Seminars in neurology
-
Seminars in neurology · Sep 2006
ReviewPostresuscitative intensive care: neuroprotective strategies after cardiac arrest.
Cardiac arrest is a common disease in the United States, and many patients will die as a result of the neurological damage suffered during the anoxic period, or will live in a neurologically debilitated state. When cardiopulmonary-cerebral resuscitation results in the return of spontaneous circulation, intensive care is required to optimize neurological recovery. Such "brain-oriented" therapies include routine care, such as positioning and maintenance of volume status; optimization of cerebral perfusion, with the use of vasopressors if needed; management of increased intracranial pressure with agents such as hypertonic saline; assuring adequate oxygenation and avoiding hypercapnia; aggressive fever control; intensive glucose control, with the use of an insulin drip if needed; and management of seizures if they occur. ⋯ Induced moderate therapeutic hypothermia is utilized as a neuroprotective maneuver. Future treatment options and advanced monitoring techniques are also discussed. Further study to optimize neuroprotective strategies when treating patients who survive cardiac arrest is needed.
-
Seminars in neurology · Sep 2006
ReviewPrehospital interventions to improve neurological outcome following cardiac arrest.
As many cases of cardiac arrest occur outside of the health care setting, prehospital treatment may dramatically affect patient outcomes. The three major interventions that have been studied are chest compressions and ventilation, electrical defibrillation, and medications. Recent studies show that increasing the rate of cardiopulmonary resuscitation (CPR), decreasing the rate of ventilation, and initiation of CPR prior to defibrillation may result in improved survival. ⋯ Public access to automatic defibrillators has been shown to increase the survival of cardiac arrest patients. Medications such as amiodarone, vasopressin, and thrombolytics also may have a role in the prehospital treatment of cardiac arrest. Recent advances in these areas will be reviewed with a discussion of the effect of each intervention on the restoration of circulation and neurological outcomes.
-
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.
-
Seminars in neurology · Apr 2006
Review Historical ArticleParoxysmal hemicrania, SUNCT, and hemicrania continua.
The trigeminal autonomic cephalalgias (TACs) are a group of primary headache disorders characterized by unilateral pain in the somatic distribution of the trigeminal nerve and ipsilateral autonomic signs, which reflect activation of the cranial parasympathetic pathway. The group includes cluster headache, paroxysmal hemicrania, and short-lasting unilateral neuralgiform headache with conjunctival injection and tearing. Hemicrania continua was previously classified as one of the TACs. Despite their common elements, individually these headaches differ with respect to attack duration, frequency, and response to indomethacin.