The role of sodium channels in chronic pain

Levinson, S. Rock; Luo, Songjiang; Henry, Michael

doi:10.1002/mus.23314

Cited by 69 publications

(54 citation statements)

References 86 publications

(106 reference statements)

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“…After nerve injury, the expression of some of these channels increases de novo, the expression of others diminishes, and some translocate into different cellular compartments. 24 The proliferation of heterotopic sodium channels, such as Nav1.3, Nav1.7, and Nav1.8, may lower the stimulation threshold and provoke ectopic discharge, resulting in spontaneous pain. In addition, the spread of sodium channels may trigger central sensitization, leading to allodynia.…”

Section: Expression Of Ion Channelsmentioning

confidence: 99%

Neuropathic pain: mechanisms and their clinical implications

Cohen

Mao

2014

BMJ

608

570

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Section: Expression Of Ion Channelsmentioning

confidence: 99%

Neuropathic pain: mechanisms and their clinical implications

Cohen

Mao

2014

BMJ

608

570

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“…(28) Voltage-gated sodium (Na) channels in membranes are crucial for initiation and propagation of action potentials in excitable tissues. (29-31) To date, ten voltage-gated Na channels (Na v 1.1-1.9 and Na v 2.x), encoded by separate genes ( SCN1ASCN5A and SCN7A-SCN11A ), are expressed in mammals; (32) eight (Na v 1.1-1.3, Na v 1.6-1.9 and Na v 2.x) in sensory neurons. (31-33) Defects in three sodium channels (Na v 1.7, Na v 1.8 and Na v 1.9, encoded by SCN9A, SCN10A, and SCN11A , respectively) cause pain disorders in humans.…”

Section: V) Discussionmentioning

confidence: 99%

“…(32) It functions primarily to transmit pain signals from the periphery to the CNS. This large tetrodotoxin-resistant polypeptide comprises a 260 kDa α-subunit and an auxillary β-subunit.…”

Section: V) Discussionmentioning

confidence: 99%

Congenital insensitivity to pain: Fracturing without apparent skeletal pathobiology caused by an autosomal dominant, second mutation in SCN11A encoding voltage-gated sodium channel 1.9

Phatarakijnirund

Mumm

McAlister

et al. 2016

Bone

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Congenital insensitivity to pain (CIP) comprises the rare heritable disorders without peripheral neuropathy that feature inability to feel pain. Fracturing and joint destruction are common complications, but lack detailed studies of mineral and skeletal homeostasis and bone histology. In 2013, discovery of a heterozygous gain-of-function mutation in SCN11A encoding voltage-gated sodium channel 1.9 (Nav1.9) established a distinctive CIP in three unrelated patients who suffered multiple painless fractures, self-inflicted mutilation, chronic diarrhea, and hyperhidrosis. Here, we studied a mother and two children with CIP by physical examination, biochemical testing, radiological imaging including DXA, iliac crest histology, and mutation analysis. She suffered fractures primarily of her lower extremities beginning at age two years, and had Charcot deformity of both ankles and joint hypermobility. Nerve conduction velocity and biopsy and electromyography were normal. Her children had recurrent major fractures beginning in early childhood, joint hypermobility, and chronic diarrhea. She had an excoriated external nare, and both children had hypertrophic scars from scratching. Skin collagen studies were normal. Radiographs revealed fractures and deformities. However, lumbar spine and total hip BMD Z-scores, biochemical parameters of mineral and skeletal homeostasis, and iliac crest histology of the mother (after in vivo tetracycline labeling) were normal. Genomic DNA from the children revealed a unique heterozygous missense mutation in exon 23 (c.3904C>T, p.Leu1302Phe) of SCN11A that is absent in SNP databases and alters an evolutionarily conserved amino acid. This autosomal dominant CIP reflects the second gain-of-function mutation of SCN11A. Perhaps joint hypermobility is an unreported feature. How mutation of Nav1.9 causes fracturing remains unexplained. Lack of injury awareness is typically offered as the reason, and was supported by our unremarkable biochemical, radiological, and histological findings indicating no skeletal pathobiology. However, low-trauma fracturing in these patients suggests an uncharacterized defect in bone quality.

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“…A number of different sodium channel isoforms exist with distinct tissue distribution and possibly distinct physiological functions. Some of these isoforms have been shown to be up-regulated in inflammatory and neuropathic pain states [28,[154][155][156].…”

Section: The Rationale For Ivlt In the Management Of Painmentioning

confidence: 99%

“…Dorsal-horn neurons are more sensitive to lidocaine compared with peripheral neurons [135]. The high susceptibility of hyper-excitable neurons to lidocaine may be attributed to the changed expression of sodium channels during nerve injury [28].…”

Section: The Rationale For Ivlt In the Management Of Painmentioning

confidence: 99%

A Review of Intravenous Lidocaine Infusion Therapy for Paediatric Acute and Chronic Pain Management

Lauder¹

2017

Pain Relief - From Analgesics to Alternative Therapies

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Pediatric acute and chronic pain experiences involve the interaction of physiological, psychological, behavioural, developmental, pharmacological and situational factors. In the acute perioperative pain setting preventative multimodal analgesia is required to provide comfort and minimise the potential for "wind-up" and central sensitisation. When pain is recurrent, ongoing or chronic some children embark on a downward spiral of decreased physical, psychological and social functioning. The multidisciplinary team management approach is a well-established standard of care for children with complex chronic pain. Intravenous lidocaine has peripheral and central mediated analgesic, anti-inflammatory and anti-hyperalgesic properties. Intravenous lidocaine infusion therapy (IVLT) has been shown to be effective in the management of acute and chronic pain in adults. This chapter will present the rational for IVLT in pediatric pain management with emphasis on preventative multimodal therapy in acute pain and the multidisciplinary treatment approach in chronic pain. Large multi-centre randomised controlled trials are required to provide the evidence-base to confirm that IVLT is indeed an effective and safe treatment option in acute preventative multimodal analgesia and as an adjunct in the multidisciplinary care of chronic pain in the pediatric population. Keywords

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The role of sodium channels in chronic pain

Cited by 69 publications

References 86 publications

Neuropathic pain: mechanisms and their clinical implications

Neuropathic pain: mechanisms and their clinical implications

Congenital insensitivity to pain: Fracturing without apparent skeletal pathobiology caused by an autosomal dominant, second mutation in SCN11A encoding voltage-gated sodium channel 1.9

A Review of Intravenous Lidocaine Infusion Therapy for Paediatric Acute and Chronic Pain Management

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