ABSTRACT
Objective To explore the postoperative recovery of the patients with glioma-related epilepsy and the possible risk factors for recurrence of epilepsy.Methods To collect clinical data of 89 patients with glioma-related epilepsy,we recorded Engle grade score of all patients underwent resection of tumor and seizure focus in a week,1,3 and 6 month after surgery Repeated measures ANOVA was used to analysis the difference within group.Kaplan-Meier method and Cox regression analysis were used to analysis seizure recurrence risk curve and the epileptic recurrence related factors,respectively.Results The postoperative recurrence rate was 26.97％ (24/89).Engle grade scores were 2.966±0.081.2.202±0.080,1.730±0.093 and 1.313±0.042 in a week,1,3 and 6 month after surgery.The difference was statistically significant (Ftime=96.076,P=0.000).Cox regression model showed that tumor accumulation site (RR =2.908,CI:1.083 ～7.806),postoperative edema formation (RR =4.769,CI:1.737 ～ 13.096),tumor relapse (RR=8.309,CI:3.379～20.432)were the important risk factors for recurrence epileptic seizures (all P＜ 0.05).Conclusions Surgical treatment can significantly reduce or even eliminate seizures postoperative and its long term efficacy is superior to short term efficacy.Appropriate measures should be taken to treat risk factors associated with recurrence epileptiform seizure to improve the prognosis of patients quality of life.
ABSTRACT
Objective Few studies are reported on the clinical characteristics of glioma-related epilepsy (GRE).Postoperative recurrence of epilepsy in some patients seriously affects their recovery.We aimed to explore the duration, frequency and type of the epileptic seizure as well as possible factors for postoperative recurrence of epilepsy.Methods We recorded the frequency and duration of epileptic seizures, analyzed the recurrence-related factors using the Cox regression model, and investigated the risk factors of recurrent epilepsy.Results The postoperative recurrence of epilepsy was found in 24 (26.97%) of the 89 cases, which, compared with the 65 non-recurrence cases, had a significantly longer seizure duration (7[3-10] vs 5[2-9] min, P2 cm) (HR=2.867, 95% CI: 1.210-6.795), brain wave type (HR=2.501, 95% CI: 1.058-5.914), and preoperative frequency of epileptic seizure (>6 times/mo) (HR=5.100, 95% CI: 2.437-10.677).Conclusion Postoperative recurrence of epilepsy is associated with the clinical pathological parameters, and the changes of the frequency and duration of epileptic seizures before and after surgery may provide some new theoretical reference for the treatment and prognosis of the disease.
ABSTRACT
Objective To explore expression of HMGB1 in glioma tissue of glioma-related epilepsy patients. Methods Immunohistochemistry was used to detect the expression of HMGB1 in the tissues from 82 glioma-related epi?lepsy patients (glioma-related epilepsy group), 80 glioma patients (glioma without epilepsy group), 80 intractable epilepsy patients (epilepsy control group) epileptogenic foci tissue and 20 normal controls (negative control group). Results HMGB1 in glioma tissue of glioma-related epilepsy group was significantly higher than that in glioma tissue of glioma without epilepsy grou p (χ2=16.944, P<0.001), especially in low pathological grade glioma tissue. HMGB1 was higher in glioma tissue of glioma-related epilepsy group than in epileptogenic foci tissue of epilepsy control group (χ2=26.094, P<0.001). Expression of HMGB1 in glioma tissue of glioma without epilepsy group (χ2=32.273, P<0.001) and epileptogenic foci tissue of epilepsy control group ( χ2=22.236,P<0.001) was higher than in normal brain tissue of negative control group. In glioma-related epilepsy group, HMGB1 was positively correlated with seizures duration(r=0.365,P=0.001), sei? zures frequency (r=0.531,P=0.000) and pathological grade of glioma tissue (r=0.265,P=0.016). Conclusions HMGB1 is highly expressed in glioma tissues of glioma-related epilepsy; HMGB1 expression is closely related with seizures; and HMGB1 in glioma tissue may contribute to the formation of glioma-related epilepsy.