Diabetes care · 2009
Role of intrinsic muscle atrophy in the etiology of claw toe deformity in diabetic neuropathy may not be as straightforward as widely believed.
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Bus Sicco A, Maas Mario, Michels Robert P J, Levi Marcel
Аннотация
OBJECTIVE: Clawing of the toes in the diabetic neuropathic foot is believed to be caused by muscle imbalance resulting from intrinsic muscle atrophy. However, experimental data that support this mechanism are lacking. The aim of this study was to evaluate this hypothesis using magnetic resonance imaging (MRI).
RESEARCH DESIGN AND METHODS: In 20 neuropathic diabetic patients, 10 with claw toe deformity and 10 with normally aligned toes, multiple plane images of the foot and lower leg were acquired using T1-weighted spin-echo MRI. Atrophy of the intrinsic and extrinsic muscles controlling the toes was assessed using a semiquantitative 5-point atrophy scale. An intrinsic-to-extrinsic foot muscle imbalance score was derived from these atrophy scores, and correlation coefficients were established.
RESULTS: The mean +/- SD intrinsic muscle atrophy score was 3.1 +/- 1.1 for the toe deformity group and 2.6 +/- 1.2 for the non-deformity group (not significantly different). The intrinsic muscle atrophy score was not significantly correlated with degree of toe deformity (r = -0.18). The muscle imbalance score was not significantly different between study groups and was not significantly correlated with degree of toe deformity (r = -0.14).
CONCLUSIONS: Neither intrinsic muscle atrophy nor muscle imbalance discriminated between neuropathic patients with or without claw toe deformity, suggesting that the role of these muscle factors in claw toe development may not be primary or as straightforward as previously believed. These findings shed new light on the etiology of foot deformity in diabetes and suggest a more complex nature of development, potentially involving anatomical and physiological predisposing factors.
RESEARCH DESIGN AND METHODS: In 20 neuropathic diabetic patients, 10 with claw toe deformity and 10 with normally aligned toes, multiple plane images of the foot and lower leg were acquired using T1-weighted spin-echo MRI. Atrophy of the intrinsic and extrinsic muscles controlling the toes was assessed using a semiquantitative 5-point atrophy scale. An intrinsic-to-extrinsic foot muscle imbalance score was derived from these atrophy scores, and correlation coefficients were established.
RESULTS: The mean +/- SD intrinsic muscle atrophy score was 3.1 +/- 1.1 for the toe deformity group and 2.6 +/- 1.2 for the non-deformity group (not significantly different). The intrinsic muscle atrophy score was not significantly correlated with degree of toe deformity (r = -0.18). The muscle imbalance score was not significantly different between study groups and was not significantly correlated with degree of toe deformity (r = -0.14).
CONCLUSIONS: Neither intrinsic muscle atrophy nor muscle imbalance discriminated between neuropathic patients with or without claw toe deformity, suggesting that the role of these muscle factors in claw toe development may not be primary or as straightforward as previously believed. These findings shed new light on the etiology of foot deformity in diabetes and suggest a more complex nature of development, potentially involving anatomical and physiological predisposing factors.