Duration of effect of botulinum toxin type A in adult patients with cervical dystonia: a retrospective chart review

Brashear, Allison; Watts, Maureen Wooten; Marchetti, Albert; Magar, Raf; Lau, Helen; Wang, Liping

doi:10.1016/s0149-2918(00)83049-0

Cited by 42 publications

(40 citation statements)

References 16 publications

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“…50 The beneficial effects of each treatment with botulinum toxin type A last approximately 3 to 5 months in neuromuscular conditions, at which time reinjection is typically requested. [51][52][53] The duration of botulinum toxin type B (Elan) is somewhat shorter than that of type A 50,54 and has been reported as 6 to 8 weeks with 1000 U and 10 to 12 weeks with 2000 U in the management of facial lines. 50 …”

Section: Time Course Of Clinical Effectsmentioning

confidence: 99%

Pharmacology and Immunology of Botulinum Neurotoxins

Aoki¹

2005

International Ophthalmology Clinics

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The first clinical uses of botulinum toxin type A were in ophthalmology for the treatment of strabismus and blepharospasm. 1,2 These uses established the safe and effective focal relaxation of extraocular and facial muscles that would later form the basis for the management of facial lines with botulinum toxin type A. Over the past decade, the use of botulinum toxin type A in facial aesthetics has grown tremendously, and today such injections are the most popular nonsurgical cosmetic procedures in the United States. 3 Currently only one product, BOTOX Cosmetic (Allergan, Irvine, CA), is approved for cosmetic use (eg, indicated for the temporary improvement in the appearance of moderate to severe glabellar [frown] lines associated with corrugator and/or procerus muscle activity in adult patients aged 65 years or younger) in the United States.The effects of botulinum toxin type A in facial aesthetics and ophthalmology are a result of its inhibition of acetylcholine release at the neuromuscular junction after local injection. 4 Specific features of the botulinum neurotoxin preparation, such as serotype and formulation, also contribute to its clinical profile. This chapter describes the basic features of botulinum neurotoxins and their pharmacology, with a focus on issues relevant for oculofacial and aesthetic plastic surgeons.n Synthesis and Structure of Botulinum Neurotoxins Botulinum neurotoxins are proteins that are produced by several different clostridial bacterial species and are related to tetanus toxin. 5 The neurotoxin proteins are synthesized along with several hemagglutinin and/or nontoxin nonhemagglutinin proteins that together form a protein complex that has been referred to as progenitor toxin. 6 The associated 25

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Section: Time Course Of Clinical Effectsmentioning

confidence: 99%

Pharmacology and Immunology of Botulinum Neurotoxins

Aoki¹

2005

International Ophthalmology Clinics

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“…Furthermore, we have investigated aspects of the duration of action of retargeted endopeptidases because a number of reports (14,15) highlight the significant longevity of action of BoNT/A when used therapeutically. As a model system we have chosen to study the effects of selectively targeting the endopeptidase domain to nociceptive afferents.…”

mentioning

confidence: 99%

Inhibition of Release of Neurotransmitters from Rat Dorsal Root Ganglia by a Novel Conjugate of a Clostridium botulinumToxin A Endopeptidase Fragment and Erythrina cristagalliLectin

Duggan¹,

Quinn²,

Chaddock³

et al. 2002

Journal of Biological Chemistry

108

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Clostridial neurotoxins potently and specifically inhibit neurotransmitter release in defined cell types. Here we report that a catalytically active derivative (termed LH N /A) of the type A neurotoxin from Clostridium botulinum has been coupled to a lectin obtained from Erythrina cristagalli to form a novel conjugate. This conjugate exhibits an in vitro selectivity for nociceptive afferents compared with the anatomically adjacent spinal neurons, as assessed using in vitro primary neuronal culture systems to measure inhibition of release of neurotransmitters. Chemical conjugates prepared between E. cristagalli lectin and either natively sourced LH N /A or recombinant LH N /A purified from Escherichia coli are assessed, and equivalence of the recombinant material are demonstrated. Furthermore, the dependence of inhibition of neurotransmitter release on the cleavage of SNAP-25 is demonstrated through the use of an endopeptidase-deficient LH N /A conjugate variant. The duration of action of inhibition of neurotransmitter released by the conjugate in vitro is assessed and is comparable with that observed with Clostridium botulinum neurotoxin. Finally, in vivo electrophysiology shows that these in vitro actions have biological relevance in that sensory transmission from nociceptive afferents through the spinal cord is significantly attenuated. These data demonstrate that the potent endopeptidase activity of clostridial neurotoxins can be selectively retargeted to cells of interest and that inhibition of release of neurotransmitters from a neuronal population of therapeutic relevance to the treatment of pain can be achieved. The clostridial neurotoxin (CNT)1 family includes tetanus toxin (TeNT), produced by Clostridium tetani, and the seven antigenically distinct botulinum neurotoxins produced from strains of Clostridium botulinum (BoNTs). These proteins are responsible for the conditions of tetanus and botulism, respectively, that develop as a direct result of inhibition of Ca 2ϩ -dependent neurotransmitter release, a mechanism of action common to all the CNTs. In the case of BoNTs, intoxication of the neuromuscular junction is thought to occur in at least three phases: an initial binding phase, an internalization phase, and finally a neurotransmitter blockade phase (1).All CNTs have a similar structure and consist of a heavy chain (ϳ100 kDa) covalently joined to a light chain (ϳ50 kDa) by a single disulfide bond. Proteolytic cleavage of the heavy chain of C. botulinum neurotoxin type A (BoNT/A) generates two fragments of ϳ50 kDa each. The C-terminal domain (H C ) is required for target cell binding, with the N-terminal domain (H N ) being proposed to be involved in intracellular membrane translocation (2). Under conditions in which the disulfide bond between the light and heavy chains is maintained, trypsin cleavage results in a 100-kDa species termed LH N /A (light chain plus N-terminal heavy chain domain) representing a catalytically active, non-cell binding, non-toxic derivative of BoNT/A. In addition to obtainin...

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“…25 Neuromuscular blockade using botulism toxin is emerging as the most viable conservative treatment option. 22,[26][27][28] Unfortunately, like other treatments of CD, this is palliative and must be repeated, as the blockade wears off in several weeks to months. 11,26 Failure of adequate palliation after 1 to 2 years of conservative care is considered an indication for surgical interventions.…”

Section: Introductionmentioning

confidence: 99%

“…22,[26][27][28] Unfortunately, like other treatments of CD, this is palliative and must be repeated, as the blockade wears off in several weeks to months. 11,26 Failure of adequate palliation after 1 to 2 years of conservative care is considered an indication for surgical interventions. 25 Current surgical procedures include muscle denervation 22,25,27 and, more recently, deep brain stimulation similar to those procedures used for Parkinson disease.…”

Section: Introductionmentioning

confidence: 99%

Reduction of Cervical Dystonia After an Extended Course of Chiropractic Manipulation: A Case Report

Kukurin¹

2004

Journal of Manipulative and Physiological Therapeutics

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Duration of effect of botulinum toxin type A in adult patients with cervical dystonia: a retrospective chart review

Cited by 42 publications

References 16 publications

Pharmacology and Immunology of Botulinum Neurotoxins

Pharmacology and Immunology of Botulinum Neurotoxins

Inhibition of Release of Neurotransmitters from Rat Dorsal Root Ganglia by a Novel Conjugate of a Clostridium botulinumToxin A Endopeptidase Fragment and Erythrina cristagalliLectin

Reduction of Cervical Dystonia After an Extended Course of Chiropractic Manipulation: A Case Report

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