Spectrum of MR Imaging Findings in Spinal Tuberculosis
Tuberculosis, caused by Mycobacterium tuberculosis, remains a major public health hazard, especially in developing countries in which poverty, malnutrition, and the presence of drug-resistant strains have combined to aid the spread of the disease. Infection with HIV increases the risk of reactivation of dormant tuberculosis and the risk of acquiring the primary infection. In those coinfected, a high frequency of extrapulmonary disease has been observed [1, 2]. tuberculosis of the spine accounts for more than 50% of musculoskeletal tuberculosis [3]. In the developing countries, the disease commonly afflicts children and young adults and tends to be more aggressive in extent and abscess formation. Consequently, neurologic complications and spinal deformities are seen frequently [4]. In the developed countries, musculoskeletal tuberculosis is uncommon, but its incidence is reported to be greater in older individuals [2]. The relative rarity and varied presentations of spinal tuberculosis pose diagnostic difficulty, warranting its inclusion in the differential diagnosis of any spinal disorder [4]. However, immigration, an aging population, and the association of spinal tuberculosis with HIV infection can be expected to increase its prevalence. MR imaging is usually performed to evaluate suspected spinal abnormalities, and the disease may first be detected when symptomatic patients undergo this examination. The purpose of our pictorial essay is to review the various typical and atypical findings of spinal tuberculosis on MR imaging. All patients included were HIV negative.
Pathology
Spinal tuberculosis is usually a secondary infection from a primary site in the lung or genitourinary system. Spread to the spine is thought to be hematogenous in most instances. Tuberculosis infection is characterized by a delayed hypersensitivity immune reaction. The first stage is a pre-pus inflammatory reaction with Langerhans' giant cells, epithelioid cells, and lymphocytes. The granulation tissue proliferates, producing thrombosis of vessels. Tissue necrosis and breakdown of inflammatory cells result in a paraspinal abscess. The pus may be localized, or it may track along tissue planes. Progressive necrosis of bone leads to a kyphotic deformity. Typically, the infection begins in the anterior aspect of the vertebral body adjacent to the disk. The infection then spreads to the adjacent vertebral bodies under the longitudinal ligaments. Noncontiguous (skip) lesions are also occasionally seen [4, 5].
Site
Patterns of Vertebral Involvement
The primary focus of infection in the spine can be either in the vertebral body or in the posterior elements. Three patterns of vertebral body involvement are recognized: paradiskal, anterior, and central lesions [4].
Paradiskal Lesions
A paradiskal lesion is adjacent to the intervertebral disk leading to a narrowing of the disk space (Fig. 1A,1B). The disk space narrowing is caused either by destruction of subchondral bone with subsequent herniation of the disk into the vertebral body or by direct involvement of the disk [6]. This is the most common pattern of spinal tuberculosis. MR imaging shows low signal on T1-weighted images and high signal on T2-weighted images in the endplate, narrowing of the disk, and large paraspinal and sometimes epidural abscesses (Figs. 1A,1B and 4A,4B).
Anterior Lesions
The anterior type is a subperiosteal lesion under the anterior longitudinal ligament (Figs. 4A,4B and 5A,5B,5C). Pus spreads over multiple vertebral segments, stripping the periosteum and anterior longitudinal ligament from the anterior surface of the vertebral bodies. The periosteal stripping renders the vertebrae avascular and susceptible to infection. Both pressure and ischemia combine to produce anterior scalloping [4] (Fig. 5A,5B,5C). MR imaging shows the subligamentous abscess, preservation of the disks, and abnormal signal involving multiple vertebral segments representing vertebral tuberculous osteomyelitis.
Central Lesions
The central lesion is centered on the vertebral body. The disk is not involved (Fig. 6). Vertebral collapse can occur, producing a vertebra plana appearance (Fig. 7). MR imaging shows a signal abnormality of the vertebral body with preservation of the disk. The appearance is indistinguishable from that of lymphoma or metastasis.
Posterior Element
Complications of the Tuberculous Spine
Paraplegia and sometimes quadriplegia are serious complications of the tuberculous spine seen in approximately 10% of patients [7]. Copious epidural pus and granulation tissue alone or in combination with vertebral collapse, subluxation, or dislocation (Figs. 10 and 11A,11B) produce cord compression. Rarely, the pus penetrates the dura resulting in severe meningomyelitis [8] (Fig. 12A,12B).
Conclusion
The differential diagnosis of the tuberculous spine includes pyogenic and fungal infections, sarcoidosis, metastasis, and lymphoma. No pathognomonic imaging signs allow tuberculosis to be readily distinguished from other conditions. Typically, infectious spondylitis is characterized by involvement of the intervertebral disk. A history of chronicity and slow progression is suggestive of tuberculosis. Moreover, inflammatory collections tend to be larger in tuberculosis than in pyogenic spondylitis. In the central and posterior element forms of tuberculosis, only biopsy can achieve a provide diagnosis [2, 6].
MR imaging is sensitive for detecting vertebral osteomyelitis and is therefore the imaging technique of choice in spinal infections [2]. In spinal tuberculosis, the superior contrast resolution of MR imaging is useful for showing contiguous vertebral involvement, skip lesions, and paraspinal collections. MR imaging provides critical information about the spinal cord and the extent of the epidural pus in patients presenting with neurologic deficits. Familiarity with the spectrum of MR findings in tuberculosis spondylitis, especially in a high-risk patient population, can prevent a delay in diagnosis and may limit the morbidity that can be caused by this aggressive but curable infectious disease.
Footnote
Address correspondence to S. Moorthy.
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Submitted: January 28, 2002
Accepted: March 29, 2002
First published: November 23, 2012
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