Etiology and prognostic significance of ictal EEG patterns in patients with non-convulsive seizures.

We aimed to study the ictal EEG patterns in patients with non-convulsive seizures (NCS) and their relationship with underlying etiology and patient outcome. We conducted a retrospective review of EEG studies from patients undergoing continuous EEG (cEEG) monitoring for indication of altered mental status with a suspicion of NCS. Ictal EEG findings of NCS were categorized as three patterns: focal or generalized epileptiform discharges (EDs) at frequencies >2.5 Hz (Pattern 1); EDs at frequencies of ≤2.5 Hz or rhythmic activity >0.5 Hz with spatiotemporal evolution (Pattern 2); and EDs with ≤2.5 Hz with subtle clinical correlate during the ictal EEG or clinical and EEG improvement after a trial of IV anti-seizure drugs (Pattern 3). Patients with anoxic brain injury were excluded from the study. Associations between ictal EEG patterns and underlying etiology and their impact on in-hospital mortality was measured. Of 487 patients included in the study, NCS was recorded on cEEG monitoring in 57 (12%). The ictal EEG Pattern 2 was the most commonly seen ictal EEG finding in our cohort of patients with NCS (70%, n=40/57), followed by Pattern 3 (15%, n=9/57) and Pattern 1(14%, n=8/57). In patients with acute brain injury, Pattern 2 (67%, n=27/40) was a commonly seen ictal EEG finding, whereas Pattern 1 (62% n=5/8) was seen in patients with underlying acute medical illness. No statistically significant difference was found between ictal EEG patterns and underlying neurological versus medical etiologies (p=0.27) or in-hospital mortality (p=0.5). Spatiotemporal evolution of epileptiform discharges at a lower frequency was the most commonly recorded ictal EEG pattern in our cohort. Further prospective studies with a larger sample size of patients with NCS may provide valuable clinical data that could be used to evaluate the etiologic correlate of the various ictal EEG patterns and their effect on outcome.

Intravenous Thrombolysis in Acute Ischemic Stroke Patients with Unsuspected Infective Endocarditis.

OBJECTIVE: Infective endocarditis (IE) is considered to be an absolute contraindication for intravenous tissue plasminogen activator treatment (IVtPA) in acute ischemic stroke (AIS). However, during the hyperacute stroke evaluation, the exclusion of IE may be difficult. We sought to report the prevalence of undiagnosed IE in AIS patients who received IVtPA. METHODS: We reviewed consecutive patients hospitalized at our comprehensive stroke center from January 1, 2014 to March 31, 2019 who received IVtPA for suspected AIS and identified patients diagnosed with IE. Data was abstracted on demographics, medical history, clinical presentation, last known normal (LKN) time, initial National Institutes of Health Stroke Scale (NIHSS), neuroimaging, culture results, and 90 day modified Rankin Scale (mRS). Good functional outcome was defined as mRS ≤ 2. RESULTS: Among 1022 AIS patients who received IVtPA, 5 patients (0.5%) were ultimately diagnosed with IE. Among the 5 patients with IE, the mean age was 53.4 years (range, 25-74) and 3 (60%) were female. The majority 4 (80%) were white. Medical risk factors for IE were present in 3 (60%) and included intravenous drug use (1) and dialysis (2). Initial NIHSS was 4.6 (range, 1 to 8). Fever was present on initial presentation in only 1 patient (102.7 F). The mean time from LKN to IVtPA was 3.0 hours (range, 1.9 to 4.4). Vascular imaging showed middle cerebral artery (MCA) occlusion in 4 (80%) and no occlusion in 1 (20%). One patient underwent endovascular thrombectomy. Two patients (40%) developed hemorrhagic complications, including 1 patient who developed subarachnoid hemorrhage due to mycotic cerebral aneurysm rupture. Blood culture results included MRSE (1), Streptococcus viridans (2) and negative (2). TEE in all patients showed vegetations on the mitral valve. No patients had good functional outcomes, and the mean 3 month mRS was 4.8 (range, 3 to 6). The 90 day mortality was 60%. CONCLUSION: In a series of AIS patients who received IVtPA by academic vascular neurologists, the risk of undiagnosed IE was low (0.5%). Fever was not commonly present during initial evaluation in IE presenting with AIS. Despite affecting younger patients with initial mild deficits, AIS patients with IE who received IVtPA had poor functional outcomes.

Lorazepam timing for acute convulsive seizure control (LoTASC).

INTRODUCTION: Guidelines specify early administration of benzodiazepines (BZD) for the management of convulsive status epilepticus. The distinction between acute convulsive seizure and status epilepticus can be misconstrued resulting in BZD administration prior to a patient meeting criteria of status epilepticus. Early BZD administration may theoretically lead to systemic vital instability. Our study aims to assess if administering lorazepam, for convulsive seizures <5 min, causes vital instability. METHODS: This is a retrospective study analyzing patients who presented with a seizure lasting <5 min between 2011 and 2016. Continuous variables of lorazepam receivers versus non- receivers were analyzed using t-test for parametric and Mann-Whitney U test for nonparametric data. Categorical variables were analyzed using Chi-Square Test. Subsequently, subjects were analyzed through univariate and multivariate regression models to determine predictors of vital instability. RESULTS: Out of 1052 subjects initially screened, 165 were included. Of these, 91 (55 %) received lorazepam, and 74 (45 %) did not. Through univariate and multivariate analyses, there was a significantly higher incidence of vital instability (defined as receipt of a vasopressor or intubation) in patients who received lorazepam (OR = 6.76, 95 % CI = 1.48, 30.95) (p = 0.014). This was dose-dependent (p < 0.0001). It was responsible for 22.5 % of the vital instability. Lorazepam administration significantly prolonged the intensive care unit (ICU) length of stay (0 days [IQR 0 - 0] vs [IQR 0-2.3]; p = 0.038). CONCLUSION: Our study suggests that lorazepam administration for acute convulsive seizures not meeting convulsive status epilepticus criteria may lead to iatrogenic vital instability and need for ICU admission.

Acute Psychosis as Main Manifestation of Central Pontine Myelinolysis.

Central pontine myelinolysis (CPM) is an acute demyelinating neurological disorder affecting primarily the central pons and is frequently associated with rapid correction of hyponatremia. Common clinical manifestations of CPM include spastic quadriparesis, dysarthria, pseudobulbar palsy, and encephalopathy of various degrees; however, coma, "locked-in" syndrome, or death can occur in most severe cases. Rarely, CPM presents with neuropsychiatric manifestations, such as personality changes, acute psychosis, paranoia, hallucinations, or catatonia, typically associated with additional injury to the brain, described as extrapontine myelinolysis (EPM). We present a patient with primarily neuropsychiatric manifestations of CPM, in the absence of focal neurologic deficits or radiographic extrapontine involvement. A 51-year-old female without significant medical history presented with dizziness, frequent falls, diarrhea, generalized weakness, and weight loss. Physical examination showed no focal neurological deficits. Laboratory data showed severe hyponatremia, which was corrected rather rapidly. Subsequently, the patient developed symptoms of an acute psychotic illness. Initial brain magnetic resonance imaging (MRI) was unremarkable, although a repeat MRI two weeks later revealed changes compatible with CPM. This case demonstrates that acute psychosis might represent the main manifestation of CPM, especially in early stages of the disease, which should be taken into consideration when assessing patients with acute abnormalities of sodium metabolism.