Trigeminal Nerve Control of Cerebral Blood Flow: A Brief Review.

Timothy G White,Henry H Woo,Kevin A Shah,Keren Powell,Chunyan Li,Raj K Narayan

doi:10.3389/fnins.2021.649910

Timothy G White, Henry H Woo + Show 4 more

Open Access

https://doi.org/10.3389/fnins.2021.649910

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Abstract

The trigeminal nerve, the fifth cranial nerve, is known to innervate much of the cerebral arterial vasculature and significantly contributes to the control of cerebrovascular tone in both healthy and diseased states. Previous studies have demonstrated that stimulation of the trigeminal nerve (TNS) increases cerebral blood flow (CBF) via antidromic, trigemino-parasympathetic, and other central pathways. Despite some previous reports on the role of the trigeminal nerve and its control of CBF, there are only a few studies that investigate the effects of TNS on disorders of cerebral perfusion (i.e., ischemic stroke, subarachnoid hemorrhage, and traumatic brain injury). In this mini review, we present the current knowledge regarding the mechanisms of trigeminal nerve control of CBF, the anatomic underpinnings for targeted treatment, and potential clinical applications of TNS, with a focus on the treatment of impaired cerebral perfusion.

Highlights

Disordered cerebral perfusion, inadequate perfusion leading to neurological injury, plays a major role in multiple disease processes including, but not limited to, acute ischemic stroke (AIS) (Prabhakaran et al, 2015), subarachnoid hemorrhage (SAH) (Ciurea et al, 2013; Baggott and Aagaard-Kienitz, 2014), and traumatic brain injury (TBI) (Vella et al, 2017; O’leary and Nichol, 2018)
It has been demonstrated in the setting of experimental TBI that stimulation of the nasociliary branch of the ophthalmic division of the trigeminal nerve can increase both Cerebral blood flow (CBF) and brain tissue oxygenation (Chiluwal et al, 2017), and trigeminal nerve via electrical stimulation (TNS) following SAH retains the effect of elevated CBF and decreased cerebrovascular resistance (CVR) (Atalay et al, 2002)
Many studies to date have demonstrated the successful regulation of CBF by TNS (Figure 1 and Table 1), providing the basic framework upon which to build future investigations into its potential applicability to various disorders of cerebral perfusion

Summary

INTRODUCTION

Disordered cerebral perfusion, inadequate perfusion leading to neurological injury, plays a major role in multiple disease processes including, but not limited to, acute ischemic stroke (AIS) (Prabhakaran et al, 2015), subarachnoid hemorrhage (SAH) (Ciurea et al, 2013; Baggott and Aagaard-Kienitz, 2014), and traumatic brain injury (TBI) (Vella et al, 2017; O’leary and Nichol, 2018). The sensory branches of the trigeminal nerve spread across most of the face and directly innervate much of the cerebral vasculature (Shankland, 2000) Stimulation of these sensory nerves activates a pathway originating at the trigeminal ganglion that leads to antidromic release of neurotransmitters, vasodilation, and increases in CBF (Goadsby et al, 1988; Mense, 2010; Goto et al, 2017). Though immunohistochemical studies have demonstrated that CGRP-containing sensory neurons are found in the SPG (Csati et al, 2012), parasympathetic nerve fibers have been found to release vasoactive molecules including acetylcholine (Ebersberger et al, 2006; Shelukhina et al, 2017), vasoactive intestinal peptide (Edvinsson et al, 1988; Goadsby and Shelley, 1990), PACAP (Uddman et al, 1993; Zagami et al, 2014), and NO (Goadsby et al, 1996), but not the aforementioned CGRP This does result in increased CBF, decreased CVR, and cerebral vasodilation, but not via the same operative vasodilator (Goadsby et al, 1984).

Result of stimulation on CBF

CONCLUSION