Abstract Details

Title Focal Painful Neuropathies Treated with Rimabotulinumtoxin B

Topic Ethics, Pain and Palliative Care

Presentation(s) P02 - (-)

Poster/Presentation
Number 012

Objective

Background BACKGROUND: Studies have demonstrated clinical improvement in patients with diabetic peripheral neuropathy1, postherpetic neuralgia2, and posttraumatic neuropathies2 following intradermal injections of onabotulinumtoxin A(obtxA). The proposed mechanism of action is disrupted neuroexocytotic release of calcitonin gene-related peptide (CGRP), substance-P, and other pain neurotransmitters. A more effective blockade of CGRP-release in mouse trigeminal ganglia was demonstrated using serotype-B botulinum toxin compared to serotype-A, implicating potential differences in pain modulation between serotypes. There are no published reports on rbtxB for painful neuropathies.

Design/Methods DESIGN/METHODS: Case Series. 18 patients were evaluated, with specific diagnoses including: notalgia paresthetica(N=6), brachioradial pruritis(N=3), complex regional pain syndrome(CRPS; N=2), postherpetic neuralgia(N=2), and posttraumatic neuropathy(N=5). Patients received intradermal rbtxB injections, 5000units/1cc volume, distributed in a 2x2cm grid pattern over primary pain sites, similar to injections for hyperhidrosis. Effective rbtxB dosages ranged from 1000-15000units total per treatment session (average: 4500units). Responsiveness was measured by (1) subjective account of pain, and (2) change in pain visual-analog-scale (VAS) before/after injections.

Results RESULTS: Most patients reported substantial reductions in pain and paresthesias. VAS scores were reduced by an average of 4.3 points comparing before/after injections. CRPS patients required higher rbtxB dosage and responded less (VAS score decreased by 2 points averaged) compared to other indications. All injections were well-tolerated. No adverse effects were reported.

Conclusions CONCLUSIONS: Similar to obtxA, rbtxB can be an effective and safe treatment for focal painful neuropathies. That CRPS was less responsive may suggest a different pathophysiologic mechanism underlying the origin of pain compared to other focal neuropathies. Future studies will be required to investigate these findings further.

Authors/Disclosures
Patrick M. Grogan, MD, FAAN (Neurology Associates) PRESENTER	No disclosure on file
Maria V. Alvarez, MD (Neurology Assciates)	No disclosure on file
Wendy Chao, DO	No disclosure on file
Marijean Buhse (Stony Brook University)	Marijean Buhse has received personal compensation in the range of $5,000-$9,999 for serving on a Speakers Bureau for Biogen.

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