Diffuse axonal injury without direct head trauma and with delayed onset of coma.

A 16-year-old female was involved in a jet ski (water craft) accident resulting in bilateral lower extremity fractures but no loss of consciousness or any other evidence of head trauma. Thirty hours later she became comatose. Magnetic resonance imaging was consistent with diffuse axonal injury.

The effects of acetyl-L-carnitine and sorbinil on peripheral nerve structure, chemistry, and function in experimental diabetes.

Nerve conduction velocity (NCV) increased with age in nondiabetic male Wistar rats for the first 26 weeks of life. The NCV of animals made hyperglycemic at age 6 weeks by administration of streptozotocin (STZ) also increases, but at a slower rate. Animals with 4 weeks of hyperglycemia and reduced NCV treated with an aldose reductase inhibitor (sorbinil) or a short-chain acyl-carnitine (acetyl-L-carnitine [ALC]) daily for 16 weeks showed an improvement in NCV.

Nerve and muscle damage after experimental thrombosis of large artery. Electrophysiology and morphology.

The effect of the terminal aorta thrombosis on the spinal cord and hind limb nerves and muscles morphology, and the sciatic-tibial motor nerve conduction was studied in cats. The effect of the iliac and femoral artery thrombosis on nerve morphology and conduction was also examined. Aortic thrombosis usually caused severe nerve and muscle lesions while spinal cord was spared.

The effect of hyperglycemia on nerve conduction and structure is age dependent.

The nerve conduction velocity (NCV) of nondiabetic male Wistar rats continues to increase until approximately 26 weeks of age. Rats made hyperglycemic at 6 weeks of age manifest reduced NCV by 10 weeks of age and show morphological differences in the sciatic tibial nerve after 5 months of hyperglycemia when compared with age-matched controls. Fiber diameter, myelin width, and the number of large myelinated fibers were decreased in the tibial nerves of the hyperglycemic animals.