Cervical myelopathy with false localizing sensory levels.

BACKGROUND: The diagnosis of cervical myelopathy is not always initially recognized. Only a few reports have described the discrepancy between sensory level and the site of cord compression, but none, to our knowledge, have used magnetic resonance imaging (MRI) for localization. OBJECTIVE: To identify a syndrome of compressive cervical myelopathy with false localizing thoracic sensory levels. DESIGN: Case series. SETTING: A university hospital referral center. RESULTS: Four men, aged 24 to 60 years, presented with progressive weakness and hyperreflexia involving the lower extremities and distinct thoracic sensory levels ranging from T-4 to T-10. None of these patients had cervical pain, history of trauma, or upper extremity symptoms. Results of MRI scans of the thoracic spinal cord were unremarkable. Initially, 1 patient was suspected of having transverse myelitis and was treated with high-dose steroids. All 4 patients were eventually found to have cervical spinal cord compression, diagnosed by MRI. Three patients underwent surgery for decompression of the cervical lesion. While all 3 improved in lower extremity strength, 2 had persistent discrete thoracic sensory levels postoperatively. CONCLUSIONS: Failure to diagnose cervical myelopathy because of the presence of a thoracic sensory level can delay appropriate treatment or lead to incorrect therapy. Persistence of a thoracic sensory level following surgery can occur.

Human and behavioral factors contributing to spine-based neurological cockpit injuries in pilots of high-performance aircraft: recommendations for management and prevention.

In high-performance aircraft, the need for total environmental awareness coupled with high-g loading (often with abrupt onset) creates a predilection for cervical spine injury while the pilot is performing routine movements within the cockpit. In this study, the prevalence and severity of cervical spine injury are assessed via a modified cross-sectional survey of pilots of multiple aircraft types (T-38 and F-14, F-16, and F/A-18 fighters). Ninety-five surveys were administered, with 58 full responses. Fifty percent of all pilots reported in-flight or immediate post-flight spine-based pain, and 90% of fighter pilots reported at least one event, most commonly (> 90%) occurring during high-g (> 5 g) turns of the aircraft with the head deviated from the anatomical neutral position. Pre-flight stretching was not associated with a statistically significant reduction in neck pain episodes in this evaluation, whereas a regular weight training program in the F/A-18 group approached a significant reduction (mean = 2.492; p < 0.064). Different cockpit ergonomics may vary the predisposition to cervical injury from airframe to airframe. Several strategies for prevention are possible from both an aircraft design and a preventive medicine standpoint. Countermeasure strategies against spine injury in pilots of high-performance aircraft require additional research, so that future aircraft will not be limited by the human in control.

Endotoxin treatment inhibits glucocorticoid induction of hepatic enzymes at a late induction step.

Bacterial endotoxin inhibits the glucocorticoid induction of several hepatic enzymes including phosphoenolpyruvate carboxykinase (PEPCK). Experiments were performed to elucidate the mechanism of this inhibition by examination of the early events in the glucocorticoid induction process. At a dose of endotoxin 2-to 10-fold greater than that required to inhibit the induction of PEPCK activity, no effect on the entry of glucocorticoids into hepatocytes or their ability to form complexes with glucocorticoid receptors could be measured. Binding data showed no effect of endotoxin treatment on the association or dissociation kinetics of the steroid-receptor binding reaction. Scatchard analysis revealed no effect on the affinity and number of hepatic glucocorticoid receptor binding sites, indicating that down-regulation of receptors is not responsible for inhibition of induction. Finally, activation of receptor complexes was unaffected as well by endotoxin treatment. We conclude from these data that endotoxin does not act at the early events in the glucocorticoid induction process and must therefore intervene at a subsequent step.