Neurologic clinics
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Data from randomized therapeutic trials often provide little relevant evidence for therapeutic decisions physicians make daily. By illustrating the nuances of these four complex cases involving cerebrovascular disease, the authors stress the importance of more time spent by specialists at the bed-side, exploring patients' symptoms and learning their thoughts, fears, biases, and wishes.
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In this series of clinical vignettes, the authors have attempted to provide a "feel" for the varied causes of syncope. The neurologist should be able to diagnose most causes of syncope using a simple algorithmic approach. Initial evaluation includes detailed clinical history, physical examination, and 12-lead ECG. ⋯ Patients with heart disease will need the most comprehensive evaluations, possibly including exercise testing, cardiac electrophysiology, and tilt-table testing. As better understanding of pathophysiology and epidemiology emerge, under-standing of the diagnosis and treatment of syncope will improve. In the meantime, there is no substitute for astute clinical acumen.
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Considerable progress has been made in providing high-quality prehospital and emergency cardiac care for OHCA victims. The use of early CPR, early defibrillation, early ACLS, and state-of-the-art postresuscitation care offers the best promise for improved community survival and neurologic outcome statistics in the future. The NIH-sponsored Resuscitation Outcomes Consortium represents the largest governmentally sponsored effort of its kind that that will test the value of promising pharmacologic and device interventions on improving survival and neurologic outcome in OHCA patients.
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Intensive care technologies have led to an increase in patients who are neurologically devastated and deceased. The practical, moral, and ethical situations encountered can be varied and challenging to manage. Decisions and discussions surrounding withdrawal of care, death by neurologic criteria, and organ donation require significant knowledge of the prognosis, ancillary testing, and definitions of these processes. Experience and skill are often required on the part of physicians and staff to guide families through these most difficult of circumstances.
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It is difficult to predict precisely the final neurologic outcome from cardiac arrest and accompanying cerebral hypoxia. Although rare, several movement disorders may arise as a consequence of hypoxic injury, including myoclonus, dystonia, akinetic-rigid syndromes, tremor, and chorea. ⋯ Many outstanding questions remain, however. What factors promote susceptibility to the development of posthypoxic movement disorders? Why do patients who have similar clinical hypoxic insults develop markedly dis-similar movement disorders? Why are the basal ganglia especially vulnerable to cerebral hypoxia? Why do some movement disorders occur in delayed fashion and progress for years after the hypoxic insult? Is the pathogenesis of progressive posthypoxic movement disorders related to that of neurodegenerative diseases? What are the most effective medications for the various posthypoxic movement disorders? Is there a role for deep brain stimulation in the treatment of posthypoxic movement disorders? We anticipate that current and future research in the area of posthypoxic movement disorders will reveal answers to some of these important questions.