Long-Term Effects of Botulinum Toxin Complex Type A Injection on Mechano- and Metabo-Sensitive Afferent Fibers Originating from Gastrocnemius Muscle

Abstract

The aim of the present study was to investigate long term effects of motor denervation by botulinum toxin complex type A (BoNT/A) from Clostridium Botulinum, on the afferent fibers originating from the gastrocnemius muscle of rats. Animals were divided in 2 experimental groups: 1) untreated animals acting as control and 2) treated animals in which the toxin was injected in the left muscle, the latter being itself divided into 3 subgroups according to their locomotor recovery with the help of a test based on footprint measurements of walking rats: i) no recovery (B0), ii) 50% recovery (B50) and iii) full recovery (B100). Then, muscle properties, metabosensitive afferent fiber responses to potassium chloride (KCl) and lactic acid injections and Electrically-Induced Fatigue (EIF), and mechanosensitive responses to tendon vibrations were measured. At the end of the experiment, rats were killed and the toxin injected muscles were weighted. After toxin injection, we observed a complete paralysis associated to a loss of force to muscle stimulation and a significant muscle atrophy, and a return to baseline when the animals recover. The response to fatigue was only decreased in the B0 group. The responses to KCl injections were only altered in the B100 groups while responses to lactic acid were altered in the 3 injected groups. Finally, our results indicated that neurotoxin altered the biphasic pattern of response of the mechanosensitive fiber to tendon vibrations in the B0 and B50 groups. These results indicated that neurotoxin injection induces muscle afferent activity alterations that persist and even worsen when the muscle has recovered his motor activity.

Characteristic Variation of Electromechanical Delay After the Botulinum Toxin Injection in Spastic Biceps Brachii Muscles

“…We have also found that the EMD values were inversely proportional to the contraction level for all the subjects in our test cohort; the measured value at 30% MVC is 45 ± 21% higher than the value at 50% MVC. The driving hypothesis behind this study was that due to the BT-induced chemodenervation of the fibers, the limited availability of the active fibers in an MU results in a reduced twitch strength ( 39 ). Additionally, a complete denervation of all the fibers from the associated motor neuron (MN) results in an absence of twitch.…”

Very Long Persistence of Botulinum Toxin B in a Patient’s Serum

“…In our case, such prolonged excretion in faeces was not observed although the toxin was still present in the serum. A recent study suggests that the persistence of BoNT intoxication can be influenced both by the ability of the toxin protease or its cleaved SNARE protein substrate to resist turnover [5].…”

Mitochondrial transplantation ameliorates acute limb ischemia

“…This evaluation has been primarily used in crushed nerve injuries to show decreased peripheral limb function due to nerve damage. [46][47][48] We did not evaluate nerve function in our study; however, this cannot be ruled out because of 2 hours of ischemia time. Some nerve damage may have contributed to limb dragging observed in mitochondria mice.…”