Handbook of clinical neurology
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Most ischemic strokes are managed on the ward or on designated stroke units. A significant proportion of patients with ischemic stroke require more specialized care. Several studies have shown improved outcomes for patients with acute ischemic stroke when neurocritical care services are available. ⋯ In this chapter, we discuss aspects of acute ischemic stroke care that are of particular relevance to a neurointensivist, covering neuropathology, neurodiagnostics and imaging, blood pressure management, glycemic control, temperature management, and the selection and timing of antithrombotics. We also focus on the care of patients who have received intravenous thrombolysis or mechanical thrombectomy. Complex clinical decision making in decompressive hemicraniectomy for hemispheric infarction and urgent management of basilar artery thrombosis are specifically addressed.
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The application of targeted temperature management has become common practice in the neurocritical care setting. It is important to recognize the pathophysiologic mechanisms by which temperature control impacts acute neurologic injury, as well as the clinical limitations to its application. Nonetheless, when utilizing temperature modulation, an organized approach is required in order to avoid complications and minimize side-effects. ⋯ Shivering is the most common side-effect of hypothermia and is best managed by adequate monitoring and stepwise administration of medications specifically targeting the shivering response. Due to the impact cooling can have upon pharmacokinetics of commonly used sedatives and analgesics, there can be significant delays in the return of the neurologic examination. As a result, early prognostication posthypothermia should be avoided.
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The human prion diseases comprise Creutzfeldt-Jakob disease, variably protease-sensitive prionopathy, Gerstmann-Sträussler-Scheinker disease, fatal familial insomnia, and kuru. Each is a uniformly fatal rare neurodegenerative disease in which conformational changes in the prion protein are thought to be the central pathophysiologic event. The majority of cases of human prion diseases occur worldwide in the form of sporadic Creutzfeldt-Jakob disease and a minority of around 10-15% are associated with mutations of the prion protein gene, termed PRNP, in the forms of genetic Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker disease, and fatal familial insomnia. ⋯ Despite having a high public profile, human prion diseases are both rare and heterogeneous in their clinicopathologic phenotype, sometimes making a diagnosis challenging. A combined clinical, genetic, neuropathologic, and biochemical approach to diagnosis is therefore essential. The intensive study of these diseases continues to inform on neurodegenerative mechanisms and the role of protein misfolding in more common neurodegenerative diseases such as Parkinson disease and Alzheimer disease.
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Dural arteriovenous fistulas are a heterogeneous group of lesions that comprise 10-15% of intracranial vascular malformations. The treatment strategy is devised after careful consideration of the arterial supply, venous drainage, clinical presentation, and risk of progression, hemorrhage, or neurologic decline. With recent advancements in endovascular technology, the majority of dural arteriovenous fistulas can be treated with either transarterial or transvenous embolization. Those that cannot be fully treated by endovascular means are approached with either adjuvant surgery or radiotherapy.
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Review Case Reports
Natural history of cerebral cavernous malformations.
Cerebral cavernous malformations (CCM) are vascular abnormalities of the central nervous system with an incidence of 0.4-0.5% and an annual rate of hemorrhage ranging from 0.7% to 1%. Most lesions are located in the cerebral hemisphere but some occur in deeper locations such as the basal ganglia and pons. The most common symptoms during presentation are headache, seizures, and focal neurologic deficits. ⋯ This finding, however, is not consistent in all natural history studies evaluated. During follow-up, the most important and consistent risk factor for rebleed was a prior hemorrhage. Here, we provide an indepth but concise review of the literature regarding the natural history of CCMs.