Abstract
In 1951 — in the early days of clinical electroencephalography — Lennox [21] showed in family and twin studies that the risk for manifesting spikes and waves (SW) is, in part, genetic. In identical twins, he found a concordance rate of 84%, as opposed to 0% in dizygotic twins [22]. Since then, SW have been considered a specific, prototypical marker of the genetic liability to manifest seizures. Familial incidence and distribution of SW are used as one basis for genetic modelling in this context. For the most part, efforts to develop explanatory genetic models have started from the assumption that SW were a genetically simple, homogeneous bioelectric phenomenon. This assumption then led to the concept of a homogeneous centrencephalic trait. Later findings, however, disproved this concept: SW during rest and hyperventilation on the one hand and SW elicited by photic stimulation on the other hand could be differentiated genetically [8, 30]. Furthermore, there are a number of arguments supporting the complex and heterogeneous nature of spontaneous — not photically evoked — SW. Meanwhile, this alternative to initial simple assumptions can be supported.
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Doose, H., Baier, W.K. (1989). Generalized Spikes and Waves. In: Beck-Mannagetta, G., Anderson, V.E., Doose, H., Janz, D. (eds) Genetics of the Epilepsies. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-95553-2_13
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