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Cardinal motor features of Parkinson’s disease (PD) include bradykinesia, rest tremor, and rigidity, which appear in the early stages of the disease and largely depend on dopaminergic nigrostriatal denervation. Intermediate and advanced PD stages are characterized by motor fluctuations and dyskinesia, which depend on complex mechanisms secondary to severe nigrostriatal loss and to the problems related to oral levodopa absorption, and motor and nonmotor symptoms and signs that are secondary to marked dopaminergic loss and multisystem neurodegeneration with damage to nondopaminergic pathways. Nondopaminergic dysfunction results in motor problems, including posture, balance and gait disturbances, and fatigue, and nonmotor problems, encompassing depression, apathy, cognitive impairment, sleep disturbances, pain, and autonomic dysfunction. There are a number of symptomatic drugs for PD motor signs, but the pharmacological resources for nonmotor signs and symptoms are limited, and rehabilitation may contribute to their treatment. The present review will focus on classical notions and recent insights into the neuropathology, neuropharmacology, and neurophysiology of motor dysfunction of PD. These pieces of information represent the basis for the pharmacological, neurosurgical, and rehabilitative approaches to PD.

Introduction. Telerehabilitation enables patients to access remote rehabilitation services for patient-physiotherapist videoconferencing in their own homes. Home-based virtual reality (VR) balance training has been shown to reduce postural instability in patients with Parkinson’s disease (PD). The primary aim was to compare improvements in postural stability after remotely supervised in-home VR balance training and in-clinic sensory integration balance training (SIBT). Methods. In this multicenter study, 76 PD patients (modified Hoehn and Yahr stages 2.5–3) were randomly assigned to receive either in-home VR telerehabilitation (n=38) or in-clinic SIBT (n=38) in 21 sessions of 50 minutes each, 3 days/week for 7 consecutive weeks. VR telerehabilitation consisted of graded exergames using the Nintendo Wii Fit system; SIBT included exercises to improve postural stability. Patients were evaluated before treatment, after treatment, and at 1-month follow-up. Results. Analysis revealed significant between-group differences in improvement on the Berg Balance Scale for the VR telerehabilitation group (p=0.04) and significant Time × Group interactions in the Dynamic Gait Index (p=0.04) for the in-clinic group. Both groups showed differences in all outcome measures over time, except for fall frequency. Cost comparison yielded between-group differences in treatment and equipment costs. Conclusions. VR is a feasible alternative to in-clinic SIBT for reducing postural instability in PD patients having a caregiver.

Post-stroke lower limb spasticity impairs balance and gait leading to reduced walking speed, often increasing wheelchair use and caregiver burden. Several studies have shown that appropriate treatments for lower limb spasticity after stroke include injections of botulinum toxin type A (BoNT-A), phenol or alcohol, surgical correction and a rehabilitation program. In the present article, we review the safety and effectiveness of BoNT-A for the treatment of lower limb spasticity after stroke, with a focus on higher doses of BoNT-A. The cumulative body of evidence coming from the randomized clinical trials and open-label studies selected in the article suggest BoNT-A to be safe and efficacious in reducing lower limb spasticity after stroke. Studies of high doses of BoNT-A also showed a greater reduction of severe post-stroke spasticity. In stroke survivors with spasticity of the ankle plantar-flexor muscles, a combined approach between surgery and BoNT-A can be indicated. However, controversy remains about improvement in motor function relative to post-stroke spasticity reduction after BoNT-A treatment.

This study aimed to explore the potential role of artificial intelligence in optimizing botulinum toxin type A treatment for spasticity and to evaluate its alignment with expert clinical decisions. A comparative analysis was conducted using thirty hypothetical clinical cases involving individuals with spasticity resulting from various neurological conditions. Five rehabilitation physicians, each with more than five years of experience, participated in the study. An artificial intelligence model trained on scientific literature and clinical guidelines generated treatment recommendations, including target muscles and dosages, which were compared with those proposed independently by the physicians. The primary outcome was the level of agreement in muscle selection and dosage. The model demonstrated consistency and adherence to guidelines but showed limited adaptability in complex presentations, such as an adducted thigh and equinovarus foot. It generally recommended lower dosages and differed significantly from physicians in both muscle selection and treatment strategies. Artificial intelligence shows promise as a clinical support tool in spasticity management, offering standardized and reproducible recommendations. However, its limited capacity to interpret clinical subtleties currently restricts its practical application. Future models should integrate multimodal clinical data and real-time clinician feedback to better emulate expert decision-making processes.

Spasticity after stroke impairs motor control, delays recovery, and reduces quality of life. Botulinum toxin type A is the first-line treatment, but it is often administered in the chronic phase, potentially limiting its impact on rehabilitation. Emerging evidence suggests that earlier treatment may enhance recovery, though functional benefits remain uncertain. We conducted a secondary analysis of a multicenter, open-label, longitudinal cohort study to investigate whether the timing of the first botulinum toxin type A injection influences outcomes in post-stroke patients naïve to this treatment. All participants received botulinum toxin injections combined with conventional rehabilitation. Assessments were performed at baseline and at 4, 12, and 24 weeks post-injection. The primary outcome was muscle tone; secondary outcomes included motor strength, sensorimotor recovery, and global disability. Statistical analyses used mixed-effects models and trend tests. Patients treated within 90 days of stroke onset showed greater reductions in spasticity at 4 and 12 weeks compared with later treatment. Despite having more severe baseline impairments, early treated patients demonstrated faster and more pronounced improvements in upper-limb strength, sensorimotor recovery, and global disability. Early toxin administration is associated with enhanced reduction in spasticity and improved motor recovery, particularly in patients with severe initial deficits.

Botulinum toxin type-A (BoNT-A) has emerged as a key therapeutic agent for the management of spasticity. This paper presents a comprehensive bibliometric and visual analysis of research concerning BoNT-A treatment of spasticity to elucidate current trends and future directions in this research area. A search was conducted in the Web of Science database for articles focused on the use of BoNT-A in spasticity published between 2000 and 2022. We extracted various metrics, including counts of publications and contributions from different countries, institutions, authors, and journals. Analytical methods in CiteSpace were employed for the examination of co-citations, collaborations, and the co-occurrence of keywords. Our search yielded 1489 publications. Analysis revealed a consistent annual increase in research output. The United States, United Kingdom, and Italy were the leading contributors. The top institution in this research was Assistance Publique Hopitaux, Paris. The journal containing the highest number of relevant publications was Toxins. Key frequently occurring keywords were ‘stroke’, ‘cerebral palsy’, ‘adult spasticity’, and ‘upper extremity’. This study identified 12 clusters of keywords and 15 clusters of co-cited references, indicating the main focus areas and emerging themes in this field. This study comprehensively analyzed and summarized trends in BoNT-A research in the field of spasticity over the past 22 years.

Botulinum toxin type A is a first-line treatment for post-stroke spasticity, with selective action at nerve endings and minimal effects beyond the injection site. However, concerns about potential adverse reactions due to toxin diffusion and spread can significantly influence physicians’ therapeutic decisions in managing post-stroke spasticity. Current evidence shows that while the main formulations of botulinum toxin type A have different molecular weights and sizes, they do not exhibit differing diffusion profiles. Instead, the key factors determining botulinum toxin type A diffusion and spread in post-stroke spasticity management are the dose (i.e., the actual amount of 150 kDa neurotoxin protein injected), dilution, and injection volume. Other injection-related factors, such as the needle gauge and injection speed, have also been suggested to have a secondary influence on botulinum toxin type A diffusion and spread. The needs of patients with post-stroke spasticity may vary, and depending on treatment goals, botulinum toxin type A diffusion and spread can be something to avoid or may offer therapeutic benefits by reaching a greater number of nerve terminals in the target muscle, enhancing the toxin’s effect. These factors should be carefully evaluated in spasticity clinics.

Botulinum toxin type A1 is a first-line treatment for adult and pediatric spasticity. However, when considering the quantity of 150 kDa neurotoxin protein in relation to patient weight and the maximum recommended dose for treating adult and pediatric patients with spasticity, several concerns arise. First, the therapeutic margin (the ratio of the actual maximum quantity of toxin recommended for treating adult spasticity to its median lethal dose) appears to be relevant. Second, there is no consistency between adult and pediatric dosing of botulinum toxin type A1 for spasticity. The third point concerns the suitability of the recommended doses for treating spasticity in pediatric patients. Based on the average body weight of American children and adolescents, the maximum weight-based doses for abobotulinumtoxinA and onabotulinumtoxinA could be administered to children as young as 9 years old. Additionally, the maximum weight-based dose for incobotulinumtoxinA could be administered to children as young as 6 years old. The final point concerns managing the maximum dose of BoNT/A1 in pediatric patients with spasticity who weigh more than 25 kg for incobotulinumtoxinA, or more than 34 kg for abobotulinumtoxinA and onabotulinumtoxinA. No labeled recommendations are given on the weight cut-off for transitioning to adult dosing in pediatric patients.

Clonus is characterized by involuntary, rhythmic, oscillatory muscle contractions, typically triggered by rapid muscle stretching and is frequently associated with spastic equinovarus foot (SEVF), where it may increase risk of falls and cause discomfort, pain, and sleep disorders. We hypothesize that selective diagnostic nerve block (DNB) of the tibial nerve motor branches can help identify which muscle is primarily responsible for clonus in patients with SEVF and provide useful information for botulinum neurotoxin type A (BoNT-A) treatment. This retrospective study explored which calf muscles contributed to clonus in 91 patients with SEFV after stroke (n = 31), multiple sclerosis (n = 21), and cerebral palsy (n = 39), using selective DNB. We found that SEVF-associated clonus was most commonly driven by the soleus muscle, followed by the gastrocnemius lateralis and medialis, tibialis posterior, and flexor digitorum longus, and that frequency differed according to SEVF etiology. Our data suggest that identifying the muscles involved in SEVF-associated clonus may aid clinicians in personalizing BoNT-A treatment to single patients. Also, the findings of this study suggest that applying a ‘stroke model’ to treating spasticity secondary to other etiologies may not always be appropriate.

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 <12 months) with PSS who received BoNT-A for the first time according to routine practice. The main outcome was the modified Ashworth scale (MAS). Patients were evaluated before BoNT-A injection and then at 4, 12, and 24 weeks of follow-up. Eighty-three patients with PSS were enrolled. MAS showed a significant decrease in PSS at 4 and 12 weeks but not at 24 weeks after treatment. Among the patients with a time between stroke onset and BoNT-A injection >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.