The effect of different vigabatrin treatment regimens on CSF biochemistry and seizure control in epileptic patients.

Ben‐Menachem, Elinor; Persson, Liselott; Schechter, Paul J.; Haegele, K.D.; Huebert, Norman; Hardenberg, J.; Dahlgren, Lena; Mumford, J. P.

doi:10.1111/j.1365-2125.1989.tb03466.x

Cited by 82 publications

(29 citation statements)

References 18 publications

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“…However, in nonhuman primates, brain GABA levels were unchanged after 6 years of treatment at 50 and 100 mg/kg/day. These results are in contrast to the human, where single daily doses of 50 m g k g for 1 month resulted in a threefold increase in CSF GABA levels (41). The same dose level (50 mg/kg/day) resulted in two-to fourfold increases in CSF GABA in rats after 2 weeks of treatment and dogs after 16 weeks of treatment (1 I).…”

Section: Possible Pathologic Mechanisms Of Ime and Myelin Toxicitycontrasting

confidence: 48%

The Potential for Vigabatrin‐Induced Intramyelinic Edema in Humans

Cohen¹,

Fisher²,

Brigell³

et al. 2000

Epilepsia

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Purpose: Vigabatrin (Sabril, Hoechst Marion Roussel) is an antiepilepsy drug (AED) presently marketed in 64 countries for the treatment of partial and secondarily generalized seizures. Vigabatrin (VGB) is marketed in a subset of these countries for the treatment of infantile spasms. Clinical experience in humans has shown that VGB provides effective seizure control with a wide margin of safety. However, animal toxicity studies raised concern when prolonged administration of VGB was shown to induce intramyelinic edema (IME) in some laboratory animal species. Methods: Animal and human data were reviewed with respect to the potential for VGB-induced IME. Surveillance of patients receiving VGB in clinical trials or by prescription has been conducted for >15 years to identify patients developing clinical abnormalities that might be IME related. Results: The histologic lesions of VGB-induced IME in animals are reliably reproduced and correlate with changes in multimodality evoked potentials (EPs) and magnetic resonance imaging (MRI). Numerous studies of the effects of VGB on EP and MRI in epilepsy patients have demonstrated no clear-cut IME-related changes in these modalities. Additionally, autopsy and surgical brain samples from VGB-treated patients have been scrutinized for potential IME histopathology. In an estimated 350,000 patient-years of VGB exposure (-1 75,000 pa

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Section: Possible Pathologic Mechanisms Of Ime and Myelin Toxicitycontrasting

confidence: 48%

The Potential for Vigabatrin‐Induced Intramyelinic Edema in Humans

Cohen¹,

Fisher²,

Brigell³

et al. 2000

Epilepsia

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“…VGB has been found to be particularly effective in patients with drug-resistant epilepsy, a large proportion of whom suffer from complex partial seizures (11)(12)(13)(14)(15).…”

Section: Discussionmentioning

confidence: 99%

Electro‐Oculography, Electroretinography, Visual Evoked Potentials, and Multifocal Electroretinography in Patients with Vigabatrin‐Attributed Visual Field Constriction

et al. 2000

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Summary: Purpose: Symptomatic visual field constriction thought to be associated with vigabatrin has been reported. The current study investigated the visual fields and visual electrophysiology of eight patients with known vigabatrin‐attributed visual field loss, three of whom were reported previously. Six of the patients were no longer receiving vigabatrin. Methods: The central and peripheral fields were examined with the Humphrey Visual Field Analyzer. Full visual electrophysiology, including flash electroretinography (ERG), pattern electroretinography, multifocal ERG using the VERIS system, electro‐oculography, and flash and pattern visual evoked potentials, was undertaken. Results: Seven patients showed marked visual field constriction with some sparing of the temporal visual field. The eighth exhibited concentric constriction. Most electrophysiological responses were usually just within normal limits; two patients had subnormal Arden electro‐oculography indices; and one patient showed an abnormally delayed photopic b wave. However, five patients showed delayed 30‐Hz flicker b waves, and seven patients showed delayed oscillatory potentials. Multifocal ERG showed abnormalities that sometimes correlated with the visual field appearance and confirmed that the deficit occurs at the retinal level. Conclusion: Marked visual field constriction appears to be associated with vigabatrin therapy. The field defects and some electrophysiological abnormalities persist when vigabatrin therapy is withdrawn.

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“…DISCUSSION Vigabatrin (7-vinyl-GABA) was developed as a structural analogue of GABA to inhibit GABA transaminase activity, which increases the CSF concentration of GABA, an inhibitory neurotransmitter. The GABA increase correlates with a reduced seizure frequency according to several studies (Schechter et al 1984;Ben-Menachem et al 1989;Riekkinen et al t989). Vigabatrin was first introduced as a treatment modality in SSADH deficiency by Jaeken et al (1989).…”

Section: Resultsmentioning

confidence: 92%

Seizures in a boy with succinic semialdehyde dehydrogenase deficiency treated with vigabatrin (γ‐vinyl‐GABA)

Matern¹,

Lehnert²,

Gibson

et al. 1995

J of Inher Metab Disea

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Succinic semialdehyde dehydrogenase (SSADH) deficiency is an autosomal recessive disease involving the catabolism of the neurotransmitter gamma-aminobutyric acid (GABA). The main symptoms include retardation of psychomotor and language development, muscle hypotonia and non-progressive ataxia. Therapy consisting of approximately 75 mg/kg per day of vigabatrin, an irreversible inhibitor of GABA-transaminase, is reported to lead to some improvement of the clinical condition in affected patients. We report on a 12-year-old boy with SSADH deficiency who, when treated with 75 mg/kg per day of vigabatrin, showed marked amelioration of symptoms but also EEG changes and two generalized seizures. On discontinuing vigabatrin therapy, the seizures resolved and the EEG improved, but the patient's clinical condition deteriorated to its pre-treatment state. A stable EEG without the recurrence of seizures as well as renewed improvement of cognitive and behavioural functions was achieved with a reduced vigabatrin dose of 25 mg/kg per day. We conclude that vigabatrin in SSADH deficiency should be administered in a gradually increasing dosage combined with frequent evaluation of the clinical condition and the EEG.

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The effect of different vigabatrin treatment regimens on CSF biochemistry and seizure control in epileptic patients.

Cited by 82 publications

References 18 publications

The Potential for Vigabatrin‐Induced Intramyelinic Edema in Humans

The Potential for Vigabatrin‐Induced Intramyelinic Edema in Humans

Electro‐Oculography, Electroretinography, Visual Evoked Potentials, and Multifocal Electroretinography in Patients with Vigabatrin‐Attributed Visual Field Constriction

Seizures in a boy with succinic semialdehyde dehydrogenase deficiency treated with vigabatrin (γ‐vinyl‐GABA)

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