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Introducción: la espasticidad, como signo clínico de daño de motoneurona superior, cobra gran importancia al momento de definir su impacto en el proceso rehabilitador. Los objetivos de esta revisión bibliográfica son: analizar la evolución de la espasticidad como concepto, describir los hallazgos actuales en relación con su fisiopatología y analizar su importancia en el proceso rehabilitador. Métodos: búsqueda bibliográfica durante el segundo semestre del 2017 en bases de datos Pubmed, Scielo, Cochrane y Google Académico, utilizando los términos MeSH: muscle spasticity, physiopathology y stroke. Los límites de búsqueda fueron: textos completos en idioma inglés y español, en humanos y publicados durante los últimos cinco años. Resultados: la fisiopatología de la espasticidad no es causada por un solo mecanismo, sino más bien una intrincada cadena de alteraciones en diferentes redes nerviosas interdependientes. Existiendo dos mecanismos principales: la alteración del control espinal y suprasegmentario y los cambios en las propiedades del sistema músculo-esquelético. Conclusión: la evidencia científica es amplia y aborda el concepto de espasticidad, sus implicancias fisiopatológicas y clínicas. Sin embargo, futuras investigaciones deberían orientar y apoyar las decisiones del equipo rehabilitador, en relación con el manejo clínico.

Neuroinflammation is a common event in degenerative diseases of the central and peripheral nervous system, triggered by alterations in the immune system or inflammatory cascade. The pathophysiology of these disorders is multifactorial, whereby the therapy available has low clinical efficacy. This review propounds the relationship between the deregulation of T helper cells and hypoxia, mainly Th17 and HIF-1α molecular pathways, events that are involved in the occurrence of the neuroinflammation. The clinical expression of neuroinflammation is included in prevalent pathologies such as multiple sclerosis, Guillain–Barré syndrome, and Alzheimer’s disease, among others. In addition, therapeutic targets are analyzed in relation to the pathways that induced neuroinflammation.

Introduction: Because of the the complex physiopathology of spasticity, it is distinguished as one of the most significant positive clinical signs of upper motor neuron syndrome, constituting a clinical feature that has great impact in the neurorehabilitation setting. Thus, the current study aimed to determine the prevalence, onset, evolution, and prediction of spasticity after a stroke. Materials and Methods: A correlational, longitudinal design was used. A total of 136 patients were evaluated at the following times: 10 days (T1), 3 months (T2), and 12 months (T3) poststroke. The initial evaluation included sociodemographic and clinical data (T1). Muscle tone was measured (T1, T2, and T3) using the Modified Ashworth Scale. Results: The prevalence of poststroke spasticity in the elbow was 37.5% at T1 and 57.4% at T2 and T3. Among patients with motor damage, the onset of spasticity occurred at T1 in 44.7%, between T1 and T2 in 23.7%, and between T2 and T3 in 0.9%. Significant predictors of the alteration in muscular tone for at least two of the evaluation times were ethnic self-classification, type, area, extent of stroke, and number of sessions. Conclusions: Spasticity onset occurs during the first 10 days after a stroke. More clinical than sociodemographic variables predicted spasticity.

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