Current neurology and neuroscience reports
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Curr Neurol Neurosci Rep · Nov 2018
ReviewPrognostic Factors in Pediatric Sport-Related Concussion.
Sport-related concussion (SRC) and mild traumatic brain injury (mTBI) have been thrust into the national spotlight, with youth athletes bearing the burden of this public health problem. The current review aims to provide a practical summary of pediatric SRC, including key terminology, return to play/school, and risk factors for post-concussion syndrome (PCS). ⋯ While the majority of youth athletes recover within 2 to 4 weeks, approximately 10% of athletes experience a protracted recovery with symptoms lasting months, impacting social, scholastic, and sporting activities. In the pediatric population, the strongest predictors of PCS are initial symptom burden and prior concussion, with mixed results behind the factors of gender, headaches, and learning disability. The role of psychiatric, family history, sports, and socioeconomic factors remain in their infancy.
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This review provides an updated summary of blunt cerebrovascular injury (BCVI) to guide clinicians in its early diagnosis and prevention and treatment of stroke associated with such injury. ⋯ Untreated BCVI causes stroke in 10-40% of patients, but more than half will not present with stroke symptoms initially. Risk of stroke is highest in the first 7 days, with a peak in the first 24 h. Computed tomography (CT) angiography is currently the screening modality of choice, although digital subtraction angiography may still be required in some cases. Antithrombotic therapy is the mainstay of treatment and has proven safety in trauma patients. In carefully selected patients, endovascular intervention may also be beneficial. BCVI is a potentially preventable cause of stroke. A high index of suspicion is needed as emergent screening during initial evaluation can provide a window for stroke prevention. Screening all patients with injuries that would otherwise prompt CT scans of the neck or chest is recommended. Treatment is guided by grade of injury. Early treatment with antithrombotics has been shown to be both effective and safe.
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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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To discuss the diagnostic approach to patients with septic encephalopathy as well as the need for specific neuro-monitoring and the perspectives on future therapeutic approaches in this setting. ⋯ Most of data-concern experimental studies evaluating the pathophysiology of septic encephalopathy. A combination of neurodegenerative pathways with neurovascular injury is the cornerstone for the development of such complication and the long-term neurological sequelae among survivors. Septic encephalopathy is a common complication in septic patients. Clinical presentation may range from mild confusion and disorientation to convulsions and deep coma. The diagnosis of septic encephalopathy is made difficult by the lack of any specific clinical and non-clinical feature, in particular among sedated patients in whom neurological examination is unreliable. In spite of the high mortality rate associated with this condition, there is no prophylactic or targeted therapy to reduce or minimize brain damage in septic patients and clinical management is limited to the treatment of the underlying infection.
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For millennia, there has been interest in the use of cannabis for the treatment of epilepsy. However, it is only recently that appropriately powered controlled studies have been completed. In this review, we present an update on the research investigating the use of cannabidiol (CBD), a non-psychoactive component of cannabis, in the treatment of epilepsy. ⋯ While the anticonvulsant mechanism of action of CBD has not been entirely elucidated, we discuss the most recent data available including its low affinity for the endocannabinoid receptors and possible indirect modulation of these receptors via blocking the breakdown of anandamide. Additional targets include activation of the transient receptor potential of vanilloid type-1 (TRPV1), antagonist action at GPR55, targeting of abnormal sodium channels, blocking of T-type calcium channels, modulation of adenosine receptors, modulation of voltage-dependent anion selective channel protein (VDAC1), and modulation of tumor necrosis factor alpha release. We also discuss the most recent studies on various artisanal CBD products conducted in patients with epilepsy in the USA and internationally. While a high percentage of patients in these studies reported improvement in seizures, these studies were either retrospective or conducted via survey. Dosage/preparation of CBD was either unknown or not controlled in the majority of these studies. Finally, we present data from both open-label expanded access programs (EAPs) and randomized placebo-controlled trials (RCTs) of a highly purified oral preparation of CBD, which was recently approved by the FDA in the treatment of epilepsy. In the EAPs, there was a significant improvement in seizure frequency seen in a large number of patients with various types of treatment-refractory epilepsy. The RCTs have shown significant seizure reduction compared to placebo in patients with Dravet syndrome and Lennox-Gastaut syndrome. Finally, we describe the available data on adverse effects and drug-drug interactions with highly purified CBD. While this product is overall well tolerated, the most common side effects are diarrhea and sedation, with sedation being much more common in patients taking concomitant clobazam. There was also an increased incidence of aspartate aminotransferase and alanine aminotransferase elevations while taking CBD, with many of the patients with these abnormalities also taking concomitant valproate. CBD has a clear interaction with clobazam, significantly increasing the levels of its active metabolite N-desmethylclobazam in several studies; this is felt to be due to CBD's inhibition of CYP2C19. EAP data demonstrate other possible interactions with rufinamide, zonisamide, topiramate, and eslicarbazepine. Additionally, there is one case report demonstrating need for warfarin dose adjustment with concomitant CBD. Understanding of CBD's efficacy and safety in the treatment of TRE has expanded significantly in the last few years. Future controlled studies of various ratios of CBD and THC are needed as there could be further therapeutic potential of these compounds for patients with epilepsy.