LAMOTRIGINE - AN UPDATE

Authors
Citation
Mj. Brodie, LAMOTRIGINE - AN UPDATE, Canadian journal of neurological sciences, 23(4), 1996, pp. 6-9
Citations number
48
Categorie Soggetti
Clinical Neurology
ISSN journal
03171671
Volume
23
Issue
4
Year of publication
1996
Pages
6 - 9
Database
ISI
SICI code
0317-1671(1996)23:4<6:L-AU>2.0.ZU;2-X
Abstract
Lamotrigine (LTG) inhibits repetitive high frequency Firing in depolar ised neurones by selectively prolonging slow inactivation of the sodiu m channel, thereby suppressing the release of excitatory amino acids. it has been shown to be effective in 11 pivotal double-blind add-on tr ials in patients with refractory partial seizures with or without seco ndary generalisation. Subsequent anecdotal data support its efficacy f or typical and atypical absences, myoclonic jerks, tonic or clonic sei zures, Lennox-Gastaut syndrome and infantile spasms, Most recently LTG has been compared with carbamazepine and plenytoin in double-blind tr ials in patients with newly diagnosed partial and primary and secondar y generalised tonic-clonic seizures. At the doses used, its efficacy w as similar to the older agents for all seizure types, bat LTG was bett er tolerated than both of the older agents. The commonest side-effects with LTG include headache, nausea, diplopia, dizziness, ataxia and tr emor: Rash occurs in fewer than 5% patients. Its incidence can be redu ced by starting treatment with a low dose, particularly in patients re ceiving concomitant sodium valproate which inhibits LTG metabolism. En zyme inducers, such as carbamazepine, phenytoin and phenobarbital, acc elerate its elimination, but LTG itself has no effect on hepatic metab olic processes. A pharmacodynamic interaction with carbamazepine neces sitates a dosage reduction in some patients when LTG is introduced, LT G is a new antiepileptic agent with a long elimination half-life, a br oad spectrum of activity, and a wide therapeutic ratio.