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  1. Article: Super-Refractory Status Epilepticus: Prognosis and Recent Advances in Management.

    Kirmani, Batool F / Au, Katherine / Ayari, Lena / John, Marita / Shetty, Padmashri / Delorenzo, Robert J

    Aging and disease

    2021  Volume 12, Issue 4, Page(s) 1097–1119

    Abstract: Super-refractory status epilepticus (SRSE) is a life-threatening neurological emergency with high morbidity and mortality. It is defined as "status epilepticus (SE) that continues or recurs 24 hours or more after the onset of anesthesia, including those ... ...

    Abstract Super-refractory status epilepticus (SRSE) is a life-threatening neurological emergency with high morbidity and mortality. It is defined as "status epilepticus (SE) that continues or recurs 24 hours or more after the onset of anesthesia, including those cases in which SE recurs on the reduction or withdrawal of anesthesia." This condition is resistant to normal protocols used in the treatment of status epilepticus and exposes patients to increased risks of neuronal death, neuronal injury, and disruption of neuronal networks if not treated in a timely manner. It is mainly seen in patients with severe acute onset brain injury or presentation of new-onset refractory status epilepticus (NORSE). The mortality, neurological deficits, and functional impairments are significant depending on the duration of status epilepticus and the resultant brain damage. Research is underway to find the cure for this devastating neurological condition. In this review, we will discuss the wide range of therapies used in the management of SRSE, provide suggestions regarding its treatment, and comment on future directions. The therapies evaluated include traditional and alternative anesthetic agents with antiepileptic agents. The other emerging therapies include hypothermia, steroids, immunosuppressive agents, electrical and magnetic stimulation therapies, emergent respective epilepsy surgery, the ketogenic diet, pyridoxine infusion, cerebrospinal fluid drainage, and magnesium infusion. To date, there is a lack of robust published data regarding the safety and effectiveness of various therapies, and there continues to be a need for large randomized multicenter trials comparing newer therapies to treat this refractory condition.
    Language English
    Publishing date 2021-07-01
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2152-5250
    ISSN 2152-5250
    DOI 10.14336/AD.2021.0302
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Mechanisms of levetiracetam in the control of status epilepticus and epilepsy.

    Deshpande, Laxmikant S / Delorenzo, Robert J

    Frontiers in neurology

    2014  Volume 5, Page(s) 11

    Abstract: Status epilepticus (SE) is a major clinical emergency that is associated with high mortality and morbidity. SE causes significant neuronal injury and survivors are at a greater risk of developing acquired epilepsy and other neurological morbidities, ... ...

    Abstract Status epilepticus (SE) is a major clinical emergency that is associated with high mortality and morbidity. SE causes significant neuronal injury and survivors are at a greater risk of developing acquired epilepsy and other neurological morbidities, including depression and cognitive deficits. Benzodiazepines and some anticonvulsant agents are drugs of choice for initial SE management. Despite their effectiveness, over 40% of SE cases are refractory to the initial treatment with two or more medications. Thus, there is an unmet need of developing newer anti-SE drugs. Levetiracetam (LEV) is a widely prescribed anti-epileptic drug that has been reported to be used in SE cases, especially in benzodiazepine-resistant SE or where phenytoin cannot be used due to allergic side-effects. Levetiracetam's non-classical anti-epileptic mechanisms of action, favorable pharmacokinetic profile, general lack of central depressant effects, and lower incidence of drug interactions contribute to its use in SE management. This review will focus on LEV's unique mechanism of action that makes it a viable candidate for SE treatment.
    Language English
    Publishing date 2014-01-31
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564214-5
    ISSN 1664-2295
    ISSN 1664-2295
    DOI 10.3389/fneur.2014.00011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: An organotypic hippocampal slice culture model of excitotoxic injury induced spontaneous recurrent epileptiform discharges.

    Ziobro, Julie M / Deshpande, Laxmikant S / Delorenzo, Robert J

    Brain research

    2010  Volume 1371, Page(s) 110–120

    Abstract: Stroke is the major cause of acquired epilepsy in the adult population. The mechanisms of ischemia-induced epileptogenesis are not completely understood, but glutamate is associated with both ischemia-induced injury and epileptogenesis. The objective of ... ...

    Abstract Stroke is the major cause of acquired epilepsy in the adult population. The mechanisms of ischemia-induced epileptogenesis are not completely understood, but glutamate is associated with both ischemia-induced injury and epileptogenesis. The objective of this study was to develop an in vitro model of epileptogenesis induced by glutamate injury in organotypic hippocampal slice cultures (OHSCs), as observed in stroke-induced acquired epilepsy. OHSCs were prepared from 1-week-old Sprague-Dawley rat pups. They were exposed to 3.5 mM glutamate for 35 minutes at 21 days in vitro. Field potential recordings and whole-cell current clamp electrophysiology were used to monitor the development of in vitro seizure events up to 19 days after injury. Propidium iodide uptake assays were used to examine acute cell death following injury. Glutamate exposure produced a subset of hippocampal neurons that died acutely and a larger population of injured but surviving neurons. These surviving neurons manifested spontaneous, recurrent epileptiform discharges in neural networks, characterized by paroxysmal depolarizing shifts and high frequency spiking in both field potential and intracellular recordings. This model also exhibited anticonvulsant sensitivity similar to in vivo models. Our study is the first demonstration of a chronic model of acquired epilepsy in OHSCs following a glutamate injury. This in vitro model of glutamate injury-induced epileptogenesis may help develop therapeutic strategies to prevent epileptogenesis after stroke and elucidate some of the mechanisms that underlie stroke-induced epilepsy in a more anatomically intact system.
    MeSH term(s) Action Potentials/drug effects ; Animals ; Anticonvulsants/pharmacology ; Cell Survival ; Epilepsy/etiology ; Epilepsy/physiopathology ; Ethosuximide/pharmacology ; Glutamic Acid/toxicity ; Hippocampus/drug effects ; Hippocampus/physiopathology ; Nerve Net/drug effects ; Nerve Net/physiology ; Neurons/drug effects ; Neurons/physiology ; Neurotoxins/toxicity ; Organ Culture Techniques/methods ; Patch-Clamp Techniques ; Phenobarbital/pharmacology ; Phenytoin/pharmacology ; Rats ; Rats, Sprague-Dawley ; Stroke/complications
    Chemical Substances Anticonvulsants ; Neurotoxins ; Glutamic Acid (3KX376GY7L) ; Ethosuximide (5SEH9X1D1D) ; Phenytoin (6158TKW0C5) ; Phenobarbital (YQE403BP4D)
    Language English
    Publishing date 2010-11-25
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1200-2
    ISSN 1872-6240 ; 0006-8993
    ISSN (online) 1872-6240
    ISSN 0006-8993
    DOI 10.1016/j.brainres.2010.11.065
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 161: Show issues Location:
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  4. Article: Epileptogenesis causes an N-methyl-d-aspartate receptor/Ca2+-dependent decrease in Ca2+/calmodulin-dependent protein kinase II activity in a hippocampal neuronal culture model of spontaneous recurrent epileptiform discharges.

    Blair, Robert E / Sombati, Sompong / Churn, Severn B / Delorenzo, Robert J

    European journal of pharmacology

    2008  Volume 588, Issue 1, Page(s) 64–71

    Abstract: Alterations in the function of Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) have been observed in both in vivo and in vitro models of epileptogenesis; however the molecular mechanism mediating the effects of epileptogenesis on CaM kinase ... ...

    Abstract Alterations in the function of Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) have been observed in both in vivo and in vitro models of epileptogenesis; however the molecular mechanism mediating the effects of epileptogenesis on CaM kinase II has not been elucidated. This study was initiated to evaluate the molecular pathways involved in causing the long-lasting decrease in CaM kinase II activity in the hippocampal neuronal culture model of low Mg2+-induced spontaneous recurrent epileptiform discharges (SREDs). We show here that the decrease in CaM kinase II activity associated with SREDs in hippocampal cultures involves a Ca2+/N-methyl-d-aspartate (NMDA) receptor-dependent mechanism. Low Mg2+-induced SREDs result in a significant decrease in Ca2+/calmodulin-dependent substrate phosphorylation of the synthetic peptide autocamtide-2. Reduction of extracellular Ca2+ levels (0.2 mM in treatment solution) or the addition of dl-2-amino-5-phosphonovaleric acid (APV) 25 microM blocked the low Mg2+-induced decrease in CaM kinase II-dependent substrate phosphorylation. Antagonists of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainic acid receptor or L-type voltage sensitive Ca2+ channel had no effect on the low Mg2+-induced decrease in CaM kinase II-dependent substrate phosphorylation. The results of this study demonstrate that the decrease in CaM kinase II activity associated with this model of epileptogenesis involves a selective Ca2+/NMDA receptor-dependent mechanism and may contribute to the production and maintenance of SREDs in this model.
    MeSH term(s) Animals ; Calcium/physiology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Cells, Cultured ; Cellulose/analogs & derivatives ; Electrophysiology ; Enzyme Inhibitors/pharmacology ; Epilepsy/chemically induced ; Epilepsy/physiopathology ; Hippocampus/cytology ; Hippocampus/drug effects ; Hippocampus/enzymology ; Immunohistochemistry ; Magnesium Deficiency/physiopathology ; Neurons/drug effects ; Neurons/enzymology ; Okadaic Acid/pharmacology ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/drug effects ; Recurrence ; Status Epilepticus/physiopathology
    Chemical Substances Enzyme Inhibitors ; Receptors, N-Methyl-D-Aspartate ; Okadaic Acid (1W21G5Q4N2) ; Cellulose (9004-34-6) ; phosphocellulose (9015-14-9) ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2008-04-12
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80121-5
    ISSN 1879-0712 ; 0014-2999
    ISSN (online) 1879-0712
    ISSN 0014-2999
    DOI 10.1016/j.ejphar.2008.04.021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 522: Show issues Location:
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  5. Article: Cellular mechanisms underlying acquired epilepsy: the calcium hypothesis of the induction and maintainance of epilepsy.

    Delorenzo, Robert J / Sun, David A / Deshpande, Laxmikant S

    Pharmacology & therapeutics

    2004  Volume 105, Issue 3, Page(s) 229–266

    Abstract: Epilepsy is one of the most common neurological disorders. Although epilepsy can be idiopathic, it is estimated that up to 50% of all epilepsy cases are initiated by neurological insults and are called acquired epilepsy (AE). AE develops in 3 phases: (1) ...

    Abstract Epilepsy is one of the most common neurological disorders. Although epilepsy can be idiopathic, it is estimated that up to 50% of all epilepsy cases are initiated by neurological insults and are called acquired epilepsy (AE). AE develops in 3 phases: (1) the injury (central nervous system [CNS] insult), (2) epileptogenesis (latency), and (3) the chronic epileptic (spontaneous recurrent seizure) phases. Status epilepticus (SE), stroke, and traumatic brain injury (TBI) are 3 major examples of common brain injuries that can lead to the development of AE. It is especially important to understand the molecular mechanisms that cause AE because it may lead to innovative strategies to prevent or cure this common condition. Recent studies have offered new insights into the cause of AE and indicate that injury-induced alterations in intracellular calcium concentration levels [Ca(2+)](i) and calcium homeostatic mechanisms play a role in the development and maintenance of AE. The injuries that cause AE are different, but they share a common molecular mechanism for producing brain damage-an increase in extracellular glutamate concentration that causes increased intracellular neuronal calcium, leading to neuronal injury and/or death. Neurons that survive the injury induced by glutamate and are exposed to increased [Ca(2+)](i) are the cellular substrates to develop epilepsy because dead cells do not seize. The neurons that survive injury sustain permanent long-term plasticity changes in [Ca(2+)](i) and calcium homeostatic mechanisms that are permanent and are a prominent feature of the epileptic phenotype. In the last several years, evidence has accumulated indicating that the prolonged alteration in neuronal calcium dynamics plays an important role in the induction and maintenance of the prolonged neuroplasticity changes underlying the epileptic phenotype. Understanding the role of calcium as a second messenger in the induction and maintenance of epilepsy may provide novel insights into therapeutic advances that will prevent and even cure AE.
    MeSH term(s) Animals ; Brain Injuries/classification ; Brain Injuries/complications ; Calcium/metabolism ; Calcium/physiology ; Electroencephalography ; Epilepsy/drug therapy ; Epilepsy/etiology ; Epilepsy/metabolism ; Homeostasis/physiology ; Humans
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2004-12-09
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S. ; Review
    ZDB-ID 194735-7
    ISSN 1879-016X ; 0163-7258
    ISSN (online) 1879-016X
    ISSN 0163-7258
    DOI 10.1016/j.pharmthera.2004.10.004
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    Zs.A 1183: Show issues Location:
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  6. Article: Calcium/calmodulin-dependent kinase II phosphorylation of the GABAA receptor alpha1 subunit modulates benzodiazepine binding.

    Churn, Severn B / Rana, Aniruddha / Lee, Kangmin / Parsons, J Travis / De Blas, Angel / Delorenzo, Robert J

    Journal of neurochemistry

    2002  Volume 82, Issue 5, Page(s) 1065–1076

    Abstract: gamma-Aminobutyric acid (GABA) is the primary neurotransmitter that is responsible for the fast inhibitory synaptic transmission in the central nervous system. A major post-translational mechanism that can rapidly regulate GABAAR function is receptor ... ...

    Abstract gamma-Aminobutyric acid (GABA) is the primary neurotransmitter that is responsible for the fast inhibitory synaptic transmission in the central nervous system. A major post-translational mechanism that can rapidly regulate GABAAR function is receptor phosphorylation. This study was designed to test the effect of endogenous calcium and calmodulin-dependent kinase II (CaM kinase II) activation on both allosteric modulator binding and GABAA receptor subunit phosphorylation. Endogenous CaM kinase II activity was stimulated, and GABAA receptors were subsequently analyzed for bothallosteric modulator binding properties and immunoprecipitated and analyzed for subunit phosphorylation levels. A significant increase in allosteric-modulator binding of the GABAAR was observed under conditions maximal for CaM kinase II activation. In addition, CaM kinase II activation resulted in a direct increase in phosphorylation of the GABAA receptor alpha1 subunit. The data suggest that the CaM kinase II-dependent phosphorylation of the GABAA receptor alpha1 subunit modulated allosteric modulator binding to the GABAA receptor.
    MeSH term(s) Allosteric Regulation/physiology ; Animals ; Benzodiazepines/metabolism ; Benzodiazepines/pharmacokinetics ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/chemistry ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Detergents/chemistry ; Electrophoresis, Gel, Two-Dimensional ; Enzyme Activation/physiology ; Male ; Phosphates/metabolism ; Phosphorylation ; Precipitin Tests ; Prosencephalon/chemistry ; Protein Binding/physiology ; Protein Subunits ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA-A/chemistry ; Receptors, GABA-A/metabolism ; Synaptosomes/chemistry ; Synaptosomes/enzymology
    Chemical Substances Detergents ; Phosphates ; Protein Subunits ; Receptors, GABA-A ; Benzodiazepines (12794-10-4) ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17) ; Calcium-Calmodulin-Dependent Protein Kinases (EC 2.7.11.17)
    Language English
    Publishing date 2002-08-23
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 80158-6
    ISSN 1471-4159 ; 0022-3042 ; 1474-1644
    ISSN (online) 1471-4159
    ISSN 0022-3042 ; 1474-1644
    DOI 10.1046/j.1471-4159.2002.01032.x
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    Ui II Zs.170: Show issues Location:
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