Acute symptomatic status epilepticus: Splitting or lumping? A proposal of classification based on real‐world data

Author:

Lattanzi Simona1ORCID,Giovannini Giada23ORCID,Brigo Francesco456ORCID,Orlandi Niccolò27ORCID,Trinka Eugen8910ORCID,Meletti Stefano27ORCID

Affiliation:

1. Department of Experimental and Clinical Medicine, Neurological Clinic Marche Polytechnic University Ancona Italy

2. Neurology Unit OCB Hospital, AOU Modena Modena Italy

3. PhD Program in Clinical and Experimental Medicine University of Modena and Reggio Emilia Modena Italy

4. Department of Neurology Hospital of Merano (SABES‐ASDAA) Merano Italy

5. Lehrkrankenhaus der Paracelsus Medizinischen Privatuniversität Salzburg Austria

6. Innovation, Research and Teaching Service (SABES‐ASDAA) Bolzano Italy

7. Department of Biomedical, Metabolic, and Neural Science, Center for Neuroscience and Neurotechnology University of Modena and Reggio Emilia Modena Italy

8. Department of Neurology, Christian Doppler Klinik Paracelsus Medical University Salzburg Austria

9. Center for Cognitive Neuroscience Salzburg Austria

10. Public Health, Health Services Research, and HTA University for Health Sciences, Medical Informatics, and Technology Hall in Tirol Austria

Abstract

AbstractThis study aimed to group acute symptomatic etiologies of consecutive episodes of status epilepticus (SE) into different subcategories and explore their associations with clinical outcome. Etiologies were first categorized as “acute,” “remote,” “progressive,” “SE in defined electroclinical syndromes,” and “unknown.” Four subcategories of acute etiologies were then defined: (1) withdrawal, low levels, or inappropriate prescription of antiseizure medications, or sleep deprivation in patients with pre‐existing epilepsy; (2) acute insults to central nervous system (CNS; “acute‐primary CNS”); (3) CNS pathology secondary to metabolic disturbances, systemic infection, or fever (“acute‐secondary CNS”); and (4) drug/alcohol intoxication or withdrawal. Poor outcome at discharge, defined as worsening of clinical conditions (modified Rankin Scale [mRS] at discharge higher than mRS at baseline), was reported in 55.6% of cases. The etiological categories of acute‐primary CNS (odds ratio [OR] = 3.61, 95% confidence interval [CI] = 2.11–6.18), acute‐secondary CNS (OR = 1.80, 95% CI = 1.11–2.91), and progressive SE (OR = 2.65, 95% CI = 1.57–4.47), age (OR = 1.05, 95% CI = 1.04–1.06), nonconvulsive semiology with coma (OR = 3.06, 95% CI = 1.52–6.17), and refractoriness (OR = 4.31, 95% CI = 2.39–7.77) and superrefractoriness to treatment (OR = 8.24, 95% CI = 3.51–19.36) increased the odds of poor outcome. Heterogeneity exists within the spectrum of acute symptomatic causes of SE, and distinct etiological subcategories may inform about the clinical outcome.

Publisher

Wiley

Subject

Neurology (clinical),Neurology

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