Table 1.
Drug | Mechanism | Frequency effect | Sample | Study (year) |
---|---|---|---|---|
Ethosuximide | Calcium channels: blockade of low voltage-activated channel | – δ, + α | 6 patients | Rosadini and Sannita (1978) [22] |
Diphenylhydantoin | Sodium channels: blockade by stabilizing fast-inactivated state | Nothing | 5 patients | Rosadini and Sannita (1978) [22] |
Carbamazepine | Sodium channels: blockade by stabilizing fast-inactivated state | + δθ | 45 uncontrolled partial and generalized epilepsy patients | Wilkus et al. (1978) [26] |
+ General, + δθ, – α | 10 untreated patients | Besser et al. (1992) [42] | ||
Mild slowing | 15 healthy subjects | Meador et al. (1993) [43] | ||
+ δθ, slowing | 31 healthy, 6 patients | Salinsky et al. (1994) [39] | ||
– PF | 16 untreated children | Frost et al. (1995) [71] | ||
+ θ, – uα | 10 healthy, 10 patients | Wu and Xiao (1996) [38] | ||
+ δθ, – PF | 11 healthy | Salinsky et al. (2002) [37] | ||
+ δθ, – α | 20 difficult-to-treat partial epilepsy patients | Clemens et al. (2004) [41] | ||
+ θ, – PF | 41 untreated patients | Clemens et al. (2006) [40] | ||
+ θ, – α, + P3 latency | 60 healthy | Meador et al. (2016) [55] | ||
Phenytoin | Sodium channels: blockade by stabilizing fast-inactivated state | – δθ, + αβ | 12 healthy males | Fink et al. (1979) [85] |
+ δθ | 27 patients | Herkes et al. (1993) [44] | ||
Mild slowing | 15 healthy subjects | Meador et al. (1993) [43] | ||
– α | 7 healthy | Chung et al. (2002) [52] | ||
Clonazepam | Benzodiazepine; activation of GABAA receptor | + β | 21 children with epilepsy | Dumermuth et al. (1983) [67] |
+ Fast activity | 4 children with epilepsy | Wang and Wang (2002) [49] | ||
Milazemide | Increasing glycine concentrations | – δ, + α, + PF | 12 healthy | Saletu and Grünberger (1984) [34] |
Gabapentin | Calcium channels: blockade of high voltage activated channel | – General, + δθ, – α | 10 healthy | Saletu et al., (1986) [72] |
+ δθ, – PF | 12 healthy | Salinsky et al. (2002) [37] | ||
Valproate | Synaptic vesicle protein 2A actions | – General, – uαβγ | 10 untreated patients | Sannita et al. (1989) [35] |
+ Power of PF | 12 patients, 12 healthy | Wu and Ma (1993) [48] | ||
+ General, – uαβ | 12 patients | Sannita et al. (1993) [45] | ||
+ uα, – β | 10 untreated patients | Wu and Xiao (1997) [46] | ||
Nothing | 4 long-term treated children | Wang and Wang (2002) [49] | ||
– δθα | 42 untreated patients | Clemens et al. (2006) [40] | ||
Oxcarbazepine | Sodium channels: blockade by stabilizing fast-inactivated state | – PF | 9 untreated patients | Clemens et al. (2006) [40] |
Lamotrigine | Sodium channels: blockade by stabilizing fast-inactivated state | – δθαβ, +PF | 25 untreated patients | Clemens et al. (2006) [40] |
Lacosamide | Sodium channels: blockade by stabilizing slow-inactivated state | + θ, – α | 41 healthy | Meador et al. (2016) [55] |
Drugs are ordered by chronological order of pharmaco-electroencephalography research conducted with the respective drug
Frequency ranges are according to the definitions in the referenced articles
α alpha 8–12 Hz, β beta 13–30 Hz, γ gamma > 30 Hz, δ delta ≤ 4 Hz, θ theta 5–7 Hz, GABA γ-aminobutyric acid, general broadband, nothing no effects detected, PF peak frequency, uα upper α 10–13 Hz, + indicates increase in activity, – indicates decrease in activity