Therapeutic effects of vagus nerve stimulation in epilepsy and implications for sudden unexpected death in epilepsy

Schachter, Steven C.

doi:10.1007/s10286-006-0275-1

Cited by 22 publications

(12 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…24 Another potential application of VNS in heart diseases is in the rate and rhythm control of AF. 10, 25, 26 VNS has been reported to reduce the incidence of sudden unexpected death in epilepsy (SUDEP), 1, 2 but others failed to confirm that finding. 27 …”

Section: Discussionmentioning

confidence: 99%

“…1, 2 Recent studies showed that there is significant interictal cardiac electrical instability (elevated T wave alternans) in patients with drug-resistant epilepsy, which was effectively suppressed by VNS. 3 Because T wave alternans is enhanced by sympathetic activation, 4 these findings suggest that VNS might be associated with reduced sympathetic tone.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Left cervical vagal nerve stimulation reduces skin sympathetic nerve activity in patients with drug resistant epilepsy

et al. 2017

View full text Add to dashboard Cite

Background We recently reported that the skin sympathetic nerve activity (SKNA) can be used to estimate the sympathetic tone in humans. In animal models, vagal nerve stimulation (VNS) can damage the stellate ganglion, reduce stellate ganglion nerve activity and suppress cardiac arrhythmia. Whether or not VNS can suppress sympathetic tone in humans remain unclear. Objective To test the hypothesis that VNS suppresses SKNA in patients with drug resistant epilepsy. Methods We used electrocardiogram (ECG) patch electrodes to continuously record SKNA in 26 patients with drug resistant epilepsy who were admitted for video electroencephalographic monitoring. Among them, 6 (2 men, age 40±11 years) were previously treated with VNS and 20 (7 men, age 37±8 years) did not. The signals from ECG leads I and II were filtered to detect SKNA. Results The VNS had an ON-time of 30 s and OFF-time of 158±72 s, with output of 1.92±0.42 mA at 24.17±2.01 Hz. The average SKNA (aSKNA) during VNS OFF-time was 1.06 μV [95% confidence interval, CI, 0.93 to 1.18] in lead I and 1.13 μV [CI, 0.99 to 1.27] in lead II, which was significantly lower than 1.38 μV [CI, 1.01 to 1.75, p=0.036] and 1.38 μV [CI, 0.98 to 1.78, p=0.035] of the control Group, respectively. The heart rate was 65 bpm [CI, 59 to 71] in VNS group, significantly lower than 77 bpm [95% CI, 71 to 83] in control group. Conclusion Patients with VNS had significantly lower SKNA than patients without VNS.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Left cervical vagal nerve stimulation reduces skin sympathetic nerve activity in patients with drug resistant epilepsy

et al. 2017

View full text Add to dashboard Cite

show abstract

“…[35] Most patients are currently stimulated at 30 Hz, with a constant stimulation cycle of 30 seconds on and 5 minutes off. [26] Clinical trials have found the device to reduce the incidence of complex partial seizures in the majority of patients tested, with 20–40% of patients achieving a greater than 50% reduction in seizure frequency. [1133] The number of responders increases with time,[719] while the number of anti-epileptic drugs (AEDs) necessary to maintain satisfactory seizure control decreases after VNS.…”

Section: Introductionmentioning

confidence: 99%

Vagus nerve stimulation for epilepsy: A review of the peripheral mechanisms

Krahl

2012

Surg Neurol Int

125

View full text Add to dashboard Cite

Vagus nerve stimulation (VNS) is a unique epilepsy treatment in that a peripheral intervention is used to treat a disease that is entirely related to pathological events occurring within the brain. To understand how stimulation of the vagus nerve can be used to stop seizures, an understanding of the peripheral anatomy and physiology of the vagus nerve is essential. The peripheral aspects of the vagus nerve are discussed in this review, with an explanation of which fibers and branches are involved in producing these antiepileptic effects, along with speculation about the potential for improving the therapy.

show abstract

“…Intermittent VNS with such a device has become a well-established, safe, and effective adjunct to medical therapyfor refractory epilepsy (Ben-Menachem, 2002; Schachter, 2006). Observations of mood elevation during VNS therapy for pharmacoresistant epilepsy (Ben-Menachem, 2002; Elger et al, 2000; Harden, 2002; Harden et al, 2000) suggested that such treatment might also show efficacy for refractory major depression.…”

Section: Introductionmentioning

confidence: 99%

Chronic vagus nerve stimulation induces neuronal plasticity in the rat hippocampus

Biggio

Gorini

Utzeri

et al. 2009

Int. J. Neuropsychopharm.

163

View full text Add to dashboard Cite

Vagus nerve stimulation (VNS) is used to treat pharmacotherapy-resistant epilepsy and depression. The mechanisms underlying the therapeutic efficacy of VNS remain unclear, however. We examined the effects of VNS on hippocampal neuronal plasticity and behavior in rats. Cell proliferation in the hippocampus of rats subjected to acute (3 h) or chronic (1 month) VNS was examined by injection of bromodeoxyuridine (BrdU) and immunohistochemistry. Expression of doublecortin (DCX) and brain-derived neurotrophic factor (BDNF) was evaluated by immunofluorescence staining. The dendritic morphology of DCX+ neurons was measured by Sholl analysis. Our results show that acute VNS induced an increase in the number of BrdU+ cells in the dentate gyrus that was apparent 24 h and 3 weeks after treatment. It also induced long-lasting increases in the amount of DCX immunoreactivity and the number of DCX+ neurons. Neither the number of BrdU+ cells nor the amount of DCX immunoreactivity was increased 3 weeks after the cessation of chronic VNS. Chronic VNS induced long-lasting increases in the amount of BDNF immunoreactivity and the number of BDNF+ cells as well as in the dendritic complexity of DCX+ neurons in the hippocampus. In contrast to chronic imipramine treatment, chronic VNS had no effect on the behavior of rats in the forced swim or elevated plus-maze tests. Both chronic and acute VNS induced persistent changes in hippocampal neurons that may play a key role in the therapeutic efficacy of VNS. However, these changes were not associated with evident behavioral alterations characteristic of an antidepressant or anxiolytic action.

show abstract

Therapeutic effects of vagus nerve stimulation in epilepsy and implications for sudden unexpected death in epilepsy

Cited by 22 publications

References 29 publications

Left cervical vagal nerve stimulation reduces skin sympathetic nerve activity in patients with drug resistant epilepsy

Left cervical vagal nerve stimulation reduces skin sympathetic nerve activity in patients with drug resistant epilepsy

Vagus nerve stimulation for epilepsy: A review of the peripheral mechanisms

Chronic vagus nerve stimulation induces neuronal plasticity in the rat hippocampus

Contact Info

Product

Resources

About