Neurologic clinics
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Electrophysiologic testing continues to play an important role in injury stratification and prognostication in patients who are comatose after cardiac arrest. As discussed previously, however, the adage about treating whole patients, not just the numbers, is relevant in this situation. EEG and SSEP can offer high specificity for discerning poor prognosis as long as they are applied to appropriate patient populations. ⋯ Aside from prognostication, electrophysiologic testing holds great promise in defining the basic anatomy and physiology of coma emergence after cardiac arrest. In addition, quantitative EEG and automated evoked potentials have the potential to render these tools less subjective and arcane and more applicable for monitoring patients in the period during and immediately after resuscitation. Quantitative EEG also has great potential asa tool to define the time window for neuroprotective intervention and the means to track the response to such therapies in real time.
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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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Neuronal injury following global cerebral ischemia continues to bea central problem of patients in the postresuscitation phase following cardiocirculatory arrest. In addition to measures focusing on rapid restoration of spontaneous circulation, the most effective treatment after cardiac arrest, as shown by large randomized trials,is the use of therapeutic mild hypothermia. ⋯ At present there is no specific neuroprotective treatment available. Promising animal experimental data concerning the use of thrombolytic agents during cardiopulmonary resuscitation have led to a large European multicenter trial (TROICA trial) that will provide its data in 2006.
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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.
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Nocturnal sleep-related ventilatory alterations may occur in dis-proportion to the severity of the neuromuscular disorder. Diaphragm paralysis occurring with a neuromuscular disorder is an overlooked complication. ⋯ Polysomnographic evaluation is recommended for patients who have neuromuscular disorder who develop symptoms and signs of sleep-wake abnormality or nocturnal respiratory failure. Application of noninvasive positive airway ventilation and, in some cases, administration of supple-mental oxygen may improve quality of life and prolong survival of patients who have neuromuscular disorder.