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

We report two cases of traumatic cerebral vascular disease which were treated successfully with barbiturate. The first case sustained blunt trauma to the bilateral vertebral arteries, resulting in complete occlusion of both arteries. After ligation of the injured vertebral arteries, multiple cerebral infarction appeared. Cerebral angiography revealed dissection and stenosis of the bilateral internal carotid arteries. We treated this case with barbiturate (Thiamylal) in combination with administration of heparin. The second case sustained cerebral contusion and traumatic subarachnoidal hemorrhage as a result of a motor cycle accident. This patient deteriorated and cerebral angiography showed diffuse cerebral arterial vasospasms. When this was treated with induced hypertension, he developed recurrent subarachnoid hemorrhage. In order to protect the brain from ischemia without elevating blood pressure, we employed barbiturate therapy and the patient recovered without major neurological deficit. The condition of severe head injury with cerebral ischemia is complicated. Therefore it has been hard for neurosurgeons to cure the patient with this condition. But we treated it with barbiturate successfully. Barbiturate therapy in severe head injury with cerebral ischemia may decrease the mortality in that group of patients considered difficult to treat with the usual therapeutic modalities.
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PMID:[Barbiturate therapy in traumatic cerebral vascular disease: report of two cases]. 261 99

Barbiturate coma is still recommended for brain protection during periods of temporary focal ischaemia such as during carotid endarterectomy. We tested the hypothesis that a single dose of barbiturate given before a period of protracted severe focal ischaemia would protect against focal cerebral infarction. Sixteen cats had the proximal left middle cerebral artery (MCA) occluded. Eight cats received halothane alone titrated to keep their pulse and blood pressure within the normal range. Eight cats received, in addition to halothane, a bolus of thiopentone sufficient to produce an isoelectric EEG immediately prior to MCA occlusion. Six hours after the occlusions the animals were sacrificed and the brains scored histologically to assess both size and severity of ischaemia. There was no statistically significant difference in the size or severity of the infarcts between the groups. We conclude from this study that the extent of the histological injury was not reduced by a single prophylactic bolus of thiopentone given before prolonged focal cerebral ischaemia.
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PMID:A prophylactic bolus of thiopentone does not protect against prolonged focal cerebral ischaemia. 369 13

Barbiturate therapy has been shown to be of benefit in certain instances for focal cerebral ischemia. This therapy can, however, result in a deleterious outcome. Early institution in combination with revascularization appears to be important for successful barbiturate application. Whether combinations of agents designed to act on different mechanisms in the pathophysiology of cerebral ischemia can prolong the 'therapeutic window' of barbiturate application is an area for future investigation.
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PMID:Barbiturate resuscitation from focal cerebral ischemia--A review. 702 25

The use of barbiturates to induce coma as a means of extending the period of reversible cerebral ischemia is reviewed. Barbiturate use in patients who had had strokes or were undergoing aneurysm surgery was initially encouraging. In uncontrolled feasibility trials in patients with cardiopulmonary arrest or in deep coma, 40 patients received 10 mg/kg thiopental sodium by i.v. push followed by 20 mg/kg thiopental sodium i.v. over the next 30 minutes; 60% of these patients regained consciousness. In a subgroup of 22 patients who had ischemia normally associated with a 90% mortality rate, 14 recovered completely. In the largest clinical trial, 45 patients with severe head injury and elevated intracranial pressure received 3--5 mg/kg pentobarbital over 10--20 minutes. A serum barbiturate level of 2.5--4.0 mg/dl was maintained for 14 days, and 30% of these patients recovered but with neurologic deficits. Other results in stroke and drowning victims were not as encouraging. It is concluded that barbiturate therapy is beneficial in the lowering of intracranial pressure. Focal and global cerebral ischemia have been shown amenable to barbiturate therapy in isolated cases. The prophylactic use of barbiturates in surgical procedures requiring focal cerebral anoxia appears to be beneficial. Controlled trials of the use of barbiturate-induced coma are clearly indicated.
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PMID:Barbiturate-induced coma to protect against cerebral ischemia and increased intracranial pressure. 702 14

The pathophysiology of brain trauma regarding disturbances of energy and transmitter metabolism, development of intra- and extracellular cerebral oedema are briefly outlined. Possible mechanisms of action of barbiturates in amelioration of cerebral ischaemia, decrease of cerebral metabolism, preservation of membrane stability, reduction of cerebral oedema and intracranial pressure are reviewed. We report on 6 patients with severe brain trauma due to head injury whose intracranial pressure despite conventional treatment with hyperventilation, steroids and osmotic diuresis remained above 25 mm Hg. They were infused with thiopentone 6--12 mg/kg x h for 6 to 15 days, to reduce cerebral electrical activity to the point of "burst suppression" in the electroencephalogram. Three patients survived, two of them regaining their previous good health. The results in these patients are discussed as regards thiopentone dosage and severity of trauma. Marked cardiovascular instability in one case and cholostatic jaundice due to barbiturate administration in two cases were the most important side effects. Barbiturate infusion seems to be indicated in brain trauma with sustained elevation of intracranial pressure above 25 mm Hg despite vigorous conventional therapy. Monitoring most essential to this aggressive treatment scheme comprises measurement of intracranial pressure and continuous observation of the EEG.
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PMID:[Barbiturate infusion in severe brain trauma (preliminary report) (author's transl)]. 741 48