Handbook of clinical neurology
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Cardiac arrest is a common and serious medical emergency affecting upwards of 450000 Americans on an annual basis. It causes a substantial strain on the physical and financial resources of the medical system. ⋯ This review focuses on epidemiologic data, current management recommendations, clinical and ancillary testing to suggest long-term prognosis, and common complications of cardiac arrest. Particular attention has been paid to updates, including therapeutic hypothermia, since this topic was last reviewed in 1993.
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Cardiac manifestations of neurologic diseases are common in clinical practice. There are numerous anatomic and pathophysiologic links between the normal and abnormal function of both systems. ⋯ This is exemplified in the area of vascular neurology where knowledge of the brain-heart connection is essential not only for bedside management but where collaborative efforts between neurology and cardiology are key in developing new strategies for ischemic stroke prevention and treatment, atrial fibrillation, and interventional techniques. This chapter will focus on cardiac manifestations of neurologic disease, with special emphasis on vascular and intensive care neurology, epilepsy, and neurodegenerative and peripheral nervous system diseases.
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There is an increasing incidence and prevalence of patients with chronic kidney disease (CKD) in Western industrialized countries and currently is estimated at approximately 10% of adults aged over 20 years. Renal failure causes an excessively increased risk of cerebrovascular and cardiovascular complications. Moreover, renal failure leads to a number of the neurologic symptoms neurologists are often confronted with. ⋯ Complications of the central nervous system (e.g., uremic encephalopathy, disequilibrium syndrome, and drug induced disorders) are reviewed. It has long been known that uremia leads to peripheral nerve injury. Frequent neurological diseases such as uremic polyneuropathy, autonomic neuropathy, and a range of mononeuropathies are discussed.
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Painful diabetic distal symmetrical polyneuropathy (painful DPN) is a puzzle with two important missing pieces: Firstly we still do not understand why only some patients with neuropathy experience painful symptoms; Secondly we still do not have a complete understanding of how nociception generated in the peripheral nervous system is processed by the central nervous system (CNS). Available treatments offer only symptom relief and there is currently no effective treatment based on arresting or reversing the progression of disease. Therefore the management of painful DPN remains less than optimal because the complex pathophysiology of nociception and pain perception in health and disease is incompletely understood. ⋯ Combining the knowledge from these two streams of enquiry we will soon be able to predict accurately who will develop painful DPN, how we can halt or reverse the condition, or who will respond to symptomatic treatments. Future developments in the treatment of painful DPN will be underpinned by decoding the peripheral and central mechanisms of pain. Research is focusing on these areas of enquiry in the hope that answers will lead to effective treatments to alleviate pain and reverse pathology for those suffering from painful DPN.
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Patients with hemophilia and other congenital bleeding disorders are at risk for development of central nervous system (CNS) hemorrhage and can present with acute or chronic neurologic symptoms. These disorders are generally caused by qualitative or quantitative deficiency of components of hemostasis such as coagulation proteins, von Willebrand factor, or platelets. ⋯ Since hemophilia is the most common bleeding disorder encountered in clinical practice, more emphasis is placed on management of hemophilia. Additionally, neurologic manifestations related to the bleeding diathesis in patients with hemophilia are elaborated.