Outcome from coma caused by cerebral hypoxia-ischemia (eg, cardiac arrest) was compared with serial neurological findings in 210 patients. Thirteen percent of patients regained independent function at some point during the first postarrest year. Computer application of new multivariate techniques to the prospectively observed findings generated easily utilized rules that classified patients by likely outcome. At the time of initial examination, 52 patients (one fourth of the total population) had absent pupillary light reflexes, and none of these patients ever regained independent daily function. By contrast, the initial presence of pupillary light reflexes, the development of spontaneous eye movements that were roving conjugate or better, and the findings of extensor, flexor, or withdrawal responses to pain identified a smaller group of 27 patients, 11 (41%) of whom regained independence in their daily lives. By 24 hours after onset, 93 poor-outcome patients were identified by motor responses that were absent, extensor, or flexor and by spontaneous eye movements that were neither orienting nor roving conjugate; only one regained independent function. This contrasts with recovery in 19 (63%) of 30 patients who at that time showed improvement in their eye-opening responses and obeyed commands or had motor responses that were withdrawal or localizing. Similarly simple rules distinguished between good- and poor-prognosis patients on postarrest days 3, 7, and 14.
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"Quite recently, several advances in cerebral imaging, in biochemical markers and in neurophysiological testing have been studied in OHCA    . However, despite promising results, the neurological examination remains in most ICUs the cornerstone of the outcome assessment and relies on absent pupillary or corneal reflexes or absent or no better than extensor motor response at day 3    . The prognostic value of the Glasgow Coma Scale (GCS) has been previously studied  . "
"Transient ischemia in the brain causes irreversible cognitive deficits, including memory disturbances (Levy et al., 1985; Volpe and Petito, 1985), since neurons are extremely susceptible to injury caused by low oxygen and glucose concentrations (Rakic, 1985). Consequently, neuronal protection is an important issue in neurosurgery, cardiac surgery, and intensive care for the management of patients with traumatic brain injuries, where the brain is frequently exposed to ischemia (Arrowsmith et al., 2000; Hoffman et al., 1997; Levine, 1989; Levy et al., 1985; Nussmeier, 1996). Since hippocampal pyramidal neurons are particularly vulnerable to ischemic events, cultured hippocampal slices are often used for the evaluation of neuronal vulnerability, as well as to assess the neuroprotective effects of drugs (Feiner et al., 2005; Gray et al., 2005; Holopainen, 2005; Lee et al., 2006; Son et al., 2004). "
[Show abstract][Hide abstract] ABSTRACT: JM-1232(-) (JM) is a novel isoindoline derivative with sedative and hypnotic activities that are mediated by binding to the benzodiazepine site of the Gamma-aminobutyric acid type A (GABA(A)) receptor. Although the neuroprotective effects of other GABAA receptor agonists are well known, there is no published report regarding JM. Thus, we examined the effects of JM on neurons exposed to oxygen-glucose deprivation (OGD) using rat hippocampal slice cultures. Hippocampal slices were assigned to either control or JM-administered groups. To assess the neuroprotective effects of JM from necrotic changes, we measured the fluorescence of propidium iodide and compared the cell mortality 24 h following OGD between the control and JM-administered groups. We also verified that the effects of JM were mediated by GABAA receptors by adding flumazenil, a benzodiazepine receptor antagonist, in the same experimental settings. JM, at concentrations of 250 and 500 mu M, significantly reduced cell mortality in pyramidal neurons after OGD; however, flumazenil did not inhibit this effect. To analyze more immediate effects of JM, we next measured the fluorescence of Oregon Green 488 BAPTA-1 during the OGD and re-oxygenation periods, and evaluated changes in intracellular Ca2+ in single CA1 pyramidal neurons. JM reduced the elevation of intracellular Ca2+ concentration during OGD, and this effect was antagonized by flumazenil. These findings indicate that JM suppressed the elevation of intracellular Ca2+ concentration during OGD through GABAA receptors, but its neuroprotective effects from necrotic changes also involve other unknown mechanisms.
"Early prediction of outcome may be, in fact, an important aspect to be considered during the postresuscitation care in order to avoid the likelihood of unnecessary prolongation of TH when a good functional recovery has already been achieved or to avoid unjustified withdrawal of care if the protection has not been fully achieved yet. For years, neurological examination and electrophysiological studies have guided physicians in predicting outcome in comatose survivors of CA, including pupillary light response, serum neuron-specific enolase, somatosensory evoked potentials, and combinations thereof [11–14]. But early prognostication remains challenging, especially because the predictive values of clinical, biochemical, and electrophysiological variables have become uncertain after the introduction of TH [15–17]. "
[Show abstract][Hide abstract] ABSTRACT: Purpose:
To investigate the effect of hypothermia on 96 hr neurological outcome and survival by quantitatively characterizing early postresuscitation EEG in a rat model of cardiac arrest.
Materials and methods:
In twenty male Sprague-Dawley rats, cardiac arrest was induced through high frequency transesophageal cardiac pacing. Cardiopulmonary resuscitation was initiated after 5 mins untreated arrest. Immediately after resuscitation, animals were randomized to either 2 hrs of hypothermia (N = 10) or normothermia (N = 10). EEG, ECG, aortic pressure, and core temperature were continuously recorded for 6 hrs. Neurological outcome was evaluated daily during the 96 hrs postresuscitation period.
No differences in the baseline measurements and resuscitation outcome were observed between groups. However, 96 hr neurological deficit score (204 ± 255 versus 500 ± 0, P = 0.005) and survival (6/10 versus 0/10, P = 0.011) were significantly better in the hypothermic group. Quantitative analysis of early postresuscitation EEG revealed that burst frequency and spectrum entropy were greatly improved in the hypothermic group and correlated with 96 hr neurological outcome and survival.
The improved burst frequency during burst suppression period and preserved spectrum entropy after restoration of continuous background EEG activity for animals treated with hypothermia predicted favorable neurological outcome and survival in this rat model of cardiac arrest.