The objective of this study was to evaluate the conditions of ankle stability and the morphological and/or lesional factors in sprains that determine when instability becomes chronic. It is based on a review of the literature and the data from the 2008 Sofcot symposium. The biomechanics of the ankle cannot be reduced to a simple flexion-extension movement with one degree of freedom as characterized by the talocrural joint: its function cannot be dissociated from the subtalar joint, allowing the foot to adapt to the ground surface. Functional stability is related to the combination of the particular biometry of the joint surfaces and a multiaxial ligament system. The bone morphology of the talus, shaped like a truncated cone, explains the potential instability in plantar flexion; the radii of curvature of the talar dome have a variable mediolateral distribution: most often the medial radius of curvature is inferior to the lateral radius of curvature (66%), sometimes equal (19%), or inverted (15%). Joint kinematics, combining rotation and slide, can therefore be modulated by the talar morphology, explaining the occurrence of at-risk ankles. Ligament stability relies on the organization in three parts of the lateral collateral ligament and the specific subtalar ligaments: the cervical and the talocalcaneal interosseous ligament. The different injury mechanisms are largely responsible for the sequence of ligament lesions: the most frequent is inversion. The first ligament stabilizers correspond to the cervical and anterior talofibular ligaments; the talocalcaneal ligament, by its oblique orientation, is solicited when there is a dorsal varus-flexion component. In chronic instability, these mechanisms explain the onset of associated lesions (impingement, osteochondral lesions, fibular tendon pathology), which can play a role in instability syndrome. Ligament lesions determine laxity, characteristic of mechanical instability. Functional instability goes along with proprioceptive deficiency. There are postural factors such as varus of the hindfoot that favor instability. Knowledge of all these factors, often associated, will provide a precise lesional assessment and treatment adapted to the instability.
On the basis of 100 brachial plexus dissections in adult subjects, the angular variations of roots in their intrarachidian and cervical portions are examined. Serial histological sections of 21 brachial plexuses allow one to define fascicular histologic organization. These descriptions of biometric anatomical variation and complexity in histological fascicular organization help to elucidate the difficulties that must be overcome following nerve suture in order to achieve a satisfactory functional recovery.
Cognitive dysfunction in the elderly commonly observed following anesthesia has been attributed to age-related neuronal changes exacerbated by pharmacotoxic effects. However, the extent to which these changes may persist following recovery from surgery is still largely unknown. This study investigates the long-term effects of anesthesia on cognitive functioning after orthopedic surgery in 270 elderly patients over the age of 65 who completed a computerized cognitive battery before and 8 days, 4 and 13 months after surgery. Their performance was compared to those of 310 elderly controls who completed the same neuropsychiatric evaluation at baseline and one-year interval. Multivariate analyses adjusted for socio-demographic variables, depressive symptomatology, vascular pathology as well as baseline cognitive performance. We found early and transient post-operative decline in reaction time and constructional praxis. With regard to long-term changes we observed improvement compared to controls in most verbal tasks (probably due to learning effects). On the other hand, a clear dissociation effect was observed for several areas of visuospatial functioning which persisted up to the 13-month follow-up. This specific pattern of visuospatial deficit was found to be independent of apolipoprotein E genotype and closely resembles what has recently been termed vascular mild cognitive impairment, in turn associated with subtle sub-cortical vascular changes. The observation of only minor differences between persons operated by general and regional anesthesia makes it difficult to attribute these changes directly to the anesthetic agents themselves, suggesting that cognitive dysfunction may be attributable at least in part to peri-operative conditions, notably stress and glucocorticoid exposure.
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