Authors :
Presenting Author: Jie Deng, MD – Beijing Children's Hospital
Jun Zhang, MD – Henan Children’s Hospital
Lili Zheng, BS – Beijing Children's Hospital
Xiaoyi Chen, MD – Henan Children’s Hospital
Rationale:
Idiopathic generalized epilepsy (IGE) is a group of epilepsy syndromes characterized by generalized seizures and specific electroencephalographic (EEG) patterns of generalized 2.5-5.5 Hz spike-and-wave discharges (SWDs). Sodium channel blockers (SCBs) are narrow-spectrum anti-seizure medications (ASMs), and their use in IGEs is contraindicated due to their potential to exacerbate seizures and EEG abnormalities. This study aims to analyze the clinical and EEG consequences of SCB misuse in IGEs, and to provide recommendations for preventing diagnostic and therapeutic errors.
Methods:
A retrospective cohort analysis was conducted at Beijing Children's Hospital and Henan Children's Hospital from January 2019 to January 2024. Clinical and EEG data were collected from patients diagnosed with IGEs who had received SCB treatment. Prognostic follow-up was performed until January 2025.
Results:
A total of 10 patients (5 males and 5 females) were collected. The median age at onset of epilepsy was 9.2 years (range 5.0~13.3 years). The epilepsy syndromes included 4 cases of childhood absence epilepsy (CAE), 5 cases of juvenile absence epilepsy (JAE), and 1 case of epilepsy with generalized tonic-clonic seizures alone (GTCA). All patients had generalized tonic-clonic seizures (GTCS), and absence seizures were present in 9. Focal epileptiform discharges were recorded on the interictal EEG in all patients, with frontal predominance in 8 and occipital/temporal predominance in 2; polyspike-wave complexes were observed in 3 cases (Figure 1).
SCBs were initiated 0.5~24 months after presentation, with a median time of 1.5 months. Oxcarbazepine was prescribed to 7 patients and was the first ASM in 2 patients, carbamazepine to 2 patients and lacosamide to 1 patient. The reasons for SCB prescription were atypical GTCS semiology (e.g., head/eye turning aside mimicking focal onset) and focal EEG abnormalities. Clinical deterioration occurred during SCBs treatment, including an increase in absence seizure frequency in 9 patients, GTCS recurrence in 7 patients, and new onset tonic seizures during sleep in 1 patient with JAE (Figure 2). There was also EEG worsening, including multifocal spikes in 8 and fast rhythmic activity in 6 cases.
Discontinuation of SCBs and optimization of ASMs to valproate, lamotrigine, levetiracetam, perampanel or clobazam resulted in seizure control in 9 patients after a median time of 9.5 months. The rechecked EEG also improved, with generalized SWD disappearing in 5, polyspike-wave discharges disappearing in 3 and focal spikes reduction in 4 cases. However, patients exposed to SCBs had prolonged clinical remission compared with our previous cohort of patients with IGEs, with median remission delayed from 3.5 months to 6.5 months in patients with CAE, and from 5.5 months to 11 months in patients with JAE.
Conclusions:
SCBs exacerbate seizures and EEG abnormalities in IGEs. Focal EEG features and atypical semiology can lead to the misuse of SCBs. Adherence to IGE treatment guidelines, which involve avoiding SCBs and prioritizing broad-spectrum ASMs, is essential to prevent disease progression and reduce the healthcare burden.
Funding: N/A