Carbamazepine-Induced Drowsiness

A quantitative study of daytime sleepiness induced by carbamazepine and add-on vigabatrin in epileptic patients

“…MSLT score analysis by MDSL and DAST indicated a lack of correlation with some variables, namely CBZ daily doses and serum levels. This finding is consistent with some data, indicating a large interpatient variability to occur in daytime sleepiness, which seems to be largely independent on a direct dose effect of CBZ (8,25). However, the general lack of correlation between the MSLT scores and nocturnal sleep profiles observed in our cases is in favour of a direct effect of anticonvulsants, unrelated to nocturnal sleep quality.…”

Acute effect of carbamazepine on corticothalamic 5–9‐Hz and thalamocortical spindle (10–16‐Hz) oscillations in the rat

“…The present study demonstrates that CBZ is a sleep spindle‐promoting agent, and this property is probably responsible for provoking persistent somnolence and attention deficit, some of the drug's major side effects (Levy et al ., ). These findings raise a number of questions requiring further investigation.…”

“…Despite the effective use of CBZ in the treatment of focal seizures, the mechanisms underlying significant side effects of the drug, such as drowsiness and severe alteration of sleep architecture (Levy et al, 1985;Yang et al, 1989), remain unclear. Pharmacotherapies that induce drowsiness or sedation, whether as the primary therapeutic mechanism of action or as an adverse effect, commonly involve GABA A receptor-mediated neurotransmission.…”

“…CBZ is ineffective in the treatment of typical absence epilepsy, aggravating the seizures in some patients (Genton, 2000) and in animal models (Liu et al, 2006), and has even been reported to trigger the de novo generation of epileptic discharges in humans (Monji et al, 2004). Owing to the tricyclic structural features of CBZ, it is also has a broad spectrum of action, resulting in significant side effects, including drowsiness, weight gain, and seizure aggravation (Levy et al, 1985;Brady, 1989;Liu et al, 2006). Apart from its primary therapeutic mechanism of use-dependent Na + channel blockage, CBZ interacts directly with several molecular targets, including GABA A receptors (Granger et al, 1995;Liu et al, 2006), adenosine A1 receptors (Biber et al, 1999), and Ca 2+ currents (Walden et al, 1993).…”