Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mild hypothermia is effective in the prevention of brain edema associated with cerebral ischemia and traumatic brain injury. Brain edema is also a serious complication of acute liver failure (ALF). To assess the effectiveness of hypothermia in ALF, groups of rats were subjected to hepatic devascularization (portacaval anastomosis, followed 48 hours later by hepatic artery ligation), and body temperatures were maintained at either 35 degrees C (hypothermic) or 37 degrees C (normothermic). Mild hypothermia resulted in a significant delay in the onset of severe encephalopathy and in reduction of brain water content compared with normothermic ALF rats (control [n = 8] 80.22%; ALF-37 degrees C [n = 8] 81.74%; ALF-35 degrees C [n = 8] 80.48% [P <.01 compared with ALF-37 degrees C]). This protective effect was accompanied by a significant reduction of cerebrospinal fluid (CSF) (but not plasma) ammonia concentrations (CSF ammonia: control: 0.05 mg/dL; ALF-37 degrees C: 1.01 mg/dL; ALF-35 degrees C: 0.07 mg/dL, P <.01 compared with ALF-37 degrees C). In vivo cerebral microdialysis studies revealed that mild hypothermia resulted in a significant reduction of extracellular glutamate concentrations in the brains of rats with ALF (control: 1. 06 micromol/L; ALF-37 degrees C: 2.74 micromol/L; ALF-35 degrees C: 1.49 micromol/L [P <.01 compared with ALF-37 degrees C]). These findings suggest that: 1) mild hypothermia is an effective approach to the prevention of the central nervous system consequences of experimental ALF; and that 2) the beneficial effect of hypothermia is mediated via mechanisms involving reduced blood-brain transfer of ammonia and/or reduction of extracellular brain glutamate concentrations. Mild hypothermia may be an effective approach to delay the onset of brain edema in patients with ALF awaiting liver transplantation.
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PMID:Mild hypothermia delays the onset of coma and prevents brain edema and extracellular brain glutamate accumulation in rats with acute liver failure. 1073 42

The characteristics of accumulation of autoantibodies (aAbs) on NMDA-type glutamate receptors were studied in blood of patients at different stages (1-4 days, 5-7 days, 8-14 days, up to 28 days) of acute period of ischemic or hemorrhagic stroke. The stability of low values (1.29 +/- 0.31 ng/ml) of the titer of aAbs to NMDA-receptors was revealed in patients with acute cerebral hemorrhage. Two types of titer of Abs to NMDA-receptors were revealed in case with cerebral ischemia. The undulating nature of Abs titer changes was revealed in acute ischemic strokes caused by hypertension and cerebral atherosclerosis (from 2.23 +/- 0.53 ng/ml on the 1-st day with increase up to 3.23 +/- 0.90 ng/ml and up to the 3-4 day), following fluctuations with less pronounced increase on 7-8th day were found out. High titer of aAbs to NMDA-receptors (up to 10.0 ng/ml) were observed on 3-4th day in cases of acute ischemic strokes on the background of chronic alcohol encephalopathy caused by intoxication or dysmetabolism with their retention up to 10-14th day.
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PMID:[Autoantibodies to NMDA-type glutamate receptors in the blood of patients with acute ischemic and hemorrhagic stroke]. 1151 78

Forty one 41-82 year-old patients with chronic cerebrovascular diseases were examined neurologically, using ultrasonic dopplerography (USD) of extracranial cerebral vessels and transcranial dopplerography (TCD) of intracranial cerebral vessels. Changes of the blood flow through major cerebral arteries as well as peculiarities of the venous circulation were evaluated. A significant decrease of the cerebral blood flow velocity (BFV) was found by TCD on early stages of cerebrovascular diseases, while USD revealed it on the III stage of dyscirculatory encephalopathy. The changes in the regulation of the venous circulation increase from latent to obvious alterations of both BFV and the pulsatility index. The conclusion is made that manifestation of clinical symptomatology in the diseases studied is undoubtedly connected with cerebral ischemia and TCD plays an important role in its determination.
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PMID:[Transcranial dopplerography in chronic disorders of cerebral circulation]. 1155 32

For studying diagnostic possibilities of a new laboratory test for cerebral ischemia (CIS-test), thirty patients have been examined. The level of autoantibodies to NMDA type glutamate receptors is shown to increase significantly (3-5 times) in patients with stage 2 dyscirculatory encephalopathy. Parallel measurements of free glutamate and homocysteine levels in the patients blood plasma did not reveal any substantial changes of the given parameters, comparing to indices of autoantibodies to NR2a glutamate receptor. The titer of autoantibodies to this receptor type did not change significantly in patients with epilepsy; the titer dependence on dyscirculatory encephalopathy severity level and its decrease during treatment have been found as well. The possibilities of CIS using for diagnosis and therapy control in patients with chronic cerebral circulation disorders are discussed.
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PMID:[Significance of the level of auto-antibodies for the NMDA type glutamate receptors in diagnosis of chronic cerebral circulation disorders]. 1176 13

The cerebral blood flow velocities (CBFV) of infants with perinatal asphyxia and hypoxic ischemic encephalopathy (HIE) in the first 12 hours of their lives have been the chief focus of our concern in this study. Cerebral ischemia which can develop in the earlier hours of HIE, and the detection and diagnosis of this condition with color Doppler ultrasonography (cD-USG) will be put into discussion. Twenty-three full-term newborn infants who had perinatal asphyxia and HIE together with a control group constituting twenty full-term newborn infants who produced no problems, were included in our study. All of the infants underwent cD-USG in the postpartum period of the first 12 hours (mean 8.4 hours). Measurements being based upon peak systolic velocity (PSV), end diastolic velocity (EDV) and Pouecelout's resistive index (RI) in anterior and middle cerebral arteries were conducted. The infants, having been discharged from the unit they were followed up for mean 9.8 months in the outpatient clinic. PSV and EDV counts in the postpartum first 12 hours of 23 infants who were detected to have HIE were found to be significantly lower compared to the control group, whereas RI counts were found to be significantly higher (p < 0.05). The counts obtained from the right and left cerebral arteries of the infants with HIE were found to be corraleted with each others. The neonates in the patient group were observed to have gone through this prognosis: Three of them died, three of them had cerebral palsy, one of them had infantile spasms, and three of them had developmental retardation. When we compared the CBFV of the 10 neonates who had poor prognosis, retrospectively with the other 13 neonates who had good prognosis, PSV and EDV were found to be significantly lower and RI significantly higher (p < 0.05). In the light of the data we have obtained, cD-USG can be considered to be a highly practical device in evaluating CBVF of the infants with HIE. A skillful detection of the decrease in cerebral blood flow which can develop in the postasphyxial first 12 hours and the prospective treatments being based upon this approach would contribute to the diagnosis, treatment and prognosis of such cases.
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PMID:Clinical value of color Doppler ultrasonography measurements of full-term newborns with perinatal asphyxia and hypoxic ischemic encephalopathy in the first 12 hours of life and long-term prognosis. 1218 Jul 90

The mechanisms of action of hyperbaric oxygenation (HBO) in toxic hypoxic encephalopathy (THE) were studied using clinical psychopathological examinations, functional and laboratory tests in 268 patients with THE treated by a therapeutic complex including HBO and 75 patients with THE treated routinely (controls). The earliest possible addition of HBO to a complex of treatment of THE patients led to involution of signs of brain edema shown by computer tomography (CT) and improvement of its functional activity, while in patients exposed to HBO later the psychoorganic symptoms and CT signs of cerebral ischemia did not disappear. Detoxifying, neuroimmunomodulating, and neuroimmunostimulating effects of HBO in THE were demonstrated. Early HBO treatment decreased the dysfunction of various compartments of the brain characteristic of THE. The technology of HBO developed by the authors prevented the development of socially dysadapting psychoneurological disorders and reduced the mortality of THE patients.
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PMID:[Time course of toxic hypoxic encephalopathy during combined therapy including hyperbaric oxygenation]. 1222 91

We present a 72 year old patient who underwent an esophagectomy uneventfully. At the end of the procedure the anaesthetist diagnosed a mydriasis not reacting to light. The mydriasis lasted for 3 hours. 30 minutes after diagnosis a cranial computed tomography scan showed no abnormalities. The tracheal tube was removed after 16 h of artificial ventilation, the patient was awake and responded to questions. The neurological examination was normal, as well as the control CT scan. With regard to a mydriasis the following differential diagnosis have to be considered: cerebral ischemia, cerebral hematoma, metabolic encephalopathy, shock, and a drug side effect. We state that an alpha-mimetic effect of the drug mixture Akrinor, the patient had received shortly before diagnosis of the mydriasis, is the most likely explanation. One 2 mls syringe contents of 200 mg norephedrine-ethyl-theophylline and 10 mg noradrenaline-ethyl-theophylline.
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PMID:[Mydriasis not reacting to light during an uneventful esophagectomy--drug-related side effect of Akrinor?]. 1263 42

23% of all septic patients develop septic encephalopathy which is associated with an increased mortality rate. Symptoms such as agitation, confusion and disorientation ranging from stupor to coma often develop in early sepsis. Severe hypotension is significantly associated with the development of septic encephalopathy. Several other factors which may play a role are also discussed: effects of inflammatory mediators on the brain, inadequate cerebral perfusion pressure, blood-brain barrier derangements, disturbances of the cerebral microcirculation, cerebral ischemia e.g. due to hypocapnia,metabolic changes, altered amino acid levels, transmitter imbalances, liver insufficiency, multiple organ failure and infections of the CNS, respectively. Compared to patients with an isolated infection,patients in septic shock have increased levels of aromatic amino acids such as phenylalanine and tryptophan in the plasma and brain as well as decreased levels of branched chain amino acids. Patients who died had higher levels of aromatic amino acids than the survivors. The correlation between aromatic amino acids and the APACHE II score was significant. The tryptophan metabolite quinolinic acid which can be synthesized in activated macrophages could act as an excitatory transmitter on the N-methyl-D-aspartate (NMDA) -receptor. Observations from experimental models indicate that activated NMDA receptors activate the neuronal isoform of the NO-synthase and other calcium dependent enzymes. This releases free radicals which may damage the DNA and activate the nuclear enzyme Poly-ADP-ribose-synthetase (PARS), resulting in energy depletion and cell death. Sepsis is the main cause of metabolic encephalopathies in critically ill patients. The differential diagnoses include hepatic, renal,hypoxic-ischemic or cardiovascular encephalopathies as well as encephalopathies,metabolic disorders and organ dysfunctions of other origin. Therapeutic interventions are numerous,however, so far only investigated in few controlled studies. The primary therapeutic goal is to maintain an adequate perfusion pressure and to prevent hypoxia and hypocapnia. Although the infusion of branched chain amino acids is controversial, experimental investigations demonstrated improvements improvements in an animal model with septic encephalopathy. Further investigations with respect to glutamate receptor antagonists, new radical scavengers, NO- and PARS-inhibitors may show whether these substances are suitable for the prophylaxis or early therapy of septic encephalopathy.
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PMID:[Septic encephalopathy. Diagnosis und therapy]. 1275 14

Neuroserpin is a member of the serine proteinase inhibitor (serpin) gene family that reacts preferentially with tissue-type plasminogen activator (tPA) and is primarily localized to neurons in regions of the brain where tPA is also found. Outside of the central nervous system (CNS) tPA is predominantly found in the blood where its primary function is as a thrombolytic enzyme. However, tPA is also expressed within the CNS where it has a very different function, promoting events associated not only with synaptic plasticity but also with cell death in a number of settings, such as cerebral ischemia and seizures. Neuroserpin is released from neurons in response to neuronal depolarization and plays an important role in the development of synaptic plasticity. Following the onset of cerebral ischemia there is an increase in both tPA activity and neuroserpin expression in the area surrounding the necrotic core (ischemic penumbra), and treatment with neuroserpin following ischemic stroke or overexpression of the neuroserpin gene results in a significant decrease in the volume of the ischemic area as well as in the number of apoptotic cells. TPA activity and neuroserpin expression are also increased in specific areas of the brain by seizures, and treatment with neuroserpin slows the progression of seizure activity throughout the CNS and results in significant neuronal survival in the hippocampus. Mutations in human neuroserpin result in a form of autosomal dominant inherited dementia which is characterized by the presence of intraneuronal inclusion bodies and is known as Familial Encephalopathy with Neuroserpin Inclusion Bodies.
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PMID:Neuroserpin: a selective inhibitor of tissue-type plasminogen activator in the central nervous system. 1498 20

Infective endocarditis involves the brain in 20-40% of cases. The neurologic syndrome often is the presenting feature. The most frequent neurologic complication is cerebral ischemia. In these patients and those with intracranial hemorrhage, a heart murmur as well as systemic signs of inflammation point to endocarditis. The encephalopathy in endocarditis is mostly due to cerebral infarction. In bacterial meningitis and brain abscess an uncommon isolate arouses suspicion. The most important therapy is antibiotic treatment. Valve replacement improves outcome; in the acute phase of endocarditis, however, it is only necessary in a third of the patients. Neurologic complications interfere with the timing of the valve replacement. If it is urgently required, its risk is reasonable within 3 days after cerebral ischemia; if possible 2-4 weeks should be waited. Cases of successful valve replacement within 4 weeks after intracranial hemorrhage have been reported, but it is recommended to postpone it for 4-6 weeks. There are no data available for the other neurologic complications. Even today patients with endocarditis challenge the diagnostic and therapeutic capacity of various disciplines.
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PMID:[Neurological complications of infective endocarditis]. 1503 58


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