Peripheral neuropathy in chronic venous insufficiency

Reinhardt, Frank; Wetzel, Tobias; Vetten, Sabine; Radespiel‐Tröger, Martin; Hilz, M. J.; Heuss, Dieter; Neundörfer, B.

doi:10.1002/(sici)1097-4598(200006)23:6<883::aid-mus6>3.0.co;2-t

Cited by 45 publications

(36 citation statements)

References 23 publications

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“…Nerve conduction studies were performed on a Keypoint electroneurographical system (Dantec, Denmark) using standard techniques as described elsewhere 10. The base to peak amplitude of the sensory nerve action potential (SNAP) of the left sural nerve, the sensory conduction velocity (CV) of the left sural nerve, the base to peak amplitude of the compound muscle action potential (CMAP) of the right extensor digitorum brevis muscle after stimulation of the peroneal nerve at the ankle, and the motor CV of the right peroneal nerve were determined.…”

Section: Methodsmentioning

confidence: 99%

Axonal polyneuropathy in obstructive sleep apnoea

Lüdemann

Dziewas²,

Sörös³

et al. 2001

Journal of Neurology, Neurosurgery &Amp; Psychiatry

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Chronic hypoxaemia in chronic obstructive pulmonary disease is a well known risk factor for polyneuropathy but the impact of intermittent hypoxaemia on peripheral nerve function has not been established so far. A case-control study was performed to evaluate the prevalence of polyneuropathy in obstructive sleep apnoea (OSA). Out of 24 patients with OSA, 17 (71%) had clinical signs of polyneuropathy versus seven (33%) out of 21 matched controls. The mean amplitude of the sural sensory nerve action potential was smaller in the OSA group than in the control group, indicating axonal nerve damage. The diVerences were significant and could not be attributed to other known risk factors for polyneuropathy. The severity of axonal damage in patients with OSA correlated with the percentage of the night time with an O 2 saturation below 90%. It is assumed that recurrent intermittent hypoxaemia in OSA is an independent risk factor for axonal damage of peripheral nerves. (J Neurol Neurosurg Psychiatry 2001;70:685-687)

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Section: Methodsmentioning

confidence: 99%

Axonal polyneuropathy in obstructive sleep apnoea

Lüdemann

Dziewas²,

Sörös³

et al. 2001

Journal of Neurology, Neurosurgery &Amp; Psychiatry

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“…13 Skin temperature was maintained at 34˚C during measurement. The base to peak amplitude of SNAP of both sural nerves was determined.…”

Section: Controlsmentioning

confidence: 99%

Treatment for obstructive sleep apnoea: effect on peripheral nerve function

Dziewas

Schilling

Engel

et al. 2006

Journal of Neurology, Neurosurgery & Psychiatry

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Background and objective: Obstructive sleep apnoea (OSA) is suggested to be associated with peripheral nerve damage. A case-control study was conducted to provide further support to this observation. In a longitudinal intervention study, it was examined whether treatment for OSA has a possible beneficial effect on peripheral nerve function. Methods: Participants were 23 patients with OSA and 23 controls matched for age and body mass index (BMI), all without any known cause of peripheral nerve damage. The sensory nerve action potential (SNAP) amplitudes of both sural nerves were determined. After 6 months of treatment for OSA, treatment compliance was evaluated and nerve conduction studies were repeated. Results: Patients with OSA had significantly lower mean (standard deviation) sural SNAP amplitudes than controls (6.3 (3.5) v 11.2 (5.0), p,0.001). Multivariate regression analysis including the variables age, BMI and Apnoea-Hypopnea Index (AHI) showed that both age (p,0.01) and AHI (p,0.05) were inversely related to the SNAP amplitude. On follow-up, the sural SNAP showed an increase of 2.6 mV on average (p,0.001). Multivariate regression analysis including the variables age, BMI, AHI, pretreatment SNAP and treatment compliance identified only treatment compliance as being significantly related to the SNAP increase (p(0.005). Conclusion: OSA is an independent risk factor for axonal dysfunction of peripheral sensory nerves. Impaired neural function is at least partly reversible with treatment for sleep apnoea.

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“…This is a sympathetic reflex and loss implies a sympathetic neuropathy. Ardron et al [12] suggested there was a ''C'' Evidence of neuropathy comes from recently conducted clinical studies by Padberg et al [13] and Reinhardt et al [14]. Padberg et al [13] suggested that the involvement of the deep tendon reflexes implied a global effect of CVI rather than a purely local phenomenon.…”

Section: Discussionmentioning

confidence: 99%

“…Padberg et al [13] suggested that the involvement of the deep tendon reflexes implied a global effect of CVI rather than a purely local phenomenon. Reinhardt et al [14] demonstrated that a disturbance of A-alpha fibers, A-beta fibers, A-delta fibers, and thermoafferent C fibers, possibly induced by ischemia resulting from venous microangiopathy and increased endoneurial pressure.…”

Section: Discussionmentioning

confidence: 99%

Confirmation of peripheral neuropathy in patients withvenous ulceration through immunohistochemistry

et al. 2011

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Patients with venous ulceration demonstrate clinical signs of peripheral neuropathy. Using immunohistochemistry we investigated cutaneous innervations immediately adjacent to chronic and healing venous ulcers. Punch biopsies (4 mm) were taken from sites adjacent to venous ulcers: (1) from nonhealing ulcers (n = 15), (2) from healing ulcers and (n = 14), and (3) from control patients with varicose veins (n = 12). Immunohistochemistry using anti-protein gene product 9.5 (PGP) antibody was used to assess total nerve fibers. Antibodies against the neuropeptides calcitonin generelated protein (CGRP) and substance P (SP) were used to assess distribution of CGRP and SP-containing fibers. Innervations of the epidermis and papillary dermis were quantified with image analysis by two blinded investigators. Using PGP 9.5, total nerve fibers are decreased in the dermis adjacent to healing ulcers but not in nonhealing group. The total nerve fibres of the epidermis are decreased in non-healing group but not in healing group. PGP-positive fibers are shorter in the dermis in both groups, but more in the nonhealers. CGRP-positive fibers are decreased in the dermis in both groups and in the epidermis in healing group. The epidermal fibers are shorter in both groups. There were few SP-positive fibers in all groups. Reduced dermal and epidermal innervations may contribute to the initial development of a venous ulcer. The decrease in epidermal fibers in chronic ulcers suggests that epidermal innervations may be important in healing. This study confirms the clinical studies with immunohistochemical evidence of peripheral neuropathy in venous ulceration. IntroductionIt is somewhat surprising that patients with venous ulceration do not experience more pain and discomfort.

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Peripheral neuropathy in chronic venous insufficiency

Cited by 45 publications

References 23 publications

Axonal polyneuropathy in obstructive sleep apnoea

Axonal polyneuropathy in obstructive sleep apnoea

Treatment for obstructive sleep apnoea: effect on peripheral nerve function

Confirmation of peripheral neuropathy in patients withvenous ulceration through immunohistochemistry

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