Hyperexcitable C nociceptors in fibromyalgia

Serra, Jordi; Collado, Antonio; Solà, Romà; Antonelli, Francesca; Torres, Xavier; Salgueiro, Mónika; Quiles, Cristina; Bostock, Hugh

doi:10.1002/ana.24065

Cited by 229 publications

(176 citation statements)

References 41 publications

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“…Microneurography of the peroneal nerve revealed abnormal cutaneous C nociceptor function similar to that seen in patients with small fiber neuropathy in 77 % of FMS patients [541]. More specifically, while mechanosensitive type 1A nociceptors functioned normally, a high proportion of the usually silent mechanoinsensitive type 1B nociceptors exhibited spontaneous activity, but also enhanced activity-dependent slowing of conduction velocity, and this distinguished FMS patients from patients with small-fiber neuropathy.…”

Section: Further Potential Peripheral Nociceptive Inputmentioning

confidence: 67%

Fibromyalgia: A Critical and Comprehensive Review

Borchers

Gershwin

2015

Clinic Rev Allerg Immunol

225

217

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Fibromyalgia is a disorder that is part of a spectrum of syndromes that lack precise classification. It is often considered as part of the global overview of functional somatic syndromes that are otherwise medically unexplained or part of a somatization disorder. Patients with fibromyalgia share symptoms with other functional somatic problems, including issues of myalgias, arthralgias, fatigue and sleep disturbances. Indeed, there is often diagnostic and classification overlap for the case definitions of a variety of somatization disorders. Fibromyalgia, however, is a critically important syndrome for physicians and scientists to be aware of. Patients should be taken very seriously and provided optimal care. Although inflammatory, infectious, and autoimmune disorders have all been ascribed to be etiological events in the development of fibromyalgia, there is very little data to support such a thesis. Many of these disorders are associated with depression and anxiety and may even be part of what has been sometimes called affected spectrum disorders. There is no evidence that physical trauma, i.e., automobile accidents, is associated with the development or exacerbation of fibromyalgia. Treatment should be placed on education, patient support, physical therapy, nutrition, and exercise, including the use of drugs that are approved for the treatment of fibromyalgia. Treatment should not include opiates and patients should not become poly pharmacies in which the treatment itself can lead to significant morbidities. Patients with fibromyalgia are living and not dying of this disorder and positive outlooks and family support are key elements in the management of patients.

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Section: Further Potential Peripheral Nociceptive Inputmentioning

confidence: 67%

Fibromyalgia: A Critical and Comprehensive Review

Borchers

Gershwin

2015

Clinic Rev Allerg Immunol

225

217

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“…As fibromyalgia affects several percent of the population, the public health and economic implications are considerable. Initial pathology skin biopsy studies identifying loss of cutaneous innervation were followed by electrophysiologic evidence that C-fibers fire spontaneously and excessively in patients with fibromyalgia as in positive-control patients with SFPN but not normal controls [74,[92][93][94]. Subsequent studies have so far all been supportive (e.g., [95]), so biological overlap between fibromyalgia and High-dose corticosteroids resulted in immediate improvement in all signs and symptoms, including pain.…”

Section: Small-fiber Polyneuropathymentioning

confidence: 99%

Immunotherapy Prospects for Painful Small-fiber Sensory Neuropathies and Ganglionopathies

Oaklander

2016

Neurotherapeutics

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The best-known peripheral neuropathies are those affecting the large, myelinated motor and sensory fibers. These have well-established immunological causes and therapies. Far less is known about the somatic and autonomic "small fibers"; the unmyelinated C-fibers, thinly myelinated A-deltas, and postganglionic sympathetics. The small fibers sense pain and itch, innervate internal organs and tissues, and modulate the inflammatory and immune responses. Symptoms of small-fiber neuropathy include chronic pain and itch, sensory impairment, edema, and skin color, temperature, and sweating changes. Small-fiber polyneuropathy (SFPN) also causes cardiovascular, gastrointestinal, and urological symptoms, the neurologic origin of which often remains unrecognized. Routine electrodiagnostic study does not detect SFPN, so skin biopsies immunolabeled to reveal axons are recommended for diagnostic confirmation. Preliminary evidence suggests that dysimmunity causes some cases of small-fiber neuropathy. Several autoimmune diseases, including Sjögren and celiac, are associated with painful small-fiber ganglionopathy and distal axonopathy, and some patients with "idiopathic" SFPN have evidence of organ-specific dysimmunity, including serological markers. Dysimmune SFPN first came into focus in children and teenagers as they lack other risk factors, for example diabetes or toxic exposures. In them, the rudimentary evidence suggests humoral rather than cellular mechanisms and complement consumption. Preliminary evidence supports efficacy of corticosteroids and immunoglobulins in carefully selected children and adult patients. This paper reviews the evidence of immune causality and the limited data regarding immunotherapy for small-fiberpredominant ganglionitis, regional neuropathy (complex regional pain syndrome), and distal SFPN. These demonstrate the need to develop case definitions and outcome metrics to improve diagnosis, enable prospective trials, and dissect the mechanisms of small-fiber neuropathy.

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“…Spontaneous ongoing discharges of C-nociceptors are considered to be pathological causes of pain, and microneurography has been used to demonstrate that such spontaneous discharge is present in patients in whom pain is associated with SFN 200 . The same technique has been used to reveal spontaneous discharge of C-nociceptors in fibro myalgia 200,202,203 , thereby widening the spectrum of disorders that have been related to SFN.…”

Section: Microneurographymentioning

confidence: 99%

New technologies for the assessment of neuropathies

et al. 2017

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Peripheral neuropathies are among the most common neurological disorders 1 . In routine clinical practice, diagnosis of peripheral neuropathies is typically based on clinical assessment, nerve conduction studies and needle electromyography, which can determine whether symptoms are caused by primary axonal damage or demyelinating damage. This distinction is often relevant to therapeutic choices and to prognosis, as axonal damage typically reflects an inflammatory (for example, vasculitic) or degenerative (for example, hereditary or idiopathic) process that correlates with disability, whereas demyelinating damage can reflect a hereditary neuro pathy, but more often reflects an acquired immunemediated neuropathy. Besides metabolic, inflammatory or primary degenerative neuropathies, peripheral nerves can also be damaged by compression from adjacent tissue structures, such as tendons, cysts or haematomas. In this case, proper identification of the site, nature and degree of the lesion might be challenging, but is relevant to treatment and prognosis. Moreover, some patients present with symptoms that suggest damage to small nerve fibres, which nerve conduction studies cannot be used to detect.In the past 15 years, several techniques have become available to investigate focal and diffuse peripheral neuropathies, and their reliability has widened the spectrum of diagnostic tools for clinicians and improved assessment of neuropathies. In this Review, we provide an overview of these new and emerging technologies. We first discuss peripheral nerve imaging with MRI and ultrasonography, which can provide information about the precise localization of neuro pathies and the pathological processes involved in large-fibre neuropathies, and can complement clinical and electrophysiological evaluation. We then consider techniques that can provide diagnostic information when the pathological process is restricted to small nerve fibres and is consequently not detectable with nerve conduction studies or neuroimaging. These include skin biopsy, which is established in clinical practice, and the emerging techniques of corneal confocal microscopy, laser-evoked potentials and heat-related and pain-related evoked potentials, and microneurography.Nerve imaging technology Advances in imaging techniques have made it possible to gain great insight into nerve pathology with magnetic resonance and ultrasound. Each approach offers distinct advantages, and can provide different information about damage to large myelinated fibres. Abstract | Technical advances are rapidly changing the clinical and instrumental approach to peripheral nerve diseases. Magnetic resonance neurography, diffusion tensor imaging and nerve ultrasonography are increasingly entering the diagnostic workup of peripheral neuropathies as tools that complement neurophysiology and enable investigation of proximal structures, such as plexuses and roots. Progress in the design of magnetic resonance scanners and sequences, and the development of high-frequency ultrasound probes mean th...

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Hyperexcitable C nociceptors in fibromyalgia

Cited by 229 publications

References 41 publications

Fibromyalgia: A Critical and Comprehensive Review

Fibromyalgia: A Critical and Comprehensive Review

Immunotherapy Prospects for Painful Small-fiber Sensory Neuropathies and Ganglionopathies

New technologies for the assessment of neuropathies

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