Faculty Bibliography

A wide spectrum of abnormalities can affect the throwing shoulder. The injuries are often particular to a specific phase of the throw and are well demonstrated with MR imaging. In this article, the authors review the phases of the throw, MR imaging techniques, and the MR appearances of the injuries associated with particular phases

Rotator cuff tears are a common cause of shoulder pain. Clinical and radiographic findings can suggest the presence of a rotator cuff tear. The most sensitive clinical findings are impingement and the 'arc of pain' sign. Radiographic findings are usually normal in the acute setting, although the 'active abduction' view may show decreased acromiohumeral distance. In more chronic cases, an outlet view may show decreased opacity and decreased size of the supraspinatus muscle due to atrophy. In late cases, the humeral head may become subluxated superiorly, and secondary degenerative arthritis of the glenohumeral joint may ensue. Ultrasonography (US), with over 90% sensitivity and specificity, can help confirm the diagnosis in clinically or radiographically equivocal cases. US can also reveal the presence of other abnormalities that may mimic rotator cuff tear at clinical examination, including tendinosis, calcific tendinitis, subacromial subdeltoid bursitis, greater tuberosity fracture, and adhesive capsulitis

OBJECTIVE: The purpose of our study is to describe shifting bone marrow edema in the knee as the MR imaging feature of intra-articular regional migratory osteoporosis of the knee. PATIENTS AND METHODS: Five men, aged 45-73 years, were referred by orthopedic surgeons for MR imaging evaluation of knee pain, which had been present for 2 weeks to 6 months. One patient had a prior history of blunt trauma. None had risk factors for osteonecrosis. Four patients had two MR examinations and the patient with prior blunt trauma had four. Plain radiographs were obtained in all patients. RESULTS: In all cases, a large area of marrow edema initially involved a femoral condyle, with migration of the bone marrow edema to the other femoral condyle, tibia, and/or patella occurring over a 2- to 4-month period. Adjacent soft tissue edema was present in all five patients, while none had a joint effusion. Radiographs of two patients showed generalized osteopenia. CONCLUSION: In the absence of acute trauma or clinical suspicion of infection, a large area of bone marrow edema without a zone of demarcation may represent intra-articular regional migratory osteoporosis. Demonstration of shifting bone marrow edema on follow-up examinations suggests this diagnosis

BACKGROUND: MI is a rare complication of trauma. We anticipate that the aging of the population and the concomitant rise in geriatric trauma will result in an increase in acute illnesses of the elderly (such as MI) complicating recovery from injury. The purpose of this article is to define the presentation of MI in the immediate postinjury period. STUDY DESIGN: Medical records of all trauma patients in whom MI developed during their hospitalizations at a single Level I trauma center, the Barnes Hospital/Washington University Medical Center, between 1990 and 1999 were screened through the trauma registry. Nineteen patients with possible postinjury MI were identified. Of these, five had bona fide cases of postinjury MI, five had ambiguity about whether MI preceded or followed trauma, one had an MI resulting in trauma, and eight were excluded because they did not meet strict diagnostic criteria for MI. RESULTS: The five patients with posttraumatic MI were older than the general trauma population with ages ranging from 51 to 81 years (mean +/- SD = 72 +/- 14 years). Each had preexisting medical illnesses, some of which are recognized to predispose to coronary artery disease. There were no identifiable precipitants other than the recent injury. Importantly, only one of the five patients had chest pain as a presenting symptom and each of the five cases was complicated by acute congestive heart failure. CONCLUSIONS: MI remains a rare but important complication of injury and may increase owing to the changing demographics of trauma victims. Methods for thorough history-gathering to identify preexisting conditions, for early hemodynamic monitoring and anticoagulation for MI in the setting of trauma, and for identifying preexisting conditions should be defined. The presentation of MI in the setting of injury is atypical and complications are frequent

The closely linked IGF2 and H19 genes on human chromosome 11p15.5 are monoallelically expressed as a result of genomic imprinting and show altered expression in Wilms' tumors (WTs). To map regional imprinting we have sought to isolate additional human genes close to IGF2/H19 and to characterize their allelic expression patterns. Here we report a novel gene, provisionally named L23MRP [L23 (mitochondrial)-related protein], which is oriented 'tail-to-tail' with H19 and is transcribed to within 40 kb of the last H19 exon. L23MRP is expressed biallelically in many mid-fetal and adult human tissues. This gene is also expressed at normal levels in WTs which have lost expression of H19 either via loss of the maternal chromosome 11p15.5 or via an epigenetic pathway involving site-specific DNA hypermethylation. These data indicate that, at least in post-embryonic stages, L23MRP is functionally insulated from the IGF2/H19 imprinted domain.

To test the potential role of H19 as a tumour suppressor gene we have examined its expression and DNA methylation in Wilms' tumours (WTs). In most WTs (18/25), H19 RNA was reduced at least 20-fold from fetal kidney levels. Of the expression-negative tumours ten retained 11p15.5 heterozygosity: in nine of these, H19 DNA was biallelically hypermethylated and in two cases hypermethylation locally restricted to H19 sequences was also present in the non-neoplastic kidney parenchyma. IGF2 mRNA was expressed in most but not all WTs and expression patterns were consistent with IGF2/H19 enhancer competition without obligate inverse coupling. These observations implicate genetic and epigenetic inactivation of H19 in Wilms' tumorigenesis.