RESUMO
It is proposed that the higher incidence of chronic stress-adaptation failure in patients with Alzheimer's disease is of specific etiopathological significance. Such chronic stress-adaptation failure leads to a vicious circular reaction, namely: intense, stressful stimuli----neocortico-limbic excitation----hypothalamo-pituitary-adrenocortical (HPA) axis activation----excessive secretion of neurohormones including cortisol----stimulation of inhibitory glucocorticoid sensitive hippocampal neurons----failure to terminate the HPA axis response----chronic excessive secretion of neurohormones including cortisol----overstimulation degeneration of glucocorticoid sensitive hippocampal inhibitory neurons----progressive cognitive-affective behavioral disorganizational failure which is typical of dementia of the Alzheimer's type. Possibilities of neuropharmacological corrections and neurobehavioral re-education are suggested.
Assuntos
Doença de Alzheimer/etiologia , Adaptação Fisiológica , Doença de Alzheimer/fisiopatologia , Biomarcadores , Hipocampo/fisiopatologia , Hormônios/metabolismo , Humanos , Hidrocortisona/metabolismo , Sistema Hipotálamo-Hipofisário/fisiopatologia , Sistema Límbico/fisiopatologia , Modelos Biológicos , Sistema Hipófise-Suprarrenal/fisiopatologia , Estresse Fisiológico/fisiopatologiaRESUMO
Circulating microembolic index (CMI) was determined by drawing one blood sample into EDTA-formalin and the other into DTA alone in patients with migraine and compared with matched normal controls. Platelet aggregates, if any, are fixed in EDTA-formalin but disaggregated by EDTA. Ratios of these two counts approximate "unity" in normals and are proportionately less than unity, depending on the number of platelet aggregates. 26 untreated migraineurs and 19 migraineurs with history of self-medication with aspirin taken within 72 hours of the test, were studied in headache-free intervals. Results were compared with those from 20 healthy, age and sex matched volunteers, without migraine, who were medication-free for at least one week. Mean CMI in untreated migraineurs (0.77 +/- 0.03 SEM) was significantly lower than the mean in normal controls (0.94 +/- 0.02, p. less than 0.002). Migraineurs with self administration of aspirin had mean CMI of 0.88 +/- 0.02, differing significantly from untreated migraineurs (p less than 0.01) but not from normal controls (0.1 less than p less than 0.2). Results suggest excessive platelet aggregation in migraineurs which tends to be corrected by treatment with platelet inhibitors such as aspirin.