Background <p>The frontalis muscle, the only elevator of the eyebrow, is essential for upper facial aesthetics and visual field preservation. Both natural aging and chronic botulinum toxin type A (BoNTA) use can contribute to frontalis atrophy and brow ptosis, but their relative impacts remain unclear. This study used large-scale computational modelling to compare long-term structural and functional changes in the frontalis muscle under different BoNTA exposure patterns and across age groups.</p> Methods <p>A 20-year in silico longitudinal simulation of 20,000 virtual subjects was conducted using the AesthetiSIM™ biomechanical platform. Subjects were stratified by baseline age (20–30, 31–40, 41–50 years) and randomized to four treatment arms: Control (no BoNTA), Low-Frequency BoNTA (20 U every 6 months), High-Frequency BoNTA (20 U every 4 months), or Focal Overuse (high-frequency for 10 years then cessation). Primary outcomes included frontalis muscle volume, static brow position, dynamic lift capacity, ptosis incidence, and surgical-threshold brow descent. Analyses employed mixed-effects models, ANOVA, Cox regression, and sensitivity testing.</p> Results <p>At 20 years, mean muscle volume loss was greatest in Controls (61.2%) and least in Low-Frequency BoNTA (38.3%), though reduced loss in BoNTA groups reflected early chemodenervation rather than muscle preservation. Brow descent was highest in Controls (4.1&#xa0;mm) and lowest in Low-Frequency BoNTA (2.3&#xa0;mm). Ptosis incidence reached 58.3% in Controls versus 20.9% in Low-Frequency BoNTA. Younger age at onset correlated with greater atrophy and earlier ptosis in all groups except Low-Frequency BoNTA. Supplemental modelling confirmed that smaller descent in BoNTA groups was attributable to functional suppression, not protective effects.</p> Conclusions <p>Both aging and BoNTA cause progressive frontalis atrophy and brow descent. Frequent, early BoNTA use accelerates functional decline, with incomplete recovery after discontinuation. Conservative, low-frequency dosing better preserves muscle volume and brow position, particularly in younger patients. Long-term clinical imaging studies are warranted to validate these findings. </p> <p>Level of Evidence: Not gradable.</p>

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Frontalis atrophy and brow ptosis in aging vs. chronic BoNTA use: a large-scale facial computational modelling study

  • Eqram Rahman,
  • Alain Michon,
  • Parinitha Rao,
  • Patricia E. Garcia,
  • Sotirios Ioannidis,
  • Jean D. A. Carruthers,
  • William Richard Webb

摘要

Background

The frontalis muscle, the only elevator of the eyebrow, is essential for upper facial aesthetics and visual field preservation. Both natural aging and chronic botulinum toxin type A (BoNTA) use can contribute to frontalis atrophy and brow ptosis, but their relative impacts remain unclear. This study used large-scale computational modelling to compare long-term structural and functional changes in the frontalis muscle under different BoNTA exposure patterns and across age groups.

Methods

A 20-year in silico longitudinal simulation of 20,000 virtual subjects was conducted using the AesthetiSIM™ biomechanical platform. Subjects were stratified by baseline age (20–30, 31–40, 41–50 years) and randomized to four treatment arms: Control (no BoNTA), Low-Frequency BoNTA (20 U every 6 months), High-Frequency BoNTA (20 U every 4 months), or Focal Overuse (high-frequency for 10 years then cessation). Primary outcomes included frontalis muscle volume, static brow position, dynamic lift capacity, ptosis incidence, and surgical-threshold brow descent. Analyses employed mixed-effects models, ANOVA, Cox regression, and sensitivity testing.

Results

At 20 years, mean muscle volume loss was greatest in Controls (61.2%) and least in Low-Frequency BoNTA (38.3%), though reduced loss in BoNTA groups reflected early chemodenervation rather than muscle preservation. Brow descent was highest in Controls (4.1 mm) and lowest in Low-Frequency BoNTA (2.3 mm). Ptosis incidence reached 58.3% in Controls versus 20.9% in Low-Frequency BoNTA. Younger age at onset correlated with greater atrophy and earlier ptosis in all groups except Low-Frequency BoNTA. Supplemental modelling confirmed that smaller descent in BoNTA groups was attributable to functional suppression, not protective effects.

Conclusions

Both aging and BoNTA cause progressive frontalis atrophy and brow descent. Frequent, early BoNTA use accelerates functional decline, with incomplete recovery after discontinuation. Conservative, low-frequency dosing better preserves muscle volume and brow position, particularly in younger patients. Long-term clinical imaging studies are warranted to validate these findings.

Level of Evidence: Not gradable.