Risk factors for stroke due to cerebral infarction in young adults.

BACKGROUND AND PURPOSE: Stroke in the young is particularly tragic because of the potential for a lifetime of disablement. More than 10% of patients with stroke due to cerebral infarction are aged 55 years or younger. While a number of studies have addressed the issue of stroke mechanism in the young, quantitation of risk factors has rarely been undertaken. Given the importance of risk factor assessment in primary prevention, we aimed to assess this using case-control methodology in a hospital-based series and community-based control subjects. METHODS: A total of 201 consecutive patients with first-onset stroke due to cerebral infarction aged 15 to 55 years (mean, 45.5 years) were accrued from four teaching hospitals during 1985 to 1992 and compared with their age- and sex-matched neighborhood controls. Information concerning potential risk factor exposure status was collected by structured questionnaire at interview. Stroke risks were estimated by calculating the odds ratios with multivariate logistic regression. RESULTS: Significantly increased risk of stroke was found among those with diabetes (odds ratio, 11.6 [95% confidence intervals, 1.2 to 115.2]), hypertension (6.8 [3.3 to 13.9]), heart disease (2.7 [1.1 to 6.4]), current cigarette smoking (2.5 [1.3, 5.0]), and long-term heavy alcohol consumption (> or = 60 g/d) (15.3 [1.0 to 232.0]). However, heavy alcohol ingestion (> or = 60 g) within 24 hours preceding stroke onset was not a risk factor (0.9 [0.3 to 3.4]). CONCLUSIONS: Diabetes, hypertension, heart disease, current smoking, and long-term heavy alcohol consumption are major risk factors for stroke in young adults. Given that the majority of these factors are either correctable or modifiable, prevention strategies may have the potential to reduce the impact of stroke in this age group.

Transcranial Doppler detected cerebral microembolism following carotid endarterectomy. High microembolic signal loads predict postoperative cerebral ischaemia.

Cerebral ischaemia, the most frequent serious complication of carotid endarterectomy (CEA), usually occurs in the early postoperative period and is often the result of thromboembolism. We hypothesized that the early postoperative detection of microembolic ultrasonic signals (MES) with transcranial Doppler ultrasound (TCD) may be of value in identifying patients at risk of postoperative cerebral ischaemia and that the MES rate may be an important determinant in risk prediction. Sixty-five patients undergoing CEA were studied at intervals up to 24 h postoperatively with TCD insonation of the middle cerebral artery ipsilateral to the operation side. Study design was open and prospective with blinded off-line analysis of MES counts. End-points were any focal ischaemic neurological deficit and/or death up to 30 days postoperatively. MES were detected in 69% of cases during the first hour postoperatively with counts ranging from 0 to 212 MES/h (means 19 MES/h; SEM +2- 4.5; median 4 MES/h). In seven cases (10.8%) counts were > 50 MES/h. Five of these seven cases developed ischaemic neurological deficits in the territory of the insonated middle cerebral artery during the monitoring period. The positive predictive value of counts > 50 MES/h for cerebral ischaemia was 0.71. Frequent signals (> 50 MES/h) occur in approximately 10% of cases in the early postoperative phase of CEA and are predictive for the development of ipsilateral focal cerebral ischaemia.

Risk factors for lacunar infarction syndromes.

BACKGROUND AND PURPOSE: Lacunar infarction is an important stroke subgroup with unique clinical and pathologic features, but its relative risks for associated risk factors have been rarely documented. To address this matter, we studied 203 consecutive patients with first-ever stroke due to lacunar infarction admitted to four general hospitals during the period 1985 to 1992. METHODS: We obtained information concerning risk factor exposure status among the patients by interview using a structured questionnaire and by comparison with age- and sex-matched neighborhood controls. Odds ratios were estimated with adjustment for confounding variables by using multivariate logistic regression. RESULTS: Significantly increasing the risk of lacunar stroke were hypertension (with an odds ratio of 8.9 [95% confidence intervals 4.2, 18.8]), current smoking (6.6 [2.9, 14.8]), and diabetes (2.3 [1.0, 5.5]), whereas frequent physical exercise was associated with a significantly decreased risk (0.3 [0.1, 0.7]). There was no risk of lacunar stroke associated with heart disease (odds ratio 1.0 [0.5, 1.9]). CONCLUSIONS: Patients with hypertension or diabetes, and those who currently smoke, are at a higher risk of lacunar stroke, whereas those who undertake regular physical exercise may be at lower risk. The high risk associated with hypertension but absent risk with heart disease supports the "lacunar hypothesis" of a unique pathophysiologic mechanism for lacunar stroke.

The capsular warning syndrome: pathogenesis and clinical features.

Transient ischemic attacks (TIAs) are not homogeneous and may consist of subsets with mechanisms as varied as their stroke counterparts. We describe a form of TIA in 50 patients where crescendo episodes of ischemia were restricted to the region of the internal capsule, usually causing symptoms affecting face, arm, and leg. These patients composed 4.5% of a consecutive series of patients admitted with TIAs over a 15-year period and 33% of all TIAs classified as subcortical. We believe that the ischemia was most often due to hemodynamic phenomena in diseases, single, small penetrating vessels. When cerebral infarction developed, it was usually lacunar and involved a single penetrating vessel, although occasionally striatocapsular or anterior choroidal artery territory infarction occurred. There was no evidence of artery-to-artery or heart-to-artery embolism. Resistance to various forms of therapy, including hemodiluting, anticoagulant, and thrombolytic agents, was common. Because of dramatic and easily recognizable clinical presentation, apparent specific pathophysiologic mechanism, and the development of early capsular stroke in a high proportion of cases (42%), we have termed this the "capsular warning syndrome."

Smoking as a risk factor for cortical ischaemia presumably due to carotid occlusive disease.

Smoking is now a well established risk factor for ischaemic stroke. However, the risk associated with smoking may differ between subgroups of ischaemic stroke. To test the hypothesis that cortical ischaemia due to carotid artery occlusive disease, the latter of which has previously been linked to smoking, may have a higher smoking risk compared to other forms of cerebral ischaemia, we identified 178 cases of cortical ischaemia presumably due to carotid occlusive disease in our previous case-control population and compared the odds ratios (OR) for smoking risk in this group with that in group of 244 cases of other forms of cerebral ischaemia combined. All cases were individually matched for age (+/- 5 years) and sex with neighbourhood controls. Multiple conditional logistic regression was used to adjust for potentially confounding factors. The OR for current smokers in the cortical group was higher than that in the non-cortical group [OR 4.4, 95% confidence interval 2.2, 8.9 vs. 2.1 (1.1, 4.1)], particularly for those who smoked more than 60 pack-years [5.5 (2.2, 14.0) vs. 1.5 (0.6, 3.8)] and those who currently smoked more than one pack per day [20.2 (3.3, 122.3) vs. 2.6 (0.8, 8.2)], but not significantly. Overall, there is some evidence to suggest that smoking may be a more potent risk factor for cortical than for other forms of cerebral ischaemia, particularly at high smoking rates. Further studies are needed to substantiate this finding.

The influence of age on atrial fibrillation as a risk factor for stroke.

To determine the influence of age on atrial fibrillation as a risk factor for cerebral infarction, the Austin Hospital Stroke Unit Register from 1977 to 1990 was reviewed. There were 2279 patients with cerebral infarction (excluding lacunar infarction syndromes) with a mean age of 68.3 years who were identified as subjects, and 800 patients with pseudostroke and lacunar infarction syndromes with a mean age of 64.7 years who were identified as controls. Data concerning potential risk factors for stroke (including sex, age, atrial fibrillation, cardiac disease, hypertension, diabetes, peripheral vascular disease and smoking) were analyzed using multivariate regression techniques. It was found that atrial fibrillation was a significant risk factor for cerebral infarction (excluding lacunar infarction) for all age groups, after adjusting for the effects of other risk factors (P less than .001). However, when age was stratified into four groups, the age-specific odds ratios for atrial fibrillation were not significantly different and no significant interactions between atrial fibrillation and age or other risk factors were found (P greater than 0.1). It was concluded that, although with increasing age atrial fibrillation becomes a more frequent cause of stroke, its potency as a risk factor does not increase correspondingly. There was no significant influence of age on the relationship between atrial fibrillation and cerebral infarction.

Smoking as a risk factor for cerebral ischaemia.

To assess whether a rigorous clinical classification, based on computerised tomography, of patients with cerebral ischaemia would identify subgroups at higher or lower risk with respect to cigarette smoking habits, a case-control study was carried out on 422 cases of first-episode cerebral ischaemia matched for age and sex with 422 community-based neighbourhood controls. Patients with ischaemic stroke due to extracranial or intracranial vascular disease were at higher risk from smoking than has previously been reported for stroke (relative risk 5.7, 95% confidence interval 2.8, 12.0) whereas those with stroke due to cardiac emboli had no excess risk associated with smoking (relative risk 0.4 [0.1, 1.8]). After cessation of smoking, the relative risk declined gradually over 10 years, at the end of which time a significant risk was still evident. This finding may imply that the risk incurred by smoking is due mainly to atheroma formation, rather than transient haematological effects. Exposure to smoking by a spouse was an independent risk factor for the whole group of cerebral ischaemia patients (relative risk 1.7 [1.1, 2.6]), but this was not so for smoking by either parent (relative risk 1.2 [0.8, 1.8]). These findings suggest that smoking is a more potent risk factor for the most common form of ischaemic stroke than has previously been appreciated. The persistent nature of the risk even after cessation of smoking and the possible risk associated with passive exposure strengthens public health arguments against smoking.