Inhibitory effect of high-frequency greater occipital nerve electrical stimulation on trigeminovascular nociceptive processing in rats

2016 ◽  
Vol 124 (2) ◽  
pp. 171-183 ◽  
Author(s):  
Olga A. Lyubashina ◽  
Sergey S. Panteleev ◽  
Alexey Y. Sokolov
Keyword(s):  
Electrical Stimulation ◽  
High Frequency ◽  
Inhibitory Effect ◽  
Occipital Nerve ◽  
Greater Occipital Nerve ◽  
Nociceptive Processing

Reduction of Calcitonin Gene-Related Peptide in Jugular Blood Following Electrical Stimulation of Rat Greater Occipital Nerve

Cephalalgia ◽  
1992 ◽  
Vol 12 (5) ◽  
pp. 275-279 ◽  
Author(s):  
Maurice B Vincent ◽  
Rolf Ekman ◽  
Lars Edvinsson ◽  
Trond Sand ◽  
Ottar Sjaastad
Keyword(s):  
Electrical Stimulation ◽  
Calcitonin Gene Related Peptide ◽  
Trigeminal System ◽  
Occipital Nerve ◽  
Related Peptide ◽  
System Reduction ◽  
Calcitonin Gene ◽  
Greater Occipital Nerve ◽  
Ocular Signs ◽  
Stimulation Of

Although it is known that pain in the forehead may be induced by neck abnormalities, the actual neck-head connections responsible for development of pain in trigeminal areas are poorly understood. Vasoactive neuropeptides released from sensory fibres, such as substance P (SP) and calcitonin gene-related peptide (CGRP), have been considered as important elements in headache pathophysiology. The levels of CGRP-like immunoreactivity (LI) were measured bilaterally in the jugular blood (52 rats) and intraocular aspirates (66 rats) following electrical stimulation of the left greater occipital nerve, and in the jugular blood of 13 control animals. One-third of the stimulated rats had varying combinations of conjunctival injection, tearing, diminished eye aperture and miosis or mydriasis on the stimulated side. The other two-thirds exhibited no ocular signs. Significantly lower levels of CGRP-LI were present in the jugular blood on the stimulated side in comparison with control rats. There was comparatively lower CGRP-LI on the non-stimulated side as well, but to a lesser extent. Significant differences between the stimulated and the non-stimulated side were present, particularly in the tearing/diminished eye cleft group. It is proposed that stimulation of the rat GON inhibits the trigeminal system (reduction of CGRP-LI) and possibly activates parasympathetic fibres (ocular changes).

scholarly journals Deep Brain Stimulation of the Posterior Insula in Chronic Pain: A Theoretical Framework

2021 ◽  
Vol 11 (5) ◽  
pp. 639
Author(s):  
David Bergeron ◽  
Sami Obaid ◽  
Marie-Pierre Fournier-Gosselin ◽  
Alain Bouthillier ◽  
Dang Khoa Nguyen
Keyword(s):  
Chronic Pain ◽  
Electrical Stimulation ◽  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
High Frequency ◽  
Brain Lesion ◽  
Low Frequency ◽  
Posterior Insula ◽  
Deep Brain ◽  
Stimulation Of

Introduction: To date, clinical trials of deep brain stimulation (DBS) for refractory chronic pain have yielded unsatisfying results. Recent evidence suggests that the posterior insula may represent a promising DBS target for this indication. Methods: We present a narrative review highlighting the theoretical basis of posterior insula DBS in patients with chronic pain. Results: Neuroanatomical studies identified the posterior insula as an important cortical relay center for pain and interoception. Intracranial neuronal recordings showed that the earliest response to painful laser stimulation occurs in the posterior insula. The posterior insula is one of the only regions in the brain whose low-frequency electrical stimulation can elicit painful sensations. Most chronic pain syndromes, such as fibromyalgia, had abnormal functional connectivity of the posterior insula on functional imaging. Finally, preliminary results indicated that high-frequency electrical stimulation of the posterior insula can acutely increase pain thresholds. Conclusion: In light of the converging evidence from neuroanatomical, brain lesion, neuroimaging, and intracranial recording and stimulation as well as non-invasive stimulation studies, it appears that the insula is a critical hub for central integration and processing of painful stimuli, whose high-frequency electrical stimulation has the potential to relieve patients from the sensory and affective burden of chronic pain.

scholarly journals Modulation of torque evoked by wide-pulse, high-frequency neuromuscular electrical stimulation and the potential implications for rehabilitation and training

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Chris Donnelly ◽  
Jonathan Stegmüller ◽  
Anthony J. Blazevich ◽  
Fabienne Crettaz von Roten ◽  
Bengt Kayser ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
High Frequency ◽  
Neuromuscular Electrical Stimulation ◽  
Motor Units ◽  
Progressive Increase ◽  
Great Promise ◽  
Measured Parameter ◽  
Time Integral ◽  
Spinal Circuitry ◽  
Evoked Force

AbstractThe effectiveness of neuromuscular electrical stimulation (NMES) for rehabilitation is proportional to the evoked torque. The progressive increase in torque (extra torque) that may develop in response to low intensity wide-pulse high-frequency (WPHF) NMES holds great promise for rehabilitation as it overcomes the main limitation of NMES, namely discomfort. WPHF NMES extra torque is thought to result from reflexively recruited motor units at the spinal level. However, whether WPHF NMES evoked force can be modulated is unknown. Therefore, we examined the effect of two interventions known to change the state of spinal circuitry in opposite ways on evoked torque and motor unit recruitment by WPHF NMES. The interventions were high-frequency transcutaneous electrical nerve stimulation (TENS) and anodal transcutaneous spinal direct current stimulation (tsDCS). We show that TENS performed before a bout of WPHF NMES results in lower evoked torque (median change in torque time-integral: − 56%) indicating that WPHF NMES-evoked torque might be modulated. In contrast, the anodal tsDCS protocol used had no effect on any measured parameter. Our results demonstrate that WPHF NMES extra torque can be modulated and although the TENS intervention blunted extra torque production, the finding that central contribution to WPHF NMES-evoked torques can be modulated opens new avenues for designing interventions to enhance WPHF NMES.

Vascular effects of free radicals generated by electrical stimulation

1984 ◽  
Vol 247 (5) ◽  
pp. H709-H714 ◽  
Author(s):  
F. S. Lamb ◽  
R. C. Webb
Keyword(s):  
Electrical Stimulation ◽  
Free Radical ◽  
Experimental System ◽  
Electrical Field Stimulation ◽  
Oxygen Metabolism ◽  
Inhibitory Effect ◽  
Oxygen Free Radical ◽  
Vascular Effects ◽  
Electrical Field ◽  
Rat Tail

Electrical field stimulation (9 V, 1.0 ms, 4 Hz) of isolated segments of rat tail arteries and dog coronary arteries inhibits contractile responses to exogenous norepinephrine and elevated potassium concentration. This inhibitory effect of electrical stimulation is blocked by various agents that alter oxygen metabolism: superoxide dismutase, catalase, glutathione, ascorbate, and dimethyl sulfoxide. The observations suggest that the inhibitory effect is due to an action of oxygen free radical metabolites that are generated by the electrical stimulation of the oxygen-rich buffer. These free radical metabolites have two actions: 1) they oxidize drugs in the experimental system, and 2) they exert a direct inhibitory action on vascular smooth muscle.

Somatostatin modulates cholinergic neurotransmission in canine antral muscle

1988 ◽  
Vol 254 (2) ◽  
pp. G201-G209 ◽  
Author(s):  
C. B. Koelbel ◽  
G. van Deventer ◽  
S. Khawaja ◽  
M. Mogard ◽  
J. H. Walsh ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Substance P ◽  
Prostaglandin E2 ◽  
Positive Inotropic Effect ◽  
Mechanical Response ◽  
Inhibitory Effect ◽  
Inotropic Effect ◽  
Inotropic Response ◽  
Cholinergic Neurotransmission

Somatostatin has been shown to inhibit antral motility in vivo. To examine the effect of somatostatin on cholinergic neurotransmission in the canine antrum, we studied the mechanical response of and the release of [3H]acetylcholine from canine longitudinal antral muscle in response to substance P, gastrin 17, and electrical stimulation. In unstimulated tissues, somatostatin had a positive inotropic effect on spontaneous phasic contractions. In tissues stimulated with substance P and gastrin 17, but not with electrical stimulation, somatostatin inhibited the phasic inotropic response dose dependently. This inhibitory effect was abolished by indomethacin. Somatostatin stimulated the release of prostaglandin E2 radioimmunoreactivity, and prostaglandin E2 inhibited the release of [3H]acetylcholine induced by substance P and electrical stimulation. Somatostatin increased the release of [3H]acetylcholine from unstimulated tissues by a tetrodotoxin-sensitive mechanism but inhibited the release induced by substance P and electrical stimulation. These results suggest that somatostatin has a dual modulatory effect on cholinergic neurotransmission in canine longitudinal antral muscle. This effect is excitatory in unstimulated tissues and inhibitory in stimulated tissues. The inhibitory effect is partially mediated by prostaglandins.

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