The Utility of Quantitative EEG in Detecting Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage.

SUMMARY: In this review, we discuss the utility of quantitative EEG parameters for the detection of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage in the context of the complex pathophysiology of DCI and the limitations of current diagnostic methods. Because of the multifactorial pathophysiology of DCI, methodologies solely assessing blood vessel narrowing (vasospasm) are insufficient to detect all DCI. Quantitative EEG has facilitated the exploration of EEG as a diagnostic modality of DCI. Multiple quantitative EEG parameters such as alpha power, relative alpha variability, and alpha/delta ratio show reliable detection of DCI in multiple studies. Recent studies on epileptiform abnormalities suggest that their potential for the detection of DCI. Quantitative EEG is a promising, continuous, noninvasive, monitoring modality of DCI implementable in daily practice. Future work should validate these parameters in larger populations, facilitated by the development of automated detection algorithms and multimodal data integration.

Stroke Prevention After Intracerebral Hemorrhage: Where Are We Now?

PURPOSE OF REVIEW: Patients after intracerebral hemorrhage (ICH) are at high risk of both ischemic stroke and recurrent ICH, and stroke prevention after ICH is important to improve the long-term outcomes in this patient population. The objective of this article is to review the current guidelines on stroke prevention measures after ICH as well as the new findings and controversies for future guidance. RECENT FINDINGS: Intensive blood pressure reduction might benefit ICH survivors significantly. Cholesterol levels and the risk of ICH have an inverse relationship, but statin therapy after ICH might be still beneficial. Anticoagulation in atrial fibrillation after ICH specifically with novel oral anticoagulants may be associated with better long-term outcomes. Left atrial appendage occlusion may be an alternative for stroke prevention in ICH survivors with atrial fibrillation for whom long-term anticoagulation therapy is contraindicated. While complete individualized risk assessment is imperative to prevent stroke after ICH, future research is required to address current controversies and knowledge gap in this topic.

Risk of seizure clusters and status epilepticus following rapid and ultra-rapid medication discontinuation during intracranial EEG monitoring.

OBJECTIVE: Anti-seizure medications (ASMs) are discontinued in the course of intracranial EEG (iEEG) monitoring for presurgical evaluation. The ASM withdrawal facilitates an emergence of seizures but may also precipitate seizure clusters (SC) and status epilepticus (SE). The aim of this study was to compare the rates of SC and SE during the ultra-rapid withdrawal (URW) and rapid withdrawal (RW) of ASMs during iEEG. METHODS: We performed a retrospective observational study of all consecutive patients with drug resistant epilepsy who completed iEEG at our comprehensive epilepsy center from 2012-2018. SC was defined as three or more seizures in 24 h with a return to baseline between the events. SE was defined as ≥ 5 min of clinical seizure or ≥ 10 min of ictal electrographic activity or series of seizures with no return to the neurological baseline between the events. RESULTS: Of 107 patients who completed iEEG with intracranial grid or strip electrodes, 46 (43%) were male. Median age at the time of iEEG was 35.4 years (interquartile range [IQR], 26.4 - 44.9). Ninety patients (84.1%) had all AEDs held on admission, while 16 patients (15%) underwent a rapid taper. The median time to first seizure was 15.1 (8.2 - 22.6) h. Sixty-two patients (57.9%) developed SC, while 10 (9.4%) developed SE. Twenty-six patients (36.1%) with these complications required intravenous lorazepam or other rescue ASMs, while the remaining patients had spontaneous resolution of seizures; intubations were not required. While there were differences in the proportions in patients who experienced SC, SE, or neither in the URW and RW groups, these differences were not significant at the 0.05 alpha level. SIGNIFICANCE: Ultra-rapid and rapid ASM withdrawal are accompanied by SC and SE the majority of which terminate spontaneously. These data support the use of either approach of the medication taper for seizure provocation in iEEG.

Towards Successes in the Management of Nonconvulsive Status Epilepticus: Tracing the Detection-to-Needle Trajectories.

PURPOSE: Data on the timeliness of emergent medication delivery for nonconvulsive status epilepticus (NCSE) are currently lacking. METHODS: Retrospective chart reviews (between 2015 and 2018) and analyses of all patients with NCSE were performed at the University of Nebraska Medical Center, a level 4 epilepsy center, to determine the latencies to order and administration of the first, second, and third antiepileptic drugs (AEDs). Recurrent NCSE cases were considered independently and classified as comatose and noncomatose. RESULTS: There were 77 occurrences of NCSE in 53 patients. The first, second, and third AEDs were delivered with substantial delays at median times of 80 (25%-75% interquartile range, 44-166), 126 (interquartile range, 67-239), and 158 minutes (interquartile range, 89-295), respectively, from seizure detection. The median times to the order of the first and second AEDs were 33 and 134.5 minutes longer in comatose NCSE patients compared with those with noncomatose forms, respectively (P = 0.001 and 0.004, respectively). The median times between the AED orders and their administration in these two groups were the same (P = 0.60 and 0.37, respectively). With bivariate analysis, the median latencies to administration of the first, second, and third AEDs were significantly increased by 33, 109.5, and 173 minutes, respectively, in patients who died within 30 days compared with those who survived (P = 0.047, P = 0.02, P = 0.0007, respectively). CONCLUSIONS: The administration of the first, second, and third AEDs for NCSE was delayed. Slow initiation of acute treatment in comatose patients was caused by delays in the placement of the medication order.