Spike‐associated networks and intracranial electrographic findings

Aims. Functional connectivity is providing new insights into the network nature of epilepsy with growing clinical applications. Our objective was to validate a novel magnetoencephalography‐based method to non‐invasively measure the epileptic network. Methods. We retrospectively identified pediatric and adult patients with refractory focal epilepsy who underwent pre‐surgical magnetoencephalography with subsequent intracranial electrographic monitoring. Magnetoencephalography tracings were visually reviewed, and interictal epileptiform discharges (“spikes”) were individually marked. We then evaluated differences in whole‐brain connectivity during brief epochs preceding the spikes and during the spikes using the Network‐Based Statistic to test differences at the network level. Results. In six patients with statistically‐significant network differences, we observed substantial overlap between the spike‐associated networks and electrographically active areas identified during intracranial monitoring (the spike‐associated network was 78% and 83% sensitive for intracranial electroencephalography‐defined regions in the irritative and seizure onset zones, respectively). Conclusion. These findings support the neurobiological validity of the spike‐associated network method. Assessment of spike‐associated networks has the potential to improve surgical planning in epilepsy surgery patients by identifying components of the epileptic network prior to implantation.     

Sensory evoked potentials in patients with Rett syndrome through the lens of animal studies: Systematic review

ObjectiveSystematically review the abnormalities in event related potential (ERP) recorded in Rett Syndrome (RTT) patients and animals in search of translational biomarkers of deficits related to the particular neurophysiological processes of known genetic origin (MECP2 mutations).MethodsPubmed, ISI Web of Knowledge and BIORXIV were searched for the relevant articles according to PRISMA standards.ResultsERP components are generally delayed across all sensory modalities both in RTT patients and its animal model, while findings on ERPs amplitude strongly depend on stimulus properties and presentation rate. Studies on RTT animal models uncovered the abnormalities in the excitatory and inhibitory transmission as critical mechanisms underlying the ERPs changes, but showed that even similar ERP alterations in auditory and visual domains have a diverse neural basis. A range of novel approaches has been developed in animal studies bringing along the meaningful neurophysiological interpretation of ERP measures in RTT patients.ConclusionsWhile there is a clear evidence for sensory ERPs abnormalities in RTT, to further advance the field there is a need in a large-scale ERP studies with the functionally-relevant experimental paradigms.SignificanceThe review provides insights into domain-specific neural basis of the ERP abnormalities and promotes clinical application of the ERP measures as the non-invasive functional biomarkers of RTT pathophysiology.     

脑电监测（24小时）对头痛型癫痫的诊断意义

对６０例临床疑为头痛型痛痫的患者进行２４ｈ脑电监测。结果表明：２４ｈ脑电监测对痛痫特殊类型的检出率明显高于常规ＥＥＧ。在１４例（２３．３％）有痫样放电的患者中，出现痫样放电以睡眠期多于清醒期；且睡眠周期中以ＮＲＥＭⅠ，Ⅱ期最常见。对６例（１６．２％）反复阵发出现高波幅额中线θ节律而无痫性放电的患者亦应考虑头痛型癫痫的诊断。     

Pathophysiology of idiopathic dystonia: findings from genetic animal models

Dystonia is a common movement disorder which is thought to represent a disease of the basal ganglia. However, the pathogenesis of the idiopathic dystonias, i.e. the neuroanatomic and neurochemical basis, is still a mystery. Research in dystonia is complicated by the existence of various phenotypic and genotypic subtypes of idiopathic dystonia, probably related to heterogeneous dysfunctions.In neurological diseases in which no obvious neuronal degeneration can be found, such as in idiopathic dystonia, the identification of a primary defect is difficult, because of the large number of chemically distinct, but functionally interrelated, neurotransmitter systems in the brain.The variable response to pharmacological agents in patients with idiopathic dystonia supports the notion that the underlying biochemical dysfunctions vary in the subtypes of idiopathic dystonia. Hence, in basic research it is important to clearly define the involved type of dystonia.Animal models of dystonias were described as limited. However, over the last years, there has been considerable progress in the evaluation of animal models for different types of dystonia.Apart from animal models of symptomatic dystonia, genetic animal models with inherited dystonia which occurs in the absence of pathomorphological alterations in brain and spinal cord are described.This review will focus mainly on genetic animal models of different idiopathic dystonias and pathophysiological findings. In particular, in the case of the mutant dystonic (dt) rat, a model of generalized dystonia, and in the case of the genetically dystonic hamster (dt^sz), a model of paroxysmal dystonic choreoathetosis has been used, as these show great promise in contributing to the identification of underlying mechanisms in idiopathic dystonias, although even a proper animal model will probably never be equivalent to a human disease.Several pathophysiological findings from animal models are in line with clinical observations in dystonic patients, indicating abnormalities not only in the basal ganglia and thalamic nuclei, but also in the cerebellum and brainstem. Through clinical studies and neurochemical data several similarities were found in the genetic animal models, although the current data indicates different defects in dystonic animals which is consistent with the notion that dystonia is a heterogenous disorder.Different supraspinal dysfunctions appear to lead to manifestation of dystonic movements and postures. In addition to increasing our understanding of the pathophysiology of idiopathic dystonia, animal models may help to improve therapeutic strategies for this movement disorder.     

重症肌无力患者IgG脑室内注射对大鼠EEG及BAEP的影响

目的 观察重症肌无力(myasthenia gravis，MG)患者IgG(AChRAb)经大鼠脑室内注入对其脑电图(electroencephalography，EEG)及脑干听觉诱发电位(brain stem auditory evoked potential，BAEP)的影响，并探讨AChRAb影响大鼠中枢神经系统(CNS)的机制。方法将从确诊的、AChRAb阳性的MG患者血清中提纯的IgG(AChRAb)，注射到实验组大鼠侧脑室，对照组大鼠则注射健康人IgG，观察大鼠行为学、BAEP、EEG改变。结果实验组大鼠术后出现类似于实验性自身免疫性MG的行为学改变，部分大鼠出现癫痫发作BAEP峰间潜伏期(IPLs)延长EEG异常，即δ、θ增多与痫性波发放增加。结论 MGAChRAb可致大鼠CNS损害，AChRAb与大鼠CNS神经元型乙酰胆碱受体结合，可能是其病理生理机制。     

熵指数对异氟烷麻醉中切皮体动反应的预测作用

目的 研究熵指数(包括反应熵和状态熵)对异氟烷复合麻醉中切皮体动反应的预测作用并与双频谱指数(BIS)比较.方法 ASA Ⅱ级择期腹部手术患者20例,按切皮有无体动反应分为体动组(9例)和非体动组(11例).入室后常规监测,然后静注异丙酚、琥珀胆碱、芬太尼快诱导气管插管,持续吸入异氟烷,维持呼气末异氟烷浓度为1.3MAC,维持10min后开始手术,切皮前不用神经肌肉阻滞剂,如果发生体动,则按10%提高下一个患者异氟烷呼气末浓度,如果不动则按10%降低下一个患者异氟烷呼气末浓度.分别于入室、切皮前60s、30s、切皮后45s、120s对每例患者同时行熵指数和BIS监测.结果 两组患者的熵指数值有显著性差异(P＜0.05),而BIS无显著性差异(P＞0.05).反应熵和状态熵可以预测切皮体动,其预测概率(Pk)值分别为0.893 7和0.885 2,BIS不能预测切皮体动,Pk值是0.591 9,熵指数和BIS的Pk值之间有显著性差异(P＜0.05),Pk与反应熵和状态熵的Logistic回归方程分别为ln [Pk/(1-Pk)]=32.517-0.481x和ln [Pk/(1-Pk)]=28.728-0.438x.结论 熵指数监测可以预测异氟烷麻醉中的切皮体动反应,值得临床推广应用.     

EEG reactivity correlates with neuropsychological test scores in Down's syndrome

Introduction – Down's syndrome patients express a neurodegenerative disorder and mental retardation. We studied the reactivity of EEG and its correlation with neuropsychological test score in Down's syndrome. Material and methods – We studied 32 patients with Down's syndrome and 31 controls for blocking of occipital EEG activity. The temporo-occipital EEG with eyes open (EO) was compared with resting EEG with eyes closed (EC), (EC/EO ratio). Results – Both Down patients and controls showed significant diminution of alpha, beta and theta activity and decrease of EEG frequency with EO. However, there was a significant impairment in Down patients in the EC/EO ratio in alpha band, compared to controls. The controls had no correlation of the alpha EC/EO ratio with age or gender. The Down patients showed a significant correlation of this variable with age which is in accordance with a gradually progressing disease. They had also significant correlations of the alpha EC/EO ratio and neuropsychological test scores which indicates that this ratio may be a more general measure of cerebral or hemispherical dysfunction than a mere impairment of visual activation. Down patients also showed significant differences in resting EEG variables, compared to the controls, even if the conventional EEG showed normal or mildly slowed dominant occipital rhythm in most of the patients. The correlation analysis between resting EEG and EC/EO ratio variables pointed out that they are relatively independent, representing different factors in the regulation of EEG. Conclusions – We believe that the alpha EC/EO ratio of EEG add a new domain in the assessment of cerebral dysfunction in Down's syndrome.     

Acute hemodynamic responses to electroconvulsive therapy are not related to the duration of seizure activity

Study Objective: To test the hypothesis that the magnitude of the acute hemodynamic response to electroconvulsive therapy (ECT) is related to the duration of the seizure activity in patients receiving different dosages of intravenous (IV) lidocaine.

Design: Randomized, double-blind, placebo-controlled, cross-over study.

Setting: University-affiliated hospital.

Patients: 21 ASA physical status I, II, and III patients undergoing four consecutive maintenance ECT treatments for chronic depression.

Interventions: Patients received lidocaine 50 mg, 100 mg, 200 mg IV, or saline prior to induction of anesthesia via a standardized anesthetic technique.

Measurements and Main Results: Noninvasive blood pressure (BP) and heart rate (HR), as well as the duration of motor and electroencephalographic (EEG) seizure, were measured. The duration of motor and EEG seizures (means ± SD) were 37 ± 13 sec and 64 ± 21 sec, 25 ± 11 sec and 52 ± 43 sec, 17 ± 12 sec and 32 ± 17 sec, 1 ± 3 sec and 18 ± 10 sec in the saline, lidocaine 50 mg, 100 mg, 200 mg groups, respectively. Although the duration of seizure activity was decreased in a dose-related fashion after lidocaine pretreatment, the peak increases in BP and HR were similar in the lidocaine and saline treatment groups.

Conclusions: Despite producing dose-related decreases in the duration of both motor and EEG seizure activity, lidocaine failed to attenuate the acute hemodynamic response to ECT. Thus, the acute hemodynamic response to ECT is not related to the duration of seizure activity.     

Topographical analysis of the EEG effects of a subconvulsive dose of lidocaine in healthy volunteers

Background: The purpose of the present study was to assess the effects of intravenous lidocaine on spatial changes of electroen-cephalographic power and on psychomotoric status in conscious volunteers.
Methods: In 11 healthy volunteers lidocaine (2-min bolus, 100 mg; 15-min infusion, 40 μg kg^-1 min^-1) or placebo were given intravenously in a randomized, single-blinded, two-way crossover study. Haemodynamics and lidocaine plasma concentrations were measured at baseline and within a period of 30 min following bolus injection. Vigilance and emotional status were tested using visual analogue scales (VAS). Toxic CNS effects were evaluated by a questionnaire. The raw EEG (17 leads, reference C_z) and computed power spectra were continuously recorded.
Results: The chosen lidocaine dosage led to nearly constant plasma concentrations (unbound lidocaine 2.5 min and 15 min after bolus 0.36±0.14 μg/ml and 0.30±0.06 μg/ml, respectively [mean±SD]). The placebo caused no symptoms, changes in VAS-scores or EEG-parameters. Lidocaine induced pronounced subjective symptoms and significant increases in delta activity for 15 min, most dominant at the frontotemporal and occipital leads (max. +219% O₁). Frontal and occipital beta1 and beta2 power (max. +131% and +124% at O₁, respectively) was immediately increased after the bolus injection. No EEG changes occurred at central region C_z, and no interhemispheric EEG differences were noted. Theta, alphal, and alpha2 power remained unchanged.
Conclusion: The current data demonstrate simultaneous changes in psychomotoric status as well as delta and beta spectral power during lidocaine infusion. These data could be an indication that the pronounced frontotemporal and occipital EEG changes are the electroencephalographic expression of subjective sensations.