Characteristics of Lower Extremity Pressure Sensation Impairment in Developing Diabetic Sensory Polyneuropathy

Rader, Andrew J.; Barry, Timothy P.; Stanley, Otis L.

doi:10.1177/1938640007312383.

Cited by 7 publications

(10 citation statements)

References 27 publications

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“…The diagnosis of DSPN was made based on presence of combination of symptoms (screening questionnaire) and signs of neuropathy including decreased distal sensation and/or decreased or absent ankle reflexes after elimination of confounding factors (inclusion/exclusion criteria) [ 7 , 9 , 15 ]. All the sensory measurements were performed by a single clinician in a patient in supine position.…”

Section: Methodsmentioning

confidence: 99%

Evaluation of oxidative stress markers in pathogenesis of diabetic neuropathy

et al. 2012

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Experimental evidences suggest that hyperglycaemia-induced overproduction of reactive oxygen species and subsequent damage to proteins, lipids and DNA may play a key role in the development of distal symmetric polyneuropathy (DSPN)—the most common complication of diabetes mellitus. The study population consisted of 51 individuals aged 52–82 years classified into 3 groups: 16 patients diagnosed with type 2 diabetes mellitus (T2DM) with DSPN, 16 T2DM patients without DSPN and 19 control subjects without diabetes and neuropathy. The study was conducted to determine the activity of antioxidant enzymes: catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX) and total antioxidant status (TAS) in the examined groups. An alkaline comet assay was used to determine the extent of DNA damage of oxidized purines as glicosylo-formamidoglicosylase (Fpg) sites, and oxidized pyrimidines as endonuclease III (Nth) sites. A significant decrease of SOD (P < 0.05), GPX (P < 0.05) and nonsignificant decrease of CAT (P > 0.05), and TAS status (P > 0.05) were seen in T2DM patients with neuropathy compared to T2DM patients as well as controls. T2DM patients with or without neuropathy revealed significantly lower (P < 0.05) plasma concentration of nitrous oxide compared to the control subjects. Endogenous level of oxidative DNA damage in T2DM patients with DSPN was significantly higher compared both to the controls and T2DM patients without DSPN (P < 0.001). Moreover, lymphocytes isolated from T2DM patients with DSPN were more susceptible to oxidative DNA lesions induced by hydrogen peroxide than from T2DM patients without DSPN (P < 0.001). Our results confirm hypothesis that oxidative stress may play a substantial role in the development and progression of diabetic distal symmetric polyneuropathy.

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Section: Methodsmentioning

confidence: 99%

Evaluation of oxidative stress markers in pathogenesis of diabetic neuropathy

et al. 2012

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“…The predominant pattern of sensory loss involved the plantar foot, even after adjusting for sensitivity differences between the dorsal, lateral, and plantar skin. 19 This is intriguing in that a purely metabolic explanation for DSPN would seem unlikely if all pedal nerves were not damaged to similar degrees at similar axonal lengths.…”

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confidence: 99%

Symmetry of Sensory Loss in Developing Diabetic Sensory Polyneuropathy

Rader

Barry

2009

Foot & Ankle Specialist

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The medical literature presents diabetic sensory polyneuropathy (DSPN) as an axonal length-dependent symmetric pathology producing a stocking-like pattern of anesthesia in the lower extremities. This has been based on anecdotal reports. Objective research has shown that damage may not occur in a purely length-dependent manner. A stocking distribution of sensory loss is atypical, and plantar sensory loss predominates. A single-blinded, age-matched, control/experimental study was performed of the symmetry of nerve damage in developing DSPN. Control (n = 46) and experimental (n = 83) subjects were examined. The patterns of sensory loss and the severity of axonal damage were evaluated. The right/left symmetry of pathology was recorded for each individual. Although there was not a stocking pattern of anesthesia found in developing DSPN, the pattern and severity of anesthesia were found to be generally symmetric. The severity of sensory impairment was symmetric at the dorsal foot (93%), lateral foot (95%), and plantar foot (69%). The most predominant site of sensory impairment was also symmetric (81%). This argues against a purely metabolic etiology for axonal damage. An anatomic component is implied. Further research will need to include examination of the unique physical characteristics of predominantly affected nerves.

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“…• For the hypothesized nerve enlargement in DSPN by strong objective level I evidence; 47,48 • Asymmetry and variability of global foot sensibility, Oxford EBM level II-1; 45,52 • High perineural tissue pressures within inflexible anatomic tunnel structures, and relief of pressure by ND, Level II-1; 35 • Subjective relief of DSPN pain, recovery of lost sensibility, and improved symptom scores, Level II-2 and II-3 evidence; 36,42 • Improved objective outcomes, including balance, perineural pressure, NCV, ulcer occurrence, prolonged protection from recurrence, and amputation risk, are supported by Level II-1 to Level II-2 evidence.…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

“…Proponents believe instead they are decompressing focal nerve entrapments at anatomic chokepoints. Limited appreciation of variable, asymmetric, and non-global sensory changes 45 prevented recognition of entrapments and contemplation that length-dependent axonopathy (LDA) might fail to adequately explain numbness patterns. The Dellon hypothesis of frequent, metabolically induced, superimposed subclinical entrapment challenges the LDA paradigm as incomplete or inaccurate.…”

Section: Discussionmentioning

confidence: 99%

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Reconsidering Nerve Decompression: An Overlooked Opportunity to Limit Diabetic Foot Ulcer Recurrence and Amputation

Nickerson

2013

J Diabetes Sci Technol

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Nerve decompression for relief of subjective diabetic sensorimotor polyneuropathy pain and numbness has been labeled of "unknown" benefit. Objective outcomes in treatment and prevention of diabetic foot complications are reviewed. There is growing evidence that plantar foot ulceration and recurrence in high-risk feet are minimized with this operation. Avoiding neuropathic and neuroischemic ulcer wounds should theoretically reduce amputations and perhaps mortality risk. Protective effects are hypothesized to act via relief of neurovascular entrapment, thereby improving neurally modulated tissue homeostasis factors. Nerve decompression deserves considerable research attention to understand its role in limiting foot complications. Its apparent benefits challenge the paradigm that diabetic neuropathy is a purely length-dependent axonopathy and may necessitate appreciation of superimposed nerve entrapment as an significant operant factor.

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Characteristics of Lower Extremity Pressure Sensation Impairment in Developing Diabetic Sensory Polyneuropathy

Cited by 7 publications

References 27 publications

Evaluation of oxidative stress markers in pathogenesis of diabetic neuropathy

Evaluation of oxidative stress markers in pathogenesis of diabetic neuropathy

Symmetry of Sensory Loss in Developing Diabetic Sensory Polyneuropathy

Reconsidering Nerve Decompression: An Overlooked Opportunity to Limit Diabetic Foot Ulcer Recurrence and Amputation

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