Mice with type I interferon signaling deficiency are prone to epilepsy upon HSV-1 infection.

Viral encephalitis continues to be a significant public health concern. In our previous study, we discovered a lower expression of antiviral factors, such as IFN-ß, STING and IFI16, in the brain tissues of patients with Rasmussen's encephalitis (RE), a rare chronic neurological disorder often occurred in children, characterized by unihemispheric brain atrophy. Furthermore, a higher cumulative viral score of human herpes viruses (HHVs) was also found to have a significant positive correlation with the unihemispheric atrophy in RE. Type I IFNs (IFN-I) signaling is essential for innate anti-infection response by binding to IFN-α/ß receptor (IFNAR). In this study, we infected WT mice and IFNAR-deficient A6 mice with herpes simplex virus 1 (HSV-1) via periocular injection to investigate the relationship between IFN-I signaling and HHVs-induced brain lesions. While all mice exhibited typical viral encephalitis lesions in their brains, HSV-induced epilepsy was only observed in A6 mice. The gene expression matrix, functional enrichment analysis and protein-protein interaction network revealed four gene models that were positively related with HSV-induced epilepsy. Additionally, ten key genes with the highest scores were identified. Taken together, these findings indicate that intact IFN-I signaling can effectively limit HHVs induced neural symptoms and brain lesions, thereby confirming the positive correlation between IFN-I signaling repression and brain atrophy in RE and other HHVs encephalitis.

The clinicopathological features of ganglioglioma with CD34 expression and BRAF mutation in patients with epilepsy.

Objective: The aim of the study was to evaluate the clinicopathological features, as well as the surgical prognosis, of epilepsy-associated gangliogliomas (GG) with CD34 expression and BRAFV600E mutation. Methods: Clinical data of patients who underwent epilepsy surgery for GG were retrospectively studied. Univariate and multivariate analyses were performed to evaluate the correlations of clinical and pathological factors with molecular markers of CD34 expression and BRAFV600E mutation in GG. Results: A total of 208 patients with GG had immunohistochemical detection of CD34 expression (positive/negative: 184/24), and among them, 89 patients had immunohistochemical detection of BRAFV600E mutation (positive/negative: 54/35). By univariate and multivariate analyses, seizure aura (p = 0.025), concordance of ictal electroencephalogram (EEG) findings (p = 0.045) and medial temporal tumor (p = 0.030) were found to be related to CD34 expression, but only hospitalization time (p = 0.042) was different for BRAF-mutated status. In addition, drug-resistant epilepsy (p = 0.040) and concordance of interictal EEG findings (p = 0.009) were found to be associated with tumor progression-free survival (PFS) in univariate analysis, but only concordance of interictal EEG findings was with significance in multivariate analysis. However, CD34 expression or BRAFV600E mutation in GG was not found to be associated with surgical outcomes of seizure control and tumor PFS. Conclusion: The CD34 expression or BRAFV600E mutation in GG may partly influence the distribution of clinicopathological features of patients with epilepsy, but they may be not able to predict the surgical prognosis of seizure outcome and tumor recurrence.

Translocation of High Mobility Group Box 1 From the Nucleus to the Cytoplasm in Depressed Patients With Epilepsy.

Depression is a common psychiatric comorbidity in patients with epilepsy, especially those with temporal lobe epilepsy (TLE). The aim of this study was to assess changes in high mobility group box protein 1 (HMGB1) expression in epileptic patients with and without comorbid depression. Sixty patients with drug-resistant TLE who underwent anterior temporal lobectomy were enrolled. Anterior hippocampal samples were collected after surgery and analyzed by immunofluorescence (n = 7/group). We also evaluated the expression of HMGB1 in TLE patients with hippocampal sclerosis and measured the level of plasma HMGB1 by enzyme-linked immunosorbent assay. The results showed that 28.3% of the patients (17/60) had comorbid depression. HMGB1 was ubiquitously expressed in all subregions of the anterior hippocampus. The ratio of HMGB1-immunoreactive neurons and astrocytes was significantly increased in both TLE patients with hippocampal sclerosis and TLE patients with comorbid depression compared to patients with TLE only. The ratio of cytoplasmic to nuclear HMGB1-positive neurons in the hippocampus was higher in depressed patients with TLE than in nondepressed patients, which suggested that more HMGB1 translocated from the nucleus to the cytoplasm in the depressed group. There was no significant difference in the plasma level of HMGB1 among patients with TLE alone, TLE with hippocampal sclerosis, and TLE with comorbid depression. The results of the study revealed that the translocation of HMGB1 from the nucleus to the cytoplasm in hippocampal neurons may play a previously unrecognized role in the initiation and amplification of epilepsy and comorbid depression. The direct targeting of neural HMGB1 is a promising approach for anti-inflammatory therapy.

The long-term surgical outcomes of low-grade epilepsy-associated neuroepithelial tumors.

OBJECTIVE: This study aimed to evaluate the surgical outcomes and relevant prognostic factors in patients with low-grade epilepsy-associated neuroepithelial tumors (LEAT) and, especially, to develop a scoring system to predict postoperative seizure outcomes. METHODS: The clinical data of patients who underwent epilepsy surgery for LEAT were retrospectively studied. The surgical outcomes of seizure and neurological statuses in patients were evaluated using Engel classification and modified Rankin Scale (mRS) scoring, respectively. A scoring system of seizure outcomes was constructed based on the weight of the ß-coefficient estimate of each predictor in the final multivariate predicting model of seizure outcomes. RESULTS: Of the 287 patients (106 female) enrolled, the median age was 19 years at surgery and 10 years at seizure onset, with a median duration of epilepsy of 60 months. Among 258 patients who were followed up for at least 12 months, 215 (83.3%) patients had a favorable seizure outcome (Engel class I) after surgery, and 43 (16.7%) patients had an unfavorable seizure outcome; longer duration of epilepsy, discordant magnetoencephalography (MEG) findings, and acute postoperative seizures were significantly included in the scoring system to predict unfavorable seizure outcomes, and in the scoring system, accumulated scoring of 0-19 scores was recorded, which were finally grouped into three risk levels: low risk (risk < 30%), medium risk (30% ≤ risk < 70%), and high risk (risk ≥ 70%). In addition, favorable neurological outcomes (mRS score 0-1) were recorded in 187 (72.5%) patients, while unfavorable neurological outcomes were recorded in 71 (27.5%) patients, which were significantly related to poor seizure control, older age at surgery, and longer duration of epilepsy and hospitalization time. SIGNIFICANCE: The long-term surgical outcomes of LEAT after surgery were satisfactory. A scoring system for predicting unfavorable seizure outcomes with different risk levels was developed, which could partly guide clinical treatments of LEAT.

Rasmussen's encephalitis is characterized by relatively lower production of IFN-ß and activated cytotoxic T cell upon herpes viruses infection.

BACKGROUND: The etiology of Rasmussen's encephalitis (RE), a rare chronic neurological disorder characterized by CD8+ T cell infiltration and unihemispheric brain atrophy, is still unknown. Various human herpes viruses (HHVs) have been detected in RE brain, but their contribution to RE pathogenesis is unclear. METHODS: HHVs infection and relevant immune response were compared among brain tissues from RE, temporal lobe epilepsy (TLE) and traumatic brain injury (TBI) patients. Viral antigen or genome, CD8+ T cells, microglia and innate immunity molecules were analyzed by immunohistochemical staining, DNA dot blot assay or immunofluorescence double staining. Cytokines were measured by multiplex flow cytometry. Cell apoptosis was visualized by TUNEL staining. Viral infection, immune response and the severity of unihemispheric atrophy were subjected to correlation analysis. RESULTS: Antigens of various HHVs were prevalent in RE and TLE brains, and the cumulative viral score of HHVs positively correlated with the unihemispheric atrophy in RE patients. CD8+ T cells infiltration were observed in both RE and TLE brains and showed co-localization with HHV antigens, but their activation, as revealed by Granzyme B (GZMB) release and apoptosis, was found only in RE. In comparison to TLE, RE brain tissues contained higher level of inflammatory cytokines, but the interferon-ß level, which was negatively correlated with cumulative viral score, was relatively lower. In line with this, the DNA sensor STING and IFI16, rather than other innate immunity signaling molecules, were insufficiently activated in RE. CONCLUSIONS: Compared with TBI, both RE and TLE had prevalently HHV infection and immune response in brain tissues. However, in comparison to TLE, RE showed insufficient activation of antiviral innate immunity but overactivation of cytotoxic T cells. Our results show the relatively lower level of antiviral innate immunity and overactivation of cytotoxic T cells in RE cases upon HHV infection, the overactivated T cells might be a compensate to the innate immunity but the causative evidence is lack in our study and need more investigation in the future.

Regulation of TWIK-related K+ channel 1 in the anterior hippocampus of patients with temporal lobe epilepsy with comorbid depression.

Epilepsy with comorbid depression has recently attracted increasing attention. Temporal lobe epilepsy (TLE) may represent an increased risk of developing depression, especially if the seizures do not generalize. The two-pore domain potassium channel-TWIK-related K+ channel (TREK-1) plays important roles in both epilepsy and depression. However, the changes in its expression in patients with epilepsy with comorbid depression remain unclear. In the present study, we analyzed depressive symptoms using neuropsychiatric scales in forty-two patients with drug-resistant TLE, who also underwent EEG in waking and sleeping states, as well as 3.0 T brain MRI. We tested for TREK-1 positive neurons and microglial cells in the anterior hippocampi of patients with drug-resistant TLE with and without comorbid depression (n=5/group). Approximately 31% of patients with TLE had comorbid depression (13/42). Meanwhile, the patients who had hippocampal sclerosis had much higher scores on the depression rating scale. The results indicated the contribution of hippocampal sclerosis to the development of depression. Immunostaining of TREK-1 channels was observed in neurons and glia in the anterior hippocampus. Increased immunoreactivity of TREK-1 neurons was observed in the hippocampi of patients with TLE with comorbid depression compared with nondepressed patients with TLE. TREK-1 was expressed in almost all microglia. Curiously, more activated TREK-1-positive microglia were observed in patients with TLE with depression than in those without depression. The results suggested that a change in TREK-1 immunoreactivity was involved, at least partly, in the development of depression as a comorbidity of TLE. Imbalance of the TREK-1 channel may be a potential target for the treatment of patients with epilepsy with comorbid depression.

HCMV infection and IFITM3 rs12252 are associated with Rasmussen's encephalitis disease progression.

OBJECTIVE: Rasmussen's encephalitis (RE) is a rare and severe progressive epileptic syndrome with unknown etiology. Infection by viruses such as human cytomegalovirus (HCMV) has been hypothesized to be a potential trigger for RE. Interferon-induced transmembrane protein-3 (IFITM3) single-nucleotide polymorphism (SNP) rs12252 is associated with the severity of viral infection disease. This study aimed to address the possibility that HCMV infection and IFITM3 rs12252 might be associated with RE disease progression. METHODS: The expression of HCMV and IFITM3 was detected with immunohistochemical staining, in situ hybridization and immunofluorescence double staining. The genotype of IFITM3 rs12252 was detected using the Sanger sequencing method. A genetic association analysis was carried out for this SNP and HCMV antigen expression. The relationship between this SNP and the clinical characteristics of these patients was further analyzed. In in vitro study, HCMV replication in SH-SY5Y cells with overexpressed IFITM3 variant was detected by immunofluorescence and real-time RT-PCR. RESULTS: Elevated expression of HCMV and IFITM3 was observed in the brain tissue of RE patients. Moreover, the IFITM3 polymorphism rs12252-C was found to associate with HCMV high detection and rapid disease progression in RE patients with the IFITM3 rs12252-CC genotype. In vitro study showed the overexpressed IFITM3 variant was associated with HCMV high infection level. CONCLUSION: These results suggest that the IFITM3 rs12252-C is associated with the disease progression of RE patients via facilitating persistent HCMV infection in brain tissue and provides new insight into understanding the pathogenesis of RE.

Comparison of Awake and Asleep Deep Brain Stimulation for Parkinson's Disease: A Detailed Analysis Through Literature Review.

OBJECTIVES: Deep brain stimulation (DBS) for Parkinson's disease (PD) has been applied to clinic for approximately 30 years. The goal of this review is to explore the similarities and differences between "awake" and "asleep" DBS techniques. METHODS: A comprehensive literature review was carried out to identify relevant studies and review articles describing applications of "awake" or "asleep" DBS for Parkinson's disease. The surgical procedures, clinical outcomes, costs and complications of each technique were compared in detail through literature review. RESULTS: The surgical procedures of awake and asleep DBS surgeries rely upon different methods for verification of intended target acquisition. The existing research results demonstrated that the stereotactic targeting accuracy of lead placement obtained by either method is reliable. There were no significant differences in clinical outcomes, costs, or complications between the two techniques. CONCLUSION: The surgical and clinical outcomes of asleep DBS for PD are comparable to those of awake DBS.

Asymmetry of Cerebral Peduncles for Predicting Motor Function Restoration in Young Patients Before Hemispherectomy.

OBJECTIVE: Hemispherectomy has been used successfully for patients with medically intractable epilepsy. However, it is difficult to predict postoperative motor function. The aim of the present study was to analyze whether the preoperative asymmetry of cerebral peduncles could be used to predict motor function restoration before hemispherectomy for young patients with medically intractable epilepsy. METHODS: The clinical record and magnetic resonance imaging data of 53 patients were analyzed retrospectively. The correlation between preoperative cerebral peduncle asymmetry ratio (pCPAR) and pre- and postoperative changes in motor function was evaluated, as well as the influencing factors for pCPAR, such as duration and etiology factors. The restoration of motor function was defined as changes in pre- and postoperative hemiparesis. RESULTS: The pCPARs of patients with improved and unchanged hemiparesis were significantly greater than that of worsened patients. Patients with a pCPAR of more than 1.5 had an obvious restorative capacity of motor function of the intact hemisphere, and these patients had a lower risk of worsening hemiparesis. The duration in the improved/unchanged and worsened groups was 5.84 ± 3.85 years and 2.67 ± 2.03 years, respectively. Furthermore, there were more patients with no-progressive pathology in the group in whom pCPAR was more than 1.5. CONCLUSIONS: pCPAR is a useful and objective indicator for predicting the restoration of motor function in pediatric patients with medically intractable epilepsy before hemispherectomy. Most patients with nonprogressive pathology and a duration of more than 5 years presented with greater pCPARs, exhibited better restoration of motor function, and had less risk of worsening hemiparesis.

Preoperative Heart Rate Variability as Predictors of Vagus Nerve Stimulation Outcome in Patients with Drug-resistant Epilepsy.

Vagus nerve stimulation (VNS) is an adjunctive treatment for drug-resistant epilepsy (DRE). However, it is still difficult to predict which patients will respond to VNS treatment and to what extent. We aim to explore the relationship between preoperative heart rate variability (HRV) and VNS outcome. 50 healthy control subjects and 63 DRE patients who had received VNS implants and had at least one year of follow up were included. The preoperative HRV were analyzed by traditional linear methods and heart rhythm complexity analyses with multiscale entropy (MSE). DRE patients had significantly lower complexity indices (CI) as well as traditional linear HRV measurements than healthy controls. We also found that non-responders0 had significantly lower preoperative CI including Area 1-5, Area 6-15 and Area 6-20 than those in the responders0 while those of the non-responders50 had significantly lower RMSSD, pNN50, VLF, LF, HF, TP and LF/HF than the responders50. In receiver operating characteristic (ROC) curve analysis, Area 6-20 and RMSSD had the greatest discriminatory power for the responders0 and non-responders0, responders50 and non-responders50, respectively. Our results suggest that preoperative assessment of HRV by linear and MSE analysis can help in predicting VNS outcomes in patients with DRE.

Downregulation of adult and neonatal Nav1.5 in the dorsal root ganglia and axon of peripheral sensory neurons of rats with spared nerve injury.

Previous studies demonstrated that Nav1.5 splice variants, including Nav1.5a and Nav1.5c, were expressed in dorsal root ganglia (DRG) neurons. However, since nine Nav1.5 isoforms have been identified, whether other Nav1.5 splice variants, especially the neonatal Nav1.5 splice variant, express in the DRG neurons is still unknown. In this study, we systematically investigated the expression of adult and neonatal Nav1.5 isoforms in the DRG neurons and axon of peripheral sensory neurons of rats with spared nerve injury (SNI) by RT-PCR, DNA sequencing, restriction enzyme digestion, immunohistochemistry and immunofluorescence methods. The results demonstrated that both adult and neonatal Nav1.5 isoforms were expressed in the DRG neurons, but their expression ratio was ~2.5:1. In SNI rat models, the expression of both adult and neonatal Nav1.5 decreased by approximately a half in both mRNA and protein levels. In contrast, the expression of protein kinase C (PKC)-γ, one of the negative modulators for sodium currents, increased by ~1-fold. Taken together, this study first confirmed the expression of both adult and neonatal Nav1.5 isoforms in the DRG neurons and axon of peripheral sensory neurons of rat, but their expression level decreased in pain models. The upregulation of PKC-γ may directly or indirectly downregulate the expression of Nav1.5 isoforms in SNI rat models, which may further involve in the pathological process of neuropathic pain.

Identification of the epileptogenic zone of temporal lobe epilepsy from stereo-electroencephalography signals: A phase transfer entropy and graph theory approach.

The aim of this research is to apply an approach based on phase transfer entropy (PTE) and graph theory to study the interactions between the stereo-electroencephalography (SEEG) activities recorded in multilobar origin, in order to evaluate their ability to detect the epileptogenic zone (EZ) of temporal lobe epilepsies (TLE). Forty-three patients were included in this retrospective study. Five to sixteen (median = 12) multilead electrodes were implanted per patient, and, for each patient, a sub-set of between 10 and 32 (median = 22) bipolar derivations was selected for analysis. The leads were classified into the onset leads (OLs), the early propagation leads (EPLs), and the rest of the leads (RLs). The results showed that a significantly different dynamic trend of the out/in ratio (more obvious in the gamma band) distinguishes the OLs from RLs in the 23 patients who were seizure-free not only during the ictal event (significant elevation), but also during the inter-,pre-, late-ictal periods, and especially in the post-ictal (sharp decline) state. However, in the 20 patients who were not-seizure-free, the differences between the OLs and RLs during the post-ictal period were not found in any frequency band. The dynamic trend was used to predict surgical outcome, and the results showed that the sensitivity was 91% and the specificity was 70%. In brief, this study indicates that our approach may add new and valuable information, providing efficient quantitative measures useful for localizing the EZ.

Multiple Nav1.5 isoforms are functionally expressed in the brain and present distinct expression patterns compared with cardiac Nav1.5.

It has previously been demonstrated that there are various voltage gated sodium channel (Nav) 1.5 splice variants expressed in brain tissue. A total of nine Nav1.5 isoforms have been identified, however, the potential presence of further Nav1.5 variants expressed in brain neurons remains to be elucidated. The present study systematically investigated the expression of various Nav1.5 splice variants and their associated electrophysiological properties in the rat brain tissue, via biochemical analyses and whole­cell patch clamp recording. The results demonstrated that adult Nav1.5 was expressed in the rat, in addition to the neonatal Nav1.5, Nav1.5a and Nav1.5f isoforms. Further studies indicated that the expression level ratio of neonatal Nav1.5 compared with adult Nav1.5 decreased from 1:1 to 1:3 with age development from postnatal (P) day 0 to 90. This differed from the ratios observed in the developing rat hearts, in which the expression level ratio decreased from 1:4 to 1:19 from P0 to 90. The immunohistochemistry results revealed that Nav1.5 immunoreactivity was predominantly observed in neuronal cell bodies and processes, whereas decreased immunoreactivity was detected in the glial components. Electrophysiological analysis of Nav1.5 in the rat brain slices revealed that an Na current was detected in the presence of 300 nM tetrodotoxin (TTX), however this was inhibited by ~1 µM TTX. The TTX­resistant Na current was activated at ­40 mV and reached the maximum amplitude at 0 mV. The results of the present study demonstrated that neonatal and adult Nav1.5 were expressed in the rat brain and electrophysiological analysis further confirmed the functional expression of Nav1.5 in brain neurons.

Altered expression of neuropeptide Y receptors caused by focal cortical dysplasia in human intractable epilepsy.

Focal cortical dysplasia (FCD) is a common cause of pharmacologically-intractable epilepsy, however, the precise mechanisms underlying the epileptogenicity of FCD remains to be determined. Neuropeptide Y (NPY), an endogenous anticonvulsant in the central nervous system, plays an important role in the regulation of neuronal excitability. Increased expression of NPY and its receptors has been identified in the hippocampus of patients with mesial temporal lobe epilepsy, presumed to act as an endogenous anticonvulsant mechanism. Therefore, we investigated whether expression changes in NPY receptors occurs in patients with FCD. We specifically investigated the expression of seizure-related NPY receptor subtypes Y1, Y2, and Y5 in patients with FCD versus autopsy controls. We found that Y1R and Y2R were up-regulated at the mRNA and protein levels in the temporal and frontal lobes in FCD lesions. By contrast, there was no significant change in either receptor detected in parietal lesions. Notably, overexpression of Y5R was consistently observed in all FCD lesions. Our results demonstrate the altered expression of Y1R, Y2R and Y5R occurs in FCD lesions within the temporal, frontal and parietal lobe. Abnormal NPY receptor subtype expression may be associated with the onset and progression of epileptic activity and may act as a therapeutic candidate for the treatment of refractory epilepsy caused by FCD.

Analysis of Altered Micro RNA Expression Profiles in Focal Cortical Dysplasia IIB.

Focal cortical dysplasia type IIB is a commonly encountered subtype of developmental malformation of the cerebral cortex and is often associated with pharmacoresistant epilepsy. In this study, to investigate the molecular etiology of focal cortical dysplasia type IIB, the authors performed micro ribonucleic acid (RNA) microarray on surgical specimens from 5 children (2 female and 3 male, mean age was 73.4 months, range 50-112 months) diagnosed of focal cortical dysplasia type IIB and matched normal tissue adjacent to the lesion. In all, 24 micro RNAs were differentially expressed in focal cortical dysplasia type IIB, and the microarray results were validated using quantitative real-time polymerase chain reaction (PCR). Then the putative target genes of the differentially expressed micro RNAs were identified by bioinformatics analysis. Moreover, biological significance of the target genes was evaluated by investigating the pathways in which the genes were enriched, and the Hippo signaling pathway was proposed to be highly related with the pathogenesis of focal cortical dysplasia type IIB.

Treatment of epilepsy with bipolar electro-coagulation: an analysis of cortical blood flow and histological change in temporal lobe.

BACKGROUND: Bipolar electro-coagulation has a reported efficacy in treating epilepsy involving functional cortex by pure electro-coagulation or combination with resection. However, the mechanisms of bipolar electro-coagulation are not completely known. We studied the acute cortical blood flow and histological changes after bipolar electro-coagulation in 24 patients with intractable temporal lobe epilepsy. METHODS: Twenty-four patients were consecutively enrolled, and divided into three groups according to the date of admission. The regional cortical blood flow (rCBF), electrocorticography, the depth of cortex damage, and acute histological changes (H and E staining, neuronal staining and neurofilament (NF) staining) were analyzed before and after the operation. The t-test analysis was used to compare the rCBF before and after the operation. RESULTS: The rCBF after coagulation was significantly reduced (P < 0.05). The spikes were significantly reduced after electro-coagulation. For the temporal cortex, the depth of cortical damage with output power of 2-9 W after electro-coagulation was 0.34 ± 0.03, 0.48 ± 0.06, 0.69 ± 0.06, 0.84 ± 0.09, 0.98 ± 0.08, 1.10 ± 0.11, 1.11 ± 0.09, and 1.22 ± 0.11 mm, respectively. Coagulation with output power of 4-5 W completely damaged the neurons and NF protein in the molecular layer, external granular layer, and external pyramidal layer. CONCLUSIONS: The electro-coagulation not only destroyed the neurons and NF protein, but also reduced the rCBF. We concluded that the injuries caused by electro-coagulation would prevent horizontal synchronization and spread of epileptic discharges, and partially destroy the epileptic focus.

Refractory temporal lobe epilepsy caused by angiocentric glioma complicated with focal cortical dysplasia: a surgical case series.

Angiocentric glioma (AG) is a rare, epilepsy-associated, low-grade neoplasm with a characteristic perivascular growth pattern. Here, we review the histological types, surgical interventions, and postoperative seizure in our three cases of AG with drug-resistant epilepsy. Some patients with AG present focal cortical dysplasia. For these patients, extended lesionectomy including the adjacent cortical dysplasia is necessary to achieve a seizure-free outcome. Surgical planning based on comprehensive evaluation of epilepsy and cortical dysplasia is therefore an important step for all patients.

Treatment of drug-resistant epilepsy with vagus nerve stimulation -- review of 45 cases.

BACKGROUND: Vagus nerve stimulation (VNS) is an alternative treatment for drug-resistant epilepsy (DRE). The study aimed to explore the potential factors of prognosis, safety and effect of VNS treatment in patients with DRE. METHODS: We retrospectively examined 45 cases of DRE that received VNS treatment in our center from June 2004 to June 2010 and analyzed the parameters (age of patient receiving VNS, seizure frequency before and after VNS as well as treatment duration) by Student's t test, Fisher's exact and Mann-Whitney U tests, and multivariate Logistic regression. RESULTS: The overall response rate was 64% (29/45), 67% (6/9) for adults and 64% (23/36) for children, with no significant difference (P = 0.28). Twenty-two cases had been in VNS therapy for over 1 year with a treatment efficacy of 73% (16/22), whereas 23 cases had been in VNS therapy no more than 1 year with a treatment effecacy of 57% (13/23), and has statistically significant difference (P = 0.03). The main side effect included hoarseness of voice and cough. One patient's device was removed due to infection. One patient's VNS was half-way terminated due to seizure aggravation. One patient died due to status epilepticus. CONCLUSIONS: VNS is a safe and effective treatment for DRE. Duration of VNS therapy may be a crucial factor on prognosis.

[Pediatric intractable epilepsy surgery].

OBJECTIVE: To explore the strategy of pediatric intractable epilepsy surgery. METHODS: The clinical data of 96 pediatric cases with intractable epilepsy and epilepsy syndromes underwent surgical treatment from April 2004 to April 2006 were retrospectively analyzed. RESULTS: The surgical treatments were performed based on the results of comprehensive data from neurological, neurosurgical and pediatric departments. Among of them, 78 cases were performed with curative procedure, 17 cases with palliative procedure and 1 case with stereotactic damage procedure. The surgical effect was judged with Engel's standard, 58 cases had no seizure during 14 to 26 months follow-up, 26 cases had significantly improved in seizure control and the total efficiency was 87.5%. 81 cases had improvements in neuropsychological tests. 22 cases had postoperative complications such as neuro-dysfunctions and 15 cases were gradually recovered after the period of follow-up ended, 1 case died of CSF over drainage after operation 3 months. CONCLUSIONS: Pediatric patients with symptomatic epilepsy and epilepsy syndromes are suitable to surgical treatment, the results are satisfactory in seizure control and neuropsychological function tests.