Lacosamide

Lacomax is indicated for the treatment of partial-onset seizures in patients 1 month of age and older.
Lacomax is indicated for adjunctive therapy in the treatment of primary generalized tonic-clonic seizures in patients 4 years of age and older.

Recommended Dosages for Partial-Onset Seizures (Monotherapy or Adjunctive Therapy) in Patients 1 Month and Older, and for Primary Generalized Tonic-Clonic Seizures (Adjunctive Therapy) in Patients 4 Years of Age and Older.
Age and Body Weight
Initial Dosage
Titration
(Incremental Steps)
Maintenance Dosage
Adults (≥17 years)
Monotherapy:
100 mg twice daily
(200 mg per day)
Adjunctive therapy:
50 mg twice daily
(100 mg per day)
Increase by 50 mg
twice daily
(100 mg per day)
every week
Monotherapy:
150-200 mg twice daily
(300-400 mg per day)
Adjunctive therapy:
100-200 mg twice daily
(200-400 mg per day)
Pediatric patients (≥50 kg)
50 mg twice daily
(100 mg per day)
Pediatric patients (30-50 kg)
1 mg/kg twice daily
(2 mg/kg per day)
Increase by 1 mg/kg
twice daily
(2 mg/kg/day)
every week
2-4 mg/kg twice daily
(4-8 mg/kg/day)
Pediatric patients (6-30 kg)
3-6 mg/kg twice daily
(6-12 mg/kg/day)
Pediatric patients <6 kg)
3.75-7.5 mg/kg twice daily
(7.5-15 mg/kg/day)
Lacosamide tablets and oral solution may be taken with or without food.

The most common adverse reactions of Lacomax are dizziness, headache, somnolence, ataxia, tremor, nausea, vomiting, fatigue, diplopia, blurred vision etc.

It is proposed that lacosamide's inhibition of sodium channels is responsible for analgesia. Lacosamide may be selective for inhibiting depolarized neurons rather than neurons with normal resting potentials. Pain and nociceptor hyperexcitability are associated with neural membrane depolarization. Lacosamide binds to collapsin response mediator protein-2 (CRMP-2), a phosphoprotein which is expressed primarily in the nervous system and is involved in neuronal differentiation and control of axonal outgrowth. The role CRMP-2 of binding in seizure control is hasn't been elucidated.
The precise mechanism by which Lacosamide exerts its anti-epileptic effects in humans remains to be fully elucidated. In vitro electrophysiological studies have shown that Lacosamide selectively enhances slow inactivation of voltage-gated sodium channels, resulting in stabilization of hyperexcitable neuronal membranes and inhibition of repetitive neuronal firing.