NCSE frequently complicate acute neurological lesions and systemic illness in ICU, more than 59% with no previous history of epilepsy. Incidence is estimated as high as 30% in neurological ICU. NCSE encompasses a broad spectrum of etiologies: post-anoxic coma, PLEDs, toxic metabolic encephalopathy, drugs, multiple organ failure and following convulsive SE (CSE). Identification of these subgroups is very important. NCSE represents an epileptic state lasting more than 30 minutes with two principal components:
1) some clinically evident alteration in mental status or behavior from baseline, and 2) seizure activity on the EEG. Some include 3) a response to AED, with significant improvement.
Complications of this definition: what constitutes “behavioral changes from baseline” and what is “seizure on EEG”. EEG is the gold standard for NCSE diagnosis. Criteria supporting EEG diagnosis of seizures are: a) repetitive generalized or focal discharges; b) sequence of rhythmic waves. Critical activity shows increment in the beginning, decrement in the end, post-seizure slowing or attenuation and duration greater than 10 seconds.
Some EEG characteristics in NCSE deserve further discussion. EEG waveforms are not specific. Either toxic metabolic encephalopathy or NCSE can present atypical or typical triphasic waves and rhythmic delta activity with intermittent spiking, rendering distinction difficult. NCSE must show continuous EEG epileptiform activity? Which is the accepted interval?
Very frequent discharges could represent NCSE? Which spiking frequency corresponds to NCSE? What level of EEG reactivity is expected?
Therapeutic test: small doses recommended, e.g. midazolam 1.5–3 mg IV, minimizing patient sedation. Monitoring is a very important, prompting timely intervention. Our preliminary work is based on simultaneous raw EEG, spectral analysis (CSA) and index alpha, allowing either seconds or hourly evaluation.