Dorsal root ganglia, sodium channels, and fibromyalgia sympathetic pain

Martı́nez-Lavı́n, Manuel; Solano, Carla

doi:10.1016/j.mehy.2008.07.055

Cited by 29 publications

(33 citation statements)

References 18 publications

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“…A single Nav1.7 mutation (L858H) induces electrical hyperactivity of sensory neurons in dorsal root ganglia and, at the same time, produces hyporeactivity of sympathetic ganglia neurons. Several sodium “channelopathies” have been associated to rare painful dysautonomic syndromes such as primary erythermalgia and paroxysmal extreme pain disorder (formerly familial rectal pain syndrome) [18]. …”

Section: Animal Models Linking the Development Of Sympathetic Painmentioning

confidence: 99%

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Fibromyalgia: When Distress Becomes (Un)sympathetic Pain

Martı́nez-Lavı́n

2012

Pain Research and Treatment

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Fibromyalgia is a painful stress-related disorder. A key issue in fibromyalgia research is to investigate how distress could be converted into pain. The sympathetic nervous system is the main element of the stress response system. In animal models, physical trauma, infection, or distressing noise can induce abnormal connections between the sympathetic nervous system and the nociceptive system. Dorsal root ganglia sodium channels facilitate this type of sympathetic pain. Similar mechanisms may operate in fibromyalgia. Signs of sympathetic hyperactivity have been described in this condition. Genetic factors and/or distressful lifestyle may lead to this state of sympathetic hyperactivity. Trauma and infection are recognized fibromyalgia triggers. Women who suffer from fibromyalgia have catecholamine-evoked pain. Sympathetic dysfunction may also explain nonpain-related fibromyalgia symptoms. In conclusion, in fibromyalgia, distress could be converted into pain through forced hyperactivity of the sympathetic component of the stress response system.

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Section: Animal Models Linking the Development Of Sympathetic Painmentioning

confidence: 99%

“…Currently available sodium channel blockers are weak and nonspecific. Selective tetrodotoxin-resistant channel blockers are being developed and may in the future constitute an important therapeutic option for FM pain [18]. …”

Section: Genetic and Clinical Data Suggesting That Fm Is A Sympathmentioning

confidence: 99%

Fibromyalgia: When Distress Becomes (Un)sympathetic Pain

Martı́nez-Lavı́n

2012

Pain Research and Treatment

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“…The background information leading to the present investigation has been already published as a hypothesis [1] and is summarized here: A consistent line of investigation suggests that autonomic nervous system dysfunction may explain the multi-system features of fibromyalgia (FM); and that FM is a sympathetically maintained neuropathic pain syndrome. Trauma and infection are two recognized FM triggers.…”

Section: Introductionmentioning

confidence: 97%

“…Trauma and infection are two recognized FM triggers. In animal models; trauma or infection can induce phenotypic changes in the dorsal root ganglia (DRG) leading to a persistent sympathetically-maintained pain state [1]. …”

Section: Introductionmentioning

confidence: 99%

A SCN9A gene-encoded dorsal root ganglia sodium channel polymorphism associated with severe fibromyalgia

Vargas‐Alarcón

Álvarez-León

Fragoso

et al. 2012

BMC Musculoskelet Disord

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Background: A consistent line of investigation suggests that autonomic nervous system dysfunction may explain the multi-system features of fibromyalgia (FM); and that FM is a sympathetically maintained neuropathic pain syndrome. Dorsal root ganglia (DRG) are key sympathetic-nociceptive short-circuit sites. Sodium channels located in DRG (particularly Nav1.7) act as molecular gatekeepers for pain detection. Nav1.7 is encoded in gene SCN9A of chromosome 2q24.3 and is predominantly expressed in the DRG pain-sensing neurons and sympathetic ganglia neurons. Several SCN9A sodium channelopathies have been recognized as the cause of rare painful dysautonomic syndromes such as paroxysmal extreme pain disorder and primary erythromelalgia. The aim of this study was to search for an association between fibromyalgia and several SCN9A sodium channels gene polymorphisms. Methods: We studied 73 Mexican women suffering from FM and 48 age-matched women who considered themselves healthy. All participants filled out the Fibromyalgia Impact Questionnaire (FIQ). Genomic DNA from whole blood containing EDTA was extracted by standard techniques. The following SCN9A single-nucleotide polymorphisms (SNP) were determined by 5' exonuclease TaqMan assays: rs4371369; rs4387806; rs4453709; rs4597545; rs6746030; rs6754031; rs7607967; rs12620053; rs12994338; and rs13017637. Results: The frequency of the rs6754031 polymorphism was significantly different in both groups (P = 0.036) mostly due to an absence of the GG genotype in controls. Interestingly; patients with this rs6754031 GG genotype had higher FIQ scores (median = 80; percentile 25/75 = 69/88) than patients with the GT genotype (median = 63; percentile 25/75 = 58/73; P = 0.002) and the TT genotype (median = 71; percentile 25/75 = 64/77; P = 0.001). Conclusion: In this ethnic group; a disabling form of FM is associated to a particular SCN9A sodium channel gene variant. These preliminary results raise the possibility that some patients with severe FM may have a dorsal root ganglia sodium channelopathy.

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“…22 Recent studies have focused on the role of the DRGs in the mechanisms of pain sensitivity and neurological pain. [23][24][25] In one type of peripheral neuropathy, acquired sensory ganglionopathy, the sensory nerve cell bodies in the DRGs were damaged, resulting in sensory loss in the large fibers. 26 Most of the distal axonpathies have been shown to display simultaneous distal degeneration of both the peripheral and central axons of DRGs, a condition termed central-peripheral distal axonopathy, whereas others display only selective distal degeneration of the peripheral axons.…”

Section: Discussionmentioning

confidence: 99%

Acute spinal cord injury could cause activation of autophagy in dorsal root ganglia

et al. 2013

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Objectives: Dorsal root ganglia (DRGs) have an important role in the peripheral mechanism of sensation by primary afferent neurons, which are widely used to research the processes of cell death, axonal regeneration, signal transmission of growth factors and the mechanism of pain. Methods: In the present study, we investigated the activation of autophagy in DRGs in a rat model of acute spinal cord injury at different time points. Results: Expression of microtubule-associated protein light chain 3, a marker of autophagy was increased after 8 h in DRGs, peaked after 3 days, and then gradually decreased after 7 days. Furthermore, the toluidine blue staining has proven that after acute spinal cord injury, the myelin sheathes of DRGs undergo histopathological changes over time, with axonal swellings, disorderly arrangement and uneven distribution. Conclusion: Potential treatment aimed at recovery of behavioral locomotor and sensory perception should target the process of autophagy in DRGs.

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Dorsal root ganglia, sodium channels, and fibromyalgia sympathetic pain

Cited by 29 publications

References 18 publications

Fibromyalgia: When Distress Becomes (Un)sympathetic Pain

Fibromyalgia: When Distress Becomes (Un)sympathetic Pain

A SCN9A gene-encoded dorsal root ganglia sodium channel polymorphism associated with severe fibromyalgia

Acute spinal cord injury could cause activation of autophagy in dorsal root ganglia

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