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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this prospective study proton magnetic resonance spectroscopy (1H MRS) was used to test the hypothesis that lactate can be detected later than 1 mo after birth in the brains of infants who display severe neurodevelopmental impairment 1 y after transient perinatal hypoxia-ischemia. Data were obtained from three groups of infants: 1) eight infants suffering birth asphyxia followed by perinatal encephalopathy and abnormal neurodevelopmental outcome at 1 y of age (defined as major neurologic impairment, Griffiths quotient <85%, and low optimality score); 2) 10 infants with signs of perinatal hypoxia-ischemia but normal neurodevelopmental outcome at 1 y; and 3) six control infants with uneventful perinatal courses and normal neurodevelopment at 1 y. Between one and four examinations (median 1) were performed at median (range) 11 (4-68) wk after birth, and the cerebral concentration ratio of lactate to creatine plus phosphocreatine (Cr) calculated from each spectrum. Lactate was detected later than the 1st mo after birth in seven of eight infants with abnormal neurodevelopmental outcome [maximum detected lactate/Cr was median (range) 0.44 (0.24-0.67)]. No lactate was detected later than the 1st mo after birth in infants with normal neurodevelopmental outcome, nor in five of six control subjects, although a small amount of lactate was detected in one control infant (lactate/Cr=0.04). These results suggest that the pathologic postasphyxial process, indicated by persistent cerebral lactate, may not be confined to the period immediately after injury.
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PMID:Persistent increases in cerebral lactate concentration after birth asphyxia. 972 5

Intensive efforts are presently directed toward developing pharmacologic therapy to protect the ischemic brain. Preclinical data from animal models indicate that insulin, already available for human use, may reduce damage in both global and focal ischemia. Two kinds of mechanisms may be involved: one in which insulin interacts directly with brain tissue and one in which insulin acts indirectly by reducing peripheral blood glucose levels. Animal data indicate that part of the former, direct mechanism is mediated by insulin-like growth factor-1 receptors. The direct effect appears to predominate in global ischemia. In focal ischemia, unlike global ischemia, the effect of insulin is predominantly via peripheral hypoglycemia, because neuroprotection is largely annulled by co-administration of glucose. The two clinical counterparts of global and focal ischemic models are, respectively, cardiac arrest encephalopathy and focal ischemic stroke. Insulin use in both of these clinical situations could be evaluated in clinical trials that attempt to reduce ischemic brain damage, because insulin has a long and safe history of human use in diabetes treatment.
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PMID:Insulin, blood glucose levels, and ischemic brain damage. 974 32

Rhabdomyolysis results from muscular fibre lysis with release of cellular contents (myoglobin, enzymes, electrolytes) into the plasma. Traumatic (crush syndrome) and non-traumatic rhabdomyolysis have been mostly reported in adults. Traumatic rhabdomyolysis are mostly due to ischemic and reperfusion injuries. Non-traumatic rhabdomyolysis include several factors: muscular compression (comas), cytotoxic injury (infections and poisonings), ischemia (shock, cardiorespiratory arrest) or excessive muscular activity (seizures, strenuous exercise). The main etiologies reported in children are: anoxic-ischemic encephalopathy (including sudden infant death and life threatening events); electrolyte disorders; severe hyperthermia; poisonings; hereditary myopathies. Non-traumatic rhabdomyolysis must be suspected in these circumstances, requiring blood creatinine phosphokinase measurements. Indeed, clinical signs are inconstant and non-specific, and functional signs are difficult to appreciate in children. During the initial phase, the main risk is arrhythmias secondary to hyperkalemia. The two main complications are the compartmental syndrome leading to irreversible vasculo-nervous injuries and acute renal failure. Treatment of traumatic and non-traumatic rhabdomyolysis includes correction of hyperkalemia, active fluid loading in order to prevent acute renal failure and alkalinisation. Prognosis of rhabdomyolysis relates to the aetiology and the presence of acute renal failure.
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PMID:[Acute rhabdomyolysis in the child]. 975 96

Two young women who had encephalopathy that resembled reversible posterior leukoencephalopathy syndrome are presented. The brain magnetic resonance imaging (MRI) of these patients exhibited similar T2-high signal lesions, mostly in the white matter of the posterior hemispheres. Xe-SPECT during the patients' symptomatic period showed hypoperfusion in the corresponding areas, and angiography demonstrated irregular narrowing of the posterior cerebral artery. Clinical manifestations subsided soon after treatment, and the abnormal radiological findings also were almost completely resolved. Thus, we concluded that transient hypoperfusion followed by ischemia and cytotoxic edema might have had a pivotal role in these cases.
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PMID:Two similar cases of encephalopathy, possibly a reversible posterior leukoencephalopathy syndrome: serial findings of magnetic resonance imaging, SPECT and angiography. 1005 33

The changes of cytokinis status and C-reactive protein were evaluated in cerebrospinal fluid of 50 patients in the acute period of ischemic hemispheric stroke with consideration of influence of the remote consequences of the ischemia, established experimentally, on the mechanisms of cerebral infarction development as well as on the progression of both atherogenesis and vascular encephalopathy in the period after the stroke. Significance both of a surplus releasing of the proinflammatory cytokines and deficiency of the protective antiinflammatory and trophotropic factors in the development of an inflammatory response was established. Immunobiochemical criteria were proposed for grading of process for stroke course prediction and for recovery of the altered neurologic functions. More favourable prognosis was anticipated in the patients in which a the treatment started within of the "therapeutic window".
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PMID:[Clinico-immunobiochemical monitoring of factors of focal inflammation in the acute period of hemispheric ischemic stroke]. 1035 15

The authors examined EEG findings and clinical factors for their association with outcome in comatose patients in their general intensive care unit. The following individual and combinations of factors were strongly related to mortality, with positive predictive values of >0.80 and odds ratios >2.0: age over 65 years, anoxic/ischemic encephalopathy, EEG suppression, lack of EEG reactivity; anoxia-ischemia with partial or complete cranial nerve areflexia, anoxia-ischemia with EEG suppression; anoxia-ischemia and generalized epileptiform activity; anoxia-ischemia with partial cranial nerve areflexia and EEG suppression. Conversely, the following factors favored survival rather than death: systemic infection/sepsis, metabolic derangement (excluding anoxic-ischemic insult), trauma; dysrhythmia, focal epileptiform activity, and regional delta and reactivity on EEGs. The findings of this study support the integration of these data into intensive care unit prognostic scoring systems, such as later versions of the Acute Physiology and Chronic Health Evaluation (APACHE).
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PMID:EEG and clinical associations with mortality in comatose patients in a general intensive care unit. 1047 8

This investigation determined if a short interval of modest hypothermia (1 h) initiated 30 min after brain ischemia provided neuroprotection. The rationale for the time and duration of brain cooling reflects the likelihood that the implementation of neuroprotective strategies will occur at an interval shortly after ischemia, and that long-term maintenance of normothermia is a cornerstone of neonatal stabilization. Studies were performed in 22 ventilated neonatal mini-swine in a superconducting magnet to obtain 31P magnetic resonance spectra. After a control period all animals underwent 15 min of global brain ischemia and were maintained normothermic for the first 30 min post-ischemia. In one group of 11 swine normothermia was continued. In the other group of 11 swine, modest hypothermia was initiated at 30 min post-ischemia, continued for 1 h and followed by resumption of normothermia. Animals were subsequently weaned from ventiltor support, removed from the magnet, and underwent neurobehavioral and histologic assessment at 72 h post-ischemia. Both groups had similar severity of ischemia, as indicated by identical changes in arterial blood pressure and pH, alterations in brain beta-nucleotide triphosphate (% of control where control = 100%, 32 +/- 28 vs 27 +/- 26% for normothermic and hypothermic groups, respectively), and the extent of intraischemic brain acidosis (6.13 +/- 0.19 vs 6.14 +/- 0.14 for normothermic and hypothermic groups, respectively). In both groups the distribution of stages of encephalopathy were the same: 1 normal and 10 abnormal (4 mild, 2 moderate, and 4 severe) normothermic, and, 3 normal and 8 abnormal (4 mild, 2 moderate, and 2 severe) hypothermic animals. There was no difference in the extent of neuronal injury between groups. We conclude that a 1-h interval of modest hypothermia initiated at 30 min post-ischemia does not confer neuroprotection.
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PMID:A limited interval of delayed modest hypothermia for ischemic brain resuscitation is not beneficial in neonatal swine. 1050 57

Nitric oxide (NO) produced by inducible NO synthase contributes to ischemic brain damage. However, the role of inducible NO synthase-derived NO on neonatal hypoxic-ischemic encephalopathy has not been clarified. We demonstrate here that aminoguanidine, a relatively selective inhibitor of inducible NO synthase, ameliorated neonatal hypoxic-ischemic brain damage and that temporal profiles of NO correlated with the neuroprotective effect of aminoguanidine. Seven-day-old Wister rat pups were subjected to left carotid artery occlusion followed by 2.5 h of hypoxic exposure (8% oxygen). Infarct volumes (cortical and striatal) were assessed 72 h after the onset of hypoxia-ischemia by planimetric analysis of coronal brain slices stained with hematoxylin-eosin. Aminoguanidine (300 mg/kg i.p.), administered once before the onset of hypoxia-ischemia and then three times daily, significantly ameliorated infarct volume (89% reduction in the cerebral cortex and 90% in the striatum; p<0.001). NO metabolites were measured by means of chemiluminescence using an NO analyzer. In controls, there was a significant biphasic increase in NO metabolites in the ligated side at 1 h (during hypoxia) and at 72 h after the onset of hypoxia (p<0.05). Aminoguanidine did not suppress the first peak but significantly reduced the second one (p<0.05), and markedly reduced infarct size in a neonatal ischemic rat model. Suppression of NO production after reperfusion is a likely mechanism of this neuroprotection.
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PMID:Protective effect of aminoguanidine on hypoxic-ischemic brain damage and temporal profile of brain nitric oxide in neonatal rat. 1062 86

Migraine, a common disorder of uncertain pathogenesis, is linked to ischemia in a variety of ways. In some cases the relationship is coincidental. In others, migraine may be causally related to stroke, although the mechanism of migrainous stroke, if not due to arterial dissection, is unclear. In young women, additional risk factors for stroke such as cigarette smoking, use of combined oral contraceptives and anticardiolipin antibody immunoreactivity may potentiate migraine, especially migraine with aura, as a stroke risk factor. The complexity of the relationship is highlighted in certain genetic conditions such as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy and mitochondrial encephalopathy with lactic acidosis and stroke in which migraine and stroke are both prominent clinical features.
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PMID:The relationship of migraine and stroke. 1065 84

To study the kidney lesions complicated by hypoxic ischemic encephalopathy (HIE) in newborn, we successfully established a neonatal pig model of HIE. Changes in brain tissue similar to those of newborn in HIE were detected after 2 hours of hypoxia and ischemia. Meanwhile, swelling of kidneys, hemorrhage below encapsules, swellin of tubular epithelial cells, necrosing and falling of a few tubular epithelial cells, and narrowing of tubular lumens were observed. The basement membranes of renal tubules remained normal serum BUN and creatinine increased significantly after experiment compared with before (P < 0.025 and P < 0.05 respectively). The results showed that the kidney of neonatal pig was damaged in HIE. But the injury was not severe. After 72 hours free from hypoxia, the structure and function recovered approximately from the injury.
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PMID:[Kidney lesions complicated by hypoxic ischemic encephalopathy of neonatal pig]. 1068 35


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