ObjectiveThe research goal: to study the diagnostic value of T2-flair sequence of magnetic resonance imaging (MRI) in hippocampal sclerosis. MethodsThe clinical data of 135 patients with epilepsy caused by hippocampal sclerosis in the Epilepsy Center of Tianshui Third People's Hospital from March 2019 to December 2020 were analyzed retrospectively, studying the correlation between the changes of hippocampal sclerosis signal and the frequency of epileptic seizures in MRI T2-flair sequence multi axial scanning. ResultsThere were 109 cases of simple hippocampal sclerosis and 26 cases of hippocampal sclerosis with other lesions, including 8 cases of cavernous hemangioma, 9 cases of traumatic or infectious malacia, 2 cases of focal cortical dysplasia, 1 case of cerebral fissure malformation, 1 case of giant gyrus and 5 cases of perinatal brain injury. MRI features of hippocampal sclerosis were as follows: ① hippocampal volume increased slightly, structure blurred, and T2-flair showed slightly increased hippocampal signal in 15 cases, accounting for 11.11%; ② The hippocampal formation was fuzzy, T2-flair was punctate hyperintense, and the volume did not change in 17 cases (12.59%); ③ Hippocampal pyknosis into small lumps, T2-flair sequence showed high signal in 103 cases, accounting for 76.30%. Statistics showed that there was a correlation between hippocampal sclerosis signal and seizure frequency (χ2=94.94, P<0.05). The higher the hippocampal sclerosis signal, the more the seizure frequency. ConclusionMRI T2-flair sequence multi axial scanning can improve the diagnostic accuracy of hippocampal sclerosis. As the change of hippocampal sclerosis signal becomes more obvious, the trend of seizure frequency increases.
ObjectiveTo investigate the status and prognosis effect of surgical operation for Temporal lobe epilepsy.MethodsRetrospective analyses were performed on 24 patients with intractable temporal lobe epilepsy who were treated by surgery in Zibo Changguo Hospital and had complete clinical and follow-up data, during the period from April 2011 to June 2014. Among them, 14 were male and 10 were female, 16 to 44 years old, the average age was (24.40±6.26) years old, and the average course of disease was (12.50±8.42) years old. The clinical characteristics and prognosis of the patients were analyzed.ResultsAll 24 patients had hippocampal sclerosis and underwent "anterior temporal lobe and medial temporal structural resection". Patients were followed up for 5~7 years, the postoperative epileptic seizure of the patient reached grade Engel Ⅰ in 20 cases (83.3%), grade Engel Ⅱ in 2 cases (8.3%) and grade Engel Ⅳ in 2 cases (8.3%).ConclusionHippocampal sclerosis and cortical dysplasia were common in 24 patients, and the operation controlling intractable epilepsy was better. In order to improve the prognosis of patients, surgical treatment should be carried out as soon as possible.
ObjectiveTo investigate the effects of hippocampal long-term potentiation (LTP) on cognitive dysfunction in immature epileptic rats. MethodsImmature epileptic rats were established by intraperitoneal injection of lithium chloride-pilocarpine (li-pilo). Racine classification standard modified by Becker was used to evaluate behavior of epileptic seizure, and the survival rats within RacineⅣmagnitude were selected in the experiment. The function of learning and memory of epileptic rats when they were adult was assessed using Morris water maze experiment, and their independent exploratory behavior was evaluated by the open-field test. Field potential was recorded by electrophysiological technology to detecte whether hippocampal LTP was essential of cognitive dysfunction. ResultsThe function of learning and memory was significantly impaired when compared with controls(n=8, t=10.86, P < 0.05;n=8, t=9.98, P < 0.05). In addition, independent exploratory behavior was significantly reduced when compared with controls(n=8, t=12.89, P < 0.05). Besides, CA1 hippocampal LTP induced by high-frequency stimulation presented the significant inhibition in epileptic rats with cognitive dysfunction when compared with controls(Slope:n=8, t=13.32, P < 0.05;Amplitude:n=8, t=20.02, P < 0.05). ConclusionInhibition of CA1 hippocampal LTP may be implicated in cognitive dysfunction of epileptic rats.
ObjectiveTo investigate the effect of dexamethasone on mammalian target of rapamycin (mTOR) expression of astrocytes in hippocampus of rats with sepsis associated encephalopathy (SAE). MethodsTotally, 90 cases of 30-day-old male Wistar rats were randomly divided into sham-operation group (n=10) and cecal ligation and puncture (CLP) group (n=80). Models of rats with sepsis were established by CLP. At 12 hours after CLP, if rats appeared lower neurobehavioral scores, abnormal electroencephalogram (EEG) and somatosensory evoked potential (SEP), they were diagnosed with SAE. And then, they were randomly divided into non-treated group and dexamethasone group. Rats in the dexamethasone group were injected with dexamethasone (1 mg/kg) via tail vein every other day for a total of 3 times. The same dose of saline was used in the non-treated group. The neurobehavioral score was measured, SEP and EEG were examined in the age of 40 days, and then the rats were killed and the hippocampus was taken. Expressions of mTOR protein were measured by Western blot. The glial fibrillary acidic protein (GFAP) and mTOR were detected by immunofluorescence assay, and the number of positive cells was calculated by image analysis system software. ResultsSix of 80 CLP rats died in 12 hours after operation, and 28 of 74 rats were diagnosed as SAE because they appeared lower neurobehavioral scores, abnormal EEG and SEP at 12 hours after CLP. The incidence of SAE was 37.84% (28/74). In the age of 40 days, compared with non-treated group, neurobehavioral score of rats in the dexamethasone group was low, the amount of alpha waves in EEG reduced, delta waves increased, the amplitude of P1 waves in SEP was decreased, and the latencies of P1 and N1 waves were prolonged (P＜0.05). GFAP immunofluorescence staining showed astrocytic body and processes were small in the sham operation group. However, astrocytes in the non-treated group had large body and hypertrophic processes, and compared with the sham operation group, the number of these cells increased significantly (P＜0.05). Astrocytic body and processes were small in the dexamethasone group compared with the non-treated group, and the number of cells also decreased (P＜0.05). The mTOR positive astrocytes in the non-treated group were more than those in the sham operation group (P＜0.05). But mTOR positive astrocytes in the dexamethasone group were fewer than those in the non-treated group (P＜0.05). ConclusionsAstrocytes are activated in the hippocampus of rats with SAE. They show features of reactive hyperplasia, and the expression of mTOR is up-regulated, while dexamethasone can inhibit effects on these.
ObjectiveTo explore the dynamic expression changes of neuronal growth and differentiation-associated miR-124a and miR-9 in the process of epileptogenesis. MethodsEstablish the lithium-pilocarpine induced status epilepticus (SE) rat model. Animal behavior change induced by SE as well as in the period of chronic epilepsy was observed by naked-eye or video-recording. Major time points for the study were chosen at 1d, 7d, 14d and 28d post-SE, on which the post-SE rats were decapitated and their hippocampal specimens were obtained. Total RNA from each specimen was extracted and qPCR was exploited to detect miR-124a and miR-9 expression in the specimens. Statistical analysis was used to show the dynamic expressional changes of miR-124a and miR-9 in rat hippocampus at 1d, 7d, 14d and 28d post-SE during the process of epileptogenesis. ResultsCompared with normal rats, the expression level of miR-124a in rat hippocampus did not show a significant difference at 1d post-SE, but it had shown markedly differences at 7d, 14d and 28d post-SE(P < 0.05), with a declining trend. Compared with normal rats, the expression level of miR-9 had demonstrated significant differences at 1d, 7d, 14d and 28d post-SE(P < 0.05)with a generally increasing trend, although there was slight fluctuation of expressional up-regulation at 7d post-SE. ConclusionNeuronal growth and differentiation-associated miR-124a and miR-9 had shown dynamic changes of down-regulation or up-regulation in the process of epileptogenesis. It can be suspected that miR-124a and miR-9 take part in hippocampal neurogenesis post-SE and be involved in epileptogenesis process.
Physiological studies have revealed that rats perform spatial localization relying on grid cells and place cells in the entorhinal-hippocampal CA3 structure. The dynamic connection between the entorhinal-hippocampal structure and the prefrontal cortex is crucial for navigation. Based on these findings, this paper proposes a spatial navigation method based on the entorhinal-hippocampal-prefrontal information transmission circuit of the rat’s brain, with the aim of endowing the mobile robot with strong spatial navigation capability. Using the hippocampal CA3-prefrontal spatial navigation model as a foundation, this paper constructed a dynamic self-organizing model with the hippocampal CA1 place cells as the basic unit to optimize the navigation path. The path information was then fed back to the impulse neural network via hippocampal CA3 place cells and prefrontal cortex action neurons, improving the convergence speed of the model and helping to establish long-term memory of navigation habits. To verify the validity of the method, two-dimensional simulation experiments and three-dimensional simulation robot experiments were designed in this paper. The experimental results showed that the method presented in this paper not only surpassed other algorithms in terms of navigation efficiency and convergence speed, but also exhibited good adaptability to dynamic navigation tasks. Furthermore, our method can be effectively applied to mobile robots.