Characterization of non–length‐dependent small‐fiber sensory neuropathy

Khan, Sara; Zhou, Lan

doi:10.1002/mus.22255

Cited by 87 publications

(118 citation statements)

References 23 publications

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“…The most commonly etiology reported for SFN is diabetes mellitus 2,4. Other possible etiologies include impaired glucose tolerance (IGT),5,6 connective tissue disease,7,8 celiac disease,9 thyroid dysfunction,10,11 vitamin B12 deficiency,10 monoclonal gammopathy,12,13 HIV and hepatitis C infections,14,15 amyloidosis,16 toxicity due to alcohol or drugs,17,18 and hereditary neuropathies 19. Despite knowledge of these factors, the reported etiology of SFN has remained unclear in 23-93% of investigated patients 1,4,13,20.…”

Section: Introductionmentioning

confidence: 99%

Idiopathic Small Fiber Neuropathy: Phenotype, Etiologies, and the Search for Fabry Disease

et al. 2014

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Background and PurposeThe etiology of small fiber neuropathy (SFN) often remains unclear. Since SFN may be the only symptom of late-onset Fabry disease, it may be underdiagnosed in patients with idiopathic polyneuropathy. We aimed to uncover the etiological causes of seemingly idiopathic SFN by applying a focused investigatory procedure, to describe the clinical phenotype of true idiopathic SFN, and to elucidate the possible prevalence of late-onset Fabry disease in these patients.MethodsForty-seven adults younger than 60 years with seemingly idiopathic pure or predominantly small fiber sensory neuropathy underwent a standardized focused etiological and clinical investigation. The patients deemed to have true idiopathic SFN underwent genetic analysis of the alpha-galactosidase A gene (GLA) that encodes the enzyme alpha-galactosidase A (Fabry disease).ResultsThe following etiologies were identified in 12 patients: impaired glucose tolerance (58.3%), diabetes mellitus (16.6%), alcohol abuse (8.3%), mitochondrial disease (8.3%), and hereditary neuropathy (8.3%). Genetic alterations of unknown clinical significance in GLA were detected in 6 of the 29 patients with true idiopathic SFN, but this rate did not differ significantly from that in healthy controls (n=203). None of the patients with genetic alterations in GLA had significant biochemical abnormalities simultaneously in blood, urine, and skin tissue.ConclusionsA focused investigation may aid in uncovering further etiological factors in patients with seemingly idiopathic SFN, such as impaired glucose tolerance. However, idiopathic SFN in young to middle-aged Swedish patients does not seem to be due to late-onset Fabry disease.

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Section: Introductionmentioning

confidence: 99%

Idiopathic Small Fiber Neuropathy: Phenotype, Etiologies, and the Search for Fabry Disease

et al. 2014

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“…However, occasionally, SFN may present with an asymmetrical patchy pattern of sensory symptoms starting in the arms or even in the face, which suggest a non-length-dependent ganglionopathy. [4][5][6] In up to 47% of cases, no underlying cause is revealed at the time point of diagnosis, 7 therefore these cases are classified as "idiopathic." Making the diagnosis of SFN often poses a challenge because routine electrophysiological measures remain normal.…”

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confidence: 99%

Small-Fiber Neuropathy Is Associated With Corneal Nerve and Dendritic Cell Alterations

Bucher

Schneider

Blau

et al. 2015

Cornea

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“…It has been suggested that hyperactivity of small, unmyelinated C-fibers results in hyperalgesia and allodynia (36). Also, Khan et al (38) reported that A-fiber afferents in diabetic rats developed abnormal spontaneous discharges and increased sensitivity to mechanical stimuli, suggesting a role of large A-fiber neurons in addition to nociceptive C-fibers in the development of diabetic neuropathic pain in early stage of DM. In our opinion, according to results of previous studies in the literature, a few weeks after induction of hyperglycemia, there is an increased expression and/or activation of Na v Chs that play an important role on developing of hyperexcitability in early stage of DM, but the possible role of Na v Chs on occured hypoexcitability and hyposensation as major symptoms of the later stage of DM 6-8 weeks after induction of hyperglycemia is still unknown.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the Effects of Novel Nafimidone Derivatives on Thermal Hypoalgesia in Mice with Diabetic Neuropathy

et al. 2013

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The worldwide diabetes epidemic has shown no signs of abatement. Its prevalence has more than doubled since 1980 (1). Diabetic neuropathy (DN) is the most common diabetic complication, afflicting over 50% of all diabetics. The possible biochemical pathomechanisms include oxidative stress, activation of the polyol pathway, increased advanced glycation end products (AGEs) and their receptors, impaired ionic homeostasis of cells and activation of protein kinases (PKC and PKA), and mitogen-activated protein kinases (MAPK), and inducible nitric oxide synthase (2-6).Understanding the biochemical mechanisms underlying diabetic neuropathic pain and sensory disorders requires preclinical studies in animal models. The streptozotocin (STZ)-induced diabetic rodent is the most commonly used animal model of diabetes (7,8). On the other hand, existing animal models of diabetic painful and insensate neuropathy, however, have serious limitations. Diabetic rats and mice have limited life span and rarely show evidence of overt neuropathy, such as demyelination, axonal degeneration, fiber loss, or axonal regeneration in their peripheral nerves. This makes diabetic rodents unsuitable for studying the contribution of these phenomena of DN to pain or to loss of sensory function (9). Nonetheless, despite these limitations, assessment of behavioral responses to external stimuli in diabetic rats and mice (i.e., thermal and mechanical hyper and hypoalgesia, tactile allodynia, as well as formalin-induced spontaneous nociceptive behavior) has led to identification of a number of mechanisms of loss of sensation and/or pain in diabetes (10).Decades of research elucidating the pathophysiology of diabetic neuropathy have failed, thus far, to produce a treatment that prevents or reverses its development and progression. Recently, however, numerous competing or parallel pathological pathways have begun to intersect and complement each other, illuminating potential pharmacologic targets. The current foci of diabetic neuropathy research are excessive activation of sodium channels and corrupted molecular mechanisms of cellular pathways of related kinases (11).Voltage-gated sodium channels (Na v Chs) are a necessary component of normal sensation, emotions, thoughts and movements and are of particular interest as target for neuro- ABSTRACTObjective: Diabetic neuropathy (DN) is a common complication in Diabetes Mellitus. The streptozotocin-induced diabetic rodent is the most commonly used animal model of diabetes and increased sodium channel expression and activity were revealed in this model. At this study, we evaluated the effect of three different nafimidone derivatives which have possible anticonvulsant activity on disorders of thermal pain sensation in diabetic mice.Study Design: Randomized animal experiment.Material and Methods: Mice were divided randomly into five groups (5 mice per group): Control, Diabetes, Dibetes+C1, Diabetes+C2, Diabetes+C3. We used hot and cold plate, and tail-immersion tests for assessment of thermal nociceptive response...

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Characterization of non–length‐dependent small‐fiber sensory neuropathy

Abstract: NLD-SFSN is more common in women, presents at a younger age, and is more likely to be associated with immune-mediated conditions than LD-SFSN.

Cited by 87 publications

References 23 publications

Idiopathic Small Fiber Neuropathy: Phenotype, Etiologies, and the Search for Fabry Disease

Idiopathic Small Fiber Neuropathy: Phenotype, Etiologies, and the Search for Fabry Disease

Small-Fiber Neuropathy Is Associated With Corneal Nerve and Dendritic Cell Alterations

Evaluation of the Effects of Novel Nafimidone Derivatives on Thermal Hypoalgesia in Mice with Diabetic Neuropathy

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