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Most primary epilepsies are thought to have a genetic basis and, as in many other idiopathic diseases such as diabetes and atherosclerosis, the mode of inheritance is complex, ie, polygenic That a genetic factor is operative in primary generalized tonic-clonic seizures is suggested by the nding of a familial incidence in 5 to 10 percent of such patients and, in particular families, the inheritance of a generalized seizure disorder through speci c chromosomal regions (Berkovic) The importance of genetic factors in the primary (idiopathic) epilepsies is also underscored by evidence from twin studies; in six major series, the overall concordance rate was 60 percent for monozygotic twins and 13 percent for dizygotic pairs In only a few of the idiopathic seizure disorders is a simple (mendelian) pattern of inheritance recognized These include a subgroup of benign neonatal familial convulsions inherited as an autosomal dominant trait (Leppert) and a similar disorder of infantile onset and a benign myoclonic epilepsy of childhood (autosomal recessive) Particularly informative are a special group of epileptic disorders in which monogenic genetic defects have been found to be related to ion channels or neurotransmitter receptors (Table 16-3) These were mentioned earlier in the discussion of the physiology of seizures and, despite their rarity, they suggest that idiopathic epilepsy may be due to a disruption in the function of these channels Functional studies suggest that the consequences of almost all of these mutations are to enhance overall neuronal excitability Examples include nocturnal frontal lobe epilepsy, which may present as a partial seizure (in which the offending mutations are in sub-
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units of the nicotinic acetylcholine receptor subunit); generalized epilepsy with febrile seizures (subunits of a neuronal sodium channel); benign familial neonatal convulsions (two different potassium channels); and forms of juvenile myoclonic epilepsy and childhood absence epilepsy (subunits of the brain GABAA receptor) These are summarized in Table 16-3 and their number will almost certainly expand in the next few years As with numerous other genetic neurologic disorders, a single mutation may produce different seizure types, and a single type may be the result of one of several different mutations This is particularly true in a group that has been termed generalized epilepsy with febrile seizures plus This denotes various combinations of uncomplicated febrile seizures, febrile seizures persisting beyond childhood, generalized, absence, myoclonic, atonic, and temporal lobe seizures Several of the mutations mentioned above, two in sodium channels and one in a GABA receptor subunit, produce this constellation, the manifestations of any one of these mutations varying between members of a single family Also notable is the low penetrance of some monogenic epileptic disorders, particularly the autosomal dominant one associated with nocturnal frontal seizures Another group of epilepsies with mendelian inheritance has been ascribed to genetic defects that do not implicate ion channels Most of these are primarily myoclonic disorders in which the epilepsy is symptomatic Thus, two forms of progressive myoclonic epilepsy, Unverricht-Lundborg disease and Lafora body disease, are the result respectively of mutations in genes encoding cystatin B and a protein, tyrosine phosphatase Other forms of myoclonic epilepsy are presumably related to primary defects that cause different forms of ceroid lipofuscinosis (see Chap 37) To these inherited forms of epilepsy may be added diseases such as tuberous sclerosis, which have a strong proclivity to cause seizures A more complex genetic element is also identi ed in several other classic childhood seizure disorders absence epilepsy with three-per-second spike-and-wave discharges and benign epilepsy of childhood with centrotemporal spikes both of which are transmitted as autosomal dominant traits with incomplete penetrance or perhaps in a more complicated manner In the partial, or focal, epilepsies (which is the form that seizures take in two-thirds of adults and almost half of the children with epilepsy), the role of heredity is not nearly so clear Yet in numerous studies there has been a greater-than-expected incidence of seizures, EEG abnormalities, or both among rst-degree relatives Among the familial cortical epilepsies, both a temporal and frontal lobe type are inherited in a polygenic fashion or in an autosomal dominant pattern Undoubtedly also inherited is the tendency to develop simple febrile convulsions, though the mode of inheritance is uncertain The genetics of the epileptic disorders has been reviewed in detail by Steinlein, Delgado-Escueta and colleagues, Hirose and associates, Malafosse and Moulard, and Anderson and Hauser, whose articles are recommended
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