Frontal nonconvulsive status epilepticus associated with high-dose tiagabine therapy in a child with familial bilateral perisylvian polymicrogyria

Citation
P. Piccinelli et al., Frontal nonconvulsive status epilepticus associated with high-dose tiagabine therapy in a child with familial bilateral perisylvian polymicrogyria, EPILEPSIA, 41(11), 2000, pp. 1485-1488
Citations number
16
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EPILEPSIA
ISSN journal
00139580 → ACNP
Volume
41
Issue
11
Year of publication
2000
Pages
1485 - 1488
Database
ISI
SICI code
0013-9580(200011)41:11<1485:FNSEAW>2.0.ZU;2-B
Abstract
Purpose: Antiepileptic drugs are known to exacerbate absence and myoclonic seizures, especially in patients with idiopathic generalized epilepsies. Ex acerbation of nonconvulsive generalized seizures in patients with partial e pilepsy is less common. Recently, however, a number of cases of putative ge neralized nonconvulsive status epilepticus (NCSE) or NCSE without further s pecification have been reported in patients with chronic partial epilepsy t reated with the gamma -aminobutyric acid reuptake inhibitor tiagabine, Alth ough complex partial status epilepticus during tiagabine therapy has also b een reported, possible precipitation of NCSE specifically associated with f rontal lobe discharges does not appear to have been recognized. In this com munication, we describe the case of a boy with familial bilateral perisylvi an polymicrogyria who developed frontal NCSE after being stabilized on high -dose tiagabine Methods: A 12-year-old boy with familial bilateral perisylvian polymicrogyr ia, mental retardation, and refractory partial seizures was administered ti agabine in addition to sodium valproate. The tiagabine dosage was increased gradually up to 10 mg t.i.d. (1 mg/kg per day), resulting in complete seiz ure control. Results: After 1 week on maintenance treatment, seizures were completely co ntrolled, but the child developed hypoactivity, decreased reactivity, and a ffective detachment. An EEG recording revealed subcontinuous sharp-wave dis charges with irregular runs of atypical spike-wave complexes over the anter ior regions of both hemispheres, consistent with a diagnosis of frontal NCS E. A reduction in tiagabine dosage to 15 mg/day Led to complete regression of the behavioral and affective changes and to disappearance of the subcont inuous EEG discharges. Conclusions: Although tiagabine-induced NCSE has been described previously, particularly in patients with preexisting spike-wave abnormalities, this i s the first report that identifies its potential role in the precipitation of frontal NCSE.