Comparison of Midazolam or Dexmedetomidine on Epileptiform EEG During Sevoflurane Mask Induction

Comparison of Intranasal Midazolam or Dexmedetomidine on Epileptiform EEG During Sevoflurane Mask Induction in Children

Induction with high sevoflurane concentrations may trigger epileptiform electroencephalographic activity without motor or cardiovascular manifestations in healthy patients. No other symptoms were associated in this series, and only electroencephalographic monitoring allowed the diagnosis. Midazolam and dexmedetomidine are sedatives commonly used in children before surgery. Although the mechanisms are different, both have been reported in antiepileptic effects. This study was designed to compare the effects between intranasal midazolam or dexmedetomidine on epileptiform EEG during sevoflurane mask induction in children. Anaesthesia was induced with 8% sevoflurane. The patients were randomly assigned to Group A (n=15, preoperative intranasal normal saline), Group B (n=15, preoperative intranasal 0.25mg/kg midazolam), and Group C (n=15, preoperative intranasal 1μg/kg dexmedetomidine). An electroencephalogram was recorded before and during induction up to 10 min after the start of induction.

Patients in Group A receive intranasal normal saline before anesthesia. Anaesthesia was induced with 8% sevoflurane initially. Sevoflurane concentration decreased to 2% after intubation. An electroencephalogram was recorded before and during induction up to 10 min after the start of induction.

Patients in Group B receive intranasal 0.25mg/kg midazolam before anesthesia. Anaesthesia was induced with 8% sevoflurane initially. Sevoflurane concentration decreased to 2% after intubation. An electroencephalogram was recorded before and during induction up to 10 min after the start of induction.

Patients in Group C receive intranasal 1μg/kg dexmedetomidine before anesthesia. Anaesthesia was induced with 8% sevoflurane initially. Sevoflurane concentration decreased to 2% after intubation. An electroencephalogram was recorded before and during induction up to 10 min after the start of induction.

EEG were visually analyzed off-line by a neurophysiologist familiar with anesthesia EEG and blinded to the randomization. EEG abnormalities related to epileptic features were classified according to the description of Vakkuri and Jaaskelainen, and the recommendations of Constant: spikes and spikes with slow wave complexes (SW), rhythmic polyspikes corresponding to waveforms appearing at regular intervals (RPS) and periodic epileptiform discharge (PED), which refers to periodic hypersynchronized complexes occurring bilaterally. These entire electroencephalographic phenomena were considered as epileptiform EEG if their duration was longer than three seconds.

the delay between the start of induction and the first changes in electroencephalographic activity (appearance of β, θ, or δ rhythms)

Inclusion Criteria: ASA physical status 1-2 Scheduled for general anesthesia Exclusion Criteria: Patients with a history of neurological, mental illnes Patients with a history of congenital heart disease Patients with a history of allergies to related drugs