RESUMO
Diabetes mellitus, a kind of chronic metabolic disease, has become one of major threats to human health with an increasing incidence. As a basic pathology of chronic complications related to diabetes mellitus, cerebral microangiopathy is mainly found in patients with Alzheimer's disease and lacunar infarction, and becomes one of the main reasons of death and disability in diabetic patients. The pathogenesis of cerebral microangiopathy is complicated, involving such signal pathways as metabolic abnormalities of polyol, saccharification hyperactivity, oxidative stress, abnormal transport of amyloid-β across blood-brain barrier and protein kinase C activation. Treatment targeting at related pathogenesis may bring a new hope to prevention and delay of the occurrence and development of cerebral microangiopathy of diabetes mellitus. Currently, pathogenesis, diagnosis and therapies for cerebral microangiopathy of diabetes mellitus have become hot topics in medical studies. This article reviews pathogenesis, clinical diagnosis and treatment for cerebral microangiopathy of diabetes mellitus, in order to provide new ideas for the prevention and treatment of cerebral microangiopathy of diabetes mellitus.
RESUMO
BACKGROUND: Neurological deterioration following acute lacunar infarction is not uncommon. Its association with poor clinical outcome is well-known, but little is known about what causes it. This study aimed to elucidate whether 3 stigmas of cerebral microangiopathy, a pathogenesis of lacunar infarction, are associated with neurological deterioration in patients with acute lacunar infarction. METHODS: Patients with acute lacunar infarction who were admitted within 24 hours of onset were identified using a prospective stroke registry. Patients who presented neurological deterioration within 7 days of hospitalization (progressive lacune group) were matched to 4 controls (non-progressive lacune group) for 'onset to arrival time'. Three stigmas of cerebral microangiopathy (leukoaraiosis, cerebral microbleeds, and silent lacunes) were measured using initial brain MRI, and their associations with neurological deterioration were analyzed. RESULTS: During 45 months, a total of 23 patients were identified and matched to 80 controls. Simple comparison of 2 groups showed that those 3 stigmas of cerebral microangiopathy were not significantly associated with neurological deterioration. Hyperlipidemia (p=0.18), history of transient ischemic attack or stroke (p=0.01), initial NIH stroke scale (p=0.07), white blood cell counts (p=0.16), and lesion volume (p=0.03) were possibly different (p's0.5). CONCLUSIONS: This study did not find a relationship between cerebral microangiopathy and neurological deterioration following acute lacunar infarction. The possibility of inadequate power should be noted.