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This paper presents a probabilistic power flow model subject to connection temperature constraints. Renewable power generation is included and modelled stochastically in order to reflect its intermittent nature. In contrast to conventional models that enforce connection current constraints, short-term current overloading is allowed. Temperature constraints are weaker than current constraints, and hence the proposed model quantifies the overload risk more realistically. Using such a constraint is justified the more by the intermittent nature of the renewable power source. Allowing temporary current overloading necessitates the incorporation of a time domain in our model. This substantially influences the choice of model for the renewable power source, as we explain. Wind power is modelled by use of an ARMA model, and appropriate accelerations of the power flow solution technique are chosen. Several IEEE test case examples illustrate the more realistic risk analysis. An example shows that a current constraint model may overestimate these risks, which may lead to unnecessary over-investments by grid operators in grid connections.

The generation by renewables and the loading by electrical vehicle charging imposes severe challenges in the redesign of today’s power supply systems. Indeed, accommodating these emerging power sources and sinks requires traditional power systems to evolve from rigid centralized unidirectional architectures to intelligent decentralized entities allowing a bidirectional power flow. In the case study proposed by ENDINET, we investigate how the penetration of solar panels and of battery charging stations on large scale affects the voltage quality and loss level in a distribution network servicing a residential area in Eindhoven, NL. In our case study we take the average household load during summer and winter into account and consider both a radial and meshed topology of the network. Our study results for both topologies considered in a quantification of the levels of penetration and a strategy for electrical vehicle loading strategy that meet the voltage and loss requirements in the network. Keywords: power systems, load flow computations, distributed generation, electrical vehicle charging

Vagus nerve stimulation (VNS) is an effective adjunctive treatment for medically refractory epilepsy. In this study, we measured VNS-induced changes in hippocampal neurotransmitter levels and determined their potential involvement in the anticonvulsive action of VNS, to elucidate the mechanism of action responsible for the seizure suppressing effect of VNS in an animal model for limbic seizures. We used in vivo intracerebral microdialysis to measure VNS-induced changes in hippocampal extracellular concentrations of noradrenaline, dopamine, serotonin and GABA in freely moving, male Wistar rats. During the same experiment, the effect of VNS on pilocarpine-induced limbic seizures was assessed using video-EEG monitoring. The involvement of VNS-induced increases in hippocampal noradrenaline in the mechanims of action of VNS was evaluated by blocking hippocampal alfa(2)-receptors. VNS produced a significant increase in hippocampal noradrenaline concentration (69 ± 16% above baseline levels). VNS also increased the latency between pilocarpine infusion and the onset of epileptiform discharges, and reduced the duration and severity of pilocarpine-induced limbic seizures. A strong positive correlation was found between the noradrenergic and anticonvulsive effects of VNS. Blockade of hippocampal alfa(2 -receptors reversed the seizure-suppressing effect of VNS. VNS induces increases in extracellular hippocampal noradrenaline, which are at least partly responsible for its seizure-suppressing effect in a model for limbic seizures, and constitute a potential biomarker for the efficacy of VNS in temporal lobe epilepsy.

Purpose: Hippocampal deep brain stimulation (DBS) is an experimental therapy for patients with pharmacoresistant temporal lobe epilepsy (TLE). Despite the successful clinical application of DBS, the optimal stimulation parameters are undetermined. We evaluate the efficacy of a new form of DBS, using continuous stimuli with Poisson distributed intervals (Poisson distributed stimulation, PDS) in the kainate (KA) rat model, a validated model for human TLE. Methods: Status epilepticus was elicited by injection of KA (i.p.). After development of spontaneous seizures, rats were implanted with hippocampal DBS- and depth electroencephalography (EEG) electrodes. After baseline EEG monitoring, one group of rats (n = 13) was treated with PDS and a second (n = 11) received regular high frequency stimulation (HFS) at 130 Hz. Stimulation intensity was 100 μA below the threshold for induction of epileptiform EEG activity. Results: Stimulation intensity was significantly lower for PDS (156 ± 20 μA) than HFS (207 ± 23 μA; p < 0.02). Seven (54%) of 13 rats treated with PDS and 5 (45%) of 11 rats treated with HFS experienced a significant reduction in seizure frequency. In PDS-improved rats, seizure frequency was reduced to 33% (p < 0.01) of baseline value and in HFS-improved rats to 50% (p < 0.01). After termination of PDS, seizure rate returned to baseline value. Discussion: Continuous hippocampal PDS significantly reduces the number of spontaneous seizures. Compared to regular HFS, there is a slightly larger number of improved rats and a larger efficacy at a considerably lower stimulus intensity. The first two observations leave room for optimization, whereas a lower intensity is beneficial for battery life.

Purpose: Despite different treatment options for patients with refractory epilepsy such as epilepsy surgery and neurostimulation, many patients still have seizures and/or drug-related cerebral and systemic side effects. Local intracerebral delivery of antiepileptic compounds may represent a novel strategy with specific advantages such as the option of higher local doses and reduced side effects. In this study we evaluate the antiepileptic effect of local delivery of adenosine in the kainic acid rat model, a validated model for temporal lobe epilepsy. Methods: Fifteen rats, in which intraperitoneal kainic acid injection had induced spontaneous seizures, were implanted with a combination of depth electrodes and a cannula in both hippocampi. Cannulas were connected to osmotic minipumps to allow continuous hippocampal delivery. Rats were freely moving and permanently monitored by video-EEG (electroencephalography). Seizures were scored during 2 weeks of local hippocampal delivery of saline (baseline), followed by 2 weeks of local adenosine (6 mg/ml) (n = 10) or saline (n = 5) delivery (0.23 μl/h) (treatment). In 7 of 10 adenosine-treated rats, saline was also delivered during a washout period. Results: During the treatment period a mean daily seizure frequency reduction of 33% compared to the baseline rate was found in adenosine-treated rats (p < 0.01). Four rats had a seizure frequency reduction of at least 50%. Both nonconvulsive and convulsive seizures significantly decreased during the treatment period. In the saline-control group, mean daily seizure frequency increased with 35% during the treatment period. Conclusions: This study demonstrates the antiseizure effect of continuous adenosine delivery in the hippocampi in rats with spontaneous seizures.

Aims: Although vagus nerve stimulation (VNS) is an approved treatment for patients with refractory epilepsy, its mechanism of action is still unclear. The aim of this study was to test the effect of VNS on seizure activity induced by intrahippocampal pilocarpine infusion and to evaluate changes in extracellular, hippocampal neurotransmitter concentrations (norepinephrine, dopamine, serotonin, GABA) in response to VNS. By using a selective alfa2-adrenoreceptor antagonist, SKF-86466, the role of norepinephrine in the anticonvulsant effect of VNS was tested. Methods: Rats (n=37) were implanted with a stimulation electrode around the left vagal nerve. A microdialysis probe was stereotactically inserted in the left hippocampus. One week after surgery video recording and microdialysis were started. Rats were randomly devided in 4 groups: SHAM (n=7), VNS (n=12), VNS/SKF (n=8) and SKF (n=10). Two hours after the start of the experiment VNS was initiated in the VNS group and SKF-86466 (SKF) was administrated via themicrodialysis probe in the VNS/SKF and the SKF group. One hour later, VNS was started in the VNS/SKF group. Both SKF administration and VNS was continued until the end of the experiment. Four hours (SHAM and VNS group) or five hours (VNS/SKF and SKF group) after the start of the experiment pilocarpine was administrated via the microdialysis probe. Behavioral and electrographical changes indicative of seizure activity were monitored using video-electo-encephalogram (EEG) recording. Extracellular concentration of noradrenalin, dopamine, serotonin and GABA were determined. Results: Epileptiform EEG activity and behavioural seizures, induced by intrahippocampal pilocarpine infusion, were significantly reduced by VNS. VNS induced a highly significant increase of hippocampal norepinephrine concentration (80% higher compared to baseline). The suppression of epileptiform EEG and behavioural seizures was positively correlated with the extend of norepinephrine increase in the hippocampus in response to VNS. Selective blocking of the alfa2-adrenoreceptor using SKF completely reverted the anticonvulsant effects of VNS. Conclusion: VNS has seizure suppressive effects in the intrahippocampal pilocarpine model for limbic seizures. These anti-epileptic effect are the result of an increase in hippocampal norepinephrine concentration induced by VNS. Increased norepinephrine concentration could be a biomarker for the anti-epileptic effect of VNS.

Aims: Although vagus nerve stimulation (VNS) is an approved treatment for patients with refractory epilepsy, its mechanism of action is still unclear. The aim of this study was to test the effect of VNS on seizure activity induced by intrahippocampal pilocarpine infusion and to evaluate changes in extracellular, hippocampal neurotransmitter concentrations (norepinephrine, dopamine, serotonin, GABA) in response to VNS. By using a selective alfa2-adrenoreceptor antagonist, SKF-86466, the role of norepinephrine in the anticonvulsant effect of VNS was tested. Methods: Rats (n=37) were implanted with a stimulation electrode around the left vagal nerve. A microdialysis probe was stereotactically inserted in the left hippocampus. One week after surgery video recording and microdialysis were started. Rats were randomly devided in 4 groups: SHAM (n=7), VNS (n=12), VNS/SKF (n=8) and SKF (n=10). Two hours after the start of the experiment VNS was initiated in the VNS group and SKF-86466 (SKF) was administrated via themicrodialysis probe in the VNS/SKF and the SKF group. One hour later, VNS was started in the VNS/SKF group. Both SKF administration and VNS was continued until the end of the experiment. Four hours (SHAM and VNS group) or five hours (VNS/SKF and SKF group) after the start of the experiment pilocarpine was administrated via the microdialysis probe. Behavioral and electrographical changes indicative of seizure activity were monitored using video-electo-encephalogram (EEG) recording. Extracellular concentration of noradrenalin, dopamine, serotonin and GABA were determined. Results: Epileptiform EEG activity and behavioural seizures, induced by intrahippocampal pilocarpine infusion, were significantly reduced by VNS. VNS induced a highly significant increase of hippocampal norepinephrine concentration (80% higher compared to baseline). The suppression of epileptiform EEG and behavioural seizures was positively correlated with the extend of norepinephrine increase in the hippocampus in response to VNS. Selective blocking of the alfa2-adrenoreceptor using SKF completely reverted the anticonvulsant effects of VNS. Conclusion: VNS has seizure suppressive effects in the intrahippocampal pilocarpine model for limbic seizures. These anti-epileptic effect are the result of an increase in hippocampal norepinephrine concentration induced by VNS. Increased norepinephrine concentration could be a biomarker for the anti-epileptic effect of VNS.

Introduction: Although vagus nerve stimulation (VNS) is an approved treatment for patients with refractory epilepsy, its mechanism of action is still unclear. Enhancement of noradrenalin release in the hippocampus, caused by altered activity in the locus coeruleus, might contribute to the anti-convulsive effect of VNS. The aim of this study was to evaluate the effects of VNS on pilocarpine-induced limbic seizures and on hippocampal extracellular neurotransmitter concentrations in vivo in rats. Materials and Methods: Rats (n=14) were implanted with a stimulation electrode around the left vagal nerve. Depth EEG electrodes and a microdialysis probe were stereotactically inserted into the left hippocampus. One week after surgery EEG recording and microdialysis was started. Two hours after the start of the experiment VNS was initiated in half of the rats and continued until the end of the experiment. Two hours after VNS initiation, limbic seizures were evoked in both the control and stimulated group by intrahippocampal administration of pilocarpine via the microdialysis probe. Behavioral changes indicative of seizure activity and hippocampal EEG were monitored. Concentration of noradrenalin, dopamine, serotonin and GABA were measured. Results: In the stimulated group, the scores of behavioral seizures were significantly (pDiscussion and Conclusion: Vagus nerve stimulation (VNS) induces a rapid increase in hippocampal extracellular noradrenalin concentration and a reduction in behavioral scores and duration of pilocarpine-induced limbic seizures. It needs to be investigated whether there is a causal relationship between the increased noradrenalin concentration and the anticonvulsant effect of VNS.