Anticonvulsant; Mood stabiliser.
Mechanism of action still not fully understood.
Binds to voltage-dependent sodium channels and lowers the nerve response and high frequency repetitive firing of neurons. Decrease of action potential in the nucleus ventralis thalami and inhibition of the lingual mandibular reflex were also observed.
Mood stabilising effect is caused probably by increased GABA transmission and dopamine turnover.
Onset of action:
Half-life of elimination: 36 hours, shortens to 12 hours over time
Metabolism: Hepatic
Elimination: Kidneys (72 %), faeces (28 %)
Oral suspension should be shaken before use.
Tablets – 100 mg, 200 mg, 400 mg
Oral suspension – 100 mg/5 ml
CNS: dizziness, blurred vision, muscle twitch, unconsciousness, respiratory arrest
CVS: decreased cardiac output, heart block, hypotension, bradycardia, ventricular arrhythmias, cardiac arrest
Nystagmus, diplopia
Ataxia
Benign leukopenia
Skin rash
Stevens-Johnson syndrome
Hyponatraemia
Hepatic dysfunction
References