Epileptiform Abnormalities in Acute Ischemic Stroke: Impact on Clinical Management and Outcomes

Abstract

Purpose:

Studies examining seizures (Szs) and epileptiform abnormalities (EAs) using continuous EEG in acute ischemic stroke (AIS) are limited. Therefore, we aimed to describe the prevalence of Sz and EA in AIS, its impact on anti-Sz drug management, and association with discharge outcomes.

Methods:

The study included 132 patients with AIS who underwent continuous EEG monitoring >6 hours. Continuous EEG was reviewed for background, Sz and EA (lateralized periodic discharges [LPD], generalized periodic discharges, lateralized rhythmic delta activity, and sporadic epileptiform discharges). Relevant clinical, demographic, and imaging factors were abstracted to identify risk factors for Sz and EA. Outcomes included all-cause mortality, functional outcome at discharge (good outcome as modified Rankin scale of 0–2 and poor outcome as modified Rankin scale of 3–6) and changes to anti-Sz drugs (escalation or de-escalation).

Results:

The frequency of Sz was 7.6%, and EA was 37.9%. Patients with Sz or EA were more likely to have cortical involvement (84.6% vs. 67.5% P = 0.028). Among the EAs, the presence of LPD was associated with an increased risk of Sz (25.9% in LPD vs. 2.9% without LPD, P = 0.001). Overall, 21.2% patients had anti-Sz drug changes because of continuous EEG findings, 16.7% escalation and 4.5% de-escalation. The presence of EA or Sz was not associated with in-hospital mortality or discharge functional outcomes.

Conclusions:

Despite the high incidence of EA, the rate of Sz in AIS is relatively lower and is associated with the presence of LPDs. These continuous EEG findings resulted in anti-Sz drug changes in one-fifth of the cohort. Epileptiform abnormality and Sz did not affect mortality or discharge functional outcomes.

The incidence of clinical seizures (Sz) complicating acute ischemic stroke (AIS) varies from 5% to 6%.¹ The main risk factors for the development of Sz in AIS include cortical involvement and presence of hemorrhage.¹ Over the last decade, a 10-fold increase in the use of continuous EEG (cEEG) in critically ill patients has led to increased detection of Sz, most of which are nonconvulsive seizures (NCSzs).^2,3 The rate of NCSz in patients with AIS has varied from 6% to 12% in prior studies.^4,5 Additionally, cEEG monitoring has identified various epileptiform abnormalities (EAs), which include rhythmic and periodic patterns of unclear clinical significance.⁶ A multicenter study of >4,500 patients demonstrated that the incidence of EAs in a heterogeneous cohort of patients is 30% to 40%.⁷ This incidence varies based on the etiology of acute brain injury,⁵ location of injury,^8,9 and mental status.¹⁰ Moreover, EAs have been shown to be associated with a high risk of Sz and worse functional outcomes in patients with intracerebral and subarachnoid hemorrhage.^8,11 However, the risk of development of EA and its impact on outcomes has not been well characterized in a large cohort of AIS patients. Further, whether this increased detection of Sz and EA impacts clinical management with anti-Sz drugs (ASDs) has also not been studied in AIS. Therefore, in this study, we aimed to examine the prevalence and risk factors for EAs and Szs on cEEG in a large cohort of AIS patients at a tertiary care stroke center, its impact on clinical management with ASDs and association with functional outcomes at discharge.

METHODS

Patient Selection

All patients ≥ 18 years of age with a primary diagnosis of AIS admitted to Grady Memorial Hospital who underwent cEEG of at least 6 hours duration between February 1, 2017 and January 30, 2019 were identified by retrospective chart review. Patients with a primary diagnosis of intracranial hemorrhage or infection with surrounding ischemic changes were excluded. The study was approved by the Emory University Institutional Review Board and Grady Memorial Hospital Research Oversight Committee. Because of the retrospective nature, consent was not required.

Clinical and Radiologic Variables

All acute ischemic strokes were confirmed radiologically by either head computed tomography or MRI. Clinical variables such as age, sex, National Institute of Health Stroke Scale (NIHSS), mental status at the time of cEEG, prior stroke, history of epilepsy, clinical Szs before cEEG, ASD use during hospitalization and at discharge, modified Rankin Scale (mRS) before admission, and any surgical intervention such as decompressive craniectomy were extracted. Details of stroke such as location (anterior circulation vs. posterior circulation), mechanism of stroke according to TOAST classification,¹² treatment interventions such as IV alteplase, and thrombectomy were also collected. Computed tomography without contrast or MRI when available, which was closest to cEEG monitoring, was reviewed by an independent reviewer (E.L.) masked to the EEG data and patient variables. Images were analyzed for the presence of cortical involvement, midline shift as measured in mm, and the presence of hemorrhagic transformation. Hemorrhagic transformation was defined as the presence of any hemorrhage in the area of infarction in two consecutive slides. Decompressive craniectomy and hemorrhagic transformation were considered only when seen on scans before or during cEEG.

EEG Acquisition and Interpretation

All patients underwent cEEG using the 10 to 20 international system of electrode placement with 21-disk scalp electrodes and acquired using Natus NeuroWorks EEG Software. A single investigator (D.D.) masked to the clinical data reviewed the EEG reports and abstracted the following variables: duration of recording, the day of recording from admission, EEG background (alpha, beta, delta, theta, or mixed frequency background) as assessed by the predominant frequencies, presence of sleep structures (vertex waves, spindles, and K complexes), posterior dominant rhythm, and focal slowing. The interictal EEG patterns were classified according to the American Clinical Neurophysiology Society nomenclature.⁶ Patterns that were considered as EAs included lateralized periodic discharges (LPDs), lateralized rhythmic delta activity (LRDA), generalized periodic discharges (GPDs), bilateral independent periodic discharges, and sporadic epileptiform discharges (sEDs). Patients with both periodic patterns and sEDs were counted as having periodic pattern and were not included into sEDs. Generalized rhythmic delta activity with or without plus modifiers was excluded from EA.⁷ Ictal findings included electrographic or electroclinical Szs.

Treatment and ASD Management

Patients with AIS were treated per National Institute of Neurological Disorders and Stroke guidelines and recommendations. Anti-Sz drugs were used at the judgment of the treating physician for clear motor Szs, other spells suggestive of Szs such as forced gaze deviation, clinical deterioration of mental status presumed to be Szs, or for Sz prophylaxis in patients undergoing decompressive craniectomy. Management of Szs and EAs were up to the discretion of treating teams. Data regarding initiation of ASD before cEEG and any changes made during or after cEEG. Escalation of ASD treatment was defined initiation of new ASD or increase in the maintenance dose or additional loading dose by bolus administration and de-escalation was defined as decrease or discontinuation of prior ASD.

Outcomes

Outcome measures were all-cause mortality and functional outcome at discharge. Good functional outcome was defined as mRS of 0 to 2 and poor outcome as mRS of 3 to 6. We also examined the association of Sz/EA with ASD management in patients on and not on ASD before cEEG. Other outcomes included length of stay and discharge disposition among survivors, and the number of patients discharged on ASD.

Statistical Analysis

Baseline characteristics were compared between patients with versus without Sz/EA using Fisher exact test for categorical variables and Mann–Whitney U test for continuous variables. Multivariable stepwise logistic regression analysis was performed to identify the predictors of poor outcomes at discharge. Categorical variables are expressed as frequencies and percentages and continuous variables as median (interquartile range [IQR]). Statistical analysis was performed using IBM SPSS Statistics 20.0 (IBM Corp, Armonk, NY). For all analyses, a two-sided P value <0.05 was used for assessing statistical significance.

RESULTS

Baseline Characteristics

The overall study cohort included 132 patients. The median age was 66.5 years, 52.3% (n = 69) were women, and 59.1% (n = 78) were African American. Table 1 summarizes the demographic and clinical characteristics of patients. History of prior stroke was present in 34.1% (n = 45) of patients, and 6.8% (n = 9) had epilepsy. Median NIHSS on admission was 16.0 (IQR, 10.0–23.0). The majority (87.9%, n = 116) of patients had anterior circulation stroke, with 74.2% (n = 98) having cortical involvement. Cardioembolism was the most common etiology of AIS (44.7%, n = 59). Thrombolytics were administered in 21.2% (n = 28), mechanical thrombectomy was performed in 25.0% (n = 33), and 14.4% (n = 19) underwent decompressive craniectomy. The median time from admission to cEEG was 2.0 days (IQR, 1.0–5.0) and median overall duration being 24.0 hours (IQR, 19.0–43.8).

TABLE 1.

Baseline Characteristics of Patients With and Without Szs or EAs

Variables	Overall Cohort (n = 132)	Without Sz or EA (n = 80)	With Sz or EA (n = 52)	P
Age, years, median (IQR)	66.5 (55.3–77.8)	64.0 (56.0–75.0)	68.0 (53.3–82.0)	0.367
Women, n (%)	69 (52.3)	35 (43.8)	34 (65.4)	0.015*
Race, n (%)
Black	78 (59.1)	49 (61.3)	29 (55.8)	0.185
White	33 (25.0)	20 (25.0)	13 (25.0)
UTD	18 (13.6)	9 (11.3)	9 (17.3)
Others	3 (2.3)	2 (2.5)	1 (1.9)
History of epilepsy, n (%)	9 (6.8)	2 (2.5)	7 (13.5)	0.028*
Preadmission mRS	1.0 (0.0–3.0)	1.0 (0–3.0)	1.0 (1.0–3.0)	0.737
Prior stroke, n (%)	45 (34.1)	27 (33.8)	18 (34.6)	0.981
Coma, n (%)	35 (26.5)	19 (23.8)	16 (30.8)	0.372
Clinical seizure before cEEG, n (%)	41 (31.1)	23 (28.7)	18 (28.7)	0.477
ASDs initiated before cEEG, n (%)	66 (50.0)	39 (48.8)	27 (51.9)	0.722
Anesthetics during cEEG, n (%)	22 (16.7)	15 (18.8)	7 (13.5)	0.426
Use of ASDs during cEEG, n (%)	77 (58.3)	39 (48.8)	38 (73.1)	0.006*
Time to EEG, days, median (IQR)	2.0 (1.0–5.0)	2.0 (0.3–4.8)	2.5 (1.0–5.0)	0.375
Duration of cEEG, hours, median (IQR)	24.0 (19.0–43.8)	21.0 (18.0–27.3)	40.0 (24.0–64.0)	<0.001*
NIHSS, median (IQR)	16.0 (10.0–23.0)	16.0 (8.0–22.0)	18.0 (11.0–23.0)	0.306
IV thrombolysis (tPA), n (%)	28 (21.2)	17 (21.3)	11 (21.2)	0.989
Mechanical thrombectomy, n (%)	33 (25.0)	19 (23.8)	14 (26.9)	0.681
Decompressive hemicraniectomy, n (%)	19 (14.4)	8 (10.0)	11 (10.0)	0.082
Imaging, n (%)
Cortical involvement	98 (74.2)	54 (67.5)	44 (84.6)	0.028*
Hemorrhagic transformation	27 (20.5)	18 (22.5)	9 (17.3)	0.515
Midline shift	24 (18.2)	12 (15.0)	12 (15.0)	0.240
Anterior circulation stroke	116 (87.9)	69 (86.3)	47 (90.4)	0.477
Mechanism of stroke, n (%)
Large artery atherosclerosis	39 (29.5)	23 (28.7)	16 (30.8)	0.753
Cardio embolism	59 (44.7)	38 (47.5)	21 (40.4)
Small vessel disease	4 (3.0)	3 (3.8)	1 (1.9)
Stroke of other determined etiology	13 (9.8)	6 (7.5)	7 (13.5)
Cryptogenic stroke	17 (12.9)	10 (12.5)	7 (13.5)

^*P < 0.05.

ASD, anti-seizure drug; cEEG, continuous EEG; EA, epileptiform abnormalities (lateralized periodic discharges; lateralized rhythmic delta activity, generalized periodic discharges and sporadic epileptiform discharges); IQR, interquartile range; IV, intravenous; mRS, modified Rankin scale; NIHSS, NIH stroke scale; Sz, seizure; tPA, tissue plasminogen activator; UTD, unable to determine.

Patients with Sz or EA were more likely to be women (65.4% vs. 43.8%, P = 0.015), have cortical involvement (84.6% vs. 67.5%, P = 0.028), and had a longer duration of cEEG recording (40.0 hours [IQR, 24.0–64.0] vs. 21.0 hours [IQR, 18.0–27.3], P < 0.001) compared with those without Sz or EA (Table 1). There were no differences between patients with and without Sz or EA in mental status, clinical Szs before EEG, use of ASDs before EEG, severity of stroke in NIHSS, hemorrhagic transformation, etiology of stroke, and treatment interventions for stroke. Among the patients who were on ASD before cEEG, 32 were initiated on ASD because of witnessed clinical Sz, 5 had history of epilepsy, 4 had history of epilepsy and had a clinical seizure before cEEG, 20 patients had altered mental status presumed to be because of seizure, and 5 were started on ASD for Sz prophylaxis of unclear reasons.

Seizures and Epileptiform Abnormalities

The overall incidence of Sz and EA was 39.4%; Sz in 7.6% (n = 10), and EA in 37.9% (n = 50) of patients (Table 2). The time to occurrence of first Sz was variable ranging from 0 minutes to 33 hours and 45 minutes. The median time to first Sz was 104 minutes with IQR of 7 to 1,230 minutes. Of the 10 patients with seizures, 2 had <1 seizure per hour and 8 patients had >1 seizure per hour. Seizures were purely electrographic in eight patients and electroclinical in two patients, all with focal onset. Among those with Sz burden of >1 per hour, 6 had purely electrographic Szs and 2 had electroclinical Szs. By using the ILAE 2015 definition of status epilepticus, 3 patients had focal status epilepticus.¹³ Except for one, all Szs required treatment with ASD. The most common EAs seen were LPDs (20.5%, n = 27), followed by GPDs (12.9%, n = 17), LRDA (7.6%, n = 10), and sED in 3.0% (n = 4). Generalized rhythmic delta activity was seen in 7.6% (n = 10) and was not considered to be epileptiform based on previous studies.⁷ On univariate analysis, only LPDs were associated with occurrence of Sz (25.9% in LPD group vs. 2.9% without LPD, P = 0.001) and clinical Sz before EEG showed a trend toward increased risk of Sz but did not reach statistical significance (14.6% vs. 4.4%, P = 0.069). There was no difference in the risk of Sz in patients with and without LRDA (0.0% vs. 10%, P = 1.00), GPD (11.8% vs. 7.0%, P = 0.62), and sEDs (25.0% vs. 7.0%, P = 0.27).

TABLE 2.

Continuous EEG Findings in Acute Ischemic Stroke

EEG Variables	Seizure	LPD	LRDA	GPD	GRDA	Sporadic ED	Focal Slowing	Focal Attenuation
N (%)	10 (7.6)	27 (20.5)	10 (7.6)	17 (12.9)	10 (7.6)	4 (3.0)	70 (53.0)	33 (25.0)

ED, epileptiform discharge; GPD, generalized periodic discharge; GRDA, generalized rhythmic delta activity; LPD, lateralized periodic discharge; LRDA, lateralized rhythmic delta activity.

Impact on ASD Treatment

After cEEG, changes to ASDs regimen occurred in 21.2% (n = 28) of patients: escalation of treatment in 16.7% (n = 22) of the patients, and de-escalation in 4.5% (n = 6). We further analyzed the changes in treatment patterns in patients who were on ASDs before EEG and those who were not. In both groups, findings of Sz and EA resulted in significant ASD changes compared with patients who did not have Sz or EA (P < 0.001). Figure 1 summarizes the changes to ASDs in both groups according to the EEG findings. In both groups, Sz resulted in an escalation of treatment (initiation of ASD or an increase in existing ASD) in 100% of patients. For cEEG with EA alone without Sz, escalation of treatment occurred in 4 of 20 patients (20.0%) who were already on ASD and in 8 of 22 patients (36.7%) who were not on prior ASD. In patients on prior ASDs who had nonepileptiform EEG (i.e., no Sz or EA), ASDs were discontinued in 6 of 39 patients (15.4%). In patients not on ASDs who had nonepileptiform EEG, 0 of 4 (0%) were started on ASDs.

FIG. 1.

Anti-Sz drug changes by continuous EEG findings. ASD, anti-seizure drug; EA, epileptiform abnormalities (include lateralized periodic discharges, generalized periodic discharges, lateralized rhythmic delta activity, and sporadic epileptiform discharges); Sz, seizure.

Outcomes

In-hospital mortality was 17.4% (n = 23) in the overall study cohort. There was no statistically significant difference in mortality, poor functional outcome (mRS, 3–6), length of stay, or discharge disposition between patients with versus without Sz or EA (Table 3).We further analyzed patients with good outcomes (mRS, 0–2) between those with EA/Sz (6/52) and without EA/Sz (8/80) and found no statistically significant difference among them at discharge (11.5% vs. 10.0%, P = 0.780). Among survivors (n = 109), there was a trend toward worse median mRS (5.0 [IQR, 4.0– 5.0]) in patients with Sz or EA compared with those without Sz or EA (4.0 [IQR, 4.0–5.0]); however, this did not reach statistical significance (P = 0.055). Overall, 42.2% of patients were discharged on ASDs. Patients with Sz or EA were more likely to be discharged on ASDs compared with those without Sz or EA (56.8% vs. 32.3%, P < 0.011).

TABLE 3.

Outcomes at Discharge

All Patients	Overall Cohort (n = 80)	Without Sz or EA (n = 80)	With Sz or EA (n = 52)	P
Poor outcome at discharge (mRS ≥ 3)	118 (89.4%)	72 (90.0%)	46 (88.5%)	0.779
Inhospital mortality	23 (17.4%)	15 (18.8%)	8 (15.4%)	0.815
Survivors	Overall Cohort (n = 109)	Without Sz or EA (n = 65)	With Sz or EA (n = 44)	P
Length of stay	17.0 (10.0–27.5)	16.0 (11.0–25.0)	17.5 (9.0–30.75)	0.795
Discharge disposition
Home	24 (22.0%)	17 (26.2%)	7 (26.2%)	0.627
Acute rehab	23 (21.1%)	12 (18.5%)	11 (25.0%)
LTAC/SNF	45 (41.3%)	26 (40.0)	19 (43.2%)
Hospice	16 (14.7%)	9 (13.8%)	7 (15.9)
ASDs at discharge	46 (42.2%)	21 (32.3%)	25 (56.8%)	0.011*
mRS at discharge	5.0 (4.0–5.0)	4 (3.5–5.0)	5 (4.0–5.0)	0.055

^*P < 0.05.

ASD, anti-seizure drug; EA, epileptiform abnormalities (lateralized periodic discharges; lateralized rhythmic delta activity, generalized periodic discharges, and sporadic epileptiform discharges); LTAC, long-term acute care facility; mRS, modified Rankin scale; SNF, skilled nursing facility; Sz, seizure.

On univariate analysis, higher NIHSS (17.0 [IQR, 10.5– 23.0] vs. 5.5 [IQR, 3.0–18.25], P = 0.011), worse preadmission mRS (1 [IQR, 1.0–3.0] vs. 0.0 [IQR, 0.0–1.0], P = 0.019), and lack of posterior dominant rhythm on EEG (74.6% vs. 25.4%, P = 0.025) were associated with poor functional outcome (mRS, 3–6). On multivariable analysis using a stepwise logistic regression model after adjusting for various baseline factors (age, sex, mental status, prior stroke, and history of epilepsy), the only factor predictive of poor outcome was higher NIHSS (adjusted odds ratio, 1.10; 95% confidence interval, 1.02–1.18; P = 0.019). Clinical Szs before cEEG monitoring were not associated with poor outcomes.

DISCUSSION

In our study of patients with AIS who underwent cEEG monitoring, the incidence of Sz and EA was 7.6% and 37.9%, respectively. Patients with Sz or EA were more likely to have cortical involvement and more likely to be treated with ASDs during hospitalization and at discharge. Further, ours is the first study to demonstrate changes in acute ASD management based on cEEG findings, which occurred in 21.2% of patients. Finally, we found that the presence of Sz, EA, or any of the background EEG features were not associated with outcomes at discharge, and only admission NIHSS independently predicted poor functional outcome at discharge.

In the studies using EEG in AIS, the incidence of electrographic Sz has been variable ranging from 6.0% to 16.8%.^4,5,14,15 Some of these differences in the rates of Sz among these studies and ours are likely attributable to the variations in duration of recording. Studies using routine 30-minute EEGs had a lower incidence of Sz 6.5%,¹⁴ whereas those with cEEGs had a higher rate up to 12% to 16.8%.^4,15 Although we used longer duration recordings (>6 hours), the incidence of Sz was significantly lower compared with other recent studies.^4,15 There are several other plausible reasons for these differences. First, the selection criteria of patients undergoing cEEG were perhaps different in each study. In a study of 81 patients with AIS, Scoppettuolo et al.⁴ examined only patients who had neurologic deterioration and hence likely had higher rates of Sz compared with our study, which did not include such criteria for cEEG. Second, the variable proportion of patients who received ASDs before EEG could have influenced the rate of Sz. In the previous studies, it is unclear what percentage of patients received ASDs before cEEG.^4,15 In our study, half of the patients were on ASDs before EEG either because of witnessed clinical Sz, neurologic deterioration attributed to Sz, or other indications for prophylaxis. However, the incidence of EA in our study is similar to prior studies using American Clinical Neurophysiology Society intensive care unit EEG nomenclature in the range of 40% to 50%, indicating that though the risk of Sz is variable, EAs are highly prevalent in this population.

Our study confirms the previously identified association of Sz with cortical involvement in ischemic stroke¹⁶ and intracranial hemorrhage.^8,17 However, because of the few patients and many having multiple lobe involvement, we could not discern if the involvement of specific brain areas such as temporal lobe or insula have a higher propensity to Sz or EA. Likewise, the presence of LPDs was associated with increased risk of Sz as compared with LRDA, GPD, and sED. This finding is consistent with previous studies in which LPDs carried a higher risk of Sz at any frequency compared with LRDA and GPD, which was associated with Sz only when related to plus modifiers and higher frequency.⁷ Interestingly, on univariate analysis, women were more likely to have Sz and EA as compared with men. While this association has not been found consistently across studies,^4,15,18 it is found that women tend to have delays in stroke treatment, often resulting in large stroke size and poor outcomes.^19,20 Further studies are needed to examine sex-specific differences in EA/Sz in patients with AIS.

To our knowledge, ours is the first study to examine the impact of cEEG on ASD management in AIS patients. We found that cEEG resulted in ASD changes in 21.2% of the patients. This is lower compared with a previous study of 300 patients with heterogenous etiology who underwent cEEG in which ASD modification occurred in 51.7% of patients.²¹ This difference is likely because of the higher incidence of electrographic Sz (28.0%) in this study, compared with our study, which included patients with AIS and had lower (7.6%) rates of Sz. As expected, the detection of Sz resulted in an escalation of ASD in 100% of patients in our study. However, treatment patterns in patients with EAs were variable. Epileptiform abnormalities resulted in ASD changes in 20.0% to 36.7% of patients, which is consistent with findings from a multicenter study that found wide variability in ASD treatment.²² In our study, 28.6% of the ASD escalations were because of EA alone without any Sz. This is not surprising given that majority of EA were LPD, LRDA, and GPDs, which lie on the spectrum ictal–interictal continuum (only 3% being sED), and physicians likely have a different threshold of treating ictal–interictal continuum patterns compared with sEDs. When the ASD escalation was because of EA alone, we speculate that the goals of treatment were variable. Anti-Sz drugs may have been given for prevention of electrographic and electroclinical Szs, as certain periodic and rhythmic patterns have been shown to be associated with a high risk of Szs. But a proportion of ASD escalations may have been because of the concern that the patterns themselves may represent nonconvulsive status epilepticus. Moreover, at the time of discharge, 42.2% of patients were discharged on ASD, half of whom did not have any EA or Sz on cEEG. These findings indicate that a large proportion of patients with suspected acute symptomatic Szs or EA/Sz on cEEG are discharged on ASDs. With the wide variability in ASD use and its potential for cognitive side effects,²³ future studies should examine the short- and long-term impact of ASD treatment on outcomes including cognition and rehabilitation.

Despite the high prevalence of EAs in our cohort, similar to previous studies, we did not find a significant association of EA or Sz with outcomes. The only predictive factor associated with poor functional outcome on admission was NIHSS, which is consistent with findings from previous studies using routine EEGs.²⁴ Although there is emerging evidence to suggest that EAs and Sz are associated with metabolic crisis,²⁵ lower brain tissue oxygen,²⁶ and worsening ischemia,²⁷ their association with the poor outcome has not been conclusively proven because of conflicting reports.^4,15,18,28 It has been observed that in severe neurologic injury, the Sz or EAs are too small to be detected on scalp EEG and that severe injury causes less Sz and EA in animal models.^29,30 In a prospective study of 100 patients with sepsis undergoing cEEG, EA and Sz were indeed more common in patients with less severe critical illness.³¹ Given that our overall cohort consisted of severe strokes with median NIHSS of 16.0, which is significantly higher compared with previous studies, it is likely that we were not able to replicate the findings from earlier studies.^15,18 Further, it should be noted that perhaps cognitive outcomes are more likely to be affected by Sz and EAs³² rather than functional outcomes, which were not examined in our study.

Study Limitations

Our study has several limitations such as retrospective design, single-center data, the minimum duration of 6 hours, and inclusion of severe strokes with higher rates of thrombectomy and decompressive craniectomy than the reported nationwide rates,³³ which limits the generalizability of our findings. First, since cEEG was ordered at the discretion of treating teams, this may have led to the inclusion of sicker AIS patients, the majority of whom had poor outcomes. It is possible that the study was underpowered to detect a statistically significant difference in outcomes. Second, the impact on ASD changes in response to cEEG findings was abstracted by retrospective chart review, which may have limited examining other factors that could have influenced the decision making. Third, additional modifiers for the rhythmic and periodic patterns such as their prevalence, frequency and plus features were not analyzed. Finally, we did not account for the Sz burden or the burden of EAs, which could have affected outcomes.

CONCLUSIONS

In patients with severe AIS who underwent cEEG monitoring, the incidence of Sz and EA was 7.6% and 37.9%, respectively. Among the EAs, only LPDs was associated with an increased risk of Sz. Patients with Sz or EA were more likely to have cortical involvement and more likely to be treated with ASDs during hospitalization and at discharge. The presence of Sz or EA on cEEG resulted in changes in ASD treatment in 21.2% of patients. There was no significant association of Sz or EA with mortality or functional outcome. Future prospective studies targeting a broader patient population with variable stroke severity and examining further characteristics such as frequency, prevalence, and modifiers of EA are needed to understand further the impact of EA and Sz on treatment and outcomes.