IntroductionVertebral end-plate (Modic) changes were first described independently by de Roos et al. [9] and Modic et al. [15] as being a feature associated with degenerative intervertebral disc disease. Type I changes consist of reduced signal intensity (SI) in the vertebral end-plates on T1-and increased SI on T2-weighted sequences (Fig. 1). They are associated with fissuring of the cartilaginous end-plate and increased vascularity within the subchondral bone marrow on histological examination. Type II changes consist of increased SI on T1-and either increased SI or isointensity on T2-weighted sequences (Fig. 2). In such cases, biopsy reveals fatty replacement of the marrow [15], which is thought to be the result of marrow ischaemia [9]. Type III changes consist of reduced SI on both T1-and T2-weighted sequences due to subchondral sclerosis ( Fig. 3). Type I changes commonly progress to Type II changes and rarely revert back to normal, whereas Type II changes appear not to change with time [15]. Modic changes are identified in 20-50% of patients, with the incidence increasing with age [9,15]. However, it is not known why some degenerative discs are associated with Modic changes while others are not.Crock [6,7] proposed the concept of "internal disc disruption", suggesting that repeated trauma to the intervertebral disc could result in the production of inflammatory substances within the nucleus pulposus. Diffusion of such toxic chemicals through the vertebral end-plate could then result in a local inflammatory reaction resulting in back pain.Inflammation in the subchondral bone adjacent to the end-plate would result in reduced SI on T1-weighted MRI sequences and increased SI on T2-weighted MRI sequences, equivalent to a Type 1 Modic change. The possiAbstract The vertebral end-plate has been identified as a possible source of discogenic low back pain. MRI demonstrates end-plate (Modic) changes in 20-50% of patients with low back pain. The aim of this study was to investigate the association between Modic changes on MRI and discogenic back pain on lumbar discography. The MRI studies and discograms of 58 patients with a clinical diagnosis of discogenic back pain were reviewed and the presence of a Modic change was correlated with pain reproduction at 152 disc levels. Twenty-three discs with adjacent Modic changes were injected, 21 of which were associated with pain reproduction. However, pain was also reproduced at 69 levels where no Modic change was seen. The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) for a Modic change as a marker of a painful disc were 23.3%, 96.8%, 91.3% and 46.5% respectively. Modic changes, therefore, appear to be a relatively specific but insensitive sign of a painful lumbar disc in patients with discogenic low back pain.

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Spinal deformity is the commonest orthopaedic manifestation in neurofibromatosis type-1 and is categorized into dystrophic and non-dystrophic types. Management should be based on a meticulous assessment of the spine with plain radiography and magnetic resonance imaging (MRI) to rule out the presence of dysplastic features that will determine prognosis and surgical planning. MRI of the whole spine should also be routinely obtained to reveal undetected intraspinal lesions that could threaten scheduled surgical interventions. Non-dystrophic curvatures can be treated with similar decision-making criteria to those applied in the management of idiopathic scoliosis. However, close observation is necessary due to the possibility of modulation with further growth and due to the increased reported risk of pseudarthrosis after spinal fusion. The relentless progressive nature of dystrophic curves necessitates aggressive operative treatment, which often has a significant toll on the quality of life of affected patients through their early childhood. Bracing of dystrophic curves has been unsuccessful. Combined anterior/posterior spinal arthrodesis including the entire structural component of the deformity is indicated in most cases, particularly in the presence of associated sagittal imbalance. This should be performed using abundant autologous bone graft and segmental posterior instrumentation to minimize the risk of non-union and recurrence of the deformity.

Magnetic resonance imaging (MRI) is the mainstay of diagnosis, staging and follow-up of much musculoskeletal pathology. Diffusion-weighted magnetic resonance imaging (DWI) is a recent addition to the MR sequences conventionally employed. DWI provides qualitative and quantitative functional information concerning the microscopic movements of water at the cellular level. A number of musculoskeletal disorders have been evaluated by DWI, including vertebral fractures, bone marrow infection, bone marrow malignancy, primary bone and soft tissue tumours; post-treatment follow-up has also been assessed. Differentiation between benign and malignant vertebral fractures by DWI and monitoring of therapy response have shown excellent results. However, in other pathologies, such as primary soft tissue tumours, DWI data have been inconclusive in some cases, contributing little additional information beyond that gained from conventional MR sequences. The aim of this article is to critically review the current literature on the contribution of DWI to musculoskeletal MRI.