Peripheral axonal neuropathies are important but poorly understood causes of neuromuscular disease. Our limited understanding of the circumstances under which axons fail in neuropathies reflects an incomplete knowledge of the physiology and metabolism of normal nerves and the compensatory metabolic responses that follow nerve injury. The present studies will begin by characterizing the perfusion, glucose utilization and bioenergetic status of normal nerves. We will then assess the effects of graded ischemia on nerve metabolism, conduction, axonal transport and fiber degeneration. Finally, we will extend these studies by measuring reactive changes in perfusion and glucose metabolism that follow crush-induced Wallerian degeneration and subsequent regeneration. These investigations will allow us to better define the metabolic requirements of normal nerves and the alterations that occur after neural injury.
| Bird, S J; Sladky, J T (1991) Corticosteroid-responsive dominantly inherited neuropathy in childhood. Neurology 41:437-9 |
| Sladky, J T; Tschoepe, R L; Greenberg, J H et al. (1991) Peripheral neuropathy after chronic endoneurial ischemia. Ann Neurol 29:272-8 |
| Epstein, M A; Sladky, J T (1990) The role of plasmapheresis in childhood Guillain-Barre syndrome. Ann Neurol 28:65-9 |
| Glauser, T A; Maguire, H C; Sladky, J T (1990) Relapse of infant botulism. Ann Neurol 28:187-9 |
| Clancy, R R; Sladky, J T; Rorke, L B (1989) Hypoxic-ischemic spinal cord injury following perinatal asphyxia. Ann Neurol 25:185-9 |
| Maguire, H C; Sladky, J T (1989) Diagnosis and management of diseases affecting the motor unit in infancy. R I Med J 72:361-6 |
| Xu, Y; Sladky, J T; Brown, M J (1989) Dose-dependent expression of neuronopathy after experimental pyridoxine intoxication. Neurology 39:1077-83 |
