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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.
Computerized tomography scans are rapid, readily available, and relatively inexpensive. Volume of hemorrhage on computerized tomography (CT) is an important predictor of mortality and functional ability after intracerebral hemorrhage (ICH). Computerized tomography angiography (CTA) offers many clinical advantages over cerebral digital subtraction angiography (DSA) for the evaluation of intracranial vascular abnormalities in cases of ICH. CTA must be shown to have similar sensitivity and specificity as DSA in the detection of secondary causes of ICH. The use of non-contrast CT in the initial evaluation of patients presenting with suspected ICH is well established and universally accepted. Recently, advances in CTA have enabled this modality to gain wide acceptance in evaluating possible secondary causes of ICH, such as aneurysm or vascular malformation. As scanner technology and software rendering capabilities continue to improve, CTA appears poised to replace DSA and become the new gold standard for such evaluations.
This chapter reviews the epidemiology of non-traumatic intracerebral hemorrhage (ICH) in light of modern neuroimaging and discusses the incidence, etiology, clinical presentation, and natural history of this condition. Risk for ICH appears to be marginally greater in men than in women, driven by an excess of deep hemorrhages. Incidence rates increase dramatically among persons older than 60. Hypertension is the most important and prevalent modifiable risk factor for ICH. The clinical features used to define ICH are presentation with a gradual progression (over minutes or days) or sudden onset of focal neurological deficit, usually accompanied by signs of increased intracranial pressure such as vomiting or diminished consciousness. A variety of reports have examined clinical and radiographic factors associated with prognosis after ICH. Primary intraventricular hemorrhage (IVH) is rare among adults, comprising 2-3% of ICH admissions. Signs and symptoms of IVH frequently include headache, vomiting, and altered level of consciousness.
Clinical outcomes prediction in rudimentary form began as clinical observations of associations between single characteristics and pertinent outcomes. Multivariate modeling in intracerebral hemorrhage (ICH) has focused on determining outcomes and examining the independent effects of specific characteristics (e.g., intraventricular hemorrhage (IVH)) that could help explicate pathophysiological mechanisms and identify potential targets for intervention. Prognostic models have fostered the development of prognosis-based clinical trial methodology in which prognostic models are used to stratify patients. Models can be used to provide a sophisticated historical comparison for data collection in observational studies. Models are also used to define patient groups suitable for specific clinical trials and help to define relevant endpoints that can be prespecified for a particular group according to their expected outcome. Finally, mathematical outcome models have been used to identify specific findings or other characteristics that may affect outcome and be targets for intervention.
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.
Acute hypertensive response is the elevation of blood pressure above normal and premorbid values that initially occurs within the first 24 hours of symptom onset in patients with intracerebral hemorrhage (ICH). Hypertension is the most frequent and most important risk factor for ICH. Hypertensive patients suspected of primary intraparenchymal hematoma died and were subsequently autopsied in order to assess the alterations of extraparenchymal and intraparenchymal vascular structures. Stroke patients with a history of hypertension are at risk of critical hypoperfusion for mean arterial pressure levels usually well tolerated by normotensive individuals. Drugs recommended for use in lowering blood pressure in acute stroke include labetalol, hydralazine, nicardipine, and nitroprusside. The Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH) trial is a prospective, open label phase I safety and tolerability study started in 2005 that plans to study 60 patients.
Perihematomal brain edema (PHBE) plays an important role in secondary brain injury after intracerebral bleeding. Perihematomal brain edema is commonly observed during the acute and subacute phases in patients with intracerebral hemorrhage (ICH). In human studies, early CT scans demonstrate that PHBE develops within three hours of symptom onset. Magnetic resonance imaging is playing an evermore important role in the evaluation of hyperacute cerebrovascular disease. Several mechanisms are implicated in the development of neurological deterioration in patients with ICH. Single-photon emission computerized tomography (SPECT) is useful in the study of PHBE evolution. Several drugs have demonstrated their benefit in PHBE treatment in animal models, and in the future may block PHBE development in clinical practice. Deferoxamine and other iron chelators attenuate brain edema in ICH, and may be potential therapeutic agents for treating ICH, reducing the oxidative stress caused by the release of iron from the hematoma.
This chapter discusses the basic principles of management of intracerebral hemorrhage (ICH), including initial stabilization, the prevention of hematoma growth, and hemodynamic goal-setting. It also talks about the treatment of potential complications such as cerebral edema, herniation and seizures, and identification of the underlying etiology. The occurrence of ICH is strongly related to premorbid blood pressure; however, the relationship between the growth of hematoma and uncontrolled blood pressure remains to be clarified. The medical management of acute ICH revolves around the concept of hematoma stabilization. Recently published research may help identify patients that are at greater risk of hematoma expansion by the presence of tiny enhancing foci following CT angiography. Amyloid angiopathy is a common etiological factor in older patients, especially those older than 65 years who have multiple lobar hemorrhages. In hemorrhages in patients who are on anticoagulation, a risk-benefit ratio needs to be established before restarting anticoagulation.
Intracerebral hemorrhage (ICH) presents clinically in a variety of ways, depending primarily on the location and size of the hematoma. Several studies have correlated the anatomical location of putaminal hemorrhages with their clinical presentation. Caudate hemorrhage presents with sudden onset of headache, vomiting, and altered level of consciousness, resembling subarachnoid hemorrhage (SAH) from ruptured cerebral aneurysm. Behavioral and neuropsychological abnormalities can be a prominent part of the clinical picture of caudate hemorrhage. Lobar ICHs occur in any of the cerebral lobes, generally favoring the parietal and occipital areas although some series have reported a predominance of frontal or temporal locations. Primary hemorrhage into the medulla oblongata is the least common of all brain hemorrhages. The most consistent clinical profile in medullary hemorrhage has been with sudden onset of headache, vertigo, dysphagia, dysphonia or dysarthria, and limb incoordination.
Considerable interest has developed over the past decade in experimental studies of intracerebral hemorrhage (ICH) in animal models. This chapter describes the classical blood infusion ICH models and reviews the collagenase model. It first details the findings from individual species. The chapter then discusses the brain neuropathological responses to ICH in these models, and compares them to observations in human ICH. It addresses the limitations of animal models, and discusses their ability to fully capture the complexities of ICH development in humans. Intraparenchymal infusion (or injection) of autologous arterial blood has been the traditional technique to generate an intracerebral hematoma. The collagenase ICH model, which has been commonly used in the rat and more recently in the mouse, has shed light on various pathochemical events following ICH. Large animal models also permit studies of surgical treatments that could be combined with pharmacological approaches.
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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