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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty patients suffering from post-ischaemic encephalopathy were treated with high doses of barbiturates during the period immediately following resuscitation. The duration of cerebral ischaemia was assessed retrospectively. The degree of ischaemic damage was evaluated on the one hand by the pupillary signs seen 10 minutes after the reestablishment of the circulation and secondly by enzyme levels in the CSF. This barbiturate load was not associated with major complications and the excretion of barbiturate continued for several days. The clinical signs seen 12 hours after ischaemia and continuous observation of the tracing of the cerebral function monitor made it possible to give an early favourable prognosis from a neurological standpoint. In all the patients (apart from one) in whom there was total cerebral ischaemia for less than 10 minutes, neurological recovery was complete.
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PMID:[Clinical use of thiopental in post-ischemic encephalopathy; preliminary report]. 3 55

Irreversible brain damage after a short period of cerebral ischemia is a clinical drama. Not neuronal dead in se, but a hemodynamic event, described as no reflow phenomenon (NRF) seems to be the primary pathogenetic factor towards fatal outcome. A combination of four flow promoting therapeutic measures (heparinisation, hemodilution, systemic arterial hypertension and brainflushing with dextran 40) greatly improves recovery of the brain function after 12 min. of cardiac arrest in dogs. Short acting barbiturates provide remarkable amelioration of postischemic encephalopathy in the monkey.
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PMID:Recent advances in the treatment of postischemic encephalopathy. A review. 82 14

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
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PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

Recent advances in the molecular biology of excitatory amino acid receptors are reviewed. Evidence that drugs blocking the excitatory action of glutamate at the N-methyl-D-aspartate (NMDA) and non-NMDA receptors may be of clinical use in epilepsy, Parkinson's disease, cerebral ischaemia and trauma, acquired immune deficiency syndrome (AIDS) encephalopathy and neuropathic pain is summarized.
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PMID:Excitatory amino acid receptors and disease. 132 24

The neurometric method as introduced by John was used to study three groups of patients with cerebral ischemia, three groups of patients with renal disease and an additional normal control group. The traditional neurometric approach was slightly modified: relative band power values were not expressed as a percentage of the total power per derivation but as a percentage of the "global power"; frequency matrices were used in addition to power matrices. From the study of the three groups of patients with one-sided supratentorial ischemia it appeared that sensitivity and specificity are completely satisfactory when using neurometrics in patients with severe ischemia in the middle cerebral artery territory studied within 48 hours of the onset of the stroke. However, in ischemia patients with less pronounced clinical signs and especially in patients without persistent neurological deficit the sensitivity is much lower. In studying dialysed and non-dialysed renal patients signs of an (often subclinical) encephalopathy could be detected in approximately 37% of all patients. Follow-up studies of the ischemia patients and the renal patients over a period of several years revealed a parallelism between clinical scores and qEEG scores in the ischemia patients; almost all qEEG improvement occurred in the first three months after the stroke. The qEEG profile of the groups of dialysed patients tended to be more or less stable over a period of several years.
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PMID:Neurometrics in cerebral ischemia and uremic encephalopathy. 151 Aug 71

We describe a case of fatal hypoxic-ischemic encephalopathy, leading to brain death following the modified Fontan procedure in a child with asymptomatic subclavian steal syndrome (SSS). This patient's brain death was most likely multifactorial in view of his postoperative course. However, we believe that the presence of the SSS contributed to the abnormal cerebral circulation during surgery and postoperatively, leading to brain death. The presence of SSS in patients undergoing an open-heart procedure may be a risk factor for cerebral ischemia or brain death.
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PMID:Asymptomatic subclavian steal syndrome in children following cardiac surgery: a potential hazard with re-operation? 161 13

Cerebral ischemia in the neonate is an important cause of hypoxic-ischemic encephalopathy. Thus, it is important to have an economical and readily available animal model in which to study the local control of the cerebral circulation in the perinatal period. This study demonstrates that the newborn rabbit, a rather immature species at birth, is a suitable neonatal model in which to measure local cerebral blood flow with quantitative iodo[14C]antipyrine autoradiography. One or 2 d after birth, local cerebral blood flow in the newborn rabbit is low, but flow varies distinctly between regions [e.g. 8.9 +/- 1.5 mL.kg-1.s-1 (53 mL.100 g-1.min-1) in the nucleus tractus solitarius and 3.4 +/- 0.7 mL.kg-1.s-1 (20 mL.100 g-1.min-1) in the frontal cortex]. During early postnatal development (i.e between 1 and 8 d), local cerebral blood flow does not change greatly. However, by 17 d, 22 of 26 brain regions exhibit significant marked increases (200-350%) in local cerebral blood flow when compared with blood flow in the newborn. Between 17 and 40 d postnatally, cerebral blood flow continues to increase in 16 of 26 regions (e.g. thalamic areas). In four of the cerebral cortical areas, elevations in flow continue during the period between 40 d of age and adulthood. In contrast to the generalized increases in flow occurring postnatally, a few brain regions (i.e. within the pons and medulla) exhibit only minor changes in cerebral blood flow. The differential pattern and lower basal levels of cerebral blood flow in the neonate compared with the adult may be important determinants in regional susceptibility of the brain to ischemia.
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PMID:Local cerebral blood flow in the newborn rabbit: an autoradiographic study of changes during development. 189 57

A total of 112 patients with ischemic stroke and 115 patients of different sexes and age with dyscirculatory encephalopathy were examined for the main risk factors of cardiovascular diseases. Hypokinesia and obesity were most common in chronic vascular brain pathology whereas frequently occurring and prolonged psychoemotional overstrain, aggravated heredity and alcohol abuse promoted the occurrence of acute disorders of brain circulation. The combination of 4 and more risk factors significantly raises the probability of acute cerebral ischemia.
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PMID:[Risk factors of acute and chronic cerebral ischemia]. 215 17

The authors studied the effects of hypocapnic-hyperventilation on cerebral blood flow (CBF) (study 1) and on cerebral oxygenation (study 2) during mechanical ventilation in 8 patients, 4 with hepatic (HE) and 4 with septic encephalopathy (SE). In study 1, a positive linear relationship between CBF(y) and PaCO2 (x) was observed (y = 2.44x - 55.5, r = 0.6276, P less than 0.01, n = 18). In the study 2, hypocapnic-hyperventilation produced a reduction in CBF below the level required to meet the demand in 4 of 8 patients. A good linear relationship was observed between CBF/CMRO2 (CMRO2 = cerebral oxygen consumption, y) and jugular venous PO2 (PjVO2, x) (y = 0.99x - 15.53, r = 0.8962, P less than 0.01, n = 18). It is concluded that cerebrovascular reactivity to CO2 was preserved in these patients, therefore, intentional or inadvertant hyperventilation may produce cerebral ischemia. Moreover, JPVO2 may be useful in monitoring cerebral oxygenation in such patients.
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PMID:Cerebrovascular reactivity to CO2 in patients with hepatic or septic encephalopathy. 216 Jul 9

We studied the patterns of cerebral blood flow (CBF), over time, in patients with systemic lupus erythematosus and varying neurologic manifestations including headache, stroke, psychosis, and encephalopathy. For 20 paired xenon-133 CBF measurements, CBF was normal during CNS remissions, regardless of the symptoms. CBF was significantly depressed during CNS exacerbations. The magnitude of change in CBF varied with the neurologic syndrome. CBF was least affected in patients with nonspecific symptoms such as headache or malaise, whereas patients with encephalopathy or psychosis exhibited the greatest reductions in CBF. In 1 patient with affective psychosis, without clinical or CT evidence of cerebral ischemia, serial SPECT studies showed resolution of multifocal cerebral perfusion defects which paralleled clinical recovery.
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PMID:Cerebral blood flow variations in CNS lupus. 229 89


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