Citations

Background The diagnosis of a painful partial tear of the medial collateral ligament in overhead-throwing athletes is challenging, even for experienced elbow surgeons and despite the use of sophisticated imaging techniques. Hypothesis The “moving valgus stress test” is an accurate physical examination technique for diagnosis of medial collateral ligament attenuation in the elbow. Study Design Cohort study (diagnosis); Level of evidence, 2. Methods Twenty-one patients underwent surgical intervention for medial elbow pain due to medial collateral ligament insufficiency or other abnormality of chronic valgus overload, and they were assessed preoperatively with an examination called the moving valgus stress test. To perform the moving valgus stress test, the examiner applies and maintains a constant moderate valgus torque to the fully flexed elbow and then quickly extends the elbow. The test is positive if the medial elbow pain is reproduced at the medial collateral ligament and is at maximum between 120 ° and 70 °. Results The moving valgus stress test was highly sensitive (100%, 17 of 17 patients) and specific (75%, 3 of 4 patients) when compared to assessment of the medial collateral ligament by surgical exploration or arthroscopic valgus stress testing. The mean shear range (ie, the arc within which pain was produced with the moving valgus stress test) was 120 ° to 70 °. The mean angle at which pain was at a maximum was 90 ° of elbow flexion. Conclusions The moving valgus stress test is an accurate physical examination technique that, when performed and interpreted correctly, is highly sensitive for medial elbow pain arising from the medial collateral ligament.

Abstract OBJECTIVE AND IMPORTANCE We report the case of a 29-year-old man with Gardner syndrome and an isolated, giant cerebellopontine angle craniopharyngioma. Our description of this patient is only the second case report of a craniopharyngioma arising primarily in the cerebellopontine angle. CLINICAL PRESENTATION The patient presented with a 1-year history of progressive neurological impairment and headache. On the basis of the patient's history of multiple dermal fibromas, a cranial osteoma, familial adenomatous polyposis (FAP), a total abdominal colectomy, and an adenoma of the ampulla of Vater, we diagnosed the patient's condition as Gardner syndrome. INTERVENTION Magnetic resonance imaging showed a large cerebellopontine angle tumor, which was removed through a suboccipital retromastoid craniotomy. The pathological features were those of an adamantinomatous craniopharyngioma. The patient has done well postoperatively and has no new neurological deficits. A careful retrospective review of the preoperative imaging shows that this tumor was located exclusively in the posterior fossa and was not an extension of a sellar, suprasellar, or clival craniopharyngioma. CONCLUSION We present the second reported case of FAP and craniopharyngioma. There is no known genetic link between FAP and craniopharyngioma. Now that the patient has manifested a primary tumor of the central nervous system with FAP, it is unclear whether he should be classified as having Turcot syndrome. For this patient, we recommended vigilant follow-up imaging and forgoing external beam radiotherapy unless there is a documented recurrence of his craniopharyngioma.

Abstract Compressive neuropathies of the radial nerve at the elbow can lead to one of 2 clinical entities. Posterior interosseous syndrome is primarily a motor deficiency of the posterior interosseous nerve, and radial tunnel syndrome presents as pain along the radial tunnel and extensor muscle mass. The radial nerve can be compressed at a number of sites around the elbow. In addition, numerous mass lesions reported in the literature can cause compressive neuropathy of the radial nerve at the elbow. Standard surgical management for persistent radial tunnel syndrome that is refractory to nonsurgical treatment is open decompression of the radial nerve. Cysts occurring in other joints are commonly treated arthroscopically. Supraglenoid cysts of the shoulder, meniscal cysts in the knee, and dorsal wrist ganglia are routinely treated with arthroscopic decompression or excision with management of the underlying etiology of the cyst. We present a case of radial tunnel syndrome caused by a ganglion cyst of the proximal radioulnar joint that was treated using arthroscopic excision of the cyst and decompression of the radial nerve.

OBJECTIVEThis study reviewed patients with unilateral facial paralysis and normal clinical and imaging findings who underwent diagnostic facial nerve exploration.STUDY DESIGN AND SETTINGFifteen patients with facial paralysis and normal findings were seen in the Mayo Clinic Department of Otorhinolaryngology.RESULTSEleven patients were misdiagnosed as having Bell palsy or idiopathic paralysis. Progressive facial paralysis with sequential involvement of adjacent facial nerve branches occurred in all 15 patients. Seven patients had a history of regional skin squamous cell carcinoma, 13 patients had surgical exploration to rule out a neoplastic process, and 2 patients had negative exploration. At last follow‐up, 5 patients were alive.CONCLUSIONSPatients with facial paralysis and normal clinical and imaging findings should be considered for facial nerve exploration when the patient has a history of pain or regional skin cancer, involvement of other cranial nerves, and prolonged facial paralysis.SIGNIFICANCEOccult malignancy of the facial nerve may cause unilateral facial paralysis in patients with normal clinical and imaging findings. (Otolaryngol Head Neck Surg 2004;130:459–65.)

Abstract The compliance, capacity, and the position of minimum intraarticular pressure were measured in 13 thawed, fresh‐frozen human elbows. The capacity of the joint capsule was 23 ± 4 ml. The intraarticular pressure was the lowest at 80° of flexion. Capsular rupture occurred at relatively low intraarticular pressures—80 ± 42 mm Hg. Knowledge of the capacity of the normal elbow joint combined with the fact that this joint capsule tends to rupture or permit extravasation of fluid into the periarticular soft tissues should be considered when infusing fluids during arthroscopy. Finally, the “resting position” of 80° of flexion minimizes capsular tension and therefore might contribute to the development of joint contracture associated with prolonged immobilization in this position. This would be consistent with the observation that patients with posttraumatic elbow stiffness have an average arc of flexion of 60–90°.

Reduced shoulder endurance in rotator cuff tear patients has been observed clinically. A simple and inexpensive shoulder endurance test protocol was developed. This study reports the test-retest reliability of the protocol. Twenty healthy volunteers without a history of shoulder pathology participated in the study. Each subject was tested twice, each on a separate day. Test-retest correlation coefficients of the arm endurance times were 0.59 and 0.60 for the dominant and nondominant sides, respectively. The protocol appears promising for assessing shoulder function.

Abstract Purpose: Painful snapping of the elbow joint is usually attributed to intra‐articular loose bodies, instability, or medial dislocation of the triceps muscle over the medial epicondyle. We report our experience with 14 patients who were treated arthroscopically for snapping elbow that was found to be caused by hypertrophic synovial folds associated with radiocapitellar chondromalacia. Type of Study: Case series. Methods: The records of 14 patients who were treated arthroscopically for painful snapping elbows caused by intra‐articular plicae were reviewed. There were 6 women and 8 men with an average age of 36 years (range, 27 to 48 years). Nine patients had had some type of trauma to the joint. Four patients had been previously diagnosed with lateral epicondylitis and 5 with intra‐articular loose bodies. The average time from initial onset of symptoms to treatment was 13 months (range, 8 to 36 months). Average follow‐up was 24 months (range, 6 to 66 months). Results: All patients complained of painful snapping in the posterolateral or anterolateral aspect of the elbow. The snapping occurred between 90° and 110° of flexion with the forearm in pronation. In 7 patients, the snapping was reproducible by passively flexing the pronated elbow, which we refer to as the flexion‐pronation test. At the time of arthroscopic surgery, all patients had a thickened synovial plica that would snap back and forward over the radial head, usually associated with a chondromalacic area on the radial head. Twelve patients had complete relief of their snapping after surgery. One patient in whom there was associated posterolateral rotatory elbow instability did not improve. One patient became asymptomatic for 4 years but then had recurrence of her symptoms, which persisted despite 2 subsequent arthroscopies. Conclusions: The presence of synovial plicae in the radiocapitellar joint must be considered in the differential diagnosis of painful snapping elbow. Arthroscopy confirms the diagnosis and allows excision of the plica.

Abstract Purpose: The purpose of this study was to investigate the difference in contact geometry at the undersurface of acromion in shoulders with and without a rotator cuff (RC) tear. Type of Study: Case‐control study. Methods: Forty fresh cadaveric shoulders (average age at death, 61 years) without gross osteoarthritic changes were divided into the intact RC group (n = 20) and the RC tear group (n = 20). Clinical impingement was simulated by compressing the humeral head and the intact portion of the RC against the coracoacromial arch with an axial compressive force of 25 kg while the humerus was held abducted 20° in the scapular plane. The contact pattern between the acromion and the RC was measured with Fuji Prescale super low‐pressure–sensitive film (Fuji Photo Film Co, Ltd, Tokyo, Japan). The imprint image was analyzed using Global Lab image software (Automatix, Marlboro, MA). Results: The percentage of the maximum anteroposterior dimension of the imprint on Fuji film to the anteroposterior diameter of the acromial undersurface was 29% ± 9% in intact RC shoulders, and 39% ± 13% in shoulders with an RC tear ( P >.05). The percentage of the maximum mediolateral dimension of the imprint to the mediolateral diameter of the corresponding part of the acromial undersurface was 27% ± 12% in intact RC shoulders, and 48% ± 11% in shoulders with an RC tear. This difference was statistically significant ( P <.005). Conclusions: The contact geometry of the acromial undersurface with the underlying RC in the anteroposterior dimension, which might be related to the appearance in supraspinatus outlet view, was not significantly different between shoulders with and without an RC tear. These findings suggest that factors other than acromial shape play a significant role in the pathogenesis of RC tears. The implication regarding the role of acromioplasty remains to be clarified.

Background — Autosomal dominant hypertrophic cardiomyopathy (HCM) is caused by inherited defects of sarcomeric proteins. We tested the hypothesis that homozygosity for a sarcomeric protein defect can cause recessive HCM. Methods and Results — We studied a family with early-onset cardiomyopathy in 3 siblings, characterized by mid-cavitary hypertrophy and restrictive physiology. Genotyping of DNA markers spanning 8 genes for autosomal dominant HCM revealed inheritance of an identical paternal and maternal haplotype at the essential light chain of myosin locus by the affected children. Sequencing showed that these individuals were homozygous for a Glu143Lys substitution of a highly conserved amino acid that was absent in 150 controls. Family members with one Glu143Lys allele had normal echocardiograms and ECGs, even in late adulthood, whereas those with two mutant alleles developed severe cardiomyopathy in childhood. These findings, coupled with previous studies of myosin light chain structure and function in the heart, suggest a loss-of-function disease mechanism. Conclusions — Distinct mutations affecting the same sarcomeric protein can cause either dominant or recessive cardiomyopathy. Electrostatic charge reversal of a highly conserved amino acid may be benign in the heterozygous state as the result of compensatory mechanisms that preserve cardiac structure and function. By contrast, homozygous carriers of a sarcomeric protein defect may have a malignant course. Recognizing recessive inheritance in children with cardiomyopathy is essential for appropriate family counseling.