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Radiological imaging of degenerative and inflammatory disease of the spine. Dr/ ABD ALLAH NAZEER. MD.
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Abnormality in disc morphology. Disc degeneration can include drying, fibrosis, diffuse bulging, cracking, osteophytes etc. Therefore, by observing, it cannot be determined if it is only aging, or if they are pathological changes Sagittal T2-weighted image showing L5-S1 left foramen, intervertebral disc dehydration, shrinking of the conjugation foramen, and the anterior complex marginal osteophyte disc L5-S1.
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Disc degeneration.
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Annular fissure A fissure is the separation of the annular fibers insertion into the vertebral body. According to the orientation of the fibers it can be concentric, radial or transverse. The term fissure describes a spectrum of these lesions, and does not imply that the injury is the result of a wound. The terms "tear" and "annular rupture" are not recommended because they make direct reference to trauma. In radiological description and clinical diagnosis, the correct term that is recommended to be used is “annular fissure” Axial spin echo T2-weighted: Fissure concentric annular core L4-L5.
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Axial T2 WI: High signal intensity in annulus fibroses at medial position of L3- L4 disc suggestive of Annular Fissure(open white arrow). Narrowing of spinal canal & bilateral lateral recess with compression of bilateral exiting nerve roots noted.
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1 Concentric fissure. Fissure of the annulus characterized by separation of annular fibers in a plane roughly parallel to the curve of the periphery of the disc, creating fluid filled spaces between adjacent annular lamellae. Sagittal (A) and axial (B) T2-Weighted lumbar spine MRI image showing L4-L5 concentric fissure (arrows).
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2. Radial fissure Disruption of annular fibers extending from the nucleus outward toward the periphery of the anulus, usually in the vertical plane, with occasional horizontal components. Axial spin echo T2-weighted: Radial fissure L4-L5.
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3. Transverse fissure Fissure of the anulus in the axial plane, usually limited to rupture of the outer annular attachments to the ring apophysis Sagittal T2-weighted: Transverse fissure.
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Bulging", by definition, is NOT considered a form of herniation. Bulging is sometimes a normal variant (usually at L5-S1); can result from advanced disc degeneration or from vertebral body remodeling (as consequent to osteoporosis, trauma, or adjacent structural deformity); can occur with ligamentous laxity in response to loading or angular motion; can be an illusion caused by posterior central subligamentous disc protrusion; or can be an illusion from volume averaging (particularly with CT axial images).
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T2 Weighted Axial MR Image: L3-L4 Disc bulge. Narrowing of spinal canal and bilateral recess (open white arrow) with compression of exiting nerve roots is present. Ligamentum flavum appears thickened (solid white circle) with bilateral facetal arthropathy.
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CT and MRI images for diffuse disc bulge.
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Abnormalities in disc morphology. Herniation: Localized displacement of the disc material beyond the edge of the disc. Displacement can only occur in association with disruption of the normal annulus or, as in the case of intervertebral herniation. A break in the vertebral body endplate. Herniated nucleus pulposus is inaccurate because disc material other than nucleus (cartilage, fragmented apophyseal bone and fragmented annulus) are common component of the displaced disc material.
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Disc Herniation Is defined as a localized (<25% or 90º of disc circumference) displacement of disc material beyond body endplates or apophysis. The location of the hernia is described as central, right/left subarticular, right/left foraminal and right/left extraforaminal Disc hernia nomenclature: central (blue); subarticular (yellow); foraminal (red); extraforaminal (green).
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Axial T1WI (A) and T2WI (B-D). A,B,C: Broad based posterior-central disc herniation producing moderate canal stenosis and left lateral recess stenosis (arrowheads in B). The base of the herniated disc represents about 56º of the disc circumference. D: another patient with narrow based central disc hernia.
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Migration: displacement of the herniated material away from the opening in the annulus through which the material has extruded. There is connection with the disc of origin. Can occur cranial or caudal at different levels. Although less frequently, migration can occur in the axial plane (paracentral, foraminal, extraforaminal or posterior epidural). Intradural migration occurs in less than 1% of hernias and its diagnosis sometimes cannot be made on imaging. A beaklike like contour of the intrathecal herniated material is considered characteristic.
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Sagittal T2WI in two different patients (A,B). Examples of cranial migration of disc hernias reaching the pedicle level (pedicles not shown).
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Disc herniation with caudal migration.
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Disc sequestration. Note the inferiorly migrated fragment (arrows) that has lost its continuity with the parent L4-L5 disc.
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Left postero-lateral disc herniation at C6-7 level.
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These terms (“protrusion” and “extrusion”) do NOT imply knowledge of the mechanism by which the changes occurred and thereby DIFFER from definitions that base the distinction on whether and how disc material has passed through a defect in the annulus. Protrusion : The greatest distance , in any plane between the edge of the disc material beyond the disc space is less than the distance between the edges of the base in the same plane. The base is defined as the cross- sectional area of disc material at the outer margin of the disc space of origin, where disc material displaced beyond the disc space is continuous with disc material within the disc space.
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Disc Osteophyte Complex This is a displacement of the intervertebral disc (bulging, protrusion or extrusion) associated with calcification or ossification crests. It is important to distinguish between marginal and non- marginal osteophyte, considering that marginal osteophyte protrudes from the vertebral endplate margins and non-marginal osteophyte protrudes from sites other than vertebral endplate margins. The terms ossified disc, hard disc, and chronic disc herniation, are not recommended. This new classification was implemented in the lumbar spine. Sagittal CT, axial, scheme: In L4-L5 Disk Osteophyte Complex left with decreased range of lateral recess on the same side.
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Vertebral body marrow changes (Modic's classification) Reactive vertebral body modifications associated with disc inflammation and degenerative disc disease, as seen on MR images. Type 1 refers to decreased signal intensity on T1-weighted spin-echo images and increased signal intensity on T2-weighted images. Type 2 refers to increased signal intensity on T1-weighted images and isointense or increased signal intensity on T2-weighted images. Type 3 refers to decreased signal intensity on both T1 and T2-weighted images. Sagittal T1-weighted (A) and sagittal T2- weighted (B) images showing vertebral body marrow changes Modic type 1 (arrows).
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Sagittal T2-weighted (A) and sagittal T1- weighted (B) images showing vertebral body marrow changes Modic type 2 (arrows). Sagittal T2-weighted (A) and sagittal T1- weighted (B) images showing vertebral body marrow changes Modic type 3 (arrows).
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Calcified disc Calcification within the disc space, not inclusive of osteophytes at the periphery of the disc space. Plain X-rays of lumbosacral spine (lateral and anteroposterior views) showing T9-T10 intervertebral disc calcification.
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Intravertebral herniation. A disc displacement in which a portion of the disc projects through the vertebral end plate into the centrum of the vertebral body. Intervertebral herniation at L3 superior endplate (white arrows) on T1-weighted (A), T2-weighted (B) and STIR (C) Images.
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Limbus vertebra. Separation of a segment of rim of vertebral body ring apophysis. Sagittal T1- weighted images demonstrate a limbus vertebra in the anterosuperior corner of L2,L3 and L4 vertebral bodies.
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Lumbar spinal canal stenosis central canal stenosis. lateral recess stenosis. neural foramen stenosis. Central canal stenosis central canal stenosis can be: 1) Congenital: e.g., short pedicle syndrome, achondroplasia 2) Acquired: usually degenerative and almost always the result of several degenerative processes occurring in concert. Normal canal > 15mm. Stenosis(a)relative stenosis :13- 14mm. (b)absolute stenosis >12 mm.
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CT sagittal (A) and axial (B) images and corresponding axial T2WI (C). Diffuse disc bulging with a concomitant disc hernia cranially migrated to the pedicle level (arrowheads). Secondary severe canal stenosis, given the CSF absence around the nerve roots.
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Sagittal and axial T2WI (A,B) and axial T1WI (C). Degenerative retrolisthesis, diffuse disc bulging, epidural fat hypertrophy and secondary severe central canal stenosis.
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Qualitative grading of lumbar spinal stenosis to Schizas classification. Mild stenosis: there is dural sac area reduction with sufficient CSF surrounding the rootlets. Moderate stenosis: dural sac reduction and almost complete loss of perineural CSF. Rootlets are still visible. Severe stenosis: no rootlets nor CSF can be individualized. Dark dural sac on MRI. Posterior epidural fat present. Extreme stenosis: severe stenosis with loss of posterior epidural fat.
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MRI scan showing cervical spondylosis and multi-level spinal canal stenosis and cord compression.
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(a) T2 weighted sagittal MRI of a 68- year-old gentleman with significant spinal cord compression and signal change. (b) T2 weighted sagittal MRI of a 56-year-old patient with significant spinal cord compression without signal change.
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Osteoarthritis of the facet joints.
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Osteoarthritis of the facet joints.
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Osteoarthritis of the facet joints with vacuum phenomenon.
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Osteoarthritis of the facet joints with vacuum phenomenon.
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Degenerative synovial cyst.
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Degenerative synovial cyst.
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Degenerative synovial cyst.
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Hypertrophy of the ligamentum flavum.
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Ossification of the ligamentum flavum.
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Hypertrophy of the ligamentum flavum.
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DISH.
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OPL.
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OPL.
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Lateral Recess Stenosis: LRS can be produced by the combined action, in variable proportion, of degenerated discs and osteophytes and hypertrophic facet joints and ligament flava. Although we don’t routinely use a grading system, Bartynski developed an interesting and illustrative MRI classification as follows Grade 0: normal LR in which the nerve root is bathed in cerebrospinal fluid. There is no contact to the adjacent structures. Grade 1: LRS without root deformation. Grade 2: LRS with root flattening and some CSF present in the lateral recess. Grade 3: LRS with root flattening with complete obliteration of any CSF at the lateral recess.
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Axial T2WI. Bilateral facet joint osteoarthritis with right synovial cyst (arrow) producing right lateral recess stenosis.
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The lateral recess is delimited between the more medial margin of the superior facet process (or ligamentum flavum if hypertrophic) and the vertebral posterior wall or herniated disc. Lateral recess stenosis produces descending root impingement (red dots in diagram), generating radiculopathy in the inferior level (i.e.; L4-5 lateral recess stenosis, L5 symptoms).
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Foraminal Stenosis: Stenosis of the neuroforamen is usually the result of: disc material and osteophytes protruding within neural foramen, facet osteoarthritis, ligamentum flavum hypertrophy and spondylolisthesis. When symptomatic it produces radiculopathy. Grade 0: absence of foraminal stenosis Grade 1: mild foraminal stenosis showing perineural fat obliteration in the two opposing directions, vertical or transverse. Grade 2: moderate foraminal stenosis showing perineural fat obliteration in the four directions without morphologic change, both vertical and transverse directions. Grade 3: severe foraminal stenosis showing nerve root collapse or morphologic change.
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Mild stenosis: partial perineural fat obliteration due to ligamentum flavum hypertrophy or disc/osteophytic protrusion. Moderate stenosis: complete perineural fat obliteration. Severe stenosis: nerve root collapse or deformation in the foraminal zone due to extrinsic compression.
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Sagittal T1WI (A) and T2WI (B). Moderate foramen stenosis. A certain amount of perineural fat remains. On T2WI it may be difficult to differentiate perineural fat and the signal from small amounts of perineural fluid.
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Sagittal reformatted CT depicts the osteophyte component in this L5-S1 severe foraminal stenosis. Although nerve root is not clearly seen in the foramen, the foraminal fat is lost at the roof of the foramen
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Listhesis refers to the displacement of a vertebral body relative to the inferior one, anterolisthesis when anterior slippage occurs and retrolisthesis when the slippage occurs backwards. When related to degenerative changes is called spondylolisthesis, often associated with canal stenosis. Meyerding classification of anterolisthesis. Grade I: < 25% displacement of vertebral body. Grade II: 25-50% displacement of vertebral body. Grade III: 50-75% displacement of vertebral body. Grade IV: 75-100% displacement of vertebral body. Grade V: spondyloptosis. The entire vertebral body lies beyond the inferior one.
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Grade I lytic spondylolisthesis.
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Grade II lytic spondylolisthesis.
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Degenerative grade II spondylolisthesis and severe central canal stenosis. Note the pronounced facet joint hypertrophy.
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Grade II1 spondylolisthesis
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Baastrou’s disease.
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SPINAL INFECTION: CRITICAL FINDINGS AND PROGNOSTIC FACTORS Spinal infection encompasses several entities that have characteristic presentations and clinical courses. These can be pyogenic (bacterial), granulomatous (tuberculosis or fungal) or parasitic (Echinococcosis). Pyogenic spinal infection can be thought of as a spectrum of disease comprising spondylitis, discitis, spondylodiscitis, pyogenic facet arthropathy, and epidural abscess. Mortality associated with spinal infections has significantly decreased to <5% in developed countries and early mortality is generally related to uncontrolled sepsis. Epidural abscess can complicate a pyogenic infection of the spine. Spinal epidural abscess (SEA) is a collection of pus or inflammatory granulation tissue between the dura mater and the surrounding fatty tissue. SEA is a rare entity. If it is not diagnosed and treated promptly, it results in high morbidity and mortality. Spinal epidural abscess is one of the most morbid and mortal diseases among spinal infections, and its prognosis is the worst among these diseases.
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Diagnostic workout Imaging evaluation of patients with suspected spinal infection begins with plain films. Initial plain radiographs may be normal but, as infection spreads from the disc space to one or both adjacent vertebral bodies, end-plate erosion occurs, then, disc space collapse and it begins destruction of the vertebral body adjacent to the disc. Sequelae changes of vertebral body can predispose instability. CT provides information about the extension of disease referring to bony destruction and differentiating infection from other spinal lesions as tumors or vascular lesions. Nevertheless in cases without concomitant bony changes in the affected level or the adjacent vertebrae, CT scan alone can not rule out an infectious compromise or the presence of spinal epidural abscess. Magnetic resonance imaging is the diagnostic method of choice. It allows to establish the diagnosis and rule out other differential diagnoses. Bony infections or abscesses in the paravertebral soft tissue can be visualized and the extent of the infection can be determined.
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54 year old patient undergoing febrile syndrome and lumbar pain studies. CT shows no relevant findings. Same-day MRI shows inflammatory process in L1-L2 segment compatible with spondylodiscitis. There is dural thickening with anterior epidural abscess.
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Lumbar radiography showing anterior osteophytic formations in the lower and lumbar dorsal vertebral bodies, decreased intervertebral space predominantly in L1-L2 and L2-L3 segments and vertebral collapse. Insufficiency fracture is suggested. Same day MRI showing L1-L2 spondylodiscitis and epidural abscess extending from L1 to L4.
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50 year old man under investigation of intense cervicodorsal pain and bacteremia. Gammagraphy showing focal increase of uptake in the right facet joint C3–C4, indicating arthritic changes. Cervical spine MRI showing changes of spondylodiscitis of C5–C6, with anterior epidural abscess and significant dural reaction that narrows the spinal canal, causing compression myelopathy. Despite the marked inflammatory changes in the MRI, there were no such findings in the Gammagraphy , showing its low sensitivity in spondylodiscitis diagnosis.
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Contrast enhanced MRI Showing C5-C6 spondylodiscitis complicated with spinal epidural abscess extending from C4 to C7. MRI T1C and axial 3D fiesta sequence, showing anterior cervical medullar cord compression from spinal epidural abscess, with thecal sac compression (Arrows) more than 50%. No neurologic deficits was seen. Note how, in cervical spine, a moderate amount of epidural collection can cause a markedly medullar compression when compared to lumbar or thoracic spine.
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Patient 22 months old, with trauma antecedent. The patient is taken to the emergency department complaining ambulation limitation and local lumbar pain that persists even after pain relievers. Top row. Contrast enhanced MRI, shows inflammatory changes at L4-L5 level. Patient is diagnosed spondylodiscitis. Antibiotic was therapy started. Bottom row. Mild improvement of inflammatory signs after established antibiotic therapy. The patient ambulate within 5 days of treatment. He had no neurologic sequels in follow up.
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Inflammatory process comprising T8-T9 segment with paravertebral collection and epidural empyema, however, despite extensive inflammatory changes, there is thecal space enough to not cause myelopathy, unlike the cervical spine.
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Control contrast enhanced MRI shows extensive intradural and epidural abscesses and vertebral bodies inflammatory changes.
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a. Non contrast enhanced MRI shows bone marrow edema and enhancement of T2-T3 with preserved disco vertebral space, compatible with spondylodiscitis. b. Contrast enhanced shows progression of inflammatory changes with epidural spinal abscess and signs of myelopathy. Soft tissues compromise have increased. c. Scoliotic anterior curve increase within 7 days indicating spine instability d. Postsurgical changes showing, T3 – T4 fixation and lateral osteosynthesis.
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Spondylodiscitis at T8-T9 level with lithic changes on the adjacent vertebral bodies. Those changes are associated with formation of prevertebral collection and epidural empyema that rejects the thoracic thecal sac and the medulla. There are no signs of compressive myelopathy.
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T8-T9 tuberculosis spondylodiscitis, paraspinal and epidural abscesses. There is vertebral collapse of T8 vertebral body and great compression of the spinal cord with signs of myelopathy.
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Inflammatory changes in C5-C6 segment with anterior epidural abscess and dural thickening. There is a decrease of approximately 60% of the amplitude of the teal sac causing spinal cord compression and signs of myelopathy. The patient lasted 1 week with a slight decrease in the osteotendinous reflexes that were then fully recovered.
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Cervical MRI showing Inflammatory process involving mainly the C3-C4 and C4-C5 segments, associated with anterior prevertebral abscess that extends from C2 to T1. There is great risk of mediastinal extension and secondary mediastinitis. Same patient thoracic MRI showing extension of the prevertebral abscess (Arrows) from the cervical segments to thoracic prevertebral segments.
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MRI STIR sequences 2 weeks follow up, showing Inflammatory changes that compromise the entire thoracic vertebral body at T2 and T3 levels and prevertebral abscess. Progressive follow-up demonstrates progression of anterior scoliosis deformity, even after drainage surgery (arrow).
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Patient of 62 years with paraparesis of lower limbs. Contrast resonance of thoracic spine showing extensive anterior epidural abscess extending from T5 to lumbar segments. There is a significant decrease in the amplitude of the spinal canal at the T5 level and there are also signs of myelopathy. The patient fully recovered from his motor deficit after 8 months of follow-up.
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A 63-year-old patient with a history of chronic renal failure. Decreased sensitivity of the left lower limb. The images show the spondylodiscitis at C4-C5 segments and epidural and prevertebral abscess and signs of myelopathy. The patient was taken to surgical management. Staphylococcus aureus meteciline sensitive strain was isolated. Patient fully recovered of left lower limb sensitivity after 1 year follow up.
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CT showing lytic lessons on T1 - T2 vertebral bodies. Lytic metastases were suspected. MRI showing multiple lytic lessons in lumbar (Not showing) and thoracic spine, those lessons are low signal in T1, high signal in T2, high signal in fat saturation sequences and they had contrast enhancement. Those lesions where interpreted as metastatic lytic lesions on MRI.
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Thank You.