Intrinsic Muscle Atrophy and Toe Deformity in the Diabetic Neuropathic Foot A magnetic resonance imaging study
ABSTRACT 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.
- SourceAvailable from: Jorge Futoshi Yamamoto
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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. "
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.Journal of Biomechanics 04/2014; 47(10). DOI:10.1016/j.jbiomech.2014.04.007 · 2.50 Impact Factor
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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). "
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.Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology 10/2013; 125(4). DOI:10.1016/j.clinph.2013.09.037 · 2.98 Impact Factor
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- "Two other studies did not find a relationship between IFM deterioration and MTPJ angle, where decreases in total muscle cross sectional area accounted for deformity in only 2 of 8 DMPN subjects, and where a semi-quantitative 5-point atrophy scale did not correlate with MTPJ angle (r = −0.14, P = 0.56) (Bus et al., 2002, 2009). Our study used a quantitative volumetric analysis, and measured both the adipose tissue infiltration and the remaining muscle tissue (Cheuy et al., 2013). "
ABSTRACT: Metatarsophalangeal joint deformity is associated with skin breakdown and amputation. The aims of this study were to compare intrinsic foot muscle deterioration ratios (ratio of adipose to muscle volume), and physical performance in subjects with diabetic neuropathy to controls, and determine their associations with 1) metatarsophalangeal joint angle and 2) history of foot ulcer. 23 diabetic, neuropathic subjects [59 (SD 10) years] and 12 age-matched controls [57 (SD 14) years] were studied. Radiographs and MRI were used to measure metatarsophalangeal joint angle and intrinsic foot muscle deterioration through tissue segmentation by image signal intensity. The Foot and Ankle Ability Measure evaluated physical performance. The diabetic, neuropathic group had a higher muscle deterioration ratio [1.6 (SD 1.2) vs. 0.3 (SD 0.2), P<0.001], and lower Foot and Ankle Ability Measure scores [65.1 (SD 24.4) vs. 98.3 (SD 3.3) %, P<0.01]. The correlation between muscle deterioration ratio and metatarsophalangeal joint angle was r=-0.51 (P=0.01) for all diabetic, neuropathic subjects, but increased to r=-0.81 (P<0.01) when only subjects with muscle deterioration ratios >1.0 were included. Muscle deterioration ratios in individuals with diabetic neuropathy were higher for those with a history of ulcers. Individuals with diabetic neuropathy had increased intrinsic foot muscle deterioration, which was associated with second metatarsophalangeal joint angle and history of ulceration. Additional research is required to understand how foot muscle deterioration interacts with other impairments leading to forefoot deformity and skin breakdown.Clinical biomechanics (Bristol, Avon) 10/2013; 28(9-10). DOI:10.1016/j.clinbiomech.2013.10.006 · 1.88 Impact Factor