Early management of spasticity may improve stroke outcome. Botulinum toxin type A (BoNT-A) is recommended treatment for post-stroke spasticity (PSS). However, it is usually administered in the chronic phase of stroke. Our aim was to determine whether the length of time between stroke onset and initial BoNT-A injection has an effect on outcomes after PSS treatment. This multicenter, longitudinal, cohort study included stroke patients (time since onset 90 days, the MAS were higher at 4 and 12 weeks than at 24 weeks compared to those injected ≤90 days since stroke. Our findings suggest that BoNT-A treatment for PSS should be initiated within 3 months after stroke onset in order to obtain a greater reduction in muscle tone at 1 and 3 months afterwards.

The loss of a hand disrupts the sophisticated neural pathways between the brain and the hand, severely affecting the level of independence of the patient and the ability to carry out daily work and social activities. Recent years have witnessed a rapid evolution of surgical techniques and technologies aimed at restoring dexterous motor functions akin to those of the human hand through bionic solutions, mainly relying on probing of electrical signals from the residual nerves and muscles. Here, we report the clinical implementation of an interface aimed at achieving this goal by exploiting muscle deformation, sensed through passive magnetic implants: the myokinetic interface. One participant with a transradial amputation received an implantation of six permanent magnets in three muscles of the residual limb. A truly self-contained myokinetic prosthetic arm embedding all hardware components and the battery within the prosthetic socket was developed. By retrieving muscle deformation caused by voluntary contraction through magnet localization, we were able to control in real time a dexterous robotic hand following both a direct control strategy and a pattern recognition approach. In just 6 weeks, the participant successfully completed a series of functional tests, achieving scores similar to those achieved when using myoelectric controllers, a standard-of-care solution, with comparable physical and mental workloads. This experience raised conceptual and technical limits of the interface, which nevertheless pave the way for further investigations in a partially unexplored field. This study also demonstrates a viable possibility for intuitively interfacing humans with robotic technologies.

Brain lesions caused by cerebral ischemia lead to network disturbances in both hemispheres, causing a subsequent reorganization of functional connectivity both locally and remotely with respect to the injury. Quantitative electroencephalography (qEEG) methods have long been used for exploring brain electrical activity and functional connectivity modifications after stroke. However, results obtained so far are not univocal. Here, we used basic and advanced EEG methods to characterize how brain activity and functional connectivity change after stroke. Thirty-three unilateral post stroke patients in the sub-acute phase and ten neurologically intact age-matched right-handed subjects were enrolled. Patients were subdivided into two groups based on lesion location: cortico-subcortical (CS, n = 18) and subcortical (S, n = 15), respectively. Stroke patients were evaluated in the period ranging from 45 days since the acute event (T0) up to 3 months after stroke (T1) with both neurophysiological (resting state EEG) and clinical assessment (Barthel Index, BI) measures, while healthy subjects were evaluated once. Brain power at T0 was similar between the two groups of patients in all frequency bands considered (δ, θ, α, and β). However, evolution of θ-band power over time was different, with a normalization only in the CS group. Instead, average connectivity and specific network measures (Integration, Segregation, and Small-worldness) in the β-band at T0 were significantly different between the two groups. The connectivity and network measures at T0 also appear to have a predictive role in functional recovery (BI T1-T0), again group-dependent. The results obtained in this study showed that connectivity measures and correlations between EEG features and recovery depend on lesion location. These data, if confirmed in further studies, on the one hand could explain the heterogeneity of results so far observed in previous studies, on the other hand they could be used by researchers as biomarkers predicting spontaneous recovery, to select homogenous groups of patients for the inclusion in clinical trials.

It is widely known that nervous and muscular systems work together and that they are strictly dependent in their structure and functions. Consequently, muscles undergo macro and microscopic changes with subsequent alterations after a central nervous system (CNS) disease. Despite this, only a few researchers have addressed the problem of skeletal muscle abnormalities following CNS diseases. The purpose of this review is to summarize the current knowledge on the potential mechanisms responsible for changes in skeletal muscle of patients suffering from some of the most common CSN disorders (Stroke, Multiple Sclerosis, Parkinson’s disease). With this purpose, we analyzed the studies published in the last decade. The published studies show an extreme heterogeneity of the assessment modality and examined population. Furthermore, it is evident that thanks to different evaluation methodologies, it is now possible to implement knowledge on muscle morphology, for a long time limited by the requirement of muscle biopsies. This could be the first step to amplify studies aimed to analyze muscle characteristics in CNS disease and developing rehabilitation protocols to prevent and treat the muscle, often neglected in CNS disease.

By blocking the release of neurotransmitters, botulinum toxin A (BoNT-A) is an effective treatment for muscle over-activity and pain in stroke patients. BoNT-A has also been reported to increase passive range of motion (p-ROM), the decrease of which is mainly due to muscle shortening (i.e., muscle contracture). Although the mechanism of action of BoNT-A on p-ROM is far from understood, pain relief may be hypothesized to play a role. To test this hypothesis, a retrospective investigation of p-ROM and pain was conducted in post-stroke patients treated with BoNT-A for upper limb hypertonia. Among 70 stroke patients enrolled in the study, muscle tone (Modified Ashworth Scale), pathological postures, p-ROM, and pain during p-ROM assessment (Numeric Rating Scale, NRS) were investigated in elbow flexors (48 patients) and in finger flexors (64 patients), just before and 3–6 weeks after BoNT-A treatment. Before BoNT-A treatment, pathological postures of elbow flexion were found in all patients but one. A decreased elbow p-ROM was found in 18 patients (38%). Patients with decreased p-ROM had higher pain-NRS scores (5.08 ± 1.96, with a pain score ≥8 in 11% of cases) than patients with normal p-ROM (0.57 ± 1.36) (p < 0.001). Similarly, pathological postures of finger flexion were found in all patients but two. A decreased finger p-ROM was found in 14 patients (22%). Pain was more intense in the 14 patients with decreased p-ROM (8.43 ± 1.74, with a pain score ≥ 8 in 86% of cases) than in the 50 patients with normal p-ROM (0.98 ± 1.89) (p < 0.001). After BoNT-A treatment, muscle tone, pathological postures, and pain decreased in both elbow and finger flexors. In contrast, p-ROM increased only in finger flexors. The study discusses that pain plays a pivotal role in the increase in p-ROM observed after BoNT-A treatment.

Various degrees of neural reorganization may occur in affected and unaffected hemispheres in the early phase after stroke and several months later. Recent literature suggests to apply a stratification based on lesion location and to consider patients with cortico-subcortical and subcortical strokes separately: different lesion location may also influence therapeutic response. In this study we used a longitudinal approach to perform TMS assessment (Motor Evoked Potentials, MEP, and Silent Period, SP) and clinical evaluations (Barthel Index, Fugl-Meyer Assessment for upper limb motor function and Wolf Motor Function Test) in 10 cortical-subcortical and 10 subcortical ischemic stroke patients. Evaluations were performed in a window between 10 and 45 days (t0) and at 3 months after the acute event (t1). Our main finding is that 3 months after the acute event patients affected by subcortical stroke presented a reduction in contralateral SP duration in the unaffected hemisphere; this trend is related to clinical improvement of upper limb motor function. In conclusion, SP proved to be a valid parameter to characterize cortical reorganization patterns in stroke survivors and provided useful information about motor recovery within three months in subcortical patients.