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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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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Spinal cavernous malformations are intramedullary vascular lesions. They have low pressure and flow, so they may take many years to present with clinical symptoms. Because of their relatively benign nature, surgical intervention is not always indicated. ⋯ Sensory symptoms correlated with worse outcome. Given the natural history of spinal cavernous malformations, surgery may be considered for symptomatic patients, when general medical health and lesion location permit safe resection. The severity of symptoms must also be considered, as the natural history of the disease can be benign.
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Developmental venous anomalies (DVAs) are relatively common lesions, present in up to 3% of the population. The defining characteristic of these lesions is the confluence of radially oriented veins into a single dilated venous channel. DVAs are also known as cerebral venous angiomas, cerebral venous malformations, and cerebral venous medullary malformations. ⋯ DVAs are congenital lesions thought to arise from aberrations that occur during venous development, but continue to provide the normal venous drainage to the cerebral territory in which they reside. Although the natural history of DVAs is benign, they may be associated with cavernous malformations or other vascular abnormalities, which can lead to hemorrhage in the vicinity of the DVA. Surgical or endovascular obliteration of DVAs carries a significant risk of venous infarction; thus, conservative management is the treatment of choice for patients with these lesions.
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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.