Citations

We describe four patients with episodic bilateral vision impairment related exclusively to light exposure. Each had angiographically documented bilateral high-grade stenosis or occlusion of the internal carotid arteries. This phenomenon appears to be related to bilateral simultaneous retinal ischemia delaying regeneration of visual pigments in the pigment epithelial layer. It must be distinguished from bilateral occipital lobe ischemia caused by vertebrobasilar system disease.

In cats in which one middle cerebral artery was occluded, cortical blood flow (CBF) was measured and the superficial cortical microvasculature was observed bilaterally before and after the intravenous injection of a vasoactive drug. Aminophylline produced decreased CBF in the nonischemic cerebral hemispheres of five of seven animals and arterial constriction in three. Ergotamine tartrate produced arterial constriction in the nonischemic hemispheres of four animals and decreased CBF in three. Neither drug consistently produced increased CBF in ischemic cerebral tissue. Acetazolamide caused vasodilatation in the nonischemic hemispheres of seven animals and increased CBF in five. Increased CBF was not due entirely to changes of Pa CO 2 . CBF also increased in ischemic hemispheres of four of the seven animals given acetazolamide.

Previous studies have shown that occlusion of the middle cerebral artery (MCA) of the squirrel monkey results in a consistent large infarct; that in the initial two hours after occlusion of the MCA, blood flow in the central area of ischemia continues at a reduced rate (20% to 50% of normal); and that restoration of normal flow within three hours results in a survival rate of 65% without infarction. In this study, cerebral adenosine triphosphate (ATP), lactate, and pyruvate concentrations were measured at various time intervals after occlusion of the MCA. ATP decreased slowly during a three-hour period to 30% of normal, and lactate, after an initial rapid accumulation, increased slowly to about eight times normal. This compares to the effects of circulatory arrest which, in the dog, results in a reduction of the ATP level to 25% of normal within four minutes and a reciprocal increase in the lactate level. Because the effects of total cerebral anoxia are potentially reversible prior to four minutes, and, therefore, at an ATP concentration above 25% of normal, the slow rate of ATP depletion observed in the ischemic monkey brain supports the view that a significant period exists after occlusion of a major intracranial vessel wherein the ischemic effects are potentially reversible. Using the methods of this study, future investigations should permit a meaningful evaluation of the relative merits of those measures recommended for the treatment of acute cerebral ischemia.

Precise use of categorical terms and definitions is mandatory in discussing the use of anticoagulants in treating occlusive cerebrovascular disease. The components of the temporal profile of the disease are described. Six reports have appeared which describe the results of anticagulant therapy in transient cerebral ischemic attacks. From these six studies it is concluded that anticoagulant therapy significantly decreased the risk of cerebral infarction in patients who had attacks of transient focal cerebral ischemia. In the few carefully performed investigations of the use of anticoagulant for acute progressing stroke the evidence points to the lack of progression in patients receiving treatment when compared to individuals not getting such drugs. There continues to be a definite difference of opinion about the results of anticoagulant therapy in completed stroke. If anticoagulant is to be administered on a long-term basis, it must be considered dangerous and every effort made to control the level of anticoagulant action precisely. Hypertension must be effectively controlled.

A 15-year follow-up of 140 patients who had transient cerebral ischemic attacks and were first seen at the Mayo Clinic for this complaint in 1950 through 1954 is reported. There was no significant difference in mortality related to sex or location of residence. Patients hypertensive at onset of symptoms had no significant increase in mortality compared to normotensive patients but the survival trend favored normotensive patients. Probability of surviving 15 years was significantly less than expected for patients less than 65 years old. Patients who were 65 or older at their first attack had a survival similar to that of the standard population. The difference between the expected and observed 15-year survivals for patients with primarily motor symptoms was about the same as that difference for patients with primarily sensory symptoms. Information concerning stroke occurrence was incomplete but 37% of local residents are known to have had a stroke, a higher rate than expected. Among patients who died during this study, 50% died of a cardiac cause and 36% died of a stroke.

To assess the effects of Pa CO CO 2 on cerebral ischemia and reactive hyperemia, the right middle cerebral artery was occluded in 18 cats. Four to six hours later, Pa CO 2 was adjusted by mechanical ventilation, with or without CO 2 , to less than 20 torr in four cats, 31 to 38 torr in six, and 46 to 68 torr in eight. Regional cerebral blood flow (CBF) then was measured at multiple sites in each hemisphere by autoradiography. In regions of brain tissue outside the distribution of the occluded middle cerebral artery, log 10 CBF correlated positively with Pa CO CO 2 . In ischemic regions, CBF was higher in normocapnic cats. Reactive hyperemia occurred in two cats of the hypocapnic group, in four cats of the normocapnic group, but in only one hypercapnic cat (Pa CO CO 2 = 46 torr). Hyperemia also was found outside potentially ischemic regions in five cats. Multiple hyperemic foci developed in six cats. Neither hypocapnia nor hypercapnia was associated with a smaller size or higher CBF of regions of cerebral ischemia produced by occlusion of a middle cerebral artery, although hypercapnia inhibited the development of hyperemia.

The records of the Mayo Clinic have been used as the primary basis for the study of stroke in the population of Rochester, Minnesota, from 1945 through 1954. The incidence rate for first stroke of all types was 1947/100,000/year. The rates increased with age, and at age 65 to 74 years, about 1% of the population was affected annually. No significant differences were noted between men and women. The rate for cerebral thrombosis was 146/l00,000/year for all ages. Cerebral hemorrhage represented less than 10% of all strokes and occurred in less than 15% of those who died; this is contrary to what is published in the U.S. Mortality Statistics . The prevalence rate was 547/100,000 on January 1, 1955. Twenty-one percent of these persons who had previously had a stroke were functioning with no incapacity on the date of prevalence determination and only 3% were bedridden. Death certificates were reviewed for all those who died after a stroke. Among those who died within a month after a stroke, some type of stroke was noted as the underlying or an associated cause of death in 91%. However, among those who died more than a month after a stroke, only 54% had such a diagnosis recorded. Probability of surviving after each type of stroke was determined and compared with survival in a normal population. The curve showing probability of surviving from cerebral thrombosis diverges throughout its course from that of the expected survival but diverges more sharply in the first several months. Among those patients with stroke who died, 41% died of causes related to the acute stroke and 10% died of a subsequent stroke. Heart disease was the cause of nearly twice as many deaths as was a subsequent stroke among those who survived the initial stroke. Autopsies were performed on approximately 50% of those persons who died following a stroke, and information from these studies confirmed the high degree of accuracy of the clinical appraisals.

A method was developed to predict the severity of cerebral ischemia before permanent occlusion of a common carotid artery in gerbils by observing the diameter and appearance of the artery after temporary occlusion and observing clinical signs after permanent occlusion. The severity of cerebral ischemia was confirmed by a sensitive immunohistochemical method and measurement of focal cerebral blood flow after 30 minutes' ischemia. All gerbils with greater than 40% reduction of the diameter and a white arterial margin distal to temporary occlusion developed severe neurologic signs following permanent occlusion, but no gerbils with reduction of less than 30% and a red arterial margin developed neurologic signs. With the cumulative neurologic score, gerbils could be divided into classes with no, mild, moderate, and severe symptoms, mostly after 10 minutes. Severely symptomatic gerbils were identified in 3 minutes. Extensive ischemic damage was observed in severely symptomatic gerbils, but no immunohistochemical lesion was detected in mildly symptomatic gerbils. Cerebral blood flow was markedly reduced in severely symptomatic gerbils but more selectively reduced in the cortical structures of moderately symptomatic gerbils. This prediction method is useful for investigating early cerebral ischemia and for evaluating the effectiveness of pharmacologic agents.

The effects of the calcium ionophore A23187, arachidonic acid, and acetylcholine were studied in isolated canine basilar arteries. Rings with and without endothelium were suspended for isometric tension recording in physiological saline. In unstimulated rings, A23187, arachidonic acid, and acetylcholine caused endothelium-dependent contractions. The contractions of rings caused by uridine 5'-triphosphate were not affected by removal of the endothelium. An inhibitor of cyclooxygenase, indomethacin (10(-5) M), prevented excitatory responses to A23187, arachidonic acid, and acetylcholine but did not alter contractions caused by KCl. An inhibitor of thromboxane synthetase, dazoxiben (10(-4) M), significantly reduced endothelium-dependent contractions to A23187 and arachidonic acid but did not significantly affect contractions caused by acetylcholine. These results demonstrate that A23187, arachidonic acid, and acetylcholine cause excitatory endothelium-dependent responses in canine cerebral blood vessels by increasing the release of product(s) of cyclooxygenase from endothelial cells; in the case of A23187 and arachidonic acid, thromboxane A2 contributes to the endothelium-dependent contractions.

The purposes of this study were to determine the trend in stroke recurrence over time and the effect of the prestroke blood pressure and management of hypertension on stroke recurrence in 1,680 incidence cases of stroke in residents of Rochester, Minnesota. Recurrent, primarily ischemic, stroke occurred in 267 cases. Stroke recurrence rates did not change during the 30-year period 1950-1979, in contrast to the decline in initial stroke incidence rates during this time. The overall stroke recurrence rates were less than 5%/yr, with cumulative rates of 5.7%, 19.3%, and 28.8% at 1, 5, and 10 years, respectively. Neither level of blood pressure before the first stroke nor management of hypertension had any apparent effect on stroke recurrence rates throughout the follow-up.