Seminars in neurology
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Seminars in neurology · Sep 2006
ReviewEthical issues in critical care and cardiac arrest: clinical research, brain death, and organ donation.
Cardiac arrest results in global hypoxic-ischemic brain injury from which there is a range of possible neurological outcomes. In most cases, patients may require a surrogate to make decisions regarding end-of-life care, including the withdrawal of life-sustaining therapies. This article reviews ethical considerations that arise in the clinical care of patients following cardiac arrest, including decisions to continue or withdraw life-sustaining therapies; brain death determination; and organ donation in the context of brain death and cardiac death (so-called non-heart-beating donation). This article also discusses ethical concerns pertaining to the design and conduct of resuscitation research that is necessary for the development of effective therapies to prevent anoxic brain injury or promote neurological recovery.
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Seminars in neurology · Sep 2006
ReviewElectrophysiological prognostication and brain injury from cardiac arrest.
Anoxic coma after cardiorespiratory arrest warrants precocious investigation to establish probable outcome. Electroencephalogram (EEG) may uncover subclinical seizures; EEG grades have provided accurate prognosis of poor and favorable outcomes, but are weakest in those patients in between. ⋯ Combining clinical examination with electrophysiology has increasingly yielded multimodality approaches to early prognostication of coma after cardiorespiratory arrest, with more recent studies using event-related and middle-latency potentials showing promise for distinguishing good outcome (to consciousness), from awake but vegetative states. Further studies are warranted for this multimodality approach which, hopefully, may yield more widespread practical use of these testing modalities.
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Seminars in neurology · Sep 2006
ReviewLong-term neurological complications after hypoxic-ischemic encephalopathy.
Hypoxic-ischemic encephalopathy accompanying cardiac arrest is a common cause of long-term neurological dysfunction. With the improvement in prehospital emergency systems, larger numbers of people are resuscitated from cardiac arrests, although with the increased prospect of neurological sequelae. Neurological impairment after cardiac arrest is dependent on the degree of brain damage suffered during the arrest. ⋯ Neurological impairments range from mild cognitive deficits to severe motor and cognitive deficits that preclude independence in many activities of daily living. Several neurological syndromes have been described in patients who awaken from hypoxic-ischemic coma with lasting motor and cognitive deficits. This review will address many of the common syndromes after hypoxic-ischemic encephalopathy, including persistent vegetative states, seizures, myoclonus, movement disorders, cognitive dysfunction, and other neurological abnormalities.
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Seminars in neurology · Sep 2006
ReviewMechanisms of injury in hypoxic-ischemic encephalopathy: implications to therapy.
Cardiac arrest survivors commonly suffer ischemic brain injury, and understanding the mechanisms of injury is essential to providing insight for effective therapies for brain protection. Injury can occur at the time of the cardiac arrest and is dependent not only on the duration but also the degree of impaired circulation. ⋯ This section will review the molecular basis of injury with cardiac arrest and will elucidate the different mechanisms of injury between cardiac arrest, pure respiratory arrest, and arrest secondary to toxins (e.g., carbon monoxide). The rationale for multiple postarrest therapies, such as hypothermia and induced hypertension, will also be reviewed.
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Seminars in neurology · Sep 2006
ReviewTherapeutic hypothermia for brain injury after cardiac arrest.
Morbidity and mortality in patients successfully resuscitated from cardiac arrest primarily depends on neurological outcome. Clinical trials of therapies directed toward reducing the extent of neuronal damage by means of pharmacological agents have been disappointing. To date, the only clinically effective tool for amelioration of brain damage by ischemia and reperfusion is mild to moderate induced hypothermia. The pathophysiology of global hypoxic-ischemic brain injury, the mechanisms by which hypothermia confers neuroprotection, and the encouraging beneficial effects of mild to moderate hypothermia in experimental studies and clinical trials are discussed.