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. Issue 3 (September 2015)

• Record Type: Journal Article
• Authors: Yin, D.; Slavin, K.V.
• Is Part Of: Medical hypotheses. Volume 85:Issue 3(2015)
• Page Start: 355
• Page End: 358
• Publication Date: 2015-09
• Subjects: Medicine -- Periodicals; Medicine -- Periodicals; Médecine -- Périodiques; Medicine; Periodicals; 610
• DOI: 10.1016/j.mehy.2015.06.014
• Languages: English
• ISSNs: 0306-9877

Abstract

<abstract xml:lang="en" abstract-type="author" id="ab005"> <title id="st005">Abstract</title> <sec> <p id="sp0005">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.</p> </sec> </abstract>