**3.4 NCSE proper and comatose NCSE**

The NCSE group was further subdivided into two: NCSE proper without coma (n = 39) and comatose NCSE (n = 26) [32, 36]; NCSE proper is defined as clinical symptoms suggestive of SE with mild impairment of consciousness (absence status or complex focal SE); NCSE with coma-lateralized epileptiform discharges, NCSE with coma-generalized epileptiform discharges is defined as deep coma of various etiology with characteristic epileptiform EEG pattern but with no clinical motor signs of SE; NCSE proper patients are significantly younger than the comatose NCSE ones (**Table 5**). NCSE in comatose patients was often recorded after the first day of cEEG monitoring: during the first 24 hours in only 54% (n = 14/26), later but within 48 hours in 35% (n = 9/26), and in the third day in 11% (n = 3/26) of the patients; comparatively, NCSE proper was recorded during the first day in 77% (n = 30/39), later but within 48 hours in 10% (n = 4/39), and during the third day in 13% (n = 5/39) of patients.

The 14 patients with early comatose NCSE (first 24 hs) suffered from head injury (n = 4), stroke (n = 4), and cardiac arrest (n = 3); and no etiology was found in three patients; comparatively, in the NCSE proper group (n = 30), 18 patients suffered from previous seizures, 5 from stroke, 3 from sepsis, 2 from head injury, and 2 from cardiac arrest.


**51**

**Table 5.**

Hospital stay (days)

Complete recovery

*Nonconvulsive Status Epilepticus in Patients with Altered Mental Status Admitted to Hamad…*

Patients with NCSs (n = 20) were treated as follows: 18 with benzodiazepines, 10 with valproate IV, and 8 with levetiracetam plus valproate IV. The 65 NCSE patients received the following: lorazepam 4–8 mg IV or diazepam 10 mg IV (n = 45), levetiracetam IV or PO (n = 22), phenytoin IV (n = 21), valproate IV or PO (n = 18), topiramate PO (n = 5), phenobarbitone IV (n = 7), midazolam IV (n = 15), propofol

NCSE group (n = 65): 69% (n = 45, m 25, f 20) responded to treatment within

Control group (n = 185): 19% (n = 35, m 20, f 15) died. Thus, compared to the control group, death was more frequent in the NCSE group; there was additional statistical significance when NCSE proper was compared to comatose NCSE and when comatose NCSE was compared to controls (**Table 5**), with comatose patients exhibiting a more ominous outcome. The majority of patients with early occurrence of NCSs/NCSE = 65% (40 minutes to 3 hours) died (n = 13/20). Causes of death in NCSE (n = 20) group were distributed as follows: cardiac arrest (n = 6), hemorrhagic and ischemic strokes (n = 5), sepsis (n = 3), head injury (n = 4), subarach-

Compared to controls, NCSE achieved complete recovery in 40% (n = 26, m 15, f 11) compared to controls 53% (n = 98, m 55, f 43); **Table 5** shows that this achieved statistical significance when comatose NCSE was compared to controls; NCSE group (NCSE proper plus comatose NCSE) had a longer hospital stay than the controls.

Deaths 20 (31%) 8 (21%)\* 12 (46%)\*§ 35 (19%)§ \* 0.05, §

Age (years) 45.7 ± 19§ 36.9 ± 24& 51.3 ± 16.9& 52.3 ± 15.8 § § 0.001, &

*Note: P values are calculated using Chi-square tests, Fisher exact tests and Student t tests wherever appropriate. \* and § compare Death occuring respectively in NCSE without coma to NCSE with coma and also Death occurring in* 

*§ and & compare patients and controls 's age respectively in NCSE group to controls and also in NCSE without coma* 

*# and ^ compare hospital stay respectively in NCSE group to controls and also in NCSE with coma to controls* 

*(respectively 0.02 and 0.03); symbol a compares complete recovery in NCSE with coma to controls (0.04)*

*Occurrence and comparison of the listed variables in the NCSE groups and control group.*

**NCSE with coma (n 26)**

15.2 ± 7.7# 14.6 ± 7.8 16.4 ± 7.7^ 12.7 ± 5.5#^ # 0.02,

26 (40%) 18 (46%) 8 (31%)a 98 (53%)a a 0.04

**Control (n 185)**

**P value**

0.0007

0.006

^0.03

**(=without coma) (n 39)**

Gender male 37 (57%) 23 (59%) 14 (54%) 101 (55%)

*DOI: http://dx.doi.org/10.5772/intechopen.83580*

**3.5 Antiseizure drug (ASD) treatment**

**3.6 Outcome**

*3.6.1 Primary outcome*

*3.6.2 Secondary outcome*

(n = 5), fentanyl (n = 2), and thiopental (n = 3).

48 hours, whereas 31% (n = 20, m 12, f 8) died.

noid hemorrhage (n = 1), and cerebral abscess (n = 1).

**Variable NCSE (n 65) NCSE proper** 

*NCSE with coma to controls (respectively 0.05 and 0.0007).*

*to NCSE with coma (respectively 0.001 and 0.006).*

### **Table 4.**

*Head CT and MRI findings (some patients had both CT and MRI).*

*Nonconvulsive Status Epilepticus in Patients with Altered Mental Status Admitted to Hamad… DOI: http://dx.doi.org/10.5772/intechopen.83580*

### **3.5 Antiseizure drug (ASD) treatment**

Patients with NCSs (n = 20) were treated as follows: 18 with benzodiazepines, 10 with valproate IV, and 8 with levetiracetam plus valproate IV. The 65 NCSE patients received the following: lorazepam 4–8 mg IV or diazepam 10 mg IV (n = 45), levetiracetam IV or PO (n = 22), phenytoin IV (n = 21), valproate IV or PO (n = 18), topiramate PO (n = 5), phenobarbitone IV (n = 7), midazolam IV (n = 15), propofol (n = 5), fentanyl (n = 2), and thiopental (n = 3).

### **3.6 Outcome**

*Epilepsy - Advances in Diagnosis and Therapy*

first 48 hours of cEEG monitoring.

**3.4 NCSE proper and comatose NCSE**

and 2 from cardiac arrest.

Ischemia, intracerebral hemorrhage, subarachnoid & subdural hemorrhage

Polymicrogyria, cortical dysplasia,

comatose.

group than controls (NCSE 15%, controls 4%, p 0.004).

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

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

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

The NCSE group was further subdivided into two: NCSE proper without coma (n = 39) and comatose NCSE (n = 26) [32, 36]; NCSE proper is defined as clinical symptoms suggestive of SE with mild impairment of consciousness (absence status or complex focal SE); NCSE with coma-lateralized epileptiform discharges, NCSE with coma-generalized epileptiform discharges is defined as deep coma of various etiology with characteristic epileptiform EEG pattern but with no clinical motor signs of SE; NCSE proper patients are significantly younger than the comatose NCSE ones (**Table 5**). NCSE in comatose patients was often recorded after the first day of cEEG monitoring: during the first 24 hours in only 54% (n = 14/26), later but within 48 hours in 35% (n = 9/26), and in the third day in 11% (n = 3/26) of the patients; comparatively, NCSE proper was recorded during the first day in 77% (n = 30/39), later but within 48 hours in 10% (n = 4/39), and during the third day in 13% (n = 5/39) of patients. The 14 patients with early comatose NCSE (first 24 hs) suffered from head injury (n = 4), stroke (n = 4), and cardiac arrest (n = 3); and no etiology was found in three patients; comparatively, in the NCSE proper group (n = 30), 18 patients suffered from previous seizures, 5 from stroke, 3 from sepsis, 2 from head injury,

**Variable CT (n pts) MRI (n pts)**

Abnormal 32 (62%) 49 (49%) 0.17 33 (80%) 53 (55%) 0.01

Cortical atrophy 5 (10%) 10 (10%) 1.0 3 (7%) 6 (6%) 1.0

Hippocampal sclerosis 3 (6%) 0 0.04 3 (7%) 1 (1%) 0.08 Encephalomalacia 3 (7%) 10 (10%) 0.04 Meningeal/cortical enhancement 1 (2%) 2 (2%) 1.0 1 (2%) 2 (2%) 1.0

*Note: P values are calculated using Chi-square tests or Fisher's exact test wherever appropriate.*

*Head CT and MRI findings (some patients had both CT and MRI).*

**Controls (n 101)**

**P value**

14 (27%) 18 (18%) 0.21 16 (39%) 32 (33%) 0.56

**NCSE (n 41)**

**Controls (n 97)**

3 (7%) 0 0.02

**P value**

**NCSE (n 52)**

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

**50**

**Table 4.**

heterotopia

### *3.6.1 Primary outcome*

NCSE group (n = 65): 69% (n = 45, m 25, f 20) responded to treatment within 48 hours, whereas 31% (n = 20, m 12, f 8) died.

Control group (n = 185): 19% (n = 35, m 20, f 15) died. Thus, compared to the control group, death was more frequent in the NCSE group; there was additional statistical significance when NCSE proper was compared to comatose NCSE and when comatose NCSE was compared to controls (**Table 5**), with comatose patients exhibiting a more ominous outcome. The majority of patients with early occurrence of NCSs/NCSE = 65% (40 minutes to 3 hours) died (n = 13/20). Causes of death in NCSE (n = 20) group were distributed as follows: cardiac arrest (n = 6), hemorrhagic and ischemic strokes (n = 5), sepsis (n = 3), head injury (n = 4), subarachnoid hemorrhage (n = 1), and cerebral abscess (n = 1).

### *3.6.2 Secondary outcome*

Compared to controls, NCSE achieved complete recovery in 40% (n = 26, m 15, f 11) compared to controls 53% (n = 98, m 55, f 43); **Table 5** shows that this achieved statistical significance when comatose NCSE was compared to controls; NCSE group (NCSE proper plus comatose NCSE) had a longer hospital stay than the controls.


*Note: P values are calculated using Chi-square tests, Fisher exact tests and Student t tests wherever appropriate.*

*\* and § compare Death occuring respectively in NCSE without coma to NCSE with coma and also Death occurring in NCSE with coma to controls (respectively 0.05 and 0.0007).*

*§ and & compare patients and controls 's age respectively in NCSE group to controls and also in NCSE without coma to NCSE with coma (respectively 0.001 and 0.006).*

*# and ^ compare hospital stay respectively in NCSE group to controls and also in NCSE with coma to controls (respectively 0.02 and 0.03); symbol a compares complete recovery in NCSE with coma to controls (0.04)*

### **Table 5.**

*Occurrence and comparison of the listed variables in the NCSE groups and control group.*

### **Figure 1.** *(a) EEG shows left LPDs; patient received 4mg lorazepam IV and (b) EEG and clinical improvement following lorazepam IV.*

**53**

**Figure 2.**

*(possible NCSE ?).*

*Nonconvulsive Status Epilepticus in Patients with Altered Mental Status Admitted to Hamad…*

*(a) EEG shows left LPDs in a comatose patient following cardiac arrest; patient receives 10 mg Diazepam IV and (b) EEG shows dramatic improvement following Diazepam IV; however the patient remains comatose* 

*DOI: http://dx.doi.org/10.5772/intechopen.83580*

*Nonconvulsive Status Epilepticus in Patients with Altered Mental Status Admitted to Hamad… DOI: http://dx.doi.org/10.5772/intechopen.83580*

*Epilepsy - Advances in Diagnosis and Therapy*

**52**

**Figure 1.**

*following lorazepam IV.*

*(a) EEG shows left LPDs; patient received 4mg lorazepam IV and (b) EEG and clinical improvement* 

### **Figure 2.**

*(a) EEG shows left LPDs in a comatose patient following cardiac arrest; patient receives 10 mg Diazepam IV and (b) EEG shows dramatic improvement following Diazepam IV; however the patient remains comatose (possible NCSE ?).*

### **Figure 3.**

*(a) EEG shows evolving GPDs with triphasic morphology and (b) EEG demonstrates some improvement following Diazepam; however the patient remained comatose.*

**55**

**Figure 4.**

*Nonconvulsive Status Epilepticus in Patients with Altered Mental Status Admitted to Hamad…*

*(a) EEG shows predominantly left sided LPDs with triphasic morphology; 32 years old male given baclofen 30 mg for spasticity the first day of admission; 2 days later he presented an altered mental status with "akinetic mutism"; patient was given 6 mg lorazepam IV bolus. (b) Dramatic improvement in EEG and clinical status following IV lorazepam ; patient recovered completely, started talking and moving around normally; he was* 

*found to have a moderate to severe renal impairment (responsible for baclofen intoxication ?).*

*DOI: http://dx.doi.org/10.5772/intechopen.83580*

*Nonconvulsive Status Epilepticus in Patients with Altered Mental Status Admitted to Hamad… DOI: http://dx.doi.org/10.5772/intechopen.83580*

*Epilepsy - Advances in Diagnosis and Therapy*

**54**

**Figure 3.**

*(a) EEG shows evolving GPDs with triphasic morphology and (b) EEG demonstrates some improvement* 

*following Diazepam; however the patient remained comatose.*

### **Figure 4.**

*(a) EEG shows predominantly left sided LPDs with triphasic morphology; 32 years old male given baclofen 30 mg for spasticity the first day of admission; 2 days later he presented an altered mental status with "akinetic mutism"; patient was given 6 mg lorazepam IV bolus. (b) Dramatic improvement in EEG and clinical status following IV lorazepam ; patient recovered completely, started talking and moving around normally; he was found to have a moderate to severe renal impairment (responsible for baclofen intoxication ?).*
