Summary:The effects of the glutamate N-methyl-D aspartate (NMDA) receptor antagonist, MK-801, upon ischemic brain damage has been examined in anesthe tized cats. Focal cerebral ischemia was produced by per manent occlusion of one middle cerebral artery and the animals were killed 6 h later. The amount of early isch emic damage was assessed in coronal sections at 16 pre determined stereotactic planes. Pretreatment with MK-801 (5 mg/kg, i.v.). 30 min before occlusion of the Glutamate is a major excitatory neurotransmitter in the mammalian central nervous system. The ac tions of glutamate are mediated via three pharma cologically distinct subtypes of receptor, the no menclature of which reflects the preferred agonist at each receptor subtype viz. the quisqualate-, kainate-, and N-methyl-D-aspartate-(NMDA)-pre ferring receptor (Greenamyre et aL, 1985). Gluta mate has recently been implicated in the patho physiology of cerebral ischemia (Meldrum 1985; Rothman and Olney, 1986). Glutamate itself is neu rotoxic when injected into cerebral tissue (Rothman and Olney, 1986). Cerebral ischemia is associated with a massive increase in extracellular glutamate concentrations (Benveniste et aL, 1984;Hagberg et aL, 1985). Destruction of glutamatergic afferent pathways or intracerebral administration of NMDA receptor antagonists can reduce the early ischemic damage to the hippocampus in cerebral ischemia and the neuronal necrosis which is observed sev eral days after a period of cerebral ischemia or se-

Recent arouse of interest indicated that drug resistant proteins are markedly over-expressed in the epileptogenic tissue and they may be responsible for the one-third of the epileptic patients who were refractory to anti-epileptic drugs (AEDs). Since several AEDs may act as substrates for these drug resistant proteins, the enhanced function of such proteins may increase drug extrusion, resulting in inadequate response to drug therapy in patients with epilepsy. We studied expression of the multidrug resistance protein 1 (MDR1) and multidrug resistance-associated protein 1 (MRP1) in the epileptic tissues resected surgically in 28 patients with focal cortical dysplasia (FCD) by immunohistochemistry. The results were compared with 10 normal necropsy brain tissues. Normal brain showed no MDR1 expression in neurons and astrocytes, while MRP1 expression was very weak, which were encountered in a few samples. MDR1 expression was mainly localized on the vascular endothelial cells. In contrast to normal brain, we found intense MDR1 and MRP1 expression in both neurons and reactive astrocytes in the vast majority of dysplastic tissues. The majority of the dysplastic neurons demonstrated moderate to strong MRP1 immunoreactivity. Endothelial cells showed both MDR1 and MRP1 expression in the majority of the specimens studied. Multidrug transporters are over-expressed in the epileptogenic zone in patients with FCD. These results are concordant with previous studies, in which over-expression of multidrug proteins were shown in epileptogenic brain tissue in patients with FCD, that the over-expression of drug transport proteins in tissue from patients with refractory epilepsy may explain one possible mechanism for drug resistant in these pathologies.

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SUMMARYSeizure outcome in mesial temporal lobe epilepsy related to hippocampal sclerosis (MTLE-HS) that was evaluated according to a noninvasive protocol was assessed in 165 patients and reported using both Engel's and ILAE classifications. The mean postoperative follow-up was 5.0 ± 2.7 years. At the end of first year, 77.1% of patients were in Engel-I, and 52.7% were in ILAE-I. Antiepileptic drugs (AEDs) were discontinued in 41 patients (42.7%), all remained seizure-free for >2 years that could be accepted as "cure." Thirty-six patients had recurrences, 19 had running-down phenomena. Anterior temporal lobectomy (ATL) was performed in 27 patients with a better outcome when compared to patients operated by selective anterior hippocampectomy. Clinical risk factors for better and worse outcome, which show some similarity in different reports, seem to veil the main reason, which is the accurate delineation of epileptogenic zone considering the presence of different subgroups and underlying developmental pathologies. KEY WORDS: Hippocampal sclerosis, Temporal lobe epilepsy, Surgery.Mesial temporal lobe epilepsy (MTLE) is a form of focal seizure disorder that is refractory to antiepileptic drug (AED) therapy and known to be remediable by surgery, and hippocampal sclerosis (HS) is the most frequent substrate obtained from the surgical specimens in these patients. About 55-70% of patients undergoing temporal resection become completely seizure-free (Engel et al., 1993), where 20-30% of patients still experience seizures following surgery (Wyler et al., 1995;. Moreover, it is difficult to obtain the information solely on patients with MTLE-HS in the literature due to the format of published reports usually providing data on various etiologies, missing number of patients cured or with either recurrence or running-down phenomena.In this study, we present a large surgical cohort data, examining the year-by-year seizure outcome, during a longterm postsurgical follow-up in patients with MTLE-HS evaluated nonivasively according to a standard protocol METHODSOut of 183 patients with MTLE-HS who underwent surgery since 1995, 165 patients who were followed for at least 1 year were included. Patients with normal MRI or with structural lesions other than HS were excluded. Two patients were reoperated due to insufficient seizure control and excluded at the time of second surgery. All patients were evaluated according to a noninvasive protocol including clinical assessment, ictal video-EEG, MRI, neuropsychological, and psychiatric investigations. The intracarotid amobarbital procedure was performed in 65 patients with bilateral memory deficits, left-sided focus, or discordant findings. Patients were followed for 6 months after surgery and then yearly when possible. Seizure outcome was classified according to the Engel's (Engel et al., 1993) and ILAE classifications (Wieser et al., 2001). AEDs were discontinued in patients who remained seizure-free for at least 2 years. 696

Study Design: The e ect of epidural space perfusion with chilled saline solution (% 0.9 NaCl) on lipid peroxidation after experimental spinal cord injury in rats was evaluated. Objectives: The extent of lipid peroxidation is a useful parameter for evaluating the cellular disturbance caused by spinal cord trauma in experimental conditions. The protective e ects of hypothermia against neurological injury resulting from trauma or ischemia both in experimental and clinical situations have been demonstrated. Setting: Departments of Neurosurgery and Biochemistry, Cerrahpasa Medical School, Istanbul, Turkey. Methods: Twenty-®ve female Wistar Albino rats were used. There were ®ve rats in group I (sham-operated), seven rats in group II (trauma), and eight rats in group III (epidural cooling). The remaining ®ve rats were used for the pilot study to determine the spinal cord and body temperature. A clip compression method was used to produce acute spinal cord injury. In group III, 30 min after the trauma the injured spinal cord was cooled by perfusion of the epidural space with chilled saline solution (% 0.9 NaCl) with a¯ow rate of 5 ml/min for 30 min. At 2 h after trauma, all rats other than the ones used in the pilot study, were sacri®ced and the spinal cords were excised. The extent of lipid peroxidation in the spinal cord was assessed by measuring the tissue content of malonil dialdehyde (MDA). Results: The tissue MDA contents were 1.58 micromol MDA/gram wet weight (gww) in group 1 (sham-operated), 2.58 micromol MDA/gww in group 2 (trauma), and 1.77 micromol/ gww in group 3 (epidural cooling), the di erences being statistically signi®cant. Conclusion:The results indicated that epidural cooling of traumatized spinal cord is e ective in preventing secondary damage due to the peroxidation of lipid membranes.

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To evaluate the hypothetical link between apolipoprotein E (APOE) polymorphisms and mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) and whether presence of APOE epsilon4 allele shortens the latent period between febrile seizures and epilepsy. A further interest is whether presence of APOE epsilon4 allele has an impact on severity of the disease. Forty-seven patients with MTLE-HS were compared with 62 controls. APOE polymorphisms were determined from lymphocytes by standard methods. Eight patients (17%) and 10 controls (16.1%) were demonstrated to have one APOE epsilon4 allele. There was not any statistically significant difference in APOE epsilon4 frequency between patients and controls (P > 0.05). There was not any difference statistically according to onset age of epilepsy and the presence of APOE epsilon4 allele within patient group. APOE epsilon4 polymorphisms did not influence the severity of epilepsy. APOE epsilon4 polymorphisms had no impact on outcome after surgery. Patients with bilateral memory deficits, bilateral hippocampal atrophy and with bilateral epileptiform interictal EEG transients, were independently compared with patients having unilateral features and there were not any statistically significant differences. This study has found no association between APOE epsilon4 polymorphisms and presentation of MTLE-HS in a group of Turkish patients.