## 1 Introduction  
The term Plagiocephaly is Greek (plagios = obliqua, kefale' = head) and stands for all alterations in the shape of the head, which can originate from multiple causes [1]. Plagiocephaly predominantly affects the infant [2]. Two forms of plagiocephaly can be distinguished: that due to premature fusion of cranial sutures (synostotic plagiocephaly) and that generated by external pressures affecting the pre- and postnatal growth orientation of the skull (deformational and/or positional plagiocephaly) [1; 3; 4; 5]. Pediatrics are obligated to examine children with plagiocephaly, which can never be surpassed by impulsive and erroneous assumptions or therapy [6]. Prompt clinical experience is the cornerstone of cranial deformity treatment. In syndromic associations and skeletal dysplasia textbooks and articles, many syndromic entities fulfill the search criteria [7]. Characteristics of plagiocephaly, in addition to non-instantaneous and perplexing versions of sclerosing diseases of the skeleton, craniotubular abnormalities include a lengthy list [8; 9; 10]. The order of precedence management should consist of the following: pediatricians and doctors must first conduct a thorough examination of the youngster, which should involve the parents; clinical observations are required regardless of severity for any uncommon craniofacial/musculoskeletal anomalies; secondly, they must conduct a clinical evaluation of the siblings and information collection for the remainder of the family; thirdly, doctors must rule out every kind of aberrant craniofacial shape and their causes and related syndromic connections [11]. Positional Plagiocephaly (PP) also can involve one or both sides of the occupit [12; 13; 14; 15] (Figure 1). Cranial sutures are classified as synarthrosis, a fixed joint type that allows no movement [16]. In the fetal skull, these sutures are non-rigid and permit some mobility during birth [17]. At birth, the skull's bones can overlap, a process known as _molding_. Physiologically, the skull adapts to the progressive development of the brain, increasing in volume during the infant's growth [18]. PP does not cause abnormal brain development or neuropsychological problems [19; 20; 21]. The infant's plastic, malleable skull can have intentional, pathological, or parabysiological deformities [22]. The latter occurrence usually happens during delivery, at the passage of the vaginal canal, and is usually reversible with the recovery of shape after a few weeks of life [23]. Neonatal PP occurs in those infants who show a preferential side of head support in the first few months of life [24; 25]. Male sex, twin pregnancies, preterm deliveries, use of forceps in assisted delivery, and torticollis are thought to be risk factors [26; 27; 28]. Figure 1: The pathogenic mechanism of skull deformation. Once posterior flattening has occurred, spontaneous correction of the skull does not occur because the external pressure of the bearing surface acts more incisively and continuously on the flattened part, despite the later, more frequent change in the position of the child's head [13; 29; 30]. Since 1992, when the American Academy of Pediatrics declared the prone position responsible for sudden infant deaths and recommended a supine position (Back to Sleep campaign), the percentage of PP and DB has increased from 0.3% to 48% [31; 32]. Interventions by pediatric plastic surgeons and neurosurgeons in the treatment of PP have markedly increased, because parents are concerned about the consequences of PP on the child's appearance, development, and future relationships [32; 33; 34; 35]. The functional consequences of plagioclase are postural and musculoskeletal disorders, sensory disorders, and impact on neurological development [36]. Therapy, which involves different protocols, depends on the level of asymmetry, estimated according to Argenta's classification [37; 38; 39]. Argenta's classification recognizes five levels of PP severity (Figure 2) [40]. 1.