
(202) Paralytic Effects of BoNT‐A VS BoNT‐B in Injected and Non‐Injected Muscles: Implications to Toxin Therapy
Author(s) -
Arezzo Joseph C.,
Litwak Mona S.,
Caputo Florence A.,
Shopp George M.,
Meyer Kathleen E.
Publication year - 2001
Publication title -
pain medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.893
H-Index - 97
eISSN - 1526-4637
pISSN - 1526-2375
DOI - 10.1111/j.1526-4637.2001.pme01039-3.x
Subject(s) - medicine , toxin , pharmacology , anesthesia , microbiology and biotechnology , biology
Botulinum toxin (BoNT) injections are a promising new therapeutic approach for treatment of various pain syndromes (eg, myofascial pain, pain from chronic muscle spasm). The toxin acts by inhibiting acetylcholine release at neuromuscular junctions thereby alleviating excessive contraction in injected muscles, but at higher doses results in a “spread” of partial paralysis to surrounding muscles. This study compared the effects of a single injection of BoNT‐B (Myobloc™) vs BoNT‐A (Botox®) in injected and non‐injected muscles. Using quantitative electrophysiologic methods, the degree of paralysis was assessed by measuring the amplitude of the evoked compound muscle action potential (CMAP) in the injected muscle (abductor pollicis brevis [APB]), in neighboring muscles (first dorsal interosseous [FDI]), and in relatively distant muscles (abductor digiti minimi [ADM]) of the monkey hand. Induced paralysis was determined by comparing data at baseline and 2 weeks post‐injection. Preliminary studies established a minimum effective dose (MED) (~70% reduction in CMAP) for each compound (BoNT‐A, 0.09 U; BoNT‐B, 0.44 U). In this study, doses included the MED, 5×, and 25× the MED. One APB of each monkey (n = 10/group) was injected with 100 μL of BoNT‐B and the contralateral APB with an equivalent dose of BoNT‐A. Both compounds were associated with a dose‐dependent “spread” of induced paralysis to the neighboring FDI muscle, but the effect was greater with BoNT‐A (92.7% vs 57.3%, P < 0.002). Similarly, in the distant ADM muscle, mean percent reduction in CMAP was 58.3% in the BoNT‐A group compared with only 2.0% in the BoNT‐B group (P < 0.0001). None of the monkeys receiving 25× MED of BoNT‐B had functional paralysis in the ADM muscle, whereas this level of dysfunction occurred in 30% of those treated with BoNT‐A. Overall, BoNT‐B exhibited less spread to non‐injected muscles, suggesting advantages in terms of “control” and “safety.” Support of Elan Pharmaceuticals is gratefully acknowledged.