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Pulsed Radiofrequency: A Review of the Basic Science as Applied to the Pathophysiology of Radicular Pain: A Call for Clinical Translation.

Reg Anesth Pain Med. 2014 March/April;39(2):149-159

Authors: Van Boxem K, Huntoon M, Van Zundert J, Patijn J, van Kleef M, Joosten EA

Radicular pain is an important health care problem, with only limited evidence-based treatments available. Treatment selection should ideally target documented pathophysiological pathways. In herniated discs, a sequence in the inflammatory cascade can be observed that initiates and maintains increased nociceptive signal input. Inflammatory mediators including tumor necrosis factor α are released from the nucleus pulposus and the degenerating peripheral nerve, which, in turn, induces production of neurotrophins like nerve growth factor and brain-derived neurotrophic factor. Neurotrophins interfere not only with the generation of ectopic firing of nociceptive neurons in the dorsal root ganglion but also with the excitability and sensitization of neuronal transmission in the dorsal spinal horn. Radicular pain is further characterized by the electrophysiological spreading of the afferent nociceptive input over different spinal nerve roots. Both the complex pathophysiological pathways involved and the spreading of the nociceptive signal make radicular pain difficult to treat. Pulsed radiofrequency (PRF) is considered an option in treatment of radicular pain. To understand and increase the efficiency of PRF interventional treatments in radicular pain, both in vitro and in vivo studies aiming at elucidating part of the mechanism of action of PRF are described. Potential factors that may improve the efficacy of PRF treatment in radicular pain are discussed.

PMID: 24553305 [PubMed – as supplied by publisher]

[Treatment of lumbar intervertebral disc herniation with coblation combined with ozone nucleus pulposus ablation].
Zhongguo Gu Shang. 2013 Oct;26(10):815-8
Authors: Ren XC, Wang XY, Zhang SH, Yang ZQ, Wei XC

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Response of Cervicogenic Headaches and Occipital Neuralgia to Radiofrequency Ablation of the C2 Dorsal Root Ganglion and/or Third Occipital Nerve.
Headache. 2014 Jan 16;
Authors: Hamer JF, Purath TA

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Pulsed radiofrequency modulates pain regulatory gene expression along the nociceptive pathway.

Pain Physician. 2013 Sep-Oct;16(5):E601-13

Authors: Vallejo R, Tilley DM, Williams J, Labak S, Aliaga L, Benyamin RM

BACKGROUND: Pulsed radiofrequency (PRF) therapy is a clinical treatment utilizing electromagnetic energy aimed to relieve neuropathic pain. This is the first study examining the modulated expression of pain regulatory genes following the induction of the spared nerve injury (SNI) pain model and subsequently treated with PRF therapy.
OBJECTIVES: The present study investigated the behavioral efficacy of PRF therapy in rats exhibiting sciatic nerve injury and examined gene expression changes in the sciatic nerve, ipsilateral L5 dorsal root ganglia (DRG), and spinal cord.
STUDY DESIGN: A randomized, experimental trial.
SETTING: Department of Biological Sciences, Illinois State University and Department of Psychology, Illinois Wesleyan University.
METHODS: An SNI model was used in male Sprague-Dawley rats (weight 260-310 g). A sham surgery was also performed as a control group. After 3 days development of the SNI model, an RF electrode was applied to the sciatic nerve proximal to the site of injury and stimulated for 3 minutes. The response to mechanical stimuli was assessed throughout the duration of the study. Furthermore, changes in gene expression along the nociceptive tract (sciatic nerve, DRG, and spinal cord) were assessed 24 hours post-PRF therapy.
RESULTS: It was observed that the mechanical allodynia, induced by SNI model, was reversed to control values within 24 hours post-PRF therapy. Additionally, modulated expression of pain regulatory genes was observed after induction of the SNI model. Following PRF therapy, expression of many of these genes returned to control values (sham) in each of the tissues tested. Increased proinflammatory gene expression, such as TNF-α and IL-6, observed in the sciatic nerve (site of injury) in the SNI group was returned to baseline values following PRF therapy. Up-regulation of GABAB-R1, Na/K ATPase, and 5-HT3r as well as down regulation of TNF-α and IL-6 were also observed in the DRG in the SNI-PRF group relative to the SNI group. Up-regulation of Na/K ATPase and c-Fos was found in the spinal cord following PRF treatment relative to the SNI group.
LIMITATIONS: Immediate changes in gene expression were observed at 24 hours to better determine the mechanism with no long-term data at this time. Protein expression was not assessed in addition to gene expression changes.
CONCLUSION: These results indicate that the electromagnetic energy applied via PRF therapy influences the reversal of behavioral and molecular effects of hypersensitivity developed from a peripheral nerve injury.

PMID: 24077210 [PubMed – in process]

In Situ Measurement of Tissue Impedance Using an Inductive Coupling Interface Circuit.

IEEE Trans Biomed Circuits Syst. 2013 Jun;7(3):225-235

Authors: Hung-Wei Chiu, Jia-Min Chuang, Chien-Chi Lu, Wei-Tso Lin, Chii-Wann Lin, Mu-Lien Lin

In this work, a method of an inductive coupling impedance measurement (ICIM) is proposed for measuring the nerve impedance of a dorsal root ganglion (DRG) under PRF stimulation. ICIM provides a contactless interface for measuring the reflected impedance by an impedance analyzer with a low excitation voltage of 7 mV. The paper develops a calibration procedure involving a 50-Ω reference resistor to calibrate the reflected resistance for measuring resistance of the nerve in the test. A de-embedding technique to build the equivalent transformer circuit model for the ICIM circuit is also presented. A batteryless PRF stimulator with ICIM circuit demonstrated good accuracy for the acute measurement of DRG impedance both in situ and in vivo. Besides, an in vivo animal experiment was conducted to show that the effectiveness of pulsed radiofrequency (PRF) stimulation in relieving pain gradually declined as the impedance of the stimulated nerve increased. The experiment also revealed that the excitation voltage for measuring impedance below 25 mV can prevent the excitation of a nonlinear response of DRG.

PMID: 23853322 [PubMed – as supplied by publisher]

Foot Orgasm Syndrome: A Case Report in a Woman.

J Sex Med. 2013 Jun 19;

Authors: Waldinger MD, de Lint GJ, van Gils AP, Masir F, Lakke E, van Coevorden RS, Schweitzer DH

INTRODUCTION: Spontaneous orgasm triggered from inside the foot has so far not been reported in medical literature. AIMS: The study aims to report orgasmic feelings in the left foot of a woman. METHODS: A woman presented with complaints of undesired orgasmic sensations originating in her left foot. In-depth interview, physical examination, sensory testing, magnetic resonance imaging (MRI-scan), electromyography (EMG), transcutaneous electrical nerve stimulation (TENS), and blockade of the left S1 dorsal root ganglion were performed. MAIN OUTCOME MEASURES: The main outcomes are description of this clinical syndrome, results of TENS application, and S1 dorsal root ganglion blockade. RESULTS: Subtle attenuation of sensory amplitudes of the left suralis, and the left medial and lateral plantar nerve tracts was found at EMG. MRI-scan disclosed no foot abnormalities. TENS at the left metatarso-phalangeal joint-III of the left foot elicited an instant orgasmic sensation that radiated from plantar toward the vagina. TENS applied to the left side of the vagina elicited an orgasm that radiated to the left foot. Diagnostic blockade of the left S1 dorsal root ganglion with 0.8 mL bupivacaine 0.25 mg attenuated the frequency and intensity of orgasmic sensation in the left foot with 50% and 80%, respectively. Additional therapeutic blockade of the same ganglion with 0.8 mL bupivacaine 0.50 mg combined with pulsed radiofrequency treatment resulted in a complete disappearance of the foot-induced orgasmic sensations. CONCLUSION: Foot orgasm syndrome (FOS) is descibed in a woman. Blockade of the left S1 dorsal root ganglion alleviated FOS. It is hypothesized that FOS, occurring 1.5 years after an intensive care emergency, was caused by partial nerve regeneration (axonotmesis), after which afferent (C-fiber) information from a small reinnervated skin area of the left foot and afferent somatic and autonomous (visceral) information from the vagina on at least S1 spinal level is misinterpreted by the brain as being solely information originating from the vagina. Waldinger MD, de Lint GJ, van Gils APG, Masir F, Lakke E, van Coevorden RS, and Schweitzer DH. Foot orgasm syndrome: A case report in a woman. J Sex Med **;**:**-**.

PMID: 23782523 [PubMed – as supplied by publisher]

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