Handbook of clinical neurology
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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.
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Cavernous malformations, accounting for approximately 5-15% of all vascular abnormalities in the central nervous system, are angiographically occult lesions which most often present with seizures, rather than acute hemorrhage. Widely variable across populations, the incidence of cavernous malformations has been reported to be 0.15-0.56 per 100 000 persons per year, with an annual hemorrhage rate of 0.6-11% per patient-year. Seen in 0.17-0.9% of the population, up to one-half are familial, and at least three gene loci have been associated with a familial form, more common among Hispanic Americans. Most cavernous malformations are supratentorial, with 10-23% in the posterior fossa, and approximately 5% found in the spine.
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Critical care medicine came into sharp focus in the second part of the 20th century. The care of acutely ill neurologic patients in the USA may have originated in postoperative neurosurgical units, but for many years patients with neurocritical illness were admitted to intensive care units next to patients with general medical or surgical conditions. Neurologists may have had their first exposure to the complexity of neurocritical care during the poliomyelitis epidemics, but few were interested. ⋯ Most neurointensivists had a formal neurology training. This chapter is a brief analysis of the development of the specialty critical care neurology and how it gained strength, what it is to be a neurointensivist, what the future of care of these patients may hold, and what it takes for neurointensivists to stay exemplary. This chapter revisits some of the earlier known and previously unknown landmarks in the history of neurocritical care.
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When critically ill, a severe weakness of the limbs and respiratory muscles often develops with a prolonged stay in the intensive care unit (ICU), a condition vaguely termed intensive care unit-acquired weakness (ICUAW). Many of these patients have serious nerve and muscle injury. This syndrome is most often seen in surviving critically ill patients with sepsis or extensive inflammatory response which results in increased duration of mechanical ventilation and hospital length of stay. ⋯ In this chapter we discuss the current knowledge on the pathophysiology and risk factors of ICUAW. Tools to diagnose ICUAW, how to separate ICUAW from other disorders, and which possible treatment strategies can be employed are also described. ICUAW is finally receiving the attention it deserves and the expectation is that it can be better understood and prevented.
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Delirium is common in critically ill patients and associated with increased length of stay in the intensive care unit (ICU) and long-term cognitive impairment. The pathophysiology of delirium has been explained by neuroinflammation, an aberrant stress response, neurotransmitter imbalances, and neuronal network alterations. Delirium develops mostly in vulnerable patients (e.g., elderly and cognitively impaired) in the throes of a critical illness. ⋯ Nonpharmacologic strategies with early mobilization, reducing causes for sleep deprivation, and reorientation measures may be effective in the prevention of delirium. Antipsychotics are effective in treating hallucinations and agitation, but do not reduce the duration of delirium. Combined pain, agitation, and delirium protocols seem to improve the outcome of critically ill patients and may reduce delirium incidence.