A New Paradigm for Neurological Lead Cyclic Testing

Author(s):  
Paul Wisnewski

The feasibility of electrical stimulation of the nervous system to treat chronic pain was proven with implantation of the first device for this purpose by Norm Shealy, MD in 1967. Since then, neurological stimulation has become a standard therapy for pain management.

2021 ◽  
Vol 11 (5) ◽  
pp. 639
Author(s):  
David Bergeron ◽  
Sami Obaid ◽  
Marie-Pierre Fournier-Gosselin ◽  
Alain Bouthillier ◽  
Dang Khoa Nguyen

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.


2016 ◽  
Vol 1 (1) ◽  

Low-level electrical stimulation (LL-ES) of aortic root ventricular ganglionated plexi (GP) was proved to be antiarrhythmic in the initiation of AF mediated by autonomic nervous system. However,it is still uncertain whether LL-ES of the ventricular GP can reverse the structural remodeling of myocardial fibrosis and atrial enlargement following heart failure by attenuating the sympathetic tone. Therefore,this review will give an general argument on this topic.


Author(s):  
Stanisa Raspopovic ◽  
Marco Capogrosso ◽  
Silvestro Micera

2014 ◽  
Vol 307 (7) ◽  
pp. G719-G731 ◽  
Author(s):  
Guo-Du Wang ◽  
Xi-Yu Wang ◽  
Sumei Liu ◽  
Meihua Qu ◽  
Yun Xia ◽  
...  

Mast cells express the substance P (SP) neurokinin 1 receptor and the calcitonin gene-related peptide (CGRP) receptor in guinea pig and human small intestine. Enzyme-linked immunoassay showed that activation of intramural afferents by antidromic electrical stimulation or by capsaicin released SP and CGRP from human and guinea pig intestinal segments. Electrical stimulation of the afferents evoked slow excitatory postsynaptic potentials (EPSPs) in the enteric nervous system. The slow EPSPs were mediated by tachykinin neurokinin 1 and CGRP receptors. Capsaicin evoked slow EPSP-like responses that were suppressed by antagonists for protease-activated receptor 2. Afferent stimulation evoked slow EPSP-like excitation that was suppressed by mast cell-stabilizing drugs. Histamine and mast cell protease II were released by 1) exposure to SP or CGRP, 2) capsaicin, 3) compound 48/80, 4) elevation of mast cell Ca2+ by ionophore A23187, and 5) antidromic electrical stimulation of afferents. The mast cell stabilizers cromolyn and doxantrazole suppressed release of protease II and histamine when evoked by SP, CGRP, capsaicin, A23187, electrical stimulation of afferents, or compound 48/80. Neural blockade by tetrodotoxin prevented mast cell protease II release in response to antidromic electrical stimulation of mesenteric afferents. The results support a hypothesis that afferent innervation of enteric mast cells releases histamine and mast cell protease II, both of which are known to act in a diffuse paracrine manner to influence the behavior of enteric nervous system neurons and to elevate the sensitivity of spinal afferent terminals.


2017 ◽  
Vol 16 (1) ◽  
pp. 169-169
Author(s):  
E. De Martino ◽  
L. Petrini ◽  
S. Schabrun ◽  
T. Graven-Nielsen

Abstract Background and aims Maladaptive plasticity in neural circuits has been proposed in chronic musculoskeletal pain and has been discussed as a key component of the transition from acute to chronic pain. The induction of delayed onset muscle soreness (DOMS) in healthy individuals is one method that can be used to investigate the adaptations of neural circuits in response to several days of muscle hyperalgesia. The aim of this study was to determine the adaptations of the sensory cortex in response to muscle hyperalgesia induced by eccentric exercise of the wrist extensor muscles. It was hypothesized that muscle hyperalgesia would result in a facilitation of cortical somatosensory excitability, based on sensory evoked potentials evoked by electrical stimulation of the radial nerve. Methods Twelve healthy subjects performed eccentric exercise of the wrist extensors. Muscle soreness, pressure pain thresholds (PPTs) on the extensor carpi radialis (ECR) muscle, somatosensory evoked potentials (SEPs) based on 10 channel EEG recorded during electrical stimulation of the radial nerve were recorded before (Day0Pre), 2h (Day0Post), 2 days (Day2), and 6 days (Day6) after exercise. Results Compared to Day0Pre: (i) Muscle soreness increased at Day0Post and increased further at Day2 (both P < 0.05). (ii) Pressure pain thresholds decreased at Day2 (P < 0.05), (iii) the peak-to-peak N30-P45 and P45-N60 amplitude of the sensory evoked potential from the central-parietal recording sites were increased at Day2 (both P < 0.05); (iv) reduction in ECR PPTs was correlated with an increase of the post-central P45 wave. ConclusionsThese data demonstrate that hyperalgesia developing across several days is accompanied by an increase in sensory cortical excitability. In addition, sensory cortical adaptation followed a similar temporal profile to increased sensitivity to pressure (PPTs). This model may be relevant for further understanding neural adaptation in the transition from acute to chronic pain.


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