Stimulation of vagal nerve in intracranial hypertension: A literature review

Abstract

Background: Pathologies that affect the central nervous system (CNS) and increases intracranial pressure may develop into fatal outcomes. There are physiological properties of neurons that are susceptible to modify, such as neuronal plasticity. The vagus nerve stimulation (VNS) has focused on the modification of these variables in order to restore the homeostasis of the CNS. In this article, we aimed to review the general concept of VNS, the pathology of intracranial hypertension and the effects of combining treatment to the pathology. Literature review: VNS activates several neuromodulatory pathways and centers in the brain, which associated with plasticity. They are including cholinergic and noreadrenergic system, which are transcendental for neural plasticity. One of the mechanisms by which VNS decreases ICP is due to the attenuation of the systemic inflammatory response and the signaling of proinflammatory cells induced by TBI, whose possible mechanism is the inhibition of cytokines such as tumor necrosis factor (TNF), IL-1b, IL-6 and IL-18. In addition, it had been shown that VNS stimulated the locus coeruleus with a consequent release of noreepinephrine, which act as an endogenous anti-inflammatory agent. VNS requires neuroanatomical knowledge of the entire vagal network and its physiology. The surgery is relatively simple and the complication rates are very low conferring a great effectiveness in several neural diseases. Neural and non-neural pathways have been well-characterized to avoid the immune response through VNS. Conclusion: Different experimental studies have concluded that VNS reduces intracranial pressure, although the mechanism is not completely specified. Further studies evaluating the clinical role of VNS in intracranial hypertension are necessary.