Fig. 2. Spinal cord lumbar segment proximal to catheter tip. Hematoxylin and eosin–stained sections for N -methyl-d-aspartate antagonist–treated and saline-treated control animals. ( A ) Saline-treated animal at the thoracic level. Bar = 100 mm. ( B ) Ketamine (10 mg/day)–treated animal. Bar = 25 mm. ( C ) Amitriptyline (8 mg)–treated animal. Bar = 50 mm. ( D ) Memantine (8 mg)–treated animal. Bar = 50 mm. ( E ) S -Methadone (1 mg/day)–treated animal. Bar = 50 mm. ( F ) AP5 (1 mg/day)–treated animal. Bar = 50 mm. Moderate to severe necrosis and inflammation of peripheral and central spinal cord elements is present in N -methyl-d-aspartate antagonist–treated animals compared with the control animal. B : This segment of submeningeal parenchyma of a ketamine-treated animal demonstrates the perivascular inflammation that extends into the Virchow-Robbins space and the edema within the white matter parenchyma. C : Memantine treatment resulted in the extensive coagulative necrosis and fibrinoid vasculitis that surrounds the parenchymal infarct seen in figure 1C. D : Amitriptyline induced a significant perivascular inflammation surrounding the meningeal and parenchymal vessels. Note the expanded meninges with necrosis and inflammation. E : Methadone treatment resulted in a large, focal infarct within the white matter parenchyma. A dense accumulation of inflammation surrounds the necrotic tissue. F : The edge of the catheter tract is illustrated here in the AP5-treated animal with extensive hemorrhage and necrosis adjacent to the fibrotic inflammatory reaction at the catheter tip that compresses the parenchyma. There is generalized edema of the subjacent white matter parenchyma.