Luisa Fernanda García-Salazar

Objetivo: Determinar quais biomarcadores têm sido relacionados à funcionalidade do membro superior na fase aguda, subaguda ou crônica de pessoas que sofreram acidente vascular cerebral (AVC) isquêmico ou hemorrágico. Métodos: Protocolo de revisão sistemática, registrado no PROSPERO (CRD42021274244), com busca de dados sem corte de tempo na PubMed, PubMed PMC, Embase, Web of Science, Scopus, Cinahl e ProQuest. Os revisores avaliarão independentemente títulos, resumos e artigos de texto completo recuperados de bases de dados para identificar estudos potencialmente elegíveis. Os artigos relevantes serão avaliados quanto ao risco de viés e qualidade por meio do uso da ferramenta Quality In Prognosis Studies (QUIPS). A revisão incluirá estudos primários (original), do tipo Ensaios Controlados ou Observacionais (transversal, caso-controle ou estudos longitudinais) com análises de biomarcadores nas diferentes fases de AVC quanto à funcionalidade ou predição de recuperação. Serão excluídos pacientes com menos de 18 anos, diagnóstico de ataque isquêmico transitório e artigos que não explicitam os critérios de forma detalhada da avaliação dos biomarcadores. A qualidade e o risco de viés dos estudos serão avaliados de forma independente por dois pesquisadores. A síntese de dados será realizada utilizando um resumo narrativo e uma análise quantitativa. Modelos de meta-análise de efeitos aleatórios poderão ser empregados com base nas variáveis de resultados encontrados.

Despite the relative success of constraint-induced movement therapy in the recovery of injury-/trauma-related populations, the mechanisms by which it promotes its results are still unknown. From a dynamical systems approach, we investigated whether the induced exploratory patterns within and between trials during an exercise in Shaping (the therapy’s practice) could shed light on this process. We analyzed data from four chronic spinal-cord injury patients during a task of placing and removing their feet from a step. We assessed the within and between trial dynamics through recurrent quantification analyses and task-space analyses, respectively. From our results, individuals found movement patterns directed to modulate foot height (to accomplish the task). Additionally, when the task was manipulated (increasing step height), individuals increased coupling and coupling variability in the ankle, hip, and knee over trials. This pattern of findings is in consonance with the idea of Shaping inducing exploration of different movements. Such exploration might be an important factor affording the positive changes observed in the literature.

This study aimed to assess the effect of the Lower Extremity Constraint-Induced Movement Therapy (LE-CIMT) intervention on the intra-limb hip-knee coordination and its variability in walking in chronic post-stroke individuals considering the lenses of the dynamic systems approach to motor behavior. Twelve chronic post-stroke individuals received the LE-CIMT intervention for 10 days following all protocol’s recommendations and designed according to individuals’ needs. Before, three days, and 30 days after the intervention, angular kinematics in the sagittal plane of the trunk, hip and knee of both extremities were analyzed. We analyzed joint angles for swing and stance phases of walking, and the intra-limb coordination of hip-knee joints through the vector coding technique. For separate joint angular kinematics, we found differences between affected extremities but no effects of the intervention. However, we observed changes in intra-limb coordination pattern as a function of increased variability after intervention and increased stability at follow-up. These changes follow the predicted pattern from the dynamic systems approach to motor behavior. The immediate decreased stability of the initial pattern could be due to the active exploration of space solution offered by the LE-CIMT and, posteriorly, the stability increased after finding new movement solutions in the real-life environment.

High concentrations of matrix metalloproteinase-2 (MMP-2) and −9 (MMP-9) are associated with inflammation early after stroke. In chronic stages, the elevation of some cytokines is related to the presence of co-morbid conditions in these individuals. In addition to this, some characteristics such as sensorimotor impairment, atrophy, and sedentary lifestyle predispose the system to an inflammatory response. To quantify MMP-2 and −9 serum activity in chronic post-stroke individuals and correlate it with variables of physical activity level, body composition, functional and walking capacity, and with inflammatory biomarkers. Additionally, gelatinase activity was characterized according to motor impairment. Fourteen patients with stroke onset >6 months and seven healthy individuals were enrolled in this study. The clinical assessment included: body composition, measure by bioelectrical impedance analyzer; Fugl-Meyer Motor Assessment Scale; six-minute and ten-meter walk tests, and physical activity level assessed by the StepWatch® Activity Monitor. Blood samples were collected from antecubital vein and serum MMP-2 and −9 activity was analyzed using gelatin Zymography, and the TNFα, IL-6, IL-1β, IL-10 biomarkers using ELISA kits. Chronic post-stroke individuals presented an increased activity of MMP-2 and −9 compared to healthy individuals. Positive correlations with time and steps in low cadence and negative ones with medium cadence and peak activity index were observed. According to the motor impairment, the MMP-2 activity was increased in the mild-moderate group compared to the control group. Increased gelatinases in chronic post-stroke individuals could describe an inflammation process related to the limited capacity of walking in high intensities.

Background: Research over the last two decades has highlighted the critical role of Brain-derived neurotrophic factor (BDNF) in brain neuroplasticity. Studies suggest that physical exercise may have a positive impact on the release of BDNF and therefore, brain plasticity. These results in animal and human studies have potential implications for the recovery from damage to the brain and for interventions that aim to facilitate neuroplasticity and, therefore, the rehabilitation process. Purpose: The aim of this study was to carry out a systematic review of the literature investigating how aerobic exercises and functional task training influence BDNF concentrations post-stroke in humans and animal models. Data Sources: Searches were conducted in PubMed (via National Library of Medicine), SCOPUS (Elsevier), CINAHL with Full Text (EBSCO), MEDLINE 1946—present with daily updates (Ovid) and Cochrane. Study Selection: All of the database searches were limited to the period from January, 2004 to May, 2017. Data Extraction: Two reviewers extracted study details and data. The methodological quality of the studies that used animal models was assessed using the ARRIVE Guidelines, and the study that evaluated human BDNF was assessed using the PEDro Scale. Data Synthesis: Twenty-one articles were included in this review. BDNF measurements were performed systemically (serum/plasma) or locally (central nervous system). Only one study evaluated human BDNF concentrations following physical exercise, while 20 studies were experimental studies using a stroke model in animals. A wide variation was observed in the training protocol between studies, although treadmill walking was the most common type of intervention among the studies. Studies were of variable quality: the studies that used animal models scored from 8/20 to 15/20 according to the ARRIVE Guidelines. The only study that evaluated human subjects scored 5/10 according to the PEDro scale and, which indicates a quality classified as “fair”. Conclusions: The results of the current systematic review suggest that aerobic exercise promotes changes in central BDNF concentrations post-stroke. On the other hand, BDNF responses following functional exercises, such as reaching training and Constraint Induced Movement Therapy (CIMT), seem to be still controversial. Given the lack of studies evaluating post-stroke BDNF concentration following physical exercise in humans, these conclusions are based on animal work.