Many factors are thought to cause ankle ligament injuries. The purpose of this study was to examine injury risk factors prospectively and determine if an abnormality in any one or a combination of factors identifies an individual, or an ankle, at risk for subsequent inversion ankle injury. We examined 145 college-aged athletes before the athletic season and measured generalized joint laxity, anatomic foot and ankle alignment, ankle ligament stability, and isokinetic strength. These athletes were monitored throughout the season. Fifteen athletes incurred inversion ankle injuries. Statistical analyses were performed using both within-group (uninjured versus injured groups) data and within-subject (injured versus uninjured ankles) data. No significant differences were found between the injured (N = 15) and uninjured (N = 130) groups in any of the parameters measured. However, the eversion-to-inversion strength ratio was significantly greater for the injured group compared with the uninjured group. Analysis of the within-subject data demonstrated that plantar flexion strength and the ratio of dorsiflexion to plantar flexion strength was significantly different for the injured ankle compared with the contralateral uninjured ankle. Individuals with a muscle strength imbalance as measured by an elevated eversion-to-inversion ratio exhibited a higher incidence of inversion ankle sprains. Ankles with greater plantar flexion strength and a smaller dorsiflexion-to-plantar flexion ratio also had a higher incidence of inversion ankle sprains.

Chronic lateral ankle instability may be present in as many as 10% to 30% of people suffering from acute lateral ankle ligament injuries. Ankle instability has been referred to as either functional instability or mechanical instability. Management options consist of either nonoperative or operative treatment, with the majority of the literature emphasizing operative management for chronic instability. Long-term studies assessing the different types of available operative repairs have now been published. This review article discusses chronic lateral ankle ligament instability from a functional, anatomical point of view. The indications for treatment, nonoperative and operative treatment, as well as the biomechanical information available regarding these methods of treatment are considered. The major emphasis of this review is discussion and analysis of the many different surgical treatment options. Following this review, we presently recommend anatomical repair to the bone of both the anterior talofibular ligament and the calcaneofibular ligament, together with imbrication of the ligaments. In patients with hypermobility, long-standing instability, or arthritis, reconstruction using the Chrisman-Snook technique is recommended.

Plantar fasciitis is the most common cause of inferior heel pain (fig 1). Its aetiology is poorly understood by many, which has led to a confusion in terminology.1 It is said to affect patients between the ages of 8 and 80, but is most common in middle aged women and younger, predominantly male, runners. 2The role of the doctor in the management of plantar fasciitis is to make an appropriate diagnosis and to allow enough time for the condition to run its course, with the aid of supportive measures. If treatment is begun soon after the onset of symptoms, most patients can be cured within six weeks. MethodsThis article is based largely on our experience and recent concepts that have changed our management of inferior heel pain. Reviews written by experts have been supplemented by selected original articles cited in Medline between 1976 and 1995 and published in high quality journals. We used the following keywords for the Medline search: plantar fasciitis, inferior heel pain, heel spur, calcaneodynia. AetiologyThe plantar fascia is a strong band of white glistening fibres which has an important function in maintaining the medial longitudinal arch: spontaneous rupture or surgical division of the plantar fascia will lead to a flat foot.4 5 The plantar fascia arises predominantly from the medial calcaneal tuberosity on the undersurface of the calcaneus, and its main structure fans out to be inserted through several slips into the plantar plates of the metatarso-phalangeal joints, the bases of the proximal phalanges of the toes and the flexor tendon sheaths. Just after heel strike during the first half of the stance phase of the gait cycle, the tibia turns inward and the foot pronates to allow flattening of the foot. This stretches the plantar fascia. The flattening of the arch allows the foot to accommodate to irregularities in the walking surface and also to absorb shock.If there is a predisposing or aggravating factor (box), the repetitive traction placed on the plantar fascia during walking or running may lead to microtears (fig 2), which induce a reparative inflammatory response. 6 Biopsy specimens of the inflamed fascia show fibroblastic proliferation and chronic granulomatous tissue.1 6 A normal plantar fascia has a dorsoplantar thickness of 3 mm; in plantar fasciitis this can be 15 mm.

Radiographs of 12 normal cadaveric lower extremities were prepared with each extremity in seven increments of axial rotation, ranging from 5 degrees of external rotation to 25 degrees of internal rotation. The tibiofibular clear space, the tibiofibular overlap, the width of the tibia and fibula, and the medial clear space were measured on each film. The width of the tibiofibular clear space (syndesmosis A) averaged 3.9+/-0.9 mm (range, 2 to 5.5 mm), but did not change significantly with rotation. Its size was independent of the size of tibia and fibula. All other measurements changed dramatically with rotation. In our specimens, a true mortise view of the ankle joint was obtained by internally rotating the extremity an average of 13.6+/-0.7 degrees (range, 12.0 degrees to 17.0 degrees). Based on our results the width of the tibiofibular clear space on the anterior-posterior view is the most reliable parameter for detecting widening of the syndesmosis on plain radiographs. However, due to its variability among different individuals, comparison views of the contralateral extremity are warranted for confirmation of clinical suspicion of syndesmosis disruption.

The purposes of the project were to monitor the development of the lower extremities and the longitudinal arch of the foot and to determine whether or not arch support footwear (three types) affected development of a neutral arch in toddlers 11 to 14 months of age until age 5 years. A total of 125 beginner walkers were recruited through the pediatrics department during a period of 1 1/2 years and divided by lot into four different footwear groups (one nonarch supportive). The group was studied for 4 years by physical examinations, x-ray films, and pedotopography (a Moire fringe technique of photography). At initial examination all of the apparently normal toddlers had pes planus by all clinical, roentgenographic, and photographic measurements. There were no cavus feet at that time or at 5 years of age. Arches developed regardless of the footwear worn but development was faster during the first 2 years (until age 3 years) with arch support footwear. The rapidity of arch development until 5 years of age continued in those children who wore longitudinal arch cookies. Ossification of the sustentaculum tali begins at approximately 5 years of age but is not complete for at least another 1 to 2 years. Hyperpronation was present in 77.9% and genu valgum in 92.3% of the 5-year-old children. These conditions are apparently the norm at this age in both boys and girls.