Parasympathetic innervation of vertebrobasilar arteries: is this a potential clinical target?

Abstract

This review aims to summarise the contemporary evidence for the presence and function of the parasympathetic innervation of the cerebral circulation with emphasis on the vertebral and basilar arteries (the posterior cerebral circulation). We consider whether the parasympathetic innervation of blood vessels could be used as a means to increase cerebral blood flow. This may have clinical implications for pathologies associated with cerebral hypoperfusion such as stroke, dementia and hypertension. Relative to the anterior cerebral circulation little is known of the origins and neurochemical phenotypes of the parasympathetic innervation of the vertebrobasilar arteries. These vessels normally provide blood flow to the brainstem and cerebellum but can, via the Circle of Willis upon stenosis of the internal carotid arteries, supply blood to the anterior cerebral circulation too. We review the multiple types of parasympathetic fibres and their distinct transmitter mechanisms and how these vary with age, disease and species. We highlight the importance of parasympathetic fibres for mediating the vasodilatory response to sympathetic activation. Current trials are investigating the possibility of electrically stimulating the postganglionic parasympathetic ganglia to improve cerebal blood flow to reduce the penumbra following stroke. We conclude that although there are substantial gaps in our understanding of the origins of parasympathetic innervation of the vertebrobasilar arteries, activation of this system under some conditions might bring therapeutic benefits.

Dynamic cerebral autoregulation is impaired in Veterans with Gulf War Illness: A case-control study

“…However, we observed similar CO 2 reactivity between-groups. This suggests that factors other than CO 2 reactivity contribute to the autoregulatory response, most notably cholinergic activation of the cerebral vasculature [ 44 ]. In support, we recently demonstrated in a randomized double-blind study that physostigmine infusion enhanced CBF velocity despite the presence of hypocapnia [ 16 ].…”

Differences in autonomic innervation to the vertebrobasilar arteries in spontaneously hypertensive and Wistar rats

“…Thus, we propose that in hypertension parasympathetic dysfunction is a major problem regarding cerebral blood flow regulation and, as we proposed recently, strategies to circumnavigate this dilatory deficit would be clinically important, especially in conditions of hypertension and stroke (Roloff et al . ).…”

“…Thus, future research should examine if harnessing parasympathetic system functionality might restore brain perfusion and alleviate hypoperfusion‐related pathologies such as hypertension, stroke and vascular dementia (Roloff et al . ).…”

“…The sources of sympathetic and parasympathetic input to the vertebrobasilar arteries are somewhat distinct from innervation to the anterior cerebral arteries/circle of Willis (Roloff et al . , for review). Whereas the anterior cerebral circulation receives sympathetic input from the superior cervical ganglion and parasympathetic input from pterygopalatine ganglion, cavernous sinus ganglia, carotid mini‐ganglion and otic ganglia, the vertebrobasilar arteries receive sympathetic input from stellate and superior cervical ganglia whereas the parasympathetic input is derived mainly from the otic ganglia.…”

In with the new and out with the old: enter multivariate wavelet decomposition, exit transfer function

“…Furthermore, these studies have relied on transfer function analyses, which assumes that perfusion pressure is the only factor influencing CBF and that perfusion pressure and CBF interactions are linear and stationary, a circumstance that is almost certainly not possible considering the multifactorial regulation of CBF (5,20). Lastly, the majority of previous studies evaluating the SNS influence on CBF regulation have used phentolamine as their drug of choice, which creates problems for interpretation, as this is a nonspecific ␣ 1 -and ␣ 2 -blocker with agonistic effects of muscarinic and histamine receptors, factors that can directly influence CBF regulation themselves (4,15).…”