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

Sclerosis of the cornu Ammonis or Ammon's horn sclerosis (AHS) is an "often-described, yet hitherto enigmatic phenomena" as Spielmyer put it in 1927. It has been found in cases with ischemia, anoxia or hypoglycemia and in more than half of the epileptic brains examined at autopsy. Various theories about its pathogenesis have been propounded. Among them, the "Pathoklise" theory of the Vogts and the vascular theory of Spielmeyer and his associates were prevailing until recently. In 1953, two articles were published to contribute to the pathogenesis of ictal automatism (a type of complex partial or temporal lobe seizures). One is the incisural sclerosis theory by Penfield and his associates and the other is the Ammon's horn sclerosis theory by Sano and Malamud. The former authors described a diffuse sclerosis of the infero-mesial temporal structures without, however, specifically relating it to AHS. They considered it was the result of localized anoxia of that portion of the brain caused by incisural herniation occurring during parturition. Sano and Malamud maintained that AHS is a result of convulsions, a distinct scar adjacent to which epileptogenic foci may develop in the course of time to cause ictal automatism. The latter theory was corroborated by Sano, Falconer and others. Falconer expanded the theory to the assertion that not only ictal automatism but other types of intractable epilepsy may be due to "mesial temporal (Ammon's horn) sclerosis". The most recent development in the pathogenesis of AHS is the excitotoxicity theory. Namely, AHS is caused by excessive excitation of neurons, probably by putative excitatory neurotransmitters, especially, glutamate. For this theory, there is a significant body of evidence. The problem of AHS, an old research subject and a matter of long-lasting controversy, has now been updated and become one of the newest topics in the field of experimental neurobiology.
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PMID:Ammon's horn sclerosis: its pathogenesis and clinical significance. 198 30

The cerebral protective actions of a new thyrotropin releasing hormone (TRH) analogue, YM-14673, [Na-[[(S)-4-oxo-2-azetidinyl-carbonyl]-L-histidyl-L-prolinamide] dihydrate), were compared with those of CDP-choline (cerebral metabolic enhancer) and naloxone in rats rats subjected to unilateral carotid artery ligation and anoxic exposure (Levine rats). Drugs were administered intraperitoneally or orally 20, 80, and 140 min after anoxia. YM-14673 (0.03 to 1 mg/kg i.p. and 0.3 to 10 mg/kg p.o.) decreased the incidence of neurological deficits, such as hemiplegia and convulsion followed by coma and death, for 48 h after ischemia and anoxia. Both the increase in the brain water content and the degeneration of neurons in the cerebral cortex and thalamus were prevented by YM-14673 at a dose of 0.1 mg/kg (i.p.). CDP-choline (400 mg/kg i.p.), which is currently used in the therapy of cerebral vascular diseases, and naloxone (3 mg/kg i.p.) also decreased the incidence of the neurological deficits. These results suggest that YM-14673 protects Levine rats against neurological deficits, presumably by attenuating the development of brain edema and preventing neuronal damage. This compound may be useful in the therapeutic treatment of cerebral vascular diseases.
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PMID:Pharmacological actions of a new TRH analogue, YM-14673, in rats subjected to cerebral ischemia and anoxia. 211 71

The HELLP syndrome (hemolysis, elevated liver enzymes, low platelet count) is a severe complication of pre-eclampsia with high risk for mother and fetus. During the last 40 months 27 parturients met the diagnostic criteria for HELLP syndrome in the University Hospital of Kiel (Tables 1-3). In 24 cases cesarean section was performed. Fetal mortality was 17.2%. In 13 women an uneventful clinical course resulted, all other patients developed complications: renal insufficiency (11 cases), disseminated intravascular coagulation (DIC) (4), intracerebral hemorrhage (1), cerebrovascular ischemia (1), eclamptic convulsions (3), reoperation due to intra- or extra-abdominal hemorrhage (4), severe blood loss ex vagina following spontaneous delivery (1), and liver rupture (1). Despite these severe complications no maternal death was observed. DIC, intrauterine death, and a rapid increase in liver enzymes are considered to be serious prognostic factors that could help to identify high-risk patients. The following recommendations for therapy of parturients suffering from HELLP syndrome are given: epidural anesthesia is not an appropriate method in HELLP syndrome because of the risk of epidural hemorrhage due to thrombopenia. At the present time general anesthesia seems to be the method of choice. Inhalation anesthetics such as halothane, enflurane, or isoflurane should probably be omitted in view of the preexisting hepatopathy. The high risk and the unpredictable postpartum course strongly indicate intensive care for parturients with HELLP syndrome. Antihypertensive, antieclamptic therapy and prophylactic measures to avoid renal insufficiency or hemorrhage (e.g. early substitution of erythrocytes, thrombocytes, and coagulation factors) deserve special attention. Co-operation between obstetrician and anesthesiologist is essential to obtain optimal therapy for these high-risk patients.
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PMID:[Anesthesia and intensive therapy of pregnant women with the HELLP syndrome]. 231 3

The pathogenesis of perinatal hypoxic-ischemic encephalopathy is poorly understood. Most insults are thought to occur before or during birth. We have investigated the evolution of parasagittal EEG activity and distribution of neuronal damage after cerebral ischemia in chronically instrumented fetal sheep (119-126 d gestation). The vertebral-carotid anastomoses were ligated and cerebral ischemia was induced by inflating occluder cuffs around the carotid arteries for 30 min. Parietal cortical EEG activity was analyzed with real-time spectral analysis with reference to control fetuses. After ischemia, EEG activity was suppressed, then rapidly increased in intensity at 8 +/- 1 h to a peak at 9 +/- 1 h postischemia. There was increased intensity of the lower frequencies (1-7 Hz) apparent as epileptiform activity with convulsions. This low-frequency hyperactivity gradually resolved by 28 +/- 7 h postinsult. After 72 h, the loss of intensity at all frequencies and laminar necrosis of the underlying parasagittal cortex indicated irreversible brain injury. Ranking the structures in order of decreasing amounts of damage: parasagittal cortex greater than hippocampal CA1, 2, and 3 regions greater than lateral cortex, hippocampal CA4 region and striatum greater than amygdala, dentate gyrus, thalamus, and cerebellum. The evolution of EEG activity and the distribution of damage after cerebral ischemia closely resembles the time course and pathology of hypoxic-ischemic encephalopathy seen in some severely asphyxiated term neonates. The consistent electrophysiologic and histologic outcome should allow this experimental approach to be valuable in testing a number of current hypotheses relating to perinatal asphyxial encephalopathy.
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PMID:Delayed seizures occurring with hypoxic-ischemic encephalopathy in the fetal sheep. 235 99

The relation between duration of ischemia, use of adjunctive ganglionic blockade and long-term recovery was studied in a rat model giving reversible subtotal forebrain ischemia. Ischemia was induced by bilateral carotid artery clamping and controlled hemorrhage to a mean arterial pressure of 50 mm Hg in animals artificially ventilated under 70% N2O. After variable lengths of time, the clamps were removed and the drawn blood was reinfused. In some animals, the ganglion blocker Arfonad was given (group A+) on induction of ischemia to facilitate hypotension. There was a strict dose-response relationship between duration of ischemia and mortality. Mortality was higher among animals not given Arfonad (group A-; 37% after 10 min of ischemia and 100% after 13 min) than in group A+ (about 20% after 12-13 min of ischemia, 50% after 15 min and 80% after 19 min). In group A+ more than half of the animals died later than 24 h after ischemia. All of them were hyperexcitable and 12% died during witnessed epileptic fits. Group A- animals regularly died within the first 24 h, with no indication of central nervous system involvement. Less blood had to be drawn to attain hypotension (mean arterial pressure 50 mm Hg) in group A+ (1.5 +/- 0.3 ml/100 g b.w.) than in group A- (2.5 +/- 0.2 ml/100 g b.w.). Group A+ also had less "washout" acidosis 5 min after reinfusion of the shed blood than group A- (15 min of ischemia: pH 7.24 +/- 0.07 v 6.96 +/- 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Forebrain ischemia in the rat. Relation between duration of ischemia, use of adjunctive ganglionic blockade and long-term recovery. 287 36

We studied the xanthine derivative propentofylline (HWA 285) to determine its protection against ischemic brain damage when administered before and after ischemia. Transient forebrain ischemia was produced in 81 Mongolian gerbils by occluding both carotid arteries. The necessary surgery was performed under anesthesia with intraperitoneal pentobarbital/chloral hydrate 2 days before occlusion. We tested the parameters delayed selective hippocampal nerve cell damage, generation of seizures, and survival. Determination of the dose-response relation revealed the optimal dose of HWA 285 to be 10 mg/kg i.p. The effect of the drug on delayed selective nerve cell damage in the hippocampus was assessed by measuring the intensity of Nissl staining in the CA1 area by means of densitometry 4 days after a 10-minute occlusion. Gerbils treated with HWA 285 revealed significant protection of the CA1 neurons even when the drug was applied 1 hour after the end of the occlusion. In contrast to HWA 285, pentobarbital provided no detectable protection of the CA1 neurons in our experimental model when administered 1 hour after occlusion, suggesting different mechanisms of action. After a 15-minute occlusion, all six untreated gerbils developed convulsions and died within 2 days. Chronic (daily) treatment of nine gerbils with HWA 285 prevented the generation of convulsions in eight and allowed seven to survive for greater than 12 days.
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PMID:Protection against ischemic brain damage using propentofylline in gerbils. 320 13

The case of a newborn presenting from birth with arthrogryposis multiplex congenita resting mainly on the legs, severe hypotonia, consciousness anomalies, clonic fits, recurrent apnea and bradycardia, absent sucking and swallowing is described. At the age 4 months a further episode of apnea and bradycardia was followed by death. The neuropathologic analysis disclosed a number of bilateral, cystic and symmetric infarcts in the thalamus and hypothalamus, spreading caudally to the tegmentum of the mesencephalon and the pons. Such distribution of lesions does suggest a vascular topography, i.e. in the territories supplied by branches of the vertebro-basilar arteries. There was light clinical and neuropathological evidence of prenatal occurrence of the vascular injuries, possibly at the end of the 7th month by a defective arterial perfusion of the fetus due to protracted menaces of premature birth. We would outline the existence and frequency of the thalamic and dorsal brain stem necrotic involvement by acute anoxia-ischemia occurring in the third trimester of gestation or at birth, and the relative peculiarity of their clinical picture.
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PMID:[Vertebrobasilar insufficiency of prenatal origin: a case report]. 329 92

The effect of the ganglioside GM1 on amplitude of the electroencephalogram, neurologic function, and histology has been studied in chronic middle cerebral artery occlusion in cats. Ischemia was produced by a 2-hour occlusion of the left middle cerebral artery and was followed by a 7-day observation period. GM1 was intravenously administered 30 minutes after occlusion and daily during the observation period. Using the reduction in the electroencephalogram amplitude to measure stroke severity, three cats with mild, three cats with moderate, and three cats with severe stroke were treated with 5 mg/kg GM1. Nine cats, three in each group, were treated with 30 mg/kg GM1, while nine cats, three in each group, received middle cerebral artery occlusion but no treatment. In all cats there was a precipitous fall in mean electroencephalogram amplitude during occlusion, followed by a secondary fall during the observation period. Treated cats showed better recovery of electroencephalogram amplitude during the first 4 hours of reperfusion and a smaller secondary fall than untreated cats. Treated cats, especially those treated with 5 mg/kg GM1, showed significant recovery of neurologic deficits compared with untreated cats. Histologic damage was less in treated cats than in untreated cats. Some cats treated with 30 mg/kg GM1 exhibited convulsions, whereas no untreated cat showed any seizure activity. Our findings suggest that gangliosides may improve the recovery of both neurologic deficits and morphologic damage in the central nervous system. These positive effects might be tentatively explained by stimulation of enzymatic activities such as Na+, K+-ATPase and adenyl cyclase.
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PMID:Effect of the ganglioside GM1 on neurologic function, electroencephalogram amplitude, and histology in chronic middle cerebral artery occlusion in cats. 340 Jan 1

Numerous laboratories have shown that hyperglycemia increases cerebral ischemic damage. This presumably results from increased lactate production and accumulation during ischemia. Although increased tissue lactic acidosis is associated with increased ischemic brain damage, this damage has not been directly linked to glycolytic flux. Because 2-deoxyglucose (2-DG) is a competitive inhibitor of glycolysis we tested its ability to reduce hyperglycemia-exacerbated ischemic brain damage. Severe forebrain ischemia was produced by the four-vessel occlusion model in rats. Four rats received 3 g/kg glucose and saline while a second group (n = 5) was injected with 3 g/kg glucose plus 1.6 g/kg 2-DG. A third group (n = 5) was treated with 1 g/kg glucose plus saline and a fourth group (n = 5) received 1 g/kg glucose and 1.6 g/kg 2-DG. All rats were injected i.p. 10 minutes prior to the ischemic insult with the same volume/kg body weight. All rats receiving the high dose of glucose alone (3 g/kg) were dead within 24 hours postischemia. Rats who received 2-DG in addition to 3 g/kg glucose showed only 40% mortality (p = 0.119 Fisher's Exact). 2-DG completely eliminated convulsions during the initial two hours of recovery which was significant (p = 0.008), however, all rats in both groups showed some convulsions by 24 hours postischemia. Among rats receiving the low glucose dose (1 g/kg), none of the rats receiving 2-DG died or convulsed by 24 hours postischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glycolytic inhibition by 2-deoxyglucose reduces hyperglycemia-associated mortality and morbidity in the ischemic rat. 376 73

Simultaneous occlusion of both common carotid arteries in female Sprague-Dawley CFY rats produced characteristic symptoms of global cerebral ischemia, such as staggering, circling, convulsions, followed by coma and death. A close correlation existed among these symptoms and the elevation of water and Na+ content, appearing at the stage of staggering; Evans blue extravasation and diminution of K+ content, detected at circling; and the increase in Ca2+ content in the total brain tissue, manifesting itself at the phase of convulsions, indicating the development of cerebral edema due to ischemia. Dexamethasone given subcutaneously in a single 2.0 mg kg-1 dose 5 hours prior to the induction of global cerebral ischemia reduced considerably the morbidity and mortality, the alterations in water and electrolyte content, and albumin leakage in the brain tissue. Actinomycin D, in a dose of 0.5 mg kg-1 injected intravenously 1 hour before steroid treatment, abolished the beneficial effect. This finding suggests that de novo protein synthesis is involved in the cerebroprotective effect of dexamethasone.
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PMID:Actinomycin D suppresses the protective effect of dexamethasone in rats affected by global cerebral ischemia. 400 66


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