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N Nicastro

Publications and source records attributed to N Nicastro.

5 recordsLinked to original sources

Developmental structure in brain evolution.

How does evolution grow bigger brains? It has been widely assumed that growth of individual structures and functional systems in response to niche-specific cognitive challenges is the most plausible mechanism for brain expansion in mammals. Comparison of multiple regressions on allometric data for 131 mammalian species, however, suggests that for 9 of 11 brain structures taxonomic and body size factors are less important than covariance of these major structures with each other. Which structure grows biggest is largely predicted by a conserved order of neurogenesis that can be derived from the basic axial structure of the developing brain. This conserved order of neurogenesis predicts the relative scaling not only of gross brain regions like the isocortex or mesencephalon, but also the level of detail of individual thalamic nuclei. Special selection of particular areas for specific functions does occur, but it is a minor factor compared to the large-scale covariance of the whole brain. The idea that enlarged isocortex could be a "spandrel," a by-product of structural constraints later adapted for various behaviors, contrasts with approaches to selection of particular brain regions for cognitively advanced uses, as is commonly assumed in the case of hominid brain evolution.

Animals↗

[Cerebral vascular autoregulatory dysfunction. Neuroradiologic aspects].

PURPOSE: We report the neuroimaging findings in a group of systemic disorders with a common pathophysiological pattern of derangements in cerebral vascular autoregulatory mechanism producting potentially reversible brain lesions. MATERIAL AND METHODS: We reviewed the brain CT and MR examinations of 14 patients with clinical diagnosis of vasculopathy not related to atherosclerosis or cardiogenic embolism. The patients were admitted at the onset of neurologic deficit and were affected with one of the following systemic disorders: thrombotic thrombocytopenic purpura (TTP, 6 cases), uremic encephalopathy (4 cases), eclampsia (2 cases), 1 chronic renal failure from systemic lupus erythematosus and 1 cyclosporin neurotoxicity. All patients underwent neuroimaging follow-up within 7-20 days of the onset of neurologic deficit and the start of anti-edema therapy. RESULTS: CT and MR findings were characterized by cortical-subcortical or deep brain lesions related to edema. Ten patients presented bilateral lesions, which were symmetric in 4 cases. Edema resolution was demonstrated on follow-up examinations after therapy in 4 patients (2 with eclampsia, 1 with TTP and 1 with uremic encephalopathy). The lesions showed no signs of regression in 10 patients. CONCLUSIONS: Brain lesions with a common pathogenesis from derangements in vascular autoregulatory mechanism--i.e., not due to atherosclerosis or cardiogenic embolism--should be properly and promptly recognized because they can be reversible and readily treatable.

Adult↗