The foot, via its structure, has the ability to adapt to various conditions, such as increased body weight and walking on uneven terrain. It is also well known that diabetic foot ulcers occur at sites of high plantar pressures that result from an alternate foot structure due to diabetic neuropathy. The most common sites of ulceration occur under the metatarsal heads and the plantar aspect of the big toe.
The aim of this study was to observe the peak plantar pressures and contact times at the above anatomical sites under the effect of increased weight in patients with diabetic neuropathy.
We recruited two groups of type 2 diabetic patients. Group A (n = 10) was composed of patients with diabetic neuropathy (vibration perception threshold [VPT] >25 V, insensitivity 5.07 SW monofilament 10 g), and group B (n = 10) was composed of patients without neuropathy, comparable in age, sex, BMI, and duration of diabetes. Using the Foot-Scan RS International barefoot pressure measurement system, peak plantar foot pressures were compared under three conditions. Baseline (C1) involved measurements without any additional weight. The second and third test conditions involved pressure measurements with an additional 5 kg (C2) and 8.5 kg (C3), respectively, evenly distributed in the pockets of a workout vest. Data recorded from under the metatarsal heads and big toe were used for analysis, and the mean peak pressures (MPP) in N/cm2 and mean contact times (MCT) in milliseconds were obtained.
Differences among groups regarding continuous variables were analyzed with Student’s t test or Mann-Whitney U test and Fisher’s exact test for categorical variables, as appropriate. Differences in MPP and MCT during the three test conditions were estimated by Friedman’s and Wilcoxon’s tests. P < 0.05 (two tailed) was considered significant. In group A there was a significant increase in mean peak plantar foot pressures for each incremental increase of weight (MPP: P < 0.001, C1 vs. C2: P = 0.017, C1 vs. C3: P = 0.005, C2 vs. C3: P = 0.005). The mean contact times were also significantly increased in patients with diabetic neuropathy (MCT: P = 0.007, C1 vs. C3: P = 0.037, C2 vs. C3: P = 0.022). In group B, there were no statistically significant differences between the three conditions (MPP: P = 0.74, MCT: P = 0.57).
The amount of increased weight must play a key role in the peak plantar pressures. With a relatively low amount of increased weight, in contrast to previous reports (1,2), our study suggests that there must be a factor or mechanism that makes the foot able to compensate for this added weight in non-neuropathic subjects. There must be an individual cutoff point for this “compensation,” but this requires further investigation. In addition, our study suggests that the ability of foot compensation to added weight must be lost or reduced in neuropathic patients.
Patients with long-term diabetes and neuropathy have been noted to have fine structural changes in their Achilles tendons when observed under electron microscopy (3). This suggests that structural reorganization could be the result of nonenzymatic glycosylation (NEG). Increased rates of NEG reduce the shock-absorbing capacity of plantar tissues. Limited joint motion (LJM) is often associated with neuropathy (4,5), and when this mobility is impaired by NEG of collagen, the foot can no longer function as a mobile adapter. As the joints cannot move adequately to accommodate for increased weight, shearing forces increase.
Collectively, dysfunction of foot compensation in added weight results in elevated mean peak plantar pressures and mean contact times in patients with diabetic neuropathy.
References
Address correspondence to Loukas Thiaspras, BSC, 6 Peloponnisou St, Argyroupolis, 164 51 Athens, Greece. E-mail: [email protected].
