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Levees are earth structures constructed along alluvial rivers and are considered to be one of the essential components of flood risk and natural hazard reduction. The preservation of their condition would require orderly monitoring. In Hungary, an over 4200 km long levee system was constructed from the 19th century on. Since then, many natural and anthropogenic processes, such as compaction, erosion, subsidence etc., could contribute to the slow but steady deformation of these structures. In the meantime , due to the lack of documentation, their structure and internal composition are still unclear in many sections. The present study uses different geophysical techniques to validate their efficiency in detecting the structure, composition and potential defects along a 3.6 km levee section of the Lower Tisza River, affected significantly by seepage and piping phenomena during floods. Measurements were made using Ground Penetrating Radar (GPR), Electrical Resistivity Tomography (ERT) and drillings. Information obtained by the different techniques was cross-checked and combined. This way, the potential of the applied survey strategy could be demonstrated, and the selected levee section could be assessed in terms of its structure and composition. Consequently, the major reasons for frequently occurring adverse flood phenomena at the site could be revealed. The survey approach outlined in the present paper can be applied extensively along lowland levee systems in the region and elsewhere.

Spreading depolarization (SD) is assumed to be the pathophysiological correlate of migraine aura, leading to spreading depression of activity and a long-lasting vasoconstriction known as spreading oligemia. Furthermore, cerebrovascular reactivity is reversibly impaired after SD. Here, we explored the progressive restoration of impaired neurovascular coupling to somatosensory activation during spreading oligemia. Also, we evaluated whether nimodipine treatment accelerated the recovery of impaired neurovascular coupling after SD. Male, 4–9-month-old C57BL/6 mice (n = 11) were anesthetized with isoflurane (1%–1.5%), and SD was triggered with KCl through a burr hole made at the caudal parietal bone. EEG and cerebral blood flow (CBF) were recorded minimally invasively with a silver ball electrode and transcranial laser-Doppler flowmetry, rostral to SD elicitation. The L-type voltage-gated Ca2+ channel blocker nimodipine was administered i.p. (10 mg/kg). Whisker stimulation-related evoked potentials (EVPs) and functional hyperemia were assessed under isoflurane (0.1%)–medetomidine (0.1 mg/kg i.p.) anesthesia before, and repeatedly after SD, at 15-min intervals for 75 minutes. Nimodipine accelerated the recovery of CBF from spreading oligemia (time to full recovery, 52 ± 13 vs. 70 ± 8 min, nimodipine vs. control) and exhibited a tendency to shorten the duration of the SD-related EGG depression duration. The amplitudes of EVP and functional hyperemia were markedly reduced after SD, and progressively recovered over an hour post-SD. Nimodipine exerted no impact on EVP amplitude but consistently increased the absolute level of functional hyperemia from 20 min post-CSD (93 ± 11% vs. 66 ± 13%, nimodipine vs. control). A linear, positive correlation between EVP and functional hyperemia amplitude was skewed by nimodipine. In conclusion, nimodipine facilitated CBF restoration from spreading oligemia and the recovery of functional hyperemia post-SD, which were linked to a tendency of an accelerated return of spontaneous neural activity after SD. The use of nimodipine in migraine prophylaxis is suggested to be re-visited. [ABSTRACT FROM AUTHOR]