Translational pediatrics · 2026
The motor endplate band as an optimal target for botulinum toxin in congenital torticollis: evidence from a rabbit model.
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Chen Ren, Zhang Ji, Duan Rurong, Fan Jinglan, Chen Hong
Аннотация
BACKGROUND: Botulinum neurotoxin type A (BoNT-A) is an established minimally invasive treatment for congenital muscular torticollis (CMT); however, current injection strategies rely on empirical anatomical landmarks rather than precise functional targets. Accurate localisation of the sternocleidomastoid muscle (SCM) motor endplate band may improve treatment efficacy by optimising toxin delivery. We aimed to investigate the therapeutic efficacy of BoNT-A injection targeting the motor endplate band of the SCM, as localised by acetylcholinesterase (AChE) whole-muscle staining, in the treatment of CMT.
METHODS: Twelve adult New Zealand rabbits underwent AChE whole-muscle staining to reveal the distribution pattern of the SCM motor endplate band. Forty-eight rabbits were randomised into four equal groups: a normal group, a model group (ethanol-induced CMT fibrosis), a conventional injection group (BoNT-A injection at the fibrotic induration), and a motor endplate band injection group (BoNT-A injection at the centre of the motor endplate band). One week after BoNT-A injection, spiral computed tomography (CT) was performed to measure SCM length. Haematoxylin and eosin (H&E) and Masson's trichrome staining were used to assess muscle fibre cross-sectional area (CSA) and collagen deposition, respectively. Western blotting was employed to detect the protein expression of alpha-smooth muscle actin (α-SMA) and muscle RING-finger protein-1 (MuRF-1).
RESULTS: AChE staining revealed that the motor endplate band was distributed between 20.25%±0.31% and 49.36%±0.41% of the SCM length, with its geometric centre located at 30.07%±0.44% of the muscle length. Two weeks after ethanol-induced modelling, the model group exhibited shortened SCM length, an elevated collagen area ratio, and upregulated α-SMA expression, confirming the successful establishment of the CMT fibrosis model. Following BoNT-A injection at different targets, the motor endplate band injection group demonstrated greater SCM length, lower collagen area ratio, lower α-SMA expression, and higher MuRF-1 expression compared with the conventional injection group; all differences were statistically significant.
CONCLUSIONS: The motor endplate band of the SCM is a promising and anatomically defined target for BoNT-A injection in the treatment of CMT. The targeted injection strategy guided by the motor endplate band was associated with significantly greater anti-fibrotic efficacy compared with the conventional injection strategy in suppressing muscle fibrosis and improving muscle function.
METHODS: Twelve adult New Zealand rabbits underwent AChE whole-muscle staining to reveal the distribution pattern of the SCM motor endplate band. Forty-eight rabbits were randomised into four equal groups: a normal group, a model group (ethanol-induced CMT fibrosis), a conventional injection group (BoNT-A injection at the fibrotic induration), and a motor endplate band injection group (BoNT-A injection at the centre of the motor endplate band). One week after BoNT-A injection, spiral computed tomography (CT) was performed to measure SCM length. Haematoxylin and eosin (H&E) and Masson's trichrome staining were used to assess muscle fibre cross-sectional area (CSA) and collagen deposition, respectively. Western blotting was employed to detect the protein expression of alpha-smooth muscle actin (α-SMA) and muscle RING-finger protein-1 (MuRF-1).
RESULTS: AChE staining revealed that the motor endplate band was distributed between 20.25%±0.31% and 49.36%±0.41% of the SCM length, with its geometric centre located at 30.07%±0.44% of the muscle length. Two weeks after ethanol-induced modelling, the model group exhibited shortened SCM length, an elevated collagen area ratio, and upregulated α-SMA expression, confirming the successful establishment of the CMT fibrosis model. Following BoNT-A injection at different targets, the motor endplate band injection group demonstrated greater SCM length, lower collagen area ratio, lower α-SMA expression, and higher MuRF-1 expression compared with the conventional injection group; all differences were statistically significant.
CONCLUSIONS: The motor endplate band of the SCM is a promising and anatomically defined target for BoNT-A injection in the treatment of CMT. The targeted injection strategy guided by the motor endplate band was associated with significantly greater anti-fibrotic efficacy compared with the conventional injection strategy in suppressing muscle fibrosis and improving muscle function.