## 1 Introduction  
Myopia is a refractive error of the eye in which images of distant objects come into focus in front of the retina in the absence of accommodation. This condition prevents the patient from seeing clearly at a distance. Myopia is progressive and can reach an advanced stage associated with a significant risk of ocular pathology [1]. For this reason, special attention has been paid in recent years to the optimization of myopia correction methods in order to adapt them and better control refractive evolution over time. It has been shown that the quality of the optical signal reaching the retina determines the eye's response to it [2]. Thus, the retina can interpret two types of defocus, either hyperopic or myopic [3]. In both cases, specific biomodulators and growth factors are released, leading to scleral remodeling [4, 5]. With prolonged exposure to hyperopic defocus, the sclera becomes softer and the eye tends to elongate, whereas myopic defocus results in greater scleral rigidity and thus resistance to axial length (AL) elongation [5, 6]. Accommodation and intraocular pressure are other factors that may modulate this response [7]. Based on the theory of the emmetropization cascade [7], which has been well studied in animal models, changes in axial length have been described as a dose-dependent response to peripheral myopic defocus [8]. In humans, [9] peripheral refraction after orthokeratology (OK) was measured, and its optical effects were shown to produce the aforementioned peripheral myopic defocus. In particular, the effectiveness of OK in controlling myopic progression appears to be related to the induction of high-order aberrations (HOAs) in the visual system after lens wear. The increase in HOAs results from topographic changes in the cornea from a prolate to an oblate shape. In particular, the effect on ocular growth may be related to the number of spherical aberrations generated by the reshaping of the corneal surface [10]. Specifically, positive spherical aberrations and coma increase progressively during the first week of overnight lens wear [11], but the induced changes may take up to 3 months to stabilize [12]. In addition, the stability of the peripheral refraction induced by OK lens wear was measured over time, and the authors showed that the amount of myopic defocus measured in the first week remained stable over the first year of wear [13]. As reported in a previous article [14], several strategies to increase myopic defocus and related HOAs can be applied and are considered effective, even more so when they are fully customized, taking into account individual and refractive factors that allow for optimization of therapeutic approaches. According to the \"Montreal Experience strategy\" [14], the type of treatment is selected according to an algorithm based on the specific characteristics of each participant. In this retrospective study, the treatment options were orthokeratology, multifocal soft contact lenses (MSCLs), and low-dose atropine. In general, for low myopia (<-2.50 D) and/or small pupil size (photopic diameter < 4.5 mm as measured with an infrared pupillometer), MSCLs were preferred. For higher myopes (\(\geq\)\(-\)2.50 D) and/or those with larger pupils (>4.5 mm), OK lenses were usually recommended. Different types of MSCLs or OK lenses were used depending on their availability at the time of dispensing or the personal preference of the practitioner. Low-dose atropine was used as an adjunct therapy if AL reached or exceeded 26 mm at adulthood based on Tideman's or San Diez growth charts. The final choice of treatment methods was made after discussion with the parents and patients. All methods used were effective in slowing AL growth and keeping AL progression below the expected progression within a myopic child population.