scholarly journals Efficacy profile of noninvasive vagus nerve stimulation on cortical spreading depression susceptibility and the tissue response

2021 ◽  
Author(s):  
Tzu-Ting Liu ◽  
Andreia Morais ◽  
Tsubasa Takizawa ◽  
Inge Mulder ◽  
Bruce J. Simon ◽  
...  
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Tissue Response ◽  
Migraine Treatment ◽  
Trigeminal Ganglia ◽  
Dependent Manner ◽  
Calcitonin Gene

Abstract Background Noninvasive vagus nerve stimulation (nVNS) has recently emerged as a promising therapy for migraine. We previously demonstrated that vagus nerve stimulation inhibits cortical spreading depression (CSD), the electrophysiological event underlying migraine aura and triggering headache; however, the optimal nVNS paradigm has not been defined. Methods Various intensities and doses of nVNS were tested to improve efficacy on KCl-evoked CSD frequency and electrical threshold of CSD in a validated rat model. Chronic efficacy was evaluated by daily nVNS delivery for four weeks. We also examined the effects of nVNS on neuroinflammation and trigeminovascular activation by western blot and immunohistochemistry. Results nVNS suppressed susceptibility to CSD in an intensity-dependent manner. Two 2-minute nVNS 5 minutes apart afforded the highest efficacy on electrical CSD threshold and frequency of KCl-evoked CSD. Daily nVNS for four weeks did not further enhance efficacy over a single nVNS 20 minutes prior to CSD. The optimal nVNS also attenuated CSD-induced upregulation of cortical cycloogenase-2, calcitonin gene-related peptide in trigeminal ganglia, and c-Fos expression in trigeminal nucleus caudalis. Conclusion Our study provides insight on optimal nVNS parameters to suppress CSD and suggests its benefit on CSD-induced neuroinflammation and trigeminovascular activation in migraine treatment.

scholarly journals Vagus nerve stimulation inhibits cortical spreading depression exclusively through central mechanisms

Pain ◽  
2020 ◽  
Vol 161 (7) ◽  
pp. 1661-1669 ◽  
Author(s):  
Andreia Morais ◽  
Tzu-Ting Liu ◽  
Tao Qin ◽  
Homa Sadhegian ◽  
Ilknur Ay ◽  
...  
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Cortical Spreading Depression ◽  
Spreading Depression

scholarly journals Vagus nerve stimulation inhibits cortical spreading depression

Pain ◽  
2016 ◽  
Vol 157 (4) ◽  
pp. 797-805 ◽  
Author(s):  
Shih-Pin Chen ◽  
Ilknur Ay ◽  
Andreia Lopes de Morais ◽  
Tao Qin ◽  
Yi Zheng ◽  
...  
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Cortical Spreading Depression ◽  
Spreading Depression

scholarly journals Cortical spreading depression as a site of origin for migraine: Role of CGRP

Cephalalgia ◽  
2018 ◽  
Vol 39 (3) ◽  
pp. 428-434 ◽  
Author(s):  
Liesl N Close ◽  
Sajedeh Eftekhari ◽  
Minyan Wang ◽  
Andrew C Charles ◽  
Andrew F Russo
Keyword(s):  
Cortical Neurons ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Calcitonin Gene Related Peptide ◽  
Trigeminal System ◽  
Migraine Treatment ◽  
Neural Connections ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
A Site

Premise Migraine is a complex neurologic disorder that leads to significant disability, yet remains poorly understood. Problem One potential triggering mechanism in migraine with aura is cortical spreading depression, which can activate the trigeminal nociceptive system both peripherally and centrally in animal models. A primary neuropeptide of the trigeminal system is calcitonin gene-related peptide, which is a potent vasodilatory peptide and is currently a major therapeutic target for migraine treatment. Despite the importance of both cortical spreading depression and calcitonin gene-related peptide in migraine, the relationship between these two players has been relatively unexplored. However, recent data suggest several potential vascular and neural connections between calcitonin gene-related peptide and cortical spreading depression. Conclusion This review will outline calcitonin gene-related peptide-cortical spreading depression connections and propose a model in which cortical spreading depression and calcitonin gene-related peptide act at the intersection of the vasculature and cortical neurons, and thus contribute to migraine pathophysiology.

Vagus Nerve Stimulation Relieves Chronic Refractory Migraine and Cluster Headaches

Cephalalgia ◽  
2005 ◽  
Vol 25 (2) ◽  
pp. 82-86 ◽  
Author(s):  
A Mauskop
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Current Strength ◽  
Migraine Treatment ◽  
Dramatic Improvement ◽  
Analgesic Effects ◽  
Migraine Headaches ◽  
Refractory Migraine ◽  
Cluster Headaches

Anticonvulsant and antidepressant medications have demonstrated efficacy in migraine treatment. Vagus nerve stimulation (VNS) is an effective treatment for drug-refractory epilepsy and possibly depression and it also has documented analgesic effects. These observations suggested a possible role for VNS in treating severe refractory headaches, and led to a trial of VNS in patients with such headaches. VNS was implanted in four men and two women with disabling chronic cluster and migraine headaches. In one man and one woman with chronic migraines VNS produced dramatic improvement with restoration of ability to work. Two patients with chronic cluster headaches had significant improvement of their headaches. VNS was well tolerated in five patients, while one developed nausea even at the lowest current strength. In conclusion, VNS may be an effective therapy for intractable chronic migraine and cluster headaches and deserves further trials.

scholarly journals Kilohertz frequency nerve block enhances anti-inflammatory effects of vagus nerve stimulation

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Yogi A. Patel ◽  
Tarun Saxena ◽  
Ravi V. Bellamkonda ◽  
Robert J. Butera
Keyword(s):  
Vagus Nerve ◽  
Nerve Block ◽  
Systemic Inflammation ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Dependent Manner ◽  
Wide Range ◽  
Inflammatory Processes ◽  
Efferent Pathways ◽  
Anti Inflammatory

Abstract Efferent activation of the cervical vagus nerve (cVN) dampens systemic inflammatory processes, potentially modulating a wide-range of inflammatory pathological conditions. In contrast, afferent cVN activation amplifies systemic inflammatory processes, leading to activation of the hypothalamic-pituitary-adrenal (HPA) axis, the sympathetic nervous system through the greater splanchnic nerve (GSN), and elevation of pro-inflammatory cytokines. Ideally, to clinically implement anti-inflammatory therapy via cervical vagus nerve stimulation (cVNS) one should selectively activate the efferent pathway. Unfortunately, current implementations, in animal and clinical investigations, activate both afferent and efferent pathways. We paired cVNS with kilohertz electrical stimulation (KES) nerve block to preferentially activate efferent pathways while blocking afferent pathways. Selective efferent cVNS enhanced the anti-inflammatory effects of cVNS. Our results demonstrate that: (i) afferent, but not efferent, cVNS synchronously activates the GSN in a dose-dependent manner; (ii) efferent cVNS enabled by complete afferent KES nerve block enhances the anti-inflammatory benefits of cVNS; and (iii) incomplete afferent KES nerve block exacerbates systemic inflammation. Overall, these data demonstrate the utility of paired efferent cVNS and afferent KES nerve block for achieving selective efferent cVNS, specifically as it relates to neuromodulation of systemic inflammation.

Acute vestibular migraine treatment with noninvasive vagus nerve stimulation

Neurology ◽  
2019 ◽  
Vol 93 (18) ◽  
pp. e1715-e1719 ◽  
Author(s):  
Shin C. Beh ◽  
Deborah I. Friedman
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Retrospective Chart Review ◽  
Preliminary Evidence ◽  
Vestibular Migraine ◽  
Migraine Treatment ◽  
Tertiary Referral Center ◽  
Headache Severity ◽  
Vestibular Symptoms

ObjectiveTo report on the benefits of noninvasive vagus nerve stimulation (nVNS) on acute vestibular migraine (VM) treatment.MethodsThis was a retrospective chart review of patients with VM treated with nVNS in a single tertiary referral center between November 2017 and January 2019. Eighteen patients (16 women) were identified (mean age 45.7 [±14.8] years); 14 were treated for a VM attack and 4 for bothersome interictal dizziness consistent with persistent perceptual postural dizziness (PPPD). Patients graded the severity of vestibular symptoms and headache using an 11-point visual analog scale (VAS; 0 = no symptoms, 10 = worst ever symptoms) before and 15 minutes after nVNS.ResultsIn those with acute VM, vertigo improved in 13/14 (complete resolution in 2, at least 50% improvement in 5). The mean vertigo intensity before nVNS was 5.2 (±1.6; median 6), and 3.1 (±2.2; median 3) following stimulation; mean reduction in vertigo intensity was 46.9% (±31.5; median 45%). Five experienced headache with the VM attack; all reported improvement following nVNS. Mean headache severity was 6 (±1.4; median 6) prior to treatment and 2.4 (±1.5; median 3) following nVNS; mean reduction in headache intensity was 63.3% (±21.7; median 50). All 4 treated with nVNS for interictal PPPD reported no benefit.ConclusionOur study provides preliminary evidence that nVNS may provide rapid relief of vertigo and headache in acute VM, and supports further randomized, sham-controlled studies into nVNS in VM.Classification of evidenceThis study provides Class IV evidence that for patients with acute VM, nVNS rapidly relieves vertigo and headache.

Effect of Transcutaneous Vagus Nerve Stimulation in Dysphagia After Lateral Medullary Infarction: A Case Report

2019 ◽  
Vol 28 (4) ◽  
pp. 1381-1387
Author(s):  
Ying Yuan ◽  
Jie Wang ◽  
Dongyu Wu ◽  
Dahua Zhang ◽  
Weiqun Song
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Rating Scale ◽  
Tube Feeding ◽  
Nasogastric Feeding ◽  
Lateral Medullary Infarction ◽  
Severe Dysphagia ◽  
Transcutaneous Vagus Nerve Stimulation ◽  
Medullary Infarction

Purpose Severe dysphagia with weak pharyngeal peristalsis after dorsal lateral medullary infarction (LMI) requires long-term tube feeding. However, no study is currently available on therapeutic effectiveness in severe dysphagia caused by nuclear damage of vagus nerve after dorsal LMI. The purpose of the present investigation was to explore the potential of transcutaneous vagus nerve stimulation (tVNS) to improve severe dysphagia with weak pharyngeal peristalsis after dorsal LMI. Method We assessed the efficacy of 6-week tVNS in a 28-year-old woman presented with persisting severe dysphagia after dorsal LMI who had been on nasogastric feeding for 6 months. tVNS was applied for 20 min twice a day, 5 days a week, for 6 weeks. The outcome measures included saliva spitted, Swallow Function Scoring System, Functional Oral Intake Scale, Clinical Assessment of Dysphagia With Wallenberg Syndrome, Yale Pharyngeal Residue Severity Rating Scale, and upper esophagus X-ray examination. Results After tVNS, the patient was advanced to a full oral diet without head rotation or spitting. No saliva residue was found in the valleculae and pyriform sinuses. Contrast medium freely passed through the upper esophageal sphincter. Conclusion Our findings suggest that tVNS might provide a useful means for recovery of severe dysphagia with weak pharyngeal peristalsis after dorsal LMI. Supplemental Material https://doi.org/10.23641/asha.9755438

Vagus nerve stimulation in rheumatoid arthritis – Authors' reply

2021 ◽  
Vol 3 (1) ◽  
pp. e14-e15
Author(s):  
Mark C Genovese ◽  
Yaakov A Levine ◽  
David Chernoff
Keyword(s):  
Rheumatoid Arthritis ◽  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation
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