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 explore the clinical and MRI features multiple system atrophy (MSA) and the significance of diagnosing its clinical subtypes.Methods Clinical data and MRI features of 28 patients with MSA were retrospectively analyzed and compared.Results Cerebellar signs (75.0%) were dominant clinic features in olivopontocerebellar atrophy (OPCA). Brain MRI showed atrophy of pontine (91.7%) and cerebellar vermis (91.7%), fourth ventricle dilatation (83.8%) and T2WI high intensity in pontocerebellar region (63.6%). Extrapyramidal signs (80.0%) were found in striatonigral degeneration (SND) with apparent basal ganglia changes such as putamen atrophy (60.0%) and lineal T2WI high intensity of the lateral margin of the putamen (putamen slit) (80.0%). Shy-Drager syndrom (SDS) presented mainly with autonomic nerve system (81.8%), and autonomic nerve system failures appeared earlier and more severe than the other two subtypes of MSA. Conclusions MRI examination may be useful in diagnosis of MSA and its subtypes. Pontine atrophy, T2WI high intensity, especially pontine cross sign may support diagnosis of OPCA. However, putamen atrophy and putamen slit are the specific imaging signs in SND.

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 investigate the rate of anxiety after str oke and study the effect of psychological intervention.Method:206 i npatients(male 126,female 80,mean age 63?16)with stroke were divided into inte rvention group(103 cases)and control group(103 cases),which matched by sex a nd age.All subjects were tested with SAS,DNF,MMSE,LES and ADL before interventi o n,3 months,6 months and 12 months later.Results:The rate of anxiety a fter 1 month of stroke in our sample was 18.4%.The reduction rate of SAS was g re ater in intervention group than control at all follow up points.Multi-factorial analysis showed,many factors including female,younger at onset,severity of strok e,poor general physical condition,less compliance with treatment,and other psych o-social factors(heavier family burden,less income,more life events,less social support)were all associated with anxiety after stroke and less reduction rate of SAS at intake and during follow up.Conclusion:Anxiety is a common c omplication after stroke,its occurrence and maintenance were associated with a v ariety of factors including severity of illness and psychosocial factors.Suppor tive psychological intervention can reduce anxiety after stroke.

Objective To study the role of GABA (? aminobutyric acid) transporters in kindled.Methods The rat's GABA model following PTZ kindled was made.The expression of GABA transporter subtype in the hippocampus(GAT 1 mRNA) was measured after PTZ (pentylenetetrazol) kindled seizures by using semiquantitative technique,reverse transcription polymerase chain reaction (RT PCR).Results GAT 1 mRNA was significantly increased in the hippocampus at 0 hour,48 hours,and 1 week after PTZ kindled seizures. Up regulation of expression of GAT 1 mRNA returned to the control levels after 1 month. No changes in the expression of GAT 1 mRNA were observed after 60 days of PTZ kindled seizures.Conclusion The expression of GAT 1 mRNA with up regulation may be associated with the epilepsy susceptibility.

Objective To investigate Guillain Barre syndrome (GBS) combined with demyelinating neuropathy in central nervous system(CNS), and explore the possible mechanism and the relationship between the two.Methods 3 cases GBS combined with demyelinating neuropathy in CNS were observed clinically and the datum of laboratory were analysed.Results Case 1, a 28 year old man had symptoms of general flaccid paralysis and coma.The result of blood gas analysis was normal. CSF showed an albuminocytological dissociation, delayed nerve conduction velocity and missed F waves. Brain MRI showed multifocal T 2 Wight Image high signs in white matter of bilateral brain and cervical spinal cord. The patient is getting recovery by treatment with plasma and immunoglobulin. Case 2 , a 5 year old girl with progressive weakness of her limbs and respiratory arrest, appeared confusion,dully light reflex and absent corneal reflex, at last she died because of rejecting treatment.Case 3,a 12 year old boy with progressive weakness of his limbs and the difficult of relieving the bowels.Brain MRI was normal.Spinal MRI showed multifocal T 2 weight imagine hight signs from T 5 to L 4.CSF showed an albuminocytological dissociation.EMG showed a delayed nerve conduction velocity.Conclusion GBS combined with disorders of consciousness are mostly severe, the pathological mechanism is unclear. It is suggested that auto immunoreaction caused by P 1 myelin basic protein can relate to around and CNS demyelination.