Effect of Kinesio Taping on gastrocnemius activity and ankle range of movement during gait in healthy adults: A randomized controlled trial.

OBJECTIVE: To examine the effect of KT on gastrocnemius surface electromyography (SEMG) activity and ankle range of motion during walking in healthy subjects. DESIGN: Randomized controlled trial, with concealed allocation and assessor blinding. SETTING: University Biomechanics Laboratory. PARTICIPANTS: Thirty six healthy physiotherapy students were randomized to KT or control group. OUTCOME MEASURES: At baseline and immediately after 72 h with the tape in situ: amplitude of LG SEMG activity during the stance phase, duration of the LG activity, onset and offset times of LG activity, ankle plantar- and dorsiflexion peaks, and the cadence of gait. RESULTS: ANOVA revealed a significant time × intervention interaction effect across two variables: duration of LG activation, F(1, 33) = 4.71, p = .037, η = .015; and onset F(1, 33) = 7.92, p = .008, η = .037. KT group showed significantly shorter duration of the LG activity as compared with control, and similar results were observed when comparing the onset of LG activation. No statistically significant differences between both groups were noted in the rest of the outcomes. CONCLUSION: KT does significantly shorten the duration of the LG activity during gait when applied 72 h in healthy adults. However, this result was not accompanied by a significant reduction in the amplitude of LG SEMG activity.

[Sleep disorders associated to prion diseases]. / El sueño en las enfermedades priónicas.

INTRODUCTION: Description of sleep disorders associated to human prion diseases. DEVELOPMENT: The recent advances on pathology, genetics and immunocytochemistry are an outstanding contribution to the knowledge of transmissible spongiform encephalopathies and identification of possible new variants. Despite decades of research, human prion diseases have remained enigmatic in many aspects. Among these, the intricate connection between infectivity and genetics, genotype-phenotype correlation, pathogenesis of brain damage and in some cases its proven dependence on the genotypic combination of a pathogenic mutation and a polymorphism. Regarding this subject we should take into consideration that Fatal Familial Insomnia (FFI) appears as an ideal model situation for answering some of these problems because of its distinctive clinicopathological phenotype based on a specific genotype as well as its transmissibility. This disease has recently enlarged the group of prion diseases. It is linked to a mutation at codon 178 of the prion protein gene, coupled with the methionine codon at position 129, the site of a methionine/valine polymorphism. The clinical aspects of FFI include a peculiar sleep-wake disorder and a autonomic hyperactivity associated with vegetative and hormonal circadian rhythm disregulation, besides cognitive and motor alteration, and it is related to the selective atrophy of limbic part of the thalamus. EEG conventional sleep studies and 24-hour polygraphic recordings can provide proof of early disappearance sleep spindles and the disturbances of sleep, which typify the disease. Epidemiologic, pathophysiologic, and histopathological aspects are also mentioned. Finally we remark the major neurophysiological features of Creutzfeldt-Jakob disease and Morvan's chorea.

El sueño en las enfermedades priónicas / Sleep disorders associated to prion diseases

Introducción. En este artículo describimos los trastornos del sueño relacionados con las enfermedades priónicas en humanos. Desarrollo. Los recientes avances en patología, genética e inmunocitohistoquimia contribuyen destacadamente en el conocimiento de las encefalopatías espongiformes y en la identificación de nuevas variantes. Tras décadas de investigación, las enfermedades priónicas siguen manteniendo en parte su carácter enigmático. Entre otros aspectos, destacan la relación entre infectividad y genética, la correlación genotipo-fenotipo, la patogénesis del daño cerebral y, en algunos casos, su dependencia respecto a un genotipo caracterizado por una determinada mutación y un polimorfismo genético. En este sentido, el insomnio familiar fatal surge como un modelo ideal para dar respuesta a algunos interrogantes debido a su peculiar fenotipo clinicopatológico, relacionado con un genotipo específico, y a su transmisibilidad. Esta enfermedad se ha incorporado recientemente al grupo de las enfermedades priónicas. Está relacionada con una mutación del codón 178 del gen de la proteína priónica, en presencia de una homocigosis metionina/metionina en el codón 129, posición del polimorfismo metionina/valina. Las características clínicas del insomnio familiar fatal incluyen un deterioro de la vigilia y el sueño, hiperactividad autónoma con desequilibrio de los ritmos circadianos hormonales y vegetativos, así como un deterioro motor y cognitivo, que se relaciona con una atrofia selectiva de la región límbica talámica. Los estudios EEG convencionales de sueño y la monitorización poligráfica durante 24 horas pueden mostrar la desaparición precoz de spindles y las alteraciones características del sueño, tipificando la enfermedad. Los aspectos epidemiológicos, fisiopatológicos e histopatológicos de esta enfermedad también son mencionados. Por último, destacamos las principales características neurofisiológicas de la enfermedad de CreutzfeldtJakob y la corea de Morvan (AU)