Bioimpedance Analysis and Type 2 Diabetes: An Overview
Abstract
Two anatomical structures are involved in the neurovascular conflict (NVK) in classical HTN: the trigeminal nerve root (CTN) and the artery (more often the superior cerebellar artery (BMA), less often the inferior anterior cerebellar artery (NPMA) and the basilar artery (BA). The occurrence of NVK occurs with a critical convergence of these structures and an increase in the traumatic effect of the artery on the CTN. The force of the artery hitting the CTN is subject to the physical laws of hydrodynamics. In turn, endothelial dysfunction contributes to atherosclerotic vascular modification with increased rigidity of the vascular wall. The existing methods of treating HTN reflect the evolution of ideas about its etiology and pathogenesis. Among the conservative methods of treatment of classical HTN, first-line drugs are anticonvulsants and, above all, carbamazepine, which suppresses cortical and stem foci of sensitization. In parallel with the increase in tolerance to the drug, the number of adverse events also increases.
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