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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Almost half of patients respond acutely to resuscitation but most die within the first several days after arrest. The incidence of survival to discharge from the hospital after cardiopulmonary arrest is about 15%; one third of those surviving have evidence of neurologic deficits. Although some prognostic variables are useful in determining which patients are most likely to die prior to discharge from the hospital, each patient needs to be evaluated on an individual basis and the various risk factors weighed carefully. As additional data accumulate, we may well be more effective at deciding which patients are more likely to benefit from CPR so that we can more judiciously apply this therapeutic modality. A number of studies have identified factors that contribute to poor outcome. Patients over 70 years of age usually fare poorly after CPR, but this is more a reflection of the number of coexisting diagnoses rather than years. Although initial survival may not be different from younger patients, fewer elderly patients live to discharge and more are likely to have neurologic sequelae. Concurrent diagnoses such as sepsis, AIDS, gastrointestinal bleeding, renal failure, cancer, and central nervous system disease have a universally poor response to CPR. If defibrillation occurs more than 6 minutes after arrest or on the general ward or if the resuscitative attempt lasts longer than 15 minutes, mortality is greater than 95%. If CPR continues for more than 30 minutes, there are no survivors. A low exhaled CO2 concentration (< 2%) during cardiac massage, asystole or EMD as the first identified rhythm, and recurrent arrest also carry a poor prognosis. On the other hand, at the time of arrest or during the immediate postarrest period, poor neurologic status is a less helpful predictor. The absence of spontaneous respiration is the only variable at the time of admission after out-of-hospital arrest that is particularly ominous. There is no evidence to suggest that the absence of spontaneous respiration implies any better prognosis for patients arresting in the hospital. Coma, hypoxic myoclonus, and absent reflexes, while not useful immediately following arrest, are of greater prognostic significance 48 hours later. Only 5% of patients who are unconscious 48 hours after arrest will have a full neurologic recovery. The Glasgow Coma Scale has also been used for prognostication.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Resuscitation: when is enough, enough? 1014 87

Hypoxic-ischemic brain injury (HI-BI) after cardiac arrest commonly results in neurological injury and long term dysfunction, with outcomes ranging from coma and vegetative states to functional disability with various degrees of dependence. Increased rates of bystander CPR and cardiac defibrillation has led to a rapid increase in successful resuscitations. Patients who reach the hospital after cardiac arrest may develop various neurological deficits or clinical syndromes that may preclude recovery to their premorbid baseline. Consequently, clinicians are faced with not only predicting outcome regarding wakefulness and independence but also with long term therapeutic management. Several neurological syndromes have been reported as consequences of HI-BI. This review will describe some of the more common syndromes seen after HI-BI, including the various levels of arousal, seizures, myoclonus, movement disorders, cognitive impairments, and other specific neurological abnormalities.
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PMID:Neurological sequelae of hypoxic-ischemic brain injury. 2013 Mar 54

Motor deficits are present in cardiac arrest survivors and injury to cerebellar Purkinje cells (PCs) likely contribute to impairments in motor coordination and post-hypoxic myoclonus. N-Methyl-D-aspartic acid (NMDA) receptor-mediated excitotoxicity is a well-established mechanism of cell death in several brain regions, but the role of NMDA receptors in PC injury remains understudied. Emerging data in cortical and hippocampal neurons indicate that the GluN2A-containing NMDA receptors signal to improve cell survival and GluN2B-containing receptors contribute to neuronal injury. This study compared neuronal injury in the hippocampal CA1 region to that in PCs and investigated the role of NMDA receptors in PC injury in our mouse model of cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Analysis of cell density demonstrated a 24% loss of PCs within 24 h after 8 min CA/CPR and injury stabilized to 33% by 7 days. The subunit promiscuous NMDA receptor antagonist MK-801 protected both CA1 neurons and PCs from ischemic injury following CA/CPR, demonstrating a role for NMDA receptor activation in injury to both brain regions. In contrast, the GluN2B antagonist, Co 101244, had no effect on PC loss while protecting against injury in the CA1 region. These data indicate that ischemic injury to cerebellar PCs progresses via different cell death mechanisms compared to hippocampal CA1 neurons.
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PMID:Region-specific role for GluN2B-containing NMDA receptors in injury to Purkinje cells and CA1 neurons following global cerebral ischemia. 2545 Sep 57