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      Ultrasound Guidance for Botulinum Neurotoxin Chemodenervation Procedures

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          Abstract

          Injections of botulinum neurotoxins (BoNTs) are prescribed by clinicians for a variety of disorders that cause over-activity of muscles; glands; pain and other structures. Accurately targeting the structure for injection is one of the principle goals when performing BoNTs procedures. Traditionally; injections have been guided by anatomic landmarks; palpation; range of motion; electromyography or electrical stimulation. Ultrasound (US) based imaging based guidance overcomes some of the limitations of traditional techniques. US and/or US combined with traditional guidance techniques is utilized and or recommended by many expert clinicians; authors and in practice guidelines by professional academies. This article reviews the advantages and disadvantages of available guidance techniques including US as well as technical aspects of US guidance and a focused literature review related to US guidance for chemodenervation procedures including BoNTs injection.

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          European consensus table on the use of botulinum toxin type A in adult spasticity.

          Paolo Manganotti, Alexander C. H. Geurts, H-F Juan … (2008)
          A group of clinicians from across Europe experienced in the use of botulinum toxin type A for the treatment of spasticity following acquired brain injury gathered to develop a consensus statement on best practice in managing adults with spasticity. This consensus table summarizes the current published data, which was collated following extensive literature searches, their assessment for level of evidence and discussion among the whole group. Published information is supplemented by expert opinion based on clinical experience from 16 European countries, involving 28 clinicians, who treat an average of approximately 200 patients annually, representing many thousand spasticity treatments with botulinum toxin per year.
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            Botulinum toxin A, brain and pain.

            Ivica Matak, Zdravko Lacković (2014)
            Botulinum neurotoxin type A (BoNT/A) is one of the most potent toxins known and a potential biological threat. At the same time, it is among the most widely used therapeutic proteins used yearly by millions of people, especially for cosmetic purposes. Currently, its clinical use in certain types of pain is increasing, and its long-term duration of effects represents a special clinical value. Efficacy of BoNT/A in different types of pain has been found in numerous clinical trials and case reports, as well as in animal pain models. However, sites and mechanisms of BoNT/A actions involved in nociception are a matter of controversy. In analogy with well known neuroparalytic effects in peripheral cholinergic synapses, presently dominant opinion is that BoNT/A exerts pain reduction by inhibiting peripheral neurotransmitter/inflammatory mediator release from sensory nerves. On the other hand, growing number of behavioral and immunohistochemical studies demonstrated the requirement of axonal transport for BoNT/A's antinociceptive action. In addition, toxin's enzymatic activity in central sensory regions was clearly identified after its peripheral application. Apart from general pharmacology, this review summarizes the clinical and experimental evidence for BoNT/A antinociceptive activity and compares the data in favor of peripheral vs. central site and mechanism of action. Based on literature review and published results from our laboratory we propose that the hypothesis of peripheral site of BoNT/A action is not sufficient to explain the experimental data collected up to now.
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              Botulinum toxin dilution and endplate targeting in spasticity: a double-blind controlled study.

              Brian D. Simpson, Steve Flanagan, D Weisz … (2008)
              To determine the effects of botulinum neurotoxin type A (BTX-A) dilution and endplate-targeting in spastic elbow flexors. Double blind randomized controlled trial; 4-month follow-up after a 160-unit injection of BTX-A into spastic biceps brachii (4 sites). Randomization into: group 1: 100 mouse units (MU)/mL dilution, 0.4cc/site, 4-quadrant injection; group 2: 100MU/mL dilution, 0.4cc/site, 4 sites along endplate band; group 3: 20MU/mL dilution, 2cc/site, 4-quadrant injection (n=7 per group). Institutional tertiary care ambulatory clinic. Referred sample of 21 adults with spastic hemiparesis. No participant withdrew due to adverse effects. A 160-unit injection of BTX-A of different dilutions and locations into biceps brachii. Primary: agonist and antagonist (cocontraction) mean rectified voltage (MRV) of elbow flexors/extensors during maximal isometric flexion/extension; secondary: maximal voluntary power of elbow flexion/extension; spasticity angle and grade in elbow flexors/extensors (Tardieu Scale); active range of elbow extension/flexion. BTX-A injection overall reduced agonist flexor MRV (-47.5%, P<0.0001), antagonist flexor MRV (-12%, P=.037), antagonist extensor MRV (-19%, P<.01), flexion maximal voluntary power (-33%, P<.001), elbow flexor spasticity angle (-30%, P<.001) and grade (-17%, P=.03), and increased extension maximal voluntary power (24%, P=.037) and active range of elbow extension (5.5%, 8 degrees , P=.002). Agonist and antagonist flexor MRV reductions in group 3 (-81% and -31%) were greater than in groups 1 and 2, whereas increase in active range of elbow extension was greater in group 2 (10%) than in groups 1 and 3 (P<.05, analysis of covariance [ANCOVA]). Elbow flexor spasticity was significantly reduced in groups 2 and 3 only (P<.05, ANCOVA). In spastic biceps, high-volume or endplate-targeted BTX-A injections achieve greater neuromuscular blockade, cocontraction and spasticity reduction, and active range of elbow extension improvement, than low volume, nontargeted injections.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Toxins (Basel)
                Journal ID (iso-abbrev): Toxins (Basel)
                Journal ID (publisher-id): toxins
                Title: Toxins
                Publisher: MDPI
                ISSN (Electronic): 2072-6651
                Publication date (Electronic): 28 December 2017
                Publication date Collection: January 2018
                Volume: 10
                Issue: 1
                Electronic Location Identifier: 18
                Affiliations
                [1 ]Functional and Applied Biomechanics Section, Rehabilitation Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892-1604, USA
                [2 ]Combined Neurosciences IRB, National Institutes of Health, Bethesda, MD 20892-1604, USA; karpb@ 123456ninds.nih.gov
                Author notes
                [* ]Correspondence: kalter@ 123456cc.nih.gov ; Tel.: +1-301-451-7529
                Author information
                https://orcid.org/0000-0002-5405-2143
                Article
                Publisher ID: toxins-10-00018
                DOI: 10.3390/toxins10010018
                PMC ID: 5793105
                PubMed ID: 29283397
                SO-VID: 0b568115-937e-434b-8421-983a6ceca092
                Copyright © © 2017 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 23 October 2017
                Date accepted : 21 December 2017
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: botulinum neurotoxin,botulinum toxin,chemodenervation,guidance,ultrasound,electrical stimulation,electromyography,motor points,anatomic localization
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: botulinum neurotoxin, botulinum toxin, chemodenervation, guidance, ultrasound, electrical stimulation, electromyography, motor points, anatomic localization

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