Welcome to the Podiatry Arena forums, for communication between foot health professionals about podiatry and related topics.
You are currently viewing our podiatry forum as a guest which gives you limited access to view all podiatry discussions and access our other features. By joining our free global community of Podiatrists and other interested foot health care professionals you will have access to post podiatry topics (answer and ask questions), communicate privately with other members (PM), upload content, view attachments, receive a weekly email update of new discussions, earn CPD points and access many other special features. Registered users do not get displayed the advertisments in posted messages. Registration is fast, simple and absolutely free so please, join our global Podiatry community today!
If you have any problems with the registration process or your account login, please contact contact us.
Atrophy of Foot Muscles in Diabetic Patients Can Be Detected With Ultrasonography
Kaare Severinsen, Annette Obel, Johannes Jakobsen and Henning Andersen Diabetes Care 30:3053-3057, 2007
Quote:
OBJECTIVE—To establish a bedside test with ultrasonography for evaluation of foot muscle atrophy in diabetic patients.
RESEARCH DESIGN AND METHODS—Thickness and cross-sectional area (CSA) of the extensor digitorum brevis muscle (EDB) and of the muscles of the first interstitium (MILs) were determined in 26 diabetic patients and in 26 matched control subjects using ultrasonography. To estimate the validity, findings were related to the total volume of all foot muscles determined at magnetic resonance imaging (MRI-FMvol). Furthermore, the relations of ultrasonographic estimates to nerve conduction, sensory perception thresholds, and clinical condition were established.
RESULTS—In diabetic patients, the ultrasonographic thickness of EDB (U-EDBt) was (means ± SD) 6.4 ± 2.1 vs. 9.0 ± 1.0 mm in control subjects (P < 0.001), the thickness of MIL (U-MILt) was 29.6 ± 8.3 vs. 40.2 ± 3.6 mm in control subjects (P < 0.001), and the CSA of EDB (U-EDBCSA) was 116 ± 65 vs. 214 ± 38 mm2 in control subjects (P < 0.001). The MRI-FMvol was directly related to U-EDBt (r = 0.77), U-MILt (r = 0.71), and U-EDBCSA (r = 0.74). U-EDBt and U-MILt were thinner in neuropathic than in nonneuropathic diabetic patients (5.8 ± 2.1 vs. 7.5 ± 1.7 mm [P < 0.05] and 28.3 ± 8.8 vs. 35.6 ± 4.3 mm [P < 0.03], respectively).
CONCLUSIONS—Atrophy of intrinsic foot muscles determined at ultrasonography is directly related to foot muscle volume determined by MRI and to various measures of diabetic neuropathy. Ultrasonography seems to be useful for detection of foot muscle atrophy in diabetes.
Intrinsic Muscle Atrophy and Toe Deformity in the Diabetic Neuropathic Foot
A magnetic resonance imaging study
Sicco A. Bus, Qing X. Yang, Jinghua H. Wang, Michael B. Smith, Roshna Wunderlich, and Peter R. Cavanagh Diabetes Care 25:1444-1450, 2002
Quote:
OBJECTIVE—The objectives of this study were to compare intrinsic foot muscle cross-sectional area (CSA) in patients with diabetic polyneuropathy and nondiabetic control subjects and to examine the association between intrinsic muscle CSA and clawing/hammering of the toes in neuropathic feet.
RESEARCH DESIGN AND METHODS—High-resolution T2-weighted fast spin-echo images and parametric T2 multiple spin-echo images were acquired using multiple spin-echo magnetic resonance imaging (MRI) of frontal plane sections of the metatarsal region of the foot in a sample of eight individuals with diabetic polyneuropathy and eight age- and sex-matched nonneuropathic nondiabetic control subjects. The configuration of joints of the second toe was obtained using a three-dimensional contact digitizer.
RESULTS—Remarkable atrophy was found in all the intrinsic muscles of neuropathic subjects as compared with nondiabetic control subjects. Quantitative T2 analysis showed a 73% decrease in muscle tissue CSA distally in the neuropathic subjects. Muscle comprised only 8.3 ± 2.9% (means ± SD) of total foot CSA compared with 30.8 ± 3.9% in control subjects. No significant differences were found between the groups in the metatarso-phalangeal and proximal and distal interphalangeal joint angles of the second ray. Moreover, clawing/hammering of the toes was found in only two of eight neuropathic subjects.
CONCLUSIONS—Although sensory neuropathy is often emphasized in considerations of diabetic foot pathology, our results show that the consequences of motor neuropathy in the feet are profound in people with diabetes. This has implications for foot function and may play a significant role in postural instability. However, intrinsic muscle atrophy does not necessarily appear to imply toe deformity.
The role of intrinsic muscle atrophy in the etiology of claw toe deformity in diabetes may not be as straightforward as widely believed.
Bus SA, Maas M, Michels RP, Levi M. Diabetes Care. 2009 Mar 11. [Epub ahead of print]
Quote:
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 supports this mechanism is lacking. The aim of this study was to evaluate this hypothesis using magnetic resonance imaging (MRI).
Research Design and Methods: In twenty neuropathic diabetic patients, ten with claw toe deformity and ten 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 were assessed using a semi-quantitative 5-point atrophy scale. An intrinsic-to-extrinsic foot muscle imbalance score was derived from these atrophy scores and correlation coefficients were established.
Results: 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). Intrinsic muscle atrophy score was not correlated with degree of toe deformity (r = -0.18). Muscle imbalance score was not significantly different between study groups and not 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. This suggests 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.
Foot Muscle Energy Reserves In Diabetic Patients Without And With Clinical Peripheral Neuropathy.
Dinh T, Doupis J, Lyons TE, Kuchibhotla S, Julliard W, Gnardellis C, Rosenblum BI, Wang X, Giurini JM, Greenman RL, Veves A. Diabetes Care. 2009 Jun 9. [Epub ahead of print]
Quote:
Objective. To investigate changes in the foot muscle energy reserves in diabetic non-neuropathic and neuropathic patients. Research Design and Methods. We measured the phosphocreatinine/inorganic phosphate (PCr/Pi) ratio, total (31)P concentration and the Lipid/Water ratio in the muscles in the metatarsal head region using MRI spectroscopy in healthy control subjects and non-neuropathic and neuropathic diabetic patients. Results. The PCr/Pi ratio was higher in the controls (3.23 +/- 0.43) followed by the non-neuropathic group (2.61 +/- 0.36) while it was lowest in the neuropathic group (0.60 +/- 1.02) (p <0.0001). There were no differences in total (31)P concentration and Lipid/Water ratio between the control and non-neuropathic groups but both measurements were different in the neuropathic group (p <0.0001). Conclusions. Resting foot muscle energy reserves are affected before the development of peripheral diabetic neuropathy and are associated with the endothelial dysfunction and inflammation.
Intrinsic muscle atrophy in diabetes
Linear Mode
