Multi-joint foot kinetics during walking in people with Diabetes Mellitus and peripheral neuropathy
Introduction
As many as 50% of people with Diabetes Mellitus (DM) will develop peripheral neuropathy (PN) (Gordois et al., 2003). In the foot, the hallmark signs of DMPN are loss of protective sensation, decreased non-contractile tissue extensibility, and intrinsic muscle atrophy and fatty infiltration (Brownlee, 1992, Cheuy et al., 2013, Pham et al., 2000). The foot-specific effects of PN are principle factors in the development of deformity, elevated plantar pressures and the increased risk for plantar ulceration (Cheuy et al., 2013, Crawford et al., 2007, Mueller et al., 2003).
The loss of intrinsic foot muscle function in people with DMPN is of particular concern because muscle atrophy is one of the earliest detectable precursors of abnormal foot function leading to pathology (Greenman et al., 2005). In healthy adults, contraction of intrinsic foot muscles attenuates, and can reverse, longitudinal arch deformation under increasingly loaded conditions (Kelly et al., 2014). Degradation of intrinsic muscle function in people with DMPN may impair the ability of the midfoot to produce positive work and attain a rigid foot posture during the push off phase of gait. Interestingly, an investigation of people with DMPN and medial column deformity demonstrated decreased forefoot plantarflexion (relative to rearfoot) (i.e. arch deformation) during single-leg heel rise tasks in comparison to healthy controls (Hastings et al., 2014). This kinematic finding suggests midfoot power produced by the interaction of the muscles and ligaments supporting the medial longitudinal arch is decreased, which may contribute to deformity. Yet, specific knowledge of diabetic foot kinetics (i.e. midfoot moments and power), during a common task like walking and prior to the onset of deformity, is limited.
Understanding of in-vivo foot kinetics in people with DMPN is derived from investigations utilizing single-segment foot modeling approaches. These studies demonstrate that people with DMPN have reduced peak ankle power generation during gait (Mueller et al., 1994, Rao et al., 2006, Rao et al., 2010, Yavuzer et al., 2006). Multi-segment foot modeling studies that assess both midfoot (MF) and rearfoot (RF) power have only been performed in the healthy adolescent population. These studies demonstrate that MF power contributes to forward propulsion during gait and that single-segment foot modeling overestimates RF power generation (Dixon et al., 2012, MacWilliams et al., 2003). Multi-joint foot modeling offers specific insight into muscle performance at the MF and a more accurate representation of RF function. The assessment of multi-joint foot kinetics is an advancement of single segment modeling approaches and a necessary next step when evaluating pathology at the forefoot and MF. Yet, an investigation of multi-joint power and work has not been performed in people with DMPN or healthy adults.
It is hypothesized that both RF and MF power generation are deficient during gait in people with DMPN. A reduction of MF power generation or positive work, as well as a greater amount of power absorption, would indicate less active muscle support of the midfoot, and potentially greater loading on passive structures. If supported, this finding in patients prior to deformity would link anticipated foot muscle and ligament changes to foot biomechanics during walking. Pathologies such as toe/midfoot deformity and forefoot tissue breakdown that are catalyzed by neuropathy may be expedited by the repetition of abnormal MF function during daily weight-bearing activity.
The purpose of this study was to compare the multi-joint kinetic profile of people with DMPN without deformity or ulceration, to healthy matched controls during walking. It was anticipated that people with DMPN would demonstrate 1) decreased MF positive work, 2) increased MF and RF negative peak power and 3) an increased negative work ratio at both the MF and RF. Detection of an abnormal kinetic pattern of MF function prior to the development of pathology may guide formulation of early foot-specific interventions aimed at reducing the progression of deformity and disability.
Section snippets
Subjects
Thirty subjects, 15 people with DMPN and 15 healthy matched controls (age, gender, BMI), participated in this case control study (Table 1). Sample size was determined from kinetic data of a pilot study of people with DMPN and controls (N=6) [α=0.05; 1−β=0.8; Cohen's d range 1.0–5.2] and is consistent with prior investigations of DMPN foot function (Rao et al., 2007).
Subjects in the DMPN group were recruited from a university health system. Review of medical records confirmed a history of DM
Power
People with DMPN demonstrated a trend of greater MF negative peak power [DMPN 0.19 (0.12) vs. Control 0.12 (0.05) W/kg; d=0.76; p=0.05] and a trend of reduced MF positive peak power [DMPN 0.29 (0.15) vs. Control 0.38 (0.12) W/kg; r=0.39; p=0.03] (Fig. 2c, Table 2). These MF power findings equated to between-group percent differences of 45% and 27% for negative and positive peak power, respectively. At the RF, the DMPN group had significantly greater negative peak power [DMPN 1.1 (0.5) vs.
Discussion
This is the first study to measure multi-joint foot kinetics in people with DMPN and a healthy adult control group. The key findings of this study include observation of reduced MF peak positive power and work, increased MF and RF negative peak powers, and a greater proportion of negative work at both the MF and RF in people with DMPN. The detected multi-joint kinetic profile of people with DMPN extends information about DMPN foot function prior to deformity or tissue breakdown that was not
Conflict of interest statement
The authors have no conflict of interests.
Acknowledgments
The University of Rochester, School of Nursing Dean's Fellowship supported this study. We thank Gary Noronha, MD Sally Nordquist, RN and Mark Cloninger, NP for their assistance with recruitment.
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