Loading…

A hypothesis on possible neurochemical mechanisms of action of cervical spinal cord stimulation in prevention and treatment of cerebral arterial vasospasm after aneurysmal subarachnoid hemorrhage

Abstract Subarachnoid hemorrhage (SAH) is associated with the high incidence of development of cerebral vasospasm that results in morbidity and mortality due to delayed cerebral ischemia. So far there are no consistently effective therapies for treatment of vasospasm in patients suffering from SAH....

Full description

Saved in:
Bibliographic Details
Published in:Medical hypotheses 2015-09, Vol.85 (3), p.355-358
Main Authors: Yin, D, Slavin, K.V
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Abstract Subarachnoid hemorrhage (SAH) is associated with the high incidence of development of cerebral vasospasm that results in morbidity and mortality due to delayed cerebral ischemia. So far there are no consistently effective therapies for treatment of vasospasm in patients suffering from SAH. It is well known that cervical spinal cord stimulation (SCS) can induce vasodilatation and increase cerebral blood flow (CBF). Based on the experiments in animals and the studies in humans, we have proposed the possibility to use SCS as a therapeutic strategy for prevention and treatment of cerebral vasospasm after SAH. However, the physiological mechanisms of action of SCS in this regard are poorly understood. Better understanding of the pathophysiology of vasospasm after SAH may provide insight into the role of SCS in such conditions. We hypothesize that effect of SCS on vasodilatation may be related to modulation of activity of phosphodiesterases 5 (PDE-5) and nitric oxide synthase (eNOS), resulting in enhancement of nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) pathway, which may help prevent and/or treat vasospasm after SAH. Further investigations on the physiological mechanisms of action of SCS would be necessary to support this hypothesis.
ISSN:0306-9877
1532-2777
DOI:10.1016/j.mehy.2015.06.014