Abnormal synergies coexist with primary motor impairments (weakness and spasticity) after stroke. They are observed during voluntary movements and are characterized by stereotyped movement patterns, a loss of independent joint control, and abnormal muscle coordination (eg, involuntary activation of distal muscles led by proximal joint movement). The structure and expression of abnormal synergies, however, are highly context-dependent (eg, influenced by gravity, body posture, and task constraints) and are not homogeneous across patients. Current evidence suggests that abnormal synergies are pathophysiologically related to damage to corticospinal tracts, upregulation of brainstem pathways (particularly the medial reticulospinal tract, but also involves the vestibulospinal tract), and maladaptive changes in spinal circuitry. These same mechanisms may overlap with those underlying spasticity and weakness. Spasticity is believed to result from overexcitability of descending excitatory brainstem pathways, the reticulospinal tract in particular, and the consequent exaggerated stretch reflexes, while muscle weakness is attributed to the reduction in corticospinal output. Recent research and clinical observations have advanced our understanding of abnormal synergies. Post-stroke abnormal synergies are not fixed motor impairments. A new framework is proposed that suggests post-stroke abnormal synergies could constitute the behavioral expression of primary impairments, including weakness and spasticity, arising from their interactions with environmental constraints, particularly antigravity control mechanisms. The term "synergy" has been used across various frameworks, with different definitions and quantification approaches. Identifying appropriate methods to quantify abnormal synergies is therefore essential to investigate their relationship with spasticity and muscle weakness, and evaluate potential abnormal synergy improvements following interventions, even if they primarily target other motor impairments.

MEGF10 biallelic variants cause early-onset myopathy, areflexia, respiratory distress and dysphagia (EMARDD), congenital myopathies with cores, and later-onset myopathies with respiratory failure. As MEGF10 plays a key role in satellite cells proliferation and differentiation, these disorders are considered primary Satellite Cell-opathies. We present clinical, genetic, and laboratory findings from three patients with MEGF10-related myopathy from two families: a 6-year-old boy with EMARDD, and two siblings with a milder myopathy with respiratory involvement. Patient 1, male, showed decreased fetal movements and profound neonatal hypotonia with respiratory failure, requiring tracheostomy soon after birth. At 6 years, he had lack of head and trunk control, scoliosis, and upper limbs antigravity movements. Muscle MRI revealed mild-to-moderate, symmetrical fibro-fatty replacement affecting scapular, paravertebral, gluteal and adductor muscles, with bilateral absence of the semimembranosus. Muscle biopsy revealed a reduction of Pax7-positive satellite cells. Genetic studies disclosed the novel homozygous MEGF10 c.337T>C, p.(Cys113Arg) variant. Patient 2 is a 24-year-old woman with myopathic facies, progressive axial and generalized weakness, and thoracolumbar scoliosis at 11 years, leading to progressive respiratory involvement necessitating tracheostomy at 14 years. Her 17-year-old brother, patient 3, experienced a threatened abortion and perinatal complications consisting of neonatal hypoxia, right arm monoplegia, and clavicle fracture, followed by motor delay, scoliosis and progressive respiratory dysfunction, requiring non-invasive ventilation at 16 years. P2 and P3 harbour the novel homozygous c.917G>C, p. (Arg306Pro) MEGF10 pathogenic variant. We describe three new patients with MEGF10-related myopathy, showing severe but variable clinical expression, associated with two novel variants.

Background: Early recovery after total hip (THA) and total knee arthroplasty (TKA) is often limited by pain and impaired antigravity function. Mechano-acoustic vibration therapy (VT) may enhance neuromuscular activation and analgesia, but evidence in arthroplasty is scarce. Methods: A total of 380 patients aged ≥65 years were retrospectively identified within 3 ± 1 days after primary unilateral total hip arthroplasty (THA) or total knee arthroplasty (TKA). All patients underwent standard inpatient physiotherapy; in the VT group, mechano-acoustic vibration therapy (ViSS®, 30 min/day for 5 days at 200-300 Hz) was added as an adjunct treatment, whereas the control group received standard physiotherapy alone. Pain (VAS, McGill), muscle strength (MRC), thigh circumferences, and 10 s Sit-to-Stand were assessed at baseline (T0), end of treatment (T1), and 3-day follow-up (T2). Results: VT produced large, early and sustained improvements in both cohorts. In THA patients, VAS decreased from 7.1 ± 1.1 to 3.8 ± 0.6 at T1 and 3.0 ± 0.7 at T2 and Sit-to-Stand repetitions increased from 3.7 ± 1.9 to 6.3 ± 1.7 at T2, with significant gains in strength and circumferences. TKA VT patients showed similar patterns. Control groups reported smaller pain reductions and no clinically relevant changes in the reported outcomes. Conclusions: integrating a short cycle of mechano-acoustic VT into early inpatient rehabilitation after THA or TKA significantly enhances pain relief and restoration of antigravity function compared with standard physiotherapy alone. VT represents a promising adjunct to conventional rehabilitation strategies and may contribute to optimizing postoperative recovery pathways in major joint replacement.

BACKGROUND Cervical spinal epidural abscesses are uncommon; ventral lesions are rare, often arising from contiguous spondylodiscitis. Atypical presentations without cranial nerve involvement or altered consciousness are easily misattributed to intracranial diseases, delaying care. CASE REPORT We report the case of a 51-year-old man with poorly controlled hypertension and recent heroin use who developed progressive back and neck pain along with 3 days of fever, followed by rapidly progressive asymmetric weakness. Neurological examination revealed a paradoxical T4/T5 sensory level with preserved mentation and cranial nerve function, an important bedside clue suggesting a spinal process despite an initial stroke workup. Cervical gadolinium-enhanced magnetic resonance imaging (MRI) later revealed a long-segment ventral-dorsal C2-C7 epidural abscess with compressive myelopathy and C4-C6 spondylodiscitis; blood cultures grew methicillin-resistant Staphylococcus aureus. The patient underwent urgent C3-C7 decompressive laminectomy with abscess drainage, followed by 6 weeks of pathogen-directed intravenous antibiotics. Adjunctive hyperbaric oxygen therapy and intravascular laser irradiation of the blood were initiated; repetitive transcranial magnetic stimulation was instituted as a rehabilitative neuromodulation strategy. Bacteremia cleared and inflammatory markers normalized; motor function improved from flaccid quadriplegia to partial antigravity strength in the selected muscle groups, although he still needed to use a wheelchair at discharge. CONCLUSIONS This case emphasizes that a thoracic sensory level with fever and preserved consciousness should prompt early spinal MRI. Standard surgical antimicrobial therapy remains important, and carefully selected adjuncts (eg, adjunctive hyperbaric oxygen therapy, intravascular laser irradiation of the blood, and repetitive transcranial magnetic stimulation) may be considered to support infection control and neurorecovery.

We report a case in which a girl diagnosed with HNRNPU-associated neurodevelopmental disorder presented with acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) and generalized hypotonia accompanied by chorea-like involuntary movements. On the first day of hospitalization, she presented with fever and generalized clonic seizures. Twenty four hours later, she continued to experience impaired consciousness and generalized hypotonia. Her consciousness improved gradually, but chorea-like involuntary movements of the limbs were observed. From the seventh day of hospitalization, the patient repeatedly experienced difficulty in making eye contact for 20-30 s for 2-3 days. Brain MRI with diffusion-weighted imaging revealed hyperintensity from the bilateral frontal cortex to subcortical white matter and the bilateral caudate nuclei. This patient presented with chorea-like involuntary movements and generalized hypotonia, and was unable to perform antigravity movements. HNRNPU-related neurodevelopmental disorders often present with congenital hypotonia. When affected children develop acute encephalopathy associated with basal ganglia lesions, the synergistic effect of these conditions may exacerbate the hypotonia.

Background/Objectives: Knee osteoarthritis (OA) is a prevalent degenerative joint disorder associated with pain, impaired proprioception, and reduced physical function. While closed kinetic chain exercises (CKCEs) are commonly prescribed to enhance joint stability, their weight-bearing nature may exacerbate symptoms. Graded weight-bearing exercises (GWBEs) using anti-gravity treadmill training provide a novel approach to reduce joint loading while maintaining functional mobility. This study aimed to evaluate the effectiveness of GWBEs compared with CKCEs and open kinetic chain exercises (OKCEs) on pain, function, proprioception, and quadricep strength in patients with knee OA. Methods: Forty-five adults aged 40-60 years with radiographically confirmed knee OA were randomized into three groups: (1) GWBE + OKCE, (2) CKCE + OKCE, or (3) OKCE alone. Interventions were conducted three times per week for six-weeks. Outcomes included pain (Visual Analogue Scale), physical function (Western Ontario and McMaster Universities Osteoarthritis Index, 6-Minute Walk Test), proprioception (joint repositioning error at 45°), and quadriceps strength (isokinetic peak torque at 60°, 120°, and 180°/s). Results: All groups demonstrated significant improvements in pain and function (p < 0.05). Proprioception improved in the GWBE + OKCE and CKCE + OKCE groups but not in the OKCE group. No significant changes were observed in quadriceps strength across groups. The GWBE + OKCE group showed significantly greater improvements in pain, function, and proprioception compared to both comparator groups (p < 0.05). Conclusions: GWBE combined with OKCE is more effective than CKCE + OKCE and OKCE alone in improving pain, function, and proprioception in patients with knee OA.

We conducted a randomized sham-controlled clinical trial from 2019 to 2024 to characterize the safety and efficacy of applying paired-associative stimulation (PAS), consisting of high-intensity transcranial magnetic stimulation and high-frequency peripheral nerve stimulation, at early stages after incomplete spinal cord injury (SCI) to enhance motor recovery. Patients with incomplete cervical SCI were randomized 1:1 within 1-4 months post-injury to receive 12 weeks of PAS or sham stimulation alongside conventional rehabilitation, which was not changed. Patients were followed up to 1.5 years after injury (about 1 year after end of stimulation). Seventeen patients (14 males, age 53 ​± ​16 years) participated. Manual Muscle Test revealed a significant effect of treatment in favor of active group (F (1, 470) ​= ​14.69; p ​< ​0.001) in muscles that had no antigravity activity before beginning of stimulation. Improvement from baseline was observed at the end of stimulation (active: 346 ​± ​53 ​%, sham: 215 ​± ​26 ​%), 1 year after injury (about 6 months after end of treatment; active: 389 ​± ​61 ​%, sham: 241 ​± ​39 ​%), and at 1.5 years after injury (about 12 months after end of treatment; active: 419 ​± ​73 ​%, sham: 210 ​± ​17 ​%). Greater improvement in fine motor skill tests was observed in the active group. Although the Spinal Cord Independence Measure showed no differences between groups (p ​= ​0.36-0.83), there was improvement in activity of daily living tests. The intervention was feasible and well-tolerated in both groups. PAS is a safe and feasible therapy that can be added to conventional rehabilitation even in early stages after SCI.

This case report describes a female in her 90s with an infarction of the left paramedian pontine artery (PPA) who presented with sudden knee buckling during gait. Upon admission to the convalescent rehabilitation ward, she exhibited motor paralysis, ataxia, and contralateral body lateropulsion, making standing difficult. At the interim evaluation, she was able to ambulate under supervision with a walker; however, knee buckling occurred at gait initiation and during turning. Surface electromyography of the right rectus femoris and biceps femoris during these episodes showed abnormal muscle activation. It was inferred that reduced antigravity muscle output via the vestibulospinal tract, impaired motor processing due to paresis, delayed activation timing from ataxia, and global postural control deficits collectively contributed to the knee buckling. A comprehensive physiotherapy program was implemented. Subsequently, her functional scores improved substantially from admission to discharge, including a marked increase in the Berg Balance Scale (BBS: 4 → 47) and motor items of the Functional Independence Measure-Motor domain (FIM-M: 17 →52). Motor paresis, ataxia, vestibular dysfunction, and postural control deficits improved, and knee buckling resolved. To our knowledge, this is the first report indicating that PPA infarction can cause sudden knee buckling during gait.