Magnetic resonance imaging of bacterial and tuberculous spondylodiscitis with associated complications and non-infectious spinal pathology mimicking infections: a pictorial review

Early bacterial infection within bone marrow typically results in minor ischemia due to septic embolism to the end arteries and the presence of inflammatory exudate. These changes result in low T1 and high T2 signal abnormalities in the bone marrow. High T2 signal intensity abnormalities within the bone marrow are made more conspicuous using fat-suppressed T2 weighted or STIR sequences. In addition, enhancement would be seen in the bone marrow (Fig. 1). The intervertebral disc will also show increased T2 signal with contrast enhancement. With progression of the disease without prompt and appropriate treatment, the end plates will show erosions with subsequent loss of disc and vertebral height. Pre- and paravertebral edema and contrast enhancement is also seen in most of the cases (Fig. 2). Extension into the adjacent soft tissue structures such as psoas muscle and diaphragmatic crura with phlegmon and abscess formation can also occur (Fig. 3). One of the major roles of MR imaging in evaluation of spinal infections is to look for spread of the infection in the epidural space and spinal canal with any effects on the cord and cauda equina nerve roots (Fig. 4). Contrast administration is necessary to differentiate phlegmon from the abscess in the epidural space (Figs. 2 and 4) as medical treatment may be sufficient in the former, while surgical drainage of abscess combined with medical treatment is necessary in cases of epidural abscesses. In patients who cannot receive gadolinium contrast or in cases where contrast enhanced MRI was not clearly diagnostic, DWI can be used to diagnose epidural abscess, as described earlier (Fig. 5).

In some cases, such as elderly patients, immunocompromised patients and following spinal procedures including facet joint steroid injections, facet joints can be the primary site of infection. This can result in abscesses which tend to be located in the posterior epidural space as compared to anterior epidural space in cases of spondylodiscitis. The MRI findings of facet joint infection includes increased signal in the joint and surrounding edema (Fig. 6). These changes can be very subtle and resemble degenerative joint disease. However, clinical presentation suggesting infective etiology and the presence of an epidural abscess favors infection over degenerative changes. In some cases, subdural abscess may be the main presentation of the spine infections, which is seen as a collection deep to the epidural fat (Fig. 7).

DWI has been shown to be useful in highlighting the extent of bacterial spondylodiscitis and distinguishing it from other pathologies which can mimic it [29]. ‘Claw sign’, described as a well-marginated, linear region of restricted diffusion at the interface of normal and abnormal marrow within the adjacent vertebral bodies, is seen in Modic type I degenerative changes and can be used to differentiate it from infection. This is due to the fact that a gradual process such as degenerative disc disease is expected to produce a well-defined response while infections usually progress quickly and diffusely giving rise to diffuse diffusion abnormalities rather than well-defined linear diffusion changes. DWI is also helpful in differentiating normal postsurgical fluid collections from the infected collections as the latter would show restricted diffusion due to thick viscous pus (Fig. 5) [30].

Frank bony and disc destruction is usually seen in chronic cases when there is a lack of initiation of prompt and appropriate treatment, either due to delay in presentation or diagnosis. Reactive bony changes, such as new bone formation and sclerosis, normalization of T1 signal intensity within a previously infected vertebral body and resolution of bone marrow edema on T2 weighted images suggest bone healing in a resolving infection.

Radiographs demonstrate reduced disc space, blurred paradiscal margins, increased paravertebral soft tissue opacity with and without calcifications, vertebral body destruction and severe kyphotic angulation in advanced progressive cases. CT is considered superior to MR imaging for visualization of small bony fragments and demonstrates more fine bony details of lytic lesions, endplate destruction and sclerotic margins, while MR imaging is considered superior for accurately defining the epidural extension of the disease and neural structure involvement. Findings of loss of vertebral body cortical definition and the presence of a calcified paraspinal mass with thick irregular rim enhancement favor tubercular over bacterial spondylodiscitis [23, 31]. Because of its superior ability to detect marrow changes before any bony destruction, MR imaging plays an important role in early diagnosis even in patients with normal radiographs. In majority of cases, tubercular spondylitis appears hyperintense on T2-weighted images and hypointense on T1-weighted images with contrast enhancement indicating marrow edema in the infected area (Fig. 8). An important imaging feature that characterizes tuberculous infection compared to bacterial infection is sparing of the intervertebral disc in the early stage of infection. Conversely, early spread to discs with loss of disc height and disc herniation favor bacterial infection [4]. Other characteristic involvement of the anterior vertebral body corner, subligamentous spread, multiple vertebral bodies, extensive paraspinal abscess formation, abscess calcification, and vertebral destruction differentiates tubercular from bacterial spondylodiscitis [17, 23, 32].

With progression of the disease classic discovertebral involvement can be seen which appear hyperintense on T2-weighted images and hypointense on T1-weighted images. In the chronic stage due to delayed diagnosis, low signal intensity on T1 and T2-weighted images indicates vertebral collapse with endplate sclerosis. During treatment, progressive increase in vertebral signal intensity on T1-weighted images suggests fatty replacement and indicates healing [23, 31, 32]. The infective process can extend into the epidural space causing cord compression, which is associated with a high mortality [23]. Extension into the spinal canal can lead to arachnoiditis (Fig. 8) and tuberculomas in the brain parenchyma in some cases.