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Aim The aim of this study was to examine foot function in the presence of diabetes-induced alterations of the anatomical and biomechanical unit formed by the Achilles tendon, plantar fascia and metatarso-phalangeal joints. More specifically, we focused on the Windlass mechanism, the physiological mechanism which entails stiffening of the foot during propulsion.
Methods Sixty-one diabetic patients, with or without neuropathy, and 21 healthy volunteers were recruited. The thickness of Achilles tendon and plantar fascia was measured by ultrasound. The main biomechanical parameters of foot–floor interaction during gait were acquired by means of dedicated platforms. The range of motion of the 1st metatarso-phalangeal joint was measured passively.
Results The plantar fascia (PF) and Achilles tendon (AT) were significantly thickened in diabetic patients [control subjects: PF 2.0 ± 0.5 mm, AT 4.0 ± 0.5 mm; diabetic patients without neuropathy: PF 2.9 ± 1.2 mm (P = 0.002), AT 4.6 ± 1.0 mm (P = 0.016); diabetic patients with neuropathy: PF 3.0 ± 0.8 mm (P < 0.0001), AT 4.9 ± 1.7 mm (P = 0.026)]. Joint mobility was significantly reduced [control subjects: 100.0 ± 10.0°; diabetic patients without neuropathy: 54.0 ± 29.4° (P < 0.0001); diabetic patients with neuropathy: 54.9 ± 17.2° (P < 0.0001)]. Loading times and force integrals under the heel and the metatarsals increased [metatarsal loading time (% stance phase): control subjects 88.2 ± 4.1%; diabetic patients without neuropathy 90.1 ± 4.7% (P = 0.146); diabetic patients with neuropathy 91.7 ± 6.6% (P = 0.048)].
Conclusions Increased thickness of Achilles tendon and plantar fascia, more evident in the presence of neuropathy, may contribute to an overall increase of tensile force and to the occurrence of an early Windlass mechanism, maintained throughout the whole gait cycle. This might play a significant role in the overall alteration of the biomechanics of the foot–ankle complex.
I fail to see how the data supports the conclusion (I have ordered but not yet read the full paper).
How does Increased thickness of Achilles tendon and plantar fascia, contribute to the occurrence of an early Windlass mechanism - from what I can read they measured tickness of the tissues and plantar loading times and forces --- they did not measure windlass timing!
__________________ Craig Payne
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Plantar fascia thickness is longitudinally associated with retinopathy and renal dysfunction: a prospective study from adolescence to adulthood.
Benitez-Aguirre PZ, Craig ME, Jenkins AJ, Gallego PH, Cusumano J, Duffin AC, Hing S, Donaghue KC. J Diabetes Sci Technol. 2012 Mar 1;6(2):348-55.
The aim was to study the longitudinal relationship between plantar fascia thickness (PFT) as a measure of tissue glycation and microvascular (MV) complications in young persons with type 1 diabetes (T1DM).
We conducted a prospective longitudinal cohort study of 152 (69 male) adolescents with T1DM who underwent repeated MV complications assessments and ultrasound measurements of PFT from baseline (1997-2002) until 2008. Retinopathy was assessed by 7-field stereoscopic fundal photography and nephropathy by albumin excretion rate (AER) from three timed overnight urine specimens. Longitudinal analysis was performed using generalized estimating equations (GEE).
Median (interquartile range) age at baseline was 15.1 (13.4-16.8) years, and median follow-up was 8.3 (7.0-9.5) years, with 4 (3-6) visits per patient. Glycemic control improved from baseline to final visit [glycated hemoglobin (HbA1c) 8.5% to 8.0%, respectively; p = .004]. Prevalence of retinopathy increased from 20% to 51% (p < .001) and early elevation of AER (>7.5 μg/min) increased from 26% to 29% (p = .2). A greater increase in PFT (mm/year) was associated with retinopathy at the final assessment (ΔPFT 1st vs. 2nd-4th quartiles, χ(2) = 9.87, p = .02). In multivariate GEE, greater PFT was longitudinally associated with retinopathy [odds ratio (OR) 4.6, 95% confidence interval (CI) 2.0-10.3] and early renal dysfunction (OR 3.2, CI 1.3-8.0) after adjusting for gender, blood pressure standard deviation scores, HbA1c, and total cholesterol.
In young people with T1DM, PFT was longitudinally associated with retinopathy and early renal dysfunction, highlighting the importance of early glycemic control and supporting the role of metabolic memory in MV complications. Measurement of PFT by ultrasound offers a noninvasive estimate of glycemic burden and tissue glycation.
Purpose/Hypothesis : Diabetes mellitus can result in deformity of the medial column of the foot. The plantar fascia functions to help create a stable medial column during walking via toe extension (windlass mechanism). Individuals with diabetes mellitus and peripheral neuropathy (DMPN) are known to have plantar fascia tissue changes, however it is unclear how the function of the plantar fascia is affected. The purpose of this study was to measure change in radiographic alignment between toe flat and extended position in subjects with DMPN and medial column deformity, and age- and weight-matched controls. We hypothesized that subjects with DMPN and medial column deformity would have impaired plantar fascia function resulting in less change in radiographic alignment from toe flat to toe extension.
Number of Subjects : 22 subjects; 12 with DMPN+deformity (7 male/5 female; age: 59±13yrs, weight: 110±24kg) and 10 controls (6 male/4 female; age: 59±15 yrs, weight: 104±32kg).
Materials/Methods : Subjects had weightbearing, lateral radiographs in a toe flat and 60 degree toe extended position. Forefoot and midfoot alignment (Meary’s angle, navicular height) and hindfoot alignment (calcaneal pitch, talar declination) were measured by a blinded rater using iSite PACS software. Within group and within position data were analyzed with a repeated measures ANOVA. Group comparison of change in alignment was analyzed with a t-test.
Results : The DMPN+deformity group demonstrated greater deformity in toe flat position compared to controls as evidenced by a more negative Meary’s angle (-20±11° versus -10±6°, p<.01), lower navicular height (28±9mm versus 40±7mm, p<.01), decreased calcaneal pitch (10±7° versus 21±6°, p≤.01) and larger talar declination (35±11° versus 21±5°, p<.01).
Amount of change in alignment between toe flat and extended conditions was significant in Meary’s angle (4±6° versus 10±3°, p≤.01), navicular height (6±4° versus 10±4°, p<.01) and calcaneal pitch (3±1° versus 2±2°, p<.01) in the DMPN+deformity and control groups. Talar declination changed between toe flat and extended conditions for control group (-5±4°, p<.01) but not the DMPN+deformity group (-1±5°, p=.32). In the DMPN+deformity group, the amount of change between conditions was smaller for Meary’s angle and navicular height compared to the control group (p<.03).
Conclusions : This study provides evidence of impaired plantar fascia function in individuals with DMPN+deformity. From toe flat to extended position, the DMPN+deformity demonstrated decreased navicular rise and forefoot plantarflexion compared to controls.
Clinical Relevance : Individuals with DMPN+deformity have impaired plantar fascia function when engaging the windlass mechanism that may contribute to progressive neuropathic foot deformity. Additional research is needed to determine if screening for plantar fascia function may assist in identifying individuals at-risk for onset or progression of neuropathic foot deformity.
Kidd and Kidd 1993, was a stroke of genius in its day, though the day has long gone. Perhaps the real story has never been told.......... I came in from work from Curtin one night,opened the fridge, took out a bottle of wine...... This is what I heard from over the room: "Put that back, right now, I have this idea in my head that wont go away". 13 hours later, we (that is she and me), left the word processor. By then it was too late for a glass, so I got showered, and went back to work. I wonder? How many of today's crowd realise how much was done with so little?
Honorary Research Associate, Institute for Human Evolution, University of Witwatersrand
Adjunct Associate Professor (Human and Comparative Anatomy), University of Western Sydney
Fellow of The Centre For Human Biology, The University of Western Australia
"Please God, deliver me whole from Creationists......."