Journal of neurosurgery
-
Journal of neurosurgery · Feb 1996
Case ReportsMiddle cerebral artery dissecting aneurysm with persistent patent pseudolumen. Case report.
The extremely rare condition of an ischemic right middle cerebral artery dissecting aneurysm with persistent patent pseudolumen is described. In the majority of cases of dissecting aneurysms, the pseudolumen persists for a very short time, probably because reentry from the pseudolumen is minimal or nonexistent. In contrast, the present case was assumed to have sufficient reentry from the bypass flow in the pseudolumen. Endothelial formation both in the true lumen and the pseudolumen was suggested as the possible mechanism of the stabilized double lumen.
-
Journal of neurosurgery · Jan 1996
Psychosocial functioning and quality of life in patients with primary brain tumors.
Perceived quality of life (QOL) was evaluated in a group of 50 patients with primary brain tumors. Participants completed two QOL measures and a demographic profile. Age was found not to be an important factor in differentiating QOL in these patients. ⋯ This study is one of the first to evaluate the multidimensional aspects of QOL in patients with primary brain tumors, an understudied group. A prospective study of QOL in this group, already underway at the authors' institution, is needed to evaluate comprehensively the effect of different treatments and interventions on the QOL functioning of primary brain tumor patients. Additionally, this study shows that the choice of QOL instruments is very important and needs to be driven by the research question.
-
To determine the incidence of, and risk factors for, the occurrence of rebleeding between admission and early operation (ultra-early rebleeding) in patients with spontaneous subarachnoid hemorrhage (SAH), the authors reviewed the cases of 179 patients admitted within 24 hours after their last attack of SAH. Thirty-one (17.3%) of these patients had ultra-early rebleeding despite scheduling of early operation (within 24 hours after admission). The incidence of rebleeding significantly decreased as the time interval between the last attack and admission increased. ⋯ Multivariate analysis revealed that the following three factors were independently associated with ultra-early rebleeding: the level of enhancement of platelet sensitivity; the time interval between the last attack and admission; and the level of thrombin-antithrombin complex. On the basis of these findings, the authors suggest that many of the risk factors for ultra-early rebleeding are interrelated. A particularly high risk of ultra-early rebleeding was observed in those patients 1) who had platelet hypoaggregability; 2) who were admitted shortly after their last SAH; and 3) whose thrombin-antithrombin complex levels were extremely high and were thus in severe clinical condition.
-
The mechanism by which intracerebral hemorrhage leads to the formation of brain edema is unknown. This study assesses the components of blood to determine if any are toxic to surrounding brain. Various solutions were infused stereotactically into the right basal ganglia of rats. ⋯ On the other hand, activation of the coagulation cascade by adding prothrombinase to plasma did produce brain edema. The edema response to whole blood could be prevented by adding a specific thrombin inhibitor, hirudin, to the injected blood. This study indicates that thrombin plays an important role in edema formation from an intracerebral blood clot.
-
Journal of neurosurgery · Jan 1996
Characterization of edema by diffusion-weighted imaging in experimental traumatic brain injury.
The objective of this study was to use diffusion-weighted magnetic resonance imaging (DWI) to help detect the type of edema that develops after experimental trauma and trauma coupled with hypotension and hypoxia (THH). Reduction in the apparent diffusion coefficients (ADCs) is thought to represent cytotoxic edema. In a preliminary series of experiments, the infusion edema model and middle cerebral artery occlusion models were used to confirm the direction of ADC change in response to purely extracellular and cytotoxic edema, respectively. ⋯ In the trauma alone group, the rise in ICP reached a maximum value (28 +/- 3 mm Hg) at 30 minutes with a significant and sustained increase in CBF despite a gradual decrease in CPP. The ADCs in this group were not significantly reduced. The data lead the authors to suggest that the rise in ICP following severe trauma coupled with secondary insult in this model is predominately caused by cytotoxic edema and that ischemia plays a major role in the development of brain edema after head injury.