The effects of methylprednisolone and the ganglioside GM1 on acute spinal cord injury in rats

Shlomo Constantini M.D.1 and Wise Young M.D., Ph.D.1
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  • 1 Department of Neurosurgery, New York University Medical Center, New York, New York
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✓ Recent clinical trials have reported that methylprednisolone sodium succinate (MP) or the monosialic ganglioside GM1 improves neurological recovery in human spinal cord injury. Because GM1 may have additive or synergistic effects when used with MP, the authors compared MP, GM1, and MP+GM1 treatments in a graded rat spinal cord contusion model. Spinal cord injury was caused by dropping a rod weighing 10 gm from a height of 1.25, 2.5, or 5.0 cm onto the rat spinal cord at T-10, which had been exposed via laminectomy. The lesion volumes were quantified from spinal cord Na and K shifts at 24 hours after injury and the results were verified histologically in separate experiments. A single dose of MP (30 mg/kg), given 5 minutes after injury, reduced 24-hour spinal cord lesion volumes by 56% (p = 0.0052), 28% (p = 0.0065), and 13% (p > 0.05) in the three injury-severity groups, respectively, compared to similarly injured control groups treated with vehicle only. Methylprednisolone also prevented injury-induced hyponatremia and increased body weight loss in the spine-injured rats. When used alone, GM1 (10 to 30 mg/kg) had little or no effect on any measured variable compared to vehicle controls; when given concomitantly with MP, GM1 blocked the neuroprotective effects of MP. At a dose of 3 mg/kg, GM1 partially prevented MP-induced reductions in lesion volumes, while 10 to 30 mg/kg of GM1 completely blocked these effects of MP. The effects of MP on injury-induced hyponatremia and body weight loss were also blocked by GM1. Thus, GM1 antagonized both central and peripheral effects of MP in spine-injured rats.

Until this interaction is clarified, the authors recommend that MP and GM1 not be used concomitantly to treat acute human spinal cord injury. Because GM1 modulates protein kinase activity, protein kinases inhibit lipocortins, and lipocortins mediate anti-inflammatory effects of glucocorticoids, it is proposed that the neuroprotective effects of MP are partially due to anti-inflammatory effects and that GM1 antagonizes the effects of MP by inhibiting lipocortin. Possible beneficial effects of GM1 reported in central nervous system injury may be related to the effects on neural recovery rather than acute injury processes.

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    Young W, , DeCrescito V, & Flamm ES, et al: Tissue Na, K, and Ca changes in regional cerebral ischemia: their measurement and interpretation. Cent Nerv Syst Trauma 3:215234, 1986 Young W, DeCrescito V, Flamm ES, et al: Tissue Na, K, and Ca changes in regional cerebral ischemia: their measurement and interpretation. Cent Nerv Syst Trauma 3:215–234, 1986

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  • 134.

    Young W, & Flamm ES: Effect of high-dose corticosteroid therapy on blood flow, evoked potentials, and extracellular calcium in experimental spinal injury. J Neurosurg 57:667673, 1982 Young W, Flamm ES: Effect of high-dose corticosteroid therapy on blood flow, evoked potentials, and extracellular calcium in experimental spinal injury. J Neurosurg 57:667–673, 1982

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  • 135.

    Young W, & Koreh I: Potassium and calcium changes in injured spinal cords. Brain Res 365:4253, 1986 Young W, Koreh I: Potassium and calcium changes in injured spinal cords. Brain Res 365:42–53, 1986

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  • 136.

    Young W, , Rappaport ZH, & Chalif DJ, et al: Regional brain sodium, potassium, and water changes in the rat middle cerebral artery occlusion model of ischemia. Stroke 18:751759, 1987 Young W, Rappaport ZH, Chalif DJ, et al: Regional brain sodium, potassium, and water changes in the rat middle cerebral artery occlusion model of ischemia. Stroke 18:751–759, 1987

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  • 137.

    Zor U, , Her E, & Braquet P, et al: A novel mechanism of glucocorticosteroid (GC) action in suppression of phospholipase A2 (PLA2) activity stimulated by Ca2+ ionophore A23187: induction of protein phosphatases. Adv Prostaglandin Thromboxane Leukot Res 21A:265271, 1991 Zor U, Her E, Braquet P, et al: A novel mechanism of glucocorticosteroid (GC) action in suppression of phospholipase A2 (PLA2) activity stimulated by Ca2+ ionophore A23187: induction of protein phosphatases. Adv Prostaglandin Thromboxane Leukot Res 21A:265–271, 1991

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