Treatment of electrical status epilepticus by short diazepam (DZP) cycles after DZP rectal bolus test

Negri, M. De; Baglietto, M. G.; Battaglia, Francesca; Gaggero, R.; Pessagno, A.; Recanati, L.

doi:10.1016/0387-7604(95)00076-n

Cited by 87 publications

(59 citation statements)

References 6 publications

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“…Concerning the CSWS-related neuropsychological disturbances, several authors have underlined the parallel, though not perfectly overlapping, course of CSWS and mental and behavioral abnormalities (De Negri et al, 1995). There is a well-documented increased incidence of attention deficit hyperactivity disorder (ADHD) and behavioral disorders, which are likely to be independent of the degree of seizure control (Schubert, 2005).…”

Section: Discussionmentioning

confidence: 99%

Sequential Prefrontal Lobe Volume Changes in Epileptic Patients with Continuous Spikes and Waves During Slow Sleep

Kanemura¹,

Aihara²

2011

Epilepsy in Children - Clinical and Social Aspects

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Section: Discussionmentioning

confidence: 99%

Sequential Prefrontal Lobe Volume Changes in Epileptic Patients with Continuous Spikes and Waves During Slow Sleep

Kanemura¹,

Aihara²

2011

Epilepsy in Children - Clinical and Social Aspects

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“…Because ␤-alanine and taurine activate both GlyRs and GABA A Rs (Choquet and Korn 1988;del Olmo et al 2000), the receptor mediating their actions in different regions of the CNS during development is unclear. Glycine, taurine, and ␤-alanine currents have similar pharmacological and physiological profiles in embryonic hippocampal neurons.…”

Section: Cultured Embryonic Mouse Hippocampal Neurons Express ␣ 2 -Comentioning

confidence: 99%

“…While the benzodiazepine concentrations needed to inhibit GlyRs are higher that those needed to augment GABA A Rs, the cerebrospinal fluid concentrations achieved clinically in neonates are unknown. Finally, this site may mediate the effects of the high dose benzodiazepine regimens used to treat electrical status epilepticus during slow wave sleep (De Negri et al 1995) and nonketotic hyperglycinemia, a condition associated with elevated cerebrospinal fluid glycine concentrations and severe neonatal seizures (Matalon et al 1983).…”

Section: Clinical Relevancementioning

confidence: 99%

Benzodiazepines Block α₂-Containing Inhibitory Glycine Receptors in Embryonic Mouse Hippocampal Neurons

Thio¹,

Shanmugam²,

Isenberg³

et al. 2003

Journal of Neurophysiology

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Inhibitory glycine receptors (GlyRs) in the mammalian cortex probably contribute to brain development and to maintaining tonic inhibition. Given their presence throughout the cortex, their modulation likely has important physiological consequences. Although benzodiazepines potentiate γ-aminobutyric acidA receptors (GABAARs), they may also modulate GlyRs because binding studies initially suggested that they act at GlyRs. Furthermore, their diminished ability to potentiate neonatal GABAARs suggests that they may exert their beneficial clinical effects at another site in the developing brain. Therefore we examined the effect of benzodiazepines on whole cell currents mediated by GlyRs in cultured embryonic mouse hippocampal neurons. First, we determined the GlyR subunit composition in this preparation. Glycine, β-alanine, and taurine activate strychnine-sensitive chloride currents in a dose-dependent manner. Maximal concentrations of the three agonists produce equal, nonadditive responses as expected of full agonists. The pharmacological properties of the GlyR currents including their pattern of modulation by picrotoxinin, picrotin, and tropisetron indicate that GlyRs consist of α2β heteromers and α2 homomers. Reverse transcriptase polymerase chain reaction (RTPCR) studies confirmed the presence of α2 and β subunits. Second, we found that micromolar concentrations of some benzodiazepines, including chlordiazepoxide and nitrazepam, inhibit GlyR currents. Nitrazepam inhibition of GlyRs is noncompetitive, is not voltage dependent, and does not reflect enhanced desensitization. Thus benzodiazepines allosterically inhibit α2-containing GlyRs in embryonic mouse hippocampal neurons via a “low”-affinity site.

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“…Patients had no neuroimaging evidence of cerebral pathology. Patients were treated with valproic acid (VPA) plus periodic short cycles of diazepam (DZP; 3-4 weeks) (22). To evaluate the presence IEDs and IEDs activation during sleep, all the subjects underwent frequent diurnal nap recordings.…”

Section: Methodsmentioning

confidence: 99%

Spindles‐Inducing Mechanism Modulates Sleep Activation of Interictal Epileptiform Discharges in the Landau—Kleffner Syndrome

et al. 2000

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Summary:Purpose: Landau-Kleffner syndrome (LKS) is characterized by a marked increase of interictal epileptiform discharges (IEDs) during sleep. During nonrapid eye movement (NREM) sleep, neuronal membrane potential oscillations lead to the appearance of spindles and delta waves in the surface EEG and might develop into paroxysmal synchronization. Spectral analysis allows the quantitative description of the dynamics of delta (slow-wave activity, SWA, 0.5-4.5 Hz) and sigma activity (SA, 12.0-16.0 Hz) and can be used to assess the relation between SA, SWA, and IEDs during sleep.Methods: We performed six overnight continuous EEGpolysomnographic studies in three patients with LKS. The temporal series of SWA and SA were obtained from a spike-free derivation lead. The IEDs count was performed on the most active lead. Relations between sigma and SWA and time series of IEDs were tested by means of correlation techniques after data normalization. Results:Our results revealed a significantly higher correlation between IEDs and SA with respect to SWA in all the subjects, in total sleep time. The same analysis limited to NREM sleep highlights the better correlation between SA and IEDs.Conclusions: Our data suggest that neural mechanisms involved in the generation of sleep spindles facilitate IEDs production in LKS. Key Words: Landau-Kleffner syndromeSleep-Spindles-Slow-wave activity-Interictal epileptic discharges.The activating properties of nonrapid eye movement (NREM) sleep on interictal epileptiform discharges (IEDs) have been attributed to the synchronizing functions of thalamocortical oscillations active during this sleep state (1). During NREM sleep, there are three main EEG rhythms: spindles, delta waves, and slow oscillations. Due to the reduction of input coming from the brainstem reticular formation in light NREM sleep, membrane potential oscillations appear in the frequency range of spindles. Approaching deep sleep, paralleling the degree of hyperpolarization of thalamocortical cells, spindles oscillations are progressively replaced by slowfrequency oscillations in the delta range (2). The slow oscillations (< 1 Hz) are generated intracortically and synchronize, trigger, and group the spindle and delta oscillations (1,2).The application of spectral analysis to sleep EEG alAccepted July 2, 1999. Address correspondence and reprint requests to Dr. L. Nobili at Cattedra di Neurofisiopatologia, Ospedale S. Martino, Largo R. Benzi 10, 16132 Genova, Italy. E-mail: nblino@dism.unige.it lowed the description of the time course of sigma activity (SA,(12)(13)(14)(15)(16) Hz) and slow-wave activity (SWA, 0.5-4.5 Hz) whose dynamics reflects, respectively, the behavior of spindles and delta waves. Within NREM sleep and especially in the first part of the night, SA and SWA oscillate inversely while they show a parallel decline during REM sleep, in both adults and children (3)(4)(5).The activating properties of spindles, delta waves, and slow oscillations on spike and waves generation was identified by experimental observations...

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Treatment of electrical status epilepticus by short diazepam (DZP) cycles after DZP rectal bolus test

Cited by 87 publications

References 6 publications

Sequential Prefrontal Lobe Volume Changes in Epileptic Patients with Continuous Spikes and Waves During Slow Sleep

Sequential Prefrontal Lobe Volume Changes in Epileptic Patients with Continuous Spikes and Waves During Slow Sleep

Benzodiazepines Block α₂-Containing Inhibitory Glycine Receptors in Embryonic Mouse Hippocampal Neurons

Spindles‐Inducing Mechanism Modulates Sleep Activation of Interictal Epileptiform Discharges in the Landau—Kleffner Syndrome

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Treatment of electrical status epilepticus by short diazepam (DZP) cycles after DZP rectal bolus test

Cited by 87 publications

References 6 publications

Sequential Prefrontal Lobe Volume Changes in Epileptic Patients with Continuous Spikes and Waves During Slow Sleep

Sequential Prefrontal Lobe Volume Changes in Epileptic Patients with Continuous Spikes and Waves During Slow Sleep

Benzodiazepines Block α2-Containing Inhibitory Glycine Receptors in Embryonic Mouse Hippocampal Neurons

Spindles‐Inducing Mechanism Modulates Sleep Activation of Interictal Epileptiform Discharges in the Landau—Kleffner Syndrome

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Benzodiazepines Block α₂-Containing Inhibitory Glycine Receptors in Embryonic Mouse Hippocampal Neurons