Vagus Nerve Stimulation in Ischemic Stroke
- PMID: 38008851
- PMCID: PMC10841711
- DOI: 10.1007/s11910-023-01323-w
Vagus Nerve Stimulation in Ischemic Stroke
Abstract
Purpose of review: Vagus nerve stimulation (VNS) has emerged as a potential therapeutic approach for neurological and psychiatric disorders. In recent years, there has been increasing interest in VNS for treating ischemic stroke. This review discusses the evidence supporting VNS as a treatment option for ischemic stroke and elucidates its underlying mechanisms.
Recent findings: Preclinical studies investigating VNS in stroke models have shown reduced infarct volumes and improved neurological deficits. Additionally, VNS has been found to reduce reperfusion injury. VNS may promote neuroprotection by reducing inflammation, enhancing cerebral blood flow, and modulating the release of neurotransmitters. Additionally, VNS may stimulate neuroplasticity, thereby facilitating post-stroke recovery. The Food and Drug Administration has approved invasive VNS (iVNS) combined with rehabilitation for ischemic stroke patients with moderate to severe upper limb deficits. However, iVNS is not feasible in acute stroke due to its time-sensitive nature. Non-invasive VNS (nVNS) may be an alternative approach for treating ischemic stroke. While the evidence from preclinical studies and clinical trials of nVNS is promising, the mechanisms through which VNS exerts its beneficial effects on ischemic stroke are still being elucidated. Therefore, further research is needed to better understand the efficacy and underlying mechanisms of nVNS in ischemic stroke. Moreover, large-scale randomized clinical trials are necessary to determine the optimal nVNS protocols, assess its long-term effects on stroke recovery and outcomes, and identify the potential benefits of combining nVNS with other rehabilitation strategies.
Keywords: Anti-inflammatory; Blood–brain barrier; Cortical spreading depolarization; Ischemic stroke; Locus coeruleus; Neuroplasticity; Non-invasive vagus nerve stimulation; Nucleus tractus solitarius; Stroke recovery; Traumatic brain injury.
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
Conflict of interest statement
Afshin A. Divani is supported by the National Institute of Neurological Disorders and Stroke (NINDS) grant # 1R21NS130423–01.
Sheharyar Baig is supported by the Association of British Neurologists Clinical Research Training Fellowship (co-funded by the Stroke Association and Berkeley Foundation). Sheharyar Baig and Arshad Majid are supported by the National Institute for Health Research (NIHR) Biomedical Research Centre, Sheffield, England. The expressed views are those of the authors and not necessarily those of the NINDS, the National Health Service (NHS), the NIHR, or the Department of Health and Social Care (DHSC).
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