TY - JOUR
T1 - The risk of unprovoked seizure occurrence after status epilepticus in adults
AU - Lattanzi, S
AU - Orlandi, N
AU - Giovannini, G
AU - Brigo, F
AU - Trinka, E
AU - Meletti, S
N1 - Lehr-KH Meran: “Franz Tappeiner” Hospital, Merano, Italy
Trinka: Department of Neurology, Neurointensive Care, and Neurorehabilitation, Christian Doppler University Hospital, Paracelsus Medical University, Member of EpiCARE, Salzburg, Austria; Neuroscience Institute, Center for Cognitive Neuroscience, Christian Doppler University Hospital Salzburg, Salzburg, Austria
PY - 2024/2/10
Y1 - 2024/2/10
N2 - ObjectiveStatus epilepticus (SE) may lead to long-term consequences. This study evaluated the risk and predictors of seizure occurrence after SE, with a focus on SE due to acute symptomatic etiologies.MethodsProspectively collected data about adults surviving a first non-hypoxic SE were reviewed. The outcome was the occurrence of unprovoked seizures during the follow-up. Kaplan-Meier survival curve analysis and log-rank test were used to analyze the time to seizure occurrence and determine the statistical significance between etiological groups. Three subcategories within acute etiology were considered according to the presence of the following: (1) structural lesion (acute-primary); (2) brain involvement during systemic disorders (acute-secondary); and (3) drug or alcohol intoxication/withdrawal (acute-toxic). Cox proportional hazards model was adopted to estimate hazard ratios (HRs) with the 95% confidence intervals (CIs).ResultsTwo hundreds fifty-seven individuals were included. Fifty-four subjects (21.0%) developed seizures after a median of 9.9 (interquartile range 4.3-21.7) months after SE. The estimated 1-, 2-, and 5-year rates of seizure occurrence according to acute SE etiologies were 19.4%, 23.4%, and 30.1%, respectively, for acute-primary central nervous system (CNS) pathology; 2.2%, 2.2%, and 8.7%, respectively, for acute-secondary CNS pathology; and 0%, 9.1%, and 9.1%, respectively, for acute-toxic causes. Five-year rates of seizure occurrence for non-acute SE causes were 33.9% for remote, 65.7% for progressive, and 25.9% for unknown etiologies. In multivariate Cox regression model, progressive etiology (adjusted HR [adjHR] 2.27, 95% CI 1.12-4.58), SE with prominent motor phenomena evolving in non-convulsive SE (adjHR 3.17, 95% CI 1.38-7.25), and non-convulsive SE (adjHR 2.38, 95% CI 1.16-4.90) were independently associated with higher hazards of unprovoked seizures. Older people (adjHR .98, 95% CI .96-.99) and people with SE due to acute-secondary CNS pathology (adjHR .18, 95% CI .04-.82) were at decreased risk of seizure occurrence.SignificanceSE carries a risk of subsequent seizures. Both the underlying cause and epileptogenic effects of SE are likely to contribute.
AB - ObjectiveStatus epilepticus (SE) may lead to long-term consequences. This study evaluated the risk and predictors of seizure occurrence after SE, with a focus on SE due to acute symptomatic etiologies.MethodsProspectively collected data about adults surviving a first non-hypoxic SE were reviewed. The outcome was the occurrence of unprovoked seizures during the follow-up. Kaplan-Meier survival curve analysis and log-rank test were used to analyze the time to seizure occurrence and determine the statistical significance between etiological groups. Three subcategories within acute etiology were considered according to the presence of the following: (1) structural lesion (acute-primary); (2) brain involvement during systemic disorders (acute-secondary); and (3) drug or alcohol intoxication/withdrawal (acute-toxic). Cox proportional hazards model was adopted to estimate hazard ratios (HRs) with the 95% confidence intervals (CIs).ResultsTwo hundreds fifty-seven individuals were included. Fifty-four subjects (21.0%) developed seizures after a median of 9.9 (interquartile range 4.3-21.7) months after SE. The estimated 1-, 2-, and 5-year rates of seizure occurrence according to acute SE etiologies were 19.4%, 23.4%, and 30.1%, respectively, for acute-primary central nervous system (CNS) pathology; 2.2%, 2.2%, and 8.7%, respectively, for acute-secondary CNS pathology; and 0%, 9.1%, and 9.1%, respectively, for acute-toxic causes. Five-year rates of seizure occurrence for non-acute SE causes were 33.9% for remote, 65.7% for progressive, and 25.9% for unknown etiologies. In multivariate Cox regression model, progressive etiology (adjusted HR [adjHR] 2.27, 95% CI 1.12-4.58), SE with prominent motor phenomena evolving in non-convulsive SE (adjHR 3.17, 95% CI 1.38-7.25), and non-convulsive SE (adjHR 2.38, 95% CI 1.16-4.90) were independently associated with higher hazards of unprovoked seizures. Older people (adjHR .98, 95% CI .96-.99) and people with SE due to acute-secondary CNS pathology (adjHR .18, 95% CI .04-.82) were at decreased risk of seizure occurrence.SignificanceSE carries a risk of subsequent seizures. Both the underlying cause and epileptogenic effects of SE are likely to contribute.
KW - acute symptomatic
KW - antiseizure medications
KW - etiology
KW - status epilepticus
KW - DEFINITION
KW - CRITERIA
KW - Seizures/epidemiology
KW - Alcoholism
KW - Humans
KW - Kaplan-Meier Estimate
KW - Proportional Hazards Models
KW - Status Epilepticus/etiology
KW - Anticonvulsants/therapeutic use
KW - Adult
KW - Aged
U2 - 10.1111/epi.17912
DO - 10.1111/epi.17912
M3 - Original Article (Journal)
C2 - 38339985
SN - 0013-9580
VL - 65
SP - 1006
EP - 1016
JO - EPILEPSIA
JF - EPILEPSIA
IS - 4
ER -