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Epilepsy: A Neurological Cramp


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1 Columbia Institute of Pharmacy, Raipur, Chhattisgarh, India
     

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Epilepsy a neurological cramp is a diverse set of neurological disorders characterized by seizures, which results from abnormal, excessive hyper synchronous neuronal activity. Nearly 50 million people have epilepsy worldwide and its 90% probability occurs in developing countries. Epilepsy syndromes are not lifelong some forms are confined to particular stages of childhood. The clinical manifestation consists of a sudden and transitory abnormal phenomenon which may include alterations of consciousness, motor, sensory, autonomic or psychic events, perceived by the patient or an observer. Thus, epileptic seizures are a sign of cerebral dysfunction. Over the last decades, there has been considerable progress in the pharmacotherapy of epilepsy, including the introduction of several new antiepileptic drugs (AEDs) and improved formulations of older drugs and newer technologies of diagnosis, prevention and treatment. Searches for epileptic mechanisms are based upon clinical approaches, and the need to know where the epileptic foci are localized. Such localization depends on both EEG and medical imageries. The latter are based upon various mechanisms, and the uptake of glucose analogs represents one of them. In future better understanding of basic mechanisms which leading to epilepsy, thus allowing to create therapies aimed at the prevention of epilepsy in patients at risk; improved understanding of pharmacoresistance mechanism, allowing to develop drugs for reversal or prevention of resistance; and development of diseasemodifying therapies, inhibiting the progression of epilepsy.

Keywords

Neuronal Activity, Epileptogenesis, Seizures, Ionic Pump, Neurotransmitters
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  • Commission on epidemiology and prognosis, International League against Epilepsy. Guidelines on epidemiology and prognosis, International League against Epilepsy. Epilepsia 1993; 34,592-596.

  • Helen E. Scharfman, The Neurobiology of Epilepsy; Curr Neurol Neurosci Rep. 2007 July 7(4),348–354

  • Schwartz RD. The GABAA receptor-gated ion channel: biochemical and pharmacological studies of structure and function. Biochem Pharmacol 1988; 37:33 69–75.

  • Everitt, A.D.; Sander, J.W. Classification of the epilepsies: time for a change A critical review of the International Classification of the Epilepsies and Epileptic Syndromes (ICEES) and its usefulness in clinical practice and epidemiological studies of epilepsy. Eur. Neurol., 1999, 42, 1-10.

  • Dreifuss, F.E. Classification of the epilepsies: influence on management. Rev. Neurol. (Paris), 1987, 143, 375-380.

  • Gastaut H. (1973) Dictionary of epilepsy. Part 1. Definitions. World Health Organization, Geneva, p. 72.

  • Hauser WA. (1990) Status epilepticus: epidemiologic considerations. Neurology 40,9–13

  • Epilepsy Foundation of America’s Working Group on Status Epilepticus. (1993) Treatment of convulsive status epilepticus. Recommendations of the Epilepsy Foundation of America’s Working Group on Status Epilepticus. JAMA 1993; 270,854– 859.

  • DeLorenzo RJ, Pellock JM, Towne AR, Boggs JG. (1995) Epidemiology of status epilepticus. J Clin Neurophysiol 12:316–325.

  • Hesdorffer DC, Logroscino G, Cascino G, Annegers JF, Hauser WA. (1998) Incidence of status epilepticus in Rochester, Minnesota, 1965-1984. Neurology 50,735–741.

  • Coeytaux A, Jallon P, Galobardes B, Morabia A. (2000) Incidence of status epilepticus in French-speaking Switzerland: (EPISTAR). Neurology 55,693–697.

  • Alldredge BK, Gelb AM, Isaacs SM. (2001) A comparison of lorazepam, diazepam, and placebo for the treatment of out-ofhospital status epilepticus. New Eng J Med 345,631–637

  • Hille B. 2001. Ion channels of excitable membranes. Sunderland (MA): Sinauer

  • Somjen GG. 2002. Ion regulation in the brain: implications for pathophysiology. Neuroscientist 8(3), 254–67.

  • Vaillend C, Mason SE, Cuttle MF, Alger BE. Mechanisms of neuronal hyperexcitability caused by partial inhibition of Na+- K+-ATPases in the rat CA1 hippocampal region. J Neurophysiol 2002; 88, 2963–2978. [PubMed: 12466422]

  • Grisar T, Guillaume D, Delgado-Escueta AV. Contribution of Na+, K(+)-ATPase to focal epilepsy: a brief review. Epilepsy Res 1992; 12 141–149. [PubMed: 1327744]

  • Haglund MM, Stahl WL, Kunkel DD, Schwartzkroin PA. Developmental and regional differences in the localization of Na, K-ATPase activity in the rabbit hippocampus. Brain Res 1985; 343 198– 203. [PubMed: 2994829]

  • Fukuda A, Prince DA. Postnatal development of electrogenic sodium pumps activity in rat hippocampal pyramidal neurons. Brain Res 1992; 65, 101–114.

  • Scharfman, H.E. The neurobiology of epilepsy. Curr. Neurol. Neurosci. Rep., 2007, 7, 348-354.

  • Vezzani, A.; Ravizza, T.; Balosso, S.; Aronica, E. Glia as a source of cytokines: implications for neuronal excitability and survival. Epilepsia, 2008, 49(Suppl 2), 24-32.

  • Ballabh, P.; Braun, A.; Nedergaard, M. The blood-brain barrier: an overview: structure, regulation, and clinical implications. Neurobiol. Dis., 2004, 16, 1-13.

  • Ueno, M. Molecular anatomy of the brain endothelial barrier: an overview of the distributional features. Curr. Med. Chem., 2007, 14, 1199-1206.

  • Ihrie, R.A.; Alvarez-Buylla, A. Cells in the astroglial lineage are neural stem cells. Cell Tissue Res., 2008, 331, 179-191.

  • Gritti, A.; Bonfanti, L. Neuronal-glial interactions in central nervous system neurogenesis: the neural stem cell perspective. Neuron Glia Biol., 2007, 3, 309-323.

  • Jordan, J.D.; Ma, D.K.; Ming, G.L.; Song, H. Cellular niches for endogenous neural stem cells in the adult brain. CNS Neurol. Disord. Drug Targets, 2007, 6, 336-341.

  • Wang, D.D.; Bordey, A. The astrocyte odyssey. Prog. Neurobiol., 2008,

  • Nagler, K.; Mauch, D.H.; Pfrieger, F.W. Glia-derived signals induce synapse formation in neurones of the rat central nervous system. J. Physiol., 2001, 533, 665-679.

  • Pfrieger, F.W.; Barres, B.A. Synaptic efficacy enhanced by glial cells in vitro. Science, 1997, 277, 1684-1687.

  • Pfrieger, F.W. Role of glia in synapse development. Curr. Opin. Neurobiol., 2002, 12, 486-490.

  • Nagler, K.; Mauch, D.H.; Pfrieger, F.W. Glia-derived signals induce synapse formation in neurones of the rat central nervous system. J. Physiol., 2001, 533, 665-679.

  • He, F.; Sun, Y.E. Glial cells more than support cells? Int. J. Biochem. Cell Biol., 2007, 39, 661-665.

  • Ullian, E.M.; Christopherson, K.S.; Barres, B.A. Role for glia in synaptogenesis. Glia, 2004, 47, 209-216.

  • Slezak, M.; Pfrieger, F.W. New roles for astrocytes: regulation of CNS synaptogenesis. Trends Neurosci, 2003, 26, 531-535.

  • Nadkarni, S.; Jung, P.; Levine, H. Astrocytes optimize the synaptic transmission of information. PLoS Comput. Biol., 2008, 4, e1000088.

  • Nadkarni, S.; Jung, P. Modeling synaptic transmission of the tripartite synapse. Phys. Biol., 2007, 4, 1-9.

  • Tritsch, N.X.; Bergles, D.E. Defining the role of astrocytes in neuromodulation. Neuron, 2007, 54, 497-500.

  • Montana, V.; Malarkey, E.B.; Verderio, C.; Matteoli, M.; Parpura, V. Vesicular transmitter release from astrocytes. Glia, 2006, 54, 700-715.

  • Chen, X.K.; Xiong, Y.F.; Zhou, Z. "Kiss-and-run" exocytosis in astrocytes. Neuroscientist, 2006, 12, 375-378.

  • Haydon, P.G.; Carmignoto, G. Astrocyte control of synaptic transmission and neurovascular coupling. Physiol. Rev., 2006, 86, 1009-1031.

  • Nadkarni, S.; Jung, P. Spontaneous oscillations of dressed neurons: a new mechanism for epilepsy? Phys. Rev. Lett., 2003, 91, 268101.

  • Halassa, M.M.; Fellin, T.; Haydon, P.G. The tripartite synapse: roles for gliotransmission in health and disease. Trends Mol. Med., 2007, 13, 54-63.

  • Halassa, M.M.; Fellin, T.; Takano, H.; Dong, J.H.; Haydon, P.G. Synaptic islands defined by the territory of a single astrocyte. J. Neurosci., 2007, 27, 6473-6477.

  • Macdonald RL, In: Engel J & Pedley TA eds. Epilepsy: A comprehensive textbook. Philadelphia: Lippincott-Raven Publishers, 1997; 265-275.

  • Podell M, Hadjiconstantinou M. Cerebrospinal fluid gammaaminobutyric acid and glutamate values in dogs with epilepsy. Am J Vet Res 1997; 58 451-456.

  • Herzog AG. Reproductive endocrine considerations and hormonal therapy for women with epilepsy. Epilepsia 1991; 32 (suppl.6):S27-S33.

  • Hopkins A. Epilepsy, mestruation, oral contraception and pregnancy. In: Hopkins A, Shorvon S, Cascino G eds. Epilepsy. London: Chapman & Hall 1995; 521-533.

  • Gastaut H. (1973) Dictionary of epilepsy. Part 1. Definitions. World Health Organization, Geneva, p. 72.

  • Shin M, Brager D, Jaramillo TC, Johnston D, Chetkovich DM. Mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsy. Neurobiol Dis 2008; 32, 26–36.

  • Noctor, S.C.; Flint, A.C.; Weissman, T.A.; Dammerman, R.S.; Kriegstein, A.R. Neurons derived from radial glial cells establish radial units in neocortex. Nature, 2001, 409, 714-720.

  • Uhlhaas, P.J.; Singer, W. Neural synchrony in brain disorders: relevance for cognitive dysfunctions and pathophysiology. Neuron, 2006, 52, 155-168.

  • Haglund MM, Stahl WL, Kunkel DD, Schwartzkroin PA. Developmental and regional differences in the localization of Na, K-ATPase activity in the rabbit hippocampus. Brain Res 1985; 343, 198– 203. [PubMed: 2994829]

  • Commission on Classification and Terminology of the International League Against Epilepsy. (1989) Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia 1989; 30 389– 399.

  • .Lai HC, Jan LY. The distribution and targeting of neuronal voltage-gated ion channels. Nat Rev Neurosci 2006; 7, 548– 562.

  • David P.D. Woldbye; antiepileptic effects of NPY on pentylenetetrazole seizures; Regulatory Peptides; 75-76 (1998) 279-282.

  • M. Maitre, L. Ciesielski, A. Lehmann, E. Kempf, P. Mandel, Protective effect of adenosine and nicotinamide against audiogenic seizures, Biochem. Pharmacol.23_1974.2807–2816.

  • Cobb SR, Buhl EH, Halasy K, Paulsen O, Somogyi P, et al. Synchronization of neuronal activity in hippocampus by individual GABAergic interneurons. Nature1996; 378, 75– 78.[PubMed:7477292]

  • T.V. Dunwiddie, T. Worth, Sedative and anticonvulsant effects of adenosine analogs in mouse and rat, J. Pharmacol. Exp. Ther. 220, 1982. 70–76.

  • Rampp, S.; Stefan, H. Fast activity as a surrogate marker of epileptic network function, Clin. Neurophysiol., 2006, 117, 2111-2117.

  • Browne, T.R., Holmes, G.L., 2001. Epilepsy New Engl. J. Med. 344, 1145–11451.

  • Dyhrfjeld-Johnsen J, Morgan RJ, Soltesz I. Double trouble? Potential for hyperexcitability following both channelopathic upand downregulation of Ih in epilepsy.Front Neurosci 2009; 3 25–33.

  • Parsons JT, Churn SB, Kochan LD, De-Lorenzo RJ, Pilocarpineinduced status epilepticus causes N-metyl-Daspartate receptor-dependent inhibition of microsomal Mg2+/Ca2+ ATPase mediated Ca2+ uptake, J Neurochem, 2000; 74 1209–18.

  • Sierra-Paredes G, Sierra-Marcuño G, Ascomycin and FK 506: Pharmacology and therapeutic potential as anticonvulsants and neuroprotectants, CNS: Neuroscience & Therapeutics, 2008; 14 36–46.

  • Sohl G., Guldenagel M., Beck H., Teubner B., Traub O., Gutierrez R., Heinemann U. and Willecke K. (2000). Expression of connexin genes in hippocampus of kainate-treated and kindled rats under conditions of experimental epilepsy. Brain Res. Mol. Brain Res. 83, 44-51.

  • Condorelli D.F., Mudo G., Trovato-Salinaro A., Mirone M.B., Amato G. and Belluardo N. (2002). Connexin-30 mRNA is upregulated in astrocytes and expressed in apoptotic neuronal cells of rat brain following kainate-induced seizures. Mol. Cell. Neurosci. 21, 94-113.

  • Condorelli D.F., Trovato-Salinaro A., Mudo G., Mirone M.B. and Belluardo N. (2003). Cellular expression of connexins in the rat brain: neuronal localization, effects of kainate-induced seizures and expression in apoptotic neuronal cells. Eur. J. Neurosci. 18, 1807- 1827.

  • Vizi ES, Mike A, Nonsynaptic receptors for GABA and glutamate, Curr Top Med Chem, 2006; 6, 941-8.

  • Vizi ES, Kiss JP, Lendvai B, Nonsynaptic communication in the central nervous system, Neurochem Int, 2004; 45,443-51.

  • Nusser Z, Mody I, Selective modulation of tonic and phasic inhibitions in dentate gyrus granule cells, J Neurophysiol, 2002; 87, 2624–8.

  • Nateri AS, Raivich G, Gebhardt C, et al., ERK activation causes epilepsy by stimulating NMDA receptor activity, EMBO J, 2007; 26, 4891–4901.

  • Namiki K, Nakamura A, Furuya M, et al., Involvement of p38alplha in Kainate-Induced Seizure and Neuronal Cell Damage, J Recept Signal Transduct Res, 2007; 27, 99–111.

  • Merlo D, Cifelli P, Cicconi S, et al., 4-Aminopyridine-induced epileptogenesis depends on activation of mitogen-activated protein kinase ERK, J Neurochem, 2004; 89, 654–9.

  • Jiang W, Van Cleemput J, Sheerin AH, et al., Involvement of Extracellular Regulated Kinase and p38 Kinase in Hippocampal Seizure Tolerance, J Neurosci Res, 2005; 81, 581–8.

  • Sierra-Paredes G, Vázquez-López A, Oreiro-García MT, et al., Neurochemistry of epileptic seizures: the role of f-actin, intercellular glutamate and glutamate ionotropic receptors location. In: KJ Hollaway (ed.), New Research on Epilepsy and Behavior, New York: Nova Biomedical, 2007; 57–93.

  • Matsumoto R, Ajmone-Marsan C. Cortical cellular phenomena in experimental epilepsy: ictal manifestations. Exp Neurol 1964; 80, 305–326. [PubMed: 14142796]

  • Brown TH, Johnston D. The synaptic nature of the paroxysmal depolarization shift in hippocampal neurons. Ann Neurol 1984; 16 S65–S71. [PubMed: 6095744]


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  • Epilepsy: A Neurological Cramp

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Authors

Parag Jain
Columbia Institute of Pharmacy, Raipur, Chhattisgarh, India
Anand Surana
Columbia Institute of Pharmacy, Raipur, Chhattisgarh, India
Ravindra Pandey
Columbia Institute of Pharmacy, Raipur, Chhattisgarh, India

Abstract


Epilepsy a neurological cramp is a diverse set of neurological disorders characterized by seizures, which results from abnormal, excessive hyper synchronous neuronal activity. Nearly 50 million people have epilepsy worldwide and its 90% probability occurs in developing countries. Epilepsy syndromes are not lifelong some forms are confined to particular stages of childhood. The clinical manifestation consists of a sudden and transitory abnormal phenomenon which may include alterations of consciousness, motor, sensory, autonomic or psychic events, perceived by the patient or an observer. Thus, epileptic seizures are a sign of cerebral dysfunction. Over the last decades, there has been considerable progress in the pharmacotherapy of epilepsy, including the introduction of several new antiepileptic drugs (AEDs) and improved formulations of older drugs and newer technologies of diagnosis, prevention and treatment. Searches for epileptic mechanisms are based upon clinical approaches, and the need to know where the epileptic foci are localized. Such localization depends on both EEG and medical imageries. The latter are based upon various mechanisms, and the uptake of glucose analogs represents one of them. In future better understanding of basic mechanisms which leading to epilepsy, thus allowing to create therapies aimed at the prevention of epilepsy in patients at risk; improved understanding of pharmacoresistance mechanism, allowing to develop drugs for reversal or prevention of resistance; and development of diseasemodifying therapies, inhibiting the progression of epilepsy.

Keywords


Neuronal Activity, Epileptogenesis, Seizures, Ionic Pump, Neurotransmitters

References