Cerebral blood supply with aging: normal, stenotic and recanalized.

UNLABELLED: The prosperity of brain parenchyma during aging depends on the preservation of cerebral blood flow (CBF) parameters. We have analysed ultrasonographic measurements of peak systolic (PSV) and end diastolic velocities (EDV) along with pulsatility (PI) and resistance indexes (RI) in common (CCA), internal (ICA) and external carotid artery (ECA) (N=199) and in vertebral arteries (VA) (N=200) in patients without any signs of stenosis. In two other cohorts patients with internal carotid artery stenosis (N=231) and patients prior to and after therapeutic recanalization (N=81) were evaluated in the same parameters. RESULTS: in the range of 21-92 years PSV in CCA decreases by 7 mm/s/year, while in ICA only by 2.31 mm/s/year. The decrease of EDV in carotid arteries occurs between 1.72 and 2.28 mm/s/year. PSV in VA drops down by 0.91 mm/s/year, EDV by 0.86 mm/s/year. PI and RI increase with age in all vessels, but not significantly. Stenotic ICAs are associated with increased PSV in the range of 0.7-2.9 m/s, but also with an increasing PSV variability along the growing stenosis in individual patients. In all degrees of stenoses some patients preserve normal velocities. In average the increment for each 10% of the stenosis below 50% makes 8 cm/s, while above 50% it makes already 50 cm/s. In persons with bilateral stenoses the increment with growing stenosis is steeper. The restoration of normal ICA lumen by means of carotid endarterectomy or by angioplasty with stenting results in an average drop by 1.23 m/s in PSV and by 0.4 m/s in EDV. We have investigated the ophthalmic artery and other substitution supplies and deduce, that the remarkable differences in blood flow velocity reactions to a compromised carotid lumen depend on the formation of collaterals in mutual interplay with peripheral resistance.

Cerebral microangiopathy in the mosaic of new discoveries.

After a short historical note on the diversion of the vascular concept of dementia from that of primary degeneration, this review describes cerebral deterioration on vascular grounds in three levels. Occlusions of big vessels with a single major infarct, middle calibre vasculopathy with multiple lacunes and finally microangiopathy causing leukoaraiosis--all these three entities produce cognitive disorders. Changes in the vessel wall, in cerebral blood flow velocity, the territorial and interterritorial rules for the location of malacia or lacunes are reviewed using neuroradiologic aspects revealed by ultrasound, by CT and MRI. Alterations in diffusion and their measurements by MRI are discussed in regard to ultrastructural reactions to ischaemia. Thresholds for tissue deterioration are shown in association with ATP depletion and with pathologic compounds in the interstitium.