Seminars in neurology
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Skill in the determination of brain death is traditionally acquired during training in an apprenticeship model. Brain death is not frequently determined, and thus exposure to the techniques used is marginal. ⋯ In this review, the authors discuss the advantages and barriers to simulation and how to develop simulation scenarios for instruction in the determination of brain death. Future research should focus on validation of brain death simulation methods and assessment tools as well as the impact of simulation on performance in clinical practice.
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Despite well-described international variabilities in brain death practices, de facto there already exists a minimum international clinical standard for the diagnosis of brain death. This remains rooted in the Harvard criteria and based on the characteristics of a permanently nonfunctioning brain. Medicine is evolving toward a single unified determination of death based on the cessation of brain function subsequent to catastrophic brain injury or circulatory arrest. ⋯ The cessation of clinical functions of the brain that will not resume is determined by the absence of capacity for consciousness, centrally mediated motor responses, brainstem reflexes, and capacity to breathe. A known proximate cause and the absence of confounding or reversible conditions must be confirmed. Regional medical, legal, cultural, religious, or socioeconomic factors may require testing beyond this minimal clinical standard.
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Seminars in neurology · Feb 2015
ReviewChronic traumatic encephalopathy: a neurodegenerative consequence of repetitive traumatic brain injury.
Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that develops as a result of repetitive mild traumatic brain injury. Chronic traumatic encephalopathy is characterized by a unique pattern of accumulation of hyperphosphorylated tau in neurons and astrocytes. The tau abnormalities begin focally and perivascularly at the depths of the cerebral sulci, spread to the superficial layers of the adjacent cortex, and eventually become widespread throughout the medial temporal lobes, diencephalon, and brainstem. ⋯ To date, CTE can only be diagnosed by postmortem neuropathological examination, although there are many ongoing research studies examining imaging techniques and biomarkers that might prove to have diagnostic utility. Currently, the incidence and prevalence of CTE are unknown, although great strides are being made to better understand the clinical symptoms and signs of CTE. Further research is critically needed to better identify the genetic and environmental risk factors for CTE as well as potential rehabilitation and therapeutic strategies.
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Despite decades of basic and clinical research, treatments to improve outcomes after traumatic brain injury (TBI) are limited. However, based on the recent recognition of the prevalence of mild TBI, and its potential link to neurodegenerative disease, many new and exciting secondary injury mechanisms have been identified and several new therapies are being evaluated targeting both classic and novel paradigms. This includes a robust increase in both preclinical and clinical investigations. ⋯ They address putative new therapies for TBI across both the spectrum of injury severity and the continuum of care, from the field to rehabilitation. They discussTBI therapy using 11 categories, namely, (1) excitotoxicity and neuronal death, (2) brain edema, (3) mitochondria and oxidative stress, (4) axonal injury, (5) inflammation, (6) ischemia and cerebral blood flow dysregulation, (7) cognitive enhancement, (8) augmentation of endogenous neuroprotection, (9) cellular therapies, (10) combination therapy, and (11) TBI resuscitation. The current golden age of TBI research represents a special opportunity for the development of breakthroughs in the field.
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Seminars in neurology · Feb 2015
ReviewNeuropathology of traumatic brain injury: comparison of penetrating, nonpenetrating direct impact and explosive blast etiologies.
The neuropathology of traumatic brain injury (TBI) from various causes in humans is not as yet fully understood. The authors review and compare the known neuropathology in humans with severe, moderate, and mild TBI (mTBI) from nonpenetrating closed head injury (CHI) from blunt impacts and explosive blasts, as well as penetrating head injury (PHI). Penetrating head injury and CHI that are moderate to severe are more likely than mTBI to cause gross disruption of the cerebral vasculature. ⋯ Neuronal injury is more prevalent in PHI and moderate to severe CHI than mTBI. Astrocyte and microglial activation and proliferation are found in all forms of animal TBI models and in severe to moderate TBI in humans. Their activation in mTBI in the human brain has not yet been studied.