Handbook of clinical neurology
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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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Decompressive surgery to reduce pressure under the skull varies from a burrhole, bone flap to removal of a large skull segment. Decompressive craniectomy is the removal of a large enough segment of skull to reduce refractory intracranial pressure and to maintain cerebral compliance for the purpose of preventing neurologic deterioration. Decompressive hemicraniectomy and bifrontal craniectomy are the most commonly performed procedures. ⋯ The ethical predicament of deciding to go ahead with a major neurosurgical procedure with the purpose of avoiding brain death from displacement, but resulting in prolonged severe disability in many, are addressed. This chapter describes indications, surgical techniques, and complications. It reviews results of recent clinical trials and provides a reasonable assessment for practice.
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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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Neurologic complications in polytrauma can be classified by etiology and clinical manifestations: neurovascular, delirium, and spinal or neuromuscular problems. Neurovascular complications include ischemic strokes, intracranial hemorrhage, or the development of traumatic arteriovenous fistulae. Delirium and encephalopathy have a reported incidence of 67-92% in mechanically ventilated polytrauma patients. ⋯ Neuromuscular complications include nerve and plexus injuries, and ICU-acquired weakness. In polytrauma, the neurologic examination is often confounded by pain, sedation, mechanical ventilation, and distracting injuries. Regular sedation pauses for examination and maintaining a high index of suspicion for neurologic complications are warranted, particularly because early diagnosis and management can improve outcomes.
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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.