Objective: The determinants of post stroke depression (PSD) have been strongly debated between proponents of a neuroanatomical model, assuming that PSD is usually caused by a cerebral lesion and supporters of a psychological model, maintaining that PSD is a result of the psychosocial adjustment required by the disease. The purpose of this study was to address the association between PSD and brain lesion localization.
Design: A clinico-pathological analysis of a large cohort of elderly patients with stroke was performed.
Materials and Methods: The study population included 104 consecutive autopsy cases (46 men and 58 women). Among them, there were 30 patients who developed PSD (mean age: 79.1±7.9 for men and 81.1±8.5 for women) and 74 patients without PSD (mean age: 83.5±7.2 for men and 86.5±5.4 for women). Subjects with stoke were included only if they lived at least one month after it and the diagnosis could be confirmed pathologically. The clinical diagnosis of depression was made according to the DSM-IV criteria. After external examination both hemispheres were cut into 1cm thick coronal slices and examined for macroscopic vascular lesions as brain infarcts, cerebral hemorrhage or lacunar infarcts. One macroscopic brain infarct or multiple lacunar infarcts in one brain region were classified as focal vascular lesions, whereas multiple brain infarcts affecting various regions were classified as multifocal vascular lesions. According to their localization focal and multi-focal vascular lesions were considered as lesions of the left or right frontal, temporal, parietal and occipital cortex, hippocampus, and substantia nigra.
Results: The two groups did not differ in men to women ratio, time interval between stroke and death, presence of vascular risk factors, dementia, and weight of brain. There was only a significant difference between the two subjects group in age of death and stroke. The severity of arteriosclerosis of the brain vessels, as well as the frequency of brain vascular lesions (focal, multi-focal), were quite similar between the two groups. Moreover, the regional distribution of vascular lesions did not differ between the two groups. In multivariate models, only age at stroke emerged as predictor of PSD, explaining 6.8% of the dependent variable.
Conclusion: To our knowledge this is the first study addressing neuropathologically the neuroanatomical model of PSD. The main finding was that there is no effect of different interhemispheric or intrahemispheric damage to PSD. The association between young age at stroke and PSD could reflect the difficulties in psychosocial adjustment consecutive to stroke-related disabilities in this particular age group.
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