Accessory Flexor Digitorum Longus Presenting as Tarsal Tunnel Syndrome: A Case Series.

ABSTRACT: Tarsal tunnel syndrome (TTS) typically occurs from extrinsic or intrinsic sources of compression on the tibial nerve. We present 3 cases of patients, all of whom have a prolonged time to diagnosis after evaluation with multiple specialties, with foot pain ultimately secondary to an accessory flexor digitorum longus muscle causing TTS. The literature describing the association between TTS and accessory musculature has been limited to single case reports and frequently demonstrate abnormal electrodiagnostic testing. In our series, 2 cases had normal electrodiagnostic findings despite magnetic resonance imaging (MRI) that later revealed TTS and improvement with eventual resection. A normal electromyogram should not preclude the diagnosis of TTS and MRI of the ankle; it should be considered a useful diagnostic tool when examining atypical foot pain.

Novel anterior coracoglenoid line utilizing magnetic resonance imaging (MRI) corresponds with critical glenoid bone loss.

OBJECTIVE: Glenoid bone loss is estimated using a best-fit circle method and requires software tools that may not be available. Our hypothesis is that a vertical reference line drawn parallel to the long axis of the glenoid and passing through the inflection point of the coracoid and glenoid will represent a demarcation line of approximately 20% of the glenoid. Our aim is to establish a more efficient method to estimate a surgical threshold for glenoid insufficiency. METHODS: Fifty patients with normal glenoid anatomy were randomly chosen from an orthopedic surgeon's database. Two orthopedic surgeons utilized T1-weighted sagittal MRIs and the coracoglenoid line technique to determine the percentage of bony glenoid anterior to vertical line. Two musculoskeletal radiologists measured the same 50 glenoids using the circle technique. Differences were determined using dependent t test. Reliability was compared using interclass correlation coefficient and Kappa. Validity was compared using Pearson correlation coefficient. RESULTS: Mean surface area of the glenoid anterior to the vertical line was on average 21.69% ± 3.12%. Surface area of the glenoid using the circle method was on average 20.86% ± 2.29%. Inter-rater reliability of the circle method was 0.553 (fair). Inter-rater reliability of the vertical line technique was 0.83 (excellent). There was a linear relationship between circle and vertical line measurements, r = 0.704 (moderate to high). CONCLUSION: The coracoglenoid line appears to represent a line of demarcation of approximately 21% of glenoid bone anterior to the coracoglenoid line. Our technique was found to be reliable, valid, and accurate.

Assessment of cortical and trabecular bone changes in two models of post-traumatic osteoarthritis.

Subchondral bone is thought to play a significant role in the initiation and progression of the post-traumatic osteoarthritis. The goal of this study was to document changes in tibial and femoral subchondral bone that occur as a result of two lapine models of anterior cruciate ligament injury, a modified ACL transection model and a closed-joint traumatic compressive impact model. Twelve weeks post-injury bones were scanned via micro-computed tomography. The subchondral bone of injured limbs from both models showed decreases in bone volume and bone mineral density. Surgical transection animals showed significant bone changes primarily in the medial hemijoint of femurs and tibias, while significant changes were noted in both the medial and lateral hemijoints of both bones for traumatic impact animals. It is believed that subchondral bone changes in the medial hemijoint were likely caused by compromised soft tissue structures seen in both models. Subchondral bone changes in the lateral hemijoint of traumatic impact animals are thought to be due to transmission of the compressive impact force through the joint. The joint-wide bone changes shown in the traumatic impact model were similar to clinical findings from studies investigating the progression of osteoarthritis in humans.

Chronic changes in the articular cartilage and meniscus following traumatic impact to the lapine knee.

The objective of this study was to induce anterior cruciate ligament (ACL) and meniscal damage, via a single tibiofemoral compressive impact, in order to document articular cartilage and meniscal changes post-impact. Tibiofemoral joints of Flemish Giant rabbits were subjected to a single blunt impact that ruptured the ACL and produced acute meniscal damage. Animals were allowed unrestricted cage activity for 12 weeks before euthanasia. India ink analysis of the articular cartilage revealed higher degrees of surface damage on the impacted tibias (p=0.018) and femurs (p<0.0001) compared to controls. Chronic meniscal damage was most prevalent in the medial central and medial posterior regions. Mechanical tests revealed an overall 19.4% increase in tibial plateau cartilage thickness (p=0.026), 34.8% increase in tibial plateau permeability (p=0.054), 40.8% increase in femoral condyle permeability (p=0.029), and 20.1% decrease in femoral condyle matrix modulus (p=0.012) in impacted joints compared to controls. Both instantaneous and equilibrium moduli of the lateral and medial menisci were decreased compared to control (p<0.02). Histological analyses revealed significantly increased presence of fissures in the medial femur (p=0.036). In both meniscus and cartilage there was a significant decrease in GAG coverage for the impacted limbs. Based on these results it is clear that an unattended combined meniscal and ACL injury results in significant changes to the soft tissues in this experimental joint 12 weeks post-injury. Such changes are consistent with a clinical description of mid to late stage PTOA of the knee.

Identification of acetabular labral pathological changes in asymptomatic volunteers using optimized, noncontrast 1.5-T magnetic resonance imaging.

BACKGROUND: Acetabular labral tears as a source of potential hip pain have received a great deal of attention in recent literature. The gold standard for identifying acetabular labral tears is hip arthroscopy, but recent advances in optimized, noncontrast magnetic resonance imaging (MRI) have proven effectiveness in identifying intra-articular hip pathological changes without the invasive nature of hip arthroscopy or gadolinium-enhanced arthrography. There are little data in the literature on imaging results in an asymptomatic population. PURPOSE: The objective of this study was to use an optimized, noncontrast 1.5-T MRI protocol to identify hip abnormalities, including paralabral cysts, in asymptomatic volunteers. STUDY DESIGN: Case series (prevalence); Level of evidence, 4. METHODS: In this study, 42 hips in asymptomatic patients with an average age of 34 years (range, 27-43 years) were prospectively imaged with optimized, noncontrast 1.5-T MRI scans. Two fellowship-trained musculoskeletal radiologists interpreted the scans at 2 different points in time and commented on the presence of labral abnormalities including paralabral cysts. The results were analyzed for both interobserver and intraobserver reliability. RESULTS: Acetabular paralabral cysts were identified in 11 of 42 (26.2%) and 9 of 42 (21.4%) hips by the 2 respective radiologists, with an interobserver reliability of 90.5% (κ = .74) and intraobserver reliability of 95.2% (κ = .87). In addition, acetabular labral tears were identified in 36 of 42 (85.7%) and 34 of 42 (80.9%) hips, with an interobserver reliability of 90.5% (κ = .70) and intraobserver reliability of 95.2% (κ = .83). CONCLUSION: Utilizing an optimized, noncontrast 1.5-T MRI protocol, we report the previously undescribed prevalence of acetabular labral pathological abnormalities and paralabral cysts in a young, asymptomatic population. This emphasizes the importance of correlating patient symptoms with history and physical examination when evaluating patients with hip pain and radiographic abnormalities as defined by MRI criteria. These data demonstrate that labral tears can occur without symptoms.

Imaging of stress injuries of the pelvis.

Stress fractures are common, representing the final stage in a continuum of bone response to continued mechanical damage. Encompassing fatigue- and insufficiency-type fractures, stress fractures of the pelvis are likely underreported. Radiographs are insensitive to stress injuries, particularly those in the pelvis, whereas scintigraphy and magnetic resonance imaging are exquisitely sensitive. In this article we discuss the pathophysiology and imaging appearances of stress injuries of the pelvis and sacrum. Relevant literature regarding risk factors, problem-solving issues, and an imaging algorithm are discussed, with the goal of improving accuracy in the diagnosis of these common injuries.

CNLAC1 is required for extrapulmonary dissemination of Cryptococcus neoformans but not pulmonary persistence.

The pathogenic yeast Cryptococcus neoformans produces a laccase enzyme (CNLAC1), which catalyzes the synthesis of melanin in the presence of phenolic compounds. A number of genes have been implicated in the regulation of laccase and melanization, including IPC1, GPA1, MET3, and STE12. Albino mutants derived from random mutagenesis techniques may contain mutations in genes that regulate multiple virulence factors, including CNLAC1. The goal of our study is to investigate the role of CNLAC1 in virulence and evasion of pulmonary host defenses after infection via the respiratory tract. Using a set of congenic laccase-positive (2E-TUC-4) and laccase-deficient (2E-TU-4) strains, we found that both strains are avirulent at a lower dose (10(4) CFU/mouse) in mice. After the infectious dose was increased to 10(6) CFU/mouse, 70% mortality was observed in mice infected with 2E-TUC-4 compared to no mortality in mice infected with 2E-TU-4 at day 30 postinfection. This observation confirms the requirement for CNLAC1 in virulence. Interestingly, we observed no differences between the two strains in pulmonary growth or in elicitation of cellular immune responses in the lung. The only measurable defect of 2E-TU-4 was in dissemination to extrapulmonary sites. To examine the role of CNLAC1 in dissemination, mice were infected intravenously. By week 3 postinfection, equal numbers of strains 2E-TUC-4 and 2E-TU-4 were recovered from the brain and spleen. This observation indicates that CNLAC1 facilitates escape from the lung, but not growth in the lungs or brain, and suggests a novel role for CNLAC1 in virulence during an infection aquired via the respiratory tract.