Painful sensory neuropathy

Periquet, Magali; Novak, Vera; Collins, Michael; Nagaraja, Haikady N.; Erdem, Sevim; Nash, Susan M.; Freimer, Miriam; Sahenk, Zarife; Kissel, John T.; Mendell, Jerry R.

doi:10.1212/wnl.53.8.1641

Cited by 363 publications

(297 citation statements)

References 38 publications

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“…Skin biopsies obtained from patients with diabetes mellitus show uniform reduction in the content of PGP 9.5 (41,42). Quantification of epidermal axon number in skin biopsies confirmed the loss of cutaneous nerve fibers in diabetic subjects with symptoms of neuropathy, and this reduction correlates with electrophysiological and somatosensory deficits (18,43,44). Consistent with these observations, we observed a severe reduction in cutaneous innervation of footpad skin of STZ-diabetic rats.…”

Section: Discussionsupporting

confidence: 85%

Erythropoietin both protects from and reverses experimental diabetic neuropathy

Bianchi

Büyükakıllı

Brines

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

235

179

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Tail-nerve conduction velocities (NCV) was assessed at 5 and 11 weeks for the preventive and therapeutic schedule, respectively. Compared to nondiabetic rats, NCV was 20% lower after 5 weeks in the STZ group, and this decrease was attenuated 50% by rhEPO. Furthermore, the reduction of Na ؉ ,K ؉ -ATPase activity of diabetic nerves (by 55%) was limited to 24% in the rhEPO-treated group. In the therapeutic schedule, NCV was reduced by 50% after 11 weeks but by only 23% in the rhEPO-treated group. rhEPO treatment attenuated the decrease in compound muscle action potential in diabetic rats. In addition, rhEPO treatment was associated with a preservation of footpad cutaneous innervation, as assessed by protein gene product 9.5 immunostaining. Diabetic rats developed alterations in mechanical and thermal nociception, which were partially reversed by rhEPO given either in a preventative or therapeutic manner. These observations suggest that administration of rhEPO or its analogues may be useful in the treatment of diabetic neuropathy.

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Section: Discussionsupporting

confidence: 85%

Erythropoietin both protects from and reverses experimental diabetic neuropathy

Bianchi

Büyükakıllı

Brines

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

235

179

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“…Therefore, routine NCV tests lack the sensitivity to detect small fiber impairment. On the contrary, footpad skin biopsy has proved to be a reliable tool to examine unmyelinated nerve fibers, as assessed by the quantification IENF density (38,(41)(42)(43), and it is now accepted as a sensitive method in assessing the presence of DPN.…”

Section: Cyclooxygenase-2 and Diabetic Neuropathymentioning

confidence: 99%

Protective Effects of Cyclooxygenase-2 Gene Inactivation Against Peripheral Nerve Dysfunction and Intraepidermal Nerve Fiber Loss in Experimental Diabetes

et al. 2007

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OBJECTIVE—Activation of the cyclooxygenase (COX) pathway with secondary neurovascular deficits are implicated in the pathogenesis of experimental diabetic peripheral neuropathy (DPN). The aim of this study was to explore the interrelationships between hyperglycemia, activation of the COX-2 pathway, and oxidative stress and inflammation in mediating peripheral nerve dysfunction and whether COX-2 gene inactivation attenuates nerve fiber loss in long-term experimental diabetes. RESEARCH DESIGN AND METHODS—Motor and sensory digital nerve conduction velocities, sciatic nerve indexes of oxidative stress, prostaglandin content, markers of inflammation, and intraepidermal nerve fiber (IENF) density were measured after 6 months in control and diabetic COX-2–deficient (COX-2−/−) and littermate wild-type (COX-2+/+) mice. The effects of a selective COX-2 inhibitor, celecoxib, on these markers were also investigated in diabetic rats. RESULTS—Under normal conditions, there were no differences in blood glucose, peripheral nerve electrophysiology, markers of oxidative stress, inflammation, and IENF density between COX-2+/+ and COX-2−/− mice. After 6 months, diabetic COX-2+/+ mice experienced significant deterioration in nerve conduction velocities and IENF density and developed important signs of increased oxidative stress and inflammation compared with nondiabetic mice. Diabetic COX-2−/− mice were protected against functional and biochemical deficits of experimental DPN and against nerve fiber loss. In diabetic rats, selective COX-2 inhibition replicated this protection. CONCLUSIONS—These data suggest that selective COX-2 inhibition may be useful for preventing or delaying DPN.

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“…Some studies in which thermal and pain thresholds have been compared with skin biopsy findings have demonstrated a correlation between cold and/or warm thresholds and IENF density 164,[214][215][216][217] , but other similar studies have not [218][219][220] . These findings suggest that QST should be considered as an additional diagnostic test for SFN, but alongside a well-characterized clinical assessment and a skin biopsy 206 .…”

Section: Box 1 | Quantitative Sensory Testingmentioning

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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Painful sensory neuropathy

Cited by 363 publications

References 38 publications

Erythropoietin both protects from and reverses experimental diabetic neuropathy

Erythropoietin both protects from and reverses experimental diabetic neuropathy

Protective Effects of Cyclooxygenase-2 Gene Inactivation Against Peripheral Nerve Dysfunction and Intraepidermal Nerve Fiber Loss in Experimental Diabetes

New technologies for the assessment of neuropathies

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