Musculoskeletal involvement of TB is estimated in 1–13 % of patients and spine is affected in more than 50 % of cases. Spinal tuberculosis is a destructive form of tuberculosis- Spondyodiscitis . Tuberculous infection of the spine - Pott’s disease/ Pott’s spine. The term ‘Pott’s paraplegia’ - paraplegia resulting from tuberculosis of the spine. The lower thoracic and upper lumbar spine are most frequently involved sites.
WHOLE SPINE Cervical – 12% Thoracic -42% Thoracolumbar-12%- most frequently involved Lumbar-26% Lumbosacral-3% Sacral Cervico –dorsal – 5% Regional distribution of spine TB
PATHOGENESIS & PATHOLOGY: Predisposing factors --- poverty, overcrowding, illiteracy, malnutrition, alcoholism, drug abuse, diabetes mellitus, immunosuppressive treatment, and HIV infection. Hematogenous spread of M. tuberculosis into the dense vasculature of cancellous bone of the vertebral bodies. Pulmonary / GU TB as primary source. Infection spreads either from arterial (Subchondral arterial arcade) or venous route ( Batsons venous plexus)
Spinal tuberculosis is initially apparent in the anterior inferior portion of the vertebral body. Later on it spreads into the central part of the body or disk. Young patients Older patients Disc – primarily involved because it is more vascularized Disc is not primarily involved because of its age related avascularity . In spinal tuberculosis, there is involvement of more than one vertebra because its segmental arteries bifurcate to supply two adjacent vertebrae.
In spinal tuberculosis, characteristically, there is destruction of the vertebral bodies and adjacent disc spaces, collapse of the spinal elements, and anterior wedging leading to the characteristic angulation and gibbus (palpable deformity because of involvement of multiple vertebrae) formation. More than one vertebra is typically affected, and the vertebral body is more frequently affected than the posterior arch.
A lack of proteolytic enzymes in mycobacterial infection has been suggested as the cause of subligamentous spread of infection and there is relativey late involvement of the disc. Early disc involvement due to highconcentration of the protelolytic enzymes . TB SPONDYLODISCITIS PYOGENIC SPONDYLODISCITIS
Type of involvement Mechanism of involvement PARADISCAL Spread of disease via the arteries CENTRAL Batsons plexus of veins ANTERIOR Abscess extension beneath the ALL and the periosteum. POSTERIOR Posterior external venous plexus of vertebral veins or direct spread SKIPPED LESIONS Batsons plexus of veins SYNOVIAL Hematogenous spread through sub synovial vessels
CLINICAL FEATURES: Local pain, tenderness, stiffness and spasm of the muscles. Cold abscess, gibbus. Slow and insidious progression. Constitutional symptoms (fever and weight loss) are also common but not as pronounced as with bacterial discitis/osteomyelitis. Atlanto -axial tuberculosis may present as torticollis. Neurologic deficits are common with involvement of thoracic and cervical regions. Left untreated, early neurologic involvement may progress to complete paraplegia or tetraplegia .
PARAPLEGIA EARLY ONSET LATE ONSET Active stage and requires active treatment. Better prognosis and is frequently seen in adults 2-3 decades a fter active infection. It is often associated with marked spinal deformities. Mechanical pressure. Tuberculous granuloma Tuberculous myelitis Spinal artery thrombosis Tuberculous arachnoiditis Transection of spinal cord by bony bridge -severe kyphosis. Fibrosis of dura (pachymeningitis) Formation of tough, fibrous membrane encircling the cord
X-RAY : Tuberculous spondylitis can be difficult to detect in early stages because of relative preservation of the disc space. Approx 1/3 rd of calcium must be lost from a particular area for osteolysis to be appreciated radiographically . A reduction in vertebral height is often seen with the irregularity of the anterosuperior endplate being relatively early and subtle sign. Due to the subligamentous extension, there may be some irregularity of the anterior vertebral margin. This is a classical appearance with TB spondylitis . Later, paraspinal collections can develop which can be remarkably large. Calcification in paraspinal masses is highly suggestive of TB . However, the height of disc space can be preserved until the later stages.
X-rays oblique view and axial CT scan show early erosive changes typically located in the anterolateral corner of the vertebral body
C-spine lateral view - narrowing at the C3-C4 level with thickening of the soft tissue in front of the cervical column (pre-vertebral soft tissue) containing foci of air .
Collapse of D9 with bulging of the paraspinal lines – Paraspinal abscess.
Cross-sectional imaging is required to assess better the extent of involvement and particularly for the presence of an epidural component and cord compression. MRI is the modality of choice for this, with contrast CT being a second choice.
CT : 4 types of V. body destruction -fragmentary, osteolytic , subperiostal and localized (sclerotic ), Fragmentary type predominates and consists of numerous residual bony fragments which frequently migrate into soft tissue masses. It is strongly suggestive of TB. Other findings include soft tissue involvement and paraspinal tissue abscess. CT helps in the demonstration of any calcification within the cold abscess, - visualizing epidural lesions containing bone fragments, - in the delineation of encroachment of the spinal canal by posterior extension of inflammatory tissue, bone or disc material. - and in the CT-guided biopsy
Axial CT scan shows the fragmentary bone pattern. Large para spinal soft tissue abscesses with initial calcification of the wall. Findings suggestive of spinal TB.
Calcified psoas abscess in a patient with tuberculous spondylitis Partially calcified right paravertebral soft-tissue mass, with expansion and bowing of the right psoas shadow , displacement of right kidney. CT scan shows vertebral destruction and a calcified right psoas abscess Axial T2W MR image demonstrates the calcified abscess with low signal intensity, along with associated vertebral destruction .
MRI: Signal changes occur early in the development of the disease, when no other image modality shows lesions. STIR sequence detects initial infective focus as inflammatory edema. It enables anatomic localization of the disease in different planes, allows early detection of disc and bone destruction, and depicts extension in bone and soft tissues, and assesses skip lesions in noncontiguous spinal TB. Four different MRI patterns of disease are found in vertebral TB: paradiskal , anterior, central and posterior lesions.
PARADISCAL: This is the most common pattern of spinal tuberculosis. Paradiscal infection begins in the vertebral metaphysis , eroding the cartilaginous end plate, leading to disc space narrowing due to the infection itself or to disc herniation into the end plate. Due to osseous resorption , end plate demineralization with loss of cortical bone. Compared to pyogenic spondylitis , TB typically shows more sharply destructive margins with absence of reactive sclerosis
Replacement of bone marrow by inflammatory exudates, cells and hyperemia . Vertebral bodies on T1W – low T2W and STIR sequence – high. The infected disc appears as decreased space showing blurring of the bone limits. On T2W- disc exhibits a very-high signal. With gadolinium the infected disk enhancement is obvious, allowing differentiation of the non-affected part.
sagittal images of thoracic spine - Paradiscal lesions with disc space narrowing which is a typical presentation of tuberculosis spine T1 W T2 W STIR Post contrast T1W
The spreading of infection into the surrounding soft tissues is common, and usually progresses in anterolateral direction. Abscess and collections - low signal intensity on T1-weighted images. high signal intensity on T2-weighted sequence. However, mixed signal intensity on both T1- and T2-weighted images can be seen in phlegmons . There is a thin smooth wall contrast enhancement in cases of abscess, whereas the phlegmon shows uniform enhancement.
Axial , sag -- dorsal vertebral end plate erosion with involvement of intervening disc, pre/ paravertebral collection and granulation tissue. Significant anterior epidural granulation tissue seen causing cord compression . T2 Post contrast T1
ANTERIOR: The infection starts in the corner of the vertebral body, it spreads to the adjacent vertebrae underneath the anterior longitudinal ligament . MRI findings consist of a subligamentous abscess with contrast enhancement, preservation of the disks, and abnormal signal involving multiple vertebral segments with heterogeneous signal intensity
Anterior subligamentous granulation tissue with involvement of anterior aspects of vertebral bodies and sparing of intervertebral discs. Subligamentous dissemination stripes the periostium and the anterior longitudinal ligament from the vertebral surface. Periostium stripping makes the avascular vertebrae more vulnerable to infection Sag STIR
CENTRAL: Affects single vertebral body and if the infection progresses, the whole vertebral body collapses. This is commonly confused with malignancy . The disc remains healthy as the nutrition is provided from the adjacent vertebra. Infection progresses to the contiguous vertebra or to the paraspinal space. MRI in this stage shows hypointense T1-weighted signal in a single vertebra and vertebral collapse with disc preservation.
: Central lesion. Sagittal T2w (A), T1w (B) and Post contrast sagittal T1w (C,D) images shows abnormal marrow signal intensity in dorsal vertebral with heterogeneous post contrast enhancement with sparing of adjacent discs and vertebral bodies. Associated peripherally enhancing anterior epidural abscess seen causing cord compression. 6 / 19 Central lesion ---Abnormal marrow signal intensity in dorsal vertebral with heterogeneous post contrast enhancement with sparing of adjacent discs and vertebral bodies. Associated peripherally enhancing anterior epidural abscess seen causing cord compression. T2 T1 Post contrast T1
Central pattern. Sagittal T2 and T1-postcontrast weighted imaging show vertebral involvement and disk preservation. Anterior epidural abscess spreading to the adjacent vertebral bodies .
POSTERIOR: Least common of all the types, as TB rarely affects the vertebral arch. When affected, the radiological pattern is frequently difficult to differentiate from metastasis, especially when disk space is preserved. This occurs in only 5% of cases, and biopsy may be necessary for the confirmation of the diagnosis
Posterior lesion. Sagittal T2 , T1 , axial T2 and post contrast axial T1 images shows destruction of lamina of L5 vertebra with associated peripherally enhancing collection seen causing spinal canal stenosis .
Posterior pattern. Axial T2-weighted imaging shows a large cold abscess located in soft tissues and associated bone infection involving vertebral arch and costovertebral joint
SKIPPED LESIONS: Usually, two or more contiguous vertebrae are involved in spinal tuberculosis owing to hematogenous spread through one intervertebral artery feeding two adjacent vertebrae. Non-contiguous multifocal tuberculous spondylitis is rare and results from spread of infection from valveless Batsons venous plexus
M ultifocal skipped involvement of upper dorsal, dorsolumbar vertebra with multiple vertebral destruction, prevertebral and anterior epidural collection with compression of spinal cord and cauda equina . Coronal STIR image show large bilateral psoas abscess STIR T1 STIR
Type of involvement Radiological appearances PARADISCAL Involves adjacent margins of two consecutive vertebrae. The intervening disk space is reduced. CENTRAL Involves central portion of a single vertebra; proximal and distal disk spaces intact. ANTERIOR Begins as destructive lesion in one of the anterior margins of the body of a vertebra, minimally involving the disk space. POSTERIOR Involves posterior arch without involvement of vertebral body SKIPPED LESIONS circumferentially involvement of two noncontiguous vertebral levels. SYNOVIAL Involves synovial membrane of atlanto -axial and atlanto -occipital joints
SPINAL MENINGEAL TUBERCULOSIS TUBERCULAR LEPTOMENINGITIS WITH ARACHNOIDITIS: Three possible pathogenesis for the occurrence of spinal TB arachnoiditis are the following: 1. TB lesion primarily arising in the spinal meninges 2. Extension of TB spondylitis 3. Downward extension of intracranial TBM (Most common) On imaging, diffuse spinal leptomeningeal , cauda equina thickening and enhancement seen. Thick enhancing exudates can be seen in lumbar spinal canal causing clumping of the cauda equina . Frequently, concomitant cranial tubercular meningitis with basal exudates and granulomata can be seen
Leptomeningitis - Sagittal post contrast T1w images show smooth enhancement of spinal leptomeninges with small ring enhancing granuloma along posterior surface of dorsal cord.
Arachnoiditis -- Sag & axial post contrast images- abnormal leptomeningeal and cauda equina enchancement with enhancing exudates seen in lumbar subarachnoid space. Post contrast cervical spine images of the same patient - significant exudates and granulomas in posterior fossa and in cervical spine.
HYPERTROPHIC PACHYMENINGITIS: Unique entity characterized by fibrosis and thickening of dura mater resulting in neurological dysfunction. It could be idiopathic or due to variety of inflammatory and infectious conditions. Tubercular pachymeningitis is uncommon manifestation of spinal tuberculosis. On MRI, thickened dura appears isointense or hypointense on T1WI and hypointense on T2WI sequence with thick post contrast enhancement Sag post contrast T1w - thick pachymeningeal enhancement with mild posterior epidural abscess causing cord compression.
ARACHNOIDITIS OSSIFICANS : Rare cause of chronic, progressive myelopathy. In contrast to the more common benign causes of meningeal calcification, arachnoiditis ossificans results in replacement of portions of the spinal arachnoid by bone as an end-stage complication of adhesive arachnoiditis. The findings of intraspinal ossification on CT are characteristics and diagnostic.
Spinal arachnoiditis ossificans. Follow up case of craniospinal tuberculosis show long segment T2 hypointense pachymeninges i.e.,areas of dural calcification on axial CT.
SPINAL CORD TUBERCULOSIS Spinal intramedullary tuberculoma and abscess present as spinal tumour syndrome and are very rare. They mimic intramedullary tumour in symptomatology with a rapidly advancing course. On imaging, they have similar characteristics as intracranial tuberculomas with solid caseating granulomas showing T2 hypointensity and ring enhancement . They can be a manifestation of military tuberculosis .
Conus medullaris tuberculoma . Intramedullary T2 hypointense lesion in conus medullaris with thick rim enhancement and significant perifocal cord edema suggesting Tuberculoma with solid caseation . Associated pulmonary tuberculosis changes can be seen on coronal post contrast images T2 Post contrast
Sagittal T2 & Post contrast T1 shows multiple small T2 hypointense intramedullary ring and nodular enhancing tuberculomas.
Tuberculous myelitis : U sually associated with tuberculous intracranial involvement of the meninges or brain parenchyma or with tuberculous arachnoiditis of the spine. It can manifest as acute transverse myelitis . In majority of patients, it affects >1 spinal segment, m/c- thoracic and cervical region. Occasionally, may affect the entire length of the spinal cord. An abnormal immune reaction against mycobacterial antigen is thought to be the main pathogenic mechanism. On imaging, Tuberculous myelitis shows long segment cord swelling with T2 hyperintensity and T1 iso to hypointensity and patchy segmental enhancement on post-contrast images. Chronic Myelitis can shows long segment myelomalacic changes or syringohydromyelia .
Sequel of Tubercular myelitis with calcific and enhancing active tubercular granulomas and long segment syrinx. Areas of pachymeningeal thickening and T2 hypointense calcifications
TUBERCULAR PYOGENIC Course Insidious rapid Location Lower thoracic, upper lumbar lumbar Disc Late involvement Early involvement Destruction of bone Partial Rapid Abscess Thin walled abscess with rim enhancement Thick walled para spinal abscess with homogenous enhancement Sclerotic reaction No/little More Posterior element involvement Yes Rarely involved. Enhancement Focal Diffuse Osteoporosis pronounced Less
Pyogenic spondylodiscits : Mild hyperintense signal on STIR Involvedendplates and increased fluid signal in L3-L4 disc. After 2 weeks - Marked hyperintense signal on STIR , Destruction of endplates and increased fluid signal in L3-L4 disc. After 2 months - Marked hyperintense signal on STIR , increased endplate destruction and fluid signal in L3-L4 disc.
Brucellosis: Zoonotic infection that is caused by small Gram-negative bacilli. Handling contaminated animal products or from unpasteurized milk. The musculoskeletal system - spine –m/c. M/C - lumbar spine. The pedicles are normally spared but the mineral bone density is decreased. Gas in discs or the vertebral body is also a characteristic finding in brucellar spondylitis . No deformity or gibbus . Minimal paraspinal soft tissue component.
A 37‑year‑old lady presented with fever and low back pain. T1, T2 sag - edema in the L2 vertebral body with air/gas, hypointense on T1 and hyperintense on T2 images. STIR - hyperintensity within L2 vertebral body and heterogeneous signal of abscesses in bilateral psoas with air/gas. CT confirmed the air/gas in the vertebra, psoas abscess and also showed generalized decreased density of the bones. Blood culture confirmed the diagnosis of brucellar spondylodiscitis
Metastsis : The common primary tumor with usual metastasis to spine is often from the lung ranging from 14%–31% and thoracic segments are the most common location for metastases compared to other vertebra. A destructive bone lesion associated with a well-preserved disc space with sharp endplates or the involvement of only one vertebral body or posterior elements suggests neoplastic infiltration.
THANK YOU
QUESTIONS?? Most common site and Route of spread of spinal TB ? Patterns of involvement ? Spectrum of findings in spinal TB? X-ray findings in spinal TB ? DD’s for spinal TB ? Differences between pyogenic and tubercular spondylodisitis ? Features of brucellar spondylitis ?