Intrinsic Muscle Atrophy and Toe Deformity in the Diabetic Neuropathic Foot A magnetic resonance imaging study

Center for Locomotion Studies, Penn State University, University Park, Pennsylvania, USA.
Diabetes Care (Impact Factor: 8.42). 09/2002; 25(8):1444-50. DOI: 10.2337/diacare.25.8.1444
Source: PubMed


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.
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.
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.
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.

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Available from: Qing X Yang, Oct 27, 2015
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    • "Although there is some controversy about the dysfunction of leg muscles and joint stiffness in the aetiology of foot deformities, they are considered potential risks for plantar ulceration[14,21,22]. A probable reason is that the leg muscles interfere with the quality and control of locomotion, affecting the absorption and transmission of forces during foot rollover[20]and leading to an inefficient load distribution[23,24]. The combination of muscle and joint disorders that affect the feet and ankles[8,25262728has often been represented by the plantar pressure distribution during gait. "
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    ABSTRACT: Diabetic polyneuropathy is an insidious and long-term complication of this disease. Synergistic treatments and preventive actions are crucial because there are no clear boundaries for determining when health professionals should intervene or what intervention would best avoid the consequences of neuropathy. Until now, most therapies to any diabetic individual were applied only after the patient's limb was ulcerated or amputated. The loss of muscle and joint functions is recognized as the main cause of plantar overloading. However, if foot and ankle exercises are performed following the early diagnosis of diabetes, they can enable the patient to maintain sufficient residual function to interact with the environment. This paper summarizes the current knowledge about the musculoskeletal deficits and biomechanical alterations caused by neuropathy. It also describes the potential benefits of foot and ankle exercises for any diabetic patient that is not undergoing the plantar ulcer healing process. We concentrate on the prevention of the long-term deficits of neuropathy. We also discuss the main strategies and protocols of therapeutic exercises for joints and muscles with deficits, which are applicable to all diabetic patients with mild to moderate neuropathy. We describe further efforts in exploiting the applicability of assistive technologies to improve the adherence to an exercise program. Following the contemporary trends towards self-monitoring and self-care, we developed a software to monitor and promote personalized exercises with the aim of improving autonomous performance in daily living tasks. Initiatives to prevent the complications of functional diabetes are highly recommended before it is too late for the patient and there is no longer an opportunity to reverse the tragic consequences of neuropathy progression. This article is protected by copyright. All rights reserved.
    Full-text · Article · Oct 2015 · Diabetes/Metabolism Research and Reviews
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    • "Therefore, fiber type grouping or " enclosed " fibers detection can be an important criterion for the diagnosis of neurogenic disorders (Engel, 1970). The metabolic changes induced by glucose imbalance lead to accumulation of glycation end-products in muscle fibers (Abboud et al., 2000), reduction of nerve conduction velocity (Almeida et al., 2008) and cross-sectional area of lower limb muscles (Wang et al., 2006), and loss of muscle mass and strength (Andersen et al., 1997; Bus et al., 2002; Lesniewski et al., 2003; Ramji et al., 2007), which result in reduction of motor units. Diabetes mellitus is also responsible for an alteration of the intracellular calcium concentration (Nakagawa et al., 1989; Watanabe et al., 2012), leading to early apoptosis. "
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    ABSTRACT: The aim of this study was to investigate muscle׳s energy patterns and spectral properties of diabetic neuropathic individuals during gait cycle using wavelet approach. Twenty-one diabetic patients diagnosed with peripheral neuropathy, and 21 non-diabetic individuals were assessed during the whole gait cycle. Activation patterns of vastus lateralis, medial gastrocnemius and tibialis anterior were studied by means of bipolar surface EMG. The signal׳s energy and frequency were compared between groups using t-test. The energy was compared in each frequency band (7-542Hz) using ANOVAs for repeated measures for each group and each muscle. The diabetic individuals displayed lower energies in lower frequency bands for all muscles and higher energies in higher frequency bands for the extensors׳ muscles. They also showed lower total energy of gastrocnemius and a higher total energy of vastus, considering the whole gait cycle. The overall results suggest a change in the neuromuscular strategy of the main extensor muscles of the lower limb of diabetic patients to compensate the ankle extensor deficit to propel the body forward and accomplish the walking task.
    Full-text · Article · Apr 2014 · Journal of Biomechanics
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    • "Although motor neurons may be more resistant than sensory axons to the dysfunction and degeneration associated with diabetes mellitus (Zochodne and Ho, 1992; Yagihashi, 1997; Toth et al., 2004; Kennedy and Zochodne, 2005; Ramji et al., 2007; Dyck et al., 2011a,b), studies in animal and human models nonetheless have shown that the motor system is affected (Hansen and Ballantyne, 1977; Bril et al., 1996; Ramji et al., 2007; Said et al., 2008; Souayah et al., 2009; Allen et al., 2013). Indeed, whereas sensory dysfunction can lead to injury resulting from lack of sensation, ulceration and amputation; dysfunction of the motor nervous system is associated with muscle atrophy and weakness (Andersen et al., 2004; Bus et al., 2002). Muscle weakness may therefore contribute to the higher risk of developing physical disability in patients with diabetes (Gregg et al., 2000). "
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    ABSTRACT: To assess the number and properties of motor units in an upper and lower limb muscle (tibialis anterior [TA] and first dorsal interosseous [FDI]) in human diabetic polyneuropathy (DPN) using decomposition-based quantitative electromyography (DQEMG). DQEMG protocols were performed in the TA and FDI of 12 patients with confirmed diabetes mellitus and associated DPN, as well as 12 age-matched control participants. Maximal dorsiflexion strength was also assessed using a dynamometer. In both muscles, patients with DPN had significantly reduced motor unit number estimates (MUNEs) (ΔTA ∼45%; ΔFDI ∼30%), compound muscle action potentials (CMAPs) (ΔTA ∼30%; ΔFDI ∼20%), and mean firing rates were reduced (ΔTA ∼15%; ΔFDI ∼15%) compared to controls (p<0.05). For the TA, patients with DPN had larger mean surface motor unit potentials (SMUPs) (ΔTA ∼40%; p<0.05), whereas in the FDI no differences were found (p>0.05). DPN may result in motor unit loss, remodeling, and altered firing rate patterns. The magnitude of changes in the neuromuscular properties of DPN patients are muscle dependent and reflect a length-dependent disease progression. DQEMG may be a clinically useful technique in identifying the presence and severity of neuromuscular pathophysiology and tracking disease progression in DPN.
    Full-text · Article · Oct 2013 · Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology
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