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Effect of diabetic neuropathy severity classified by a fuzzy model in muscle dynamics during gait

BACKGROUND: Electromyography (EMG) alterations during gait, supposedly caused by diabetic sensorimotor polyneuropathy, are subtle and still inconsistent, due to difficulties in defining homogeneous experimental groups with a clear definition of disease stages. Since evaluating these patients involve...

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Detalles Bibliográficos
Autores principales: Watari, Ricky, Sartor, Cristina D, Picon, Andreja P, Butugan, Marco K, Amorim, Cesar F, Ortega, Neli RS, Sacco, Isabel CN
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3922253/
https://www.ncbi.nlm.nih.gov/pubmed/24507153
http://dx.doi.org/10.1186/1743-0003-11-11
Descripción
Sumario:BACKGROUND: Electromyography (EMG) alterations during gait, supposedly caused by diabetic sensorimotor polyneuropathy, are subtle and still inconsistent, due to difficulties in defining homogeneous experimental groups with a clear definition of disease stages. Since evaluating these patients involve many uncertainties, the use of a fuzzy model could enable a better discrimination among different stages of diabetic polyneuropathy and lead to a clarification of when changes in muscle activation start occurring. The aim of this study was to investigate EMG patterns during gait in diabetic individuals with different stages of DSP severity, classified by a fuzzy system. METHODS: 147 subjects were divided into a control group (n = 30) and four diabetic groups: absent (n = 43), mild (n = 30), moderate (n = 16), and severe (n = 28) neuropathy, classified by a fuzzy model. The EMG activity of the vastus lateralis, tibialis anterior, and gastrocnemius medialis were measured during gait. Temporal and relative magnitude variables were compared among groups using ANOVA tests. RESULTS: Muscle activity changes are present even before an established neural involvement, with delay in vastus lateralis peak and lower tibialis anterior relative magnitude. These alterations suggest an impaired ankle shock absorption mechanism, with compensation at the knee. This condition seems to be more pronounced in higher degrees of neuropathy, as there is an increased vastus lateralis activity in the mild and severe neuropathy groups. Tibialis anterior onset at terminal stance was anticipated in all diabetic groups; at higher degrees of neuropathy, the gastrocnemius medialis exhibited activity reduction and peak delay. CONCLUSION: EMG alterations in the vastus lateralis and tibialis anterior occur even in the absence of diabetic neuropathy and in mild neuropathic subjects, seemingly causing changes in the shock absorption mechanisms at the heel strike. These changes increase with the onset of neural impairments, and the gastrocnemius medialis starts presenting altered activity in the later stages of the disease (moderate and severe neuropathy). The degree of severity of diabetic neuropathy must be taken into account when analyzing diabetic patients’ biomechanical patterns of locomotion; we recommend the use of a fuzzy model for classification of disease stages.