Dataset Information

Levetiracetam for Status Epilepticus in Adults: A Systematic Review.

ABSTRACT:

Background

Status epilepticus (SE) is a neurologic emergency with potential for substantial mortality and morbidity. Parenteral benzodiazepine is the established first-line treatment but fails to control SE in about one-third of patients. Levetiracetam may be used for SE that is refractory to benzodiazepine therapy.

Objective

To examine, by means of a systematic review, the role of IV levetiracetam for the treatment of SE in adults.

Data sources

MEDLINE, Embase, CENTRAL, and CINAHL databases were searched, from inception to August 18, 2020.

Study selection and data extraction

Included in this review were prospective randomized controlled trials comparing levetiracetam with another antiepileptic drug, given with or after a benzodiazepine, in adult patients with SE. The primary outcome was cessation of SE. Quality of evidence was assessed with the Cochrane risk-of-bias tool. Characteristics of the included studies were reported using descriptive statistics.

Data synthesis

Five studies compared IV levetiracetam with valproic acid, phenytoin (or its prodrug fosphenytoin), or both. All 5 studies found no statistically significant differences in efficacy or safety end points. There were numerically more cases of hypotension and respiratory failure with phenytoin, and more cases of psychiatric adverse effects (e.g., post-ictal psychosis) with levetiracetam.

Conclusions

Available evidence suggests that levetiracetam is as effective as valproic acid or phenytoin for the cessation of SE in adults. Other factors should therefore dictate the choice of antiepileptic drug for patients with SE, such as adverse effect profile, logistics of administration, drug cost, inclusion on hospital formularies, and drug availability.

SUBMITTER: Webb CA

PROVIDER: S-EPMC8677000 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Objective Status epilepticus (SE) is a common neurological emergency that is defined as a prolonged seizure or a series of seizures which often leads to irreversible damage. Levetiracetam (LEV) and valproate (VPA) are second-line anti-seizure drugs that are frequently used in patients with established SE (ESE). This meta-analysis compared the efficacy and safety of LEV and VPA for the treatment of ESE. Method MEDLINE, EMBASE, Central Register of Controlled Trials (CENTRAL), and clinicaltrials.gov were searched by two authors, which identified six randomized controlled trials (RCTs) that compared LEV and VPA for ESE. Results The six RCTs included 1213 patients (LEV group, n = 593; VPA group, n = 620). Integrated patient data information display LEV was not superior to VPA in terms of clinical seizure termination (63.55% vs. 64.08%, respectively; relative risk [RR] = 1.03, 95% confidence interval [CI] = 0.94–1.11, p = 0.55), with no significant differences between LEV and VPA in terms of good functional outcome at discharge (Glasgow Outcome Scale [GOS] = 4 or 5), intensive care unit (ICU) admission, adverse events, and mortality. There was no statistically significant difference between the two drugs in different age groups. Previous multicenter studies have demonstrated that VPA was slightly more effective than LEV, whereas single-center studies showed the opposite results. In addition, LEV and VPA had similar rates of clinical seizure termination, ICU admission, and adverse events between the age subgroups (ages <18 and >18 years). Conclusions Levetiracetam (LEV) was not superior to valproate (VPA) in terms of efficacy or safety outcomes. In addition, children (<18 years) and adults (>18 years) might have similar responses to LEV and VPA. Additional RCTs are required to verify our results. Highlights • Levetiracetam (LEV) was not superior to valproate (VPA) in terms of efficacy outcomes.• There were no significant differences in the safety outcomes between LEV and VPA.• The efficacy of VPA was better in children than in adults, but the safety profile was opposite.• There is no difference in efficacy and safety between children and adults with LEV.

Project description:BackgroundElectrical status epilepticus during slow-wave sleep (ESESS) which is also known as continuous spike-wave of slow sleep (CSWSS) is type of electroencephalographic (EEG) pattern which is seen in ESESS/CSWSS/epilepsy aphasia spectrum. This EEG pattern can occur alone or with other syndromes. Its etiology is not clear, however, brain malformations, immune disorders, and genetic etiologies are suspected to contribute. We aimed to perform a systematic review of all genetic etiologies which have been reported to associate with ESESS/CSWSS/epilepsy-aphasia spectrum. We further aimed to identify the common underlying pathway which can explain it. To our knowledge, there is no available systematic review of genetic etiologies of ESESS/CSWSS/epilepsy-aphasia spectrum. MEDLINE, EMBASE, PubMed and Cochrane review database were searched, using terms specific to electrical status epilepticus during sleep or continuous spike-wave discharges during slow sleep or epilepsy-aphasia spectrum and of studies of genetic etiologies. These included monogenic mutations and copy number variations (CNVs). For each suspected dosage-sensitive gene, further studies were performed through OMIM and PubMed database.ResultsTwenty-six studies out of the 136 identified studies satisfied our inclusion criteria. I51 cases were identified among those 26 studies. 16 studies reported 11 monogenic mutations: SCN2A (N?=?6), NHE6/SLC9A6 (N?=?1), DRPLA/ ATN1 (N?=?1), Neuroserpin/SRPX2 (N?=?1), OPA3 (N?=?1), KCNQ2 (N?=?2), KCNA2 (N?=?5), GRIN2A (N?=?34), CNKSR2 (N?=?2), SLC6A1 (N?=?2) and KCNB1 (N?=?5). 10 studies reported 89 CNVs including 9 recurrent ones: Xp22.12 deletion encompassing CNKSR2 (N?=?6), 16p13 deletion encompassing GRIN2A (N?=?4), 15q11.2-13.1 duplication (N?=?15), 3q29 duplication (N?=?11), 11p13 duplication (N?=?2), 10q21.3 deletion (N?=?2), 3q25 deletion (N?=?2), 8p23.3 deletion (N?=?2) and 9p24.2 (N?=?2). 68 of the reported genetic etiologies including monogenic mutations and CNVs were detected in patients with ESESS/CSWSS/epilepsy aphasia spectrum solely. The most common underlying pathway was channelopathy (N?=?56).ConclusionsOur review suggests that genetic etiologies have a role to play in the occurrence of ESESS/CSWSS/epilepsy-aphasia spectrum. The common underlying pathway is channelopathy. Therefore we propose more genetic studies to be done for more discoveries which can pave a way for proper drug identification. We also suggest development of common cut-off value for spike-wave index to ensure common language among clinicians and researchers.