Journal of neurotrauma
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Journal of neurotrauma · Jan 1993
Surface and epidural lumbosacral spinal cord evoked potentials in chronic spinal cord injury.
Nine patients were examined in the chronic stage of spinal cord injury (12 to 56 months postinjury). Surface lumbosacral spinal cord evoked potentials (LSEPs) were obtained using electrodes placed over the S1, L2, L4, and T12 vertebral levels, referenced to a T6 surface electrode. Epidural LSEPs were obtained using a multielectrode lead placed percutaneously into the epidural space for evaluation of the efficacy of spinal cord stimulation for modification of pain and spasticity. ⋯ The LSEPs for the marginal group (n = 2, 1 incomplete and 1 complete) showed similar epidural/surface amplitude ratios. In the abnormal case (n = 1, complete) surface LSEPs were absent but epidural LSEPs were present but with stationary and propagating components of low amplitude. This study demonstrates the ability of the epidural LSEP to provide more information than the surface LSEP of the functional condition of the lumbosacral spinal cord, particularly regarding the character of the propagating action potentials and in cases when the surface LSEPs appear to be of very low amplitude or absent.
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Journal of neurotrauma · Jan 1993
Lactated Ringer's solution alleviates brain trauma-precipitated lactic acidosis in hemorrhagic shock.
To determine the influence of brain trauma on blood acid-base and lactate-pyruvate responses to hemorrhage, and the effect of lactated Ringer's solution on these responses, 30 anesthetized rats were assigned to four groups: hemorrhage (n = 7), hemorrhage following fluid percussion brain trauma (trauma-hemorrhage group) (n = 7), hemorrhage treated with lactated Ringer's solution (hemorrhage-resuscitation group) (n = 8), and hemorrhage following brain trauma treated with lactated Ringer's solution (trauma-hemorrhage-resuscitation group) (n = 8). The hemorrhage group showed no significant changes in pH, HCO3, and base excess after hemorrhage. Base excess and pH were significantly reduced after the hemorrhage in the trauma-hemorrhage group but were raised after resuscitation in the hemorrhage-resuscitation group. ⋯ Lactate rose significantly after hemorrhage in the hemorrhage group and was even higher in the trauma-hemorrhage group, but there were no differences between the hemorrhage versus hemorrhage-resuscitation or trauma-hemorrhage-resuscitation groups. Both brain trauma and lactated Ringer's solution increased pyruvate with marked reduction in the ratio of lactate to pyruvate. These data indicate that brain trauma precipitates blood lactate accumulation and metabolic acidosis after hemorrhage, and infusion of lactated Ringer's solution can relieve these disturbances.
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Journal of neurotrauma · Jan 1993
Randomized Controlled Trial Clinical TrialA phase II study of moderate hypothermia in severe brain injury.
Forty-six patients with severe nonpenetrating brain injury [Glasgow Coma Scale (GCS) 4-7] were randomized to standard management at 37 degrees C (n = 22) and to standard management with systemic hypothermia to 32 to 33 degrees C (n = 24). The two groups were balanced in terms of age (Wilcoxon's rank sum test, p > 0.95), randomizing GCS (chi-square test, p = 0.54), and primary diagnosis. Cooling was begun within 6 h of injury by use of cooling blankets. ⋯ Sepsis was seen more commonly in the hypothermia group, but difference was not statistically significant (chi-square test). Mean Glasgow Outcome Scale (GOS) score at 3 months after injury showed an absolute increase of 16% (i.e., 36.4-52.2%) in the number of patients in the Good Recovery/Moderate Disability (GR/MD) category as compared with Severe Disability/Vegetative/Dead (SD/V/D) (chi-square test, p > 0.287). Based on evidence of improved neurologic outcome with minimal toxicity, we believe that phase III testing of moderate systemic hypothermia in patients with severe head injury is warranted.
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Journal of neurotrauma · Jan 1993
Behavioral protection by moderate hypothermia initiated after experimental traumatic brain injury.
The effects of postinjury hypothermia on behavioral outcome following moderate fluid percussion traumatic brain injury (TBI) were examined. In Experiment I, three groups of rats were examined. The first group was normothermic (37.5 degrees C); and hypothermia (30 degrees C) was initiated 15 min and 30 min postinjury in the second and third groups, respectively. ⋯ In Experiment II, subcortical brain temperature was compared to temporalis muscle temperature in normothermic (37.5 degrees C) and hypothermic (30 degrees C) rats subjected to TBI. In both groups brain temperature tracked within 0.4 degree C of temporalis muscle temperature. These results are similar to post-TBI excitatory receptor antagonist studies and indicate a therapeutic window for moderate hypothermia of less than 30 min after moderate fluid percussion TBI in the rat.