Neurovegetative Correction of Diencephalic – Hyperkinetic, Catabolic Adrenergic Syndrome

Abstract

Hibernation proposed by Irving and Krog (1954) was developed by H. Laborit and P. Huguenard, which, today, is very current and important in modern medicine as neurovegetative correction (NVC): Curative anesthesia, neurovegetative blockade, artificial hibernation, capable of providing the minimal metabolic rate at the parabiosis level, and phylogenetic descending cerebral activity. It is important! NVC is not block-free and inhibits excessive impulses, prevents them from attenuating, and installs normal blood pressure, heart rate, body temperature (T°C), blood (pH), adrenal-cholinergic balance, maintaining hibernation homeostasis. From the multiple neurovegetative correction (NVC) schemes of cerebral insufficiency (CI) of various causes (traumas, onco, stroke, neuroinfections, metabolic, hypoxic, etc.), ongoing 35 years, retrospectively, arranged the pattern, with three essential syndromes manifestation of CI: Diencephal -hyperkinetic (catabolic adrenergic), extrapyramidal -eukinetic (balanced), and mezencephal -hypokinetic (anabolic cholinergic). NVC is multimodal and selective inhibition, correction, and analgesia. Thus, by performing the loco-regional correction of the three symptoms of CI and systemic by appropriate medications, NVC can be obtained. Here we describe, diencephal -hyperkinetic syndrome (catabolic adrenergic) → psychic, motor, and vegetative agitation (↑blood pressure [BP], heart rate [HR], T0C) return to normal by administering the usual doses of dexmedetomidine,D with the influence of G-protein and super selective α2-Adreno agonists, as a cerebrospinal locoregional neurotransmitter, D installs anxiolysis, anesthesia, ↓ T0C (central) produces sedation without inhibiting the respiratory center (important in patients with sleep apnea) and central and systemic cerebral effect, α2-Adreno agonist (previously used clonidine) ↓BP, HR, T0C (peripheral), to optimize systemic perfusion pressure, in turn dependent on mean BP and capillary resistance, also stimulates the elimination by endotheliocytes of the NO vasorelaxant → antioxidant, which catches the superoxide O 2 -, at the same time influencing and mitochondrial permeability transition pore dependent Ca++uniporter, mPT pore.