A coordinated pattern of multi-muscle activation is essential to produce efficient reaching trajectories. Disruption of these coordinated activation patterns, termed synergies, is evident following stroke and results in reaching deficits; however, preclinical investigation of this phenomenon has been largely ignored. Furthermore, traditional outcome measures of post-stroke performance seldom distinguish between impairment restitution and compensatory movement strategies. We sought to address this by using kinematic analysis to characterize reaching movements and kinematic synergies of rats performing the Montoya staircase task, before and after ischemic stroke. Synergy was defined as the simultaneous movement of the wrist and other proximal forelimb joints (i.e. shoulder, elbow) during reaching. Following stroke, rats exhibited less individuation between joints, moving the affected limb more as a unit. Moreover, abnormal flexor synergy characterized by concurrent elbow flexion, shoulder adduction, and external rotation was evident. These abnormalities ultimately led to inefficient and unstable reaching trajectories, and decreased reaching performance (pellets retrieved). The observed reaching abnormalities in this preclinical stroke model are similar to those classically observed in humans. This highlights the potential of kinematic analysis to better align preclinical and clinical outcome measures, which is essential for developing future rehabilitation strategies following stroke.

Attention-deficit hyperactivity disorder (ADHD) may be caused by genetic or environmental factors. Among environmental factors, perinatal complications are related, such as neonatal hypoxia-ischemia (HI). Thus, the aim of this study was to investigate whether HI contributes to the development of characteristics related to ADHD in adult rats, and to correlate the behavioral results with brain damage volume. Male Wistar rats were divided into 2 groups: HI and control. The HI procedure consisted of a permanent occlusion of the right common carotid artery followed by a period of hypoxia (90 min; 8% O₂ and 92% N₂) on the 7th postnatal day. Two months later, animals were evaluated in the open field test during a single 5-min session, and in the 5-choice serial reaction time task (5-CSRTT), over 25 weeks. Our results demonstrated that animals submitted to HI manifest cognitive impairments in task acquisition, deficits in sustained attention, and increases in impulsivity and compulsivity in response to task manipulation in the 5-CSRTT. Locomotor activity observed in open field did not differ between groups. Moreover, brain volume loss in the total hemisphere, cerebral cortex, white matter, hippocampus, and striatum were observed in HI animals, especially on the side ipsilateral to the lesion. From these results, we can infer that neonatal HI is an environmental factor that could contribute to the development of behavioral characteristics observed in ADHD that are associated with general brain atrophy.

Background Impairments of functional mobility may affect locomotion and quality of life in subjects with Parkinson’s disease (PD). Movement smoothness measurements, such as the spectral arc length (SPARC), are novel approaches to quantify movement quality. Previous studies analyzed SPARC in simple walking conditions. However, SPARC outcomes during functional mobility tasks in subjects with PD and freezing of gait (FOG) were never investigated. This study aimed to analyze SPARC during the Timed Up and Go (TUG) test in individuals with PD and FOG. Methods Thirty-one participants with PD and FOG and six healthy controls were included. SPARC during TUG test was calculated for linear and angular accelerations using an inertial measurement unit system. SPARC data were correlated with clinical parameters: motor section of the Unified Parkinson’s Disease Rating Scale, Hoehn & Yahr scale, Freezing of Gait Questionnaire, and TUG test. Results We reported lower SPARC values (reduced smoothness) during the entire TUG test, turn and stand to sit in subjects with PD and FOG, compared to healthy controls. Unlike healthy controls, individuals with PD and FOG displayed a broad spectral range that encompassed several dominant frequencies. SPARC metrics also correlated with all the above-mentioned clinical parameters. Conclusion SPARC values provide valid and relevant clinical data about movement quality (e.g., smoothness) of subjects with PD and FOG during a functional mobility test. Electronic supplementary material The online version of this article (10.1186/s12984-019-0579-8) contains supplementary material, which is available to authorized users.

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Objective Chronic pain associated with osteoarthritis (OA) often leads to reduced function and engagement in activities of daily living. Current pharmacological treatments remain relatively ineffective. This study investigated the efficacy of photobiomodulation therapy (PBMT) on cartilage integrity and central pain biomarkers in adult male Wistar rats. Design We evaluated the cartilage degradation and spinal cord sensitization using the monoiodoacetate (MIA) model of OA following 2 weeks of delayed PBMT treatment (i.e., 15 days post-MIA). Multiple behavioral tests and knee joint histology were used to assess deficits related to OA. Immunohistochemistry was performed to assess chronic pain sensitization in spinal cord dorsal horn regions. Furthermore, we analyzed the principal components related to pain-like behavior and cartilage integrity. Results MIA induced chronic pain-like behavior with respective cartilage degradation. PBMT had no effects on overall locomotor activity, but positive effects on weight support ( P = 0.001; effect size [ES] = 1.01) and mechanical allodynia ( P = 0.032; ES = 0.51). Greater optical densitometry of PBMT-treated cartilage was evident in superficial layers ( P = 0.020; ES = 1.34), likely reflecting the increase of proteoglycan and chondrocyte contents. In addition, PBMT effects were associated to decreased contribution of spinal glial cells to pain-like behavior ( P = 0.001; ES = 0.38). Conclusion PBMT during the chronic phase of MIA-induced OA promoted cartilage recovery and reduced the progression or maintenance of spinal cord sensitization. Our data suggest a potential role of PBMT in reducing cartilage degradation and long-term central sensitization associated with chronic OA.