Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038379 (strabismus)
 9,317 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Botulinum neurotoxins, causative agents of botulism in humans, are produced by Clostridium botulinum, an anaerobic spore-former Gram positive bacillus. Botulinum neurotoxin poses a major bioweapon threat because of its extreme potency and lethality; its ease of production, transport, and misuse; and the need for prolonged intensive care among affected persons. A single gram of crystalline toxin, evenly dispersed and inhaled, can kill more than one million people. The basis of the phenomenal potency of botulinum toxin is enzymatic; the toxin is a zinc proteinase that cleaves neuronal vesicle associated proteins responsible for acetylcholine release into the neuromuscular junction. As a military or terrorist weapon, botulinum toxin could be disseminated via aerosol or by contamination of water or food supplies, causing widespread casualties. A fascinating aspect of botulinum toxin research in recent years has been development of the most potent toxin into a molecule of significant therapeutic utility . It is the first biological toxin which is licensed for treatment of human diseases. In the late 1980s, Canada approved use of the toxin to treat strabismus, in 2001 in the removal of facial wrinkles and in 2002, the FDA in the United States followed suit. The present review focuses on both warfare potential and medical uses of botulinum neurotoxin.
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PMID:Botulinum toxin: bioweapon & magic drug. 2114 97

This retrospective study aimed to examine the safety of botulinum toxin A (BoNT-A) treatment in a paediatric multidisciplinary cerebral palsy clinic. In a sample of 454 patients who had 1515 BoNT-A sessions, data on adverse events were available in 356 patients and 1382 sessions; 51 non-fatal adverse events were reported (3.3% of the total injections number, 8.7% of the patients). On five occasions, the adverse reactions observed in GMFCS V children were attributed to the sedation used (rectal midazolam plus pethidine; buccal midazolam) and resulted in prolongation of hospitalization. Of the reactions attributed to the toxin, 23 involved an excessive reduction of the muscle tone either of the injected limb(s) or generalized; others included local pain, restlessness, lethargy with pallor, disturbance in swallowing and speech production, seizures, strabismus, excessive sweating, constipation, vomiting, a flu-like syndrome and emerging hypertonus in adjacent muscles. Their incidence was associated with GMFCS level and with the presence of epilepsy (Odds ratio (OR) = 2.74 - p = 0.016 and OR = 2.35 - p = 0.046, respectively) but not with BoNT-A dose (either total or per kilogram). In conclusion, treatment with BoNT-A was safe; adverse reactions were mostly mild even for severely affected patients. Their appearance did not necessitate major changes in our practice.
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PMID:Safety of botulinum toxin A in children and adolescents with cerebral palsy in a pragmatic setting. 2348 50

Initially popularized for the treatment of strabismus and blepharospasm, injection of botulinum neurotoxin has become the most commonly performed cosmetic treatment in the United States. Injection techniques have been particularly well-studied in the midface and periocular region, and patient satisfaction tends to be very high. We review the salient differences among available neurotoxins, how to optimally reconstitute them, how to inject the forehead, glabella, lateral canthal lines ("crow's feet"), infralid region, and transverse nasal lines ("bunny lines"), how to sculpt the brow, and how to manage potential complications.
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PMID:The role of neurotoxins in the periorbital and midfacial areas. 2592 74

More than a century has elapsed since the identification of Clostridia neurotoxins as the cause of paralytic diseases. Clostridium botulinum is a heterogeneous group of Gram-positive, rod-shaped, spore-forming, obligate anaerobic bacteria that produce a potent neurotoxin. Eight different Clostridium botulinum neurotoxins have been described (A-H) and 5 of those cause disease in humans. These toxins cause paralysis by blocking the presynaptic release of acetylcholine at the neuromuscular junction. Advantage can be taken of this blockade to alleviate muscle spams due to excessive neural activity of central origin or to weaken a muscle for treatment purposes. In therapeutic applications, minute quantities of botulinum neurotoxin type A are injected directly into selected muscles. The Food and Drug Administration first approved botulinum toxin (BT) type A in 1989 for the treatment of strabismus and blepharospasm associated with dystonia in patients 12 years of age or older. Ever since, therapeutic applications of BT have expanded to other systems, including the gastrointestinal tract. Although only a single fatality has been reported to our knowledge with use of BT for gastroenterological conditions, there are significant complications ranging from minor pain, rash and allergic reactions to pneumothorax, bowel perforation and significant paralysis of tissues surrounding the injection (including vocal cord paralysis and dysphagia). This editorial describes the clinical experience and evidence for the use BT in gastrointestinal motility disorders in children.
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PMID:Use of Clostridium botulinum toxin in gastrointestinal motility disorders in children. 2599 83

There is a long and extensive experience with the use of Botulinum Toxin type A (BoNT-A) injection in the treatment of different types of strabismus and oculomotor palsies. The frequency of its use varies depending on the country and institution. It is a short procedure, may reduce general anesthesia exposure, causes minimal scarring compared to surgery, and can be proposed as an early treatment in unstable strabismus. Over many years, the experience of using BoNT-A indications has been refined and new applications have been reported. The use of BoNT-A in the postoperative period, after strabismus surgery or during surgery, can also be beneficial.
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PMID:The Use of Botulinum Toxin in Strabismus Treatment. 3105 79

Botulinum Neurotoxins have always existed in nature, but its paralytic effect on humans due to the consumption of poorly preserved food was not recognized until 18th century. There are 8 serotypes of botulinum neurotoxins (A, B, C, D, E, F, G, H). Serotype A have been the most recognized one and was initially developed for large scale production in 1940's. The first batch for clinical use was produced by Edward Schantz, who collaborated with Dr. Alan Scott, an ophthalmologist, evaluating botulinum neurotoxin to treat strabismus. The process Schantz used had variability and led to inconsistent batch production. However, this process is still used by various manufacturers of commercial botulinum neurotoxin products as the foundation. These manufacturers have refined the manufacturing of botulinum neurotoxins by implementing new advanced techniques, including better potency assays. Despite the improvements in the manufacturing process, botulinum neurotoxins are still one of the most potent molecules and therefore, require special handing and additional safety/security measurements during production.
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PMID:Manufacturing and Clinical Formulations of Botulinum Neurotoxins. 3193 89

Botulinum neurotoxin is widely used for the treatment of central and peripherical neurological conditions. Initially used to treat strabismus, over the years its use has been expanded also to spasticity and other neurological disorders. This review summarizes the evidence from the published literature regarding its effect on neuropathic pain. Almost all investigations were performed using onabotulinum toxin type A (BoNT/A). Most studies provided positive results, even though toxin formulation, dose, dilution, injection techniques, and sites are heterogeneous across studies. Future larger, high-quality, specifically designed clinical trials are warranted to confirm botulinum neurotoxin efficacy in neuropathic pain.
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PMID:Botulinum Neurotoxin for the Treatment of Neuropathic Pain. 3284 95


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