Complexes of epileptic activity formed by a determinant focus in the cortex isolé

Foci of increased excitability, functioning independently, were created in the neuronally isolated cortex of cats by means of weak strychnine solutions. The creation of a hyperactive focus by application of concentrated solutions or crystals of strychnine led to an increase of amplitude and discharge frequency in other foci, synchronization of the discharges in these foci, and their combination into a single functional complex of foci driven by the hyperactive focus. The later thus played the role of determinant structure. Marked generalization of paroxysmal activity also took place under the influence of the determinant focus and was manifested as the spread of epileptic discharges to areas of cortex untreated with strychnine. The results indicate that relations established between hyperactive foci in the cortex and the effects of the determinant structure can be brought about through purely cortical mechanisms.Laboratory of General Pathology of the Nervous System, Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. Department of Pathological Physiology, M. I. Pirogov Odessa Medical Institute. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 88, No. 10, pp. 408–412, October, 1979.     

大鼠癫痫发作可预测性的研究

癫痫是一种常见的神经系统疾病,其长期反复发作,使患者身心不断遭受伤害.若能提前预测到癫痫的发作,则可以使患者及时采取措施进行预防和保护.在癫痫发作预测研究中,动物模型可以提供丰富的样本,验证算法可行性,揭示癫痫发作的规律.本文制作了癫痫大鼠模型并建立了数据采集系统.利用同步性和复杂度两种非线性特征,对12次癫痫大发作进行分析,发现癫痫发作前同步性特征呈下降或上升趋势,复杂度特征则呈与同步性相反的变化趋势.这种变化在发作前几分钟出现,分析结果验证了癫痫发作的可预测性.     

Effects of delta-sleep-inducing peptide on NMDA-induced convulsive activity in rats

Acute experiments on rats showed that the ED₁₀₀ of NMDA for induction of clonic convulsions was 0.53 μg, while the ED₁₀₀ of NMDA for inducing tonic extension of the forelimbs was 5.02 μg/animal. Determination of these parameters after administration of delta-sleep-inducing peptide (100 μg/kg, i.p.) revealed 2.3- and 4.46-fold increases. These results provide evidence for a neuroprotective role of delta-sleep-inducing peptide in relation to excitatory amino acid receptor agonists. Department of Normal Physiology, State Medical University, 2 Valikhovskii Lane, 270100 Odessa, Ukraine. Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 83, No. 9, pp. 32–36, September, 1997.     

柴胡皂苷a对难治性癫痫大鼠痫性发作的影响

目的探讨柴胡皂苷a（SSa）对匹罗卡品致难治性癫痫模型大鼠痫性发作的影响。方法将制备成功的48只SD难治性癫痫大鼠模型随机分为模型组（B）、丙戊酸钠组（C）、柴胡皂苷a低剂量组（D）和高剂量组（E）4组,每组各12只,另有空白对照组（A）12只。A、B组给予等量生理盐水,C组用量为200mg/kg,D、E组用药浓度依次为1.09mg/kg、2.18mg/kg,A、B、C组灌胃给药,D、E组腹腔注射给药。分别观察给药4周、8周后痫性发作次数、平均发作时间及发作级别的变化。结果痫性发作方面,A组无痫性发作,B组大鼠痫性发作明显（P〉0.05）,C、D、E组大鼠痫性发作均有不同程度的减轻（P〈0.05）,E组大鼠痫性发作减轻最明显。结论柴胡皂苷a能减轻难治性癫痫大鼠的痫性发作,有明显的抗癫痫作用。     

Facilitation of spike-wave discharge activity by lipopolysaccharides in Wistar Albino Glaxo/Rijswijk rats

In normal rats the proinflammatory cytokines like interleukin-1beta, interleukin-6, which are induced by bacterial lipopolysaccharides, are able to control thalamo-cortical excitability by exerting strong effects on physiological synchronization such as sleep and on pathological synchronization like that in epileptic discharges. To investigate whether proinflammatory cytokines or lipopolysaccharides could modulate absence seizures resulting from a very different generator mechanism than the already investigated bicuculline-, kindling- and kainate-induced seizures, we used a genetically epileptic Wistar Albino Glaxo/Rijswijk rat strain, which is spontaneously generating high voltage spike-wave discharges. Wistar Albino Glaxo/Rijswijk rats responded with an increase of the number of spike-wave discharges to lipopolysaccharide injection (from 10 microg/kg to 350 microg/kg). Repetitive administration of 350 microg/kg lipopolysaccharides daily for 5 days increased the number of spike-wave discharges on the first, second and third days but the number of spike-wave discharges returned to the control value on day 5, at the 5th injection of lipopolysaccharides, showing a tolerance to lipopolysaccharides. The lipopolysaccharide-induced increase in spike-wave discharges was not directly correlated with the elevation of the core body temperature, as it is in febrile seizures, although lipopolysaccharide induced prostaglandin and is clearly pyrogenic at the doses used. Indomethacin, the prostaglandin synthesis inhibitor, efficiently blocked lipopolysaccharide-induced enhancement of spike-wave discharge genesis suggesting that the spike-wave discharge facilitating effect of lipopolysaccharides involves induction of cyclooxygenase 2 and subsequent synthesis and actions of prostaglandin E2. Low dose (40 mg/kg, i.p.) of competitive N-methyl-d-aspartate receptor antagonist 2-amino-5-phosphonopentanoic acid, and low dose of lipopolysaccharide (20 microg/kg) showed a synergistic interaction to increase the number of spike-wave discharges, whereas at supramaximal doses of lipopolysaccharide and the N-methyl-D-aspartate antagonist no synergy was present. The data reveal a functional connection between absence epileptic activity and lipopolysaccharide induction of prostaglandin synthesis and prostaglandin action and suggest some common cellular targets in epilepsy and lipopolysaccharide-induced inflammation.     

Simulation of determinant and dependent foci of epileptic activity in the rat cerebral cortex

Foci of increased activity with independent firing patterns were created by means of weak solutions of strychnine in acute experiments on rats. A hyperactive focus of excitation created by means of concentrated strychnine solutions played the role of determinant structure. Its role was to determine the character of activity of the other epileptogenic foci, to enhance their paroxysmal activity, to combine them into a single functional complex, and to determine the behavior of the whole complex. This complex could be destroyed by suppressing the activity of the determinant focus. Elimination of any of the dependent foci forming the complex did not disturb the complex itself. These investigations confirm, on a new model, the general concept of the role of determinant structure in the activity of the CNS.Department of Pathological Physiology, N. I. Pirogov Odessa Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR A. M. Chernukh.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 87, No. 3, pp. 217–220, March, 1979.     

Facial anomalies in D-2-hydroxyglutaric aciduria

D -2-hydroxyglutaric aciduria is a rare autosomal recessive organic aciduria with variable clinical expression. The biochemical defect is still unknown, and genetic heterogeneity has been suggested. Here, we report on facial anomalies in two unrelated cases of D -2-hydroxyglutaric aciduria presenting with epileptic encephalopathy. In a review, we found that minor facial anomalies have been mentioned in three patients. A flat face with a broad nasal bridge and external ear anomalies were present in our patients and in reported cases. We suggest giving consideration to D -2-hydroxyglutaric aciduria as a cause of minor facial anomalies in epileptic encephalopathy of unknown origin. Am. J. Med. Genet. 86:124–129, 1999. © 1999 Wiley-Liss, Inc.     

Tubulin β‐III modulates seizure activity in epilepsy

Tubulin β‐III (TUBB3) is the most dynamic β‐tubulin isoform expressed in neurons, and is highly expressed in the central nervous system. However, the relationship between TUBB3 and epileptic seizures has not been thoroughly investigated. The aims of this study were to investigate the expression of TUBB3 in patients with temporal lobe epilepsy and two different rat models of chronic epilepsy, and to determine the specific roles of TUBB3 in epilepsy. TUBB3 expression was upregulated in human and rat epileptic tissue. Moreover, TUBB3 expression was associated with inhibitory GABAergic neurons and the inhibitory postsynaptic scaffold protein gephyrin. TUBB3 downregulation attenuated the behavioural phenotypes of epileptic seizures during the pilocarpine‐induced chronic phase of epileptic seizures and the pentylenetetrazole kindling process, whereas TUBB3 overexpression had the opposite effect. Whole‐cell clamp recordings and western blotting revealed that the amplitude of GABA‐A receptor‐mediated miniature inhibitory postsynaptic currents and the surface expression of the GABA‐A receptor were increased in rats in which TUBB3 expression was downregulated. Importantly, TUBB3 interacted with GABA‐A receptor‐associated protein, which is known to be involved in GABA‐A receptor trafficking. These results indicate that TUBB3 plays a critical role in the regulation of epileptic seizures via GABA‐A receptor trafficking, suggesting a molecular mechanism for new therapeutic strategies. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.     

癫痫发作时的脑电图研究

脑电图已成为癫痫诊断中不可缺少的手段,特别是发作时的脑电图为癫痫诊断的基本要素,本文对22例癫痫发作时的脑电图进行了研究,分析了发作时的癫痫放电及发作前后的波形演变,对癫痫的分类及治疗有着重要的意义。     

安定颈动脉内注射对癫（疒/间）灶定侧的价值

目的：探讨颈动脉内注射安定对癫痫定侧的价值。方法：对12例（10例两侧同步和2例游走性痫样放电）癫痫患者进行安定颈动脉内注射试验、观察注射后痫样波受抑制情况来确定痫灶侧。结果：于痫灶侧安定颈动脉内注射，两侧痫样波同时消失；于痫灶对侧注射，则注射侧痫样波消失，而病灶侧痫样波仍存在。结论：颈动脉内注射安定对癫痫灶定侧有重要价值，可替代传统的颈动脉内阿米妥钠注射试验。     

癔症性精神障碍与癫癎性精神障碍临床及脑电图对照分析

目的：观察癔症性精神障碍与癫痫性精神障碍的临床及脑电图特点并对照分析。方法：采用日本光电5214脑电图系统，按照国际10～20系统标准放置电极，进行单极双极、过度换气、闪光试验测试的描记方法检查脑电图。结果：两组病人各30例，癔症性精神障碍组边缘状态2例，轻度异常2例，中度异常及重度异常无1人。而癫痫性精神障碍组边缘状态10例，轻度异常4例，中度异常及重度异常共12例。结论：虽然两组临床发作相似，但有明显差异，癫痫性精神障碍组EEG阳性率明显升高，疗效差。癔症性精神障碍组EEG无一例中度异常或重度异常，治疗效果好。