Epileptic disorders : international epilepsy journal with videotape · 2025
Clinical and EEG characterization of late-onset de novo absence nonconvulsive status epilepticus secondary to benzodiazepine withdrawal.
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Mayà Gerard, Muñoz-Lopetegi Amaia, Tercero Ana, Centeno María, Conde Estefanía, Montini Angelica, Arqueros Aurora, Iranzo Alex, Santamaria Joan, Gaig Carles
Аннотация
OBJECTIVE: Abrupt benzodiazepine (BDZ) withdrawal may induce nonconvulsive status epilepticus (NCSE), but information regarding its clinical and EEG features is limited. Our aim was to better characterize this condition.
METHODS: Patients with NCSE according to Salzburg criteria secondary to abrupt BDZ withdrawal identified at our center (2009-2024) were included. Clinical data, seizure semiology, and EEG, were described using ILAE, ACNS, and Salzburg criteria; clinical response to BDZ was quantified using the NCSE response scale (NRS). Recurrences at long-term follow-up were documented.
RESULTS: Fifteen patients (median age 68 years, 53% male) were identified, accounting for 4% of all NCSE cases. None had epilepsy, 80% had psychiatric disorders, and 47% had cognitive impairment. Six (40%) subjects were taking only a low-dose BDZ, and only one was above the therapeutic range. Potential seizure facilitators were identified in all but one patient, including withdrawal from other drugs (60%) or infections (33%). There were two clinical presentations: (1) recurrent absence seizures lasting ≤15 min with asymptomatic periods in-between (67%); and (2) continuous, fluctuating consciousness impairment (33%). Motor phenomena (67%) - including increased or decreased blinking, movement-induced myoclonus or automatisms-, and generalized tonic-clonic seizures (60%) were frequent. Before EEG, BDZ withdrawal was not suspected in any case. The ictal EEG activity consisted of generalized, rhythmic, or irregular polyspike-slow waves and spike-slow waves with gradual onset and offset. However, in 20%, this ictal pattern was less developed. Intravenous clonazepam induced an immediate EEG and clinical improvement, but complete control of seizures required 1-3 days. At follow-up, a new abrupt BDZ withdrawal caused absence seizures recurrence in 4/7 patients still on BDZ treatment, but in none of the eight patients who had gradually discontinued BDZ.
SIGNIFICANCE: NCSE secondary to BDZ withdrawal has distinctive clinical and EEG features but is misdiagnosed without an EEG. Reintroduction of BDZ stops seizures, but long-term management requires gradual BDZ discontinuation to prevent recurrences.
METHODS: Patients with NCSE according to Salzburg criteria secondary to abrupt BDZ withdrawal identified at our center (2009-2024) were included. Clinical data, seizure semiology, and EEG, were described using ILAE, ACNS, and Salzburg criteria; clinical response to BDZ was quantified using the NCSE response scale (NRS). Recurrences at long-term follow-up were documented.
RESULTS: Fifteen patients (median age 68 years, 53% male) were identified, accounting for 4% of all NCSE cases. None had epilepsy, 80% had psychiatric disorders, and 47% had cognitive impairment. Six (40%) subjects were taking only a low-dose BDZ, and only one was above the therapeutic range. Potential seizure facilitators were identified in all but one patient, including withdrawal from other drugs (60%) or infections (33%). There were two clinical presentations: (1) recurrent absence seizures lasting ≤15 min with asymptomatic periods in-between (67%); and (2) continuous, fluctuating consciousness impairment (33%). Motor phenomena (67%) - including increased or decreased blinking, movement-induced myoclonus or automatisms-, and generalized tonic-clonic seizures (60%) were frequent. Before EEG, BDZ withdrawal was not suspected in any case. The ictal EEG activity consisted of generalized, rhythmic, or irregular polyspike-slow waves and spike-slow waves with gradual onset and offset. However, in 20%, this ictal pattern was less developed. Intravenous clonazepam induced an immediate EEG and clinical improvement, but complete control of seizures required 1-3 days. At follow-up, a new abrupt BDZ withdrawal caused absence seizures recurrence in 4/7 patients still on BDZ treatment, but in none of the eight patients who had gradually discontinued BDZ.
SIGNIFICANCE: NCSE secondary to BDZ withdrawal has distinctive clinical and EEG features but is misdiagnosed without an EEG. Reintroduction of BDZ stops seizures, but long-term management requires gradual BDZ discontinuation to prevent recurrences.