Ischemic stroke remains a leading cause of morbidity and death for which few therapeutic options are available. The development of neuroprotective agents, a once promising field of investigation, has failed to translate from bench to bedside successfully. This work reviews the ischemic cascade, agents targeting steps within the cascade, and potential reasons for lack of translation. Additional therapeutic targets are highlighted and areas requiring further investigation are discussed. It is clear that alternative targets need to be pursued, such as the role glia play in neurological injury and recovery, particularly the interactions between neurons, astrocytes, microglia, and the vasculature. Similarly, the biphasic nature of many signaling molecules such as matrix metalloproteinases and high-mobility group box 1 protein must be further investigated to elucidate periods of detrimental versus beneficial activity.

The sural nerve is at risk of iatrogenic injury even during minimally invasive operative procedures to repair the calcaneal (Achilles) tendon. Through 107 cadaveric leg dissections, the data derived from the present study was used to develop a regression equation that will enable surgeons to estimate the intersection point at which the sural nerve crosses the lateral border of the Achilles tendon, an important surgical landmark. In most cases, the sural nerve crossed the lateral border of the Achilles tendon 8 to 10 cm proximal to the superior border of the calcaneal tuberosity. By simply measuring the leg length of the patient (from the base of the heel to the flexor crease of the popliteal fossa), surgeons can approximate the location of this intersection point with an interval length of 0.68 to 1.80 cm, with 90% confidence, or 0.82 to 2.15 cm, with 95% confidence. For example, for a patient with a lower leg length of 47.0 cm, the mean measurement in the present study, a surgeon can be 90% confident that the sural nerve will cross the lateral border of the Achilles tendon 8.28 to 8.96 cm (interval width of 0.68 cm) proximal to the calcaneal tuberosity. Currently, ultrasound and clinical techniques have been implemented to approximate the location of the sural nerve. The results of the present study offer surgeons another method, that is less intensive, to locate reliably and subsequently avoid damage to the sural nerve during calcaneal (Achilles) tendon repair and other procedures of the posterolateral leg and ankle.

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Using a standard acceleration-deceleration model of mild traumatic brain injury, we have shown successful visualization of traumatically injured axons with antibody staining of APP. Our results indicate no statistically significant effect of anabolic steroids on the number of APP-positive axons. With the use of this model, and within its limitations, we see no adverse effect or causative role of anabolic steroid administration on the brain following mild traumatic brain injury using APP counts as a marker for anatomic injury.

The present study demonstrates the wide variability within the cervical anatomy of the phrenic nerve.