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Neurologic conditions are among the more common concurrent medical conditions encountered during pregnancy. Table 44.1 shows the prevalence of several such neurologic diseases. Despite their cumulative prevalence, the relative rarity of many of these conditions limits the actual clinical experience of both the managing obstetrician and the neurologist. In addition, the individual practitioner is further hampered by the limited amount of pregnancy-specific information available. The frequent overlap of symptoms associated with common pregnancy complaints, the sometimes disabling and lethal consequences of the disease, and the fetal effects of the maternal disease and/or treatment make the diagnosis and management of neurologic disease during pregnancy an often-daunting task.
Late Pregnancy – Maternal Problems
J. Ricardo Carhuapoma, Neuroscience Critical Care Division, The Johns Hopkins Hospital, Baltimore, MD, USA,
Michael W. Varner, Department of Obstetrics & Gynecology, University of Utah School of Medicine, Salt Lake City, UT, USA,
Steven R. Levine, Departments of Neurology and Emergency Medicine, The State University of New York (SUNY) Downstate College of Medicine & Medical Center, Brooklyn, NY, USA
Advanced cerebral amyloid angiopathy (CAA) consists of vascular deposition of amyloid and secondary breakdown of amyloid-laden vessel walls. This chapter focuses on the pathogenesis of CAA, clinical and genetic risk factors, presentations and diagnosis, and prospects for treatment. CAA-related intracerebral hemorrhage (ICH) accounts for a substantial proportion of all spontaneous ICH in the elderly. CAA-related lobar ICH presents similarly to other types of lobar ICH with acute onset of neurological symptoms and the variable presence of headache, seizures, or decreased consciousness according to hemorrhage size and location. CAA-related hemorrhages can also be small and clinically silent. CAA can also present with transient neurological symptoms, another syndrome where diagnosis during life is of particular practical importance. Future treatments for CAA are likely to focus on preventive or protective therapy aimed at decreasing the deposition or toxicity of vascular amyloid.
Intracerebral hemorrhage is a neurovascular emergency associated with high mortality and morbidity. With in-depth reviews of the clinical and biological aspects of the condition, this text provides an up-to-date coverage of this form of stroke. The book covers epidemiology, causes, clinical presentation, management and prognosis, and describes the ongoing research advances aimed at improving our understanding of the condition. The book fills an existing gap in the medical literature. The chapters discussing the clinical aspects of intracerebral hemorrhage are aimed at the practitioner directing the care of stroke victims. Chapters exploring the biology of pathophysiological events triggered by this disease will provide readers with current data directed to facilitate experimental research in this field of cerebrovascular neurology. It will appeal to clinicians and those with a research interest in cerebrovascular diseases.
Vascular malformations constitute an important cause of intracranial hemorrhage especially in younger patients. These malformations may arise from any segment of the different functional units of the brain vasculature, including arteries, arterioles, capillaries, venules, and veins. Among vascular malformations causing intracranial hemorrhage, brain arteriovenous malformations (AVMs) are among the most frequently encountered. Brain AVMs commonly affect distal arterial branches and in roughly half of the cases, the malformation is found in the borderzone region shared by the distal anterior, middle, and/or posterior cerebral arteries. Cerebral angiography may help to differentiate brain AVMs from other types of intracranial anomalies with arterio-venous shunting. Resection of an associated developmental venous anomaly is contraindicated as its occlusion may lead to venous stasis, brain edema, and eventual hemorrhage. A developmental venous anomaly (DVA) is found in up to 30% of cerebral cavernous malformations (CCM) patients.
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