Vigabatrin treatment

Alanine GABA-transaminase deficiency Vigabatrin treatment Ureidopropionase deficiency... 

Zgorzalewicz M, Galas-Zgorzalewicz B. Visual and auditory evoked potentials during long-term vigabatrin treatment in children and adolescents with epilepsy. Clin Neurophysiol 2000 111(12) 2150. ... 

The longer the duration of vigabatrin treatment and the higher the dose the greater the probability of field defects (28,30,51). 

Vigabatrin does not produce enzyme induction and did not generally alter the kinetics of ethinylestradiol and levonorgestrel, although two women had an approximate 50% reduction in ethinylestradiol concentrations during vigabatrin treatment (SEDA-21, 80). 

Nousiainen I, Kalviainen R, Mantiyarvi M, Riekkinen PJ. Prevalence of concentric visual field constriction in adult epilepsy patients with vigabatrin treatment. Neurology 1999 52(Suppl. 2) A235-6. 

Harding GF, Wild JM, Robertson KA, Rietbrock S, Martinez C. Separating the retinal electrophysiologic effects of vigabatrin treatment versus field loss. Neurology 2000 55(3) 347-52. 

Erdal, J., Gram, L., Alving, J., and Loscher, W. 1999. Change in plasma GABA concentration during vigabatrin treatment of epilepsy A prospective study. Epilepsy Res. 34 145-50. 

At present, the primary indication for vigabatrin is in the treatment of patients with partial seizures, but it appears to be an effective and generally well tolerated antiepileptic medication for other seizure types as well. It should not be used in patients with absence epilepsy or with myoclonic seizures. Vigabatrin is not approved as an AED in the United States, although it is approved in many other countries. 

Drowsiness, hypotonia, and irritability were observed in 37% of infants given corticotropin in a randomized comparison of corticotropin with vigabatrin in the treatment of infantile spasms (SEDA-22, 442 11). 

Vigevano F, Cilio MR. Vigabatrin versus ACTH as first-line treatment for infantile spasms a randomized, prospective study. Epilepsia 1997 38(12) 1270-4. 

Vigabatrin is used as an adjunctive antiepileptic in patients with resistant partial epilepsy with or without secondary generalization, unresponsive to other therapy [2]. Nowadays, vigabatrin is rarely used in the treatment of partial seizures due to several irreversible visual field constrictions associated with its chronic use [57-62], It is regarded by many authorities as a drug of choice in infants with west syndrome (infantile spasms), particularly in cases associated with tuberous sclerosis [62],... 

Bromide (1857) was the first drug to be used for the treatment of epilepsy, but it is now obsolete. Phenobarbital, introduced in 1912, controlled patients resistant to bromides. The next success was the discovery in 1938 of phenytoin (a hydantoin) which is structurally related to the barbiturates. Since then many other drugs have been discovered, but phenytoin still remains a drug of choice in the treatment of major epilepsy. Over the past ten years there has been a dramatic increase in the number of new anticonvulsant drugs (vigabatrin, gabapentin, lamotrigine, topiramate, oxcarbazepine, levetiracetam), but none has been shown to be superior to the major standard anticonvulsants (phenytoin, carbamazepine and sodium valproate). 

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