Bibliografías temáticas / Botulinum toxin – Therapeutic use

Literatura académica sobre el tema "Botulinum toxin – Therapeutic use"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 29 de enero de 2023

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Artículos de revistas sobre el tema "Botulinum toxin – Therapeutic use"

Palazón-García, Ramiro y Ana María Benavente-Valdepeñas. "Botulinum Toxin: From Poison to Possible Treatment for Spasticity in Spinal Cord Injury". International Journal of Molecular Sciences 22, n.º 9 (5 de mayo de 2021): 4886. http://dx.doi.org/10.3390/ijms22094886.

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Botulism has been known for about three centuries, and since its discovery, botulinum toxin has been considered one of the most powerful toxins. However, throughout the 20th century, several medical applications have been discovered, among which the treatment of spasticity stands out. Botulinum toxin is the only pharmacological treatment recommended for spasticity of strokes and cerebral palsy. Although its use as an adjuvant treatment against spasticity in spinal cord injuries is not even approved, botulinum toxin is being used against such injuries. This article describes the advances that have been made throughout history leading to the therapeutic use of botulinum toxin and, in particular, its application to the treatment of spasticity in spinal cord injury.

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Zbrojkiewicz, Małgorzata, Agata Lebiedowska y Barbara Błońska-Fajfrowska Barbara Błońska-Fajfrowska. "Botulinum toxin in medicine and cosmetology – two hundred years’ history and new perspectives". Postępy Higieny i Medycyny Doświadczalnej 72 (16 de abril de 2018): 278–89. http://dx.doi.org/10.5604/01.3001.0011.7617.

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It has been nearly 200 years since the discovery of the botulinum toxin and the strain responsible for its synthesis Clostridium botulinum. Over this period, the knowledge about botulism and the use of botulinum toxin in medicine has been significantly expanded. Currently, eight serotypes of botulinum toxin (A-H) are known and they differ from each other by molecular weight, antigenic structure, immunogenicity, receptors, localization of coding genes and by the duration of the therapeutic effect. American physician Allan B. Scott was the first to demonstrate the use of botulinum toxin for medical purposes. Nowadays, botulinum toxin type A is widely used in medicine. Botulinum toxin injections are not only one of the most popular non-surgical aesthetic-cosmetic procedures, but are also widely used in neurology, ophthalmology and dermatology. The therapeutic potential of botulinum toxin has not been exhausted yet. Currently, many clinical trials are underway to extend the therapeutic indications of botulinum toxin and to improve its safety. Due to the huge development in medicine, botulinum toxin is today not only associated with aesthetic procedures and improvement in appearance, but also with raising the quality of life for people suffering from diseases with excessive muscle contraction and with other neuromuscular disorders.

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Tugnoli, Valeria, Roberto Eleopra, Cesare Montecucco y Domenico De Grandis. "The therapeutic use of botulinum toxin". Expert Opinion on Investigational Drugs 6, n.º 10 (octubre de 1997): 1383–94. http://dx.doi.org/10.1517/13543784.6.10.1383.

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Martina, Emanuela, Federico Diotallevi, Giulia Radi, Anna Campanati y Annamaria Offidani. "Therapeutic Use of Botulinum Neurotoxins in Dermatology: Systematic Review". Toxins 13, n.º 2 (5 de febrero de 2021): 120. http://dx.doi.org/10.3390/toxins13020120.

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Botulinum toxin is a superfamily of neurotoxins produced by the bacterium Clostridium Botulinum with well-established efficacy and safety profile in focal idiopathic hyperhidrosis. Recently, botulinum toxins have also been used in many other skin diseases, in off label regimen. The objective of this manuscript is to review and analyze the main therapeutic applications of botulinum toxins in skin diseases. A systematic review of the published data was conducted, following Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. Botulinum toxins present several label and off-label indications of interest for dermatologists. The best-reported evidence concerns focal idiopathic hyperhidrosis, Raynaud phenomenon, suppurative hidradenitis, Hailey–Hailey disease, epidermolysis bullosa simplex Weber–Cockayne type, Darier’s disease, pachyonychia congenita, aquagenic keratoderma, alopecia, psoriasis, notalgia paresthetica, facial erythema and flushing, and oily skin. Further clinical trials are still needed to better understand the real efficacy and safety of these applications and to standardize injection and doses protocols for off label applications.

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Intiso, Domenico. "Therapeutic Use of Botulinum Toxin in Neurorehabilitation". Journal of Toxicology 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/802893.

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The botulinum toxins (BTX), type A and type B by blocking vesicle acetylcholine release at neuro-muscular and neuro-secretory junctions can result efficacious therapeutic agents for the treatment of numerous disorders in patients requiring neuro-rehabilitative intervention. Its use for the reduction of focal spasticity following stroke, brain injury, and cerebral palsy is provided. Although the reduction of spasticity is widely demonstrated with BTX type A injection, its impact on the improvement of dexterity and functional outcome remains controversial. The use of BTX for the rehabilitation of children with obstetrical brachial plexus palsy and in treating sialorrhea which can complicate the course of some severe neurological diseases such as amyotrophic lateral sclerosis and Parkinson's disease is also addressed. Adverse events and neutralizing antibodies formation after repeated BTX injections can occur. Since impaired neurological persons can have complex disabling feature, BTX treatment should be viewed as adjunct measure to other rehabilitative strategies that are based on the individual's residual ability and competence and targeted to achieve the best functional recovery. BTX therapy has high cost and transient effect, but its benefits outweigh these disadvantages. Future studies must clarify if this agent alone or adjunctive to other rehabilitative procedures works best on functional outcome.

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TaniosMarrelli, LorenaCury, Daniele MazzucaDominelli, IdibertoJosé ZotarelliFilho, LeandroMoreira Tempest y PatríciaGarani Fernandes. "THERAPEUTIC USE OF BOTULINUM TOXIN IN DENTISTRY". International Journal of Advanced Research 6, n.º 10 (30 de septiembre de 2018): 1219–22. http://dx.doi.org/10.21474/ijar01/7926.

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Ghasemi, Majid, Rasul Norouzi, Mehri Salari y Bahador Asadi. "Iatrogenic Botulism After the Therapeutic Use of Botulinum Toxin-A". Clinical Neuropharmacology 35, n.º 5 (2012): 254–57. http://dx.doi.org/10.1097/wnf.0b013e31826248b8.

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Erbguth, Frank J. "Historical notes on botulism,Clostridium botulinum, botulinum toxin, and the idea of the therapeutic use of the toxin". Movement Disorders 19, S8 (2004): S2—S6. http://dx.doi.org/10.1002/mds.20003.

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Eleopra, R., O. Rossetto y C. Montecucco. "Non-A/non-B botulinum toxin for therapeutic use". Toxicon 68 (junio de 2013): 73. http://dx.doi.org/10.1016/j.toxicon.2012.07.051.

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Corsalini, Massimo, Francesco Inchingolo, Gianna Dipalma, Angelika Elzbieta Wegierska, Ioannis Alexandros Charitos, Maria Assunta Potenza, Antonio Scarano et al. "Botulinum Neurotoxins (BoNTs) and Their Biological, Pharmacological, and Toxicological Issues: A Scoping Review". Applied Sciences 11, n.º 19 (23 de septiembre de 2021): 8849. http://dx.doi.org/10.3390/app11198849.

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Botulinum toxins or neurotoxins (BoNTs) are the most potent neurotoxins known, and are currently extensively studied, not only for their potential lethality, but also for their possible therapeutic and cosmetic uses. Currently, seven types of antigenically distinct toxins are known and characterized, produced by a rod-shaped bacterium, Clostridium botulinum. Human poisoning by botulism (presenting with severe neuromuscular paralytic disease) is usually caused by toxins A, B, E, and F type. Poisoning from contaminated food preparations is the most common cause of noniatrogenic botulism. The spores are highly resistant to heat but are easily destroyed at 80 °C for thirty minutes. Type A and B toxins are resistant to digestion by the enzymes of the gastrointestinal system. After their entry, BoNTs irreversibly bind to cholinergic nerve endings and block the release of acetylcholine from the synapses. In contrast, in wound botulism, the neurotoxin is instead product by the growth of C. botulium in infected tissues. The contamination by BoNT inhalation does not occur by a natural route but it is certainly the most dangerous. It can be caused by the dispersion of the botulinum toxin in the atmosphere in the form of an aerosol and therefore can be deliberately used for bioterrorist purposes (e.g., during CBRN (chemical, biological, radiological, and nuclear) unconventional events). In addition, BoNTs are currently used to treat a variety of diseases or alleviate their symptoms, such as the onabotulinumtoxinA for migraine attacks and for cosmetic use. Indeed, this paper aims to report on updated knowledge of BoNTs, both their toxicological mechanisms and their pharmacological action.

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Tesis sobre el tema "Botulinum toxin – Therapeutic use"

Seifart, Anja. "The impact of functional electrical stimulation to the lower leg after a single botulinum toxin injection in children with a spastic equinus gait due to cerebral palsy". Thesis, Stellenbosch : Stellenbosch University, 2008. http://hdl.handle.net/10019.1/2860.

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Thesis (MScPhysio (Physiotherapy))--Stellenbosch University, 2008.
Cerebral palsy (CP) is a common neurological condition seen in children which results in childhood disability. Damage to the developing brain results in abnormal muscle tone and decreased force generation, which leads to loss of independent function. Previous studies investigating interventions targeting the typical equinus gait pattern seen in spastic CP have reported inconclusive and widespread outcomes. Objectives The objectives of the study were to determine (1) the effect of functional electrical stimulation (FES) after a single botulinum toxin injection into the triceps surae muscle as a functional orthosis on various gait parameters and economy of movement; (2) caregivers’ perceptions of the impact of the intervention on their child’s function and participation, and (3) optimal timing intervals for introducing FES after a botulinum toxin injection. Method Single-subject research with a multiple baseline approach was conducted on five ambulant subjects (average age 5.1 years, SD=1.4) in the Cape Metropole with a dynamic equinus gait due to hemiplegic CP. Two-dimensional gait analysis, isometric dynamometry, Energy Expenditure Index (EEI), and a caregiver questionnaire were used to gather data on walking speed, ankle angles at initial contact of gait, isometric plantarand dorsiflexior muscle strength, energy expenditure during gait, as well as caregiver perception on participation changes. Statistical analysis was conducted by means of ANOVA tests and graphic data illustrations. Results A statistically significant pre- to post intervention (FES after botulinum toxin) change was found for plantarflexor muscle strength. This effect was partially maintained over the withdrawal phase. Caregivers felt the intervention to have a positive influence on their children’s walking speeds, as well as on age-appropriate function and participation. Selfselected walking speed, dorsiflexor muscle strength, and ankle angles at initial contact did not change significantly. A 32-day interval between between botulinum toxin and the FES programme resulted in the most pronounced improvements in terms of walking speed, EEI scores, and plantarflexor muscle strength. Conclusion FES to the lower limb, 32 days after botulinum toxin into the triceps surae, applied for 30 minutes per day, five times a week over a total of four weeks, seemed to improve selected gait parameters as well as caregiver perception of impact on function and activities of daily living. However, further research is needed.

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Redman, Toni Annette. "Upper limb Botulinum Toxin-A in children with hemiplegic cerebral palsy : physiological corticomotor pathways and effect on health related quality of life". University of Western Australia. Faculty of Medicine and Dentistry and Health Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0123.

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[Truncared abstract] Introduction: The assessment of any therapy requires not only an understanding of how that therapy works but also how it affects health related quality of life (HRQOL). Botulinum Toxin A(BoNT-A) therapy for upper limb spasticity management in children with hemiplegic cerebral palsy(CP) is currently under trial. Despite its use for over a decade for lower limb spasticity, little is known about the mechanisms involved in improving motor function and the effect on the child and their familys HRQOL. Both central and peripheral mechanisms are hypothesised[1]. Whilst evidence of improved quality of movement and ability to perform tasks is emerging[2-4], this cannot be directly correlated with an improvement in HRQOL. In addition, the traditional method of assessing child HRQOL by parent proxy reports has come under question[5, 6]. The World Health Organisation now recommends the collection of both parent proxy and child self-reports[7]. Aims: 1. Investigate the corticomotor projections to the upper limb in school aged children with hemiplegic CP and the changes that occur with BoNT-A therapy by transcranial magnetic stimulation (TMS). 2. Investigate the effect of upper limb BoNT-A therapy on HRQOL of school aged children with hemiplegic CP by completion of the PedsQL 4.0 Generic Core Scales and 3.0 CP Module. 3. Determine the concordance between Child Self-Report and Parent Proxy Report scores for the PedsQL 4.0 Generic Core Scales and 3.0 CP Module. 4. Determine the concordance between PedsQL scores and function as assessed by the Melbourne Assessment of Unilateral Upper Limb Function (MUUL). Methods: Design: Prospective randomised pilot study. Setting: Department of Paediatric Rehabilitation, Princess Margaret Hospital, and Centre for Neurological and Neuromuscular Disorders, Perth. Participants: 22 school aged children with hemiplegic CP aged 7yr 0mth-13yr 11mth (12 treatment, 10 control). 3 Treatment: One episode BoNT-A injections (dose 1-2U/kg/muscle) into the upper limb for treatment group. The control group received usual care. ... Conclusion: This pilot study provides preliminary evidence of the effects of upper limb BoNT-A therapy at both a central physiological and a broader quality of life level in school aged children with hemiplegic CP. At a central level, corticomotor pathway reorganisation occurs in the setting of BoNT-A. However the reorganisation is not limited to the affected side pathways suggesting a systemic BoNT-A effect or developmental changes. Similarly, in this pilot study, there was no statistically significant effect of upper limb BoNT-A on the childs HRQOL as assessed by the PedsQL although positive trends were observed 4 for a number of physical and psychosocial domains. The collection of both child self-report and parent proxy reports when assessing HRQOL is recommended, and function needs to be assessed independently. Larger studies across the broader CP population, the design of CP specific HRQOL tools appropriate for use in the higher functioning CP cohort, and alternative better tolerated methods of investigating the motor system in children with movement disorders are recommended.

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Corry, Ian S. "Use of motion analysis laboratory in assessing the effects of botulinum toxin in cerebral palsy". Thesis, Queen's University Belfast, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295345.

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Lindsay, Cameron. "The early use of botulinum toxin in post stroke spasticity : developing a new approach to contracture management". Thesis, Keele University, 2018. http://eprints.keele.ac.uk/5173/.

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Introduction: Patients surviving a severe stroke are at risk of developing contractures. Evidence suggests that spasticity may be a cause of contractures, particularly in patients who have not recovered functional movement. The relationship and the time course of spasticity and contractures remain unclear. This thesis aims to identify when spasticity can be identified and investigate whether treating spasticity at onset using botulinum-toxin, might slow contracture development. Methods: A double blind randomised placebo-controlled trial with an initial six-week screening phase was conducted in an acute NHS hospital. Patients with no arm function (Action Research Arm Test grasp-score < 2) within six-weeks of stroke were eligible for screening. Screening for spasticity was carried out using a neurophysiological method. Patients who developed spasticity were randomly assigned to receive intra-muscular injections of 0.9%sodium chloride solution or onabotulinumtoxinA. Measures of spasticity and contracture development (reduced passive range of motion (PROM) and increased stiffness) were taken at the wrist and elbow at baseline, weeks-two, four, six and twelve post injection and six-months post stroke. Results: Over a 23-month period, 1143 patients were admitted with stroke and 120 consented to study participation. Of these, 100 developed spasticity without functional recovery 84%(95% confidence interval(95%CI):76%-89%). Mean time of spasticity onset was 13.5-days(SD:8.5). Of the 100 eligible for randomisation 93 were included in intention to treat analysis. At six-weeks, treatment results in a reduction in wrist spasticity (mean difference(MD):4.8μV;95%CI:1.2to8.4;p=0.009), stiffness (MD=4.2mN/deg;95%CI:0.7to7.7;p=0.02) and PROM (MD=13.8o;95%CI:6.1to21.6;p=0.01). At the elbow; four-weeks spasticity (MD=9.8μV;95%CI:4.3to15.4;p=0.001), four-week stiffness (MD=4.8mN/deg;95%CI:-0.1to9.6;p=0.056) and twelve-weeks PROM–(MD=6.5o;95%CI:0.6to12.3;p=0.03). These changes were not maintained at the six-month follow-up assessment. Conclusion: Spasticity occurs earlier and is more common than previously reported. Treating spasticity early with onabotulinumtoxinA can reduce the rate of contracture formation. Further work is required to elucidate who is at greatest risk of contractures and to explore if these treatment effects can be sustained with adjunct therapies.

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Ng, Wai-yun Louisa y 吳慧欣. "Production of variants of mitogillin with reduced IgE bindingactivity". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31972093.

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Teixeira, Natacha Betânia Alves. "Toxina botulínica, considerações em medicina dentária". Master's thesis, [s.n.], 2014. http://hdl.handle.net/10284/4398.

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Projeto de Pós-Graduação/Dissertação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Medicina Dentária
A toxina botulínica (TB) foi durante muito anos considerada um promotor de doença. No presente é considerada um agente terapêutico versátil para o tratamento de distúrbios musculares. O seu mecanismo de ação ocorre ao nível da fenda sináptica do músculo esquelético e leva a uma desnervação parcial e funcional dos neurónios motores, através da inibição da liberação do neurotransmissor de acetilcolina (Ach), juntamente com o bloqueio da libertação de outros neurotransmissores periféricos relacionados com a dor, que permite tenha uma ação antinociceptiva. Este trabalho consiste numa revisão bibliográfica narrativa que tem como objetivos abordar a estrutura e a síntese da TB, o seu mecanismo de acção e os diferentes aspectos farmacológicos e imunológicos associados à sua utilização terapêutica e abordar as diversas indicações de utilização ao nível da medicina dentária, nomeadamente, desordens temporomandibulares, distonias oromandibulares, bruxismo, sialorreia, cefaleia tensional, sorriso gengival e pós-operatório cirúrgico. As palavras-chaves utilizadas foram: ―Botulinum Toxin‖; ―Botulinum Toxin Type A‖; ―Temporomandibular Disorders‖; ―Bruxism‖; ―Gummy Smile‖; ―Myofascial Pain‖; ―Sialorrhoea‖; ―Tension Headache‖; ―Oromandibular Distonia‖; ―Masseter Hy-pertrophy‖; ―Temporoamdibular Joint Disc Displacement‖; ―Temporomandibular Joint Luxation‖; ―Pain‖; ―Clinical Use‖; ―Mechanism Of Action‖; ―Safety And Efficacy‖ combinadas de diversas formas. Nos últimos anos tem-se verificado o valor da TB no âmbito de diversas áreas da Medicina Dentária, no entanto, no seu enquadramento legal por parte da Ordem dos Médicos Dentistas, esta recomenda apenas a sua aplicação por parte de profissionais que tenham a devida formação e experiência. Botulinum toxin (BT) was for many years considered a promoter of disease. At present it is considered a versatile therapeutic agent for the treatment of muscular disorders. The mechanism of action of BT is at the level of the synaptic cleft of skeletal muscle and leads to a partial functional denervation of motor neurons by inhibiting the release of the neurotransmitter acetylcholine (Ach), together with blocking the release of other neurotransmitters related peripheral with pain, which allows it to have an antinociceptive action. This work consists in a narrative literature review that aims to deal with the structure and synthesis of BT, its mechanism of action and different pharmacological and immunological aspects related to its therapeutic use and discuss the its different uses in dentistry like in temporomandibular disorders, oromandibular dystonias, bruxism, drooling, tension headache, gummy smile surgery and postoperatively. The keywords used were: ―Toxin Botulinum‖; ―Botulinum Toxin Type A‖; ―Temporomandibular Disorders‖; ―Bruxism‖; ―Gummy Smile‖; ―Myofascial Pain‖; ―Sialorrhoea‖; ―Tension Headache‖; ―Oromandibular Distonia‖; ―Masseter Hy-pertrophy‖; ―Temporoamdibular Joint Disc Displacement‖; ―Temporomandibular Joint Luxation‖; ―Pain‖; ―Clinical Use‖; ―Mechanism Of Action‖; ―Safety And Efficacy‖ combined in various ways. In recent years BT has been used within various dentistry areas with success, however in a legal point of view, the Portuguese Dental Association leaves the recommendation that its use must be restrict to the professionals who have proper training and experience.

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Preston, Nicholas John. "Does the use of home-based assistive rehabilitation technology enhance the functional benefits of botulinum toxin in children with cerebral palsy who have upper limb movement difficulties : a single-blind randomised controlled trial". Thesis, University of Leeds, 2014. http://etheses.whiterose.ac.uk/8075/.

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Background. Spastic cerebral palsy is a common cause of childhood activity limitation that restricts children’s personal development. Botulinum toxin is a spasticity treatment that can improve upper limb activity limitation when combined with rehabilitation therapy. We investigated whether use of a computer-assisted arm rehabilitation (CAAR) device enhanced the benefits of botulinum toxin treatment of the upper limb of children with cerebral palsy. Method. Fifteen children with cerebral palsy aged 5 – 12 years old undergoing botulinum toxin treatment for spasticity of the upper limb were randomly allocated into a CAAR group and a control group using minimisation, a procedure that balances groups for prognostic factors e.g. age and disability. Children used CAAR at home for 6 weeks. Assessments were carried out by blinded assessor at baseline, six and twelve weeks. Primary outcome measure. ABILHAND-kids. Secondary outcome measure. Canadian Occupational Performance Measure (COPM). Results. ABILHAND-kids. Activity limitation worsened following botulinum toxin treatment. An ANCOVA revealed that this was not significant (median scores, all participants: baseline, 0.8084; six weeks, 0.145; twelve weeks, 0.334; p=0.462) and that there was no difference between groups (p=0.699). COPM. A Friedman’s ANOVA revealed a statistically significant improvement that was clinically non-significant (baseline score, 4/10; six week score, 4.6/10; twelve week score, 4.6/10; p=0.031). A Kruskal-Wallis ANOVA revealed no difference in scores between groups at each time point. CAAR use. Mean daily use, 7 minutes. Maximum use, 256 minutes (played over 24 days, mean daily use 10.667 minutes). Sample size. This sample size was underpowered by 75%. Conclusion. This study potentially supports evidence that botulinum treatment should be used only in combination with rehabilitation therapy but it was not adequately powered and a Type II error cannot be ruled out. The CAAR device did not engage the children enough to promote sufficient intensity and repetition of arm movements.

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Salga, Marjorie. "Inflammation et paraostéoarthropathies neurogènes Blocking neuromuscular junctions with botulinum toxin A injection enhances neurological heterotopic ossification development after spinal cord injury in mice Traumatism brain injury: if neurological damage was not the key to the development of neurogenic heterotopic ossification? Corticosteroid injection is an alternative therapeutic strategy to treat pain in Neurogenic Heterotopic Ossification: a Case Series". Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLV072.

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Les ossifications hétérotopiques (OH) sont des formations osseuses bénignes anormalement situées dans les tissus mous du corps humain. Les OH peuvent être d’origine génétique, acquise et idiopathique. Elles sont appelées paraostéoarthropathies neurogènes (POAN) lorsqu’elles se développent après une lésion du système nerveux central. Cette thèse a pour objectif de préciser les facteurs inflammatoires locaux et systémiques, impliqués dans la survenue de POAN. Nous avons tout d’abord étudié l’effet de l’injection de composants de paroi membranaire bactérienne dans un modèle de souris développant des ossifications hétérotopiques neurogènes (OHN) après section médullaire et injection intramusculaire d’un myotoxique chimique. L’injection locale intramusculaire comme systémique d’un composant de paroi d’Escherichia Coli ou de Staphylococcus Aureus a permis d’augmenter de façon significative le volume des OHN. A l’issu de ces expériences, il semble que le niveau d’inflammation intramusculaire influence de façon importante le volume des OHN, selon un effet-dose. La provenance des agents de paroi bactérienne fait supposer que l’inflammation pourrait être spécifiquement induite par des pathogènes infectieux. Il semblerait qu’il existe un niveau inflammatoire seuil à partir duquel, la section médullaire ne soit plus obligatoire à la survenue d’OH. Toujours dans le même modèle murin, nous avons montré que le blocage de la jonction neuro-musculaire par une injection de toxine botulique augmente le volume des OHN. La jonction neuro-musculaire semble réguler le développement de OHN dans un muscle pathologique chez la sourie avec section médullaire. Il est possible que cette régulation s’effectue via un mécanisme de neuro-inflammation locale. Suite à ces découvertes en recherche fondamentale, nous avons mené une étude cas-témoins recherchant des facteurs pourvoyeurs d’inflammation à la phase très précoce suivant l’accident neurologique, qui pourraient être corrélés à l’apparition de POAN. Cette étude a été la première à montrer que les patients avec POAN présentent de façon plus importante des infections à Pseudomonas Aeruginosa. La présence de traumatismes associés et de chirurgies était corrélée à la survenue de POAN, tout comme la longueur de la ventilation mécanique, du coma, du séjour en réanimation et la présence d’une trachéotomie. En revanche, aucun critère neurologique n’était associé à une augmentation du risque de POAN. A gravité neurologique égale, il semble donc que les patients développant des POAN présentent un niveau d’inflammation plus élevé (infections, polytraumatisme, chirurgies multiples, réanimation) que les patients sans POAN. Comme pour d’autres pathologies articulaires avec une composante inflammatoire, nous avons infiltrer des dérivés cortisonés localement, dans le but de traiter les douleurs induites par certaines POAN. Un mois après l’injection, 80% des patients présentaient un soulagement des douleurs. Ce traitement local parait être une alternative intéressante à la prise en charge antalgique des POAN douloureux.Les POAN sont toujours, à l’heure actuelle, diagnostiqués et prises en charge tardivement lors de l’apparition de complications. L’enjeu actuel est d’identifier les patients à risque de développer des POAN, le plus tôt possible après leur accident neurologique de façon à leur assurer un suivi et une prise en charge adaptée et précoce. En se basant sur les études cliniques et les données issues du modèle murin développant des POAN, nous allons relever des critères cliniques et biologiques reconnus comme étant corrélés à l’apparition de POAN dans une base de données clinico-biologique. Ce tout premier travail prospectif sur les POAN permettra de repérer les patients à risque de développer des POAN et peut être à terme d’identifier des cibles thérapeutiques qui permettrons de prévenir ou de guérir les POAN
Heterotopic ossifications (H0) are abnormal ectopic bone formations that develop in soft tissues. HO can be related to genetic factors or acquired pathologies. HO occurring after central nervous system lesion are called neurogenic HO (NHO). The objective of this project is to identify local and systemic inflammatory factors that may be associated with occurrence of NHO. We study first, the effect of bacterial membrane components on the development of NHO in a mouse model of spinal cord injury triggered by injection of a myotoxic compound into muscle. Local and systemic administration of membrane components from Escherichia coli or Staphylococcus aureus significantly increased the volume of NHO. Changes in the level of inflammation, which was dose responsive, correlated with changes in NHO volume suggesting that inflammation influences NHO formation. As bacterial membrane components were also linked to increased volumes of NHO, it is possible that inflammation triggered by infectious pathogens could also be involved in NHO development. Furthermore, we identified that after reaching a certain threshold of inflammation, triggered by administration of bacterial membrane components, spinal cord injury was not required for NHO formation. Further experiments with this model involved determining the effect of blocking neuromuscular signaling on NHO formation. Botulinum toxin injection increased the size of NHO. Therefore, neuromuscular signaling also modulates NHO development in damaged muscles of spinal cord-injured mice. By extension, local neuroinflammation was implicated in regulating neuromuscular signals received by affected muscles. Based on these preclinical results, we carried out a case-control study to look for factors inducing inflammation that could be linked with NHO occurrence, and which occur at early stages after neurological trauma. This study identifies for the first time that patients with Pseudomonas Aeruginosa-positive infections were more likely to develop NHO. NHO patients more frequently experience surgery and polytrauma, compared to patients without NHO. Furthermore, extended stays in intensive care, long periods of mechanical ventilation, enduring coma, or patients with a tracheotomy were more frequent in patient with NHO. In contrast, no neurological factors were associated with a higher risk of developing NHO. Patients with comparable neurological trauma severity were more susceptible to develop NHO when they were experiencing a high level of inflammation (infection, polytrauma, surgeries, intensive care). Like for other inflammatory joint pathologies, we performed a further study which involved the infiltration of NHO with corticosteroid locally, in order to treat pain induced by NHO formation. One month after treatment, 80% of patients reported an improvement of pain. Therefore, we demonstrate that corticosteroid infiltration at the site of NHO is an effective treatment for pain associated with NHO. Detecting patients that are at risk to develop NHO as early as possible after an accident is imperative, to adapt rehabilitative strategies or treatment needs specific for patients that develop NHO. However, NHO diagnosis occurs during late phase of disease, when complications are occurring. To address this shortfall in the detection of NHO formation, we are undertaking the first prospective study of NHO, where clinical and biological information will be recorded to make a database. The specific data to be collected has been defined by our previous research in the mouse model and earlier clinical studies, and will identify specific biological and clinical factors that can be monitored to identify patients at risk to develop NHO. The outcomes of this project have specific implications in the understanding the drivers of NHO formation and its detection. Global outcomes of this project include improving patient management and possibly the prevention of NHO formation in patients

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Joussain, Charles. "Construction and validation of HSV-1 vectors with selective and long-term expression in bladder afferent neurons for gene therapy of neurogenic detrusor overactivity. : A translational approach Botulinum Neurotoxin Light Chains Expressed by Defective Herpes Simplex Virus Type-1 Vectors Cleave SNARE Proteins and Inhibit CGRP Release in Rat Sensory Neurons Development and assessment of herpes simplex virus type 1 (HSV-1) amplicon vectors with expression from sensory neuron-selective promoters. Construction and properties of replication-incompetent HSV-1 recombinant vectors expressing transgenic botulinum toxins in primary cultures of human sensory neurons and displaying long-term expression in vivo. Therapeutic escalation for the neurogenic bladder in SCI patients : A bicentric study real life experience Long-term outcomes and risks factors for failure of intradetrusor onabotulinumtoxin A injections for the treatment of refractory neurogenic detrusor overactivity". Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLV057.

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Cinquante à 80% des patients atteints d'une lésion médullaire traumatique (LM) présente des d'épisodes d'incontinence urinaire liés à une hyperactivité détrusorienne neurogène (HDN). L’HDN est caractérisée par des contractions non inhibées du détrusor pendant la phase de remplissage vésical, qui conduit à une augmentation des pressions détrusoriennes, particulièrement lorsque l’HDN est associée à une dyssynergie vésico-sphinctérienne. L'objectif principal de la prise en charge de l’HDN est d'obtenir une vidange vésicale régulière, complète et à basse pression, ainsi que de maintenir la continence urinaire, afin d'améliorer la qualité de vie des patients et de prévenir les complications uro-néphrologiques dont l’insuffisance rénale. La prise en charge actuelle repose sur une pharmacothérapie agissant principalement au niveau de la branche efférente, motrice, du réflexe mictionnel, permettant ainsi un remplissage vésical à basse pression. Le traitement de première intention repose sur des antimuscariniques oraux, le plus souvent associés à la réalisation d’autosondages pluriquotidiens. En cas d’échec de cette thérapeutique, l’injection intradétrusorienne de toxine botulique A est proposée. Cependant, malgré leur efficacité, ces traitements induisent des effets secondaires et souffrent d’un échappement thérapeutique, conduisant à un traitement chirurgical de troisième ligne. La technique de Brindley, qui consiste en une désafférentation des racines postérieures sacrées innervant la vessie associée à une stimulation électrique, à la demande, des racines antérieures est une alternative prometteuse, mais reste peu proposée en raison de la complexité de la procédure chirurgicale requise. L'HDN résulte de l'émergence d'un réflexe spinal anormal médié par une plasticité des afférences vésicales de type-C dans les suites de la LM. Le projet de mon équipe est de réaliser une déafférentation vésicale par thérapie génique afin d'abolir le réflexe de miction spinale altérée. Dans un second temps, la miction sera déclenchée par une stimulation électrique à la demande, des neurones efférents de la vessie. Mon travail de thèse consistait à développer les outils nécessaires à une telle désafférentation moléculaire. En conséquence, j'ai construit des vecteurs défectifs HSV-1 délivrant comme transgène thérapeutique la chaine légère d’un toxine botulique (BoNT-LC), sous le contrôle du promoteur du gène codant pour la protéine liée au gène de la calcitonine (hCGRP), permettant une expression sélective au sein des neurones sensoriels. La cassette de transcription a été insérée dans le locus LAT du génome HSV-1, la seule région du génome du virus qui reste active sur le plan transcriptionnel pendant une infection latente. Ces vecteurs ont été évalués (i) in vitro, sur des lignées cellulaires d'origine neurale et sur des cultures primaires de neurones sensoriels embryonnaires et adultes de rats, ainsi que sur des cultures primaires de neurones sensoriels et sympathiques humains adultes, (ii) ex vivo, sur des cultures organotypiques de ganglions sensoriels, sympathiques et parasympathiques de rats adultes, et (iii) in vivo, post inoculation au niveau du coussinet plantaire de rats adultes. Nos résultats indiquent que (i) les vecteurs expriment des BoNT-LC fonctionnelles, clivant ainsi les protéines SNARE post infection de cultures primaires de neurones sensoriels de rats et d’être humain, et inhibant la libération du neuromédiateur CGRP dans les neurones sensoriels de rat, (ii) la sélectivité d’expression de ces vecteurs dans des neurones sensoriels humains, par rapport aux neurones sympathiques humains, et (iii) une expression transgénique prolongée in-vivo au sein de ganglions sensoriels (DRG), au moins pour trois mois, après injection. Par conséquent, ces vecteurs semblent présenter les trois principales spécifications requises pour le développement d’une future stratégie de thérapie génique visant à traiter l’HDN
Fifty to 80% of patients with traumatic spinal cord injury (SCI) undergo urinary incontinence episodes, mostly related to neurogenic detrusor overactivity (NDO). NDO is characterized by uninhibited detrusor contractions during the bladder-filling phase which could lead to a significant increase in bladder pressures, especially when associated to sphincter-destrusor-dyssynergia, leading to uro-nephrological complications. The main goal of NDO management following SCI is to achieve regular and complete bladder emptying, avoiding high intra-detrusor pressure and maintaining continence, in order to improve patients’ quality of life and to prevent renal failure. The current management is well characterized and relies on pharmacotherapy acting primarily at the level of efferent motor micturition reflex branch, thus allowing bladder filling at low pressure. First line treatment relies on oral antimuscarinics, often associated to clean intermittent bladder self-catheterization. When patients are refractory to antimuscarinics, injection of botulinum toxin A into the detrusor is proposed. However, despite their efficacy, these treatments fail to persist in the long term, leading to a third-line surgical treatment, which consists in cystoplasty augmentation or sacral neuromodulation. The Brindley technique, which consist in a sacral deafferentation of bladder posterior roots associated to an electrical stimulation, on demand, of anterior roots is a promising alternative, but remains seldom performed because of the complex surgical procedure required. NDO results from the emergence, secondary to neuronal plasticity following SCI, of an abnormal micturition reflex mediated by bladder afferent C-fibers, conveying aberrant sensory information to the spinal cord. The aim of the team where I developed my work is to silence these bladder afferent C-fibers in order to abolish the impaired spinal micturition reflex after SCI. In a second time, micturition would be fired, on demand, by electric stimulation of the bladder efferent neurons. My work consisted in developing the tools and methods required for such molecular deafferentation. Accordingly, I constructed replication-incompetent HSV-1 vectors conceived to deliver a therapeutic transcription cassette, consisting in the light chains of botulinum toxin (BoNT-LC) driven by the human version of the promoter of the gene encoding calcitonin gene-related protein (hCGRP), to achieve sensory neuron-selective transgenic expression. The transcription cassette was inserted into the LAT locus of the HSV-1 genome, the only region of the virus genome that remains transcriptionally active during latent infection. These vectors have been assessed (i) in vitro, on cell lines of neural origin and on primary cultures of rat embryonic and adult sensory neurons, and on primary cultures of adult human sensory and sympathetic neurons, (ii) ex vivo, on organotypic cultures of sensory, sympathetic and parasympathetic ganglia from adult rats, and (iii) in vivo, in sensory ganglia following infection at the hind footpad of adult rats.Our results indicate that (i) the vectors express functional BoNT-LC, thereby cleaving proteins of the SNARE complex in rat and human sensory neurons and inhibiting release of the neuromediator CGRP in rat sensory neurons, (ii) the transcription cassette delivered by the vectors display highly selectively expression towards human sensory neurons, as compared to human sympathetic neurons, and (iii) the vectors induced long-term transgenic expression in sensory (DRG) ganglia (at least for three months) following footpad injection. Therefore, the vectors seem to accomplish the three main specifications required for a future gene therapy strategy, allowing to restore urinary continence and micturition without catheterization and without any major surgery. This approach will represent a major breakthrough in the management of NDO in SCI patients with complete and incomplete lesion

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Silva, Cláudia Sofia Dionísio. "Use of Botulinum Toxin for Refractory Trigeminal Neuralgia". Master's thesis, 2018. https://repositorio-aberto.up.pt/handle/10216/112186.

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Libros sobre el tema "Botulinum toxin – Therapeutic use"

NIH Consensus Development Conference on Clinical Use of Botulinum Toxin (1990 Bethesda, Md.). Botulinum toxin. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, Office of Medical Applications of Research, 1990.

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Joseph, Jankovic, ed. Botulinum toxin: Therapeutic clinical practice & science. Philadelphia, PA: Saunders/Elsevier, 2008.

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Botulinum-toxin therapy. Stuttgart: Thieme, 2000.

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Botulinum neurotoxins. Heidelberg: Springer, 2013.

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Chancellor, Michael B. Botulinum toxin in urology. Heidelberg: Springer, 2011.

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Joseph, Jankovic y Hallett Mark, eds. Therapy with botulinum toxin. New York: M. Dekker, 1994.

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Cooper, Grant, ed. Therapeutic Uses of Botulinum Toxin. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-247-2.

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FRCP, Moore Peter, ed. Handbook of botulinum toxin treatment. Oxford [England]: Blackwell Science, 1995.

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Gluckstein, Fritz P. Clinical use of botulinum toxin: January 1987 through September 1990, 318 citations. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Library of Medicine, Reference Section, 1990.

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Gluckstein, Fritz P. Clinical use of botulinum toxin: January 1987 through September 1990 : 318 citations. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Library of Medicine, Reference Section ; Washington, D.C. : For sale by the Supt. of Docs., U.S. G.P.O., 1990.

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Capítulos de libros sobre el tema "Botulinum toxin – Therapeutic use"

Wan, Michael J., Sara AlShaker y David G. Hunter. "Use of Botulinum Toxin in Ophthalmology". En Botulinum Toxin Therapy, 147–60. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/164_2019_325.

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Chancellor, Michael B. y Christopher P. Smith. "Use of Botulinum Toxin in the Genitourinary System". En Botulinum Toxin Therapy, 171–84. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/164_2019_308.

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Wan, Michael J., Sara AlShaker y David G. Hunter. "Correction to: Use of Botulinum Toxin in Ophthalmology". En Botulinum Toxin Therapy, 283. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/164_2020_413.

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Wollmer, M. Axel, Michelle Magid, Tillmann H. C. Kruger y Eric Finzi. "The Use of Botulinum Toxin for Treatment of Depression". En Botulinum Toxin Therapy, 265–78. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/164_2019_272.

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Li, Sheng y Gerard E. Francisco. "The Use of Botulinum Toxin for Treatment of Spasticity". En Botulinum Toxin Therapy, 127–46. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/164_2019_315.

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Berardelli, Alfredo y Antonella Conte. "The Use of Botulinum Toxin for Treatment of the Dystonias". En Botulinum Toxin Therapy, 107–26. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/164_2019_339.

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Yuan, Hsiangkuo y Stephen D. Silberstein. "The Use of Botulinum Toxin in the Management of Headache Disorders". En Botulinum Toxin Therapy, 227–49. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/164_2020_365.

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Wollmer, M. Axel, Michelle Magid, Tillmann H. C. Kruger y Eric Finzi. "Correction to: The Use of Botulinum Toxin for Treatment of Depression". En Botulinum Toxin Therapy, 279. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/164_2020_411.

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Li, Sheng y Gerard E. Francisco. "Correction to: The Use of Botulinum Toxin for Treatment of Spasticity". En Botulinum Toxin Therapy, 281. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/164_2020_412.

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Berardelli, Alfredo y Antonella Conte. "Correction to: The Use of Botulinum Toxin for Treatment of the Dystonias". En Botulinum Toxin Therapy, 285. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/164_2020_414.

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Actas de conferencias sobre el tema "Botulinum toxin – Therapeutic use"

Figueiredo, Camila Angelo Vidal de, Kaline dos Santos Kishishita Castro y Sílvia Raimunda Costa Leite. "Therapeutic management of movement disorders present in Huntington’s Disease: a literature review". En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.430.

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Background: Huntington’s Disease (HD) is a hereditary neurodegenerative genetic disease with motor, cognitive and behavioral repercussions that interferes in several areas of the patients’ lives. Therefore, to increase the quality of life for patients the therapeutic management of symptoms is necessary. Objective: to elucidate the main forms of treatment that reduces motor disorders present in HD. Methods: an integrative literature review was conducted using scientific articles published between 2016-2020 about this topic found in Pubmed and Google Scholar databases. Results: the chorea treatment in HD can be done using Tetrabenazine, deutetrabenazine or antipsychotics. During a study by the Huntington Study Group (HSG), tetrabenazine proved its efficacy, however, due to several adverse effects, its use was reduced. Thus, deutetrabenazine was created, which consists in a tetrabenazine deuterated version, with a longer half- life and less adverse effects. Studies by the HSG found that besides reducing chorea, it also improves motor function in general in patients. Antipsychotics are used when the patient has behavioral and psychiatric symptoms that prevent him from using the other drugs. The dystonia treatment involves physiotherapy and botulinum toxin injections, which are also used in the bruxism therapy, along with mouth protectors. Abnormal gait and balance problems can be reduced with psychomotor rehabilitation, physiotherapy, and using a walker. Conclusion: the control of HD motor symptoms is an important way to increase patients’ quality of life. Therefore, more studies are necessary to expand the effective therapeutic options.

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Sternlieb, S. J., S. Ferrell, S. P. Kantrow y G. Lea. "Pyridostigmine for Therapeutic Botulinum Toxin Reversal in Adult". En American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2404.

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Garrido, João Guilherme Santos, João Gustavo dos Anjos Morais Oliveira, Luana Brandão de Sales Reis, Beatriz do Nascimento Garcia Moreno y Ricardo Moreno do Carmo Junior. "Benefits of Botulinum Toxin type A in post-stroke neurorehabilitation". En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.360.

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Background: Stroke can injure the upper motor neuron, and may develop spasticity, a speed-dependent excessive contraction that makes muscle extension difficult. The botulinum toxin type A make contraction difficult, by inhibiting acetylcholine liberation by the lower motor neuron. Thus, it is hypothesized that the botulinum toxin has benefits in post-stroke spasticity. Objective: To evaluate the benefits of botulinum toxin in post-stroke spasticity. Methods: This is a literature review, which articles were searched via PubMed, with MeSH descriptors, using the formula: (“Botulinum toxin type A”) AND (“stroke”) AND (“spasticity”). Clinical trials, systematics reviews and metanalysis, that used botulinum toxin type A as intervention were included. Results: The search resulted in 16 articles, and 5 were selected. A metanalysis, that included 10 clinical trials, evaluated 950 patients and the botulinum toxin type A in superior limbs spasticity has not shown benefits. Yet, another metanalysis which evaluated 27 clinical trials with 2793 patien ts, with both superior and inferior limbs spasticity, demonstrated improvement in levels of tonicity and deficiency evaluation scales. A prospective cohort whose outcome was based in doctor-patient goals has shown great improvement in mobility (87%), positioning (100%), pain relief and spasms (>80%). A clinical trial has also shown improvement on inferior limb function after 3 months of botulinum toxin use. Conclusions: The botulinum toxin use for improvement in inferior limbs spasticity is well described on the literature. However, its use for superior limbs is still controversial, requiring more studies.

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Taylor, Graham, Donald Leo y Andy Sarles. "Detection of Botulinum Neurotoxin/A Insertion Using an Encapsulated Interface Bilayer". En ASME 2012 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/smasis2012-8101.

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Many signaling mechanisms in living cells occur at biological boundaries via cell surface receptors and membrane proteins embedded in lipid bilayers. The coordination of actions of sensory and motor neurons in the nervous system represents one example of many that heavily depends on lipid membrane bound receptor mediated signaling. As a result, chemical and biological toxins that disrupt these neural signals can have severe physiological effects, including paralysis and death. Botulinum neurotoxin Type A (BoNT/A) is a proteolytic toxin that inserts through vesicle membranes and cleaves membrane receptors involved with synaptic acetylcholine uptake and nervous system signal conduction. In this work, we investigate the use of a Bioinspired liquid-supported interface bilayer for studying the insertion of BoNT/A toxin molecules into synthetic lipid bilayers. DPhPC lipid bilayers are formed using the regulated attachment method (RAM), as developed by Sarles and Leo, and we perform current measurements on membranes exposed to BoNT/A toxin to characterize activity of toxin interacting with the synthetic bilayer. Control tests without toxin present are also presented. The results of these tests show an increase in the magnitude of current through the bilayer when the toxin is included. We interpret these initial results to mean that incorporation of BoNT/A toxin at a high concentration in an interface bilayer increases the permeability of the membrane as a result of toxin molecules spanning the thickness of the bilayer.

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Santos, Gabriel Cerqueira, Caio de Almeida Lellis, Bruno Coelho Duarte Oliveira, Letícia Romeira Belchior, Caíque Seabra Garcia de Menezes Figueiredo y Ledismar José da Silva. "Botulinum toxin type A in the treatment of Myofascial Pain Syndrome: A Systematic Review". En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.263.

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Introduction: Myofascial pain syndrome (MPS) is a regional painful condition characterized by the presence of trigger points in the affected muscles, and botulinum toxin type A (BoNT-A) is a possible therapeutic option. Objectives: To evaluate the safety and efficacy of botulinum toxin in the management of MSD. Design and setting: A systematic review conducted at the Pontifical Catholic University of Goiás. Methodology: A systematic review was conducted in the PubMed, IBECS and VHL databases: “(Myofascial Pain Syndromes OR Myofascial Trigger Point Pain) AND Botulinum toxin”. Randomized studies, clinical trials and case reports published in the last 10 years were selected. Results: Two randomized trials concluded that application of BoNT-A, regard less of the application site, did not show significant improvement in pain intensity compared to the control group. Also, another multicenter, random ized trial reported that application of ToNB-A to the masseter muscles did not result in improvement of SDM within three months of application. Finally, a clinical trial reported improvement in visual numeric scores of myofascial pain in the scapular girdle in subjects who received a second dose (P = 0.019). Conclusion: BoNT-A was not effective in improving SDM at any site of ap plication and in any dosage studied, except in a single study, therefore insuf ficient to state whether subsequent doses have better results.

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Lemos, Gabrielle Torres Oliveira, Gabriel das Chagas Benevenuto, Gabriela Guy Duarte, Bruno Alves Pinto y Ivan Magalhães Viana. "The use of Botulinum toxin type A for the treatment of refractory chronic migraine". En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.566.

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Background: Chronic migraine is a neurological disorder described as refractory to preventive treatments. Based on the PREEMPT study, the National Institute for Health and Clinical Excellence (NICE) and the FDA approved, in 2010, the use of Botulinum Toxin type A (BoNT/A) to treat refractory chronic migraine. Objectives: To review the effectiveness of the use of BoNT/A in the treatment of refractory migraine. Methods: Bibliographic review based on PubMed database, using the descriptors “migraine” and “botulinum toxin”. Clinical trials, meta-analyzes and randomized controlled tests, from the last five years, were defined as inclusion criteria. Results: Sanz et al., (2016) infiltrated BoNT/A in 69 patients - mean age 43 years old, 88.4% women, mean infiltration rate was 2,0. The reduction of headache days and pain intensity was 48.5% and 20.5%, respectively, both statistically significant (p <0.006). Ion et al., (2018) intervened 61 patients - mean age 50 years old, 87% women, mean infiltration of 3.5. 73% showed a reduction greater than 50% for the frequency of migraine episodes, 48% for headache days and 48% for drug use. Dodick et al., (2019) applied BoNT/A in 688 patients - 696 received placebo. The severity and frequency of pain showed a statistically significant reduction (p < 0.001) after the first week of treatment in relation to the control group. Conclusions: The use of BoNT/A to treat refractory chronic migraine proves to be effective, although there is need for studies with larger samples to ensure its effectiveness.

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Popescu, Mara, Jochen Kammermeier, Rakesh Vora y Mohamed Mutalib. "G14 The use of pyloric EndoFLIP to assess response to botulinum toxin injection in children". En Abstracts of the BSPGHAN Annual Meeting, 25–27 April 2022. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/flgastro-2022-bspghan.34.

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Pinheiro, Renato Serquiz Elias, Emanuelly da Costa Nobre Soares, Maria Eduarda Bezerra Figueiredo y Stella Mandu Cicco. "Pisa syndrome in Parkinson’s disease: case description". En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.644.

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Context: Pisa Syndrome (PS) is a rare postural disorder, characterized by dystonia of the trunk muscles, lateral deviation as well as rotation of the axial axis. There is a strong association with Parkinson’s disease (PD) due to the possible imbalance between neurotransmitters. It happens either due to a decrease in dopaminergic stimuli, either because of an excess of cholinergic stimuli or drugs (an example of antidopaminergics). The diagnosis is clinical, showing at least a 10-degree trunk flexion with improvement of pharmacological and non- pharmacological measures. Case report: A 60-year-old man was diagnosed with PD five years ago due to tipical clinical complaints and physical examination. The treatment recquired an increase of Pramipexole as well as the use of Levodopa and Benserazide. After two years, he complained about neck pain, low back pain, hip pain and a slight trunk twisting. After six months, his pain was worse and he reported right hemidystonia. Thus, he was diagnosed with PS associated with PD. It was decided to optimize the therapy with Pregabalin, muscle relaxants and rehabilitation. However, it did not show any good result. In 2020, the application of botulinum toxin (BTX) evidenced excellent results, improving both the pain and the spasticity of the patient. Conclusions: Early recognition is necessary to introduce the right treatment as soon as possible, especially BTX and rehabilitation, ensuring functionality and avoiding negative outcomes.

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Informes sobre el tema "Botulinum toxin – Therapeutic use"

Cairo, Jessica, Iulia Gherman y Paul Cook. The effects of consumer freezing of food on its use-by date. Food Standards Agency, julio de 2021. http://dx.doi.org/10.46756/sci.fsa.ret874.

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The current Food Standards Agency consumer guidance states that consumers can freeze pre-packed food right up to the “use-by” date and, once food has been defrosted, it should be consumed within 24 hours. This strategic review has collated relevant data to determine whether there is an increased risk in relation to freezing ready-to-eat and non-ready-to-eat foods on the use-by date compared to the day before the use-by date. The review has focused on how the shelf-life of a food is determined and the effects of freezing, thawing and refrigeration on foodborne pathogens, including Bacillus spp., Campylobacter spp., Clostridium botulinum, Clostridium perfringens, Listeria monocytogenes, Salmonella, pathogenic Escherichia coli and Shigella spp. In the UK, food business operators are responsible for setting the safe shelf-life of a food which, in practice, should take into consideration the consumer habits, as well as the factors affecting shelf-life, such as food product characteristics, food processing techniques, transport, retail and domestic food storage temperatures, and type of packaging. Some countries, such as Ireland, New Zealand and Canada specifically recommend including safety margins within shelf lives. This is used to maintain brand integrity because it ensures that the food is consumed in its optimum condition. The FSA has collaborated with other organisations in the production of several guidance documents; however, there is no explicit requirement for the consideration of a margin of safety when setting shelf-life. There is also no legal requirement in the UK to consider a safety margin when setting shelf-life. According to regulations, pathogens should not be present in sufficient levels to cause foodborne illness on the use-by date, as food should still be safe to eat on that day. Given that these requirements are met, the risk assessed in this report arises from the processes of freezing, thawing and subsequent refrigerated storage for a further 24 hours, and the potential for these to increase pathogen levels. In this review, it was found that there is a risk of additional growth of certain pathogens during the refrigerated storage period although the impact of freezing and thawing on the extent of this growth was not readily evident. This risk would relate specifically to ready-to-eat foods as cooking of non-ready-to-eat foods after defrosting would eliminate pathogens. This report explores the potential issues related to consumer freezing on the use-by date and identifies additional information or research required to understand the risks involved. Overall, there is little evidence to suggest a significant change in risk between consumers freezing ready-to-eat food on the use-by date compared to freezing the food on the day before the use-by date. Specific areas that merit further research include the risks due to low temperature survival and growth of L. monocytogenes. There is also a lack of research on the effects of freezing, defrosting and refrigeration on the growth and toxin production of non-proteolytic C. botulinum, and the growth of Salmonella during domestic freezing and thawing. Finally, more information on how food business operators set shelf-life would enable a better understanding of the process and the extent of the safety margin when determining shelf-life of ready-to-eat and non-ready-to-eat foods.

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Safe and effective use of botulinum toxin for refractory LUTS. BJUI Knowledge, diciembre de 2016. http://dx.doi.org/10.18591/bjuik.0053.

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