13 research outputs found

    The role of the rehabilitation in subjects with Progressive Supranuclear Palsy: a narrative review

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    Progressive Supranuclear Palsy (PSP) is a progressive neurodegenerative disorder due to the deposition of abnormal proteins in neurons of the basal ganglia that limit motor ability producing disability and reduced quality of life. So far, no pharmacologic therapy has been developed and the treatment remains symptomatic. The aim of the present study was to investigate systematically literature, and to determine the types and effects of rehabilitative interventions. A search of all studies was conducted in MEDLINE/PubMed, the Cochrane Central Register of Controlled Trials, CINAHL and EMBASE. Twelve studies were individuated including 6 case reports, 3 case series, one case control, one quasi-RT crossover study and one RCT, with 88 patients investigated overall. Rehabilitative interventions varied in type, number, frequency and duration of sessions. The most commonly used clinical measures were Progressive Supranuclear Palsy-Rating Scale (PSP-RS) and Unified Parkinson's Disease Rating Scale (UPDRS). Physical exercises were the main rehabilitative strategy but were associated with other interventions and rehabilitative devices, in particular treadmill and robot-assisted gait training. All studies showed an improvement of balance and gait impairment with a reduction of falls after rehabilitation treatment. Due to poor methodological quality and the variability of rehabilitative approach with different and variable strategies, there was no evidence of the effectiveness of a specific rehabilitation intervention in PSP. Despite this finding, rehabilitation might improve balance and gait, thereby reducing falls in PSP subjects

    Effect of electrical stimulation as an adjunct to botulinum toxin type A in the treatment of adult spasticity: a systematic review

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    <p><b>Objective:</b> To investigate whether electrical stimulation (ES) as an adjunct to BTX-A boosts botulinum activity and whether the combined therapeutic procedure is more effective than BTX-A alone in reducing spasticity in adult subjects.</p> <p><b>Data sources:</b> A search was conducted in PubMed, EMBASE, Cochrane Central Register, and CINAHL from January 1966 to January 2016.</p> <p><b>Study selection:</b> Only randomized controlled studies (RCT) involving the combination of BTX-A and ES were considered. RCTs were excluded if BTX plus ES was investigated in animals or healthy subjects; certain techniques were used as an adjunct to BTX-A, but ES was not used; BTX-A or ES were compared but were not used in combination. ES was divided into neuromuscular stimulation (NMS), functional electrical stimulation (FES), and transcutaneous electrical nerve stimulation (TENS). Two authors independently screened all search results and reviewed study characteristics using the Physiotherapy Evidence Database (PEDro) scale.</p> <p><b>Results:</b> Fifteen RCTs were pinpointed and nine studies were included. Trials varied in methodological quality, size, and outcome measures used. ES was used in the form of NMS and FES in seven and two studies, respectively. No study investigating BTX-A plus TENS was found. BTX-A plus ES produced significant reduction in spasticity on the Ashworth Scale (AS) and on the modified AS in seven studies, but only four showed high quality on the PEDro scale. Significant reduction in compound muscular action potential (CMAP) amplitude was detected after BTX-A plus ES in two studies.</p> <p><b>Conclusions:</b> ES as an adjunctive therapy to BTX-A may boost BTX-A action in reducing adult spasticity, but ES variability makes it difficult to recommend the combined therapy in clinical practice.</p> <p>Implications for rehabilitation</p><p>Electrical stimulation (ES) as adjunct to botulinum toxin type A (BTX-A) injections may boost neurotoxin action in treating adult spasticity.</p><p>Given the variability of ES characteristics and the paucity of high-quality trials, it is difficult to support definitively the use of BTX-A plus ES to potentiate BTX-A effect in clinical practice.</p><p>A vast array of rehabilitation interventions combined with BTX-A have been provided in reducing spasticity, but the present evidence is not sufficient to recommend any combined therapeutic strategy.</p><p></p> <p>Electrical stimulation (ES) as adjunct to botulinum toxin type A (BTX-A) injections may boost neurotoxin action in treating adult spasticity.</p> <p>Given the variability of ES characteristics and the paucity of high-quality trials, it is difficult to support definitively the use of BTX-A plus ES to potentiate BTX-A effect in clinical practice.</p> <p>A vast array of rehabilitation interventions combined with BTX-A have been provided in reducing spasticity, but the present evidence is not sufficient to recommend any combined therapeutic strategy.</p

    Botulinum Toxin Type A for the Treatment of Neuropathic Pain in Neuro-Rehabilitation

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    Pain is a natural protective mechanism and has a warning function signaling imminent or actual tissue damage. Neuropathic pain (NP) results from a dysfunction and derangement in the transmission and signal processing along the nervous system and it is a recognized disease in itself. The prevalence of NP is estimated to be between 6.9% and 10% in the general population. This condition can complicate the recovery from stroke, multiple sclerosis, spinal cord lesions, and several neuropathies promoting persistent disability and poor quality of life. Subjects suffering from NP describe it as burning, itching, lancing, and numbness, but hyperalgesia and allodynia represent the most bothersome symptoms. The management of NP is a clinical challenge and several non-pharmacological and pharmacological interventions have been proposed with variable benefits. Botulinum toxin (BTX) as an adjunct to other interventions can be a useful therapeutic tool for the treatment of disabled people. Although BTX-A is predominantly used to reduce spasticity in a neuro-rehabilitation setting, it has been used in several painful conditions including disorders characterized by NP. The underlying pharmacological mechanisms that operate in reducing pain are still unclear and include blocking nociceptor transduction, the reduction of neurogenic inflammation by inhibiting neural substances and neurotransmitters, and the prevention of peripheral and central sensitization. Some neurological disorders requiring rehabilitative intervention can show neuropathic pain resistant to common analgesic treatment. This paper addresses the effect of BTX-A in treating NP that complicates frequent disorders of the central and peripheral nervous system such as spinal cord injury, post-stroke shoulder pain, and painful diabetic neuropathy, which are commonly managed in a rehabilitation setting. Furthermore, BTX-A has an effect in relief pain that may characterize less common neurological disorders including post-traumatic neuralgia, phantom limb, and complex regional pain syndrome with focal dystonia. The use of BTX-A could represent a novel therapeutic strategy in caring for neuropathic pain whenever common pharmacological tools have been ineffective. However, large and well-designed clinical trials are needed to recommend BTX-A use in the relief of neuropathic pain

    Botulinum Toxin—A High-Dosage Effect on Functional Outcome and Spasticity-Related Pain in Subjects with Stroke

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    Stroke patients can develop spasticity and spasticity-related pain (SRP). These disorders are frequent and can contribute to functional limitations and disabling conditions. Many reports have suggested that higher doses than initially recommended of BTX-A can be used effectively and safely, especially in the case of severe spasticity; however, whether the treatment produces any benefit on the functional outcome and SRP is unclear. Studies published between January 1989 and December 2022 were retrieved from MEDLINE/PubMed, Embase, and Cochrane Central Register. Only obabotulinumtoxinA (obaBTX-A), onabotulinumtoxinA, (onaBTX-A), and incobotulinumtoxinA (incoBTX-A) were considered. The term “high dosage” indicates ≥600 U. Nine studies met the inclusion criteria. Globally, 460 subjects were treated with BTX-A high dose, and 301 suffered from stroke. Studies had variable method designs, sample sizes, and aims. Only five (55.5%) reported data about the functional outcome after BTX-A injection. Functional measures were also variable, and the improvement was observed predominantly in the disability assessment scale (DAS). SRP pain was quantified by visual analog scale (VAS) and only three studies reported the BTX-A effect. There is no scientific evidence that this therapeutic strategy unequivocally improves the functionality of the limbs. Although no clear-cut evidence emerges, certain patients with spasticity might obtain goal-oriented improvement from high-dose BTX-A. Likewise, data are insufficient to recommend high BTX dosage in SRP

    Vitamin D serum level in subjects with critical illness polyneuropathy and myopathy

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    Critical illness polyneuropathy and myopathy (CIPNM) is a disabling neuropathy that occurs in intensive care unit (ICU) subjects. It was hypothesized that a low serum level or deficiency of 25(OH)D might be associated with CIPNM. The aim of the present study was to ascertain the 25(OH)D serum level in subjects with CIPNM

    High Dosage of Botulinum Toxin Type A in Adult Subjects with Spasticity Following Acquired Central Nervous System Damage: Where Are We at?

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    Spasticity is a common disabling disorder in adult subjects suffering from stroke, brain injury, multiple sclerosis (MS) and spinal cord injury (SCI). Spasticity may be a disabling symptom in people during rehabilitation and botulinum toxin type A (BTX-A) has become the first-line therapy for the local form. High BTX-A doses are often used in clinical practice. Advantages and limitations are debated and the evidence is unclear. Therefore, we analysed the efficacy, safety and evidence for BTX-A high doses. Studies published from January 1989 to February 2020 were retrieved from MEDLINE/PubMed, Embase, Cochrane Central Register. Only obabotulinumtoxinA (obaBTX-A), onabotulinumtoxinA (onaBTX-A), and incobotulinumtoxinA (incoBTX-A) were considered. The term &ldquo;high dosage&rdquo; indicated &ge; 600 U. Thirteen studies met the inclusion criteria. Studies had variable method designs, sample sizes and aims, with only two randomised controlled trials. IncoBTX-A and onaBTX-A were injected in three and eight studies, respectively. BTX-A high doses were used predominantly in treating post-stroke spasticity. No studies were retrieved regarding treating spasticity in MS and SCI. Dosage of BTX-A up to 840 U resulted efficacious and safety without no serious adverse events (AEs). Evidence is insufficient to recommend high BTX-A use in clinical practice, but in selected patients, the benefits of high dose BTX-A may be clinically acceptable
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