Epilepsia
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Historical Article
The Institute of Epileptology of King's College, University of London.
The Institute of Epileptology of King's College, London has arisen from need and from opportunity. The need is due to the relative neglect nationally and internationally of the most common serious brain disorder with important physical, psychological, and social complications. The relative neglect is reflected in services, research, charitable donations, public profile, and stigma and in a serious lack of professional education. ⋯ Piers Lingfield, The Institute of Psychiatry, King's College School of Medicine and Dentistry, and the School of Life, Basic Medical and Health Sciences, all under the umbrella of King's College, University of London. Further stimulus and help came from a group of dedicated supporters in private and public life. There are three strands to this initiative: (a) a charity, The Fund for Epilepsy; (b) the clinical Centre for Epilepsy, which was formally opened at the Maudsley Hospital in July 1994; and (c) the academic Institute of Epileptology for research and teaching, which was launched on November 15, 1994.
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Established antiepileptic drugs (AEDs) decrease membrane excitability by interacting with neurotransmitter receptors or ion channels. AEDs developed before 1980 appear to act on sodium channels, gamma-aminobutyric acid type A (GABAA) receptors, or calcium channels. Benzodiazepines and barbiturates enhance GABAA receptor-mediated inhibition. ⋯ The mechanism of action of oxcarbazepine (OCBZ) is not known; however, its similarity in structure and clinical efficacy to CBZ suggests that its mechanism of action may involve inhibition of sustained high-frequency repetitive firing of voltage-dependent sodium action potentials. Vigabatrin (VGB) irreversibly inhibits GABA transaminase, the enzyme that degrades GABA, thereby producing greater available pools of presynaptic GABA for release in central synapses. Increased activity of GABA at postsynaptic receptors may underline the clinical efficacy of VGB.