Middle cerebral artery occlusions (MCAo) in rats produce infarcts in the pyriform and frontoparietal cortex, extending into the lateral basal ganglia and parasagittal cortex. We estimated tissue H 2 O concentrations from wet and dry weight measurements and determined Na and K concentrations by atomic absorption spectroscopy in these areas of rat brains. Tissue samples were analyzed at 2,4, and 24 hours after MCAo and sham MCAo, compared with normal values measured in unoperated rats. In the pyriform and frontoparietal areas, H 2 O concentrations increased to 34 and 7% greater than normal by 2 hours, and 89 and 94% by 24 hours after MCAo. Na concentrations rose in these areas to 73 and 37% greater than normal by 2 hours, and 281 and 330% by 24 hours. K concentrations did not change until 4 hours, but fell to 62 and 34% of normal in these areas by 24 hours. Such large ion shifts indicate severe tissue destruction. In the parasagittal cortex and basal ganglia areas, the ion and water changes were smaller and did not become significant until 24 hours after MCAo. Rates of Na entry into the infarct site were greatest at 0-2 hours, while the rates of K loss peaked later, between 2 and 4 hours. The difference in Na influx and K efflux resulted in net ion shifts that correlated highly with water entry, yielding a correlation coefficient of 0.992 (p < 0.001) and a slope indicating that 1 ml of water entered the tissue with each 145 /xmoles of ions. These findings strongly suggest that net ion shifts cause the early edema of regional brain ischemia. To explain the dominance of Na gain over K loss, we reject the hypothesis of a selective increase of blood-brain barrier Na permeability and propose instead that glial buffering of K ions released by Ischemic neurons reduced the driving force for K clearance during the first 2-4 hours after MCAo. (Stroke 1987;18:751-759) T he middle cerebral artery (MCA) occlusion (MCAo) model in rats possesses several major advantages over other models of cerebral ischemia. First, unlike global ischemia models, 1 " 3 occlusion of cerebral arteries produces regional losses of blood flow, allowing ischemic sites to be compared with perfused tissues in the same brain. Second, the effects of severe ischemia can be investigated in animals with relatively low mortality rates. Third, unlike MCAo models in larger mammals such as cats and primates, rats can be studied in large numbers.In an earlier study, 4 we showed that tissue ion shifts in injured spinal cords can serve as quantitative indices of the severity and time course of cell damage. Here, a similar approach was applied to the rat MCAo model of regional ischemia. The time course and regional distribution of Na, K, and water changes at 2, 4, and 24 hours after unilateral MCAo were compared with measurements in sham-occluded and unoperated rats. We report below earlier and larger changes in brain Na, K, and water shifts than described previously. Received April 1, 1986; accepted February 6, 1987. Na influx exceeded K efflux, resulting in ...

The deployment of PEDs with concurrent partially dense coiling is safe and efficacious. This technique achieved early complete occlusion and endovascular reconstruction of the parent vessel, without inducing mass effect. Favorable midterm clinical results were observed in all patients.

Supratentorial cortical ependymoma (CE), a rare type of ependymoma, is located in the superficial cortex. We reported 11 patients (six female and five male) with CE. The age of the patients ranged from 2 to 63 years old with a median age of 47 years at the time of diagnosis. On MRI, enhancement was noted in all cases with solid appearance in six cases, and solid and cystic appearance in five cases. The frontal and parietal regions were the most common locations for CE. On histology, two were low-grade (WHO grade II) and nine were WHO grade III anaplastic ependymomas. Some tumors exhibited clear cell, spindle (tanycytic) and giant cell morphologies, as well as the classic ependymoma morphology. Dura-based tumor nodules and even tumor dissemination along the dura can be seen in CEs. Low grade CEs have a higher likelihood to present with seizures, a lower likelihood to cause brain edema, tumor recurrence and lower mortality than anaplastic ependymomas. While difficult, anaplastic CEs may be distinguished from glioblastoma by a clear interface between tumor and adjacent brain tissue, relative uniformity of tumor cell nuclei and immunopositivity for epithelial membrane antigen and/or CD99. As is the case for ependymomas in general, gross total resection is still the treatment of choice for CEs.

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