2019
DOI: 10.1109/jtehm.2019.2937121
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Expression of Concern: A Pilot Study of Facial Nerve Stimulation on Cerebral Artery Vasospasm in Subarachnoid Hemorrhage Patients

Abstract: This work was supported in part by the National Counsel of Science and Technology (CONACYT) of Mexico, and in part by NeuroSpring, a not-for-profit organization that supports research in the neurosciences (www.neurospring.org).

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Cited by 5 publications
(3 citation statements)
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“…This does ultimately result in increased CBF, decreased CVR, and cerebral vasodilation, but not via the same operative vasodilator (Goadsby et al, 1984). Though it has been seen that facial nerve stimulation and activation of the SPG may be protective in cerebrovascular disease (Borsody et al, 2013(Borsody et al, , 2014Borsody and Sacristan, 2016;San-Juan et al, 2019), this has not been harnessed through the trigeminal nerve. It is thought that the decrease in CVR subsequently protects against impaired perfusion and worsening ischemia, with studies suggesting a large role for the parasympathetic system in pathologic states (Hamel, 2006).…”
Section: Trigeminal Parasympathetic Pathwaymentioning
confidence: 99%
“…This does ultimately result in increased CBF, decreased CVR, and cerebral vasodilation, but not via the same operative vasodilator (Goadsby et al, 1984). Though it has been seen that facial nerve stimulation and activation of the SPG may be protective in cerebrovascular disease (Borsody et al, 2013(Borsody et al, , 2014Borsody and Sacristan, 2016;San-Juan et al, 2019), this has not been harnessed through the trigeminal nerve. It is thought that the decrease in CVR subsequently protects against impaired perfusion and worsening ischemia, with studies suggesting a large role for the parasympathetic system in pathologic states (Hamel, 2006).…”
Section: Trigeminal Parasympathetic Pathwaymentioning
confidence: 99%
“…Cerebral vasospasm is the most major cause behind morbidity (decreased cerebral blood flow, ischemic neurological deficits, and cerebral infarction) and mortality associated with aneurysmal subarachnoid hemorrhage. [1] Cerebral vasospasm develops within 48 hours after subarachnoid hemorrhage as a result of inflammatory response but is rarely detected with angiography within the first 3 days. [2] It is usually determined 5 to 14 days after subarachnoid hemorrhage and begins to improve within 2 to 4 weeks.…”
Section: Introductionmentioning
confidence: 99%
“…[5,6] Pentoxifylline and facial nerve stimulation are more recent treatment options whereas common treatment options include clazosentan, balloon dilatation, intra-arterial papaverine, and nimodipine [isopropyl (2-methoxy-ethyl) 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate]. [1,2,[7][8][9][10] Despite all these proposed treatment options, the only conventional evidence-based treatment method is hemodynamic therapy, which involves the manipulation of blood pressure, volume, and viscosity to improve cerebral blood flow. And even this treatment method is associated with a 20 to 30% risk of complications.…”
Section: Introductionmentioning
confidence: 99%