1995 Volume 17 Issue 3 Pages 232-240
Silent cerebral infarction (SCI) is often associated with the evolution of symptomatic ischemic vascular accidents and dementia. However, the longitudinal outcome of SCI is unknown. We conducted a preliminary investigation in an attempt to answer this question. Subjects without neurological abnormalities or any history suggesting vascular accident, and in whom cerebral hyperintensity (CH) was detected by magnetic resonance imaging (MRI), were diagnosed as SCI. Forty-three subjects who visited our department in 1991 with non-specific complaints such as headache or dizziness were diagnosed as SCI and enrolled in the present study. We conducted MRI studies and a series of cognitive examinations over an average period of 23 months in order to follow the clinical course, determine the risk factors, and assess the cognitive status of these subjects. The degree of CH was expressed using the rating scale proposed by Scheltens et al., which allocates points according to the size and number of CHs in the periventricular, white matter, basal ganglia and infratentorial regions. Only CHs larger than 3 mm were considered, since they are more likely to represent actual infarctions rather than enlarged perivascular spaces. Over the course of the study, 5 subjects ceased communicating with our department, 3 refused the second evaluation, 2 did not provide complete data, and one developed a fatal subarachnoid hemorrhage. None of the remaining 32 subjects developed symptomatic cerebral infarction and all continued to satisfy the criteria for a diagnosis of SCI at the time of the second evaluation. Fifteen subjects showed an increased CH score (increase group), while 17 subjects displayed no change or a decreased CH score (non-increase group). Increases were most commonly observed in the posterior half of the brain, especially in the periventricular area. Univariate analysis revealed a significantly higher frequency of antiplatelet agent ingestion and a non-significant but higher frequency of diabetes mellitus in the increase group. Multivariate analysis demonstrated that higher CH scores at the first evaluation, longer follow-up intervals, aging, ST-T changes on ECG as well as the ingestion of antiplatelet agents were factors that coincided with a CH increase. Use of antiplatelet agents did not directly cause an increase in CHs, but these agents were more likely to be prescribed to subjects with a large number of risk factors, resulting in higher CH scores. Cognitive functions were not significantly different between the two groups. However, the increase group exhibited longitudinal deterioration on the Raven Colored Progressive Matrices, while the non-increase group showed no deterioration. The results of our study suggest that (1) SCI does not signify an urgent prodrome of symptomatic infarction or dementia; (2) SCI may increase in the presence of prior SCI and ECG changes, and when subjects are aged and under observation for an extended period of time; and (3) appropriate control of associated risks is mandatory for preventing SCI increases.
