Citations

Background and Purpose —Intracerebral hemorrhage (ICH) is a highly morbid disease process. Perihematomal edema is reported to contribute to clinical deterioration and death. Recent experimental observations indicate that clotting of the intrahematomal blood is the essential prerequisite for hyperacute perihematomal edema formation rather than blood-brain barrier disruption. Methods —We compared a series of patients with spontaneous ICH (SICH) to a series of patients with thrombolysis-related ICH (TICH). All patients were imaged within 3 hours of clinical onset. We reviewed relevant neuroimaging features, emphasizing and quantifying perihematomal edema. We then analyzed clinical and radiological differences between the 2 ICH types and determined whether these factors were associated with perihematomal edema. Results —TICHs contained visible perihematomal edema less than half as often as SICHs (31% versus 69%, P <0.001) and had both lower absolute edema volumes (0 cc [25th, 75th percentiles: 0, 6] versus 6 cc [0, 13], P <0.0001) and relative edema volumes (0.16 [0.10, 0.33] versus 0.55 [0.40, 0.83], P <0.0001). Compared with SICHs, TICHs were 3 times larger in volume (median [25th, 75th percentiles] volume 69 cc [30, 106] versus 21 cc [8, 45], P <0.0001), 4 times more frequently lobar in location (62% versus 15%, P <0.001), 80 times more frequently contained blood-fluid level(s) (86% versus 1%, P <0.001), and were more frequently multifocal (22% versus 0%, P <0.001). Conclusions —The striking qualitative and quantitative lack of perihematomal edema observed in the thrombolysis-related ICHs compared with the SICHs provides the first substantial, although indirect, human evidence that intrahematomal blood clotting is a plausible pathogenetic factor in hyperacute perihematomal edema formation.

Acetazolamide was given to five of ten cats for 48 to 54 hours after extradural occlusion of a middle cerebral artery (MCA). At seven to eight days later, measurements of regional cerebral blood flow (CBF) and estimates of the sizes of the ischemic and infarcted areas of the brains were made. Neurological deficits were more severe and the ischemic and infarcted regions were larger in the cats given acetazolamide. Cerebral edema (brain swelling) was present and reactive hyperemia was common in the treated cats, even one week after MCA occlusion. The hypercapnia and decreases of pH of nonischemic brain tissue that are caused by acetazolamide are harmful for ischemic brain tissue, presumably because of vasodilatation in nonischemic brain tissue with resultant increases of intracranial pressure and decreases of CBF of ischemic regions.

The right middle cerebral artery was occluded in cats, and Pa o o2 was increased by increasing the amount of oxygen inhaled by the animals at atmospheric pressure. Cortical blood flow (CBF) was measured with Krypton-85, and observations and photographs of the superficial cortical microvasculature were made bilaterally. In two of five animals, increasing the Pa o o2 caused constriction of surface arterioles of the nonischemic hemispheres, with an associated decrease of CBF; in the three other animals, there were no circulatory responses to the increased Pa o o2 . In seven animals, increasing the Pa o o2 had no apparent effect on CBF or arteriolar caliber of the ischemic cerebral hemispheres. In four animals, at Pa o o2 greater than 400 torr, reactivity to increases of Pa CO CO2 was preserved in nonischemic cortex but impaired in ischemic cortex. Reddening of venous blood of the microvasculature of ischemic cerebral cortex occurred when Pa o o2 was increased, indicating that more oxygen was made available to the ischemic cerebral tissue. However, no beneficial effects could be demonstrated on the changes in the microvasculature produced by ischemia.

An infrared microscope was used for the remote detection of the surface temperature of the cerebral cortex of experimental cats. With this instrument a qualitative assessment of the circulation of the cerebral cortex can be made without interference with the integrity of the brain or vascular tissues or the reactivity of blood vessels. Although the instrument is sensitive enough to detect minor changes of cortical blood flow, its use appears limited to the detection of rapid or transient changes of cerebral circulation and is not suitable for long-term measurements of surface temperature of the brain.

The right seventh cranial nerve (n. VII) was exposed intracranially via a suboccipital approach in each of eight cats. Measurements of cerebral blood flow (CBF) were made from superficial cortex, sulcal cortex, basal cortex, the basal ganglia, and the centrum semiovale of each cerebral hemisphere of each cat by autoradiography using 14 Cantipyrine. In six cats, measurements of CBF were made during electric stimulation of n. VII; in two of these, the nerve was sectioned before stimulation. In the remaining two cats, measurements were made after exposure but without stimulation of n. VII; in these cats, there were no side-to-side differences of CBF. In each of the four cats with n. VII intact, CBF values were lower on the stimulated side. In each of the two cats with n. VII sectioned, CBF values were higher on the stimulated side. Thus, stimulation of n. VII causes regional increases of CBF only when centripetal effects of stimulation are prevented. Cerebral vasodilatation has been observed by others during stimulation of a sectioned or an intact n. VII. When an intact nerve is stimulated, vasodilatation apparently is unable to compensate for decreases of CBF mediated centripetally through brain stem structures and extracranial or basal cerebral vessels; moreover, such vasodilatation may be due in part to regulatory responses of vessels to decreases of perfusion pressure.

Background and Purpose —The volume of ischemic stroke on CT scans has been studied in a standardized fashion in acute stroke therapy trials with median volumes between 10.5 to 55 cm 3 . The volume of first-ever ischemic stroke in the population is not known. Methods —The first phase of the population-based Greater Cincinnati/Northern Kentucky Stroke Study identified all ischemic strokes occurring in blacks in the greater Cincinnati region between January and June of 1993. The patients in this phase of the study who had a first-ever ischemic clinical stroke were identified, and the volume of ischemic stroke was measured. Results —There were 257 verified clinical cases of ischemic stroke, of which 181 had a first-ever ischemic infarct. Imaging was available for 150 of these patients, and 79 had an infarct on the CT or MRI study that was definitely or possibly related to the clinical symptoms. For these patients, volumetric measurements were performed by means of the modified ellipsoid method. The median volume of first-ever ischemic stroke for the 79 patients was 2.5 cm 3 (interquartile range, 0.5 to 8.8 cm 3 ). There was a significant relation between location of lesion and infarct size ( P <0.001) and between volume and mechanism of stroke ( P =0.001). Conclusions —The volume of first-ever ischemic stroke among blacks in our population-based study is smaller than has been previously reported in acute stroke therapy trials. The large proportion of small, mild strokes in blacks may be an important reason for the low percentage of patients who meet the inclusion criteria for tissue plasminogen activator. Further study is necessary to see if these results are generalizable to a multiracial population.