Status epilepticus during vigabatrin treatment: A report of three cases

Krom, M.C.T.F.M. de; Verduin, N.; Visser, Elizabeth; Kleijer, M.; Scholtes, F.B.J.; Groen, Jan-Willem

doi:10.1016/s1059-1311(95)80099-9

Cited by 21 publications

(9 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…First, the functional loss of GABA A receptors resulting from subunit trafficking may explain the time-dependent development of pharmacoresistance to GABAergic agents in SE and represents a new mechanism of pharmacoresistance that might have implications beyond SE (de Krom et al, 1995;Ali and Olsen, 2001;Fitzek et al, 2001;Kumar et al, 2003). Our findings emphasize the importance of recognizing a crucial time window for delivery of GABAenhancing medications during SE, stress the role of additional pharmacotherapies for effective treatment (including those directed against glutamatergic excitation), and may explain timedependent relationships for different anticonvulsants (Walton and Treiman, 1991;Jones et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Trafficking of GABA_AReceptors, Loss of Inhibition, and a Mechanism for Pharmacoresistance in Status Epilepticus

Naylor¹,

Liu²,

Wasterlain³

2005

J. Neurosci.

498

447

View full text Add to dashboard Cite

During status epilepticus (SE), GABAergic mechanisms fail and seizures become self-sustaining and pharmacoresistant. During lithiumpilocarpine-induced SE, our studies of postsynaptic GABAAreceptors in dentate gyrus granule cells show a reduction in the amplitude of miniature IPSCs (mIPSCs). Anatomical studies show a reduction in the colocalization of the β2/β3 and γ2 subunits of GABAAreceptors with the presynaptic marker synaptophysin and an increase in the proportion of those subunits in the interior of dentate granule cells and other hippocampal neurons with SE. Unlike synaptic mIPSCs, the amplitude of extrasynaptic GABAAtonic currents is augmented during SE. Mathematical modeling suggests that the change of mIPSCs with SE reflects a decrease in the number of functional postsynaptic GABAAreceptors. It also suggests that increases in extracellular [GABA] during SE can account for the tonic current changes and can affect postsynaptic receptor kinetics with a loss of paired-pulse inhibition. GABA exposure mimics the effects of SE on mIPSC and tonic GABAAcurrent amplitudes in granule cells, consistent with the model predictions. These results provide a potential mechanism for the inhibitory loss that characterizes initiation of SE and for the pharmacoresistance to benzodiazepines, as a reduction of available functional GABAApostsynaptic receptors. Novel therapies for SE might be directed toward prevention or reversal of these losses.

show abstract

Section: Discussionmentioning

confidence: 99%

Trafficking of GABA_AReceptors, Loss of Inhibition, and a Mechanism for Pharmacoresistance in Status Epilepticus

Naylor¹,

Liu²,

Wasterlain³

2005

J. Neurosci.

498

447

View full text Add to dashboard Cite

show abstract

“…VGB aggravates absence and myoclonic seizures, and de novo myoclonic seizures, absences, and convulsive status have also been reported (34,59). In addition, exacerbations of seizures and myoclonic status have been reported in the context of an acute encephalopathy with VGB (60).…”

Section: Clinical Evidence For Aggravation Of Generalized Epilepsiesmentioning

confidence: 99%

“…The primary mechanism of action of VGB is believed to arise from irreversible inhibition of GABA‐transaminase, producing an increase in GABA. VGB may worsen IGEs (58,59). In a trial of VGB in children with uncontrolled epilepsy, 10% experienced an important increase in seizures, particularly if they had myoclonic epilepsy or LGS.…”

Section: Clinical Evidence For Aggravation Of Generalized Epilepsiesmentioning

confidence: 99%

Seizure Aggravation in Idiopathic Generalized Epilepsies

Chaves¹,

Sander²

2005

Epilepsia

View full text Add to dashboard Cite

Summary: Seizures in the idiopathic generalized epilepsies (IGEs) usually remit completely with antiepileptic drugs (AEDs). Occasionally, however, they may be aggravated by AEDs. Before attributing exacerbation of seizures to an AED, alternative explanations need to be excluded. These include natural fluctuation of seizures, irregular compliance, maladjustment to the disease, comorbid illness, and development of tolerance. Aggravation may be due to a paradoxical reaction or drug‐induced encephalopathy, sedative effects, or inappropriate use of a drug; and this need to be established, as it will guide management. An important caveat is that most data on aggravation of generalized seizures are based on anecdotal case reports or case series. Whether considering efficacy or aggravation, the interpretation of data from uncontrolled studies and case reports must be treated with caution. In practice, despite the fact that clear evidence is lacking, the possibility of seizure aggravation must be considered when treating people with IGEs. Predictive factors for seizure aggravation in a particular patient with a specific drug are yet to be fully defined. It is paramount to classify seizure type correctly in all patients. If this is not possible, a broad‐spectrum AED should be used. Drugs that modulate Na+‐channels and GABAergic drugs seem to be more prone to aggravating seizures, and therefore are best avoided in the initial management of IGE. Further studies are required to elucidate this phenomenon in full. It is interesting to speculate that paradoxical responses to AEDs may have pharmacogenetic value, serving as tools for a more precise and useful characterization of the epilepsies.

show abstract

“…Partial or generalized status epilepticus as a possible complication of VGB has been reported in a number of patients with symptomatic generalized or partial epilepsy (120)(121)(122). Although in at least some of these cases a cause-and-effect relationship with VGB treatment could not be established or was unlikely (1 23), the possibility that VGB may play a role in the precipitation of status epilepticus should be considered in individual patients.…”

Section: )mentioning

confidence: 99%

Antiepileptic Drugs as a Cause of Worsening Seizures

Perucca

Gram

Avanzini³

et al. 1998

Epilepsia

500

329

View full text Add to dashboard Cite

Summary:Purpose: Although the paradoxical ability of antiepileptic drugs (AEDs) to increase seizure activity has been recognized for decades, the underlying mechanisms are poorly understood and few systematic studies have addressed this problem. This article is intended to provide a critical review of available literature on this topic.Methods: Information was collected by means of computerized literature searches, screening of journals and textbooks, and consultation with colleagues. Mechanisms which potentially might precipitate underlying drug-induced exacerbation of seizures were considered based on available pharmacologic and clinical knowledge.

show abstract

Status epilepticus during vigabatrin treatment: A report of three cases

Cited by 21 publications

References 13 publications

Trafficking of GABA_AReceptors, Loss of Inhibition, and a Mechanism for Pharmacoresistance in Status Epilepticus

Trafficking of GABA_AReceptors, Loss of Inhibition, and a Mechanism for Pharmacoresistance in Status Epilepticus

Seizure Aggravation in Idiopathic Generalized Epilepsies

Antiepileptic Drugs as a Cause of Worsening Seizures

Contact Info

Product

Resources

About

Status epilepticus during vigabatrin treatment: A report of three cases

Cited by 21 publications

References 13 publications

Trafficking of GABAAReceptors, Loss of Inhibition, and a Mechanism for Pharmacoresistance in Status Epilepticus

Trafficking of GABAAReceptors, Loss of Inhibition, and a Mechanism for Pharmacoresistance in Status Epilepticus

Seizure Aggravation in Idiopathic Generalized Epilepsies

Antiepileptic Drugs as a Cause of Worsening Seizures

Contact Info

Product

Resources

About

Trafficking of GABA_AReceptors, Loss of Inhibition, and a Mechanism for Pharmacoresistance in Status Epilepticus

Trafficking of GABA_AReceptors, Loss of Inhibition, and a Mechanism for Pharmacoresistance in Status Epilepticus