Handbook of clinical neurology
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Chronic traumatic encephalopathy (CTE) is a neurodegenerative disorder associated with repetitive head impact exposure, such as that resulting from sports-related concussive and subconcussive brain trauma. Currently, the only way to diagnose CTE is by using neuropathologic markers obtained postmortem. ⋯ To describe the use of neuroimaging as presumed biomarkers of CTE, this chapter focuses on only those studies that report the chronic stages of sports-related brain injury, as opposed to previous chapters that described neuroimaging in the context of acute and subacute injury. Studies using positron emission tomography and magnetic resonance imaging and spectroscopy will be discussed for contact/collision sports such as American football, boxing, mixed martial arts, rugby, and soccer, in which repetitive head impacts are common.
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The clinical manifestation of drug-induced abnormalities in thermoregulation occurs across a variety of drug mechanisms. The aim of this chapter is to review two of the most common drug-induced hyperthermic states, serotonin syndrome and neuroleptic malignant syndrome. ⋯ Our goal is to both review the current literature and to provide a practical guide to identification and treatment of these potentially life-threatening illnesses. The diagnostic and treatment recommendations made by us, and by other authors, are likely to change with a better understanding of the pathophysiology of these syndromes.
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Neurocritical care has two main objectives. Initially, the emphasis is on treatment of patients with acute damage to the central nervous system whether through infection, trauma, or hemorrhagic or ischemic stroke. Thereafter, attention shifts to the identification of secondary processes that may lead to further brain injury, including fever, seizures, and ischemia, among others. ⋯ The concepts and design of each monitor, in addition to the patient population that may most benefit from each modality, will be discussed, along with the various tools that can be used together to guide individualized patient treatment options. Major clinical trials, observational studies, and their effect on clinical outcomes will be reviewed. The future of multimodal monitoring in the field of bioinformatics, clinical research, and device development will conclude the chapter.
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Traumatic brain injury (TBI) is a growing global problem, which is responsible for a substantial burden of disability and death, and which generates substantial healthcare costs. High-quality intensive care can save lives and improve the quality of outcome. ⋯ However, observational studies have informed the development of authoritative international guidelines, and the use of multimodality monitoring may facilitate rational approaches to optimizing acute physiology, allowing clinicians to optimize the balance between benefit and risk from these interventions in individual patients. Such approaches, along with the emerging impact of advanced neuroimaging, genomics, and protein biomarkers, could lead to the development of precision medicine approaches to the intensive care management of TBI.
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The cerebrospinal fluid (CSF) space consists of the intracerebral ventricles, subarachnoid spaces of the spine and brain (e.g., cisterns and sulci), and the central spinal cord canal. The CSF protects the central nervous system (CNS) in different ways involving metabolic homeostasis, supply of nutrients, functioning as lymphatic system, and regulation of intracranial pressure. CSF is produced by the choroid plexus, brain interstitium, and meninges, and it circulates in a craniocaudal direction from ventricles to spinal subarachnoid space from where it is removed via craniocaudal lymphatic routes and the venous system. ⋯ The extracellular space volume, potassium buffering, CSF circulation, and interstitial fluid absorption are mainly regulated by aquaporin-4 channels, which are abundantly located at the blood-brain and brain-CSF interfaces. The composition of CSF shows a high dynamic range, and the levels of distinct proteins vary due to several influencing factors, such as site of production (brain or blood-derived), site of sampling (ventricular or lumbar), CSF flow rate (BCB function), diurnal fluctuations of CSF production rate, and finally, molecular size of blood-derived proteins (IgM vs. albumin) and circadian rhythm (glucose, prostaglandin D synthase). Alterations of lumbar CSF are mainly influenced by processes of the CNS located adjacent to the ventricular and spinal CSF space and less by pathologies in cortical areas remote from the ventricles.