis only occurs in children,while in adults spondylitis leads to secondaryinfection of adjacent disc.

Clinical Scenario and Indicationsfor Imaging

Clinical signs are various and unspecific. Localpain is the most common initial sign (86%).Severe, lancinating pain may indicate an epiduralabscess. While the most common location of ver-tebral osteomyelitis is lumbar (58%), followed bythoracic (30%) and cervical (11%) spine, the mostcommon locations of epidural abscesses areinverse, with cervical (28%) spine followed bythoracic (22%) and lumbar (12%) spine. Fever

might be present, but is an infrequent sign(35–60%), probably due to antipyretic effect ofcommonly used nonsteroidal anti-inflammatorydrugs (NSAIDs). Neurologic deficits likehypaesthesia, paresis, radiculopathy occur inabout one third of cases. Spinal tenderness onpercussion is reported in less than one fifth ofcases (Zimmerli 2010).


Due to its superior soft-tissue-contrast, the imag-ing method of choice is MRI, being able to detectearly stages of the disease. MRI is very sensitivein detecting inflammation of the vertebral disc andbody, epi- and paraspinal tissue, when radiogra-phy and even CTmay still be without pathologicalfinding (Fig. 16). Affected vertebral discs andbodies show hyperintensity on T2-weighted andhypointensities on T1-weighted images (Fig. 17).

Fig. 14 OPLL Case 3: OPLL in a 69-year-old male.OPLL usually shows low signal intensity on all MRIpulse sequences. Spinal canal stenosis, cord compression,and potential intramedullary edema. As CT shows theexact extent of the ossifications, it is recommended priorto surgical decompression of symptomatic OPLL. Due toOPLL with high grade narrowing of the spinal canal andsymptomatic myelopathy, dorsal decompression surgery

was performed, with stabilization by implantation of aninternal fixation. (a) Sagittal T1-weighted MRI. (b) Sagit-tal T2-weightedMRI. (c) Sagittal STIR-weighted MRI. (d)Axial T2-weighted MRI. (e) Axial gradient echo sequence.(f) Sagittal CT reformat bone window. (g) Axial CT bonewindow. (h) Sagittal CT reformat bone window. (i) AxialCT bone window. (j) Lateral radiograph. (a–g) prior to and(h–j) after dorsal decompression surgery


A suggestion for an MRI pulse sequence protocolis shown in Table 3, including sagittal T1weighted, sagittal or coronal STIR-weighted, sag-ittal T2 weighted, sagittal and axial gadolinium-enhanced T1 weighted fat-saturated sequences(Prodi et al. 2016).

MRI delivers criteria with very high and highsensitivity for pyogenic osteomyelitis, includingthe presence of paraspinal or epidural inflamma-tion (97.7% sensitivity), disc enhancement(95.4% sensitivity), hyperintensity or fluid-equivalent disc signal intensity on T2-weighted

MR images (93.2% sensitivity), erosion ordestruction of vertebral endplates (84.1% sensi-tivity), and effacement of the nuclear cleft (83.3%sensitivity) (Fig. 18). Criteria with low sensitivityare decreased height of the intervertebral space(52.3% sensitivity) and disc hypointensity onT1-weighted MRI (29.5% sensitivity)(Ledermann et al. 2003).

As in the first 2 weeks, osseous signs are neg-ative on radiographs, radiography is inappropriateas initial imaging method. In early stages onlyabnormalities of paravertebral soft tissue might

Fig. 15 Spondylodiscitis. Radiographs (a and c) showdecreased height of disc space and erosions of adjacentvertebral endplates. Besides osseous structures, the para-spinal soft tissue has to be regarded carefully as well, as forexample abscess with gas inclusions in the psoas musclemay be detected on radiographs as well (c). In MRI theaffected discs show hyperintense signal intensity onfat-saturated T2-weighted (b and g), and STIR-weighted(d) images. CT (e and f) shows reduced disc space height,and erosions of the adjacent vertebral endplates (e), and

contrast-enhanced CT may detect inflammation of para-spinal and epidural soft-tissue (f) as well. Inflammation ofthe paraspinal soft tissue is best visualized on gadolinium-enhanced fat-saturated T1-weighted images (i). (a and c)a.p. radiograph. (b) Sagittal T2-weighted fat-saturatedMRI. (d) Coronal STIR-weighted MRI. (e) Sagittal CTreformat bone window. (f) Sagittal CT reformat soft tissuewindow. (g) Sagittal T2-weighted fat-saturated MRI. (h)Sagittal T1-weighted MRI. (i) Axial gadolinium-enhancedT1-weighted fat-saturated MRI


be detected, like changes in paraspinal soft tissuedensity, or loss of fat planes. Reduced height ofthe vertebral disc, and erosions of vertebralendplates, destruction of the vertebral body,fusion of vertebral body, sclerosis, and deformityonly occur in later stages and cannot be detectedin the first 2 weeks (Byrd et al. 1983; Pineda et al.2009).

CT inherits a higher spatial resolution com-pared to radiography, and thus even subtle ero-sions of the vertebral endplates can be detected,which might not be seen on plain radiography, butmight be difficult to differentiate from degenera-tive conditions in early stages of the disease.Inflammation of the epidural and paraspinal softtissue can be detected, with increased sensitivityin contrast-enhanced CT.

Magnetic resonance imaging is most sensitivefor diagnosing vertebral osteomyelitis in early

stages of the disease, thus being the imagingmodality of choice (Carragee 1997; Prodi et al.2016). In Table 3, a suggestion for an MRI pulsesequence protocol is shown.


Always evaluate spinal alignment, height of ver-tebral bodies and disc space, lining of endplates,integrity of vertebral bodies, and of course para-spinal soft tissue.

MRI– Method of choice, due to its superior soft tissue

contrast– Disc hyperintense on T2- and STIR-weighted

images

Fig. 16 Spondylodiscitis. Case 1. 80-year-old male withspondylodiscitis C6/7. Initial CTalready shows erosions ofadjacent vertebral endplates (a) and epidural empyema (b).In MRI the disc and adjacent vertebral bodies have hyper-intense signal intensity on T2-weighted images (c and d).The epidural empyema is visible on T2-weighted images(c and d), but the extent of paravertebral soft tissueinvolvement is best seen on gadolinium-enhanced,fat-saturated T1-weighted images (f). Despite initiation ofantibiotic therapy, the clinical status of the patient wors-ened, and MRI performed 8 days later (g–j) showed

progression of both, osseous and soft tissue involvementas well. (a) Sagittal CT reformat bone window. (b) Sagittalcontrast-enhanced CT reformat soft tissue window. (c)Sagittal T2-weighted fat-saturated MRI. (d) AxialT2-weighted MRI. (e) Sagittal T1-weighted MRI. (f) Sag-ittal gadolinium-enhanced T1-weighted fat-saturated MRI.(g) Sagittal T2-weighted fat-saturated MRI. (h) AxialT2-weighted MRI. (i) Sagittal T1-weighted MRI. (j) Sag-ittal gadolinium-enhanced T1-weighted fat-saturated MRI.(c–f) Initial MRI. (g–j) Second MRI after clinical worsen-ing despite antibiotic therapy


– Narrowing of disc space– Diffuse gadolinium-enhancement of vertebral

disc– Edema, later osseous erosions and destruction

of adjacent vertebral bodies/ endplates– Diffuse gadolinium-enhancement of adjacent

vertebral bodies

– Paraspinal and epidural abscess or phlegmon(Fig. 19)

– Compression of spinal cord possible

CT– Iso- to hypodense swelling of paraspinal soft

tissue– Gas inclusions in paraspinal soft tissue– Contrast-enhancement of affected disc, verte-

bral body, and adjacent paravertebral softtissue

– Reduced disc height– Erosions or sclerosis of vertebral endplates,

and later destruction of vertebral bodies, poten-tial bony sequestra

– Potential spinal deformity in late course of thedisease

Fig. 17 Spondylodiscitis. Case 2. 37-year-old male withthoracic pain and elevated inflammatory markers. Initiallyperformed radiography showed decreased height of thedisc space and subtle erosions T8/9 (arrows in a). MRIrevealed the whole extent of the inflammatory process,involving disc space, vertebral bodies, and surroundingepidural and paravertebral tissue. The destruction of the

adjacent vertebral endplates is best detected with CT. (a)a.p. radiograph. (b) Sagittal fat-saturated T2-weightedMRI. (c) Sagittal T2-weighted MRI. (d) AxialT2-weighted MRI. (e) Sagittal T1-weighted MRI. (f) Sag-ittal gadolinium-enhanced T1-weighted MRI. (g) Axialgadolinium-enhanced fat-saturated T1-weighted MRI. (h)Sagittal CT reformat

Table 3 Suggested MRI pulse sequence protocol

Pulse sequence Orientation

Slicethickness(mm)

STIRw Sagittal orcoronal

3

T1w Sagittal 3

T2w Sagittal andaxial

3

Contrast-enhanced,fat-saturated T1w

Sagittal andaxial

3


Radiography– No pathologic findings within the first weeks– Osteolysis of endplates and later vertebral bod-

ies, osteosclerosis– Changes of paraspinal soft tissue density, for

example, by edema or gas inclusions– Late stage of the disease: spinal deformity

Treatment Monitoring: Follow-upScheme and Findings/Pitfalls

Pathological MRI findings in spondylodiscitisremain present for months or may even increasedespite sufficient antibiotic therapy. In particu-lar, compared with baseline MRI, follow-up

MRI more frequently show decreased vertebralbody height. Less frequently epidural enhance-ment, epidural canal empyema, and epiduralcanal compromise are observed in routinefollow-up MRI. But gadolinium-enhancementof vertebral body and disc space and bone mar-row edema often appear equivocal or evenworse compared with baseline MRI (Kowalskiet al. 2007; Baxi et al. 2012). Thus, a lack ofcorrelation between clinical follow-up statusand MRI can be observed (Baxi et al. 2012).At least, clinical worsening is never associatedwith improvement of MRI. Consequently, rou-tine follow-up is of limited value, but repetitionof MRI is always indicated, if the clinical statusdeteriorates.

Fig. 18 Spondylodiscitis. Case 3. 81-year-old male withlumbar pain and elevated inflammatory markers. Besidesspondylodiscitis T12/L1, with T2-hyerintense liquefactionof the disc space (b and c), and destruction of the vertebralbodies, MRI revealed bilateral abscesses in the psoas mus-cle (c and d). The destruction of the vertebral bodies is

demonstrated by CT (e and f). (a) Sagittal T1-weightedMRI. (b) Sagittal T2-weighted MRI. (c) Coronal STIR-weighted MRI. (d) Axial T2-weighted MRI. (e) SagittalCT reformat bone window. (f) Axial CT bone window. (g)Sagittal CT reformat soft tissue window. (h) Axial CT softtissue window


Differential Diagnosis

Tuberculous SpondylodiscitisThe differentiation of pyogenic from tuberculousspondylodiscitis is often difficult by clinical, aswell as radiological means, but is crucial forchoosing the appropriate therapy, as tuberculosisrequires antituberculous medication to reducemorbidity. Although pyogenic and tuberculous

spondylodiscitis often show differences in clinicalpresentation, laboratory, and imaging studies(Table 4), the specificity of all these parametersmay be relatively low. The clinical onset of symp-toms usually is acute in pyogenic, versus chronic,or prolongated in tuberculous spondylodiscitis.While clinical laboratory markers, particularlyC-reactive protein (CRP), erythrocyte sedimenta-tion rate (ESR), and leucocyte count, are highly

Fig. 19 Spondylodiscitis. Case 4. 82-year-old female sep-sis caused by Staphylococcus aureus. As lancinating painof the spine and progressive tetraparesis occurred, spinalMRI was performed. Spondylodiscitis L4/5 and L5/S1(arrows in b and d) was diagnosed, accompanied by

epidural empyema extending from cervical to lumbarlevel. (a and b) Sagittal T2-weighted MRI. (c and d)Sagittal gadolinium-enhanced fat-saturated T1-weightedMRI. (e and f) Axial gadolinium-enhanced fat-saturatedT1-weighted MRI


elevated in pyogenic spondylodiscitis, they arerelatively low, or only moderately elevated inmost cases of tuberculous spondylodiscitis. Fre-quent differences between both entities can beobserved, concerning number of involved seg-ments, involvement of intervertebral discs, andparavertebral soft tissue. In pyogenic spondylo-discitis, usually only one segment is affected, theintervertebral disc is involved early in the tempo-ral course, and paravertebral involvement revealsrather small epidural abscesses, in contrary totuberculous spondylodiscitis, often affecting sev-eral segments, late involvement of theintervertebral disc, and extended involvement ofthe paravertebral soft tissue, with often large, andfrequently calcified paraspinal abscesses(Fig. 20). In cases, when clinical symptoms,inflammation markers, blood cultures, and radio-logical studies are inconclusive, image-guidedbiopsy may be necessary to gain tissue for histo-logical, or even molecular examinations.

Differential Diagnostic Considerationsin Imaging of Inflammatory Diseasesof the Spine

The two major categories of inflammatory disor-ders of the spine are infectious and noninfectious.Infectious disease can be located in the spine itself,

or the surrounding structures. Hematogenousseeding is the most common cause of pyogenicand nonpyogenic infection, but direct inoculationis possible as well. Noninfectious inflammatoryconditions of the spine are systemic diseases thatcan be divided into two main categories, rheuma-toid disorders including rheumatoid arthritis, andseronegative spondylarthropathies.

Clinical, laboratory, and also imaging findingsin infectious and noninfectious, and even non-inflammatory, degenerative diseases of the spinemay overlap. Thus, clinical neuroradiology maynot lead to a definitive diagnosis, but to certainimaging patterns, and possible differentialdiagnoses.

Seronegative spondylarthropathies can be classi-fied in ankylosing spondylitis (Bechterew disease),the most frequent seronegative spondylarthropathy,or as psoriatic spondylarthritis, reactive arthritis(formerly termed Reiter syndrome), enteropathicspondylarthritis (associated with inflammatorybowel disease), and undifferentiatedspondylarthritis. Imaging findings of differenttypes of seronegative spondylarthropathies are sim-ilar and often nonspecific. Erosions, later sclerosis ofthe anterior corners of the vertebral bodies, knownas “shiny corner” sign, and T2-hyperintensities ofthe anterior corners of the vertebral bodies, so-called“Romanus lesions” are highly suggestive for anky-losing spondylitis. “Andersson lesions,” disc-relatederosions and irregularities of the central potion withsparing of the anterior and posterior part of theendplates, frequently occur in other seronegativespondylarthropathies as well. Squaring of vertebralbodies can be observed frequently, but is alsounspecific. First subtle, later bridging syn-desmophytes, are relatively specific for ankylosingspondylitis. In later stages of ankylosing spondylitis,fusion of facet and uncovertebral joints occurs, withthe endstage of ankylosing of the whole spine(“bamboo spine”) with decreased lumbar and cervi-cal lordosis and accentuated thoracic hyper-kyphosis, and consecutive loss of sagittal balance.Osteopenia is often present in ankylosing spondyli-tis, but is very unspecific.

Ossifications of the paravertebral ligaments,resulting in ankylosis of the spine, may occur innoninflammatory conditions as well, like diffuse

Table 4 Clinical, laboratory marker, and imaging differ-ences of pyogenic versus tuberculous spondylodiscitis

Pyogenic Tuberculous

Symptoms Acute Chronic

Clinicallaboratorymarkers ofinflammation

Highly elevated Relatively low, oronly moderatelyelevated

Involvedsegments

Usuallymonosegmental

Oftenpolysegmental

Involvementofintervertebraldisc

Early Late

Paravertebralinvolvement

Rather smallepiduralabscesses

Often largeparaspinalabscesses,frequentlycalcified


idiopathic skeletal hyperostosis (DISH), ossifica-tion of the posterior longitudinal ligament(OPLL), or ossification of the flava ligament(OFL).

Imaging differential diagnoses of spondylo-discitis/pyogenic vertebral osteomyelitis includeactivated osteochondrosis, and tuberculous spondy-litis. In spondylodiscitis, MRI is the method ofchoice, due to its superior soft tissue contrast.While narrowing of disc space, edema, later

osseous erosions and destruction of adjacent verte-bral bodies/ endplates, and diffuse gadolinium-enhancement of adjacent vertebral bodies mayoccur in degenerative conditions, like activatedosteochondrosis as well, disc hyperintensities onT2- and STIR-weighted images, diffusegadolinium-enhancement of vertebral discs, andparaspinal and epidural abscess or phlegmon arehighly sensitive for spondylodiscitis.

Fig. 20 Tuberculous spondylodiscitis with large psoasabscesses. 36-year-old African male with paraplegia. Poly-segmental involvement, (a–c), large abscesses in the para-vertebral soft tissue and the psoas muscles (d–f) alreadywere suggestive for tuberculous spondylodiscitis.CT-guided drainage of the psoas abscess (g) confirmedthe diagnosis. (a) Sagittal T2-weighted MRI. (b) Sagittal

T1 weighted MRI. (c) Sagittal Gadolinium-enhancedfat-saturated T1-weighted MRI. (d) Axial T2-weightedMRI. (e) Axial Gadolinium-enhanced T1-weighted MRI.(f) Coronal Gadolinium-enhanced fat-saturatedT1-weighted MRI. (g) CT-guided drainage of psoasabscess


In pyogenic vertebral osteomyelitis, usuallyonly one segment is affected, the intervertebraldisc is involved early in the temporal course, andparavertebral involvement reveals rather smallepidural abscesses, in contrary to tuberculousspondylodiscitis, often affecting several seg-ments, late involvement of the intervertebraldisc, and extended involvement of the para-vertebral soft tissue, with often large, and fre-quently calcified paraspinal abscesses.

Imaging findings in spondylodiscitis remainpositive even months after sufficient antibiotictherapy, but clinical worsening is never associatedwith improvement of MRI. Consequently, routinefollow-up in pyogenic vertebral osteomyelitis isof limited value, but repetition of MRI is alwaysindicated, if the clinical status deteriorates.

Thus, clinical neuroradiology alone may not becapable to lead to a definitive diagnosis, but cer-tain imaging patterns may contribute to possibledifferential diagnoses. Therefore, regarding clini-cal and laboratory findings, as well, is crucial forappropriate interpretation of imaging studies.

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Further Readings

Braun J, Bollow M, Sieper J. Radiologic diagnosis andpathology of the spondyloarthropathies. Rheum DisClin N Am. 1998;24(4):697–735.. Review

Ehara S, Shimamura T, Nakamura R, YamazakiK. Paravertebral ligamentous ossification: DISH,OPLL and OLF. Eur J Radiol. 1998;27(3):196–205.

Grigoryan M, Roemer FW, Mohr A, Genant HK. Imagingin spondyloarthropathies. Curr Rheumatol Rep. 2004;6(2):102–9.

Hong SH, Choi JY, Lee JW, Kim NR, Choi JA, KangHS. MR imaging assessment of the spine: infection oran imitation? Radiographics. 2009;29(2):599–612.https://doi.org/10.1148/rg.292085137.

Nascimento FA, Gatto LA, Lages RO, Neto HM,Demartini Z, Koppe GL. Diffuse idiopathic skeletalhyperostosis: a review. Surg Neurol Int. 2014;5(Suppl3):S122–5. https://doi.org/10.4103/2152-7806.130675.eCollection 2014

Paparo F, Revelli M, Semprini A, Camellino D,Garlaschi A, Cimmino MA, Rollandi GA, LeoneA. Seronegative spondyloarthropathies: what radiolo-gists should know. Radiol Med. 2014;119(3):156–63.https://doi.org/10.1007/s11547-013-0316-5.. Epub2013 Nov 22

Prodi E, Grassi R, Iacobellis F, Cianfoni A. Imaging inSpondylodiskitis. Magn Reson Imaging Clin NAm. 2016;24(3):581–600. https://doi.org/10.1016/j.mric.2016.04.005.


https://doi.org/10.1055/s-0034-1375569

https://doi.org/10.1055/s-0034-1375569

https://doi.org/10.1136/annrheumdis-2013-203582

https://doi.org/10.1136/annrheumdis-2013-203582

https://doi.org/10.1055/s-0035-1564696

https://doi.org/10.1055/s-0035-1564696

https://doi.org/10.1056/NEJMcp0910753

https://doi.org/10.1056/NEJMcp0910753

https://doi.org/10.1148/rg.292085137

https://doi.org/10.4103/2152-7806.130675

https://doi.org/10.1007/s11547-013-0316-5

https://doi.org/10.1016/j.mric.2016.04.005

https://doi.org/10.1016/j.mric.2016.04.005

inflammatoryandinfectiousdisorders of the spine … · of the spine imaging approach marcel wolf...

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