Citations

Much of the available data on stroke occurrence, service use, and cost of care originated with hospital discharge abstracts. This article uses the unique resources of the Rochester Epidemiology Project to estimate the sensitivity and positive predictive value of hospital discharge abstracts for incident stroke. The Rochester Stroke Registry was used to identify all confirmed first strokes (hospitalized and nonhospitalized) among Rochester residents for 1970, 1980, 1984, and 1989 (n = 364). The sensitivity of discharge abstracts was estimated by following these individuals for 12 months after stroke to determine the proportion assigned a discharge diagnosis of cerebrovascular disease (International Classification of Diseases [ICD] codes 430 through 438.9). The positive predictive value of discharge abstracts was assessed by identifying all hospitalizations of Rochester residents with an ICD code of 430-438.9 in 1970, 1980, and 1989 (n = 377). Events were categorized as incident stroke, recurrent stroke, stroke sequelae, or nonstroke after review of the complete community-based medical record by a neurologist. Only 86% (n = 313) of all first-stroke patients in 1970, 1980, 1984, and 1989 were hospitalized. Of hospitalized patients, only 76% were assigned a principal discharge diagnosis code of 430-438.9. Fatal strokes and those occurring during a hospitalization were less likely to be identified. Among all hospitalizations of Rochester residents in 1970, 1980, and 1989, there were 377 with a principal diagnosis code of 430-438.9. Less than half (n = 177) were determined by the neurologist to be incident stroke; only 60% (n = 225) were either incident or recurrent stroke. Comparison of alternative approaches showed the validity of discharge abstracts was enhanced by increasing the number of diagnoses and excluding codes with poor positive predictive value. This study provides previously unavailable estimates of the sensitivity of stroke-coded hospitalizations for a US community. A model for improving the sensitivity and positive predictive value of discharge abstracts is presented.

Intracerebral hematoma may complicate treatment of acute myocardial infarction in patients treated with fibrinolytic agents. We studied the clinical presentation and computed tomographic characteristics. We studied eight patients with lobar intracerebral hematomas after fibrinolytic treatment of acute coronary occlusion. All patients had electrocardiographic and laboratory evidence of acute myocardial infarction and were treated with tissue plasminogen activator or streptokinase followed by heparin infusion to prevent reocclusion. Computed tomography scans of 17 patients with cerebral hemorrhage from other causes were used for comparison. For most patients, outcome was fatal within hours of the ictus. Computed tomography scans showed superficially large lobar hematomas in six patients. One patient had a putaminal hemorrhage, and one had a vermis hemorrhage. Multiple sites of intracerebral hemorrhage were noted in three patients. Fluid levels inside the hematoma suggesting continuing hemorrhage into multiple compartments were common. Radiologically, fluid levels in hematomas, multiple hematomas, and blood in multiple compartments served to differentiate fibrinolysis-induced hemorrhage from hemorrhage of other causes. Severe amyloid angiopathy was found in one patient who was operated on. Hemorrhages in multiple compartments and the presence of fluid levels inside the hematoma suggest fibrinolysis-associated cerebral hematomas. Severe amyloid angiopathy may be a crucial factor in this clinical entity. Outcome is poor, and a high proportion of patients have rapid progression to brain death. Therefore, emergency neurosurgical evacuation will probably be unsuccessful.

Antiphospholipid antibodies are known to be associated with increased risk of venous and arterial thrombotic events, including cerebral venous thromboses. Pseudotumor syndrome can be produced by cerebral venous thrombosis. A patient with cerebral venous thrombosis associated with antiphospholipid antibodies who exhibited pseudotumor syndrome is reported. A 49-year-old man who noted visual blurring and persistent vertical wavy lines in his fields of vision was found to have papilledema. Cerebrospinal fluid values were normal except for an opening pressure increase to 510 mm of fluid. His visual symptoms improved with lumbar puncture and the use of acetazolamide. Imaging studies showed that the transverse sinus was occluded completely on the left and partially on the right and that there was a small left cerebellar cortical venous infarction. Antiphospholipid syndrome should be considered in the differential diagnosis of pseudotumor syndrome related to cerebral venous thrombosis.

This is a study of cardiac diseases associated with the 1,382 cases of first cerebral infarction in residents of Rochester, Minn., during 1960-1984. This is a population-based study in Rochester, Minn., for which the medical record-linkage system was used to identify cardiac disease among patients with first cerebral infarction. There were 318 patients (23%) who had at least one major potential cardiac source of emboli. The proportion of patients with a cardiac source of emboli was significantly higher among patients older than age 75 years (29%) than among younger patients (17%). The 30-day stroke recurrence rate among patients with a cardiac source of emboli (2%) was not significantly different than that among those without a cardiac source of emboli (2%). Among patients with a cardiac source of emboli, there was no difference in the probability of stroke at 30 days and at 90 days for those treated or not treated with anticoagulants. During the first 30 days after cerebral infarction, the risk of death in patients with a cardiac source of emboli (23%) was 14 times that of recurrent stroke. The risk of death at 30 days in patients without a cardiac source of emboli was 8%. Significant independent predictors of death (Cox proportional-hazards analysis) were age, prior myocardial infarction, atrial fibrillation present at onset of stroke, congestive heart failure before the stroke, and an age x congestive heart failure interaction. The only significant independent predictors of recurrent stroke were cardiac valve disease and congestive heart failure.

This study evaluated the characteristics and natural history of patients with lacunar (small, deep) cerebral infarcts in a defined population for comparison of these characteristics to those in patients with nonlacunar infarcts. This is a population-based study in Rochester, Minnesota, from 1960 to 1984, that used the medical record-linkage system to identify and characterize patients with cerebral infarction. The age- and sex-adjusted average annual incidence rate of lacunar cerebral infarction was 13.4/100,000 persons, accounting for 12% of all first cerebral infarcts. Temporal trends in incidence rates, stroke recurrence rates, prevalence of diabetes mellitus, and causes of death (given survival for 30 days) for cases of lacunar infarction were not significantly different from those for cases of nonlacunar infarction. Hypertension was found in 81% of patients who had a lacunar infarct and in 70% of patients who had a nonlacunar infarct (p = 0.05). A potential cardiac source of embolism was found in 12% of patients who had a lacunar infarct and in 28% of patients who had a nonlacunar infarct (p = 0.002). Survival was significantly better after a lacunar infarct than after a nonlacunar infarct. Small, deep cerebral infarcts had many of the epidemiological characteristics of other cerebral infarcts but there was a slightly higher frequency of hypertension, significantly lower frequency of a cardiac embolic source, and significantly better survival in patients with lacunar infarction than in those with nonlacunar infarction.

This study is a prospective analysis of the predictive value of diffuse and localized carotid bruit. Patients with asymptomatic carotid bruits are compared with a population-based age- and sex-matched control group known not to have carotid bruit, in regard to subsequent transient ischemic attack, stroke, and death. Each person was followed until death or for 5 years. Among the 566 patients with asymptomatic carotid bruit, the annual stroke rate given survival was 1.5%/yr or 7.5% at 5 years by actuarial analysis. The annual stroke rate given survival for the 428 patients in the population-based cohort was 0.5%/yr or 2.4% at 5 years. Patients with localized carotid bruit were not significantly different from those with diffuse carotid bruits in regard to subsequent cerebral ischemic events (p = 0.11). These data indicate that patients with asymptomatic diffuse or localized carotid bruit are approximately three times more likely to have ischemic stroke than an age- and sex-matched population sample known not to have carotid bruit.

The effect of cigarette smoking on extracranial carotid atherosclerosis was studies by obtaining cigarette smoking histories and information on other potential risk factors from consecutive patients undergoing carotid arteriography. At least on extracranial carotid artery was visualized in 752 patients in whom the extent of carotid atherosclerosis was assessed. The total years of cigarette smoking was the most significant independent predictor of the presence of severe carotid atherosclerosis. Other independent predictors, in order of significance, were age, hypertension, diabetes mellitus, male sex, and current systolic blood pressure. By age 60 years, the risk of having severe carotid atherosclerosis for a person who had smoked for 40 years was approximately 3.5 times that for a never smoker. The major benefit of smoking cessation is in limiting the accumulation of smoking years.

We studied subarachnoid hemorrhage in the population of Rochester, Minnesota, for the 40-year period from 1945 through 1984. The average annual incidence rate of subarachnoid hemorrhage in Rochester has remained constant at approximately 11 per 100,000 population. Age-specific incidence rates increased with age. However, the average annual mortality rate for subarachnoid hemorrhage in Rochester has shown a decreasing trend, from 6.8 per 100,000 population in 1955-1964 to 4.3 in 1975-1984. It is likely that this is due to a decrease in case-fatality rates from 57% in 1945-1974 to 42% in 1975-1984 (p = 0.10). This decreasing trend was also evident in annual mortality rates from subarachnoid hemorrhage for US white men and women. The reason for the improved case-fatality rate is unclear, but it may be related to changes in management. The interval from onset of subarachnoid hemorrhage to surgery decreased from a median of 12 days in 1975-1979 to 2 days in 1980-1984, and of those who survived to receive medical attention, more patients received some form of medical treatment in 1980-1984. Whether either or both of these changes have led to the decrease in the case-fatality rate is uncertain.

Studies of the population of Rochester, Minnesota, have provided the only data on temporal trends for the incidence of stroke in North America. Among the residents of Rochester, the average annual incidence rate of stroke declined by 46%, from 213 to 115 per 100,000 population, between 1950-1954 and 1975-1979. The decline occurred in all age and sex groups, but it occurred earlier in women than in men. The rates stabilized in the 1970s, and did so earlier in women. For 1980-1984, the incidence rate of stroke was 17% higher than that for 1975-1979. The onset of the decline in incidence rates coincided with the introduction of effective antihypertensive therapy, but stabilized and increased rates were associated with continuing improvement in the control of hypertension. The increase in the incidence rates of stroke coincided with the introduction of computed tomography, which appeared to increase the detection of less severe strokes.

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.