Gait characteristics of people with diabetes-related peripheral neuropathy, with and without a history of ulceration

Highlights

• Biomechanical alterations are believed important in diabetic foot ulceration.

• Clinical and gait measures were taken in people diabetes-related ulceration.

• Altered ankle function was associated with past neuropathic plantar foot ulceration.

• Risk of biomechanically induced ulceration may be linked with neuropathy severity.

Abstract

Biomechanical alterations in diabetes are believed to contribute to plantar neuropathic ulceration. This exploratory study documents clinical measures of flexibility and strength, alongside three-dimensional biomechanical gait data of the lower limb, in 10 patients with a history of neuropathic ulceration (DNU; n = 10). Comparative data is presented from age and gender matched groups with; diabetes peripheral neuropathy and no ulcer history (DWN; n = 10), diabetes and no peripheral neuropathy (DNN; n = 10) and a non-diabetes reference group (NOND; n = 10). Biomechanical data were collected at a comfortable walking speed with a Vicon motion analysis system. Clinical measures showed a non-significant trend toward decreased static range of motion at the ankle and first metatarsophalangeal joints, with worsening neuropathy status. Of the diabetes groups, knee and ankle strength was significantly lower in those with an ulcer history (p = 0.01–0.03), with the exception of knee extension. In the DNU group, walking speed was on average 0.17 ms slower compared to NOND (p = 0.04). The DNU group demonstrated a lower range of motion than NOND at the: hips (frontal plane, by 25%: p = 0.03); hips and knees (transverse plane, 31%: p = 0.01 and 32%: p < 0.01); ankles (sagittal plane, 22%: p < 0.01) and first metatarsophalangeal joints (sagittal plane, 32%: p = 0.01), with less foot rotation (24%: p = 0.04). Kinetic alterations in DNU included lower: ankle maximum power (21%: p = 0.03) and vertical ground reaction force 2nd peak (6%: p < 0.01). The study findings identified gait alterations in people with clinically severe peripheral neuropathy and related plantar foot ulcer history. Further research is needed to explore potential casual pathways.

Introduction

Biomechanical alterations of the lower limb in diabetes are believed to be important in the etiology of plantar foot ulceration, although the mechanisms for this are not well understood [1], [2]. Diabetes-related foot ulceration is a major medical, social and economic problem, with an estimated 15% of people with diabetes likely to develop a foot ulcer during their lifetime [3]. An estimated 85% of all diabetes-related amputations are preceded by a foot ulcer, therefore great emphasis is placed on prevention and targeted management of this problem [4].

It is well known that chronic hyperglycaemia causes a heterogeneous mix of neuro-motor and connective tissue changes affecting the lower limb. These are expressed clinically in a number of ways, including loss of sensation, reduced strength, altered motor control, reduced static joint range of motion and thickening of soft tissues [5], [6], [7]. It has been hypothesized that these elements interact to alter biomechanical function and create damaging patterns of plantar loading although the pathways for this are unclear. Important questions remain regarding the exact cause and nature of diabetes-related biomechanical changes and how they might be implicated in the development of foot ulceration.

Two recent reviews of gait characteristics in diabetes concur that the adoption of conservative strategies are typically employed by those affected by peripheral neuropathy, including slower walking speeds, wider base of gait, prolonged double support time and greater step variability [1], [2]. Elevated plantar pressures, a moderate risk factor for ulceration, occur in diabetic neuropathy although the exact reasons behind this have been somewhat elusive [8], [9]. Research into kinematic gait changes in this clinical population has produced inconsistent results. One study reported no difference in gait ankle motion in participants with diabetic peripheral neuropathy [10] and another concurred when the confounding issue of walking speed was controlled for [11]. In contrast, reduced ankle motion during gait has been shown by others when consistency of walking speed was maintained [12].

Reports from gait and ulceration studies have also been inconsistent, with findings ranging from reduced dynamic motion, peak power and peak moment at the ankle [13], lower knee joint angle, vertical ground reaction force and anteroposterior force [14] and reduced gait dorsiflexion at the first metatarsophalangeal joint [15], to reports of no changes in gait motion at the ankle [15]. Research investigating gait biomechanics and ulceration is limited, however, in that; only a small number of studies nominate a group with an ulcer history [13], [14], [15], older motion analysis systems have been superseded by more recent technological advances [13], [14] and only a few studies, with relatively small and potentially underpowered sample sizes, have evaluated the entire lower limb [13], [14].

With recent developments in motion analysis technology, including improved multi-segment foot models, studies are emerging that support links between peripheral neuropathy and reductions in gait excursions of the ankle complex and sub-segments of the foot [16], [17]. Given the importance of biomechanical alterations in the development of diabetic neuropathic foot ulceration, and the inconsistency of the available literature, further research is required. This current study is exploratory in nature, aiming to document comprehensive lower limb three-dimensional biomechanical data in patients with a history of neuropathic ulceration. Data on groups of participants with and without neuropathy, and without diabetes is reported for comparative observation.