Northern Manhattan Stroke Study Research Articles

Testing the validity of the lacunar hypothesis: the Northern Manhattan Stroke Study experience.

Few studies have attempted to validate the "lacunar hypothesis." The accuracy of identifying lacunar and other nonlacunar mechanisms of infarction will be increasingly important in evaluating potential stroke treatments. The aim of this study was to determine the value of lacunar syndromes in predicting radiologic lacunes and the value of clinicoradiologic lacunes in predicting "lacunar infarction" as final stroke mechanism. From 1990 to 1994, 591 patients with cerebral infarction, who were from northern Manhattan and over the age of 39, were prospectively examined. Data were collected on the admitting clinical syndrome (lacunar or nonlacunar) and brain imaging findings. Lacunar syndromes were categorized as pure motor hemiparesis (PMH), pure sensory syndrome (PSS), sensorimotor syndrome (SMS), ataxic-hemiparesis (A-H), and other lacunar syndromes. Brain imaging findings were classified as radiologic lacune or nonlacune. Positive predictive values, sensitivities, and specificities of lacunar syndromes for identifying radiologic lacunes were calculated. The final mechanism of infarction was determined after review of all the diagnostic tests and compared among the lacunar groups. Lacunar syndromes occurred in 225 cases. PMH was the most common lacunar syndrome, accounting for 45%, SMS 20%, A-H 18%, and PSS 7%. Lacunar syndromes had an overall positive predictive value (PPV) of 87% for detecting radiologic lacune: PSS 100%, A-H 95%, SMS 87%, and PMH 79%. Among the 195 patients who presented with a lacunar syndrome and had this condition confirmed radiologically, 147 were classified as having a final diagnosis of lacunar mechanism of infarction (PPV = 75%). Atherosclerosis accounted for 17 (9%), cardioembolism 10 (5%), cryptogenic 17 (9%), and other unusual causes 4 (2%). While lacunar syndromes, especially PSS and A-H, are highly predictive of lacune, in about one in four patients presenting with lacunar syndromes confirmed radiologically the condition is associated with nonlacunar mechanisms of infarction. Noninvasive neurovascular and cardiac evaluations are still warranted even among patients with lacunes.

Predictors of mortality and recurrence after hospitalized cerebral infarction in an urban community: the Northern Manhattan Stroke Study.

To identify determinants of recurrence and mortality after ischemic stroke in a mixed-ethnic region. The determinants of ischemic stroke outcome are not uniformly characterized and will be of increasing importance as the frequency of ischemic stroke survivors increases in our aging population. A cohort of 323 patients (40% black, 34% Hispanic, 26% white) with cerebral infarction from northern Manhattan over age 39 were followed for a mean of 3.3 years, with only 6% lost to follow-up. Cumulative life table risk of mortality and recurrence was calculated. Risk factors classified at the time of index ischemic stroke were selected based on univariate analyses and then entered into a Cox proportional hazards model for mortality and for recurrence. The life table cumulative risk of mortality was 8% at 30 days, 22% at 1 year, and 45% at 5 years after ischemic stroke. The immediate cause of death was related to vascular disease in 60%. After age adjustment, the significant predictors of mortality were congestive heart failure (risk ratio [RR] = 2.6), admission glucose > 140 mg/dl (RR = 1.7), and presentation with either a large dominant, nondominant, or major basilar syndrome (RR = 2.0). Patients with a lacunar syndrome had a better survival (RR = 0.6). Recurrent strokes occurred in 72 patients. The life table cumulative risk of recurrence was 6% at 30 days, 12% at 1 year, and 25% at 5 years after ischemic stroke. Ethanol abuse (RR = 2.5), hypertension requiring discharge medications (RR = 1.6), and elevated blood glucose within 48 hours of index ischemic stroke (RR = 1.2 per 50 mg/dl) were the independent predictors of recurrence. Among 30-day survivors, the effect of ethanol abuse was greater (RR = 3.5), indicating its impact on late recurrence. After accounting for age and presenting syndrome, initial glucose predicts stroke mortality and recurrence after ischemic stroke. This association may reflect uncontrolled and undiagnosed diabetes in our urban population. Furthermore, ethanol abuse may be a determinant of ischemic stroke recurrence. Reduction of the stroke public health burden will require targeted modification of such conditions and behaviors.