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Biomedical subjects

Romergryko G Geocadin

Publications and source records attributed to Romergryko G Geocadin.

12 recordsLinked to original sources

Quantitative EEG and neurological recovery with therapeutic hypothermia after asphyxial cardiac arrest in rats.

We test the hypothesis that quantitative electroencephalogram (qEEG) can be used to objectively assess functional electrophysiological recovery of brain after hypothermia in an asphyxial cardiac arrest rodent model. Twenty-eight rats were randomly subjected to 7-min (n = 14) and 9-min (n = 14) asphyxia times. One half of each group (n = 7) was randomly subjected to hypothermia (T = 33 degrees C for 12 h) and the other half (n = 7) to normothermia (T = 37 degrees C). Continuous physiologic monitoring of blood pressure, EEG, and core body temperature monitoring and intermittent arterial blood gas (ABG) analysis was undertaken. Neurological recovery after resuscitation was monitored using serial Neurological Deficit Score (NDS) calculation and qEEG analysis. Information Quantity (IQ), a previously validated measure of relative EEG entropy, was employed to monitor electrical recovery. The experiment demonstrated greater recovery of IQ in rats treated with hypothermia compared to normothermic controls in both injury groups (P < 0.05). The 72-h NDS of the hypothermia group was also significantly improved compared to the normothermia group (P < 0.05). IQ values measured at 4 h had a strong correlation with the primary neurological outcome measure, 72-h NDS score (Pearson correlation 0.746, 2-tailed significance <0.001). IQ is sensitive to the acceleration of neurological recovery as measured NDS after asphyxial cardiac arrest known to occur with induced hypothermia. These results demonstrate the potential utility of qEEG-IQ to track the response to neuroprotective hypothermia during the early phase of recovery from cardiac arrest.

Animals↗

Intensive care after resuscitation from cardiac arrest: a focus on heart and brain injury.

Less than 3% of all patients who have out-of-hospital cardiac arrests have return of spontaneous circulation (ROSC), survive the hospitalization, and have a reasonable functional recovery. The fact that many patients who have ROSC ultimately die or fail to have favorable neurologic recovery suggests that processes that occur after hospitalization, especially in the ICU, have an impact on survival and neurologic recovery. This article addresses the acute care, with emphasis on the cardiac and neurologic aspects,that patients who have post cardiac arrest are provided in the cardiac ICU.

Arrhythmias, Cardiac↗

Postresuscitative 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. To date, no neuroprotectant medications have been shown to improve neurological outcome. 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.

Brain Infarction↗

Ethical 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.

Advance Directives↗

Quantitative EEG and effect of hypothermia on brain recovery after cardiac arrest.

In this paper, we provide a quantitative electroencephalogram (EEG) analysis to study the effect of hypothermia on the neurological recovery of brain after cardiac arrest. We hypothesize that the brain injury results in a reduction in information of the brain rhythm. To measure the information content of the EEG a new measure called information quantity (IQ), which is the Shannon entropy of decorrelated EEG signals, is developed. For decorrelating EEG signals, we use the discrete wavelet transform (DWT) which is known to have good decorrelating properties and to show a good match to the standard clinical bands in EEG. In measuring the amount of information, IQ shows better tracking capability for dynamic amplitude change and frequency component change than conventional entropy-based measures. Experiments are carried out in rodents (n = 30) to monitor the neurological recovery after cardiac arrest. In addition, EEG signal recovery under normothermic (37 degrees C) and hypothermic (33 degrees C) resuscitation following 5, 7, and 9 min of cardiac arrest is recorded and analyzed. Experimental results show that the IQ is greater for hypothermic than normothermic rats, with an IQ difference of more than 0.20 (0.20 +/- 0.11 is 95% condidence interval). The results quantitatively support the hypothesis that hypothermia accelerates the electrical recovery from brain injury after cardiac arrest.

Algorithms↗

Safety of induced hypertension therapy in patients with acute ischemic stroke.

INTRODUCTION: The management of blood pressure in acute stroke is controversial. Small pilot studies have suggested that blood pressure augmentation improves short-term neurological function, but the rate of adverse events with induced hypertension (IH) therapy is unknown. METHODS AND RESULTS: We reviewed 100 consecutive patients who underwent perfusion magnetic resonance imaging for acute ischemic stroke. IH therapy was employed in 46 patients and standard therapy (ST) in 54. The two groups had similar baseline characteristics, but more patients in the IH group had significant large-artery stenoses. The IH group achieved significantly higher mean arterial pressure (MAP) than the ST group within 3 days of initiation of therapy with a variety of vasopressor agents. Only 35% of patients in the IH group actually achieved the target MAP augmentation of 10-20% above baseline, however. All patients survived to discharge. Four patients experienced major adverse events in each group. Two patients in the IH group experienced intra cerebral hemorrhage compared to none in the ST group. Two patients in the ST group experienced myocardial ischemia, compared to none in the IH group. The National Institutes of Health Stroke Scale during the hospitalization and place of discharge were similar in both groups. Patients in the IH group were more likely to be admitted to the intensive care unit and had a longer hospital stay by nearly 4 days compared to the ST group. CONCLUSION: These data demonstrate the relative safety of IH therapy in acute stroke patients. Given the greater use of resources, however, the role of IH in improving clinical outcomes requires a prospective, randomized trial.

Aged↗

Effect of acute hypoxic preconditioning on qEEG and functional recovery after cardiac arrest in rats.

Acute hypoxic preconditioning (AHPC) can confer neuroprotection from global cerebral ischemia such as cardiac arrest. We hypothesize that acute neuroprotection by AHPC will be detected early by quantitative EEG (qEEG) entropy analysis after asphyxial cardiac arrest (aCA). Cerebral ischemia lowers EEG signal randomness leading to low entropy. A qEEG entropy index defined as the duration when the entropy measure is 15% below uninjured baseline entropy is used as a measure of injury. We compared 3 groups of adult Wistar rats: (1) untreated controls that were subjected to 5 min of aCA and were resuscitated (n = 5); (2) AHPC-treated group with 10% FI O2 for 30 min, then 25 min of room air, 5 min of aCA followed by resuscitation (n = 5); and (3) a surgical sham group (no aCA) (n = 3). Functional outcome was assessed by neurodeficit score (NDS) which consisted of level of consciousness, cranial nerve, motor-sensory function, and simple behavioral tests (best = 100 and brain dead = 0). We found that increasing entropy index of injury at 0-5 h from return of spontaneous circulation (ROSC) is associated with worsening NDS at 24 h (linear regression: r = 0.81, P < 0.001). The NDS of the group sham (84.7 +/- 2.8) (mean +/- SEM) and AHPC group (84.6 +/- 2.9, P > 0.05) was better than control injury group (52.2 +/- 8.4, P < 0.05) (ANOVA with Tukey test). We therefore conclude that AHPC confers acute neuroprotection at 24 h, which was detected by qEEG entropy during the first 5 h after injury.

Analysis of Variance↗

Rhabdoid meningioma occurring in an unrelated resection cavity with leptomeningeal carcinomatosis. Case report.

Rhabdoid meningioma (RM) is a recently described, aggressive variant of meningioma. The authors report a case of RM occurring in the resection cavity of an unrelated neurosurgical procedure, temporal lobectomy for intractable seizures. The patient presented with intractable headache 10 years after the temporal lobectomy. Imaging revealed a dura-based, uniformly enhancing lesion within the resection cavity. She underwent gross-total resection and the findings of the surgical pathological report were consistent with an RM, with a dramatically elevated MIB-1 index of approximately 50%. The patient's clinical course was complicated by severe pain and communicating hydrocephalus secondary to rapid dissemination of malignant cells throughout the CSF pathways. Despite aggressive measures, including tumor resection, ventriculoperitoneal shunt placement, and the initiation of conventional radiation therapy, the ensuing leptomeningeal carcinomatosis proved to be rapidly fatal.

Adult↗

Intracerebral hemorrhage and postpartum cerebral vasculopathy.

INTRODUCTION: Intracerebral hemorrhage (ICH) associated with pregnancy commonly occurs in the postpartum period in the setting of preeclampsia/eclampsia. We describe the clinical course of two patients with ICH due to postpartum cerebral vasculopathy in the absence of toxemia. METHODS: We reviewed two cases with ICH and postpartum vasculopathy in our hospital (1996-2001) and compared them with seven similar case reports from the literature. RESULTS: Mean age of all patients is 28.7+/-5.6 years (mean+/-S.D.). Toxemia of pregnancy was absent in all cases. ICHs were cortical in eight and putaminal in one patient. Erythrocyte sedimentation rate was elevated in two. Two cases rehemorrhaged during the same admission. No cerebral infarctions were reported. All patients had diffuse vasculopathy on conventional catheter angiography, with no clinical manifestations or laboratory data supportive of extracerebral or systemic vasculitis. Eight patients were treated with corticosteroids, two with additional cytotoxic agents and one with nimodipine alone. Improvement on follow-up cerebral angiography (catheter or MRA) and transcranial Doppler ultrasonography (TCD) was noted in eight cases. One did not have follow-up cerebral imaging but had an excellent clinical outcome. All cases had good to excellent functional recovery. CONCLUSIONS: Postpartum ICH in the absence of toxemia may be associated with isolated cerebral vasculopathy. The clinical course and functional outcome is good to excellent. This entity appears to be distinct from cerebral vasculitis, which is usually associated with poor outcome.

Adrenal Cortex Hormones↗

Neurological recovery by EEG bursting after resuscitation from cardiac arrest in rats.

INTRODUCTION: The return of neurological function during the early period after resuscitation from cardiac arrest (CA) has not been evaluated systematically. We report the temporal analysis of EEG bursting pattern during the very early periods after resuscitation. DESIGN/METHOD: A balanced group of good and poor outcome animals was selected from a population of rats subjected to either 5 or 7 min of asphyxial cardiac arrest (ACA) on the basis of a single criteria: 24 h neurobehavioral function based on the neurodeficit score (NDS). The EEGs of six consecutive good outcome rats (NDS > or = 60) and six consecutive poor outcome rats (NDS < 60) were selected for the study. The EEGs of these animals were given to two EEG examiners who were blinded to the selection process, the experimental conditions and the neurobehavioral recovery. The EEG bursting characteristics, such as rate, peak and duration of bursting were studied. RESULTS: There was significantly higher EEG bursting in the good outcome animals (P < 0.05) and the burst complexes evolved into continuous activity by 90 min. Lower frequency bursting that persisted and failed to evolve into continuous activity was observed in the poor outcome group. CONCLUSION: Increased EEG bursting during first 30-40 min after resuscitation from moderate to severe ACA was observed in rats with good neurological outcome at 24 h. Early EEG bursting patterns may provide additional prognostication after resuscitation from CA.

Analysis of Variance↗