OBJECTIVE: Epileptic attack can cause neuronal damage and increase the risk of potential seizure. Analysis of the possible mechanism of neuronal damage following epileptic seizure may provide evidences for implementing preventive measures against brain damage due to epileptic seizures.DATA SOURCES: A computer-based search of the related publications in PubMed database between June 1995 and June 2004 with different combinations of the key words of "epilepsy", "neuron damage", "necrosis"and "apoptosis", limiting the results to the language of English.STUDY SELECTION: The retrieved articles were examined at first to select reports of experimental study on human and animals related to epilepsy and the subsequent neuronal damages, and their full-text publications were obtained with the other unrelated articles excluded.DATA EXTRACTION: Eighteen articles documenting randomized controlled experiment immediately related to neuronal damage after epilepsy seizure, 4 reporting non-randomized controlled experiments related to central neuronal excitatory toxic damage, and 3 concerning neuronal damage were collected for this review.DATA SYNTHESIS: In the 14 randomized controlled experiments, chemical or electric methods were used to induce epilepsy in the animal models in which the ultrastructural changes of the neurons and cell organelles were observed and the expression of apoptosis-related factors determined.In the 4 non-randomized controlled experiments, central neuronal ischemic and hypoxic models were adopted for observing the expression of various apoptotic factors in the neurons due to different damages with the assistance of electron microscope, to provide direct evidences for the mechanism of central neuronal excitatory toxic damage. The other three related literatures introduced the pathways of neuronal damages and the expression of the related factors.CONCLUSION: Neuronal death after epileptic seizure is correlated with the severity of the damage and mitochondrial functional status, and the mitochondria constitute the control center for neuronal survival. The release of cytochrome C and the activation of caspases are the final common pathway of neuronal damage.

Objective　To study the plasticity of hippocampal formation in epilepsy.Methods　The optical density (OD)of synaptophysin positive immunoreactive product was examined by image pattern analysis instrument in hippocampus of pentylenetetrazol induced kindling epileptic rats. The examined areas included CA1,CA3 and the dentate gyrus.Results　The OD of synaptophysin positive immunoreactive product in hippocampal formation of kindling group was higher than the controls,especially in the mossy fiber layer of the area CA3 and the inner molecular layer in the dentate gyrus. Conclusion　The change of synaptophysin resulted from kindling, it also could result in the molecular elements of kindling maintenance.

Objective To observe the expression of matrix metalloproteinase-9 (MMP-9) and the regulation of neuregulin-1β (NRG-1β) in brain tissue in rats following cerebral ischemia/reperfusion injury. Methods The animal models of middle cerebral artery occlusion/reperfusion (MCAO/R) were established by a monofilament method from left external-internal carotid artery in 200 adult healthy male Wistar rats. The rat models in the treatment group (75 rats) and in control group (75 rats) were injected with 1.5%NRG-1β 5 μl and 0.1 mol/L PBS 5 μl, respectively, from internal carotid artery (ICA). The cerebral infarct volume was measured by TFC stain, the apoptosis was identified with in situ TUNEL method, and the expression of MMP-9 was detected by immunohistochemical and immunofluorescent double staining and Western blotting analysis. Results Cerebral ischemia-reperfusion can induce apoptosis and expression of MMP-9 in cerebral cortex and striatum. With the ischemic time prolonging, the number of apototic cells in cortex from ischemic 0, 0. 5, 1.0, 1.5 and 2. 0 h increased from 1.78 ± 0. 15,5. 78 ± 0. 51,10. 35 ± 0. 77, 21.50 ± 1.19 to 32. 00 ± 1.78, while the number of apoptotic cells in stratum from ischemic also increased significantly from 1.46±0.21, 4. 12±0.54, 7.33±0.71, 16.54 ± 1.63 to 19.03± 1.44 (t =9.31- 37.78, P < 0. 01) and the expression of MMP-9 increased significantly (t = 7.73-27.75, P < 0. 01) in the control group. With NRG-1β treatment, the number of apoptotie cells in cortex from ischemic 0, 0. 5,1.0, 1.5 and 2. 0 h reduced from 1.66±0. 11,4. 80±0. 61,5.63±0. 56, 9.75±1.22 to 13.54 ±1.26; while the number of apoptotic cells in striatum from ischemic also decreased significantly from 1.34 ± 0. 14, 3.35 ± 0. 32, 4. 55± 0. 50, 7. 63 ±1.41 to 10. 46 ± 0. 98 (t = 2. 74-18. 93, P < 0. 05), the expression of MMP-9 decreased (t = 3.85-12. 09, P < 0. 01), and the infarct volume decreased significantly (t = 4. 645-13. 043,P < 0. 01) compared with those in the control group at the same timepoint and the corresponding region. Conclusions The expression of MMP-9 is increased after cerebral ischemia/ reperfusion, and it may contribute to the inflammatory reaction. NRG-1β might down-regulate the expression of MMP-9 to inhibit apoptosis inducing by inflammatory reaction in cerebral ischemic reperfusion.

Objective To research the effective regions of estrogen in central nervous system of convulsive rats.Methods In two models of epilepsy with different mechanism induced by Kainic acid(KA) and flurothyl, we observed FOS expression of hippocampus, cerebral cortex and corpus striatum in the rats of convulsive group with and without estradiol (E 2) administration by means of immunohistochemistry.Results In the rats of convulsive group induced by KA and flurothyl, the FOS expression in hippocampus, cerebral cortex and corpus striatum was significant higher than those of normal control group (all P 0.05).Conclusion The FOS expression of rats'brains induced by E 2 is different in two models of epilepsy with different mechanism.

Objective To study the risk of recurrence after a first unprovoked seizure and analyze the potential predictors of recurrence. Methods 150 patients with one or more recently unprovoked seizures who attended our hospital from October, 1998 to June, 2000, which included 66 patients having a first unprovoked seizure, were followed up for 2 years. Recurrence rate was estimated by Kaplan-Meier curves. Univariate and multivariate analyses of the potential predictors of recurrence were performed for the first unprovoked seizure patients using the Cox proportional hazards model.Results All the 150 patients had 109 relapses in 2 years, Kaplan-Meier estimate of recurrence rate was 73%(?3.6%), while 66 first unprovoked seizure patients had 36 relapses, with the recurrence rate 54%(?6.1%). Cox Univariate and multivariate analyses showed that symptomatic etiology increased the risk of recurrence, and other predictors of recurrence included abnormal electroencephalogram, the occurrence of seizures during sleep and first seizure lasting longer than 10 minutes, whereas an age of 3 to 12 years decreased this risk.Conclusion The recurrence risk after the first unprovoked seizure is lower than those who have two or more recent seizures. Several factors enable us to predict the recurrence risk after a first unprovoked seizure.

Objective To observe the relations of sleep structure changes and cognitive behavior abnormalities in children with idiopathic epilepsy.Methods All night polysomnographies, day attention test and Achenbach child behavior checklist were done on 64 children with idiopathic epilepsy and 20 healthy controls the requirement. Spearman correlations were made to evaluate the correlations between the parameters of sleep structure and the results of attention and cognitive behavior abnormalities.Results All children with epilepsy had longer stage Ⅰ sleep percentage and latency of rapid eye movement (REM) sleep compared with controls (all P

Objective To observe the mitochondrion and nucleus ultrastructural damage and caspase-3 expression in hippocampal CA_3 neurons during kainic acid(KA) induced status epilepticus(SE) in rats.Methods SE was induced for 2 h with KA in adult male Wistar rats.3,12 and 24 h later the rats were killed and the hippocampal CA_3 subareas were taken out to make brain sections.The neuronal damage on the whole with light microscope and the ultrastructure of mitochondrion and nucleus with electron microscope.Caspase-3 expression of the same area was examined with immunohistochemical staining.Results 24 h after SE,by the light microscope examination,the KA group showed that the neurons put scattered disorder and nucleus shrink firmly.3 h after SE,electron microscope examination showed swelling cristae and ruptured membrane of mitochondria.The change of nucleus were significant margination of chromatin 24 h after SE.Compared to normal control group,the caspase-3 expression increased 12 h after SE,the average number of positive cell and the gray scale were obviously higher(all(P

Objective To investigate the changing features of microtubule associated protein 2 (MAP2) expression, which was a neural dendrite marker, of epileptic rat and the intervention results after using Diazepam. The relations between MAP2 and epileptogenesis were also explored.Methods Model of epileptic rat was established by Pentylenetetrazol (PTZ) and divided into PTZ-NA group,PTZ-Diazepam group, Diazepam-PTZ group and normal control group. Immunohistochemistry method was applied on hippocampus of epileptic rats to determine the change of MAP2 immunoreactivity (MAP2-IR) with or without Diazepam intervention at various time points. MAP2-IR was showed by mean optical density (COD).Results In the PTZ-NA group and PTZ-Diazepam group, MAP2-IR in molecular cell layer of hippocampal dentate gyrus increased after 3 days (all P

Objective To study the change of glutamate transporter (GluTs) function of hippocampus in seizures rats induced by KA, and explore the role of GluTs in the mechanism of epilepsy.Methods 60 adult male Wistar rats were randomly divided into two groups: KA group(Ⅰ group) and control group(Ⅱ group). Each group was randomly divided into five subgroups according to different time after kindling, including 4 h, 24 h, 48 h, 5 d,and 7 d after injection. GluTs function was studied by means of assay of 3H-L-glutamate uptake in synaptosomes and tissue sections of hippocampus.Results The function of GluTs in synaptosomes was singnificently decreased at any time (all P

Objective To investigate the clinical and electromyographic features of peripheral nerve involvement in MS. Methods The clinical and electromyographic (EMG) data of 29 MS patients were evaluated retrospectively.Results 18 (62.1%) patients showed clinical and/or electromyographic abnormalities of peripheral nerves. The clinical symptoms included extremity numbness in 16 cases (88.9%), limb inertia in 11 cases (61.1%), radicular pain in 5 cases (27.8%), autonomic nerve disorder and dysphagia in few patients. Signs included decrease of tendon reflex in 11 cases (61.1%), periphery or root form hypoesthesia in 9 cases (50%), muscle weakness in 7 cases (38.9%), myatrophy in 4 cases (22.2%), and reduced pharyngeal reflex in 1 case (5.6%). There was no difference in age of onset, course of disease, neurologic impairment and prognosis between the patients accompanied with peripheral neuropathy and the patients without peripheral neuropathy. The electromyographic abnormalities included spontaneous potential in 4 cases (13.8%), increased motor unit potential in 8 cases (27.6%), slow MCV in 15 cases (51.7%), slow SCV in 13 cases (44.8%), low amplitude in 9 cases (31.1%), and prolonged distal latency in 5 cases (17.2%). The neuropathies improved by treatment with corticosteroid in the all patients except one.Conclusions Some MS patients may accompany with peripheral nerve abnormalities, which may improve with the recovery of MS. EMG is useful to evaluale the site and degree of peripheral nerve damage.