**3.2 Characterization of NCSE and the control group**

The control group consisted of 185 patients with AMS or coma in which cEEG monitoring did not show any features of NCSE. **Table 2** shows the demographic and clinical features of NCSE and control subjects. Only age and presence of subtle motor phenomena differed between the two groups; the NCSE patients were relatively younger and displayed subtle motor phenomena more often. As for etiology and comorbid states, a history of previous seizures and presence of cortical dysplasia were significantly more common in the NCSE group (**Table 3**). Other etiologies were not informative. Head injury, stroke, and status postcardiac arrest were frequently encountered in accident and emergency patients with NCSE; CT head done in 52


### **Table 2.**

*Epilepsy - Advances in Diagnosis and Therapy*

discharges, and their responses to treatment.

**2.5 Laboratory investigations and Neuroimaging**

midazolam, and barbiturates were used [34, 35].

day by an EEG specialist.

**2.6 NCSs/NCSE treatment**

were not used in control group.

**2.7 Outcome parameters**

**2.8 Statistical methods**

parameters.

**3. Results**

**3.1 Occurrence of NCSE**

*2.4.2 EEG duration*

extraneous electrical artifact, 50 Hz notch filter was used; impedance was 100 and 5000 ohms. cEEG was done by EEG technologists and monitored at least twice a

The duration of cEEG monitoring was determined by the response to treatment

The following investigations were performed in most NCSE cases and controls: complete blood count, electrolytes, liver and renal functions, brain MRI, and/or CT

Benzodiazepines (lorazepam or diazepam) were used when NCSs/NCSE was suspected. If seizures persisted, European Federation of Neurological Sciences (EFNS) Guidelines and Glauser et al. report on NCSE treatment were followed: IV diazepam or lorazepam first and then second-line ASDs were initiated—valproic acid, phenytoin, or levetiracetam. If no results, continuous infusions of propofol,

Many patients received more than one ASD. refractory NCSE was treated with anesthetic agents; same treatment protocol was followed in comatose NCSE. ASDs

Seizure control and survival/death were considered as primary outcome parameters, while complete recovery and length of stay were secondary outcome

Descriptive statistics (mean with standard deviation) for continuous variables, frequency, and percentages for categorical variables was used; differences between mean levels of NCSE and controls, outcome and morbidity, and Student's t-test were calculated; to detect associations between categorical variables and NCSE vs controls, outcome, and morbidity, chi-square tests or Fisher's exact tests were used. For independent variables at univariate analysis, NCSE logistic regressions were performed using a significance level of 0.05. A P value of 0.05 (two tailed) was considered a statistically significant level. For statistical analysis, an SPSS 22.0 statistical software was used.

Six patients suffered from CSE; only one of them who showed later NCSE EEG features and was included in the study. Twenty patients presented NCSs; 30% of them (n = 6) responded to ASDs and did not develop NCSE on cEEG monitoring;

of NCSs/NCSE, the presence of other EEG features like rhythmic and periodic

head; imaging was performed either before or after cEEG monitoring

**48**

*Characteristics of patients with NCSE and controls.*


### **Table 3.**

*Etiology of patients with NCSE and controls.*

NCSE cases and in 101 of controls and MRI head done in 41 NCSE cases and in 97 of controls showed hippocampal sclerosis, malformations of cortical development, and encephalomalacia, which were more commonly seen in the NCSE group (**Table 4**).

Abnormal cholesterol and liver enzymes were more often abnormal in the NCSE group than controls (NCSE 15%, controls 4%, p 0.004).

### **3.3 Length of cEEG monitoring and time of occurrence of NCSs/NCSE**

Twenty patients showed NCSs; 65% of them (n = 13) had NCSs during the first 40 minutes of recording, whereas 35% (n = 7) had their seizures later but within the first 48 hours of cEEG monitoring.

In the NCSE group (n = 65), NCSE EEG patterns were recorded during the first 3 hours in 66% (n = 43), later but within the first 48 hours in 22% (n = 14), and in the third day in 12% (n = 8). Among the 22 patients with late NCSE, 17 (77%) were comatose.
