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The cerebral circulation is protected from systemic blood pressure surges by a complex branching system and two resistance elements: the first of these lies in the large cerebral arteries, and the second in vessels of diameter <100 μm. Endothelial cells in cerebral capillaries contain few pinocytic vesicles and are sealed with tight junctions, without any anatomical gap. Several endogenous substances including catecholamines and vascular growth enhancing factor can dynamically modulate blood-brain barrier (BBB) permeability. Classical cerebral autoregulation assessment does not consider the latency of autoregulatory mechanisms, focusing instead on the maintenance of cerebral blood flow (CBF) at different steady state levels of cerebral perfusion pressure (CPP). Methods of measuring CBF may be regional or global, and may be applicable either to humans or primarily to experimental animals. Severe head injury is accompanied by both direct and indirect effects on CBF and metabolism, which show both temporal and spatial variations.
The intracranial pressure (ICP) has three components: an arterial vascular component; a cerebrospinal fluid (CSF) circulatory component; and a venous outflow component. More generally, multiple variables such as the arterial pulsatile pressure, autoregulation and cerebral venous outflow all contribute to the vascular component. Intracranial compliance is a concept often associated with CSF storage. Measurement of brain compliance is classically performed using a CSF bolus injection. In sedated patients with TBI, continuous ICP monitoring is recommended, and can only be achieved by direct invasive measurement. The gold standard for ICP monitoring is a catheter inserted into the lateral ventricle and connected to an external pressure transducer. Cerebral perfusion pressure (CPP)-oriented therapy has been introduced to decrease the risk of ischaemia in post-injury care. Intracranial pressure waveforms include distinct periodic components: heart pulse waves, respiratory waves and quasi-periodic slow vasogenic waves.
Clinical neurophysiology encompasses a variety of diagnostic tests including EEG, nerve conduction studies, electromyography, evoked potentials and polysomnography. This chapter describes the tests that are most widely used for monitoring during neuroanaesthesia and neurocritical care, specifically, EEG, somatosensory evoked potentials (SSEPs), brainstem auditory evoked potentials, motor evoked potentials (MEPs) and electromyography (EMG). The main indications for EEG are in the diagnosis and management of epilepsy, sleep studies and neuromonitoring. Evoked potentials are the electrical response from the nervous system to an external stimulus. There are two types of EPs: sensory and motor. SSEPs monitor the integrity of sensory pathways, including peripheral nerves, and MEPs the motor pathways. Electromyography is a technique used to evaluate the electrical activity in muscle fibres. Two types of EMG monitoring commonly used include: recording spontaneous electrical activity and recording responses generated by stimulation of motor nerves.
Core Topics in Neuroanesthesia and Neurointensive Care is an authoritative and practical clinical text that offers clear diagnostic and management guidance for a wide range of neuroanesthesia and neurocritical care problems. With coverage of every aspect of the discipline by outstanding world experts, this should be the first book to which practitioners turn for easily accessible and definitive advice. Initial sections cover relevant anatomy, physiology and pharmacology, intraoperative and critical care monitoring and neuroimaging. These are followed by detailed sections covering all aspects of neuroanesthesia and neurointensive care in both adult and pediatric patients. The final chapter discusses ethical and legal issues. Each chapter delivers a state-of-the art review of clinical practice, including outcome data when available. Enhanced throughout with numerous clinical photographs and line drawings, this practical and accessible text is key reading for trainee and consultant anesthetists and critical care specialists.
This chapter reviews the history, evolution and organization of neurointensive care units. It emphasizes the key role that neurointensive care teams play in delivering improved outcomes for patients. Neurointensive care has evolved from its original single-system focus on the central nervous system (CNS) to a multisystem speciality providing all aspects of a patient's care. Despite the widespread availability and relative simplicity of many neuromonitoring techniques, there is considerable variation in their placement and in the application of monitoring-guided therapeutic strategies. The overall goals of neurointensive care are to resuscitate and support the acutely ill patient, minimize secondary neurological injury, and prevent or treat systemic (non-neurological) complications. Protocol-guided treatment improves clinical outcome in all areas of medicine and is effective in reducing mortality and improving outcome after brain injury. Expertise in neurointensive care involves procedural skills, proficiency with standard (systemic) monitoring and management, as well as specialized neuromonitoring techniques and interventions.
The ideal marker of organ damage or dysfunction must be specific and sensitive. Of paramount importance is also that it should be easily and reliably measured with clearly defined thresholds, and preferably independent of age, sex and other concurrent systemic disorders. In addition, the serum levels of the marker should correlate with the severity of disease so that it is possible to predict accurately recovery, further damage and the likelihood of permanent injury. The diagnosis, prognosis and natural history of central nervous system (CNS) injury relies on repeated clinical neurological examination and radiological techniques such as computed tomography (CT) and/or magnetic resonance imaging (MRI). A number of clinical scenarios exist in which the application of such assessments is not practical or feasible. Therefore, the benefits of having a reliable, sensitive and specific serum biomarker for diagnosing and predicting prognosis after CNS injury are self-evident . This chapter will discuss the merits and the potential pitfalls of protein S-100β as a useful marker of CNS damage and dysfunction.
The S-100 protein family consists of 17 members . These proteins are made of two subunit amino acid chains, α and β. S-100 ββ is found in high concentrations in glial and Schwann cells, S-100 α1β in glial cells and S-100 α1α1 in kidney, and striated and cardiac muscles. The isoform of main interest in brain damage is the homodimer which consists of two monomers (S-100 ββ) and which is usually abbreviated to S-100β.
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