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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Creatine kinase (CK) and its brain-specific isoenzyme (CK-BB), neuron-specific enolase (NSE), neural cell adhesion molecule (NCAM) and the ions sodium, potassium, chloride and calcium were measured both in CSF and serum and inorganic phosphate in CSF in order to assess their prognostic value in total brain ischemia due to cardiac arrest. The samples were collected at 4, 28 and 76 h after resuscitation. Twenty consecutive patients resuscitated from ventricular fibrillation or asystole were included in the study. Nine of the patients recovered consciousness (recovered) but eleven remained comatose (disabled). The follow-up period was 2 years after which only one patient was still alive. The earliest statistically significant differences between neurologically recovered and disabled patient groups were seen in CSF inorganic phosphate (P = 0.030) already at 4 h and CK-BB (P = 0.046) and NSE (P = 0.020) activity at 28 h. Later, at 76 h after the resuscitation CSF NSE differentiated the groups most clearly (P = 0.014). The values were higher in the disabled patients. A negative correlation between CSF parameters and Glasgow Coma scores was also seen at these timepoints. Statistically significant differences between the groups were seen in both CSF and blood pCO2, pO2, base excess (BE) and actual bicarbonate (HCO3-). CSF or serum NCAM has no prognostic value in anoxic-ischemic coma. The results suggest that in CSF CK-BB and NSE are useful prognostic indicators of hypoxic brain injury when measured 28-76 h after cardiac arrest whereas blood samples have no prognostic value.
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PMID:CSF and serum brain-specific creatine kinase isoenzyme (CK-BB), neuron-specific enolase (NSE) and neural cell adhesion molecule (NCAM) as prognostic markers for hypoxic brain injury after cardiac arrest in man. 850 98

In-vivo microdialysis has been used extensively to study the neurochemical mechanisms of ischemia, epilepsy and hypoglycemia. It is also being increasingly used to document the response of neurons to various medications. Most of the work to date has been done in small animals. In the last 2 years, the technique has been adapted for use in patients with subarachnoid hemorrhage, head trauma, Parkinson's disease, brain tumors and epilepsy. Two of the major limiting factors are the invasiveness of the technique and the resultant potential for CNS infection. We describe a simple, safe and reliable method to measure neurochemical changes in the human brain with in-vivo microdialysis. We were able to easily monitor for 4-6 h daily for up to 4 days in awake or comatose patients with subarachnoid hemorrhage or head trauma. Cerebral concentrations of glutamate, GABA, other amino acids and catecholamines were measured. This technique thus has a potential for on-line measurements of neurotoxins in patients with unstable neurological conditions.
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PMID:A new method of in-vivo microdialysis of the human brain. 854 74

Laboratory studies of moderate hypothermia (30-33 degrees C) after injury show diminished neuronal loss after ischemia, diminished excessive neurotransmitter release after ischemia, prevention of blood-brain barrier disruption after ischemia and brain injury, and behavioral improvement after brain injury. Clinical literature suggests that brief periods of moderate hypothermia (> or = 30 degrees C) in humans are not associated with cardiovascular, hematologic, metabolic, or neurological toxicity. Clinical studies were, therefore, organized to investigate the potential application of moderate systemic hypothermia in patients after severe brain injury. A study of 21 elective craniotomy patients and 11 patients with severe brain injury led to the conclusion that 32 to 33 degrees C was the lowest safe temperature in patients with severe brain injury. A randomized study of moderate hypothermia in 46 patients with Glasgow Coma Score (GCS) 4-7 gave an indication of improved neurologic outcome in the hypothermia group. A multicenter, randomized protocol to test the effect of moderate systemic hypothermia in patients with severe brain injury is in progress. Funded by the National Institutes of Health, The National Acute Brain Injury Study: Hypothermia tests the hypothesis that systemic hypothermia to 32-33 degrees C if rendered within 6 h of injury improves Glasgow Outcome Scores (GOS) at 6 months after injury in patients with severe brain injury (GCS 3-8).
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PMID:Systemic hypothermia in treatment of severe brain injury: a review and update. 859 21

Severe traumatic brain injuries are extremely heterogeneous. At least seven of the secondary derangements in the brain that have been identified as occurring after most traumatic brain injuries also occur after cardiac arrest. These secondary derangements include posttraumatic brain ischemia. In addition, traumatic brain injury causes insults not present after cardiac arrest, i.e., mechanical tissue injury (including axonal injury and hemorrhages), followed by inflammation, brain swelling, and brain herniation. Brain herniation, in the absence of a mass lesion, is due to a still-to-be-clarified mix of edema and increased cerebral blood flow and blood volume. Glutamate release immediately after traumatic brain injury is proven. Late excitotoxicity needs exploration. Inflammation is a trigger for repair mechanisms. In the 1950s and 1960s, traumatic brain injury with coma was treated empirically with prolonged moderate hypothermia and intracranial pressure monitoring and control. Moderate hypothermia (30 degrees to 32 degrees C), but not mild hypothermia, can help prevent increases in intracranial pressure. How to achieve optimized hypothermia and rewarming without delayed brain herniation remains a challenge for research. Deoxyribonucleic acid (DNA) damage and triggering of programmed cell death (apoptosis) by trauma deserve exploration. Rodent models of cortical contusion are being used effectively to clarify the molecular and cellular responses of brain tissue to trauma and to study axonal and dendritic injury. However, in order to optimize therapeutic manipulations of posttraumatic intracranial dynamics and solve the problem of brain herniation, it may be necessary to use traumatic brain injury models in large animals (e.g., the dog), with long-term intensive care. Stepwise measures to prevent lethal brain swelling after traumatic brain injury need experimental exploration, based on the multifactorial mechanisms of brain swelling. Novel treatments have so far influenced primarily healthy tissue; future explorations should benefit damaged tissue in the penumbra zones and in remote brain regions. The prehospital arena is unexplored territory for traumatic brain injury research.
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PMID:Resuscitation from severe brain trauma. 860 6

Cerebral ischemic insults in at least 30% of severely head injured patients at a very early stage following trauma and are associated with early death. To date, the threshold for ischemia of 18 mL/100g/min used in human head injury studies has been adopted from animal studies (by temporary occlusion of the middle cerebral artery). Since the traumatized brain becomes more susceptible to irreversible damage if accompanied by ischemia one may question whether the threshold for ischemic vulnerability is higher than 18 mL/100 g/min. Cerebral ischemia can cause atrophy. Therefore, the authors obtained computerized tomography (CT) scans in 33 comatose head-injured patients (Glasgow Coma Score of 8 or less) at least 3 months following injury and compared ventricle sizes (as a reflection of atrophy) with cerebral blood flow (CBF) obtained within 4 h (average 2.3 +/- 0.8 h) after injury. Ventricular measurements were performed in three fashions: the third ventricular size (cm), the bicaudate cerebral ventricular index (BCVI), and the hemispheric ventricular index (HCVI). No significant correlation was found between early CBF and any of the ventricule sizes. Applying a multiple correlation analysis with four independent parameters [CBF, CBF/time postinjury, CBF/(time postinjury)2, age], only age emerged as a significant indicator for predicting ventricle size (p < 0.001). We also compared CBF data, obtained within 4 h after trauma, from survivors at 3 months after injury (mean CBF of 32 mL/100 g/min) with CBF data from non-survivors (CBF 20 mL/100 g/min). The difference in CBF between survivors and nonsurvivors was significant at p < 0.001 (Wilcoxon rank-sum test). The proportion of patients with CBF less than or equal to 20 mL/100 g/min was 56% in the nonsurvivors and only 5% in survivors. The difference in the proportions was significant at p < 0.001 (chi-square test). We conclude that a measure of atrophy does not correlate with ultra-early CBF. However, based on the clear distinction between survivors and nonsurvivors, we suggest the threshold for ischemia after head injury be redefined as a CBF of 20 mL/100 g/min.
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PMID:Thresholds for cerebral ischemia after severe head injury: relationship with late CT findings and outcome. 871 59

Ischemia is one of the major factors causing secondary brain damage after severe head injury. We have investigated the value of continuous partial pressure of brain tissue oxygen (PbrO2) monitoring as a parameter for cerebral oxygenation in 22 patients with severe head injury (Glasgow Coma Scale score, < or = 8). Jugular bulb oxygenation, intracranial pressure, and cerebral perfusion pressure were simultaneously recorded. O2 and CO2 reactivity tests were performed daily to evaluate oxygen autoregulatory mechanisms. PbrO2 monitoring was started an average of 7.0 hours after trauma with a mean duration of 74.3 hours. No complications were seen, and the calibration of the catheters after measurement showed a zero drift of 1.2 +/- 0.8 mm Hg and a sensitivity drift of 9.7 +/- 5.3%. In 86% of patients, PbrO2 was < 20 mm Hg in the acute phase. Mean PbrO2 significantly increased during the first 24 hours after injury. Two distinct patterns of change of PbrO2 over time were noted. The first pattern was characterized by normal stable levels after 24 hours, and the second was characterized by transiently elevated levels of PbrO2 during the second and third days. PbrO2 values < or = 5 mm Hg within 24 hours after trauma negatively correlated with outcome. O2 reactivity was significantly lower in patients with good outcomes. CO2 reactivity showed no constant pattern of change over time and was not correlated with outcome. Increased hyperventilation was shown to decrease PbrO2 in some patients. Accurate detection of the moment of cerebral death was possible on the basis of the PbrO2 measurements. The correlation between PbrO2 and other parameters, such as intracranial pressure and cerebral perfusion pressure, was weak. We conclude that PbrO2 monitoring is a safe and clinically applicable method in patients with severe head injury. The early occurrence of ischemia after head injury can be monitored on a continuous basis. Deficiency of oxygen autoregulatory mechanisms can be demonstrated, and their occurrence is inversely related to outcome. For practical clinical use, the method seemed to be superior to jugular oximetry.
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PMID:Continuous monitoring of partial pressure of brain tissue oxygen in patients with severe head injury. 914 75

We report a 10-month-old boy with heat stroke because he was left in a car. He showed hyperthermia, coma and convulsions at the time of his admission. Liver dysfunction and coagulopathy were observed, but they were improved after several days. Consciousness was gradually recovered, but currently he shows neurological sequelae. Cranial CT showed brain edema until the 7th hospital day. Cranial MRI on the fortieth hospital day showed the finding of cortical laminar necrosis in the vascular boundary zones. This finding suggest that brain ischemia was related with the neurological involvement of heat stroke.
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PMID:[A case of heat stroke with cortical laminar necrosis on vascular boundary zones]. 883 Dec 47

Acute ischemia in the complete territory of the carotid artery may lead to massive cerebral edema with raised intracranial pressure and progression to coma and death due to uncal, cingulate, or tonsillar herniation. Although clinical data suggest that patients benefit from undergoing decompressive surgery for acute ischemia, little data about the effect of this procedure on experimental ischemia are available. In this article the authors present results of an experimental study on the effects of decompressive craniectomy performed at various time points after endovascular middle cerebral artery (MCA) occlusion in rats. Focal cerebral ischemia was induced in 68 rats using an endovascular occlusion technique focused on the MCA. Decompressive craniectomy was performed in 48 animals (in groups of 12 rats each) 4, 12, 24, or 36 hours after vessel occlusion. Twenty animals (control group) were not treated by decompressive craniectomy. The authors used the infarct volume and neurological performance at Day 7 as study endpoints. Although the mortality rate in the untreated group was 35%, none of the animals treated by decompressive craniectomy died (mortality 0%). Neurological behavior was significantly better in all animals treated by decompressive craniectomy, regardless of whether they were treated early or late. Neurological behavior and infarction size were significantly better in animals treated very early by decompressive craniectomy (4 hours) after endovascular MCA occlusion (p < 0.01); surgery performed at later time points did not significantly reduce infarction size. The results suggest that use of decompressive craniectomy in treating cerebral ischemia reduces mortality and significantly improves outcome. If performed early after vessel occlusion, it also significantly reduces infarction size. By performing decompressive craniectomy neurosurgeons will play a major role in the management of stroke patients.
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PMID:Decompressive craniectomy in a rat model of "malignant" cerebral hemispheric stroke: experimental support for an aggressive therapeutic approach. 889 24

Carbon monoxide (CO) poisoning still represents a frequent and severe casualty in France. Aside from the well-known effect of CO on hemoglobin, the role of CO binding to other hemoproteins like myoglobin and cytochrome a3 has been more recently recognized. Moreover, in addition to these hypoxic injuries, the reoxygenation phase may itself induce toxic effects by a mechanism close to the ischemia-reperfusion phenomenon. Clinical manifestations include neurologic disturbances, cardiac arrhythmia, respiratory and circulatory failures which usually disappear with removal from toxic atmosphere and administration of oxygen. However, long term neurologic manifestations may occur and lead to important functional impairment and disability. Hyperbaric oxygen is actually the treatment of choice to avoid the occurrence of delayed sequelae. HBO is advocated in every patient who remains comatose on hospital admission, who has lost consciousness during toxic exposure or with persisting neurologic abnormalities. CO poisoned pregnant women should also undergo HBO.
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PMID:[Carbon monoxide poisoning]. 895 70

Carbon monoxide (CO) poisoning still represents a frequent and severe casualty in France. Aside the well-known effect of CO on hemoglobin, the role of CO binding to other hemoproteins like myoglobin and cytochrome a3 have been more recently recognized. Moreover, in addition to these hypoxic injuries, the reoxygenation phase may itself induce toxic effects by a mechanism close to the ischemia-reperfusion phenomenon. Clinical manifestations include neurologic disturbances, cardiac arrythmia, respiratory and circulatory failures which usually disappear with removal from toxic atmosphere and administration of oxygen. However, long term neurologic manifestations may occur and lead to important functional impairment and disability. Hyperbaric oxygen in actually the treatment of choice to avoid the occurrence of delayed sequelae. HBO is advocated in every patient who remains comatose on hospital admission, who had lost consciousness during toxic exposure or with persisting neurologic abnormalities. CO poisoned pregnant women should also undergo HBO. Well designed prevention programs are urgently needed in our country to decrease the incidence and the consequences of CO poisoning.
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PMID:[Carbon monoxide poisoning: current aspects]. 896 14


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