Electrocorticogram can be used to define the location and extent of epileptic foci during epilepsy surgery. However, electrocorticogram can be affected by anesthetic technique. The present study found that sevoflurane concentration and hyperventilation affected the frequency and the extent of electrocorticogram spike activity in epileptic patients.

Recent investigation suggested neuroprotective efficacy of a delta-opioid agonist in the brain. We investigated the effects of intrathecal treatment with a delta-opioid agonist (SNC80) on spinal cord ischemia (SCI) in rats. SCI was induced with an intraaortic balloon catheter. The animals were randomly allocated to one of the following five groups: 1) SNC80 before 9 min of SCI (SNC-9; n = 12), 2) vehicle before 9 min of SCI (V-9; n = 12), 3) SNC80 before 11 min of SCI (SNC-11; n = 10), 4) vehicle before 11 min of SCI (V-11; n = 12), or 5) sham (n = 12). SNC80 (400 nmol) or vehicle was administered 15 min before SCI. Forty-eight hours after reperfusion, hind-limb motor function was assessed by using the Basso, Beattie, Bresnahan (BBB) scale (0 = paraplegia; 21 = normal) and histological assessment of the L4 and L5 spinal segments was performed. BBB scores in the SNC-9 group were higher compared with those in the V-9 group (P < 0.05), whereas there were no differences in BBB scores between the SNC-11 and V-11 groups. There were significantly more normal neurons in the SNC-9 and SNC-11 groups than in the V-9 and V-11 groups (P < 0.05). The results indicate that intrathecal treatment with the delta-opioid agonist SNC80 can attenuate hind-limb motor dysfunction and neuronal injury after SCI in rats.

The results in the current study show that SCI induced white matter injury as well as gray matter injury in a rabbit model of SCI. The time course for 14 days after reperfusion may differ among the gray and white matter damages and hind-limb motor function in rabbits subjected to SCI.

The results indicated that the amount of blood in the right sylvian fissure was significantly associated with the development of angiographic vasospasm after SAH.