Piccinelli P, Borgatti R, Perucca E, Tofani A, Donati G, Balottin U
Child Neuropsychiatry Unit, University of Insubria, "Fondazione Macchi" Hospital, Varese, Italy.
Epilepsia. 2000 Nov;41(11):1485-8. doi: 10.1111/j.1528-1157.2000.tb00126.x.
Antiepileptic drugs are known to exacerbate absence and myoclonic seizures, especially in patients with idiopathic generalized epilepsies. Exacerbation of nonconvulsive generalized seizures in patients with partial epilepsy is less common. Recently, however, a number of cases of putative generalized nonconvulsive status epilepticus (NCSE) or NCSE without further specification have been reported in patients with chronic partial epilepsy treated with the gamma-aminobutyric acid reuptake inhibitor tiagabine. Although complex partial status epilepticus during tiagabine therapy has also been reported, possible precipitation of NCSE specifically associated with frontal lobe discharges does not appear to have been recognized. In this communication, we describe the case of a boy with familial bilateral perisylvian polymicrogyria who developed frontal NCSE after being stabilized on high-dose tiagabine
A 12-year-old boy with familial bilateral perisylvian polymicrogyria, mental retardation, and refractory partial seizures was administered tiagabine 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 seizure control.
After 1 week on maintenance treatment, seizures were completely controlled, but the child developed hypoactivity, decreased reactivity, and affective detachment. An EEG recording revealed subcontinuous sharp-wave discharges with irregular runs of atypical spike-wave complexes over the anterior regions of both hemispheres, consistent with a diagnosis of frontal NCSE. A reduction in tiagabine dosage to 15 mg/day led to complete regression of the behavioral and affective changes and to disappearance of the subcontinuous EEG discharges.
Although tiagabine-induced NCSE has been described previously, particularly in patients with preexisting spike-wave abnormalities, this is the first report that identifies its potential role in the precipitation of frontal NCSE.
已知抗癫痫药物会加重失神发作和肌阵挛发作，尤其是在特发性全身性癫痫患者中。部分性癫痫患者的非惊厥性全身性发作加重情况较少见。然而，最近有报道称，在接受γ-氨基丁酸再摄取抑制剂替加宾治疗的慢性部分性癫痫患者中，出现了一些疑似全身性非惊厥性癫痫持续状态（NCSE）或未进一步明确的NCSE病例。尽管也有报道称替加宾治疗期间出现复杂部分性癫痫持续状态，但与额叶放电特别相关的NCSE的可能诱发情况似乎尚未得到认识。在本报告中，我们描述了一名患有家族性双侧外侧裂周多小脑回畸形的男孩，在高剂量替加宾治疗病情稳定后发生额叶NCSE的病例。
一名患有家族性双侧外侧裂周多小脑回畸形、智力发育迟缓且难治性部分性癫痫的12岁男孩，除丙戊酸钠外还给予了替加宾。替加宾剂量逐渐增加至每日3次，每次10毫克（每日1毫克/千克），癫痫发作得到完全控制。
维持治疗1周后，癫痫发作完全得到控制，但患儿出现活动减少、反应性降低和情感淡漠。脑电图记录显示双侧半球前部区域有亚持续的尖波放电，伴有不规则的非典型棘波-慢波复合波，符合额叶NCSE的诊断。将替加宾剂量减至每日15毫克后，行为和情感变化完全消退，亚持续脑电图放电消失。
尽管之前已描述过替加宾诱发的NCSE，尤其是在已有棘波-慢波异常的患者中，但这是首次报告指出其在诱发额叶NCSE中的潜在作用。
