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Objective To investigate the clinical,genetic and neuroimaging features by reporting a family with dyssynergia cerebellaris myoclonica. Methods The proband was examined clinically by neuroimaging,electromyography ( EEG),skin and muscles pathology and hematology.The patients with the illness in the family were followed up and the pedigree was drawn.Results There were 6 patients with dyssynergia cerebellaris myoclonica of the 27 family members in the family.All patients had disproportionate myoclonus,epilepsy,progressive cerebellar ataxia performance. Proband brain MRI showed cerebral atrophy.Cerebellar and cortical atrophy were more serious than other parts.There were long T,and long T2 signals in the white matter,high signal in T2FLAIR.EEG showed bursts of spike-low wave,polyspilke-low waves and polyspike waves distributing in the whole brain.Pathology of the skin and muscles was normal.Conclusions Dyssynergia cerebellaris myoclonica is an autosomal dominant disease,characterised by myoclonus,progressive cerebellar ataxia and epilepsy.Brain MRI shows cerebral cortical and cerebellar atrophy,abnormal signal in white matter.EEG showes spike and ware wave.The diagnosis is mainly based on family history,typical clinical manifestations,brain MRI and EEG changes.
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Objective To investigate the clinical and neuroimaging features of Vogt-KoyanagiHarada syndrome ( VKH ).Methods Cerebrospinal fluid ( CSF ), neuroimaging examination, clinical manifestation and pharmacotherapy features were investigated in 5 patients diagnosed as VKH. ResultsAll 5 patients were diagnosed as uveitis in the early stage of disease.All patients suffered “ headache”.Meningeal irritation sign was appeared in 3 cases. The MRI enhanced scan of all 5 cases showed abnormal enhancement of meninges. CSF examination showed increased leukocyte number ((4--196) × 106/L). All patients were alleviatedwith combination therapyof high dose of steroid with cyclophosphamide.ConclusionsVKH is a systemic disease that usually involving the uvea, central nervous system, internal ear and the skin. MRI and CSF examination are valuable for diagnosis. High dose of steroid combined with cyclophosphamide is an effective therapeutic strategy.
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AIM:To investigate the time course of nuclear factor-κB (NF-κB) and the effects of 3-aminobenzamide (3-AB) on the expressions of NF-κB,interleukin-1β (IL-1β) and cyclooxygenase-2 (COX-2) in hippocampus after seizures. METHODS:Epilepsy were induced by kainic acid through cerebral ventricular injection. Western blotting was used to detect NF-κB p65 expression in nucleus at various experiment groups. Moreover,mRNA and protein expressions of IL-1β and COX-2 in different experiment groups were determined by RT-PCR and Western blotting analysis. RESULTS:NF-κB p65 immunoreactivity began to increase in the nuclear fraction at 2 h (P<0.05),kept rising at 12 h (P<0.05) and returned to control level at 24 h after epilepsy seizures. Furthermore,3-AB sharply decreased the accumulation of NF-κB p65 in nucleus (P<0.05). In addition,3-AB significantly decreased the mRNA and protein expressions of IL-1β and COX-2 which obviously increased in hippocampus at 6 h after epilepsy seizures (P<0.05). CONCLUSION:Seizures triggers NF-κB nucleus translocation and promotes the expressions of IL-1β and COX-2 in hippocampus. In addition,poly (adenosine diphosphate-ribose) polymerase inhibition by 3-AB suppresses NF-κB associated inflammatory pathway in epileptic rat hippocampus.
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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.
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Objective To explore the role of proton MR spectroscopic imaging(1H-MRSI)and diffusion tensor imaging(DTI)in the diagnosis of adrenoleukodystrophy and to demonstrate the involvement of fibers by using the technique of DTT.Methods 1H-MRSI,DTI and routine imaging examinations were performed in 6 patients with ALD.The values of NAA,Cho,Cr,ADC,and FA were evaluated in different regions of lesion.The involved fibers were demonstrated by using the technique of DTT.Results The ratios of NAA/Cr(0.55±0.19)and NAA/Cho(0.22±0.11)were lower(F=7.693,7.751),and Cho/Cr(2.54±0.37)was higher(F=6.348)in the initial lesions,where higher ADC values(1.49±0.36,F=5.226)and the lowest FA values(0.21±0.08,F=5.139)were also observed(P＜0.05).The decreases of NAA/Cr(1.16±0.03)and NAA/Cho(0.45±0.17)in adjacent regions were more distinct than those of remote regions(t=1.769,1.842,P＜0.05).In the developing regions,the ADC values(0.89±0.03)were lower and the FA values(0.45±0.07)were the highest.There was negative correlation between NAA/Cho and ADC values(r=-0.71,P＜0.05),and there was positive correlation between NAA/Cho and FA values(r=0.31,P＜0.05).Discontinuations and fragments of fibres were observed in corpus callosum and pyramidal tract.Conclusions Combination of 1H-MRSI and DTI can offer a sensitive method for the early diagnosis and monitor the progress of white matter.DTT can be used to directly observe the involvement of fibers.
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Objective To investigate the clinical and neuroimaging futures of chorea due to nonketotic hyperglycemia.Methods Seven cases of chorea due to nonketotic hyperglycemia were clinically examined and underwent brain CT and MRI as well.Results Investigations revealed uncontrolled diabetes with absent ketones of 7 cases.They all presented with sudden onset hemiachorea or bilateral chorea or generalized chorea.The CT scan of brain could find abnormal lesions in our cases.Hyperintense lesions in the basal ganglia,on T1 WI of MRI were demonstrated in our study.Pure drugs was unable to control chorea.The symptoms of chorea and neuroimaging lesions were normal after the hyperglycemia being controlled.Conclusions Chorea caused by nonketotic hyperglycemia is mainly found in aged people with diabetes mellitus in a mechanism of causing striatal neuronal dysfunction,presenting charicristic CT scan or MRI of brain.Chorea should be considered potentially reversible when associated with nonketotic hyperglycemia,for rapid detection and early correction of hyperglycemia could lead to complete recovery of these involuntary movements.
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Objective To investigate clinicopathological and neuroimaging features of meninheal malignant melanosis.Methods The cytologic study of cerebrospinal fluid(CSF)and neuroimaging examination and meningeal histochemistry were performed in 3 cases of meningeal malignant melanosis. Results Three patients were found to have initial onsets of headache.followed by meningeal irritation.One case had huge malignant melanoma on skin.The second patient had diabrotic malignant melanoma on her face,which did not healed for a long time.The third patient had no malignant melanoma on skin and viscera.The MRI enhanced scanning of all 3 cases showed abnormal enhancement of meninge.There were a large number of abnormal shape cells in CSF.The meninxes were blackbrown or brown.The tumor cells were in various shapes with big and round irregular nucleus and rich cytoplasm.There were a great quantitv of melanosomes.The tumor cells were disarranged. Immunohistochemistry analyses found S-100 protein and Vim and HMB-45 were positive reaction. Conclusions The patients with meningeal malignant melanosis have an initial onset of headache,followed by meningeal irritation,and MRI enhanced scanning plays a valueble role in the diagnosis.A lage number of tumor cells in abnormal shape have been found in CSF.Thetumour cells of meninx presents different shapes with big and round or irregular nucleus.There are a great quantity of mellanosomes,and the tumour cells are arranged in a state of chaos.
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Objective To investigate the value of gradient echo T2'* -weighted imaging for detection of familial cerebral cavernous malformation (FCCM). Methods Twenty-six members in 2 families of FCCM were examined at 3.0 T by using CT, conventional MRI and GRE T2'*2'-WI sequences to detect numbers of FCCM. Results Twelve cases of FCCM were found by GRE T2'*-WI sequences. These patients all had multiple lesions(average of 23). The lesions were mainly located in ganglia area, followed by cortico-subcortical, thalamus, cerebellar and brain stem. These lesions appeared as special reticulated core of mixed signal intensity with a surrounding rim of decreased signal intensity representing bemosiderin from previous hemorrhages. The numbers of lesions (average of 5-17) and cases of FCCM (average of 3-9) examined by the conventional MRI were decreasing in the order of SE, DWI, T2FLAIR, T1WI and T2WI, each less than GRE T2'*-WI. CT only identified 3 cases with big lesions combined with hemorrhage and calcification.Conclusions GRE T2'*-WI could be a better choice of MRI sequence in diagnosing FCCM compared with CT and conventional MRI.
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Objective To study the role of calcium homeostatic and kinetics in the epileptogenesis activity. Methods Hippocampal neurons were acutely isolated from controls and status epilepticus (SE) models induced by lithium-pilocarpine at different time point. The [Ca2+]i levels were detected by laser scanning confocal microscope. And the ability to restore resting [Ca2+]i levels after a brief exposure to 5 μmol/L glutamate in control and epileptic neurons were evaluated. Results The [Ca2+]i level of acute separated hippocampal neurons in the control rats was (95.4±22. 1) nmol/L After injection of lithium pilocarpine, the [Ca2+]i level in hippecampal neurons increased dramatically to (867.6±35.2) nmol/L, and decreased to (292.8 ± 18.3) nmol/L on the 7th day, lasting for about 30 days ((220. 8± 17.6) nmol/L), it is higher than that in the control group (t = 12. 55, P < 0.01). The distribution of neuronal [Ca22+]i showed that 92% of control neurons were in the normal range of [Ca2+]i level (25-150 nmol/L) ; After 6 hours, however [Ca2+]i levels of all SE neurons increased, and 85% of which were higher than 500 nmol/L; After 7, 14 and 30 days, there were 75%, 60% and 52% of SE neurons still manifested an elevated [Ca22+]i level, but less than 500 nmol/L. After the exposure to 5 μmol/L glutamate treatment for 2 minutes, [Ca2+]i of the control neurons restored to baseline values in (9. 5±3.4) minutes, whereas the SE rats of acute, latent and chronic phases did not (t = 5.08, 4. 56, 4. 21, all P < 0. 01). Conclusion Lithium-pilocarpine induced epilepsy causes a long-term alteration of calcium homeostatic mechanisms of hippocampus neurons, which may play an important role in the development and maintenance of spontaneous recurrent seizures.
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Objective To investigate the clinical and neuroimaging features of hypoglycemia encephalopathy in the elderly. Methods The history and clinical features of 36 patients who had undergone brain CT and MRI were analyzed retrospectively. Results Twenty-seven patients had infections and fevers as a trigger, presenting all kinds of symptoms. Eleven cases were found to have abnormal signals in bilateral caudate nucleus and lenticular nucleus in MRL But CT examination showed no new lesions in corresponding position. Hypoglycemia encephalopathy were commanly found in the elderly who had diabetes mellitus and treated with drugs. After being followed up for 6 months, their neuroimaging did not change. Conclusions Because the patients often present unconsciousness and weakness with a sudden onset, hypoglycemia is easily mistaken for other disorders, especially in the elderly. For those with consciousness, we should pay more attations to hypoglycemia. Brain CT has no value of diagnosing hypoglycemia encephalopathy, while MRI plays an impotant role in diagnosing the disease. The characteristic MRI features predicts a bad prognosis.
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Objective To establish a primary culture method of hippocampal neurons of new-born rats,and to observe the morphological characteristics at different developmental and differential stages.Methods The hippocampus was digested and the cells were seeded in a flask.The neurons were then transferred and re-seeded on cover glasses coated with poly-L-lysine.The neurons were identified by polyclonal antibody against neuron specific enolase(NSE).The morphology was observed under phase-contrast microscope.Results A large number of hippocampal neurons began to adhere to the cover glasses after 12～24 hours.They showed different shapes-shuttle,triangle,pyramidal,or nonregular after clinging to the plate.Their processes connected into nets and different in length and thickness.They were well developed on the 7th～10th day and survived as long as 28 days after seeding.Immunocytochemistry of NSE proved high purity.Conclusion The culture method of new-born rat hippocampal neurons in vitro is successful and can be used as an in vitro model of research.
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BACKGROUND: Status epilepticus can result in neuronal injury.OBJECTIVE: To observe the mitochondrial ultrastructural damage and the changes of Fas, Bax and Caspase-3 expressions in hippocampal CA3 neurons of rats of different kindling, so as to provide theoretical evidence for the neuronal injury after epilepsy.DESIGN: A randomized c ntrol animal experiment.SETTINGS: Department of Neurology and Department of Anesthesiology,Qilu Hospital of Shandong University.MATERIALS: The experiments were carried out in the pathological laboratory of Shandong Academy of Medical Sciences between March and July2005. Totally 150 adult male SD rats of 260-300 g were provided by the experimental animal center of Shandong University (SCXK20030004), they were raised at room temperature and were free to the access of food and water.METHODS: The adult male Sprague Dawley (SD) rats were divided into intraperitoneal injection of kainic acid group and caudal venous injection of kainic acid group respectively ac cording to the method of random number table, and the rats were administrated by kainic acid injected intraperitoneally (12 mg/kg) and via caudal vein (10 mg/kg) respectively. Each group was divided into 5 subgroups, which were 3, 6, 24, 48 and 72 hours after status epilepticus groups respectively. Twelve successfully induced rats were selected from each subgroup, hippocampi were removed at different time points after the termination of status epilepticus, 2 were used for examination under electron microscope, 5 for the reverse transcription-polymerase chain reaction (RT-PCR) detection of Fas and Bax, and 5 for the immunohistochemical assay of Caspase-3. Another 12 rats were used as normal controls without any treatment. The materials were taken at24 hours after corresponding status epilepticus in the control group, and the specific distributions were the same as those in the subgroups. The mitochondrial structure was observed under electron microscope, the levels of Fas and Bax mRNA were detected with semi-quantitative RT-PCR, and the expression of Caspase-3 protein was determined with the immunohistochemical assay.MAIN OUTCOME MEASURES: ① Results of ultrathin section under transmission electron mcroscope; ② RT-PCR results; ③ Immunohistochemical results.RESULTS: Totally 132 rats were involved in the analysis of results. ①Mitochondrial structure under electron microscope: In the intraperitoneal injection group, the mitochondria swelled, and the neurons showed characters of apoptosis. In the caudal venous injection group, the mitochondria swelled, and accompanied by the membranous collapse, and the neurons manifested the necrosis. ② No expression of Fas and Bax was detected in the control group and caudal venous injection. In the intraperitoneal injection group, Fas expression appeared at 6 hours after status epilepticus, increased at 24 hours, reached the peak value at 48 hours, and lasted till 72 hours. ③ The Caspase-3 expressions began to increase 6 hours after status epilepticus in both the intraperitoneal injection group and caudal venous injection group(10.27±0.34, 15.21±0.34; P ＜ 0.001), and reached the peak values at 24 hours (25.36±0.47, 28.23±0.47; P ＜ 0.001); The higher expression of Caspase-3 lasted till 72 hours in the intraperitoneal injection group, but sharply decreased in the caudal venous injection group.CONCLUSION: Two different methods of administration result in different severity of mitochondrial damage and different expressions of Fas, Bax and Caspase-3, which further determines the molecular mechanisms of neuronal death.
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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.
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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.
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Objective To study the role of gap junctions in epileptiform activity. Methods The epileptiform activity was induced by zero-Mg 2+ medium in cultured hippocampal neurons of newborn rats. Immunocytochemistry and real time RT-PCR were introduced to evaluate the expression of gap junction Cx32 and Cx43. Results The level of Cx32 mRNA increased quickly one hour after the neurons were treated with zero-Mg 2+ medium and was raised by 10 times 5 hours later, while Cx32 protein began to develop at the 2nd hour (21.80?1.74) and was raised by 5 times at the 8th hour (47.30?5.75). The expression of Cx43 mRNA went up obviously 5 hours later, and Cx43 protein developed visibly 8 hours later. Carbenoxolone depressed the expressions of Cx32 and Cx43. Conclusions The expression of Cx32 and Cx43 increases dramatically after epileptic discharges and carbenoxolone inhibits both the discharges and the expression of gap junctions, which indicates that gap junction could contribute to epileptogenesis.
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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
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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.
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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.
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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
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Objective To observe the characteristics and onset time of seizures caused by kindling of bilateral amygdale, and to discuss its mechanism.Methods 40 adult Wistar rats were randomly assigned into bilateral amygdala kindling group and unilateral amygdala kindling group. The models were made according to Goddard's method. Results All the rats in bilateral amygdala kindling group developed stage Ⅴ convulsions after a mean of 20.9 stimulations.12 rats of which showed spontaneous seizure discharges. But in unilateral amygdala kindling group, the successful kindling rate was 60% after a mean of 8.9 stimulations. Comparing with unilateral kindling, bilateral amygdala kindling significantly increased the successful rate of kindling (P