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Wise Young, Eugene S. Flamm, Harry B. Demopoulos, John J. Tomasula and Vincent DeCrescito

identified and reversed. Recently, naloxone, an opiate receptor antagonist, 18 was reported to improve neurological function in cats subjected to cervical cord injury, even when given 45 minutes after injury. 19, 20 This effect was attributed to the beneficial influence of naloxone on systemic pressure and respiratory function. 19, 20, 27, 32, 38 Our experience with thoracic cord injury, however, suggests that neither systemic pressure nor respiratory function plays a major role in the development of posttraumatic ischemia. By the time ischemia occurs, 2 to 3 hours

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Eugene S. Flamm, Wise Young, William F. Collins, Joseph Piepmeier, Guy L. Clifton and Boguslav Fischer

A major impetus in acute spinal cord injury research has been the hypothesis that mechanical trauma initiates secondary and progressive injury processes in the spinal cord. This has created the hope that the injured spinal cord is amenable to treatment administered shortly after trauma. To test this hypothesis, experimental models of spinal cord injury have been used to assess treatments aimed at reducing the secondary damage. From those experiments, two drugs have recently been identified as useful: methyl-prednisolone 1, 4–8, 19–21, 26, 31 and naloxone. 13

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Methylprednisolone or naloxone treatment after acute spinal cord injury: 1-year follow-up data

Results of the second National Acute Spinal Cord Injury Study

Michael B. Bracken, Mary Jo Shepard, William F. Collins Jr., Theodore R. Holford, David S. Baskin, Howard M. Eisenberg, Eugene Flamm, Linda Leo-Summers, Joseph C. Maroon, Lawrence F. Marshall, Phanor L. Perot Jr., Joseph Piepmeier, Volker K. H. Sonntag, Franklin C. Wagner Jr., James L. Wilberger, H. Richard Winn and Wise Young

A randomized double-blind clinical trial of the efficacy of very high doses of methylprednisolone or naloxone, compared with placebo, in the early treatment of acute spinal cord injury was conducted. In a previous report, 8 we have shown that neurological function is significantly improved 6 weeks and 6 months after injury among patients starting methylprednisolone treatment within 8 hours of injury. In this paper, we report the 1-year follow-up results of this trial: the second National Acute Spinal Cord Injury Study (NASCIS). We provide further details

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Jerry L. Hubbard and Thoralf M. Sundt Jr.

functional. However, no one has demonstrated histological evidence of reduction in infarction size, CBF, or electroencephalographic (EEG) responses to naloxone in models of cerebral ischemia. If naloxone is beneficial, it may exert its effects by direct neuronal action (membrane stabilization by opioid receptor or nonopioid receptor antagonism), or indirectly by increasing CBF above the critical ischemic threshold. We have designed an experiment to determine if naloxone reduces infarction size following temporary unilateral middle cerebral artery (MCA) occlusion, and to

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Ronald L. Hayes, Brian J. Galinat, Pramod Kulkarne and Donald P. Becker

M any recent studies have suggested that endogenous opiate mechanisms may contribute to some cardiovascular consequences of shock. For example, in man, dogs, cats, and/or rats, the specific narcotic antagonist, naloxone, reduced the hypotension associated with hemorrhage, 10, 16, 41 injection of Escherichia coli endotoxin, 9, 26, 29, 34 splanchnic artery occlusion, 4 insulin injection, 28 or sleep. 38 Naloxone also attenuates the hypotension, hypothermia, and hypoventilation observed after spinal cord transection. 12, 25 Moreover, naloxone treatment

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Tomoo Furui, Issei Tanaka and Kinjiro Iwata

A lthough there have been a number of studies regarding the therapeutic use of naloxone for cerebral ischemia since the first encouraging report by Baskin and Hosobuchi, 1 its clinical efficacy remains controversial. The effects of naloxone on the neurological deficits, the size of infarction, and survival have been shown to vary. 2, 10, 14–16 Even if naloxone has some favorable effects on cerebral ischemia, the effect may be so slight as not to have been demonstrated in some of these evaluations. Recently, several reports were published concerning the role

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Robert J. Hariri, Elizabeth L. Supra, John Paul Roberts and Michael H. Lavyne

T he release of endogenous brain opioid peptides has been implicated in the pathophysiological cardiovascular alterations associated with both hypovolemic 7, 10, 15 and septic 4, 28, 33, 44, 46 circulatory shock. The combined autonomic activity of these centrally acting opioids to increase brain parasympathetic response and concomitantly to decrease brain sympathetic activity contributes to the observed bradycardia and hypotension in these states. 21, 25 Opiate receptor blockade with naloxone has been shown to increase mean arterial blood pressure and

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Michael B. Bracken and Theodore R. Holford

(NASCIS), established in 1977, conducts multicenter randomized controlled trials of therapies that might improve recovery from spinal trauma. Since its inception, the NASCIS has examined drug treatments that might ameliorate the complex series of biochemical processes known to occur in the spinal cord during the hours following traumatic insult. 23, 35 NASCIS 2 compared the use of large doses of methylprednisolone or naloxone to placebo and reported that patients who started treatment with methylprednisolone within 8 hours posttrauma had significantly improved motor

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Neurosurgical Forum: Letters to the Editor To The Editor David S. Baskin , M.D. Yoshio Hosobuchi , M.D. San Francisco, California 1328 1331 While Drs. Hubbard and Sundt appropriately selected the cat model of focal cerebral ischemia for the experiments they report in their article (Hubbard JL, Sundt TM Jr: Failure of naloxone to affect focal incomplete cerebral ischemia and blood flow in cats. J Neurosurg 59: 237–244, August, 1983), we believe that their experimental design compromises their

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Tomoo Furui, Kyoko Satoh, Yoshio Asano, Sadashi Shimosawa, Michiaki Hasuo and Tony L. Yaksh

R ecently naloxone, an opiate antagonist, has been reported to attenuate the neurological deficits in animals after spinal cord injury, 6, 7, 9, 29 cerebral artery occlusion 2, 17, 22 and cerebral concussive injury, 14 and in humans after cerebral ischemia. 1 Some possible explanations for the therapeutic mechanism of naloxone have been postulated. One likely explanation of these observations is that the ischemic event causes the peripheral or central release of opioid peptides; when the opioid peptides interact with an opiate receptor, the deleterious