Hemodynamic and metabolic concomitants of brain swelling and cerebral edema due to experimental cerebral infarction

1972 ◽  
Vol 36 (6) ◽  
pp. 728-744 ◽  
Author(s):  
Tetsuaki Teraura ◽  
John Stirling Meyer ◽  
Keizo Sakamoto ◽  
Kazuo Hashi ◽  
Peter Marx ◽  
...  

✓ Severe cerebral ischemia was produced in 25 baboons by clamping the carotid and vertebral arteries bilaterally for 10 minutes. Cerebral hemodynamics and metabolism were monitored throughout. Cerebral anoxia was less severe in animals in which a marked pressor response occurred due to ischemia of the vasomotor center, and a reversible type of brain swelling was usual. In those with more severe ischemic anoxia, progressive cerebral edema was a pathological entity. Evidence is presented that cerebral edema was caused by loss of autoregulation of cerebral blood flow (CBF) concomitant with hyperemia and an increase of water and chloride content of brain tissue. Cerebral edema began when CBF was reduced during occlusion and progressed for several hours after termination of occlusion. Evidence is adduced that uncoupling of oxidative phosphorylation may be an important concomitant of cerebral edema.

1971 ◽  
Vol 34 (4) ◽  
pp. 488-493 ◽  
Author(s):  
Raymond N. Kjellberg ◽  
Alberto Prieto

✓ A large bifrontal craniotomy was used in selected patients judged to carry an unusually high mortality risk due to brain swelling secondary to brain trauma. The procedure enabled exploration of both hemisphere convexities, evacuation of accumulated blood and necrotic brain, and decompression of swollen brain. This report reviews 73 cases operated on at the Massachusetts General Hospital since March, 1962; 18% of these patients survived. The largest experience was with post-traumatic cerebral edema, although intractable edema secondary to mass lesions, hemorrhage, toxic encephalopathy, and pseudotumor cerebri was also treated.


1982 ◽  
Vol 56 (3) ◽  
pp. 404-410 ◽  
Author(s):  
Antonio V. Lorenzo ◽  
Keasley Welch ◽  
Scott Conner

✓ Spontaneous hemorrhage into the ventricles in premature babies is a major problem, and neither its cause nor its pathogenesis is understood. A model is presented for the study of germinal matrix and intraventricular hemorrhage in the preterm rabbit. This animal is particularly suitable because like the human, 1) the maximal growth of the brain occurs perinatally; 2) there is an abundant germinal matrix near term, and by birth this is substantially reduced; 3) there is no rete mirabile; 4) the blood flow to the brain is via internal carotid and vertebral arteries; 5) the maturation of the lungs is completed just before term; and 6) the rabbit pup can maintain a separate existence from the dam when delivered prematurely. Eight of 64 such animals were found to have developed spontaneous germinal matrix hemorrhage with or without rupture into the ventricles. Several physiological and chemical features characteristic of the premature rabbit are presented. The hemorrhage in the lagomorph might be a paradigm of that in infants, and its study may aid in the understanding of the pathogenesis of the process.


1980 ◽  
Vol 52 (2) ◽  
pp. 153-161 ◽  
Author(s):  
Miguel A. Faria ◽  
Alan S. Fleischer

✓ Seven cases of giant posterior hemisphere arteriovenous malformations are described. The significance of meningeal feeding vessels from the external carotid artery in addition to the primary cerebral supply through the internal carotid and vertebral arteries to these malformations is discussed. The necessity of bilateral selective external carotid arteriography is stressed, and the value of preoperative embolization is questioned.


2021 ◽  
Vol 38 (01) ◽  
pp. 053-063
Author(s):  
Ananth K. Vellimana ◽  
Jayson Lavie ◽  
Arindam Rano Chatterjee

AbstractCervical carotid and vertebral artery traumatic injuries can have a devastating natural history. This article reviews the epidemiology, mechanisms of injury, clinical presentation, and classification systems pertinent to consideration of endovascular treatment. The growing role of modern endovascular techniques for the treatment of these diseases is presented to equip endovascular surgeons with a framework for critically assessing patients presenting with traumatic cervical cerebrovascular injury.


1987 ◽  
Vol 66 (4) ◽  
pp. 548-554 ◽  
Author(s):  
Seigo Nagao ◽  
Tsukasa Nishiura ◽  
Hideyuki Kuyama ◽  
Masakazu Suga ◽  
Takenobu Murota

✓ The authors report the results of a study to evaluate the effect of stimulation of the medullary reticular formation on cerebral vasomotor tonus and intracranial pressure (ICP) after the hypothalamic dorsomedial nucleus and midbrain reticular formation were destroyed. Systemic arterial pressure (BP), ICP, and local cerebral blood volume (CBV) were continuously recorded in 32 cats. To assess the changes in the cerebral vasomotor tonus, the vasomotor index defined by the increase in ICP per unit change in BP was calculated. In 29 of the 32 animals, BP, ICP, and CBV increased simultaneously immediately after stimulation. The increase in ICP was not secondary to the increase in BP, because the vasomotor index during stimulation was significantly higher than the vasomotor index after administration of angiotensin II. The vasomotor index was high during stimulation of the area around the nucleus reticularis parvocellularis. In animals with the spinal cord transected at the C-2 vertebral level, ICP increased without a change in BP. These findings indicate that the areas stimulated in the medullary reticular formation play an important role in decreasing cerebral vasomotor tonus. This effect was not influenced by bilateral superior cervical ganglionectomy, indicating that there is an intrinsic neural pathway that regulates cerebral vasomotor tonus directly. In three animals, marked biphasic or progressive increases in ICP up to 100 mm Hg were evoked by stimulation. The reduction of cerebral vasomotor tonus and concomitant vasopressor response induced by stimulation of the medullary reticular formation may be one of the causes of acute brain swelling.


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