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This article discusses the evolving definitions of seizures and status epilepticus in the critical care environment and the role of critical care EEG in both diagnosing seizure activity and serving as a predictive biomarker of clinical trajectory.

Initial screening EEG has been validated as a tool to predict which patients are at risk of future seizures. However, accepted definitions of seizures and nonconvulsive status epilepticus encourage a treatment trial when the diagnosis on EEG is indeterminate because of periodic or rhythmic patterns or uncertain clinical correlation. Similarly, recent data have demonstrated the diagnostic utility of intracranial EEG in increasing the yield of seizure detection. EEG has additionally been validated as a diagnostic biomarker of covert consciousness, a predictive biomarker of cerebral ischemia and impending neurologic deterioration, and a prognostic biomarker of coma recovery and status epilepticus resolution. A recent randomized trial concluded that patients allocatalized uses of EEG as a prognostic biomarker have emerged in traumatic brain injury for predicting language function and covert consciousness, cardiac arrest for predicting coma recovery, and subarachnoid hemorrhage for predicting neurologic deterioration due to delayed cerebral ischemia.

This article describes the causes, clinical and imaging features, management, and prognosis of posterior reversible encephalopathy syndrome (PRES) and reversible cerebral vasoconstriction syndrome (RCVS), in which the underlying pathophysiology is related to reversible dysregulation of the cerebral vasculature.

PRES and RCVS are descriptive terms, each bringing together conditions with similar clinical-imaging manifestations. Headache, visual symptoms, seizures, and confusion occur in both syndromes. RCVS is usually heralded by recurrent thunderclap headaches, whereas encephalopathy and seizures are typical in PRES. In PRES, brain imaging shows reversible vasogenic edema that is typically symmetric and located in subcortical regions (mostly posterior predominant). In RCVS, brain imaging is often normal; cerebral angiography shows segmental vasoconstriction-vasodilatation affecting the circle of Willis arteries and their branches. Aside from shared clinical features, significant imaging overlap exists. Botophysiology and risk factors for poor outcome are expected to optimize the management of these not uncommon syndromes.

Traumatic brain injury (TBI) encompasses a group of heterogeneous manifestations of a disease process with high neurologic morbidity and, for severe TBI, high probability of mortality and poor neurologic outcomes. This article reviews TBI in neurocritical care, hence focusing on moderate and severe TBI, and includes an up-to-date review of the many variables to be considered in clinical care.

With advances in medicine and biotechnology, understanding of the impact of TBI has substantially elucidated the distinction between primary and secondary brain injury. Consequently, care of TBI is evolving, with intervention-based modalities targeting multiple physiologic variables. Multimodality monitoring to assess intracranial pressure, cerebral oxygenation, cerebral metabolism, cerebral blood flow, and autoregulation is at the forefront of such advances.

Understanding the anatomic and physiologic principles of acute brain injury is necessary in managing moderate to severe TBI. Management is based on the prevention of secondary brain injury from resultant trauma. Care of patients with TBI should occur in a dedicated critical care unit with subspecialty expertise. With the advent of multimodality monitoring and targeted biomarkers in TBI, patient outcomes have a higher probability of improving in the future.

Understanding the anatomic and physiologic principles of acute brain injury is necessary in managing moderate to severe TBI. Management is based on the prevention of secondary brain injury from resultant trauma. Care of patients with TBI should occur in a dedicated critical care unit with subspecialty expertise. IC-87114 nmr With the advent of multimodality monitoring and targeted biomarkers in TBI, patient outcomes have a higher probability of improving in the future.

Nontraumatic intracerebral hemorrhage (ICH) is the second most common type of stroke. This article summarizes the basic pathophysiology, classification, and management of ICH and discusses the available evidence on therapy for hematoma, hematoma expansion, and perihematomal edema.

Current available data on potential therapeutic options for ICH are promising, although none of the trials have shown improvement in mortality rate. link2 The literature available on reversal of anticoagulation and antiplatelet agents after an ICH and resumption of these medications is also increasing.

ICH continues to have high morbidity and mortality. Advances in therapeutic options to target secondary brain injury from the hematoma, hematoma expansion, and perihematomal edema are increasing. Data on reversal therapy for anticoagulant-associated or antiplatelet-associated ICH and resumption of these medications are evolving.

ICH continues to have high morbidity and mortality. Advances in therapeutic options to target secondary brain injury from the hematoma, hematoma expansion, and perihematomal edema are increasing. Data on reversal therapy for anticoagulant-associated or antiplatelet-associated ICH and resumption of these medications are evolving.

Subarachnoid hemorrhage (SAH) remains an important cause of mortality and long-term morbidity. This article uses a case-based approach to guide readers through the fundamental epidemiology and pathogenesis of SAH, the approach to diagnosis and management, the results of clinical trials and evidence to date, prognostic considerations, controversies, recent developments, and future directions in SAH.

Historically, management of SAH focused on prevention and treatment of subsequent cerebral vasospasm, which was thought to be the primary cause of delayed cerebral ischemia. Clinical and translational studies over the past decade, including several therapeutic phase 3 randomized clinical trials, suggest that the pathophysiology of SAH-associated brain injury is multiphasic and multifactorial beyond large vessel cerebral vasospasm. The quest to reduce SAH-associated brain injury and improve outcomes is shifting away from large vessel cerebral vasospasm to a new paradigm targeting multiple brain injury mechanismsignificant variabilities in care settings and empiric treatment protocols and inconsistent scientific terminologies have limited advancement in patient care and therapeutic clinical studies. Large consensus efforts are under way to introduce clinical guidelines and common data elements to advance therapeutic approaches and improve patient outcome.

This article reviews the pathophysiology and management of cerebral edema, brain compression, and elevated intracranial pressure (ICP). It also provides a brief introduction to the concept of the glymphatic system and select cellular contributors to cerebral edema.

Cerebral edema and brain compression should be treated in a tiered approach after the patient demonstrates a symptomatic indication to start treatment. All patients with acute brain injury should be treated with standard measures to optimize intracranial compliance and minimize risk of ICP elevation. When ICP monitors are used, therapies should target maintaining ICP at 22 mm Hg or less. Evidence exists that serial clinical examination and neuroimaging may be a reasonable alternative to ICP monitoring; however, clinical trials in progress may demonstrate advantages to advanced monitoring techniques. Early decompressive craniectomy and hypothermia are not neuroprotective in traumatic brain injury and should be reserved for situations refractory e revised in response to currently evolving discoveries regarding the pathophysiology of acute brain injury.

The aim of this study was to investigate introductions and spread of different HIV-1 subtypes in the Netherlands.

We identified distinct HIV-1 transmission chains in the Netherlands within the global epidemic context through viral phylogenetic analysis of partial HIV-1 polymerase sequences from individuals enrolled in the ATHENA national HIV cohort of all persons in care since 1996, and publicly available international background sequences.

Viral lineages circulating in the Netherlands were identified through maximum parsimony phylogeographic analysis. The proportion of HIV-1 infections acquired in-country among heterosexuals and MSM was estimated from phylogenetically observed, national transmission chains using a branching process model that accounts for incomplete sampling.

As of 1 January 2019, 2589 (24%) of 10 971 (41%) HIV-1 sequenced individuals in ATHENA had non-B subtypes (A1, C, D, F, G) or circulating recombinant forms (CRF01AE, CRF02AG, CRF06-cpx). The 1588 heterosexuals were in 1224, and ry.

Patient-related clinical factors, laboratory factors, and some imaging factors may lead to statistical bias when investigating coronary plaque progression. In this study, we avoided patient characteristics by comparing morphological characteristics of plaque progression and nonprogression within the same patient with multiple plaques.

From August 2011 to December 2018, 177 consecutive patients with 424 plaques who were followed with coronary computed tomography angiography (CTA) were reviewed retrospectively. Follow-up images of the plaques were used to determine whether the plaque volume or stenosis grade increased. The plaques were divided into progressive and nonprogressive groups. link3 Logistic regression analysis was used to identify the factors associated with plaque progression. Through clinical follow-up, we analyzed whether the factors associated with plaque progression were related to major adverse cardiac events (MACEs).

There were 223 plaques that progressed during a mean follow-up period of 27.6 ± 15.9 months. The univariate logistic regression model revealed that only low attenuation plaque (LAP) volume (P = 0.02) was associated with plaque progression. After a mean post-CTA follow-up period of 36.7 ± 18.4 months, 37 patients experienced MACEs, and LAP volume was significantly related to future MACEs.

Only a high baseline LAP volume was associated with plaque progression, and patients with progressive plaques and a high LAP volume were more likely to have future MACEs. More attention should be given to plaques with LAP volumes larger than 2.4 mm3.

Only a high baseline LAP volume was associated with plaque progression, and patients with progressive plaques and a high LAP volume were more likely to have future MACEs. More attention should be given to plaques with LAP volumes larger than 2.4 mm3.

Brain metastases (BM) in soft-tissue sarcomas (STS) is associated with poor prognosis. This large population analysis presents (1) demographic and clinical variables of these patients, (2) potential risk factors, (3) impact of BM on overall survival, and (4) treatment strategies.

Patients with STS and BM were identified from the Surveillance, Epidemiology, and End Results database. Demographic and clinical variables, as well as treatment modalities, were analyzed. Overall 5-year survival was calculated using the Kaplan-Meier method, and the survival difference was assessed using the log-rank test. A multivariate analysis was performed using the Cox proportional hazard regression to determine the risk factors.

Twenty-two patients (22/8,433) with STS presented BM at diagnosis. A multivariate analysis showed that women and American Indians/Alaska Natives had a greater risk of presenting BM. The most common histological subtype to metastasize to the brain was alveolar soft part sarcoma (4/22). In 54.5% of patients with BM, the tumor had also metastasized to the lung, although having synchronous bone, liver, and lung metastases showed the greatest increase in risk for presenting BM (odd ratio [OR] = 1,857.