Current neurology and neuroscience reports
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We aimed to summarize recent findings in cervical (CeAD) and intracranial artery dissection (IAD) research. ⋯ Considered a disease of the young- and middle-aged, an analysis on the largest CeAD-population to date (n = 2391) revealed that about 1 of 14 CeAD-patients was aged ≥60 years. Distinct genetic variants were associated with CeAD. However, in clinical practice, genetic investigations are not helpful due to the small effect size. Despite the paucity of data from randomized-controlled trials in CeAD-stroke patients, both intravenous thrombolysis and endovascular treatment should be considered as acute treatment in such patients. Future research is needed to clarify which patients benefit most from each treatment modality. Whether to use antiplatelets or anticoagulants in stroke prevention in CeAD-patients is still a matter of debate. One randomized-controlled feasibility trial has been published, and another trial designed to show non-inferiority of aspirin to vitamin-K-antagonists is underway and will be terminated in late 2018. Non-vitamin-K-oral anticoagulants should not be used in CeAD outside a properly designed trial, as experience with these drugs in CeAD-patients is limited. With many IAD patients developing intracranial hemorrhage, antithrombotic therapy should be used with caution. Knowledge about CeAD and IAD has advanced substantially. Nevertheless, further research is mandatory, in particular regarding pathophysiology, acute treatment, and stroke-preventive therapy, as well as long-term outcome and prognosis.
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Curr Neurol Neurosci Rep · Nov 2018
ReviewA Precision Medicine Approach to Cerebral Edema and Intracranial Hypertension after Severe Traumatic Brain Injury: Quo Vadis?
Standard clinical protocols for treating cerebral edema and intracranial hypertension after severe TBI have remained remarkably similar over decades. Cerebral edema and intracranial hypertension are treated interchangeably when in fact intracranial pressure (ICP) is a proxy for cerebral edema but also other processes such as extent of mass lesions, hydrocephalus, or cerebral blood volume. A complex interplay of multiple molecular mechanisms results in cerebral edema after severe TBI, and these are not measured or targeted by current clinically available tools. Addressing these underpinnings may be key to preventing or treating cerebral edema and improving outcome after severe TBI. ⋯ This review begins by outlining basic principles underlying the relationship between edema and ICP including the Monro-Kellie doctrine and concepts of intracranial compliance/elastance. There is a subsequent brief discussion of current guidelines for ICP monitoring/management. We then focus most of the review on an evolving precision medicine approach towards cerebral edema and intracranial hypertension after TBI. Personalization of invasive neuromonitoring parameters including ICP waveform analysis, pulse amplitude, pressure reactivity, and longitudinal trajectories are presented. This is followed by a discussion of cerebral edema subtypes (continuum of ionic/cytotoxic/vasogenic edema and progressive secondary hemorrhage). Mechanisms of potential molecular contributors to cerebral edema after TBI are reviewed. For each target, we present findings from preclinical models, and evaluate their clinical utility as biomarkers and therapeutic targets for cerebral edema reduction. This selection represents promising candidates with evidence from different research groups, overlap/inter-relatedness with other pathways, and clinical/translational potential. We outline an evolving precision medicine and translational approach towards cerebral edema and intracranial hypertension after severe TBI.
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A major goal in neurocritical care is to monitor for and prevent secondary brain injuries. However, injuries occurring at the cellular and molecular levels evade detection by conventional hemodynamic monitoring and the neurological exam. Cerebral microdialysis (CMD) is an invasive means of providing nearly continuous measurements of cerebral metabolism and is a promising tool that can detect signs of cellular distress before systemic manifestations of intracranial catastrophe. ⋯ In this review, we describe the technique of CMD and the common biomarkers used to monitor cerebral energy metabolism. We examine the published evidence on how CMD data reflect secondary injuries and improve understanding of the pathophysiology of traumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage. We also discuss some of the caveats of the technique, including how CMD probe position affect the sensitivity of capturing energy failures, and how abnormal levels of cerebral glucose and lactate can reflect different states of cerebral energy metabolism. In order to best incorporate cerebral metabolic monitoring into the management of neurocritical care patients, neurointensivists must be familiar with the nuances in the limitations as well as the interpretations of data obtained from cerebral microdialysis.
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For many neurologists, seizures in critically ill patients represent a difficult problem. Etiology can be elusive because of the complexity of the environment, and treatment decisions can be compromised by the paucity of evidence-based guidelines. Emerging data support a higher than previously thought incidence of nonconvulsive epileptic activity in this patient population, which is another important consideration. ⋯ Although there is no reason to believe that late seizures after severe head trauma cannot be prevented with prophylactic treatment, such an approach may be useful during the first week after the injury. Physicians, however, have to individualize the treatment to the critical patient after stroke or trauma based on the presence of additional factors that increase the risk for seizures, including structural cortical injuries and medications used in critical illness with epileptogenic potential. A general therapeutic scheme for seizures in the intensive care unit and the role newer antiepileptic drugs can play are also presented in this review.
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Curr Neurol Neurosci Rep · Jul 2018
ReviewThrombectomy for Acute Ischemic Stroke: Recent Insights and Future Directions.
Mechanical thrombectomy has become the standard of care for acute ischemic stroke with proximal large vessel occlusions (LVO). This article reviews recent research relating to thrombectomy. ⋯ Thrombectomy for anterior circulation stroke with proximal LVO was first shown to be highly efficacious within 6 h of stroke onset, but "late-window" trials have further demonstrated efficacy until 24-h postonset in select patients with salvageable tissue. However, the concept of "time is brain" remains critical. Thrombectomy trials have further stimulated worldwide efforts to develop systems of care for rapid treatment of eligible patients. Thrombectomy is cost-effective and likely to have long-term efficacy for both disability and mortality outcomes. Thrombectomy is a highly efficacious acute stroke therapy. Enduring uncertainties include efficacy in patients with premorbid disability, posterior circulation, or more distal occlusions; use of bridging thrombolysis; and optimal techniques to achieve consistent revascularization and address tandem occlusions or stenoses.