Seventy-six healthy adults underwent magnetic resonance imaging (1.5 T) to investigate the effects of age on regional cerebral volumes and on the frequency and severity of cortical atrophy, lateral ventricular enlargement, and subcortical hyperintensity. Increasing age was associated with (1) decreasing volumes of the cerebral hemispheres (0.23% per year), the frontal lobes (0.55% per year), the temporal lobes (0.28% per year), and the amygdala-hippocampal complex (0.30% per year); (2) increasing volumes of the third ventricle (2.8% per year) and the lateral ventricles (3.2% per year); and (3) increasing odds of cortical atrophy (8.9% per year), lateral ventricular enlargement (7.7% per year), and subcortical hyperintensity in the deep white matter (6.3% per year) and the pons (8.1% per year). Many elderly subjects did not exhibit cortical atrophy or lateral ventricular enlargement, however, indicating that such changes are not inevitable consequences of advancing age. These data should provide a useful clinical context within which to interpret changes in regional brain size associated with "abnormal" aging.

Multiplanar spin-echo magnetic resonance imaging was performed on 54 patients with acute complete anterior cruciate ligament tears. Imaging was done within 45 days of index anterior cruciate ligament injury. Spin-echo T1- and T2-weighted images were used to determine the lesion morphology and location. Only the T2-weighted sagittal images were used for the incidence assessment; T2-weighted spin-echo imaging reflects free water shifts and best indicates the acute edema and inflammatory changes from injury. Eighty-three percent (45 of 54) of the knees had an osseous contusion directly over the lateral femoral condyle terminal sulcus. The lesion was highly variable in size and imaging intensity; however, the most intense signal was always contiguous with the subchondral plate. Posterolateral joint injury was seen in 96% (43 of 45) of the knees that had a terminal sulcus osseous lesion determined by magnetic resonance imaging. This posterolateral lesion involves a spectrum of injury, including both soft tissue (popliteus-arcuate capsuloligamentous complex) and hard tissue (posterolateral tibial plateau) injuries. The consistent location of the osseous and soft tissue injuries underscores a necessary similar mechanism of injury associated with these acute anterior cruciate ligament tears. Based on these characteristic findings, several proposed mechanisms of injury are discussed.

To better correlate the appearance of avascular necrosis (AVN) of the femoral head on magnetic resonance (MR) images with the stage of disease, MR images of 56 proved AVN lesions were compared with staging from corresponding radiographs (n = 56), Tc-99m scans (n = 41), and grade of symptoms (n = 28). Fractures complicating AVN were seen in 28 (50%) of 56 radiographs (radiographic stages III-V). With long repetition (TR) and echo delay (TE) times, a characteristic "double line sign" consisting of high signal intensity inside a low-intensity peripheral rim was seen in 45 lesions (80%). The central region within the rim was isointense with marrow fat on both short and long TR and TE images in 20 (71%) of 28 lesions uncomplicated by fracture (stages I-II) but in only four (14%) of 28 stage III-V lesions (P less than .001). Symptoms were least severe in lesions isointense with fat and most severe in lesions with low-signal central regions at short and long TRs and TEs. The peripheral double line sign on long TR/TE images may add specificity to the diagnosis of AVN by MR imaging. A chronologic pattern of central MR signal features is presented which may allow staging of AVN by MR imaging.

BACKGROUND Previous studies have suggested injury to the anterior talofibular ligament may be linked to altered kinematics and the development of osteoarthritis of the ankle joint. However, the effects of ATFL injury on the in vivo kinematics of the ankle joint are unclear. HYPOTHESIS Based on the orientation of the ATFL fibers, we hypothesized that ATFL deficiency would lead to increased anterior translation and increased internal rotation of the talus relative to the tibia. STUDY DESIGN Controlled laboratory study. METHODS The ankles of 9 patients with unilateral ATFL injuries were compared as they stepped onto a level surface. Kinematic measurements were made as a function of increasing load. Using magnetic resonance imaging and orthogonal fluoroscopy, the in vivo kinematics of the tibiotalar joint were measured in the ATFL deficient and intact ankles from the same individuals. RESULTS A statistically significant increase in internal rotation, anterior translation, and superior translation of the talus was measured in ATFL deficient ankles as compared to intact, contralateral controls. For example, at 100% body weight, ATFL deficient ankles demonstrated a statistically significant increase in anterior translation of 0.9 ± 0.5mm (p = 0.008). At 100% body weight, the ATFL deficient ankle was internally rotated relative to the intact ankle by 5.7 ± 3.6° (p = 0.008). There was a slight increase of 0.2 ± 0.2mm in the superior translation of the ATFL deficient ankle compared to the intact ankle at 100% body weight (p = 0.02). CONCLUSIONS ATFL deficiency increases anterior translation, internal rotation, and superior translation of the talus. CLINICAL RELEVANCE Altered kinematics may contribute to the degenerative changes observed with chronic lateral ankle instability. These findings might help to explain the degenerative changes frequently observed on the medial talus in patients with chronic ATFL insufficiency and provide a baseline for improving ankle ligament reconstructions aimed at restoring normal joint motion.

Despite recent attention in the literature, anterior cruciate ligament (ACL) injury mechanisms are controversial and incidence rates remain high. One explanation is limited data on in vivo ACL strain during high-risk, dynamic movements. The objective of this study was to quantify ACL strain during jump landing. Marker-based motion analysis techniques were integrated with fluoroscopic and magnetic resonance (MR) imaging techniques to measure dynamic ACL strain non-invasively. First, eight subjects’ knees were imaged using MR. From these images, the cortical bone and ACL attachment sites of the tibia and femur were outlined to create 3D models. Subjects underwent motion analysis while jump landing using reflective markers placed directly on the skin around the knee. Next, biplanar fluoroscopic images were taken with the markers in place so that the relative positions of each marker to the underlying bone could be quantified. Numerical optimization allowed jumping kinematics to be superimposed on the knee model, thus reproducing the dynamic in vivo joint motion. ACL length, knee flexion, and ground reaction force were measured. During jump landing, average ACL strain peaked 55 ± 14 ms (mean and 95% confidence interval) prior to ground impact, when knee flexion angles were lowest. The peak ACL strain, measured relative to its length during MR imaging, was 12 ± 7%. The observed trends were consistent with previously described neuromuscular patterns. Unrestricted by field of view or low sampling rate, this novel approach provides a means to measure kinematic patterns that elevate ACL strains and that provide new insights into ACL injury mechanisms.