A porcine model of neurological decompression illness (DCI) and its treatment is described.Pigs (wt. 16-22 kg) underwent a simulated dive to 200 feet of seawater (fsw) (612.6 kPa) for 24 min, then decompressed at 60 fsw/min-1 (183 kPa.min-1). Pigs that developed neurological DCI were sedated with diazepam, then treated by recompression on U.S. Navy Treatment Table 6. Functional outcome was assessed by treadmill running. At necropsy 24 h postdive, carcass density was measured by underwater weighing, and tissue samples including heart, spinal cord, and brain were taken for histopathological examination.Neurological DCI occurred in 73% of control animals and developed within 2-7 min in 50% of cases. Affected pigs had significantly earlier onset of skin DCI than unaffected pigs (means: 9.52 min vs. 17.9 min, p < 0.001). Only 16.4% of pigs made a full functional recovery after recompression treatment. Outcome at 24 h was not improved in 20 pigs randomized to receive adjunctive lidocaine infusion compared to 20 pigs that received saline alone. Following necropsy, 77% of cases had petechial hemorrhages grossly visible in the spinal cord. Multifocal, microscopic hemorrhages, predominantly of spinal cord white matter, were found in 86.6% of DCI cases. Neither weight, density, nor genetic predisposition were found to influence DCI risk.The model is analogous to severe, early-onset, neurological DCI in humans and allows prospective evaluation of risk reduction and treatment stratagems for this form of DCI. Many applied and basic science issues relevant to diving medicine may also be studied using the model, and adaptation to study hypobaric DCI and other clinical applications of hyperbaric oxygen is feasible.