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Recent investigations have indicated the importance of secondary brain damage in the pathophysiology of intracerebral hemorrhage (ICH), which includes ischemic brain damage and edema formation around a hematoma. The purpose of the current study is to investigate chronological changes of perihematomal edema in patients with human ICH and also the correlation between volume of perihematomal edema and neurological status. Fourteen patients with medium-sized putaminal hemorrhage (29.4 +/- 13.2 ml) without hematoma enlargement were included in this study. To investigate chronological changes of perihematomal edema, we performed CT scans prospectively on the day of hemorrhage and repeated them on days 1, 3, 7, 14, and 28. We evaluated the patients neurologically using the NIH stroke scale on the day a CT scan was performed. The volume of perihematomal edema in human ICH increased rapidly three days after hemorrhage and the score on the NIH stroke scale showed a deterioration. The volume of perihematomal edema then increased slowly until day 14 after hemorrhage, and decreased thereafter. Despite progression of perihematomal edema, the score on the NIH stroke scale improved gradually after day 3.

The propagation of extravasated contrast medium around 6 supratentorial meningiomas with peritumoral white matter of low density (PWL) of Lanksch II-III was investigated by repeated CT scanning at 4 h intervals, following a 1 h drip infusion of 200 ml of Iopamidol. The volume of the expanding peritumoral contrast enhancement was calculated according to a method previously described. By calculating the increase in volume from the first to the second scan, and from the second to third, we derived the rate of edema formation as well as the resolution rate of edema in the PWL. The surface area of the entire tumor (TS) and area of tumor surface facing the PWL (LS) were calculated by summating the surface areas of all CT slices, each area of which was derived from the measured length of the entire circumference of the tumor and circumference of the tumor facing the PWL, respectively, multiplied by the slice thickness of 0.5 cm. The volume of PWL, edema formation rate of entire tumor, and tumor volume x LS/TS were well correlated with each other. We concluded that the severity of peritumoral edema in meningiomas depends on the size of the tumor and the extent of tumor surface contact with the PWL.

We examined the effectiveness of high colloid oncotic pressure (COP) therapy to suppress and/or reduce brain edema associated with putaminal hemorrhage of patients whose clinical grades were grade 3 or 4a classified according to the Japanese neurological grading for putaminal hemorrhage. In the treated group of 11 patients, 25% albumin solution was intravenously administered (50-100 ml/day) with additional use of furosemide (20-40 mg/day) following hematoma removal. The serum COP was maintained at 25-30 mmHg for 2 weeks. In the untreated group of 11 patients, the COP therapy was not applied following hematoma removal. The serum COP was 20-25 mmHg for 2 weeks thereafter. During the 2-week observation period, serum osmolality, electrolyte, and hematocrit levels did not significantly differ between the two groups. The midline structure shift on CT of the treated group was 4.5 mm, which was significantly smaller than that of the untreated group (p < 0.05). The numbers of patients either in the vegetative state or death were 0 and 3, respectively, in the treated and the untreated groups. We concluded that high COP therapy for 2 weeks following hematoma removal was effective to suppress and/or reduce brain edema associated with putaminal hemorrhage, and that this therapy could be continued for 2 weeks without systemic complications.

We investigated whether prolonged high colloid oncotic therapy for two weeks can suppress contusional brain edema. Eighteen patients with cerebral contusion were randomly divided into two groups of patients receiving high oncotic pressure (HOP; 26-30 mmHg) treatment and those receiving normal oncotic pressure (NOP; 22-26 mmHg) treatment. Oncotic pressure was maintained for two weeks with administration of a 25% albumin solution with additional use of furosemide. Edema volume was calculated by summation of all measured low-density areas in each CT slice multiplied by 1.0 cm of slice of thickness. We expressed contusional brain edema volume as a percent increase based on each patient's initial CT. The mean percent increase of contusional brain edema in the NOP group was significantly higher than that in the HOP group at 9-15 days (208.9% and 14.0%, respectively) and 16-25 days (188.8% and 10.0%, respectively). There were no complications such as heart failure or renal failure during treatment. All the patients in the HOP group recovered with minimal or no neurological deficit. On the other hand, 30% of patients in the NOP group remained in poor condition. With frequent measurement of oncotic pressure and adjustment of fluids and electrolytes, continuous oncotic therapy for two weeks effectively and safely reduced contusional brain edema.

Following infusion of 200 ml of Iopamidol for 1 hour the propagation of extravasated contrast medium around different types of 12 brain tumours was examined and imaged via CT. Increasing volume of expanding peritumoural contrast enhanced brain tissue was measured by integrating volumes of planimetrically measured enhanced area on CT slice of 0.5 cm in thickness. So far our data failed to demonstrate differences in the peritumoural contrast expansion between the different types of tumours. Formation and resolution as well as the speed of oedema propagation were determined by calculation of the increasing volume of the enhanced peritumoural brain tissue. Average formation rate of oedema fluid from 1 cm3 of tumour was 0.06 ml/hr, and was lower in larger tumours, while formation rate of oedema fluid from whole tumour was higher in larger tumours. Average resolution rate of oedema fluid during the passage through 1 cm3 of the peritumoural white matter was 0.03 ml/hr, and was not affected by tumour size. Average speed of oedema propagation was 0.59 mm/hr, and was higher in larger tumours. The main therapeutic effect of steroid in peritumoural oedema was a reduction in formation rate of oedema fluid.