## 1 Introduction  
The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) defines tics as sudden, rapid, recurrent, nonrhythmic motor movements or vocalizations. They can be classified as either simple or complex, based upon their duration, ranging from short (i.e., milli-seconds) to long (i.e., seconds). A diagnosis of tic disorder (TD) is made when a subject under the age of 18 shows motor and/or vocal tics for a specific period of time, which are not attributable to another medical condition or substance use [1]. TDs are highly prevalent in the developmental age population, although prevalence estimates vary widely (0.03-5.26%) [2]. Current studies indicate that the prevalence of TDs in children and adolescents ranges between 0.3-0.9% [2, 3]. There are three main diagnostic categories of TD: Tourette's Disorder (or Tourette's Syndrome, TS), persistent (chronic) motor or vocal tic disorder (CTD), and provisional tic disorder (PTD). These categories are hierarchical, with variations in the presence and duration of motor and/or vocal tics. TS requires both motor and vocal tics, CTD requires only one type, while PTD may include either or both types of tics, differing primarily in duration. TS and CTD symptoms must occur for at least one year,whereas PTD symptoms last less than one year [1]. The worldwide prevalence of these three diagnostic categories of TD indicates that PTD is the most common with a prevalence of 2.99%, followed by CTD and TS with prevalence of 1.61% and 0.77%, respectively [4]. Given the neurodevelopmental nature of TDs, which therefore must be diagnosed before age 18, and their high prevalence in children and adolescents, this systematic review focuses on the group aged < 18 years. Understanding the etiopathogenesis of TDs provides crucial insights into their development and progression. A key factor in the pathophysiology of TDs is the dysfunction of the cortico-striatal-thalamus-cortical circuit, which involves motor, sensory, and limbic regions. A critical aspect involves the dysregulation of dopaminergic pathways, where presynaptic regulatory abnormalities, combined with phasic dysfunctions in dopaminergic transmission, seems to disrupt normal motor control. Furthermore, the serotonergic system has been repeatedly reported to be impaired, adding complexity to the neuro-chemical profile. Even though genetic studies highlight the strong hereditary nature of these disorders, the onset seems to be ultimately driven by a complex interplay between genetic predispositions and environmental factors that shapes their development and progression [5]. Moreover, tics often improve over time, with a significant reduction in adolescence continuing into adulthood, when the intensity and frequency of tics may decrease to the extent that they no longer cause impairment [6]. Although tics often resolve spontaneously over time without treatment, some individuals need interventions to reduce difficulties in social, emotional, and behavioral functioning [7]. Given the severity of tic-related impairments and their long-term implications, having a thorough understanding of the best treatment options for TDs in developmental age is highly relevant and clinically important. Historically, pharmacological interventions, including traditional and atypical antipsychotics, analgesics, and anticonvulsants, have been considered the first-line treatment for TS symptoms [8; 9]. However, long-term medication use can lead to adverse side effects and treatment discontinuation, suggesting that pharmacological treatments may not provide satisfactory outcome for all, or complete relief of symptoms [8]. Nonpharmacation treatments, therefore, emerged as viable alternative or adjunct to the pharmacological ones [7], reducing concerns associated with side effects of drug use [10].