Faculty Bibliography

The purpose of this study was to investigate the association of aortic arch calcification, a surrogate marker of atherosclerosis, with rotator cuff tendinosis and tears given the hypothesis that decreased tendon vascularity is a contributing factor in the etiology of tendon degeneration. A retrospective review was performed to identify patients ages 50 to 90 years who had a shoulder MRI and a chest radiograph performed within 6 months of each other. Chest radiographs and shoulder MRIs from 120 patients were reviewed by two sets of observers blinded to the others' conclusions. Rotator cuff disease was classified as tendinosis, partial thickness tear, and full thickness tear. The presence or absence of aortic arch calcification was graded and compared with the MRI appearance of the rotator cuff. The tendon tear grading was positively correlated with patient age. However, the tendon tear grading on MRI was not significantly correlated with the aorta calcification scores on chest radiographs. Furthermore, there was no significant correlation between aorta calcification severity and tendon tear grading. In conclusion, rotator cuff tears did not significantly correlate with aortic calcification severity. This suggests that tendon ischemia may not be associated with the degree of macrovascular disease

OBJECTIVE: The purpose of this article is to review imaging of the rotator interval, an anatomically complex region in the shoulder that plays an important role in the normal function of the shoulder joint. The rotator interval can be difficult to evaluate by imaging, and it is not routinely evaluated arthroscopically unless the clinical examination or imaging findings suggest an abnormality of the rotator interval. Rotator interval pathology is implicated in glenohumeral instability, biceps instability and adhesive capsulitis-entities which remain a challenge to diagnose and treat. CONCLUSION: Imaging can play an important role in increasing suspicion for injury to the rotator interval so that this region can be evaluated and appropriate treatment can be initiated

Entrapment neuropathies can manifest with confusing clinical features and therefore are often underrecognized and underdiagnosed at clinical examination. Historically, electrophysiologic evaluation has been considered the mainstay of diagnosis. Today, cross-sectional imaging, particularly magnetic resonance (MR) imaging and specifically MR neurography, plays an increasingly important role in the work-up of entrapment neuropathies. MR imaging is a noninvasive operator-independent technique that allows identification of the underlying cause of injury, differentiation between surgically treatable and untreatable causes, and guidance of selective diagnostic anesthetic nerve blocks. Pathologic conditions affecting the lumbosacral plexus and major motor and mixed nerves of the pelvis and hip include neuropathies of the lumbosacral plexus, femoral nerve, lateral femoral cutaneous nerve, obturator nerve, and sciatic nerve; piriformis muscle syndrome; and injury of the gluteal nerves. Diagnosis of entrapment neuropathies of the pelvis and hip with MR imaging requires familiarity with the normal MR imaging anatomy and awareness of the anatomic and pathologic factors that put peripheral nerves at risk for injury

OBJECTIVE: The objective of this study was to assess the prevalence of increased signal intensity in the pronator quadratus in the general patient population. Using region-of-interest measurements, we measured the signal intensity of the pronator quadratus and of an adjacent flexor muscle. In addition, we performed independent subjective assessments of the pronator quadratus. CONCLUSION: Increased signal intensity in the pronator quadratus is a frequent normal finding of unclear etiology and is not related to disease. Familiarity with this normal phenomenon is important to avoid overdiagnosis of denervation due to anterior interosseous nerve entrapment.

Purpose: There is insufficient understanding regarding how generalized OA involving the hand and knee differs from isolated knee OA, which may result from other factors such as obesity or trauma. The purpose of these studies is to determine whether the presence of hand OA involving interphalangeal (IP) and first carpometacarpal (CMC) joints, alone or in combination, predicts progression of patients with symptomatic knee OA. Methods: Hand radiographs were obtained on 94 patients at NYUHJD who met ACR criteria for symptomatic knee OA, and who were enrolled in a two-year NIH-sponsored prospective study. The patients completed standardized fixed-flexion knee radiographs at baseline and 24 months, with progression the signal (more painful) knee OA determined by change in joint space width (JSW) and KL score. For these analyses, the patients were separated into two groups by results on their signal knee: 17 progressors, defined by at least 30% decreased JSW over 24 months, and 77 non-progressors. For each set of hand x-rays, 2 radiologists evaluated 18 IP joints and 2 CMC joints for joint space narrowing and/or osteophytes, and whether or not there was erosive change at the IP joints; we averaged the scores from the two readers. Results: Kappa scores between the two scoring radiologists for the IP and CMC joints, and for the presence of erosive IP disease, were 0.79, 0.87 and 0.96, respectively. The overall mean IP score was 5.6 and 1st CMC score was 0.9, while medians were 5 and 1.0, respectively. The 17 progressors had a higher average IP (but not CMC) score than the non-progressors, 7.2+/- 5.4 vs. 5.0+/-4.6, p=0.13. Since the IP scores were not normally distributed, we further analyzed data by dichotomizing the study populations into two groups using the median IP total (5) as the cutoff point. When so analyzed, the presence of hand OA increased the odds ratio of knee OA progression to 2.8 (p=0.096). Of interest, the severity of knee OA correlated with hand OA scores: the average total hand OA scores (out of 20 joints) increased with baseline KL score, with mean scores of 3.8+/-5.5, 6.1+/-6.1 and 7.2+/-5.6 for KL 1 to 3 (p=0.06). There is also an increasing trend of total hand OA joint scores by KL score (p=0.042) when dichotomized around the median (5 joints), and with IP scores alone (p=0.026). The 8 patients with radiographic evidence of erosive IP disease, as compared with the 31 non-erosive IP OA patients (>5 IP joints) and the 54 without IP OA, demonstrated faster knee OA progression over 2 years by average KL increases (1.00, 0.35, 0.30) and decreases in joint space width (0.65, 0.56, 0.36), although perhaps given small numbers, this was not statistically significant (p=0.839). Conclusions: In cross-sectional analysis, the quantitative burden of hand OA correlates with the radiographic severity of knee OA (KL). Moreover, radiographic hand OA at the IP joints, but not at the 1st CMC joint, predicts more rapid progression of knee OA. Erosive IP disease may be an even stronger predictor than non-erosive IP disease of accelerated progression of knee OA

Painful total knee arthroplasty (TKA) represents a diagnostic challenge for the clinician and radiologist, as there is a wide variety of potential etiologies, with a broad range of clinical presentations, and the abnormalities on imaging studies are often subtle, absent, or nonspecific. Imaging findings of normal TKA are reviewed, in addition to a variety of complications such as loosening, infection, instability, osteolysis, heterotopic ossification, extensor mechanism disruption, and fracture. Although imaging evaluation of painful TKA is usually limited to conventional radiographs and nuclear imaging, examples of the utility of computed tomography are also illustrated, and suggested imaging strategies and algorithms are discussed

Lesions that involve the cortex of the tibia are fairly common in radiology practice. However, the number of diseases that involve the tibial cortex is great, and it can be difficult to arrive at a limited differential diagnosis from radiographic findings. Categorization of lesions of the tibia into those that cause cortical destruction and those that cause cortical proliferation can help narrow the broad differential diagnosis. Lesions that cause cortical destruction include nonossifying fibroma, fibrous dysplasia, osteofibrous dysplasia, aneurysmal bone cyst, giant cell tumor, eosinophilic granuloma, Ewing sarcoma, neurofibromatosis, adamantinoma, osteoblastoma, chondromyxoid fibroma, hemangioendothelioma, renal cell metastatic disease, hemangioma, and hemangiopericytoma. Lesions that cause cortical proliferation include osteochondroma, stress fracture, osteoid osteoma, periosteal osteogenic sarcoma, diaphyseal dysplasia, venous stasis, cellulitis, chronic osteomyelitis, osteopathia striatum, and melorheostosis. Conventional radiography along with clinical and pathologic data can aid in diagnosis of the wide variety of disease processes that involve the tibial cortex.