Roy Poblete

Neonatal Brain Hemorrhage (NBH) of Prematurity: Translational Mechanisms of the Vascular-Neural Network

Neonatal brain hemorrhage (NBH) of prematurity is an unfortunate consequence of preterm birth. Complications result in shunt dependence and long-term structural changes such as posthemorrhagic hydrocephalus, periventricular leukomalacia, gliosis, and neurological dysfunction. Several animal models are available to study this condition, and many basic mechanisms, etiological factors, and outcome consequences, are becoming understood. NBH is an important clinical condition, of which treatment may potentially circumvent shunt complication, and improve functional recovery (cerebral palsy, and cognitive impairments). This review highlights key pathophysiological findings of the neonatal vascular-neural network in the context of molecular mechanisms targeting the posthemorrhagic hydrocephalus affecting this vulnerable infant population.

Corrigendum: Targeted Temperature Management and Multimodality Monitoring of Comatose Patients After Cardiac Arrest

[This corrects the article DOI: 10.3389/fneur.2018.00768.].

Targeted Temperature Management and Multimodality Monitoring of Comatose Patients After Cardiac Arrest

Out-of-hospital cardiac arrest (CA) remains a leading cause of sudden morbidity and mortality; however, outcomes have continued to improve in the era of targeted temperature management (TTM). In this review, we highlight the clinical use of TTM, and provide an updated summary of multimodality monitoring possible in a modern ICU. TTM is neuroprotective for survivors of CA by inhibiting multiple pathophysiologic processes caused by anoxic brain injury, with a final common pathway of neuronal death. Current guidelines recommend the use of TTM for out-of-hospital CA survivors who present with a shockable rhythm. Further studies are being completed to determine the optimal timing, depth and duration of hypothermia to optimize patient outcomes. Although a multidisciplinary approach is necessary in the CA population, neurologists and neurointensivists are central in selecting TTM candidates and guiding patient care and prognostic evaluation. Established prognostic tools include clinal exam, SSEP, EEG and MR imaging, while functional MRI and invasive monitoring is not validated to improve outcomes in CA or aid in prognosis. We recommend that an evidence-based TTM and prognostication algorithm be locally implemented, based on each institutions resources and limitations. Given the high incidence of CA and difficulty in predicting outcomes, further study is urgently needed to determine the utility of more recent multimodality devices and studies.

Serum Lactic Acid Following Aneurysmal Subarachnoid Hemorrhage Is a Marker of Disease Severity but Is Not Associated With Hospital Outcomes

Background: Following aneurysmal subarachnoid hemorrhage, peripherally-drawn lactic acid has been associated with poor outcomes; however, its clinical significance is unknown. We investigated admission factors and patient outcomes associated with serum lactic acid in this population. Methods: This was a retrospective observational study of 105 consecutive patients with serum lactate collected within 24 h of admission. Primary objectives were to determine the incidence of admission lactic acidemia, and factors positively and negatively associated with lactate levels. We also sought to determine if admission lactic acidemia was associated with patient outcomes, including vasospasm, delayed cerebral ischemia, mortality, and discharge disposition. Results: Admission serum lactic acid was elevated in 56 patients (53% of the cohort). Levels were positively associated with Hunt & Hess and modified Fisher grade, glucose, troponin I and white blood cell counts, and negatively associated with GCS and ventilator-free days. Admission lactate was not associated with the development of vasospasm or delayed cerebral ischemia. Patients with elevated lactic acid more often died during hospitalization, and less often were discharged home. After adjusting for other predictors of poor outcome, the adjusted odds of inpatient mortality (OR 0.97, 95% CI 0.79–1.20; p = 0.80) and discharge to home (OR 1.00, 95% CI 0.80–1.26; p = 0.97) was not associated with admission lactic acid. Conclusions: Early serum lactic acid elevation is common following aneurysmal subarachnoid hemorrhage and is associated with the clinical and radiographic grade of hemorrhage. Levels did not independently predict short-term outcomes when adjusted for established predictors of poor outcome. Further study is needed to determine the clinical significance of peripherally-drawn lactic acid in aneurysmal subarachnoid hemorrhage.

Status Epilepticus and Beyond: A Clinical Review of Status Epilepticus and an Update on Current Management Strategies in Super-refractory Status Epilepticus

Status epilepticus and refractory status epilepticus represent some of the most complex conditions encountered in the neurological intensive care unit. Challenges in management are common as treatment options become limited and prolonged hospital courses are accompanied by complications and worsening patient outcomes. Antiepileptic drug treatments have become increasingly complex. Rational polytherapy should consider the pharmacodynamics and kinetics of medications. When seizures cannot be controlled with medical therapy, alternative treatments, including early surgical evaluation can be considered; however, evidence is limited. This review provides a brief overview of status epilepticus, and a recent update on the management of refractory status epilepticus based on evidence from the literature, evidence-based guidelines, and experiences at our institution.

Hypothermia for Acute Ischemic Stroke

The use of hypothermia as a medical therapy has been used and tested for centuries. In the modern era, its use in neurological diseases has attained significant interest and potential benefit has been found in a number of areas, particularly cerebral ischemia. In the setting of global cerebral ischemia, clinical benefit has been observed and so it seems that this may be the case in focal cerebral ischemia as well. This chapter reveals the current state of the evidence.

A Case of Acute Motor Axonal Neuropathy Mimicking Brain Death and Review of the Literature

We describe a case report of fulminant Guillain–Barré syndrome (GBS) mimicking brain death. A previously healthy 60-year-old male was admitted to the neurointensive care unit after developing rapidly progressive weakness and respiratory failure. On presentation, the patient was found to have absent brainstem and spinal cord reflexes resembling that of brain death. Acute motor axonal neuropathy, a subtype of GBS, was diagnosed by cerebrospinal fluid and nerve conduction velocity testing. An electroencephalogram showed that the patient had normal, appropriately reactive brain function. Transcranial Doppler (TCD) ultrasound showed appropriate blood flow to the brain. GBS rarely presents with weakness so severe as to mimic brain death. This article provides a review of similar literature. This case demonstrates the importance of performing a proper brain death examination, which includes evaluation for irreversible cerebral injury, exclusion of any confounding conditions, and performance of tests such as electroencephalography and TCDs when uncertainty exists about the reliability of the clinical exam.

Atypical presentation of venous infarct: Developmental venous anomaly thrombosis propagating from clot in dural venous sinus

A 42-year-old woman with systemic lupus erythematosus (SLE) presented with right hemisensory loss and aphasia beginning 3 hours prior to arrival to the hospital. Two months prior to presentation, anticoagulation was started for a left transverse sinus to internal jugular thrombosis, which was diagnosed after development of a severe headache and vomiting (figure 1, A and C). There was an incidental finding of a patent left temporal developmental venous anomaly (DVA). The DVA drained the supramarginal and superior temporal gyri extending from the Sylvian fissure to the vein of Labbe (figure 1B).