Resection of the nerves bundle from the sphenopalatine ganglia tend to increase the infarction volume following middle cerebral artery occlusion

Su, Diansan; Shifen, Zhang; Zhen, Gu; Wang, Heming; Wang, Xiangrui

doi:10.1007/s10072-010-0238-0

Cited by 19 publications

(11 citation statements)

References 19 publications

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“…The concept of the BrainsGate device is, of course, strongly supported by the numerous studies described previously examining electrical stimulation of the SPG in normal animals. The concept of the BrainsGate device is further supported by the repeated observation that lesions of the SPG or its efferents to the cerebral arteries allow for larger infarct volumes in rat stroke models,[ 68 69 70 ] a finding that also supports the proposed natural protective role for the SPG against brain ischemia. BrainsGate itself sponsored preclinical studies of SPG stimulation as a treatment for ischemic stroke that are technically comparable to studies of direct electrical stimulation of the SPG by way of cranial dissection.…”

Section: Clinical Development Of Facial Nerve Stimulator Devicesmentioning

confidence: 92%

Facial nerve stimulation as a future treatment for ischemic stroke

Borsody¹,

Sacristán²

2016

Brain Circ

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Stimulation of the autonomic parasympathetic fibers of the facial nerve system (hereafter simply “facial nerve”) rapidly dilates the cerebral arteries and increases cerebral blood flow whether that stimulation is delivered at the facial nerve trunk or at distal points such as the sphenopalatine ganglion. Facial nerve stimulation thus could be used as an emergency treatment of conditions of brain ischemia such as ischemic stroke. A rich history of scientific research has examined this property of the facial nerve, and various means of activating the facial nerve can be employed including noninvasive means. Herein, we review the anatomical and physiological research behind facial nerve stimulation and the facial nerve stimulation devices that are in development for the treatment of ischemic stroke.

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Section: Clinical Development Of Facial Nerve Stimulator Devicesmentioning

confidence: 92%

Facial nerve stimulation as a future treatment for ischemic stroke

Borsody¹,

Sacristán²

2016

Brain Circ

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“…Data in experimental models of stroke have demonstrated that stimulation of this ganglion increased blood flow, reduced infarct volume and improved functional outcomes (Henninger and Fisher, 2007, Bar-Shir et al, 2010). Conversely, severing the nerves emanating from the sphenopalatine ganglion increased infarct volume after MCAO (Diansan et al, 2010). Based on encouraging preclinical data, the safety of sphenopalatine ganglion stimulation is currently being evaluated in human stroke patients (Khurana et al, 2009).…”

Section: Collateral Circulation and Arteriogenesis As The New Thermentioning

confidence: 99%

Vascular remodeling after ischemic stroke: Mechanisms and therapeutic potentials

Liu

Wang

Akamatsu

et al. 2014

Progress in Neurobiology

268

224

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The brain vasculature has been increasingly recognized as a key player that directs brain development, regulates homeostasis, and contributes to pathological processes. Following ischemic stroke, the reduction of blood flow elicits a cascade of changes and leads to vascular remodeling. However, the temporal profile of vascular changes after stroke is not well understood. Growing evidence suggests that the early phase of cerebral blood volume (CBV) increase is likely due to the improvement in collateral flow, also known as arteriogenesis, whereas the late phase of CBV increase is attributed to the surge of angiogenesis. Arteriogenesis is triggered by shear fluid stress followed by activation of endothelium and inflammatory processes, while angiogenesis induces a number of pro-angiogenic factors and circulating endothelial progenitor cells (EPCs). The status of collaterals in acute stroke has been shown to have several prognostic implications, while the causal relationship between angiogenesis and improved functional recovery has yet to be established in patients. A number of interventions aimed at enhancing cerebral blood flow including increasing collateral recruitment are under clinical investigation. Transplantation of EPCs to improve angiogenesis is also underway. Knowledge in the underlying physiological mechanisms for improved arteriogenesis and angiogenesis shall lead to more effective therapies for ischemic stroke.

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“…One rodent study using the middle cerebral artery occlusion model of ischaemic stroke has demonstrated that perivascular nerve fibres could have a critical and possibly protective role in reducing lesion volume. 14 The reduction in lesion volume could be the result of not only short-term vasomotor effects, but also long-term effects of innervation on the growth, differentiation, and functional characteristics of cerebral arteries. Consequently, the functional denervation associated with ischaemic or haemorrhagic stroke could remove neural input to arterial smooth muscle, resulting in deleterious changes in the function and phenotype of cerebrovascular smooth muscle cells.…”

Section: The Role Of Vascular Cell Typesmentioning

confidence: 99%

The vascular neural network—a new paradigm in stroke pathophysiology

Zhang¹,

Badaut²,

Tang³

et al. 2012

Nat Rev Neurol

180

171

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The concept of the neurovascular unit as the key brain component affected by stroke is controversial, because current definitions of this entity neglect mechanisms that control perfusion and reperfusion of arteries and arterioles upstream of the cerebral microcirculation. Indeed, although definitions vary, many researchers consider the neurovascular unit to be restricted to endothelial cells, neurons and glia within millimetres of the cerebral capillary microcirculation. This Perspectives article highlights the roles of vascular smooth muscle, endothelial cells and perivascular innervation of cerebral arteries in the initiation and progression of, and recovery from, ischaemic stroke. The concept of the vascular neural network—which includes cerebral arteries, arterioles, and downstream neuronal and glial cell types and structures—is introduced as the fundamental component affected by stroke pathophysiology. The authors also propose that the vascular neural network should be considered the main target for future therapeutic intervention after cerebrovascular insult.

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Resection of the nerves bundle from the sphenopalatine ganglia tend to increase the infarction volume following middle cerebral artery occlusion

Cited by 19 publications

References 19 publications

Facial nerve stimulation as a future treatment for ischemic stroke

Facial nerve stimulation as a future treatment for ischemic stroke

Vascular remodeling after ischemic stroke: Mechanisms and therapeutic potentials

The vascular neural network—a new paradigm in stroke pathophysiology

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