Background and Purpose-A low risk of recurrent stroke and death after lacunar infarction has previously been reported, but follow-up has been limited to Յ5 years. Methods-One hundred eighty patients with pure motor stroke, collected between 1983 and 1986 from a hospital-based stroke registry, were followed up until at least 10 years after the index stroke. Two patients were lost to follow-up. Survival status was determined from the official population registry and compared with survival rates of the Swedish population, matched for age and sex. Cox proportional hazards regression analyses were used to identify independent prognostic predictors. Results-During follow-up 106 (60%) of the 178 patients died, most commonly as a result of coronary heart disease.During the first 5 years after the stroke, survival rates were similar to those of the general population. Beyond this time the risk of death was increased among patients with pure motor stroke, with an excess of 10 to 15 percent units compared with the general population. Independent determinants for death were age (PϽ0.01), male sex (PϽ0.01), and nonuse of acetylsalicylic acid (Pϭ0.02). Recurrent stroke occurred in 42 (23.5%) of the patients, corresponding to an annual risk of 2.4%. Hypertension (Pϭ0.025) and diabetes (Pϭ0.024) were independent risk factors for recurrent stroke. Conclusions-For the first few years after lacunar infarct, the risk of death was similar to that of the general population, but later a clear excess of death was observed. The long-term prognosis in lacunar infarction appears less favorable than previously reported.

Background and Purpose: The ‘capsular warning syndrome’ (CWS) of recurrent stereotyped episodes of motor or sensory dysfunction is clinically well recognized, and is associated with a high risk of imminent lacunar infarction with permanent deficits resembling those of CWS. However, the pathophysiology of CWS has not been well characterized. We report a clinicoanatomic correlation with MR imaging studies in the acute and chronic phases in patients with CWS. Material and Methods: Between April 1997 and March 2001, we prospectively studied 8 patients, mean age 73.3 years, presenting with 4–17 motor or sensorimotor transient ischemic attacks (TIAs; duration 2–90 min) up to 3 days after onset of the first episode. Four patients were free of symptoms between the attacks and had no residua, whereas 4 patients developed a pure motor or sensorimotor stroke within 1–3 days after symptom onset. Diffusion-weighted echoplanar MRI (DWI) and T₂-weighted MRI studies were performed within 1 week after symptom onset and were repeated 1–2 months later. Results: Seven of the 8 patients had an appropriate lesion on DWI in the acute phase. DWI abnormalities in the 3 patients with TIAs were 4–10 mm in diameter and confined to the lateral thalamus or medial globus pallidus without involving the internal capsule, whereas 4 patients who developed a stroke had abnormalities localized to the putamen extending to corona radiata (3 patients), or the pontomesencephalic junction (1 patient). All 6 patients who underwent follow-up MRI had an infarct on T₂-weighted images corresponding to, but usually smaller than, the acute phase DWI abnormality. Conclusions: Small infarcts in the basal ganglia or the pons, close to central motor pathways, appear to be the primary lesion in CWS. The pathophysiology of CWS is complex, and may involve hemodynamic mechanisms in penetrating arterial territories, as well as molecular mechanisms, such as peri-infarct depolarizations affecting adjacent motor pathways.

Almost all patients with acute ischemic lacunar syndromes have acute lesions on echo-planar diffusion-weighted MRI within 3 days after stroke onset. These lesions are mostly small and subcortical, compatible with lacunar infarcts caused by single penetrating artery occlusion, but in a minor proportion of patients (2 of 23 in our study) a cortical involvement is found.

No abstract

No abstract