Handbook of clinical neurology
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Major neurologic morbidity, such as seizures and encephalopathy, complicates 20-30% of organ and stem cell transplantation procedures. The majority of these disorders occur in the early posttransplant period, but recipients remain at risk for opportunistic infections and other nervous system disorders for many years. ⋯ Drug neurotoxicity accounts for a significant proportion of complications, with posterior reversible leukoencephalopathy syndrome, primarily associated with calcineurin inhibitors (i.e., cyclosporine and tacrolimus), being prominent as a cause of seizures and neurologic deficits. A thorough evaluation of any patient who develops neurologic symptoms after transplantation is mandatory, since reversible and treatable conditions could be found, and important prognostic information can be obtained.
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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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Neurocritical care has two main objectives. Initially, the emphasis is on treatment of patients with acute damage to the central nervous system whether through infection, trauma, or hemorrhagic or ischemic stroke. Thereafter, attention shifts to the identification of secondary processes that may lead to further brain injury, including fever, seizures, and ischemia, among others. ⋯ The concepts and design of each monitor, in addition to the patient population that may most benefit from each modality, will be discussed, along with the various tools that can be used together to guide individualized patient treatment options. Major clinical trials, observational studies, and their effect on clinical outcomes will be reviewed. The future of multimodal monitoring in the field of bioinformatics, clinical research, and device development will conclude the chapter.
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Arteriovenous malformations (AVMs) of the brain are diverse lesions that vary widely in location, size, and complexity. Treatment options for AVMs are correspondingly complex. Complete elimination of an AVM is required to protect patients from future hemorrhage. ⋯ Some AVMs can be managed conservatively, whereas others can be managed with microsurgical resection, radiosurgical ablation, or endovascular embolization, either individually or in combination. Some AVMs may also be treated with partial therapy to reduce the risk of hemorrhage or to ameliorate symptoms. In this chapter, we review the key factors that influence whether and how to manage AVMs with multimodality treatment.
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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.